• Loyola University Chicago, USA
  • Title:The Motor Image in Self Integration: Bridging Postural Dynamics to Egocentric Coding
  • Time :

Abstract:

Neural integration is a key mechanism for life related, clinical diagnoses, which is likely to be disrupted in serious cognitive diseases like schizophrenia. Among its singular determinants are behavioral influences that plastically shape integration through motor plans and executed movements, and which also fundamentally contribute to cognition. A key requirement of the motor plan is that of framing motions in the context of an agent, where the body is appropriated as an origin of action emergence. Embodied, motor actions propel the consumption of free energy reserves needed to sustain organismal operation in its entirety thereby driving global integration. Free energy influences, however, track energy use homeostatically and are motivationally agnostic with respect to goal selection. On the other hand, existing evidence indicates that the motor plan is teleologically oriented and that motor behaviors are structured uniquely in the context of specific goals. Current work is beginning to disentangle representational content that is globally attuned to the whole individual from that for discrete movements. These studies suggest that representations of body posture are likely to be an important proxy for global self-representation in dynamic actions and may be directly modified by goal specific content. Candidate influences for goal related modulation is likely to include egocentric coding in the posterior parietal and premotor cortices that shape self representations to yield goal directed motor movement. The physical instantiation of such strategies likely reflects a metaphysical need for increasing behavioral range that can be autonomously accessed, and positively informs psychiatric etiologies and existential psychology.

Biography:

Dr. Denis Larrivee is a Visiting Scholar at the Mind and Brain Institute, University of Navarra Medical School and Loyola University Chicago and has held professorships at the Weill Cornell University Medical College, NYC, and Purdue University, Indiana. A former fellow at Yale University’s Medical School he received the Association for Research in Vision and Ophthalmology’s first place award for studies on photoreceptor degenerative and developmental mechanisms. He is the editor of a recently released text on Brain Computer Interfacing with InTech Publishing and an editorial board member of the journals Annals of Neurology and Neurological Sciences (USA) and EC Neurology (UK). An International Neuroethics Society Expert he is the author of more than 80 papers and book chapters in such varied journals/venues as Neurology and Neurological Sciences (USA), Journal of Neuroscience, Journal of Religion and Mental Health, and IEEE Explore. In 2018 he was a finalist in the international Joseph Ratzinger Expanded Reason award. He is an international keynote speaker, frequently appearing at Neurology and Psychiatric Disease forums.

  • Jordan University of Science and Technology, Jordan
  • Title:Loss of Binocular Vision as Direct Cause for Misrouting of Temporal Retinal Fibers in Albinism
  • Time :

Abstract:
In humans, the nasal retina projects to the contralateral hemisphere, whereas the temporal retina projects ipsilaterally. The nasotemporal line that divides the retina into crossed and uncrossed parts coincides with the vertical meridian through the fovea. This normal projection of the retina is severely altered in albinism, in which the nasotemporal line shifted into the temporal retina with temporal retinal fibers cross the midline at the optic chiasm. This study proposes the loss of binocular vision as direct cause for misrouting of temporal retinal fibers and shifting of the nasotemporal line temporally in albinism. It is supported by many observations that clearly indicate that loss of binocular vision causes uncrossed retinal fibers to cross the midline.
This hypothesis may alert scientists and clinicians to find ways to prevent or minimize the loss of binocular vision that may occur in some diseases such as albinism and early squint. Hopefully, this will minimize the misrouting of temporal fibers and improve vision in such diseases.

  • McMaster University, Canada
  • Title:Pathogenesis of Neurotrauma in the Model of Spinal Cord Injury with Future Directions of Neuroprotective Therapies
  • Time :

Abstract

Spinal cord injury (SCI), traumatic brain injury (TBI) and stroke constitute the most important human diseases with no effective treatments which is related to the lack of understanding of the pathogenesis of the disease initiated by the traumatic (SCI, TBI) or by vascular (stroke) events. In the rat model of SCI studied systematically, 3 supervening phases are evident; (1) Acute Phase, lasts 2 days and is characterized by hemorrhage, poorly defined areas of cellular necrosis and edema; (2) Inflammatory Phase, begins on the day 3 with infiltration of the areas of hemorrhage and necrosis by large numbers of M1 type macrophages phagocytizing myelin and red blood cells. Depending on the location of the hemorrhagic necrosis in the injured spinal cord, there are 2 types of inflammation; (i) areas deep in the spinal cord are converted within the 1st week into a cavity of injury (COI) encompassing necrotic debris and fluid infiltrated by M1 macrophages; (ii) in superficial areas granulomatous infiltration from the subarachnoid space including macrophages, fibroblasts and blood vessels form arachnoiditis obliterating the spinal cord. Both COI and arachnoiditis are walled off by progressively severe astrogliosis mounted by the surrounding spinal cord. The severity of M1 macrophage infiltration in the COI peaks at 1-4 weeks and then slowly declines but small numbers are still present at 16 weeks post-SCI. (3) Resolution Phase overlaps with Inflammatory Phase by 12 weeks and leads to formation of mature syrinx from the COI. Arachnoiditis becomes a mature scar devoid of glial cells and macrophages. The unusual severity and extraordinarily long course of inflammation initiated by trauma in the spinal cord is related to locally massive damage to myelin sheaths, a potently immunogenic material. Its phagocytosis by M1 macrophages is associated with their activation and presence of elevated factors of inflammation such as TNF-, IL-1, IFN-, Il-6, chemokines, MMP-8, within the 1st week and their decline in levels later. The lack of M1 to M2 macrophage polarization in COI with concurrent decline in numbers of M1 macrophages during the Resolution Phase suggests that classic immune mechanisms do not play role in inhibition of severity of inflammation but rather the spinal cord tissue reaction, specifically astrogliosis does. This is supported by previous observations on the SCI in the Long Evans Shaker (LES) rat where inflammation is entirely eliminated by 7 days post-trauma. The severity of inflammation in COI with active myelin phagocytosis by M1 macrophages beyond 16 weeks indicates continuous destruction of the surrounding spinal cord and calls for anti-inflammatory treatments to provide neuroprotection beyond trauma. Since the spinal cord reaction confines the inflammation to the COI which is directly connected to the subarachnoid space, infusion of anti-inflammatory drugs; dexamethasone, Serp-1 and M-T7, immunomodulatory proteins derived from Myxoma virus, into the subdural space resulted in reduction of the numbers of macrophages by 50-80%. While dexamethasone was effective in lowering the numbers of macrophages, it was unduly toxic but both Serp-1 and M-T7 were well tolerated by recipient rats. However, when infused intraperitoneally, both proteins had little (M-T7) or no detectable (Serp-1) effect on the levels of infiltrating macrophages in the COI indicating that constant subdural infusion is an effective mode of administration and intravenous administration is not. Importantly, 1 week long infusion reducing numbers of macrophages resulted in persistence of large amounts of un-phagocytized, myelin-rich necrotic debris and numerous red blood cells that would lead to re-igniting of the severe inflammation at the premature termination of anti-inflammatory treatment. Therefore, a much longer than 1 week, subdural infusion needs to be administered to eliminate inflammation and its destructive activity following SCI and also TBI and stroke involving white matter injury.

Biography

Education: DVM (Doctor of Veterinary Medicine); 1983, University of Agriculture in Lublin, Poland
MSc; 1991, University of Guelph, Canada. Veterinary Pathology.
PhD; 1995, University of Guelph, Canada. Veterinary Pathology.
Post-Doc.; 1994-1996, University of Wisconsin-Madison, USA, Fellow National Multiple Sclerosis Society, USA. Neuroscience.
Current Status: Associate Professor, Department of Pathology and Molecular Medicine, McMaster University, Canada.
Veterinary Research Pathologists, McMaster University.
Research Interests: Pathogenesis of neurotrauma
Animal models of spinal cord injury and of traumatic brain injury
Neuroprotective treatments in neurotrauma
Mechanisms involved in neuroregeneration.

  • Amrita Vishwa Vidyapeetham University, India
  • Title:Application of Ayurveda in Acute stroke patients
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Abstract

On observation some stroke patients report improvements after Ayurvedic massage, while others did not. There is a little indexed literature to support the use of this in rehabilitation. The aim was to objectively measure the differences between patients with stroke who received Ayurvedic massage in addition to standard Physiotherapy (PT) versus those who received only standard PT. Designed as a prospective case control study, this was done in a tertiary level hospital Neuro-rehabilitation unit.
Participants- Fifty-two patients undergoing acute inpatient rehabilitation were prospectively followed post stroke. They self selected one month from the event into Ayurvedic Massage with regular PT or PT alone. Twenty five received Ayurvedic massage with PT and twenty seven received only PT. All participants completed treatment.
Duration- 2014-2017
Intervention- Age, gender, National Institute of Health Stroke Scale result, number of co-morbidities, and whether cases were deemed simple or complex were taken at baseline. All patients received 6 hours of physical therapy averaged over a week. Massage was delivered daily for a total of 10 sessions followed by steam application.
Main Outcome Measurements:- Brunnstrom Leg progression, spasticity using the Modified Ashworth Scale (MAS), time to achieve stand with minimal assistance, Functional Independence Measure (FIM) score for walking at discharge, use of antispastic drugs at discharge were followed. Patients were categorized as simple or complicated stroke based on events prior to rehabilitation. Both simple and complicated patients who received Ayurvedic massage had lower MAS and need for antispastic drugs, achieved standing with minimal assistance sooner, and had better locomotion at discharge. All these differences were significant.
Conclusion- Utilizing Ayurvedic massage in post stroke patients with flaccidity can promote faster standing with minimal assistance and lead to less need for antispastic drugs at discharge.

Biography

Ravi Sankaran MD is an Associate Professor in the Department of Physical Medicine and Rehabilitation. His areas of expertise lie in: adult and pediatric spasticity, disorders of consciousness, and peripheral nerve injury/ hand transplant rehabilitation. He trained in spasticity interventions in Tokyo, and has a primary hyperbaric medical certification from Palmetto South Carolina in the USA. He has publications and book chapters in the same areas.

  • Medical University of Varna, Bulgaria
  • Title:In Vitro Model of Ischemic Stroke: Ghrelin and Potential Intracellular Factors Preventing the Secondary Brain Damage and Ameliorating Postischemic Recovery
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Abstract

Normal brain function is highly dependent on oxygen supply, and one of the first consequences of ischemia is change in the neural network: acute episodes of hypoxia result in decreased synaptic activity, while the longer periods of oxygen deprive cause neuronal dead. Ischemic stroke, which usually results from cerebral arteries occlusion, leads to neuronal dead in the infarction core. Stroke is the second leading cause of dead above age of 60 years. Annually, 15 million people worldwide suffer a stroke, nearly six million die, and another five million get permanently disabled. Unfortunately, effective specific therapy for the ischemic brain damage is lacking. However, many patients improve in different period of time following stroke, inferring an innate capacity for brain repair. The exact mechanisms of this recovery are not clear but they may include synaptogenesis and adult neurogenesis. To test this hypothesis we used dissociated cortical neurons as a model system to study the general synaptic damage caused by temporary severe hypoxia and the possibility to restrict it by ghrelin (Ghr) treatment. Briefly, cultures were exposed to hypoxia for 6 h (pO2 lowered from 150 to 20 mm Hg). Three hours after the re-oxygenation, half of the cultures were treated with Ghr for 24 h, while the other, non-supplemented, were used as a control. All cultures were stained immunocytochemically for detection of the synaptic marker synaptophysin. Hypoxia led to drastic decline of the number and the activity of synapses, followed by partial recovery after return to normoxia, but still below the pre-hypoxic level. Ghr treatment significantly increased synapse density and activity, as compared with the controls or with the pre-hypoxic period. In addition, we investigated the effect of Ghr on the expression of some intrinsic cellular factors important for the regulation of neurogenesis – Pax6 and Zbtb20. Hypoxia reduced the percentage of cells expressing Pax6 and Zbtb20, but Ghr administration during re-oxygenation considerably upregulated their expression. Furthermore, significant number of Pax6-positive cells had features consistent with neuroepithelial/progenitor cells phenotype, which we normally do not observe in mature cultures under normoxic conditions. In conclusion, Ghr stimulates neuronal network connectivity and activity after hypoxia exposure, and activates some endogenous factors promoting neurogenesis in mature neuronal networks in vitro. Though the functional impact of postischemic neurogenesis is yet unknown, it might be a prospective therapeutic target for stroke patients.

Biography

Irina I. Stoyanova–van der Laan graduated in General Medicine at the Medical Academy, Sofia, Bulgaria and specialized at human anatomy and histology. In 1983 she was appointed as an Assistant Professor and later on, in 2004, as an Associate Professor at the Department of Anatomy, Trakia University, Bulgaria. She obtained her PhD in 2002 (thesis “Morphological and neurochemical characteristics of certain primary sensory neurons”). In 2008-2015 she worked as a postdoc at the department of Biomedical Signals and Systems, and the department of Clinical Neurophysiology, University of Twente, the Netherlands. In 2011 she was appointed as an Associate Professor in Human Anatomy and Physiology at the University College Roosevelt, the Netherlands. Since 2015 she is an Associate Professor at the department of Anatomy and cell biology, Medical University, Varna, Bulgaria.
Research interests – Neurosciences: different aspects of the structural and functional neuromorphology and their clinical implications. For her achievements she was awarded twice (at International Falk Foundation Symposium of Gastroenterology in Bucharest, Romania, 2000, and at 7th International Symposium on Cytokines and Chemokines (satellite of the 13th World Congress of Gastroenterology), Montreal, Canada, 2005). She is also a member of the editorial boards of two international journals – International Journal of Biomedical Sciences (since 2005), Adipobiology (since 2009), and a reviewer for other scientific journals.

  • Federico II University of Naples, Italy
  • Title:Amyloid Precursor Protein Tyr682 Phosphorylation is Mediated by Fyn Tyrosine Kinase and Triggers Amyloidogenesis in Neurons
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Abstract

Alzheimer’s disease (AD) is a progressively deteriorating cognitive and functional neurodegenerative disorder frequently associated with cerebral cortical atrophy, beta-amyloid plaque formation, and intraneuronal neurofibrillary tangles. Appropriate diagnostic criteria in the very early stages of the pathology is imperative thereby excluding non-AD dementias patients who cannot benefit from an AD-specific treatment and frequently make puzzling the interpretation of clinical trial results. We are interested on the potential role of APP Tyr682 residue as biomarker for AD. We previously reported that the aberrant phosphorylation of APP Tyr682 residue leads to Aβ production and neuronal degeneration. Fyn Tyrosine Kinase (TK) interacts with APP Tyr682 residue in neurons from AD patients and in AD modelling minipigs and the exposure to Fyn TK inhibitors protect AD neurons from Aβ accumulation, autophagic deficits, and neurodegeneration. Here we show that in neurons and fibroblasts from AD patients, APP Tyr phosphorylation levels are increased when compared to the heathy volunteers. We demonstrate that Fyn selectively triggers APP Tyr682 phosphorylation in neurons thus increasing APP processing to generate Aβ and APP intracellular peptides. Additionally, we provide evidence that Fe65, a previously characterized APP adaptor, is crucial in this Fyn mediated APP Tyr682 phosphorylation process. Finally, AD neurons in which Tyr phosphorylation levels are increased when exposed to Fyn tyrosine kinase inhibitors (TKI), show decreased Aβ production, whereas the same decrease is not obvious in AD neurons in which Tyr phosphorylation levels are not increased. All together these findings support previous evidence on APP Tyr682 as potential biomarker in AD and open to the new fascinating perspectives of targeting Tyr682 residue for the development of either new diagnostic or personalized therapeutic management of AD patients.

Biography

Dr Matrone Carmela obtained her PhD in the field of Biomedical sciences at the Medical faculty University Federico II of Naples where she is currently employed as associate professor in Pharmacology and where she has established her independent group, working on Alzheimer’s disease and related diseases. She was trained as post doc at European Brain Research Institute in Rome working in the prof RL Montalcini lab (Nobel prize for NGF discovery in 1986). In 2012, she moved to the University of Health in Aarhus, Dept of Biomedicine, (DK) where she became associate professor in pharmacology in 2014 and where she is currently a guest lecturer. She is involved in extensive international collaborations with eminent scientists and she is member of several associations in the Neuroscience field. She has authored more than 50 scholarly
publications (journal articles, monographs, book chapters, and copyrighted assessment instruments). She has made approximately 50 research and professional presentations at international, national, regional conferences as speaker, moderator, as well as an organizer. She is an experienced peer reviewer for international scientific journals and as well as for international granting agencies in the Alzheimer’s disease field.

