Biography:

Aliaksandr Haretski is the rector of the European Academy of Folk Medicine, Professor of the department of neurology of the International University of Science in Hannover, Germany, Doctor of naturopathy /complementary medicine of the Institute for Interdisciplinary Studies in Hannover, Germany. He is the director of the Body Regeneration Center of EAFM, Poland. He published more than 20 articles in reputed journals. He is the author of the book “A practical guide to rejuvenation and complete healing of diseases and cancer”.

Abstract:

The method of nervous system regeneration is a universal integrated method based on the use of more than 40 of our developments know-how. It is able to mobilize human abilities and make the human body restore itself. The unique advantage of the method is the absence of contraindications and adverse side effects. This method helps us not only halt the disease progression but restore lost body functions. Many patients with various chronic incurable and even genetic diseases, such as cancer, Parkinson’s disease, MS, ALS, ICP, fibromyalgia, CFS, all types of myopathy, atrophy and muscle dystrophy, undergo their treatment successfully in our center. The use of this method allow us to have an integrated impact on the whole body at once rather than on its separate damaged parts, cleanse the body of toxins, eliminate the main causes of a disease, boost immunity, provide the body with nutrients to fight against diseases, launch the mechanisms of body regeneration and self-healing in patients with various diseases practically at any age. When stimulating the immune system, the body starts to produce a large number of its own stem cells. Old damaged cells will be completely replaced with new ones in organs in a very short time. Scar tissue cells will be transformed into new healthy cells in damaged organs. As a result all organs will be completely revived again without any surgery. The unique results of treatment achieved by our patients many times are the best proof of the efficiency of this method.

Biography:

Leandro Bueno Bergantin has received his academic education from UNIFESP-EPM (Brazil) and did his MSc (2010) and PhD (2014) degrees in Biomedicine. His research involves cell signaling mediated by Ca²⁺ and cAMP, skeletal and smooth muscles, peripheral and central nervous systems. His research work solved the enigma of the paradoxical effects produced by L-type Ca²⁺ channel blockers. He is currently a Post-doctoral fellow (FAPESP) at UNIFESP-EPM.

Abstract:

The hypothesis of the so-called calcium paradox phenomenon in the sympathetic neurotransmission has its origin in experiments done in models of neurotransmission since 1970´s. Historically, calcium paradox originated several clinical studies reporting that acute and chronic administration of L-type Ca²⁺ channel blockers (CCBs), drugs largely used for antihypertensive therapy such as verapamil and nifedipine, produces reduction in peripheral vascular resistance and arterial pressure, associated with a paradoxical sympathetic hyperactivity. Despite this sympathetic hyperactivity has been initially attributed to adjust reflex of arterial pressure, the cellular and molecular mechanisms involved in this paradoxical effect of the L-type CCBs remained unclear for four decades. Also, experimental studies using isolated tissues richly innervated by sympathetic nerves showed that neurogenic responses were completely inhibited by L-type CCBs in high concentrations, but paradoxically potentiated in low concentrations, characterized as a calcium paradox phenomenon. We discovered in 2013 that this paradoxical increase in sympathetic activity produced by L-type CCBs is due to Ca²⁺/cAMP interaction. Then, the pharmacological manipulation of this interaction could represent a potential cardiovascular risk for hypertensive patients due to increase of sympathetic hyperactivity. In contrast, this pharmacological manipulation could be a new therapeutic strategy for increasing neurotransmission in psychiatric disorders such as depression, and producing neuroprotection in the neurodegenerative diseases such as Alzheimer´s and Parkinson´s diseases.

Biography:

Xagara Anastasia completed her degree in Biology at the University of Ioannina (Greece), Department of Biological Applications and Technologies (5-years, 300 ECTS). She is currently a PhD candidate in the Department of Biomedical Research, Institute of Molecular Biology and Biotechnology- Foundation for Research and Technology (FORTH/BRI), under the supervision of Assoc. Prof. Theologos Michaelidis. Her research is focused on the analysis of neuro-immune interactions that take place in human CNS and PNS and their significance for the development of neurological disorders.

