Day1

  • Federal Center of Brain Research and Neurotechnologies, Russia
  • Title:Optimization of MS Care Organization in Countries of Central and Eastern Europe, Including DMTs Biosimilars and gGenerics
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Abstract

Many countries within Central and Eastern Europe are classified as having the highest prevalence of MS. Consistent with the global trend, in the absence of reliable tests or biomarkers, progression at early stage remains undiagnosed. Due to diagnostic uncertainty and lack of a universally accepted disease definition, clinicians rely more on retrospective analysis of the clinical symptoms to confirm the diagnosis. Important problems are the lack of a universally accepted definition for different types of MS, including SPMS, as well as a lack of reliable biomarkers for the condition contribute to diagnostic uncertainty. A poor understanding of the underlying disease mechanisms and difficulty in identifying the early signs of progression make disease management more challenging for clinicians. Frequent follow-up of patients and periodic assessment of progression are recommended for the timely identification of patients transitioning from RRMS to SPMS. Progression is evaluated based on the disability status, as measured mainly by the EDSS, however, assessment of cognitive function is also important for diagnosing and evaluating disease progression, as cognitive impairment heavily influences the lives of MS patients. It is important to perform the cognitive testing from the beginning of the MS course. From a Central and Eastern European perspective, these challenges are further complicated by a longer delay in diagnosis of SPMS and fewer treatment options. Many patients are currently being treated with DMTs not working in progressive course of MS (PPMS and SPMS). The off-label use of DMTs with low effectiveness in patients with delayed diagnosis of SPMS increases the economic burden of MS in these countries. The focus should be on early treatment initiation to delay disease progression. The high cost of DMTS is another important problem in countries of Central and Eastern Europe. This limits the use of several products and decrease the number of patients, who can received DMTs covered by state. One of the possible ways of decreasing cost of MS without losing effectiveness and safety of therapy is the use of biosimilars and generics. In Russian Federation we have a long time positive experience of the use of biosimilars and generics of IFNβ, GA, teriflunomide, DMF and fingolimod, based on the data of clinical comparing studies. The special study studied the attitude of MS patients and MS neurologist to the transfer from original products to biosimilars and generics. The key role of MS specialists if forming the positive attitude and adherence to biosimilars and generics. The future developing of biosimilars and generics without lose of effectiveness and safety of therapy could be one of the important future direction in MS care in Central and Eastern Europe.

Biography
Alexey Boyko gained his MD and PhD from the Russian State Medical University, Moscow and has been Professor of the Department of Neurology and Neurosurgery at this university since 1997. He was the Chief Neurologist of the Department of Health Care of the Government of Moscow in 2001-2015. He works as the Director of the Moscow Multiple Sclerosis Centre and Director of the Institute of Clinical Neurology and Department of Neuroimmunology at the Federal Centre of Brain Research and Neurothechnologies. He was also elected as Honourable Professor of Kazan and Yaroslavl State Medical Universities. He is also a member of the Presidium of the All-Russian Society of Neurologists, Co-ordinator of the Medical Consulting Boards of Moscow and All-Russian MS Societies, President of RUCTRIMS, member of ECTRIMS Council, Member of the Board of the European Charcot Foundation (ECF). It 2017 he was elected as Honored Scientist of Russian Federation. Professor Boyko has published 17 books and more than 900 original publications, he is Co-editor of three medical journals, a member of Editorial Boards of 5 journals, including MSJ and MSRD. The main interest is epidemiology and genetic of MS, neuroimmunology, clinical trials in MS, he is a member of several Advisory Boards of ongoing and finished clinical trials.

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

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

  • CHU Research Center of Quebec-University Laval
  • Title:Insertion of a Protective Icelandic Mutation(A673T) in the APP Gene using the CRISPR/Cas9 Base Editing Technology.
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Abstract

There is currently no treatment for Alzheimer disease (AD). However, the Icelandic mutation in the APP gene (A673T) has been shown to confer a protection against the onset and development of AD 1. This single nucleotide mutation in APP exon 16 reduces the cleavage of the APP protein by the beta-secretase by 40% thus preventing the development of AD even in persons more than 95 years old.
Our research group has initially shown that the presence of the A673T mutation in an APP gene reduced the secretion of beta-amyloid peptides even if there is also a FAD mutation in the gene 2. This is the case for 14 different FAD mutations.
We have used CRISPR/Cas9 base editing and PRIME editing technologies to insert the A673T mutation in the APP gene 3. We have compared several different cytidine base editor complexes to achieve the most effective and accurate genome modification possible in HEK293T cells and in SH-SY5Y neuroblastomas. The insertion of the A673T mutation in cells containing the London mutation reduced the secretion of beta-amyloid peptides.
We are currently using lentiviral vectors to infect neurons from a mouse model and human neurons induced from fibroblasts of a patient with the London mutation.
The insertion of the protective Icelandic mutation in the APP gene using these editing technologies opens a new potential therapeutic avenue not only for Familial Alzheimer’s diseases but also for sporadic Alzheimer’s disease.

Biography
Dr. Jacques P. Tremblay is a professor of the department of Molecular Medicine at Laval university. He is working on the development of cell and gene therapies for hereditary diseases. He has published 292 peer reviewed articles and trained 64 Master degree students, 23 PhD students and 17 post-doctoral fellows.

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

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

  • 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
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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.

  • 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
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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.

  • 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.
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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.

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

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

  • 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
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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.

  • 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~
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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. 

  • 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.

  • 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.

  • 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.

  • 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.

  • 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.

  • 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 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.

 

  • 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 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

  • 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.

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

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.

  • 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.

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

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 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.

  • 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.

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

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

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

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