  • Medical University of Innsbruck, Austria
  • Title:Modifiable Risk-Factors in the Course of Alzheimer´s Disease
  • Time :

Abstract

Over the last few years, the concept of dementia Alzheimer’s type (DAT) has changed significantly.
There is increasing evidence that pathophysiologic changes already begin decades before cognitive symptoms qualifying for dementia or even mild cognitive impairment (MCI).The long ‘preclinical’ phase in the course of Alzheimer’s disease (AD) provide the opportunity for preventive interventions to reduce the risk for conversion to dementia or rather slow disease progression.1.Currently, there are no validated and generally accepted psychopharmacological nor non-pharmacological strategies to prevent patients with MCI from converting to AD. However, there is increasing evidence that the risk for conversion from MCI to AD could be reduced by modifying life style and consequent treatment of especially the metabolic syndrome. Further, depressive symptoms in old age are frequently associated with cognitive impairment and have been reported as an important risk factor for an early manifestation of dementia.2 Moreover the role of long-term use of benzodiazepines have been discussed to possible increase AD-risk. However, currently we have no approved prevention strategies for AD. Nonetheless, experts of all medical disciplines should be actively encouraged to screen for signs of cognitive impairment and to assessment known modifiable risk-factors for AD in clinical routine to lay the foundation for a successful dementia prevention in the future.

Biography

Michaela Defrancesco has completed her university education in medicine and PhD in neuroscience in 2013 at the Innsbruck Medical University and finished her psychiatric residency in 2015. She is the head of the memory clinic of the psychiatric department of the University Clinic of Innsbruck. Her scientific work focuses on early signs and predictors of conversion from Mild cognitive impairment to Alzheimer´s disease.

  • University of Haifa, Israel
  • Title:Understanding the Variability of Vulvar Pain Manifestation: The Manifestation of Neuropathic Pain Symptoms in Provoked Vestibulodynia
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Abstract

Provoked vestibulodynia (PVD), is the common chronic pain syndrome characterized by severe pain and tenderness on vestibular touch or attempted vaginal entry during sexual intercourse (dyspareunia). The incidence of PVD is estimated as 12%-16%, but the actual incidence is presumably higher than reported. The etiology of PVD is considered multifactorial, however, no single causative factor has yet been identified. Current efforts to subdivide PVD into sub-groups had led to the allocation of patients into primary and secondary forms of PVD, describing the onset of symptoms in regards to timing of first provoking physical contact. The comparison between these two types demonstrates pain-related personality features, mainly higher anxiety, among primary PVD patients as well as greater neural hypertrophy in the vestibular tissue as compared to those with secondary PVD. However, this distinction does not address mechanism-based etiology and consequently fails to establish diagnostic and treatment guidelines. Despite that the possible role of neuropathic alterations has been suggested, the precise mechanisms of such idiopathic pain disorder is still insufficiently clear. Treatments focus mainly on the pain and its effect on sexual functioning, but wide disparity in treatments efficacy is reported among PVD patients.
This presentation will focus on the notion that several distinctive sub-groups of PVD exists, such that the anatomic location of provoked vestibular pain hypersensitivity and it’s associated with specific features represent different etiological mechanisms in PVD. Data abstained from large sample of PVD patients will be presented to address whether in part of the women, vestibular pain location (circumferential or posterior vestibule alone) and the existence of vulvar allodynia/hyperalgesia and/or general pain-hypersensitivity represent neuropathic changes. Pain response to experimental stimulation (Q-tip and pressure stimuli) and self-reported pain measures (tampon insertion and penetrative intercourse) will serve to reveal whether vestibular neuroproliferation result painful intercourse. The possibility that congenital or acquired neuronal sensory alteration will be discussed form embryologically perspective in which the endodermal neuroproliferation associated with local and systemic pain sensitivity. This presentation will also highlight whether psychosocial features, sexual functioning and cognitive factors such as pain catastrophizing involved in the manifestation of vulvar pain experience. Identifying sub-groups of PVD based on the mucosal and neuropathic changes may allow better understanding about pain variability in women who suffer from chronic pelvic pain and promote individualized management.

Biography

Michal Granot, RN, PhD, is an associate professor at the Faculty of Social Welfare & Health Sciences, Department of Nursing, the University of Haifa, Israel. Her clinical background has shaped her research activity that focuses mainly on psychophysical assessment of pain modulation processing. As part of a multi-disciplinary team at the Laboratory of Clinical neurophysiology at the Technion and Rambam Medical Campus she investigates psychological, neurophysiological and cognitive features that affect pain perception and modulation in acute and chronic pain conditions, with special emphasis on pain disorders among women, such as chronic pelvic pain. Prof. Granot has been a co-Principal investigator in several research projects that focused on pain variability and the mechanisms that are involved in the transition from acute to chronic pain, using lab tests of pain induced by experimental stimulations combined with pain related personality questionnaires.

  • The Scripps Research Institute and Protego Biopharma, USA
  • Title:Treating Protein Aggregation Diseases in the Central and Peripheral Nervous Systems: Success and Failure in Familial Amyloidotic Polyneuropathy and Alzheimer’s disease
  • Time :

Abstract

It was clear almost from the first descriptions in Portugal that the hereditary autonomic and peripheral neuropathy endemic in Povoa de Vazim was due to amyloid deposits in peripheral and autonomic nerves. It remained only for the precursor to be identified as transthyretin (TTR) and the mutation characterized. We now know that there are 123 different mutations in the coding region of the protein that are associated with autosomal dominant neuropathic and/or cardiomyopathic syndromes and that without aggregation there is no clinical disease. Over the last two decades therapies directed at reducing or eliminating amyloid formation by reducing the availability of the TTR aggregation substrate have been introduced into clinical practice. Hence liver transplantation, small molecule molecular stabilizers of TTR and oligonucleotide therapies have reduced symptoms and prolonged life for the carriers of the mutations, a major advance in neurologic patient care. Nonetheless, cure has not been achieved and a significant proportion of the patients do not respond to the available therapies, representing a still unmet medical need.
The role of amyloid deposits in the pathogenesis of Alzheimer’s disease, from the very beginning, was far more contentious with the uncertain role of amyloid articulated initially by Hardy and Higgins and then by Hardy and Selkoe in the titles of their seminal papers e.g. “Alzheimer’s disease: the amyloid cascade hypothesis”. The generation of mice transgenic for mutant forms of the Aβ precursor or the mutant enzymes involved in processing AβPP in the autosomal forms of the human disease allowed the development of therapeutics based on blocking the generation of the amyloid precursor or the aggregation of the amyloidogenic peptide. Enzyme inhibitors tested in these models, as well as antibodies directed against the peptide, its oligomers or fibrils, moved from blocking the pathologic changes seen in the transgenic mouse brains to large scale clinical trials. In contrast with the findings in TTR-associated FAP, the results have been disappointing. We now await the results of trials using secretase inhibitors and/or antibodies in subjects who are carriers of genes that produce autosomal dominant AD administered well before the onset of disease, as judged by the age of onset characteristic of their kindred. The results of such trials will provide the final test of the Aβ hypothesis.

Biography

Professor Buxbaum’s laboratory at NYU School of Medicine identified TTR mutations responsible for both autosomal dominant polyneuropathic and cardiomyopathic forms of amyloidosis and developed transgenic mouse models of systemic TTR deposition. At The Scripps Research Institute he continued his extensive clinical and genetic characterization of the cardiomyopathic TTR mutation that is highly prevalent in African Americans. He served as consultant to Foldrx during its development of tafamidis (Vyndaqel, Pfizer). More recently his group has studied the interaction between TTR and Aβ, finding that neuronal production of TTR may have a salutary rather than an adverse effect on the development of Aβ deposits in the brains of both Aβ transgenic mice and humans with AD.

  • University of Virginia Health System, USA
  • Title:Success Stories Using Emergency Telestroke Services
  • Time :

Abstract

The ability to rapidly access and evaluate acute stroke patients is crucial to ensure a good clinical outcome. Time sensitive therapies, including intravenous thrombolytics (tissue plasminogen activator) and thrombectomy endovascular techniques in selected patients can improve outcome by ~30-70% versus no treatment. Telestroke, the use of live remote videoconferencing by a neurologist to distance emergency departments has allowed greater access and expertise in decision making to render these treatment options. In addition, it allows for higher accuracy in patient selection for treatment, ensuring the right treatment is provided at the right time in the right patient.
We will discuss the current state of Telestroke (international) programs, highlighting the successes, and elucidating the remaining barriers and future growth needs in the field. Clinical cases will be presented to illustrate the new neuroimaging techniques in the field (“RAPID” software brain mapping), and endovascular technical advances (stent-retrievers). Emerging acute stroke therapies, including new thrombolytics being tested, will be discussed. Patient clinical outcomes will be explored in terms of financial, humanistic and societal savings.

Biography

Nina J. Solenski, M.D., FAHA is an internationally recognized vascular neurologist with over 25 years of cerebrovascular clinical and research experience. She completed her medical training at Jefferson Medical College, Philadelphia, PA, and medical and neurology residency training at Dartmouth University, NH and at the University of Virginia (UVA), VA. She completed her Cerebrovascular Fellowship training at the University of Virginia, and was awarded a NIH K08 stroke research grant. Dr. Solenski is ABPN board certified in General Neurology and Vascular Neurology. She has been practicing since 1993, specializing in development of telestroke and teleneurology programs, stroke in the young patient, and supporting first generation college students interested in the medical field. She has been involved in over 60 clinical stroke research trials over the years. Current projects include developing a national stroke system of care in the Dominican Republic, implementing a state-wide “ECHO” Stroke program to educate primary care physicians on primary and secondary care of stroke patients. She recently was selected for the prestigious American Academy of Neurology “Women in Neurology Leadership” and has served both as the Chair of the UVA Faculty Senate and as faculty representative on the University of Virginia’s corporate Board of Visitors.

  • University of South Carolina School of Medicine, USA
  • Title:Early Effect of HIV on Cerebral Blood Flow, Autoregulation and Neurocognitive Function
  • Time :

Abstract

Human immunodeficiency virus (HIV)-infection is associated with HIV associated neurocognitive disorders (HAND) as well as a risk for ischemic stroke. We measured cerebral blood flow (CBF), oxygen extraction fraction (OEF) and autoregulation in HIV infected subjects and controls. In HIV subjects, we tested for HAND. In treatment-naive HIV infected subjects and age-, gender-, and race-matched controls, OEF was measured by using MRI T2*-weighted echo-planar imaging sequences and CBF was measured by MRI pulsed arterial spin labeling (PASL) approach. Static cerebral autoregulation tested by ~10% MAP lowering. Cerebral autoregulation was measured globally and regionally in gray matter (GM), white matter (WM) and subcortical GM. Autoregulatory Index (AI) was computed using the equation AI = %CBF change/% MAP change supplemented by CBF associated OEF changes. Fifteen neuropsychological tests were administered at baseline in treatment naïve subjects and after 12 months on treatment, for HAND categorization. Correlation between HAND and AI tested at baseline. Forty-one treatment naïve HIV-infected subjects and 47 age-, gender-, race-matched controls participated. HIV-infected subjects had higher CBF in cortical GM compared to the controls (76.8± 12 mL/100 g/min versus 71.6 ± 11 mL/100 g/min; P = .04) but not in white matter (30.9± 8 mL/100 g/min versus 30.0 ± 8 mL/100 g/min; P = .60) subcortical GM (62.8± 13 mL/100 g/min versus 61.3 ± 13 mL/100 g/min; P = .57). Whole brain (WB), GM, WM or subcortical GM, OEF were similar between the groups (p > .05). The median AI were similar between cases and controls in WB (0.40 vs 0.18, p=0.86), GM (0.10 vs. 0.16, p=0.87), WM (0.80 vs. 0.87, p=0.31), and subcortical GM (1.65 vs. 1.77, p=0.26). A 12-month follow-up (N=30) in HIV-subjects on antiretroviral therapy did not produce a significant change in CBF or OEF in the WB, GM, WM or subcortical GM (Paired sample t test p>0.05). Similarly, no changes were noted on the AI (Wilcoxon Match Rank test p>0.05). In a group with low pre-,morbid functioning, HAND diagnosis was found in 83%, with further categorization demonstrating 22% with Asymptomatic Neurocognitive Impairment (ANI), 44% with Mild Neurocognitive Disorder (MND), and 17% with HIV associated dementia (HAD). HAD was associated with lower white matter AI (Analysis of variance, ANOVA, p=0.01). A 12-month follow-up (N=30) in HIV-subjects on antiretroviral therapy revealed significant worsening of HAND categorization (X2, p=0.007) AI was similar between HIV cases and control and remained so after 12-months of antiretroviral therapy. In these early stages of HIV, we found no evidence of a defect in autoregulation to explain the high-risk of ischemic stroke documented in other studies. HAND diagnosis noted in a significant proportion of subjects with worsening after 12-months of antiretroviral therapy. At baseline HAD subjects had low white matter autoregulation.

Biography

Souvik Sen received his medicine degree from University of Calcutta, MPH in Epidemiology from the University of North Carolina (UNC), and MS in Cardiovascular Pharmacology from Wayne State University. He completed his Neurology Residency at Temple University and Post-Doctoral fellowship in Cerbrovascular Diseases from the Johns Hopkin’s Medical Institution. In 2002, he founded the stroke center at UNC. In 2010, he joined as the founding Chair and Tenured Professor of the Department of Neurology (http://neurology.med.sc.edu/) at the University of South Carolina School of Medicine. He has over 100 publications, serves on editorial boards and is funded by the National Institutes of Health

  • The first Affiliated Hospital of Nanchang University, China
  • Title:Plasma Trimethylamine N-oxide, A Gut Microbe–Generated Phosphatidylcholine Metabolite, is Associated with Autism Spectrum Disorders
  • Time :

Abstract

The compositions of the gut microbiota and its metabolites were altered in autism spectrum disorders (ASD) individuals. The aim of this study was to assess whether plasma levels of gut-derived metabolite trimethylamine N-oxide (TMAO) in relation to the risk and degree of the severity of ASD.

Biography

Lijuan Quan,MD,graduated from the Nanchangl University ,China in 2011, now is a deputy director of rehabilitation department of the First affiliated Hospital of Nanchang University, Attending and associate chief physician.
I service on the following committees:
1.Standing member of the first committee of rehabilitation assessment professional committee of China association for the rehabilitation of disabled persons;
2.Member of the third session of child rehabilitation committee of Chinese rehabilitation association;
3.Member of the first session of the advisory committee on rehabilitation medicine of the Chinese association of rehabilitation medicine;
4.Member of autism spectrum disorders group, child rehabilitation committee, Chinese academy of rehabilitation medicine;
5.Vice President of the second council of jiangxi disabled persons rehabilitation association;
6.Vice chairman of the second committee of autism rehabilitation professional committee of jiangxi disabled persons rehabilitation association;
7.Vice – chairman of child rehabilitation committee of jiangxi rehabilitation medical association;
8.Member of the second board of jiangxi rehabilitation medical association.

 

  • University of Cambridge, UK
  • Title:Compounding Nimodipine Oral Suspension for Subarachnoid Hemorrhage
  • Time :

Abstract

What happens when there is an entire patient population, not just a specific patient, which cannot take a commercial pharmaceutical product due to significant adverse effects, although the commercial product has a U.S. Food and Drug Administration-approved indication for the medical problem? What should or can be done in this situation? This presentation discusses this dilemma using subarachnoid hemorrhage as an example of a true documented medical need, and discuss the option and circumstances surrounding the compounding of a nimodipine oral suspension, a U.S. Food and Drug Administration-approved indication for the treatment of subarachnoid hemorrhage.
The learning objectives include the following:
Discuss the need for an oral nimodipine liquid.
Provide options for treating patients with subarachnoid hemorrhage.
Provide information on compounding nimodipine oral suspension to avoid adverse effects.

Biography

Dr. Mcelhiney is the Team Lead Compounding Pharmacist and a preceptor for Indiana University Health in Indianapolis, Indiana. It is one of the largest health-systems in the United States, consisting of 20 hospitals and dozens of outpatient clinics and surgery centers.She is an author for the International Journal of Pharmaceutical Compounding and contributing author in pharmacy and medical textbooks. Dr. McElhiney is a full fellow in the American College of Apothecaries (ACA), American Society of Health-System Pharmacists (ASHP), and the International Academy of Compounding Pharmacists (IACP). She has served on several national committees and board of directors in professional pharmacy organizations and received several awards. Dr. McElhiney currently serves as the President-Elect for the American College of Apothecaries.Dr. McElhiney earned a B.S. in Pharmacy from Purdue University in 1984. Dr. McElhiney earned a Pharm.D. (2002) and a Masters (2012) from the University of Florida.