Abstract:

The immune and nervous systems interact both at the cellular and molecular level, and share significant similarities in essential mechanisms and signaling pathways. IFN-γ, a cytokine that belongs to type II interferons, plays crucial role in innate and adaptive immunity whereas its aberrant expression/activity has been associated with a number of autoimmune diseases. IFNγ can enhance neurogenesis in the hippocampus of adult mice, by unknown mechanisms, possibly involving coordination between brain inflammation and repair, and can also modulate neurotransmitter release at synapses and affect memory, thereby revealing an important role of this immunological effector for the function of the adult nervous system. Using neuroblastoma cells, we are currently analyzing the influence of neuroinflammatory components in the process of aberrant activation of key signaling pathways involved in cellular proliferation and neuronal differentiation as well as in cellular heterogeneity, a hallmark of neuroblastoma which is observed in both tumors and tumor-derived cell lines. We found that IFNγ reduces neuroblastoma cell proliferation by delaying progression through the S phase of the cell cycle. Concomitantly, it promotes molecular and morphological features of early neuronal differentiation as revealed by the extended neurite outgrowth, increased formation of varicosities, and induction of specific neuronal differentiation markers. Our data also showed that chronic treatment with IFNγ alters the program of retinoic acid-induced differentiation, leading to an induction of large, nestin+, Schwann-like (S-type) cells, known to influence the biology of the adjacent neuroblastic (N-type) cells, suggesting that immune components may contribute to the phenotypic heterogeneity and tumorigenicity of neuroblastoma.

Biography:

Sushil Razdan, MBBS, MD, DM(Neurology), Honorary Professor, Acharya Shri Chander College of Medical Sciences, Sidhra, Jammu, Jammu & Kashmir, India

Abstract:

Vitamin D is increasingly recognized to have beneficial effects in several inflammatory conditions and there is some evidence to suggest that it is associated with a reduced risk of various internal malignancies, aside from its classic physiologic effects on calcium metabolism and bone homeostasis. Although vitamin D toxicity is thought to be extremely rare, and an extremely rare cause of hypercalcemia, food and nutrition board guidelines specify 2000IU as highest vitamin D intake that healthy adults can consume daily without risking hypercalcemia. For many people the word “vitamin” implies something that is beneficial, essential and not potentially poisonous. But,Vitamin D is toxic in large doses and sporadic reports of vitamin D toxicity exist in literature. We report a case series of fifteen patients with symptomatic hypercalcemia in whom toxicity occurred due to excessive administration of vitamin D by oral and parenteral route. The most frequently noted clinical manifestations in these patients was altered sensorium. In the present study we report a case series of 15 patients, nine women and six men, aged between 42–85 years who presented to the Department of Medicine, Acharya Shri Chander College of Medical Sciences and Hospital, Jammu, Jammu and Kashmir between December 2009 and September 2011. All patients were residents of Jammu and Kashmir. All the 15 patients had symptoms attributable to hypercalcemia with elevated serum calcium and serum 25-hydroxy vitamin D3 levels. All the 15 patients were suffering form hypervitaminosis D

Biography:

Ute-Christiane Meier completed her PhD at the University of Oxford, where she worked on the cytotoxic T-cell control of HIV infection. She continued her studies on persistent virus infections and immunotherapeutic cancer vaccine-strategies within Oxford University, the Edward Jenner Institute and British Biotech in Oxford. She started working in Neuroimmunology in 2007 at the Blizard Institute London. In 2012 she was appointed as lecturer in Neuroimmunology. Her main research interest focusses on the role of environmental risk factors in multiple sclerosis, the topic of her Habilitation at the Ludwig-Maximilian-University Munich and more recently on dysregulated immune responses and the role of inflammation in psychiatric disease.

Abstract:

The exact mechanisms underlying neuroinflammation and neuropathology in multiple sclerosis (MS) are still unknown, but susceptibility depends on a combination of genetic and environmental risk factors and their interactions. With little influence on genetic predisposition, the importance of modulating environmental risk factors is becoming an area of great interest. There is mounting evidence implicating both late Epstein-Barr virus (EBV) infection and hypovitaminosis-D as key environmental risk factors in MS. We have previously shown that active white matter lesions in the MS brain show signs of innate immune activation, and that latently EBV-infected cells can be found in these areas. We hypothesized that EBV-RNAs (EBERs) may promote an inflammatory milieu within the lesion. We propose that dysregulated EBV infection may be a potential risk factor and contribute to MS disease activity via the stimulation of innate immune responses by EBERs, and/or antigenic mimicry, cross-reactivity of cellular immune responses with “self” brain antigens or via the transactivation of endogenous retroviruses.