 

  • St George’s University of London, Cyprus
  • Title:Migraine Disorder in Obstetrics and Gynaecology – Where are we Now?
  • Time :

Abstract

Migraines are the third most prevalent disorder and seventh-highest specific cause of disability worldwide. Migraines have a multitude of underlying aetiologies; hormonal treatment, menstrual cycle symptoms or pregnancy, they can vary based on intensity and duration. Clinicians should be fully knowledgeable of the potential complications and well-versed in management options.
A systematic review of the incidence, symptoms, treatment options and complications for migraine sufferers in gynaecology and obstetrics cases was performed. Migraine significance in prognosis for antenatal care and contraception was also investigated.
Migraine incidence in gynaecological and obstetric cases, and contraceptive users were 11.7-12.5 %, 9-38.5 %, and 16.7-54.7% respectively. There is on average a six-fold increase in the risk of stroke in women who take combined hormonal contraception and suffer from migraines. Four papers with 1565 patients proposed the combination of triptans along with the progesterone only pill as a superior treatment. Desogestrel 75mcg/day was found to reduce the intensity of migraines compared to the combined hormonal contraceptives. The Pregnant women suffering from migraines have an increased risk of gestational hypertension, low birth weight, preterm birth, pre-eclampsia.
Migraines have a high incidence in gynaecology and obstetrics. Health care providers are obligated to include screening questions when history taking to identify women with migraines and manage them effectively. Thorough follow-up and treatment is required for all female migraine sufferers in order to minimize the risk of cerebrovascular events, and negative outcomes in pregnancy. Women with migraines are strongly advised to avoid contraception in the form of the combined pill and use progesterone only formulas.
Tanos V, Raad E, Berry K, Toney Z. Review of migraine incidence and management in obstetrics and gynaecology. European Journal of Obstetrics & Gynecology and Reproductive Biology. 2019;240:248-255.

Biography

Zara is a final year medical student, graduating in July 2020 and plans to begin her foundation medical training in the UK this year. She completed her Bachelors of Science in London in 2014, also conducting a year in industry working in clinical trial sample analysis at a contract research organisation. Zara is a Wellcome Trust and Rotary Foundation Global Grant Scholar, achieving these awards during her BSc and for her MBBS degrees. Her research interests span obstetrics and gynaecology, infectious disease and child health. Zara has presented at international conferences and meetings throughout university and hopes to continue contributing to clinical literature, having a positive impact on patient care.

  • University of Bologna, Italy
  • Title:Field Cancerization Therapy with Ingenol Mebutate Contributes to Restoring Skin-Metabolism to Normal-State in Patients with Actinic Keratosis: A Metabolomic Analysis
  • Time :

Abstract

Actinic keratosis (AK) is a skin premalignant lesion, which progresses into squamous cell carcinoma (SCC) if left untreated. Ingenol mebutate gel is approved for local treatment of nonhyperkeratotic, non-hypertrophic AK; it also has the potential to act as a field cancerization therapy to prevent the progression of AK to SCC. To understand the mechanisms of ingenol mebutate beyond the mere clinical assessment, we investigated, for the first time, the metabolome of skin tissues from patients with AK, before and after ingenol mebutate treatment, with high-resolution magic angle spinning nuclear magnetic resonance spectroscopy (HR-MAS NMR). The metabolomic profiles were compared with those of tissues from healthy volunteers. We identified a number of metabolites, the homeostasis of which became altered during the process of tumorigenesis from healthy skin to AK, and was restored, at least partially, by ingenol mebutate therapy. These metabolites may help to attain a better understanding of keratinocyte metabolism and to unmask the metabolic pathways related to cell proliferation. These results provide helpful information to identify biomarkers with prognostic and therapeutic significance in AK, and suggest that field cancerization therapy with ingenol mebutate may contribute to restore skin metabolism to a normal state in patients with AK.

Biography

Valeria Righi is a researcher at the University of Bologna since 2012. She is professor of biochemistry. Her research activity is focused on metabolomics sciences through the use of nuclear magnetic resonance (NMR). She was involved in the study of cerebral cancer pathologies and the gastrointestinal system cancer diseases. Recently, she has focused her attention on skin diseases (in particular those defined as non-melanoma skin cancer) to the study of tissues and bio-fluids and also to diseases linked to behavioural disorders due to food. Metabolomics is a science that allows us to evaluate metabolic changes even when histological analyses do not detect cellular alterations. She held part of her doctorate and post-doc at the “Instituto de Investigaciones Biomedicas Alberto Sols” Madrid (Spain) and she was post doc at the Harvard Medical School of Boston (USA) in 2008-2009. She was awarded by L’Oreal and Unesco in 2009.
She is author and co-author of over 45 publications in high-impact international scientific journals and has presented numerous works at national and international conferences.

  • Social Psychiatry Zurich University, Zurich
  • Title:Harm Reduction Policy for Autonomous Citizens : A Critical Analysis
  • Time :

Abstract :

The aim of harm reduction is to minimize damage caused by human behavior and lifestyles, be it health damage, financial damage, damage to well being. Controversial debate starts around the question how this aim should be attained and how it can be assured. One position favors the interests of public health and public order by regulations and legislation, limiting potentially harmful behavior. The other position allows people to make their own decisions, charging them to bear the responsibility for the consequences of their behavior. A third position combines the liberal preference for self-responsibility with a duty for the competent authorities to research the evidence on the type, extent and outcomes of potentially harmful behaviors, and to make such evidence public knowledge so people can learn how to protect themselves. Advantages and disadvantages of these positions are analysed, as a guidance for societies to make their choices and to determine the type and extent of harm reduction policies. A final conclusion recommends how it will best respond to the specific situation of a given society.

Biography:

Born 1928 in Basel. Studies in medicine, philosophy and social science at Zurich University, Ph.D. 1954, M.D. 1959. Specialization in psychiatry and psychotherapy. Since 1970 founder and head of the department for social psychiatry at Psychiatric University Hospital of Zurich, with in- and outpatient specialized services. Undergraduate and postgraduate teaching at Zurich Medical School. Since 1977 professor of Social Psychiatry and co-director at Psychiatric University Hospital, retired 1995.
Since 1974 research projects in the fields of psychotherapy, psychiatry, drug dependence and health policy, especially drug policy. Co-editor of several scientific journals, co-founder of „European Addiction Research“. Editor of a comprehensive handbook on Addiction Medicine (Urban & Fischer Munich). Reviewer on grant proposals and research projects, for national and international organisations and authorities. Over 290 publications.
Expert on national and international committees. Member of the Expert Panel on Drugs of World Health Organisation. Founder and past president of Swiss Society of Social Psychiatry, past board member of the European Association on Substance Abuse Research EASAR. Missions for World Health Organisation to various countries; numerous contributions to WHO expert meetings and reports since 1974.
Founder and since 1995 President of the Addiction Research Institute, now Swiss Research Institute for Public Health and Addiction, a WHO Collaborating Center, affiliated with Zurich University. Numerous research projects in epidemiology, prevention and treatment of substance dependence.

  • Virginia Commonwealth University, USA
  • Title:Microglia-Axonal Interactions and Diffuse Glial Signatures in a Translational Model of Mild Brain Trauma
  • Time :

Abstract

Traumatic brain injury (TBI) is a highly prevalent disease with devastating costs associated with long term morbidity. While this morbidity has been linked to diffuse pathologies, our knowledge regarding these TBI-initiated diffuse pathologies is limited. Further, there are currently no successful therapeutics to treat TBI, despite many promising candidates. The unsuccessful clinical translation of many promising therapeutics has triggered a call for the use of higher-order animal models prior to transitioning to large-scale clinical trials. Due to their high level of homology with humans in terms of systemic inflammatory responses, metabolic rates, and cytoarchitecture, we utilize an adult micro pig model to study the effects of mild TBI in a more translational fashion. Additionally, as thalamic damage has been suggested to play a central role in the pathogenesis of mild TBI and its various symptoms, we focus much of our investigations on the thalamic domain. In this talk we will explore the association between diffuse axonal injury and neuroinflammation, specifically investigating activated microglial process convergence onto injured axonal segments following diffuse brain injury as well as the species variation we have observed in this trauma-induced phenomenon. We will also explore histopathological signatures associated with serum biomarkers in a micro pig model of diffuse traumatic brain injury. These studies were initiated as part of the multi-institute Operation Brain Trauma Therapy (OBTT) consortium.

Biography

Audrey Lafrenaye, PhD is an Assistant Professor in the Department of Anatomy and Neurobiology at Virginia Commonwealth University (VCU), USA. Her background is in cellular and molecular neuroscience, with focuses on quantitative immunohistological approaches, glial pathology (including microglia, astrocytes and oligodendrocytes), and traumatic brain injury (TBI). Her research is currently funded by the National Institutes of Health and focuses on evaluating the progression and molecular mechanisms involved in diffuse neuronal and glial pathologies following TBI. Dr. Lafrenaye is also a site-PI for the Operation Brain Trauma Therapy (OBTT) pre-clinical therapeutic and serum biomarker discovery consortium, which is the only pre-clinical multi-institute consortium of its type in the field. She is an active member of the National Neurotrauma Society and Training, Education and Mentoring in Neurotrauma for the promotion of diversity in neurotrauma research.

  • Capital Medical University, China
  • Title:Accessory Nerve Schwannoma: A New Case Report and Systematic Review
  • Time :

Abstract

Background and Objective: Accessory nerve schwannoma is an exceedingly rare disease. It has not yet been well characterized because of the rarity of this disease. We sought to expend the knowledge of accessory nerve schwannoma by reviewing comprehensive literature and adding to it a new case that is originated from spinal root of accessory nerve at the cerebellomedullary cisterna.

Case description: A 62-year-old woman presented with a 1-month history of the right occipital pain. There were no apparent neurologic deficits in physical examination. A brain Magnetic Resonance image found a well-demarcated mass at the right cerebellomedullary cistern, extending to the cervical 1 level and moderately compressing the medullar oblongata. The mass was completely removed via a right suboccipital craniotomy with cervical 1 laminectomy. A brain Magnetic Resonance image was performed 36 months following operation. There was no radiologic and clinical evidence of regrowth in three-year follow-up.

Conclusions: To date, we report herein 63 cases of accessory nerve schwannomas, which include 62 cases reported from the literature review and a new case reported herein. Only 5 of accessory nerve schwannomas were strictly located at cerebellomedullary cisterna. We present a new case of schwannoma located at cerebellomedullary cisterna. We performed a comprehensive review of accessory nerve schwannoma, describing more cases than those previously reported. This review characterizes a rare disease and increases awareness of this disease among neurologists and otolaryngologists.

  • National Center for Biotechnology, Kazakhstan
  • Title:Case of Nervous System Damage in a Combination of 4 Infections
  • Time :

Abstract

Female, 25 years, lives in the village, has cattle, drinks raw milk. Got sick on 20.06, – headache, weakness, joint& body pain, sweating, dizziness, fever (390C), nausea, vomiting, liver enlargement. In the hospital (10 day of illness) –positive serological tests for Brucella, Herpes Simplex Virus, Cytomegalovirus, Borrelia and TBEV (all IgG). Consciousness impairment, clonic convulsions, muscles gipertonus in extrapyramidal type, meningitis symptoms appeared. On MRI-signs of stem encephalitis, in CRF-cytosis 85.2 (lymphocytes), protein – 1.65. Treated with antibiotics, antiviral drugs, glucocorticoids, immunoglobulins – human and against tick-borne encephalitis virus. She was discharged on the 39th day of illness, with residual symptoms, and fully recovered a year later.

Biography

Prof. Andrey Dmitrovskiy was born in 1950, in 1973 graduated from Almaty Medical University, worked as an infectious disease specialist in the village, then in Almaty city hospital/ He worked for 20 years at Central Asian Anti-Plague Institute, where defended PhD (Yersinioses) and doctor of science (Plague) dissertations. He worked at CDC Central Asian office (2006-2009), AECOM (2001-2016), Kazakh National Medical University. Currently, he works as head of laboratory of Almaty branch of NCB (CRL) and chief research of the National Center for Extremely Dangerous Infections, Training Department.

  • Southern Tohoku General Hospital, Japan
  • Title:Diagnosis and Treatment of Co-Existence of Pituitary Adenoma and Rathke's Cleft Cyst. ~Results of a Prospective Study~
  • Time :

Abstract

Introduction
The frequency of coexistence of pituitary adenoma and RCC was reported to be 1.9%, and it was considered to be very rare, and it was found that Rathke’s cleft cyst (RCC) was complicated with the pituitary adenoma at a high rate, since MET-PET became diagnosable to the pituitary microadenoma. Between 2011 and 2014, we initiated a prospective study with concomitant pituitary adenomas in mind in cases of RCC and examined the frequency of concomitant pituitary adenomas associated with RCC.  Based on the results, from 2015, we examined the frequency of precedent RCC lesions in cases with pituitary macroadenomas as a prospective of preoperative diagnosis.
Materials:
Part1: From 2011 to 2014, 308 surgical cases with prospective analysis for patients with RCCs were included. Male: 77 cases, female: 231 cases. The average age was 39-year-old, ranging from 11-year-old to 82-year-old. Basal pituitary hormones and the presence of abnormal findings in the sellar region on 3D-CT were screened for those with symptoms of headaches and dizziness and suspected RCCs. When abnormalities were observed in the screened items, 3T-MRI features including 3D-Flair cube images and hormonal challenge tests were added. If hormonal loading test showed abnormal ACTH, GH secretions, MET-PET was added and fused images with 3T-MRI were created. Surgical treatment of both complicated lesions was performed at the time of surgery, and pathological examination was performed.
Part2: The complication rate of RCC, which is assumed to be the antecedent lesion of pituitary adenoma, was examined for prospective in macroadenoma operation case under the result of Part1.We studied pituitary tumors in 42 consecutive surgical cases from 2015 to 2016. Scores of headache and detailed preoperative medical history were taken with the combination of RCC and adenoma in mind. Radiological image has been added to sensitive methods for detecting RCCs, namely, 64-channel 3D-CT reconstruction imaging and, more 3T-MRI, conventional imaging, plus flair cube 3D and SPGR techniques. As an intraoperative finding, in cases of suspected ruptured RCC, we check the presence or absence of indirect finding not obtained by histology (presence of fissures within the pituitary gland, ruptured foramen, and venous lake of the dura mater).
Results;
Part1: From radiological examination and operative findings, 308 cases of RCC were diagnosed. Among them, pituitary adenomas were histopathologically confirmed in 106 cases, 111 adenomas. Therefore, the rate of concomitant adenoma and RCC was 34%. 100 out of 106 pituitary adenomas showed the diameter less than 10mm (microadenoma). Of the 106 cases, 28 had adenoma confirmed by pathological examination alone, and 78 had adenoma visualized by MET-PET, which was also confirmed by surgical pathological specimens. Breakdowns of adenomas were GH production in 40 cases, ACTH production in 36 cases, PRL production in 14 cases, and others in 5 cases.
Part2: Among 42 consecutive surgical cases, 34 cases were diagnosed as pituitary adenomas. Among those 34 cases of pituitary adenoma, complication of RCC was confirmed in 9 cases, which were pituitary adenoma and suspective preceded lesion.
The complication frequency of macroadenoma and ruptured RCC was 26%. Types of adenomas included PRL production (1 case), Gonadotrpin production (1 case), and GH production (1 case), PRL & GH production (2 cases), TSH production (1 case),
plurihormonal adenoma (2 cases), and Null cell adenoma (1 case). Thus, all types of hormone-producing adenomas were seen.
Conclusion
1, Ruptured RCC has the risk of forming pituitary adenomas, and when diagnosing
and treating RCC, it is important to carry out the retrieval considering also the pituitary
adenoma preoperatively.
2, Approximately 26% of pituitary macroadenomas were expected to form based on ruptured RCCs.
3, In the medical examination of the pituitary adenoma, the combination of RCC is always kept in mind, and precise hearing, endocrine examination, diagnostic imaging are also important for understanding the disease state in deciding the treatment plan.

Biography

Prof. Ikeda Graduated from Tohoku University School of Medicine in 1981. He learned and had training both Neurosurgery and General pathology at Tohoku University and obtained MD and PhD. He worked as visiting scientist at Dept of Neuropathology, University Hospital, Zurich, Switzerland (1992) and at Dept of Molecular biology, Harvard Medical School, Boston, USA (1993). He accomplished more than 2500 cases of transsphenoidal surgery for pituitary tumors at Tohoku University, Kohnan Hospital, Ohara medical center Hospital and Southern Tohoku General Hospital during the period of 1990~2016. For this great achievement and success he had won many prizes, such as “Joseph Lister Research Awards-2015 in Neurology”, “Archimedes Research Award-2015 in surgery”, “Academic Excellence Award-2015”, “Takahashi memorial award in 2016”, and Albert Nelson Marquis Lifetime Achievement Award in 2017. 

  • Zhejiang Provincial People’s Hospital, China
  • Title:Effect of Hemodynamic Characteristic Changes of the Carotid Artery on 6-OHDA-Induced Parkinson’s Disease Model Rats Treated by Gut-Acupuncture
  • Time :

Abstract

Parkinson’s Disease , is the most common motor relateddisorders up to date. Since
the discovery of levodopa half a century ago, which may cause a ‘‘honeymoon period”as well
as side effects. Recent studies have reported that acupuncture is the most commonly used
complementary and alternative therapy (CAM) for a large number of PD patients besides
standard treatment.In recent years, the development of PD research has been focused on the
gastrointestinal tract and the related ENS. Combining findings from gut-brain axis studies
about early warning gastrointestinal (GI) symptoms in PD and the course of the ‘‘stomach
meridian” in Huangdi Neijing, we employed a 6-OHDA rat model, to elucidate the
mechanisms of acupuncture–mediated amelioration of PD symptoms.Our data show that gut- acupuncture correlates with significantly increased abundance of TH, a marker of DA
neurons compared to untreated rats. Furthermore the area of SNH in the injured side of the
acupuncture group was significantly reduced. PSV of LCCA, LICA,RICA showed that were
significantlyimproved i.e. decreased in the acupuncture group, while the diameter of LICA
and RCCA in acupuncturegroup was narrower. We also found that the PSV was significantly
increased and the vascular diameternarrowed in LCCA and LICA during treatment, whereas
after removing the acupuncture needle the PSVdecreased and the vascular diameter widened. In short,Gut-acupuncture can reduce SNH and influence TH abundance in the SN which
correlatedwith changes of hemodynamic characteristics of the lesioned side. We suggest a
regulatory mechanismwhich may affect the vagus nerve through the ENS and cause the
change of cervical hemodynamics. Itfurther induces low oxygen tension microenvironment
conducive to the proliferation of neural stem cells,which leads to the enrichment of TH in PD
model rats of acupuncture group.

Biography

Li Lihong, Associate Professor, Master’s tutor,vice-directors.Dr. Li Lihong graduated from
Zhejiang University of traditional Chinese medicine in 2009, and then worked in the
Department of acupuncture and moxibustion of Zhejiang Provincial People’s hospital. Dr. Li
Lihong graduated from Zhejiang University of traditional Chinese medicine in 2009, and
then worked in the Department of acupuncture and moxibustion of Zhejiang Provincial
People’s hospital. She has been engaged in acupuncture clinical work for 11 years, and has
been committed to the research on the mechanism of acupuncture and moxibustion on
regulating neuroimmunity. Good at acupuncture treatment of Parkinson’s disease, myasthenia
gravis, depression, anxiety, sleep disorders, tension headache, migraine, facial paralysis and
so on. She has published a textbook of acupuncture and moxibustion, serving as a member of the
sleep Management Committee of the Chinese Acupuncture Association, a member of the
meridian Committee of the acupuncture society, and a member of the pain society of
traditional Chinese medicine.

  • Virgen del Rocío University Hospital, Spain
  • Title:Antibody-Mediated Encephalitis
  • Time :

Abstract

Antibody-mediated encephalitis is a novel entity in neurology on which there are important advances in pathophysiology, diagnosis and treatment, and is currently considered a rare but with increasing frequency.
Its diagnosis is fundamentally based on antibodies, which are usually delayed, so its early diagnosis is important to reduce sequelae and mortality and requires close monitoring for at least two or three years in search of an associated neoplasm.
Its diagnosis is based on epidemiological, clinical, neuroimaging, fluid, electroencephalographic, nuclear medicine, and the antibodies described, but since they are delayed, we move to the level of certainty “Probable Antibody-Mediated Encephalitis” to start treatment in acute phase and thus reduce sequelae and mortality. It should be noted that these antibodies are not found in half of the patients, which further justifies the follow-up of these patients and the approach to alternative diagnoses.
The purpose of this Oral Communication is to review the most relevant aspects of this entity, focusing on the importance of early diagnosis and the need to have Reference Laboratories to improve efficiency in the detection of antibodies, as well as the need for Increase research items to better understand the pathophysiology of this entity and improve prescribed treatments.

Biography
I am graduated from Medical School in 1991 (Sevilla).Training as neurology resident in Hospital Virgen de las Nieves in Granada (1993-6).Ph. D in 2007 with certificate “Cum Laudem”, in University of Sevilla “ Epidemiology in Multiple Sclerosis in the island of Lanzarote and its variations in the last years”.Master’s Degree in Neuroimmunology, University of Barcelona 2009.Master’s Degree in Direction of Social-sanitary Servicies, University of Extremadura (2011). University Expert Degree in Neuropsicology, in Pablo Olavide University (Sevilla 2010).
Title “Neurologist for the future”, by Spanish Neurological Society. Current secretary of Andalusian Neurological Society. Clinic Tutor in pre/post-grade formation. Regular copy editor of the Neurología magazine.

  • West China Hospital of Sichuan University, China
  • Title:Pineal Region Glioblastomas: Clinical Characteristics, Treatment and Survival Outcome
  • Time :

Abstract

OBJECTIVE: Given the rarity in the pineal GBM patients, clinical
characteristics, treatment, and prognostic factors are not well
characterized. This study aimed to investigate these characteristics and
identify the prognostic factors of overall survival (OS). METHODS: A
retrospective analysis of newly diagnosed pineal GBM patients, including our three cases and an
additional forty-four cases from published articles, was conducted. Survival analysis was performed
by Kaplan-Meier analysis and Cox regression analysis was used to determine the prognostic factors.
RESULTS: A total of 47 patients (28 males and 19 females) were enrolled, with a median of 46
years (range, 5-74 years). Forty-four patients (90.9%) had preoperative obstructive hydrocephalus.
Among 38 patients, 21 (55.3%) had distal leptomeningeal dissemination. Forty-five (95.7%)
patients had resection/biopsy, in which 6 had GTR, 22 had STR, 7 had PR, and 10 had biopsy.
Adjuvant therapy included radiotherapy in 36 patients and chemotherapy in 27 patients. The median
OS was 10.0 months. The 6-month, 1-year and 2-year survival rates were 68.0%, 42.6% and 17.0%,
respectively. COX regression analysis revealed that patients receiving biopsy (p = 0.042) or
chemotherapy (p = 0.029) had the better OS and these were regarded as independent prognostic
factors. Further survival analysis showed that chemoradiotherapy had better survival benefit than
other regimens. CONCLUSIONS: In this study, we summarized the characteristics of pineal GBM
patients and revealed the correlation between clinical characteristics and prognosis. This study may
make the readers have a deep understanding of these rare GBMs and provide some references for
future management.

Biography

Dr. Qing Mao, Professor of Neurosurgery, West China Hospital of Sichuan University, China. Academic Positions: Vice chairman, Society for Neuro-oncology of China; Member of the Standing Committee of 3D printing technology Branch, China Medicinal Biotechnology Association; Member of the Standing Committee of Chinese Society of Neuro-oncology; Chairman, Southwest Group of Chinese Society of Glioma; Chairman Designate, Sichuan neurosurgery committee;
Chairman Designate, Chinese Glioma Cooperative Group; Academic and Technical Leader of Sichuan Province; Member of Neuro-oncology Committee, Chinese Congress of Neurological Surgeons; Member of Minimally Invasive Neurosurgery Committee, Chinese Congress of Neurological Surgeons; Member of Neuro-oncology Branch, Chinese Neuroscience Society.
Main Achievements: He has published more than 100 papers including SCI and others in world-wide professional academic journals. He has undertaken more than 10 key scientific research projects from the Sichuan provincial and Ministry of Science and Technology, and got the second prize of provincial science and technology progress award.

  • Vellore EEG Center, India
  • Title:Anterior Thalamic Nucleus Stimulation in Intractable Epilepsy: Optimization of Stimulation Parameters by EEG Based Novel Approach
  • Time :

Abstract

Deep brain stimulation (DBS) of anterior thalamic nucleus (ATN) is establishing as an effective adjunctive therapy for patients with intractable epilepsy (IE) not suitable for epilepsy brain surgery and/or vagal nerve stimulation. The judicious selection of DBS parameters (DBSPs) plays a crucial role in the success of ATN-DBS. Conventionally, DBSPs are selected by trial and error requiring multiple sessions and hospital visits warranting a strong need for optimization of the DBSPs with objective assessment of its effects. The author presents an EEG-guided novel and superior approach to the selection of effective DBSPs targeted to induce EEG-desynchronization, which is known to exert potent antiepileptic influence with possibly possession of an additional anti-kindling effect that can suppress or even arrest the ongoing process of epileptogenesis in the patients with intractable epilepsy in addition to exercising control over the intractable seizures. It is further claimed that the innovative EEG-guided approach can successfully optimize the DBSPs resulting in (a) minimum sessions of DBSP adjustments, thereby reducing the frequency of hospital visits (b) minimum side effects and (c) minimum consumption of the device battery; thus, prolonging its life. Preliminary results of the clinical application of the novel approach in the selection of the DBSPs in a small case series have been very promising and encouraging despite which it is strongly recommended that well designed large sized studies are required for its validation and successful clinical outcome.

Biography

Professor Dr Jaseja has worked as a faculty member in a Medical school for more than 33 years. His main research interest has been in epilepsy and epileptogenesis; in 2013, he was ranked Second in Epilepsy Research in India.
He has published papers on various aspects of epilepsy, especially association of epilepsy with sleep. He had advocated consideration of diagnosis of epilepsy even after the first epileptic attack (in 2009) long before the ILAE definition of epilepsy in 2014 that permits clinical diagnosis of epilepsy even after one epileptic attack associated with a 60% risk of a recurrent attack. Until this definition, clinicians usually waited for occurrence of a second attack thus delaying the initiation of anti-epileptic medication, causing anxiety and stress in the patients due to uncertainty and unpredictability of a second attack.
His current work has been on Deep brain stimulation (DBS) in intractable epilepsy (IE). He has postulated a new target for DBS, namely Pedunculopontine nucleus (PPN), claiming that its stimulation is superior in therapeutic efficacy and success over the conventional DBS of anterior thalamic nucleus (ATN) in patients with IE.
In 2005, Dr Jaseja initiated a debate on the epileptogenic potential of Meditation.Dr Jaseja has published new guidelines for treatment of patients with cerebral palsy (CP), based on EEG. He has claimed that CP, contrary to popular belief, can change its course and progression with time and therefore, observation of new guidelines, quality of life of patients with CP may be improved.
Dr Jaseja has studied the effects of vagal nerve stimulation and has shown and claimed its efficacy in patients with CP, post which, CP has been included in the list of indications of VNS, the links to which are: (http://www.aetna.com/cpb/medical/data/100_199/0191.html,http://www.anthem.com/medicalpolicies/policies/mp_pw_a053286.htm).
Dr Jaseja has worked on interpretation of an EEG and shown how its misinterpretation can be prevented; further, he has also ideated how the yield of EEG-findings can be enhanced in patients with epilepsy. He has shown that the hallmarks of epileptiform activity namely ‘spike’ and ‘sharp’ waves (which hitherto were considered having same significance) posses differential clinical significance especially in patients with epilepsy.
Interestingly, he has shown that the Indian traditional application of Shoe-smell in Epilepsy has a sound scientific basis. In a small study, shoe smell was reported to posses beneficial effect (reduction in duration and severity) during an epileptic attack.

  • University of Cambridge, UK
  • Title:Evaluation and Surgical Management of Spasticity in the Upper Extremities
  • Time :

Abstract

An injury to the upper motor neuron results in impaired regulation of motor activity that can manifest as hyper-reflexia or spasticity.  This can lead to an imbalance of forces across the joint and result in static or dynamic deformities in the upper extremities.  In severe cases, these deformities can result in hygiene issues and markedly decrease quality of life.  The goals of surgical reconstruction are to reduce pain, improve hygiene, enhance functionality, and to correct unaesthetic contractures.  The presentation will review the evaluation and management of this unique and underserved patient population.  A case-based format will be utilized to illustrate the approach to evaluating common spastic deformities in the upper extremity and review the surgical procedures that can be employed based on the functionality of the extremity.  Participants will be able to better evaluate the upper extremity in patients with spasticity and understand the possible surgical treatment options that are available to improve function and/or quality of life.

Biography

Dr. Peter Charles Rhee is a hand and microvascular surgeon within the Department of Orthopedic Surgery at the Mayo Clinic in Rochester, MN. He holds academic appointment as an Associate Professor of Orthopedic Surgery through the Mayo Clinic College of Medicine and is the Program Director for the Mayo Clinic Hand Surgery fellowship program. He is board certified in orthopedic surgery with a Certificate of Added Qualification in Hand Surgery through the American Board of Orthopedic Surgery.  Dr. Rhee graduated as Valedictorian of his medical school class at the Kirksville College of Osteopathic Medicine (Kirksville, MO). He completed his orthopedic surgery residency and hand surgery fellowship at the Mayo Clinic while obtaining his Master of Science degree in Orthopedic Research from the Mayo Graduate School.
He then served in the United States Air Force as the Chief of Hand and Microvascular Surgery at the San Antonio Military Medical Center (SAMMC, Fort Sam Houston, TX), the DoD’s only Level-1 trauma center where he instituted a microvascular surgery service to support the care of upper and lower extremity traumatic injuries.  He was also the Director of the Microvascular Surgery Research Lab (Fort Sam Houston, TX) and Chief Hand Surgeon at the Center for the Intrepid Advanced Rehabiliation Center (Fort Sam Houston, TX) from 2013 until 2017. He participated on 2 deployments to the Dominican Republic and to Bagram Air Field in Afghanistan. He was awarded the Meritorious Service Medal for his contributions to patient care both in San Antonio and in Afghanistan. During his USAF career, he was a subject matter expert in the management of the mangled upper extremity. He is currently in the USAF reserves after separation from active duty in August 2017.
A dedicated teacher, Dr. Rhee, has developed educational curricula for residents and fellows utilizing evidence-based practices to enhance objective based learning and developing independent thought and analysis.  He was awarded “Teacher of the Year” by the orthopedic surgery residents at SAMMC (2015) and by the hand surgery fellows at the Mayo Clinic (2018).  He is involved in educational committees both for the American Society for Surgery of the Hand (ASSH) and the American Association for Hand Surgery (AAHS).
Dr. Rhee has a clinical interest in the emergent management and reconstruction of traumatic injuries to the upper extremity from the brachial plexus to the fingertip.  He also has a profound interest in the management of patient with upper motor neuron injuries from cervical spinal cord or brain injuries.  He has presented over 60 regional, national, and international presentations, has authored 55 peer-reviewed articles, 2 editorials, and 5 book chapters. He also serves on 8 committees for the ASSH and 1 committee for the AAHS. Dr. Rhee is a reviewer for the Journal of Hand Surgery America, American Journal of Orthopedics, Journal of Clinical Biomechanics, and Hand Surgery.

  • Pasteur Institute, France
  • Title:Do Nicotinic Receptors Modulate High-Order Cognitive Processing?
  • Time :

Abstract

Recent studies provided strong evidence that deficits in cholinergic signaling cause disorders of cognition and affect conscious processing. Technical advances that combine molecular approaches, in vivo recordings in awake behaving animals, human brain imaging, and genetics have strengthened our understanding of the roles of nicotinic acetylcholine receptors (nAChRs) in the modulation of cognitive behavior and network dynamics. Here, we review the emergent role of nAChRs in high-order cognitive processes and discuss recent work implicating cholinergic circuits in cognitive control, including conscious processing.

Biography

Jean-Pierre Changeux worked on the bacterial regulatory enzyme, l-threonine deaminase which led to the general discovery that chemical signals that regulate the biological activity of proteins act at “allosteric” sites distinct from the biologically active sites(1961)as a Ph.D. student in Jacques Monod Laboratory, and involved a cooperative conformational transition (Monod-Wyman-Changeux 1965) viewed as a general molecular mechanism of signal transduction. His subsequent career led to the chemical identification of eukaryotic acetylcholine nicotinic receptor, the first identified neurotransmitter/drug membrane receptor and ion channel together with the demonstration of its allosteric properties and of its structural homology with prokaryotic receptors. In addition to the novel concept of allosteric modulators that creates a revolution in the field of drug design, he has brought new perspectives on nicotine addiction, the higher function of the brain and their pathologies.

  • Ben-Gurion University of the Negev, Israel
  • Title:Pyruvate Administration Reducing Lesion Volume, Brain Edema and the Extent of BBB Permeability 24 hours Post-MCAO.
  • Time :

Abstract

Introduction: It is well known that abnormalities elevated glutamate levels in the brain are associated with secondary brain injury following acute and chronic brain insults. As such, a tight regulation of brain glutamate concentrations is of utmost importance in preventing the neurodegenerative effects of excess glutamate. Pyruvate, via blood resident enzyme glutamate-pyruvate transaminase convert glutamate into its inactive form 2-ketoglutarate. This method of reducing excess glutamate, known as blood glutamate scavenging (BGC). The objective of the present study was to investigate the efficacy decrease in blood glutamate concentrations in the injured brain results in reduced cerebral edema, infarct zone and BBB breakdown.
Methods: Eighty Sprague-Dawley male rats were randomly assigned into one of three groups: Middle Cerebral Artery Occlusion (MCAO) plus pyruvate treatment (n=30), MCAO plus placebo treatment (n=30), and sham operated rats (n=20). The pyruvate was administrated intravenous after MCAO. Equal volumes of isotonic saline without pyruvate were given to the placebo group. The neurological status, brain infarct zone, brain edema, BBB breakdown (by MRI technique) and blood glutamate levels were also evaluated.
Results: Our results showed that rats after MCAO demonstrated reduced lesion volume, brain edema and the extent of BBB permeability 24 hours post-MCAO . Treatment with pyruvate also led to reduced glutamate levels 24 hours after MCAO and improved neurologic recovery.
Conclusion: Glutamate scavenging with pyruvate appears to be an effective as a method in providing neuroprotection following stroke.

Biography

Academic Education: M.D 2001 – 2007 Shevchenko Moldavian State University Faculty of Medicine; PHD 2018 – presented at Ben Gurion University in Negev, Beer Sheva, Title: “The effect of blood glutamate scavenging by pyruvate on long – term behavioral patterns after acute brain injuries in rats”.
Professional Training: 2007–2009 Therapy Residency, Republican Clinical Hospital, Tiraspol, Moldova; 2012-2017 Anesthesia Residency, Soroka University Medical Center, Beer Sheva, Israel.
Employment History: 2017 – present Attending in Department of Anesthesiology, Soroka University Medical Center, Beer Sheva, Israel. Academic Appointments: 2018-2019 Clinical Instructor, Division of Anesthesiology, Soroka University Medical Center, Ben Gurion University of the Negev, Beer Sheva, Israel. 2019 – present Lecturer. Division of Anesthesiology and Intensive Care, General Intensive Care Unit, Soroka University Medical Center Faculty of Health Science, Ben Gurion University of the Negev Beer Sheva, Israel. Educational Activities: 2015 – 2016 Pharmacist course, 4 years. Ben Gurion University of the Negev, 2017 – present Medical Student course, 6 years. Ben Gurion University of the Negev, 2018 – present Anesthesiologist resident course. Ben Gurion University of the Negev.

  • Jersey Shore University Medical Center, USA
  • Title:Cytokine Storm Induced New Onset Depression in Patients with COVID-19. A New Look into the Association Between Depression and Cytokines—Two Case Reports
  • Time :

Abstract

Background: Depression appears to be a common complication in patients during and post-COVID-19 infection. Understanding the mechanism of action of cytokines such as interleukin-6, interleukin10 and others in depression and in cytokine storm syndrome, the core component of COVID-19, could shine a new light on future treatment options for both disorders.
Objective: This review demonstrates the role of interleukins in COVID-19 pathogenesis and their role in depression.
Results: We describe cases we have treat3ed as an example for the dual role interleukins have in COVID-19 infection and depression and reviewed approximately 70 articles focusing on the role of interleukins in cytokine storm syndrome and depression
Conclusion: This review highlights the key features of cytokines in both diseases. As the scientific community has more time to recover and process the effect of the current pandemic, we believe that additional research will pave the way to diverse pathways to treat depression in these patients and others.

Biography

I am a psychiatrist who specializes in Child and Adolescent Psychiatry and Psychosomatic Medicine. I treat children and adults with depression disorder, PTSD, delirium, somatization and drug and alcohol addiction. My specialty involves the evaluation and treatment of patients with co-morbid medical illness and psychiatric symptoms. I have a special interest in organ transplantation and worked at the Children’s Hospital of Philadelphia and Yale-New Haven Hospital with liver, kidney and heart transplant candidates. During my time at the Medical College of Wisconsin, I was director of transplant services.
As a result of the COVID-19 pandemic, I have focused on patients who exhibited complications such as delirium, depression and Guillain-Barre Syndrome.
Most of my work in recent years has focused on Consultation-Liaison Psychiatry or Psychosomatic Medicine. I remain active academically and continue to publish and give lectures.
I recently received the honor of becoming a Fellow of the Academy of Consultation-Liaison Psychiatry.

  • Newcastle University, UK
  • Title:Increased Telomerase Improves Motor Function and Alpha-Synuclein Pathology In A Transgenic Mouse Model Of Parkinson’s Disease Associated with Enhanced Autophagy
  • Time :

Abstract

Protective effects of the telomerase protein TERT have been shown in neurons and brain. We previously demonstrated that TERT protein can
accumulate in mitochondria of Alzheimer’s disease (AD) brains and protect from pathological tau in primary mouse neurons. This prompted us to employ telomerase activators in order to boost telomerase expression in a mouse model of Parkinson’s disease (PD) overexpressing human wild type -synuclein. Our aim was to test whether increased Tert expression levels were able to ameliorate PD symptoms and to activate protein degradation.
We found increased Tert expression in brain for both activators which correlated with a substantial improvement of motor functions such as gait and motor coordination while telomere length in the analysed region was not changed. Interestingly, only one activator (TA-
65) resulted in a decrease of reactive oxygen species from brain mitochondria. Importantly, we demonstrate that total, phosphorylated and aggregated -synuclein were significantly decreased in the hippocampus and neocortex of activator-treated mice corresponding to enhanced markers of autophagy suggesting an improved degradation of toxic alpha- synuclein. We conclude that increased Tert expression caused by telomerase activators is associated with decreased -synuclein protein levels either by activating autophagy or by preventing or delaying degradation mechanisms which are impaired during disease progression. This encouraging preclinical data could be translated into novel therapeutic options for neurodegenerative disorders such as PD.

Biography

Dr. Saretzki graduated from Sankt Petersburg (Russia) University 1982 and did her PhD at the Department of Genetics at the Humboldt-University Berlin (Germany) in 1990.
Since 1990 she was involved in ageing research and worked on telomeres, telomerase, oxidative stress, DNA damage and cellular senescence. Since 2001 she worked at Newcastle University (UK) where she became a lecturer in Ageing Research in 2002. In particular, her research interest were functions of telomerase in cancer and stem cells as well as non-canonical functions of the telomerase protein TERT in mitochondria. She extended this work to non-canonical functions of TERT in brain with an interest in neurodegenerative diseases.

  • Nara Medical University, Japan
  • Title:Hypothalamic Neurons Modulate Behavioral Responses to a Potential Threat.
  • Time :

Abstract

Defensive behaviors are evolutionarily conserved responses to threat stimuli. There are two types of threat stimuli, actual and potential. Actual threats such as predators and intruders elicit fight, flight, and freeze responses. Otherwise, a potential threat such as a novel object evokes risk assessment behavior to correct risk information. Many studies have focused on the neural mechanisms underlying fight-flight-freeze responses, while those of risk assessment are hardly understood. Our recent study revealed that hypothalamic perifornical neurons modulate risk assessment behavior in mice. Perifornical urocortin-3 neurons respond to a novel object stimulus and their neuronal activity is associated with the risk assessment of a novel object. The activation of these neurons enhanced risk assessment and burying behavior. Burying is one of the active forms of defensive behavior and is also known to be a marker for repetitive/stereotypic behavior. The ablation of these neurons caused abnormal behaviors, such as gnawing and direct contact with novel objects. These findings indicate that hypothalamic neurons modulate defensive behaviors in response to a potential threat, which is a new function of the hypothalamus.

Biography

2016‒Present: Lecturer, Anatomy and Cell Biology, Nara Medical University
2006‒2010: Assistant professor, Anatomy and Cell Biology, Nara Medical University
2006-2010: Assistant professor, Parasitology, Nara Medical University
2006: received a Ph.D. in Kyoto Institute of Technology, Graduate School of Science and Technology
Research focus: Behavioral neuroscience, the extracellular matrix in the brain
Awards: Encouragement Award of the Japanese Association of Anatomist (2015), Young Investigator Award of the Japan Neuroendocrine Society (2013)

  • University of Brescia, Italy
  • Title:Synapsin III as a therapeutic target for Parkinson’s disease
  • Time :

Abstract

Parkinson’s disease (PD) is characterized by the progressive loss of nigral dopamine neurons and the deposition of fibrillary aggregated α-synuclein in Lewy bodies (LB).
We recently described that synapsin III (Syn III), a synaptic phosphoprotein regulating dopamine release in cooperation with α-synuclein (Zaltieri et al., 2015), composes insoluble fibrils in the LB of patients affected by PD (Longhena et al., 2018). Accumulation of Syn III occurs in the caudate/putamen of patients affected by PD when compared to matched controls and co-immunoprecipitation studies showed that Syn III interaction with α-synuclein is detectable in the brain of patients affected by α-synucleinopaties. We thus investigated whether Syn III might constitute a novel therapeutic target for PD by studying its involvement in α- synuclein aggregation and in the associated nigrostriatal synaptic damage and degeneration and motor symptom onset.
We found that Syn III ko mice did not develop fibrillary insoluble α-synuclein aggregates and that their nigrostriatal neurons were protected from both synaptic alterations and degeneration resulting from unilateral adeno-associated vector (AAV)-mediated α-synuclein overexpression (Faustini et al., 2018). Moreover, gene silencing of Syn III in a human α-synuclein mouse model of PD at pathological stage could revert α-synuclein aggregation, synaptic derangement and motor symptom onset. Finally, we observed that the monoamine inhibitor methylphenidate induced a synapsin III-reliant motor response in the human α-synuclein transgenic mice independently of its dopamine transporter inhibitory action (Faustini et al., 2020). These observations indicate that Syn III functions as an accessory mediator of α-synuclein aggregation and toxicity. In addition, our findings identify Syn III as a valid therapeutic target for PD.

Biography

Zaltieri M, Grigoletto J, Longhena F, Navarria L, Favero G, Castrezzati S, Colivicchi MA, Della Corte L, Rezzani R, Pizzi M, Benfenati F, Spillantini MG, Missale C, Spano P, Bellucci
A. Alpha-synuclein and synapsin III cooperatively regulate synaptic function in dopamine neurons. J. Cell. Sci. 2015; 128:2231-43.
Longhena F, Faustini G, Varanita T, Zaltieri M, Porrini V, Tessari I, Poliani PL, Missale C, Borroni B, Padovani A, Bubacco L, Pizzi M, Spano P, Bellucci A. Synapsin III is a key component of α-synuclein fibrils in Lewy bodies of PD brains. Brain Pathol. 2018, 28:875- 888.
Faustini G, Longhena F, Varanita T, Bubacco L, Pizzi M, Missale C, Benfenati F, Björklund A, Spano P, Bellucci A. Synapsin III deficiency hampers α-synuclein aggregation, striatal synaptic damage and nigral cell loss in an AAV-based mouse model of Parkinson’s disease. Acta Neuropathol. 2018 Oct;136(4):621-639.
Faustini G, Longhena F, Bruno A, Bono F, Grigoletto J, La Via L, Barbon A, Casiraghi A, Straniero V, Valoti E, Costantino G, Benfenati F, Missale C, Pizzi M, Spillantini MG, Bellucci
A. Alpha-synuclein/synapsin III Pathological Interplay Boosts the Motor Response to Methylphenidate. Neurobiol Dis, 2020, 138, 104789.

  • University of Cambridge, UK
  • Title:Evaluation and Surgical Management of Spasticity in the Upper Extremities
  • Time :

Abstract

An injury to the upper motor neuron results in impaired regulation of motor activity that can manifest as hyper-reflexia or spasticity.  This can lead to an imbalance of forces across the joint and result in static or dynamic deformities in the upper extremities.  In severe cases, these deformities can result in hygiene issues and markedly decrease quality of life.  The goals of surgical reconstruction are to reduce pain, improve hygiene, enhance functionality, and to correct unaesthetic contractures.  The presentation will review the evaluation and management of this unique and underserved patient population.  A case-based format will be utilized to illustrate the approach to evaluating common spastic deformities in the upper extremity and review the surgical procedures that can be employed based on the functionality of the extremity.  Participants will be able to better evaluate the upper extremity in patients with spasticity and understand the possible surgical treatment options that are available to improve function and/or quality of life.

Biography

Dr. Peter Charles Rhee is a hand and microvascular surgeon within the Department of Orthopedic Surgery at the Mayo Clinic in Rochester, MN. He holds academic appointment as an Associate Professor of Orthopedic Surgery through the Mayo Clinic College of Medicine and is the Program Director for the Mayo Clinic Hand Surgery fellowship program. He is board certified in orthopedic surgery with a Certificate of Added Qualification in Hand Surgery through the American Board of Orthopedic Surgery.  Dr. Rhee graduated as Valedictorian of his medical school class at the Kirksville College of Osteopathic Medicine (Kirksville, MO). He completed his orthopedic surgery residency and hand surgery fellowship at the Mayo Clinic while obtaining his Master of Science degree in Orthopedic Research from the Mayo Graduate School.
He then served in the United States Air Force as the Chief of Hand and Microvascular Surgery at the San Antonio Military Medical Center (SAMMC, Fort Sam Houston, TX), the DoD’s only Level-1 trauma center where he instituted a microvascular surgery service to support the care of upper and lower extremity traumatic injuries.  He was also the Director of the Microvascular Surgery Research Lab (Fort Sam Houston, TX) and Chief Hand Surgeon at the Center for the Intrepid Advanced Rehabiliation Center (Fort Sam Houston, TX) from 2013 until 2017. He participated on 2 deployments to the Dominican Republic and to Bagram Air Field in Afghanistan. He was awarded the Meritorious Service Medal for his contributions to patient care both in San Antonio and in Afghanistan. During his USAF career, he was a subject matter expert in the management of the mangled upper extremity. He is currently in the USAF reserves after separation from active duty in August 2017.
A dedicated teacher, Dr. Rhee, has developed educational curricula for residents and fellows utilizing evidence-based practices to enhance objective based learning and developing independent thought and analysis.  He was awarded “Teacher of the Year” by the orthopedic surgery residents at SAMMC (2015) and by the hand surgery fellows at the Mayo Clinic (2018).  He is involved in educational committees both for the American Society for Surgery of the Hand (ASSH) and the American Association for Hand Surgery (AAHS).
Dr. Rhee has a clinical interest in the emergent management and reconstruction of traumatic injuries to the upper extremity from the brachial plexus to the fingertip.  He also has a profound interest in the management of patient with upper motor neuron injuries from cervical spinal cord or brain injuries.  He has presented over 60 regional, national, and international presentations, has authored 55 peer-reviewed articles, 2 editorials, and 5 book chapters. He also serves on 8 committees for the ASSH and 1 committee for the AAHS. Dr. Rhee is a reviewer for the Journal of Hand Surgery America, American Journal of Orthopedics, Journal of Clinical Biomechanics, and Hand Surgery.

  • Vellore EEG Center, India
  • Title:Anterior Thalamic Nucleus Stimulation in Intractable Epilepsy: Optimization of Stimulation Parameters by EEG Based Novel Approach
  • Time :

Abstract

Deep brain stimulation (DBS) of anterior thalamic nucleus (ATN) is establishing as an effective adjunctive therapy for patients with intractable epilepsy (IE) not suitable for epilepsy brain surgery and/or vagal nerve stimulation. The judicious selection of DBS parameters (DBSPs) plays a crucial role in the success of ATN-DBS. Conventionally, DBSPs are selected by trial and error requiring multiple sessions and hospital visits warranting a strong need for optimization of the DBSPs with objective assessment of its effects. The author presents an EEG-guided novel and superior approach to the selection of effective DBSPs targeted to induce EEG-desynchronization, which is known to exert potent antiepileptic influence with possibly possession of an additional anti-kindling effect that can suppress or even arrest the ongoing process of epileptogenesis in the patients with intractable epilepsy in addition to exercising control over the intractable seizures. It is further claimed that the innovative EEG-guided approach can successfully optimize the DBSPs resulting in (a) minimum sessions of DBSP adjustments, thereby reducing the frequency of hospital visits (b) minimum side effects and (c) minimum consumption of the device battery; thus, prolonging its life. Preliminary results of the clinical application of the novel approach in the selection of the DBSPs in a small case series have been very promising and encouraging despite which it is strongly recommended that well designed large sized studies are required for its validation and successful clinical outcome.

Biography

Professor Dr Jaseja has worked as a faculty member in a Medical school for more than 33 years. His main research interest has been in epilepsy and epileptogenesis; in 2013, he was ranked Second in Epilepsy Research in India.
He has published papers on various aspects of epilepsy, especially association of epilepsy with sleep. He had advocated consideration of diagnosis of epilepsy even after the first epileptic attack (in 2009) long before the ILAE definition of epilepsy in 2014 that permits clinical diagnosis of epilepsy even after one epileptic attack associated with a 60% risk of a recurrent attack. Until this definition, clinicians usually waited for occurrence of a second attack thus delaying the initiation of anti-epileptic medication, causing anxiety and stress in the patients due to uncertainty and unpredictability of a second attack.
His current work has been on Deep brain stimulation (DBS) in intractable epilepsy (IE). He has postulated a new target for DBS, namely Pedunculopontine nucleus (PPN), claiming that its stimulation is superior in therapeutic efficacy and success over the conventional DBS of anterior thalamic nucleus (ATN) in patients with IE.
In 2005, Dr Jaseja initiated a debate on the epileptogenic potential of Meditation.Dr Jaseja has published new guidelines for treatment of patients with cerebral palsy (CP), based on EEG. He has claimed that CP, contrary to popular belief, can change its course and progression with time and therefore, observation of new guidelines, quality of life of patients with CP may be improved.
Dr Jaseja has studied the effects of vagal nerve stimulation and has shown and claimed its efficacy in patients with CP, post which, CP has been included in the list of indications of VNS, the links to which are: (http://www.aetna.com/cpb/medical/data/100_199/0191.html,http://www.anthem.com/medicalpolicies/policies/mp_pw_a053286.htm).
Dr Jaseja has worked on interpretation of an EEG and shown how its misinterpretation can be prevented; further, he has also ideated how the yield of EEG-findings can be enhanced in patients with epilepsy. He has shown that the hallmarks of epileptiform activity namely ‘spike’ and ‘sharp’ waves (which hitherto were considered having same significance) posses differential clinical significance especially in patients with epilepsy.
Interestingly, he has shown that the Indian traditional application of Shoe-smell in Epilepsy has a sound scientific basis. In a small study, shoe smell was reported to posses beneficial effect (reduction in duration and severity) during an epileptic attack.

  • Pasteur Institute, France
  • Title:Do Nicotinic Receptors Modulate High-Order Cognitive Processing?
  • Time :

Abstract

Recent studies provided strong evidence that deficits in cholinergic signaling cause disorders of cognition and affect conscious processing. Technical advances that combine molecular approaches, in vivo recordings in awake behaving animals, human brain imaging, and genetics have strengthened our understanding of the roles of nicotinic acetylcholine receptors (nAChRs) in the modulation of cognitive behavior and network dynamics. Here, we review the emergent role of nAChRs in high-order cognitive processes and discuss recent work implicating cholinergic circuits in cognitive control, including conscious processing.

Biography

Jean-Pierre Changeux worked on the bacterial regulatory enzyme, l-threonine deaminase which led to the general discovery that chemical signals that regulate the biological activity of proteins act at “allosteric” sites distinct from the biologically active sites(1961)as a Ph.D. student in Jacques Monod Laboratory, and involved a cooperative conformational transition (Monod-Wyman-Changeux 1965) viewed as a general molecular mechanism of signal transduction. His subsequent career led to the chemical identification of eukaryotic acetylcholine nicotinic receptor, the first identified neurotransmitter/drug membrane receptor and ion channel together with the demonstration of its allosteric properties and of its structural homology with prokaryotic receptors. In addition to the novel concept of allosteric modulators that creates a revolution in the field of drug design, he has brought new perspectives on nicotine addiction, the higher function of the brain and their pathologies.

  • Nara Medical University Hospital, Japan
  • Title:Searching for Baby-Friendly Phototherapy to prevent Bilirubin Encephalopathy in Premature Infants
  • Time :

Abstract

Kernicterus (bilirubin encephalopathy), a neurological complication of neonatal hyperbilirubinemia, has been reported, especially in preterm infants, and neonatal hyperbilirubinemia management remains an important issue for neonatal care. Premature infants in severe jaundice often do not have the typical kernicterus symptoms shown, and in infancy, present with hearing loss and athetoid cerebral palsy. Needless to say, phototherapy is a treatment method for neonatal hyperbilirubinemia that has spread worldwide. There is a tendency to think that phototherapy has no adverse events other than effects on the retina. However, according to Morris et al, aggressive phototherapy for extremity very low birth weight infants did not change mortality or the incidence of neurological sequelae. On the contrary, the mortality rate increased for neonates with a birth weight of 500-750 g (Morris BH, et al. N Engl J Med.359, 2008). For this reason, phototherapy is not necessarily a safe treatment. Since 2010, we have conducted clinical studies on neonatal jaundice and animal studies using young rats with jaundice models. As a result, green light has an advantage in reducing photo-oxidative stress response, but blue wavelength is essential to reduce blood bilirubin. (Uchida Y, et al. Early Hum Dev. 91, 2015).This result motivated the pursuit of what would be an effective and harmless treatment to excrete bilirubin more quickly. Under the current management of jaundice, the decision to start or stop treatment is based on blood total bilirubin and unbound bilirubin levels, and bilirubin excretion has not been directly evaluated. In newborns only a few days old, especially preterm infants, liver enzymes and circulation are immature. In addition, bilirubin excreted in the intestinal tract is absorbed into the blood again by the entero-hepatic circulation, so that it is insufficient to evaluate the phototherapy effect used for jaundice treatment only by the blood bilirubin value. That is, the effect of reducing blood bilirubin in a short period of time with phototherapy is presumed to be excreted as a photo-isomer in urine, but currently it can only be detected by a special analysis method such as high-performance liquid chromatography (HPLC). That is, it is difficult to easily measure urinary bilirubin excretion immediately at the bedside. I would also like to mention at this meeting our ongoing work to establish a new method to assess urinary bilirubin excretion using the fluorescent protein UnaG, which binds specifically and strongly to unconjugated bilirubin.

Biography

Dr. Yumiko Uchida is a lecturer of division of neonatal intensive care, maternal, fetal and neonatal medical center, Nara Medical University Hospital. She graduated from Nara Medical University in 1995 and majored in Pediatrics at Nara Medical University Hospital. She has been engaged in neonatal intensive care since 1996. She has been studying neonatal hyperbilirubinemia in the last 10 years.

  • University of Nebraska, USA
  • Title:Neuron Model with Conductance-Resistance Symmetry
  • Time :

Abstract

We will derive a mathematical model for neuron by imposing only a principle of symmetry that two modelers must obtain the same model when one models the conductances of neural channels and the other models the channels’ resistances. Conductance-voltage characteristics for ion transport channels and protein gating channels are both derived. They are expressed as products of maximal conductances and opening probabilities for both types of channel. It gives an explanation to the critical role of spontaneous firing of individual channel pores and to the origin of leak current. The model has a better fit to a classical data than the Hodgkin-Huxley model does. It can also be reduced to a 2-dimensional model qualitatively similar to the FitzHugh-Nagumo equation and be expanded to a model of three ion channels capable of spike bursts. It gives an electrical circuit design for true artificial neuron. The channel opening probability function derived can also be used in the area of AI.

Biography

Dr. Bo Deng is a mathematician working in the field of Mathematical Biology. He obtained his PhD from Michigan State University in US. He has been a professor in the Department of Mathematics, University of Nebraska – Lincoln, US, since 1988. He has done researches in a few areas of Mathematical Biology, including Evolutionary Genetics, Population Genetics, Bioinformatics, Neurosciences, Evolutionary Ecology, and Community Ecology. He has also published works in the areas of Dynamical Systems, Bifurcation Theory, and Chaos Theory.

  • Neuro-Horizon Pharma, USA
  • Title:Drug Development for the Treatment of Amyotrophic Lateral Sclerosis
  • Time :

Abstract
We have previously identified the interaction between mammalian V-ATPase a2-subunit isoform and cytohesin-2 (CTH2) and studied molecular details of binding between these proteins. In particular, we found that six peptides derived from the N-terminal cytosolic domain of a2-subunit (a2N1–402) are involved in the interaction with CTH2 [1]. However, the actual 3D binding interface was not determined in that study due to the lack of high-resolution structural information about a-subunits of V-ATPase. Here, using a combination of homology modeling and NMR analysis, we generated the structural model of complete a2N1–402 and uncovered the CTH2-binding interface. First, using the crystal structure of the bacterial M. rubber Icyt-subunit of A-ATPase as a template [2], we built a homology model of mammalian a2N1–352 fragment. Next, we combined it with the determined NMR structures of peptides a2N368–395 and a2N386–402 of the C-terminal section of a2N1–402. The complete molecular model of a2N1–402 revealed that six CTH2 interacting peptides are clustered in the distal and proximal lobe sub-domains of a2N1–402, showing that a2-subunit of V-ATPase interacts with two molecules of CTH2. Indeed, using Sec7/Arf-GEF activity assay we experimentally confirmed our model. These data are critical for drug development using: i) in silico computer-aided drug design (CADD) and ii) TR-FRET based high throughput screening (HTS) of the libraries of BBB-permeable small molecules [3,4]. In particular, it was shown that CTH2 interacts with mutant superoxide dismutase 1 (SOD1), a known cause of familial amyotrophic lateral sclerosis (ALS) [5]. Inhibition of CTH2 activity by small molecules protects against ER stress, enhances autophagic flux and reduces the burden of misfolded SOD1. These data indicate that targeting of cytohesins by peptides and/or small molecules in motor neurons may be beneficial for the treatment of ALS.

  • The Johns Hopkins University, USA
  • Title: Imaging Neurovascular Abnormalities in Neurodegenerative Diseases
  • Time :

Abstract
Energy metabolism is crucial for maintenance of normal brain functions. As the supply of adequate oxygen and energy substrates for local metabolic demands is controlled by blood vessels in the brain, neurovascular abnormalities
may contribute to the neuropathology and functional deficits in brain diseases. Here, I will discuss our work on the investigation of microvascular and metabolic abnormalities in neurodegenerative diseases measured by advanced
MRI technologies developed at ultra-high magnetic field.

Biography
Dr. Hua is an Associate Professor in the F.M. Kirby Research Center for Functional Brain Imaging at Kennedy
Krieger Institute, and the Russell H. Morgan Department of Radiology at Johns Hopkins University. Dr. Hua’s research has centered on the development of novel MRI technologies for in vivo functional and physiological imaging in the brain, and the application of such methods for studies in healthy and diseased brains. These include the development of human and animal MRI methods to measure functional brain activities, cerebral perfusion and oxygen metabolism at high (3 Tesla) and ultra-high (7 Tesla and above) magnetic fields. He is particularly
interested in novel MRI approaches to image small blood and lymphatic vessels in the brain. Collaborating with clinical investigators, these techniques have been applied 1) to detect functional, vascular and metabolic abnormalities in the brain in neurodegenerative diseases such as Huntingdon’s disease (HD), Parkinson’s disease (PD), Alzheimer’s disease (AD) and mental disorders such as schizophrenia; and 2) to map brain functions
and cerebrovascular reactivity for presurgical planning in patients with vascular malformations, brain tumors and epilepsy.

  • University of California, USA
  • Title:Integrated Stress Response Inhibitor Reverses Sex-Dependent Behavioral and Cell-Specific Deficits After Mild Repetitive Head Trauma
  • Time :

Abstract
Mild repetitive traumatic brain injury (rTBI) induces chronic behavioral and cognitive alterations and increases the risk for dementia. Currently there are no therapeutic strategies to prevent or mitigate chronic deficits associated with rTBI. We previously developed an animal model of rTBI that recapitulates some of the cognitive and behavioral deficits observed in humans. Here we report that rTBI results in an increase in risk-taking behavior in male but not female mice. This behavioral phenotype is associated with cell-specific synaptic alterations in the type A subtype of layer V pyramidal neurons in the medial prefrontal cortex (mPFC). Strikingly, by briefly treating animals’ weeks after injuries with ISRIB, a selective inhibitor of the integrated stress response (ISR), we permanently reverse the increased risk-taking behavioral phenotype and restore cell-specific synaptic function in the affected mice. Our results indicate that targeting the ISR even at late time points after injury can permanently reverse behavioral changes. As such, pharmacological inhibition of the ISR emerges as a promising avenue to combat rTBI-induced behavioral dysfunction.

Biography
Susanna Rosi is a Professor in the Departments of Physical Therapy Rehabilitation Science and Neurological Surgery and the Director of Neurocognitive Research in the Brain and Spinal Injury Center. She is a member of the UCSF Weill Institute for Neurosciences, Kavli Institute for Fundamental Neuroscience, Hellen Diller Cancer Center, Neuroscience Graduate Program, Biomedical Science Graduate Program. Originally from Tuscany, Dr. Rosi earned her undergraduate degree and PhD in Biology from the University of Florence, Italy. She trained in the Neural System Memory and Aging center at the University of Arizona before becoming a Faculty Member of UCSF. Her research is focused on understanding the mechanisms responsible for the cognitive dysfunctions observed after brain injury. Her final goal is to identify diagnostic tools for treatment and prevention. She demonstrated the key role that neuroinflammation plays in the development of cognitive deficits. Most notably, she identified therapeutic strategies able to both prevent and restore lost cognition. She received the Bridging the Gap Award from the California Institute for Quantitative Biosciences, the Innovation Award from the Weill Institute for Neurosciences. She serves as PI on NIH (NIA, NINDS and NCI) funded grants, a NASA grant and she also serves as a standing member of the Molecular Neurogenetic study section at the National Institutes of Health and Associate Editor for the Journal of Neuroinflammation.

  • University of Illinois at Chicago, USA
  • Title:Predicting Autism Spectrum Disorder Using Domain-Adaptive Cross-Site Evaluation
  • Time :

Abstract

The advances in neuroimaging methods reveal that resting-state functional fMRI (rs-fMRI) connectivity measures can be potential diagnostic biomarkers for autism spectrum disorder (ASD). Recent data sharing projects help us replicating the robustness of these biomarkers in different acquisition conditions or preprocessing steps across larger numbers of individuals or
sites. It is necessary to validate the previous results by using data from multiple sites by diminishing the site variations. We investigated partial least square regression (PLS), a domain adaptive method to adjust the effects of multicenter acquisition. A sparse Multivariate Pattern Analysis (MVVPA) framework in a leave one site out cross validation (LOSOCV) setting has been proposed to discriminate ASD from healthy controls using data from six sites in the Autism Brain Imaging Data Exchange (ABIDE). Our results showed that two or more informative connections are Dorsolateral Prefrontal Cortex, Somatosensory Association Cortex, Primary Auditory Cortex, Inferior Temporal Gyrus and Temporopolar area. These interrupted regions are involved in executive function, speech, visual perception, sense and language which are associated with ASD. Our findings may support early clinical diagnosis or risk determination by identifying neurobiological markers to distinguish between ASD and healthy controls.

Biography

Dr. Bhaumik is a research assistant professor at Biostatistical Research Center, in the Department of Psychiatry. Her research focuses on Longitudinal Data Analysis, Multivariate Statistical analysis, Graph Theory and applications of Machine Learning Algorithms to Neuroscience and other fields.

  • Cairo University, Egypt
  • Title:Renin Angiotensin System Activation in Diabetes Induced Cognitive Impairment
  • Time :

Abstract

There is a great concern in learning and memory deficits that develop over time in patients with poorly controlled diabetes. Hyperactivity of the renin- angiotensin system (RAS) is directly associated with β-cell dysfunction and diabetic complications, including cognitive impairment. There is correlation between RAS components found in areas of the brain and cognition, behavior and locomotion. RAS modifiers; aliskiren and captopril protective and molecular effects were investigated on cognitive deficits in the rat hippocampus, a key brain region responsible for memory and cognition. Poorly controlled STZ-diabetic rats were injected subcutaneously with ineffective daily doses of insulin for 4 weeks. The hyperglycemia and pancreatic atrophy caused memory disturbances that were identifiable in behavioral tests, hippocampal neurodegeneration,and the following significant changes in the hippocampus, increases in the inflammatory marker interleukin 1β, cholinesterase, the oxidative stress marker malondialdehyde and protein expression of phosphorylated extracellular-signal-regulated kinase and glycogen synthase kinase-3 beta versus decrease in the antioxidant reduced glutathione and protein expression of phosphorylated glycogen synthase kinase-3 beta. Blocking RAS with either drug along with insulin restored all previously mentioned parameters to normal. Aliskiren stabilized the blood glucose level and restored normal pancreatic integrity and hippocampal MDA level. Aliskiren showed superior protection against the hippocampal degeneration displayed in the earlier behavioral modification in the passive avoidance test and aliskiren group outperformed the control group in the novel object recognition test. We, therefore, conclude that aliskiren and captopril reversed the diabetic state and cognitive deficits through the renin inhibitory effect and blockade of
RAS. Captopril protective effect is related to a reduction in Ang II synthesis. At last, dwindling RAS activity reduce oxidative stress, inflammation state, and modulating protein expression.

Biography

Madonna Magdy Youssef, MSc, received pharmacy degree from Ain Shams University and master’s degree in the field of pharmacology at faculty of pharmacy, Cairo University in 2019. Currently employed as quality assurance specialist in Egyptian Drug Authorization (EDA), granted a quality management diploma in 2020. The Ph.D. research work is in progress in fruitful collaboration with the National Research Center and the Academy of Scientific Research. The study related to neurocognitive protection from Alzheimer’s disease for healthy aging as well as investigation of possible enhancement of insulin release and sensitivity for diabetic patients. Serve as a reviewer for Elsevier international journal “Pharmacology and Therapeutics”. Research interests are overly concerned with critical pathways and applicable drugs related to neurological and cognitive disorders, diabetes as well as immunological diseases.

  • Tongji University, China
  • Title:Multilevel Metric Rank Match for Person Re-Identification
  • Time :

Abstract

Metric learning is one of the important ways to improve the person re-identification (ReID)
accurate, of which triplet loss is the most effect metric learning method. However, triplet loss only
ranks the extracted feature at the end of the network, in this paper, we propose a multilevel metric
rank match (MMRM) method, which ranks the extracted feature on multilevel of the network. At
each rank level, the extracted features are ranked to find the hard sample pairs and the back
transfer triplet loss. Each rank level has different penalize value to adjust the network, in which
the value is bigger with the deeper level of the whole network. Experiment results on CUHK03,
Market1501 and DukeMTMC datasets indicate that The MMRM algorithm can outperform the
previous state-of-the-arts.

Biography

Chao Wang is now a Ph.D. candidate with the Institute of Machine Learning and Systems Biology,
School of Electronics and Information Engineering, Tongji University, China. He received the B.S.
degree from Anhui University, China, in 2006, and the M.S. degree from University of Science
and Technology of China, in 2009. From Nov. 2009 to Dec. 2010, he worked as Research
Associate in Nanyang Technological University. From Jan. to May 2011, he worked as Research
Associate in Jacobs University, Bremen Germany. From June 2011 to Aug. 2012, he worked as
Research Associate in Shenzhen Institute of advanced technology, Chinese Academy of Sciences.
From Sept. 2012 to Mar. 2013, he worked as Engineer in Huawei Technology Co., Ltd. He now
works at Suzhou University. His research focuses on pattern recognition, deep learning and image
processing.

  • Maastricht University Medical Center, The Netherlands
  • Title:Subclinical Myasthenia Gravis in Thymomas
  • Time :

Abstract

Background A proportion of thymoma-patients without a history of myasthenia gravis (MG) before thymectomy, appears to have positive anti-AChR-antibodies in the serum. These subclinical MG-patients could be underdiagnosed because analyzation of anti-AChR-antibodies in thymomas is not always performed in patients who did not experience neurological symptoms. The prevalence and long-term outcomes of subclinical MG are never described in literature yet.
Methods: We retrospectively analyzed 398 consecutive patients who underwent a robotic-assisted thoracoscopic surgery at the Maastricht University Medical Center+ (MUMC+) between April 2004 and December 2018. In the MUMC+, a robotic approach is the standard surgical approach in patients with thymic diseases. Inclusion criteria were thymomas, thymectomy performed in the MUMC+ with a follow-up of at least one year and age above 18 years old. Exclusion criteria were patients with thymic carcinomas, refused participation, or those who were lost to follow-up.
Results:
Of the 102 included thymoma-patients, 87 patients (85%) were tested for anti-AChR-antibodies before thymectomy, of which 57 patients were diagnosed with clinical MG and seven subclinical MG-patients were found. Of the 15 patients who were not tested for anti-AChR-antibodies, four more subclinical MG-patients were discovered in the years after thymectomy. The median follow-up time was 62 months. In total, 11 subclinical MG-patients were found, with a mean age of 54 years and predominantly females (64%). Ten subclinical MG-patients (91%) developed clinical-MG, within six years after thymectomy. Immunosuppressive drugs were prescribed in five patients. Four patients were diagnosed with a recurrence of the thymoma. No surgical mortality was reported. Two patients died due to a myasthenic crisis.
Conclusions:
The prevalence of subclinical MG in thymomas was found to be 10.8%. One in four patients who experienced no neurological symptoms before thymectomy, appeared to have anti-AChR-antibodies and 91% of these patients developed clinical MG within six years after the thymectomy. Analyzing anti-AChR-antibodies in the serum is recommended in all suspected thymomas before a thymectomy is performed.
Key words: thymomas, thymectomy, myasthenia gravis, anti-acetylcholinereceptor-antibodies

Biography

Dr. Florit Marcuse is a resident in Pulmonology and PhD Candidate in the Departments of Pulmonology of the Maastricht University Medical Center+ (MUMC+) and School for Mental Health and Neuroscience (MheNS) of the University of Maastricht. In the Netherlands, the MUMC+ is the main center of expertise for the treatment of patients with thymic disorders. Dr. Marcuse has special interest in thymic oncology and associated thymic diseases in myasthenia gravis. Her research focuses on patients who underwent a robotic thymectomy, which is a standard treatment for patients with a thymoma and in most of the patients with myasthenia gravis. The thymic team of the MUMC+ is internationally known for participation in (inter)national research and collaborations.

  • Manmohan Memorial Eastern Regional Community Hospital, Birtamode, Nepal
  • Title:Pathway to Care in Patients having Mental Illness in Eastern Nepal
  • Time :

Abstract

Background: Patients with mental illness are treated at various levels before receiving specialist treatment. In doing so, the duration of illness is prolonged, treatments received are sub-optimal, and productivity lessened impacting overall outcome. This study aimed to elaborate on the various pathways of care that a mentally ill patient has to go through and its association with socio-demographic profiles. Methods: A cross-sectional study was carried out among patients presenting to Neuropsychiatric outpatient department who along with their caregivers were interviewed using semi-structured proforma and WHO Pathway Interview Schedule. Results: Of the total participants attending the outpatient clinic, 30% were either first attended by a local practitioner or hospital doctor. The duration of illness in 40% was less than a month whereas in 1/3rd of the patients was more than 12 months before presenting to the first treatment. Similarly, 38.8% had treatment latency of at least 31 months duration before receiving specialist treatment.
Conclusion: Majority of patients with mental illness approached health-professionals at first with majority being prescribed psychotropics. Time to approach for first help seeking was better but approach to psychiatric care was delayed. There is a need for improving mental health awareness at different levels to motivate early help-seeking and proper treatment.
Keywords: Mental illness, patients, specialist, treatment

Biography

I, Dr Sandarba Adhikari, have received Masters Degree in Psychiatry from Institute Of Medicine, Tribhuvan University, Kathmandu, Nepal. I had worked as Lecturer in Department of Neuropsychiatry, B&C Medical college Teaching Hospital and Research Centre, Birtamode, Province 1 (April 2018- September 2020) and thereafter currently started Psychiatry services in Regional Community Hospital. My professional interests focus on addiction psychiatry, community Psychiatry and Researches. I am fluent in Nepali, English and Hindi. I have done my thesis on “Disulfiram and Naltrexone for Relapse Prevention in Cases of Alcohol Dependence Syndrome” (MD Psychiatry 2017) and few publications in national and international journals. I am also selected as Trainer in WHO E-mhGAP project (Emilia). I am lifetime member at Psychiatrists’ Association of Nepal (PAN).

  • Antwerp University Hospital, Belgium
  • Title:The Clinical and Genetic Spectrum in Infants with (an) Unprovoked Cluster(s) of Focal Seizures
  • Time :

Abstract

Self-limited (familial) infantile epilepsy (S(F)IE), formerly known as benign (familial) infantile convulsions (B(F)IC), is an infantile cluster epilepsy with in rule a complete recovery. It is one of common self-limited epilepsy syndromes affecting children. This large group includes benign syndromes like epilepsy with centrotemporal spikes (‘rolandic epilepsy’), Panayiotopoulos syndrome, and the occipital epilepsies (Gastaut and photosensitive types). Landau-Kleffner is a not always benign form.
In self-limited epilepsy syndromes, there is evidence there is both a role for oligogenic and polygenic component in self-limited focal epilepsies. Recently, in 20 out of 57 patients rare candidate variants were identified with typical or atypical self-limited focal epilepsies in childhood.
We analysed a cohort of 23 patients from 21 families, all with an initial diagnosis of self-limited infantile epilepsy. In 12 individuals a pathogenic variation in PRRT2 gene or complete deletion was identified. Pathogenic variants in PCDH19 and KCNQ2 were found in respectively 3 and 1 individuals. One individual had a non-pathogenic variant in ATP1A3 and in 6 others no variants were identified. Most had only one cluster of seizures. We conclude that most children with unprovoked clusters of focal seizures carry a PRRT2 mutation. When clusters reoccur frequently, when seizures are more therapy-resistant and when seizures persist beyond the age of 2 years, another diagnosis or causative gene (than PRRT2) is likely.

Bibliography

1.A. van Roest, A. Van de Vel, D. Lederer, B. Ceulemans, The clinical and genetic spectrum in infants with (an) unprovoked cluster(s) of focal seizures, Eur. J.Paediatr. Neurol. (2019 Dec 13),
2.G. Rudolf, J. de Bellescize, A. de Saint Martin, et al., Exome sequencing in 57 patients with Self-limited focal epilepsies of Childhood with typical or atypical presentations suggests novel candidate genes, Eur J Ped Neurol (2020) Volume 27, July 2020, Pages 104-110

  • Ben-Gurion University of the Negev, Israel
  • Title:New Model to Induce Diffuse Axonal Brain Injury in Adult Rats.
  • Time :

Abstract

Introduction: Traumatic brain injury (TBI) is one of the major causes of death and disability. Diffuse axonal injury (DAI) is a widespread axonal damage developed after TBI. A rapid axonal stretch injury triggers secondary axonal changes that can vary in extent and severity. The most vulnerable areas are the brainstem, thalamus, parasagittal white matter of the cerebral cortex, corpus callosum. Immunohistochemically analysis of beta-amyloid precursor protein (βAPP) accumulation is currently the gold standard clinical and experimental technique for assessment of DAI. The objective of the present study was to develop a simple reproducible, reliable model that will cause widespread white matter damage without additional skull fractions and contusions.
Methods: 30 adult male Sprague-Dawley rats weighting 350-400 gr were randomly divided in the DAI (n=15) and control (n=15) groups. The rat lateral head rotation device was used to turn the head rapidly from 0 to 90° in the coronal plane. Force applied for animal’s heads was equal for all rats. At 48 hours after injury the brains of all rats in injury and control groups were removed and evaluated for existence DAI by immunochemical staining of βAPP. 48 hours after injury was performed NSS assessment for all rats. Results: Representative photomicrographs of brains tissue sections revealing axonal and neuronal immunoreactivities following isolated diffuse axonal brain injury in rats after 48 hours post injury (section in thalamus). Small cellular strains were detected with βAPP. Rats after DAI has been developed neurologic deficits 48 hours ago after injury.
Conclusion: In the present study we developed a simple reproducible, reliable DAI model based on rotational acceleration that caused widespread white matter damage without additional skull fractions and contusions.

Biography

Academic Education: M.D 2001 – 2007 Shevchenko Moldavian State University Faculty of Medicine; PHD 2018 – presented at Ben Gurion University in Negev, Beer Sheva, Title: “The effect of blood glutamate scavenging by pyruvate on long – term behavioral patterns after acute brain injuries in rats”.
Professional Training: 2007–2009 Therapy Residency, Republican Clinical Hospital, Tiraspol, Moldova; 2012-2017 Anesthesia Residency, Soroka University Medical Center, Beer Sheva, Israel.
Employment History: 2017 – present Attending in Department of Anesthesiology, Soroka University Medical Center, Beer Sheva, Israel.
Academic Appointments: 2018-2019 Clinical Instructor, Division of Anesthesiology, Soroka University Medical Center, Ben Gurion University of the Negev, Beer Sheva, Israel. 2019 – present Lecturer. Division of Anesthesiology and Intensive Care, General Intensive Care Unit, Soroka University Medical Center Faculty of Health Science, Ben Gurion University of the Negev Beer Sheva, Israel.
Educational Activities: 2015 – 2016 Pharmacist course, 4 years. Ben Gurion University of the Negev, 2017 – present Medical Student course, 6 years. Ben Gurion University of the Negev, 2018 – present Anesthesiologist resident course. Ben Gurion University of the Negev.

  • Cedars-Sinai Medical Center, Canada
  • Title:Identification and Management of Cerebrospinal Fluid Leak after Lumbar Total Disc Replacement
  • Time :

Abstract

Lumbar total disc replacement (TDR) is an increasingly common intervention for discogenic back pain, particularly in the younger patient where motion preservation is paramount. This procedure however is not without complications. A CSF leak after lumbar TDR is rare; as such there is a paucity of literature regarding the operative approach to this uncommon pathology. Identification of the CSF leak is the primary step toward successful repair. Multiple modalities may be required such as MRI, CT myelogram, or digital subtraction myelogram (DSM). Successful CSF leak after lumbar TDR may range from simple procedures such as epidural blood patching or lumbar drain, while more significant dural injuries may require repeat operative intervention. Repeat surgery may involve transdural repair or additional measures such as replacement with an alternative implant and primary repair of the leak.

Bibliography

Julie L. Chan is currently a Neurosurgery Resident at Cedar-Sinai Medical Center. She received her B.S. in Neurobiology from the University of California, Irvine and her M.D.-Ph.D. in Neuroscience from the Medical College of Virginia. Her clinical and research interests include spinal deformity and spine outcomes.

  • SUNY Downstate Health Sciences University, USA
  • Title:Early Levetiracetam Treatment Prevents the Development of Evoked and Spontaneous Epileptiform Discharges In In Vitro and an In Vivo Model of Cortical Neurotrauma: Clinical Implications
  • Time :

Abstract

Traumatic brain injury (TBI) is a major public health problem and a significant cause of epilepsy worldwide. Effective interventions to prevent post-traumatic epilepsy have proved elusive, in part because TBI is a complex and heterogeneous condition. Our research group has studied 2 rat models of TBI associated epileptogenesis, the in vitro traumatized slice and the in vivo controlled cortical impact (CCI) model. This presentation will describe our recent investigations into the antiepileptogenic efficacy of the pyrrolidine antiseizure drug, levetiracetam (LEV) may prevent epileptogenesis after TBI.
In vitro studies were conducted on traumatized slices of rat neocortex (P21-32) that were prepared using published methods. Randomly selected traumatized slices were treated with clinically correlated concentrations of LEV added to the bath for 1 hour starting immediately after the injury or after a delay of up to 80 min. Treated and untreated slices were examined for epileptiform activity using intra- and extracellular recordings. For the in vivo model, rats (P24-32) were subjected to non-penetrating focal CCI using published methods. Immediately after injury the injured rats were then given a single dose of either LEV or the saline vehicle intraperitoneally. Ex vivo neocortical slices were prepared 2-3 weeks after CCI and examined for epileptiform activity. The results from the in vitro traumatized slice experiments showed that LEV treatment within 60 minutes of injury significantly reduced the proportion of slices that exhibited stimulus-evoked epileptiform activity by more than 50%. LEV treatment also increased the stimulus intensity required to trigger epileptiform bursts by 2-4 fold. Consistent with these findings, in vivo LEV treatment of CCI-injured rats significantly reduced the percentage of animals that exhibited spontaneous and stimulus-evoked epileptiform bursts compared to saline-treated controls. In addition, LEV also significantly increased the stimulus intensity required to evoke epileptiform bursts in slices prepared from CCI-treated animals. These results suggest that early administration of LEV has the potential to prevent or reduce posttraumatic epileptogenesis and highlights that there may be a narrow time window for successful therapeutic intervention. The challenges of using animal models for human epileptogenesis, the clinical implications and limitations of these two models of posttraumatic epileptogenesis, and potential strategies to address prevention or mitigation of post-traumatic epilepsy will be discussed.

Biography

I am a Professor of Clinical Neurology at SUNY Downstate Health Sciences University and the Chief of the Neurology Service at H+H Kings County Hospital. As a clinician-scientist I travel between the clinical and research worlds, now often by virtual means. For the past 15 years I have served as the Chief of the Neurology Service in the second largest public hospital in the United States. I have also been a Residency Program Director for Adult Neurology and an educator of residents, fellows, medical students, attending physicians, nurses, nurse practitioners, EEG technicians, EMTs, patients, and patients’ families. At Kings County Hospital we have a developing neuroscience center which, in partnership with SUNY Downstate Health Sciences University includes a neuroscience research program We have participated in the NETT, SIREN, and Neuro NeXT networks.
My recent publications include:

  • Google Health, USA
  • Title:Deep Learning in Ophthalmology
  • Time :

Abstract
The application of deep learning in healthcare has sparked tremendous interest in recent years in the fields of image recognition, speech recognition and natural language processing. This talk will cover basics of machine learning for the clinician, and discuss the potential of machine learning to empower physicians and improve healthcare through examples of models trained to detect diseases in medical images. This talk will include
examples from ophthalmology as well as other fields of medicine, focusing on algorithms for the detection of eye diseases and other health related signals from fundus photographs.

Biography Naama is a clinical research scientist in Google Health. In this role she focuses on
developing machine learning models for the detection of ocular and systemic diseases from medical images. Naama is an ophthalmologist with a subspecialty in glaucoma. She completed her medical and ophthalmology training at Tel-Aviv University; her glaucoma fellowship at the Shiley Eye Institute, UC San Diego; and her ophthalmic informatics
fellowship at the UC Davis Eye Center

  • University of Heidelberg, Germany
  • Title:Physical Activity, Oxidative DNA Damage, Colorectal Cancer Risk and Type 2 Diabetes
  • Time :

Abstract

Clinical and epidemiologic studies convincingly have demonstrated that type 2 diabetes (T2D) is associated with an elevated risk for colorectal cancer (CRC) and that outcomes and disease course of CRC are worse in T2D; posing particular challenge to prevention and management strategies. There is sufficent evidence accumulated over the last three decades, that non-pharmacologic approaches such as physical acticvtiy (PA) and exercise intervention (EI) may have clincally beneficial effects in terms of decreased cancer risk and improved outcomes in cancer patients, but further improving those strategies needs a better understanding of underlying mechanisms of action. To quantify tumor risk (including CRC) highly sensitive biomarkers modifiable by PA/EI have been proposed among them 8-oxo-2‘-deoxyguanosine (8-oxo-dG) reflecting DNA damage due to oxidative stress and found to be elevated in many metabolic, inflammatory and malignant disease conditions. The first aim of this lecture is to further define their clinical relevance by comparing urinary excretion in groups with different CRC-risk such as patients with T2D (moderate risk) and those with curatively treated CRC (high risk for recurrence). The second aim is to present more evidence concerning beneficial effects of PA/EI in terms of modification of those risk biomarkers. In our recently published study we found that urinary excretion of 8-oxo-dG was significantly elevated in T2D compared to healthy controls (average risk), but lower than in patients with curatively treated CRC who showed the highest levels. In addition, there was a positive correlation of urinary 8-oxo-dG excretion with the body mass index (BMI) in all study participants (p=0.04) suggesting that beneficial effects of PA/EI are mediated predominantly by concomitant weight reduction. The great majority of interventional studies including a previous study from our institution have shown that EI with moderate intensity is associated with decreased urinary excretion of 8-oxo-dG in the range of 20 to 30 percent, whereas high intensity EI was linked to elevated levels; these effects were found to be accompagnied by simultaneous enhancemant of antioxidant defenses at the humoral, cellular and epigenetic level. A first clinical application of our results would be the implementation of biomarker data into CRC risk prediction models to improve accuracy and hence prevention stategies, the second would be improving patient management by biomarker-giuded tailoring of individual exercise programs (moderate intensity) in risk groups such as patients with T2D.

Biography

Prof. Allgayer, born in 1948 received a Biology degree from the Technical University of Munich and graduated as an MD from Medical School, University of Munich in 1978. After residency in Internal Medicine and specializing in gastroenterology he was a postdoctoral fellow at Washington University, St. Louis, Mo. USA. He was Head of the Gastroenterology and Metabolism Department at the Klinik Ob der Tauber, Bad Mergentheim, Academic Teaching Hospital, University of Heidelberg, Germany until his retirement in 2013. Presently he is a Consultant in Gastroenterology and Diabetology at the Hartwald Klinik, Rehazentrum Bad Brückenau, Deutsche Rentenversicherung Bund, Germany. The focus of his research interest were clinical (ultrasound, endosonography) and pharmacologic studies of mechanisms of action of antiinflammatory drugs in inflammatory bowel disease and more recently, investigations of clinical and molecular effects of life style interventions (physical activity, exercise) as important aspects of cancer prevention (e.g. colorectal cancer) in patients at risk such as type 2 diabetes based on the concept of sensitive and modifiable tumor risk biomarkers. This research involved a close cooperation with the German Cancer Research Center (DKFZ), Heidelberg, Germany over a time period of more than one decade. Prof. Allgayer is member of various national and international medical and scientific societies among them the American Gastroenterology Association (AGA) and is a Fellow of this society (AGAF).

  • Ariel University, Israel
  • Title:Intensity-Dependent Effects of Exercise Training in Experimental Multiple Sclerosis
  • Time :

Abstract

Background: Exercise training (ET) has beneficial effects in Multiple Sclerosis (MS)patients and in experimental autoimmuneencephalomyelitis (EAE), the animal model of MS. However, the intensity-dependent effects of ET on the systemic immune system and/or the central nervous system (CNS) remain undefined.
Purpose: To compare the systemic immune-modulatory- and direct neuroprotectiveeffects of moderate vs. high intensity ET protocols on EAE development.
Methods: Healthy mice performed moderate- or high-intensity treadmill runningprograms. Proteolipid protein (PLP)-induced transfer EAE was utilized to enable differentiation between effects of ET on systemic autoimmunity vs. direct effects on the CNS. To investigate the immune-modulatory effects of ET, lymph-node (LN)-T cells from trained- vs. sedentary donor mice were transferred to naïve recipients. EAE severity in recipient mice was assessed by clinical assessment and histopathological analysis. LN-T cells derived from donor trained vs. sedentary PLP-immunized mice were analyzed in vitro for proliferation by flow cytometry analysis, and for cytokine and chemokine receptor gene expression using real-time PCR. To investigate the neuroprotective effects of ET, PLP-reactive, encephalitogenic T cells were transferred into recipient mice that underwent the training program prior to EAE transfer, and disease severity was compared to that in recipient sedentary mice.
Results: High-intensity training in healthy donor mice induced significantly greater inhibition than moderate-intensity training on proliferation and generation of encephalitogenic T-cells in response to PLP-immunization, and on EAE severity upon their transfer into recipient mice. Additionally, whereas moderate intensity ET did not have direct neuroprotective effects, transfer of PLP-reactive, encephalitogenic LN-T cells resulted in less severe EAE in recipient mice that were subjected to high intensity training program prior to EAE transfer.
Conclusions: Our data, obtained by using a unique experimental design, indicate superior effects of high intensity training on both systemic immune-modulation and direct neuroprotection to inhibit autoimmunity in EAE. This study is of clinical significance and may provide a basis for defining exercise recommendations (that are currently lacking) for MS patients.

Biography

Prof.Ofira Einstein graduated physical therapy school in 1999 (B.P.T.) and doctorate studies in neurobiology in 2006 (Ph.D.). She joined as a faculty of the Physical Therapy department at Ariel University in 2009 and served as the head of the department in years 2011-2017. Prof. Einstein’s research areas are neuro-immunology and neuroregeneration. Her first studies concerned on the neurobiology of neural stem cells and cell therapy, specifically on animal models of human Multiple Sclerosis (MS). Her work published in 2003 was the first to show that transplanted neural stem cells have anti-inflammatory effects on the rodent brain. This finding was a breakthrough for further research of her group, as well as other research groups around the world. Her current research focuses on neuro-immunological, neuro-protective and neuroregenerative effects of exercise training on neuro-inflammatory and neuro-degenerative diseases. These studies are particularly carried on experimental autoimmune encephalomyelitis (EAE), the animal model of MS. Prof. Einstein’s studies involve animal physical training, clinical evaluations, histopathological analyses, cell cultures and molecular biology techniques.

  • Inra Research Centre, France
  • Title:Stunning and Slaughter Techniques: Neurological Mechanisms and Indicators of Consciousness and Unconsciousness
  • Time :

Abstract

At slaughter, animals are generally stunned before bleeding, but society and field workers sometimes question efficacy. Recently, work was undertaken to understand better the neurobiological mechanisms involved in the stunning and killing process of animals. The mechanisms underlying the loss of consciousness depend on the technique used: mechanical, electrical or gas stunning. Direct exsanguination without prior stun, for religious slaughter, causes also a loss of consciousness, before inducing death. Stunning techniques use stun guns, electrified devices or gas mixtures. The principles of stunning and bleeding involve mechanical shock waves and the mechanical destruction of neurons, electrical fields, the reduction or arrest of cerebral blood circulation, or high and/or low levels of CO2 and/or O2, respectively, in inspired air. Effects involve cerebral anoxia or ischemia, the depolarisation, acidification and/or the destruction of brain neurons. Targeted brain structures are the reticular formation, the ascending reticular activating system or thalamus, or the cerebral hemispheres in a general manner. Some of the techniques induce an immediate loss of consciousness, other techniques a progressive loss of consciousness.
To ensure that the animal is unconscious, before further processing, indicators of consciousness and of unconsciousness are verified. They evaluate different aspects of cerebral functioning. As they are imprecise, it necessary to monitor several. As animals may regain consciousness, they are observed until the end of bleeding. Animals are considered unconscious if signs of consciousness are absent, and signs of unconsciousness are present.
Examples of indicators of unconsciousness are the absence of standing posture and of righting movements, the absence of a corneal reflex and respiratory arrest. Indicators of consciousness are the standing posture, coordinated righting movements, specifies-specific vocalizations and a response to the threat test. Often various movements are observed following the stun and during bleeding, including eye tracking, eyeball rotation, nystagmus, head and neck movements and leg paddling. Their presence often leads to confusion on the field as they may be reflex movements, but sometimes they indicate consciousness. Their interpretation needs further discussion.
The techniques used to diagnose brain death in humans cannot be used in the slaughterhouse. Under field conditions, at the end of bleeding, the absence of breathing and of brainstem reflexes and the adequacy of the exsanguination are verified. If these three aspects are confirmed, in the context of the slaughterhouse and at this stage of the slaughter process, the loss of vital functions is irreversible and the animal considered dead.

  • Dankook University College of Medicine, Kore
  • Title:Endovascular Treatment with Stents in Ruptured Complex Aneurysms
  • Time :

Abstract

Stent using in intracranial aneurysms has been avoided by most operators because of concerns about the risk of using dual antiplatelet therapy in the setting of acute SAH.
In case of posterior communicating artery aneurysm with fetal type artery incorporated on aneurysm or broad necked appearance, it was regarded as very difficult to treat endovascularly. However with intracranial stenting maneuver introducing recently, it can be treated completely by retrograde navigation of stent through anterior communicating artery and further coiling with staged approach.
And flow diverters also play important role to treat aneurysms.
The author introduces several technical extensions to overcome the pitfalls in treating the intracranial
complex aneurysms.

Biography

Young Joon Kim, Korean neurosurgeon, educator. Achievements include research in endovascular aneurysm coiling with stent & endovascular care of acute stroke. Member of Korean Society Neurosurgery (board directors since 1998), Korean Society Intravascular Neurosurgery (president 2002-2004).

  • Ozel Bağlar Hospital, Turkey
  • Title:COVID-19: Endogenous Retinoic Acid Theory and Retinoic Acid Depletion Syndrome
  • Time :

Abstract

This study presents two new concepts and definitions to the medical literature. One of those is “endogenous retinoic acid theory” and the other “retinoic acid depletion syndrome”. A new classification will be provided for the immune system. “retinoic acid-dependent component” and “retinoic acid non-dependent component”. If this theory is verified, all the diseases where the retinoic acid metabolism is defective and retinoic acid levels are low will be identified and new approaches will be developed fortreating such diseases. When the need for retinoic acids increases, such as acute infection, high fever, severe catabolic process, or chronic antigenic stimulation, cytochrome P450 monooxidase enzymes are inhibited by drugs or internal mechanisms. Metabolism and excretion of retinoic acids stored in the liver are prevented. In this way, retinoic acid levels in the blood are raised to therapeutic levels. This is called “Endogenous Retinoic Acid Theory”. Retinoic acids also manage their metabolism through feedback mechanisms. Despite compensatory mechanisms, causes such as high fever, serious catabolic process and excessively large viral genome (SARS-CoV-2), excessive use of RIG-I and Type- I interferon synthesis pathway using retinoic acid causes emptying of retinoic acid stores. As a result, the RIG-I pathway becomes ineffective, Type-I IFN synthesis stops, and the congenital immune system collapses. Simultaneously, the immune mechanism crosses the TLR3, TLR7, TLR8, TLR9, MDA5 and UPS pathways in monocyte, macrophage, neutrophil and dendritic cells of the adaptive immune defense system that do not require retinoic acid. This leads to excessive TNFα and cytokine discharge from the pathway. With the depletion of retinoic acid stores as a result of this overuse, the immune defense mechanism switches from the congenital immune system to the adaptive immune system, where retinoic acids cannot be used. As a result of this depletion of retinoic acids, the shift of the immune system to the NFκB arm, which causes excessive cytokine release, is called “retinoic acid depletion syndrome”. COVID-19 and previously defined sepsis, SIRS and ARDS are each retinoic acid depletion syndrome. We claim that retinoic acid metabolism is impaired in autoimmune and other chronic inflammatory diseases, and therefore the RIG-I pathway and UPS degradation system are not working properly. Endogenous retinoic acid metabolism is defective in COVID-19 (cytokine storm), sepsis, SIRS, ARDS, severe viral and bacterial infectious diseases, chronic autoimmune diseases and degenerative neurological diseases. This pathogenesis explanation brings a new perspective and treatment approach to this type of disease.

  • University of New South Wales, Australia
  • Title:Cerebral Cortex of Diprotodontids- A Quantitative Analysis and Comparison with the Eutherians
  • Time :

Abstract

The Diprotodontids which are a highly successful group of Australian metatherians with a strikingly diverse range of ecological niches from nectar and pollen feeders to grazers and folivores. They range from a small- brained nectar feeding species (Tarsipes) to the large-brained grazing and browsing species (macropods). Their diversity in all aspects of their life provides an opportunity to examine and analyse how the cerebral cortex has expanded in an adaptive radiation quite independent of that occurring among eutherians. We have used the Nelson Brain collection and online resources to perform a quantitative analysis of the isocortex, hippocampal formation and olfactory structures in diprotodontids. The scaling relationship between iso- and periallocortical grey matter and brain size, and between subcortical white matter and iso- and periallocortex grey matter, are both almost identical among diprotodontids and eutherians. By contrast, the relationship between gyrification and brain size is strikingly different between diprotodontids and eutherians, with gyrification being much lower for a given brain size among the diprotodontids, although gyrification is much more varied among macropods than other diprotodontids. The scaling of iso- and periallocortical volume with dorsal striatal and dorsal thalamic volume is almost identical among the diprotodontids and eutherians, but the claustrum is smaller, and amygdala larger, for a given brain size among diprotodontids than eutherians. The hippocampal formation and central olfactory areas (anterior olfactory region and piriform cortex) both scale more steeply with brain size among diprotodontids compared to eutherians. Our findings suggest that, although white matter scaling is identical among all therians, there are significant differences between diprotodontids and eutherians in the way that cortical folding and expansion of allocortical structures occurs with brain enlargement.

  • University of Missouri, Columbia
  • Title:Enhanced Recovery: Post-Operative Delirium and Potential Interventions
  • Time :

Abstract
Enhanced recovery programs have been developed to improve patient’s post-operative outcomes through pre-op education and preconditioning, modification of anesthetic techniques intraoperatively and multimodal pain management techniques post-operatively. The overall goal of these protocols is to decrease the use of medical interventions and time in the hospital. With a growing elderly population requiring surgical intervention, the impact of post-operative delirium and cognitive dysfunction is a growing problem and significantly increases the cost of care. The collaborative efforts of Neurology and Anesthesiology to identify patients who are at risk and modify anesthetic techniques are the next evolution for enhanced recovery protocols to improve patient outcomes and increase efficient delivery of care.

Biography

Quinn L. Johnson, MD, MBA is the Chair of the Department of Anesthesiology at the University of Missouri-Columbia, and serves as the Russel B. and Mary D. Sheldon Professor in Anesthesiology. He also serves as adjunct faculty in the School of Business where he teaches management classes on healthcare as it relates to business. Clinically he has advanced training in acute pain management and ultrasound guided regional nerve block techniques. Clinically he works at the Missouri Orthopaedic Institute. He recently served as the president of the Missouri Society of Anesthesiology and is currently a member of the American Society of Anesthesiology’s committee on Academic Anesthesiology. He has received grants, published and presented in numerous journals and conferences, on a variety of topics including enhanced recovery and post-operative delirium in the elderly.

  • Brigham and Women’s Hospital, USA
  • Title:How Self-Reported Hot Flashes May Relate to Affect, Cognitive Performance and Sleep
  • Time :

Abstract

Purpose: To explain the controversy about whether midlife women who self-report hot flashes have relatively increased affective symptoms, poor cognitive performance or worse sleep. Methods: Retrospective data from 88 women seeking relief from bothersome day and night hot flashes were submitted to mixed linear regression modeling to find if estimated hot flashes, as measured by Women’s Health Questionnaire (WHQ) items or diary-documented hot flashes recorded daily were associated with each other or with affective, cognitive or sleep measures. Results: Subjects averaged 6.3 daytime diary-documented hot flashes and 2.4 nighttime diary-documented hot flashes per 24 h. Confounder-controlled, diary-documented hot flashes but not estimated hot flashes were associated with increased Leeds anxiety scores (F = 4.9; t = 2.8; p = 0.01) and Leeds depression scores (3.4; 2.5; 0.02), decreased Stroop Color–Word test performance (9.4; 3.5; 0.001), increased subjective sleep disturbance (effect size = 0.83) and increased objective sleep disturbance(effect size = 0.35). Hot flash effects were small to moderate in size. Univariate but not multivariate analyses revealed that all hot flash measures were associated with all affect measures. Different measures of hot flashes associated differently with affect, cognition and sleep. Only nighttime diary-documented hot flashes consistently correlated with any affect measures in multivariate analyses.
Conclusions: Reported inconsistencies in menopause study outcomes may be due to the use of differing measures for hot flashes, affect, cognition and sleep. This problem impedes forging a consensus on whether hot flashes correlate with neuropsychological symptoms.

Biography

Quentin Regestein is a clinician-researcher interested in menopause and transcranial brain stimulation. He currently develops applications to improve US health care delivery.
Joan Friebely’s research has focused on menopause’s psychological effects and second-hand smoking.
Isaac Schiff is a clinician-researcher who has done prize-winning menopausal research. He co-founded founded the North American Menopause Society and is Editor-in-Chief of the journal Menopause.

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