Another potential environmental risk factor in MS is hypovitaminosis-D. Vitamin-D plays an important role not only in bone homeostasis but also in immunity and control of persistent infections. Hypovitaminosis-D, which is a hallmark of MS cohorts, has been associated with disease activity in MS. I will discuss data, which highlights interdependence between EBV- and vitamin-D status in MS. Several vitamin-D supplementation trials are currently underway to test the effect of vitamin-D supplementation on disability progression in MS.

In the final part of my presentation I will focus on psychoneuroimmunology, which studies the interactions between immunity/inflammation and mood, cognition and behaviour. I will discuss novel findings on the role of inflammation and potential environmental risk factors in schizophrenia e.g. hypovitaminosis-D. We propose that an MS-like inflammatory signature may be present in schizophrenia. This area warrants further study as it may highlight novel prevention or treatment strategies.

Biography:

Husham Bayazed has completed his PhD from University of Mosul, College of Medicine. He is now Consultant at the Scientific Research Center, University of Zakho / Kurdistan Region, Iraq. He is specialist in Immunology and has published more than 25 papers in reputed journals and has been serving as scientific reviewers of many local and international medical journals. In addition of being Fellowship of ISC, Infection, Cancer, Immunology Advisory Board Member (EUROMDnet) (Belgium), Membership of World Stroke Organization, Membership of Metabolomics (USA) and Membership of American Association of Science & Technology.

Abstract:

Anti-phospholipid syndrome (APS) is an autoimmune disease. Cerebral ischemia associated with APS occurs at a younger age than typical atherothrombotic cerebrovascular disease, is often recurrent, and is associated with high positive IgG anti-phospholipid (GPL) unit levels. This study sought to determine the frequency rates of anti-cardiolipin (aCL) dependent on the presence of β₂-GPI, anti-β₂-glycoprotein I (aβ₂-GPI) and anti-phosphatidyl serine (aPS) IgG autoantibodies among stroke patients, and thus demonstrate the importance of testing for aβ₂-GPI autoantibodies. For this study, stroke patients and control subjects recruited from Mosul, Erbil and Dohuk provinces in Northern Iraq between March 2004 and March 2005 were evaluated. All cases were under 50 years-of-age and had no recognizable risk factors. Using ELISA to evaluate the presence of IgG isotype of aCL, aβ₂-GPI and aPS autoantibodies in their blood, the results indicated that the frequency of aβ₂-GPI was 14/50 (28%), aCL was 11/50 (22%), and aPS was 9/50 (18%) among stroke patients. In contrast, aCL was detected in 2/30 (6.7%) of control subjects; each of the other anti-phospholipid antibodies (APLA) was never observed. Of all the aβ₂-GPI⁺ cases, the incidence of stroke patients having the combined profile of aβ₂-GPI + aCL was 11/14 (78.6%) and of aβ₂-GPI + aPS was 9/14 (64.3%). Only 2/14 (14.3%) of these aβ₂-GPI⁺ patients, also expressed aCL in the absence of aPS. The frequency of patients expressing all three markers was only 9/14 (64.3%). In none of the APS/stroke patients were aCL or aPS expressed in the absence of the aβ₂-GPI. Conversely, IgG aβ₂-GPI as a sole marker was seen in 3/14 (21.4%) of these patients (i.e. in absence of either other marker). It can be concluded from these studies that the among the three major forms of APLA examined, the presence of IgG aβ₂-GPI autoantibodies appeared to correlate best with stroke in patients who were concurrently suffering APS.

Biography:

José Ochoa USA Resident (1966), Citizen of Chile, national of the European Community (Spain). 50 years of specialized academic Neurology; hundreds of peer reviewed articles, book chapters, and two books; identified two syndromes of neuropathic pain; deconstructed illegitimate “neuropathic pain” disorders; competitive NIH RO1 grant awards since 1982.

Abstract:

Our current IASP President led a distinguished group who, based on science and courage, redefined “neuropathic pain” in 2008, but were reminded that such transparency excluded CRPS-I. Current authorities agree: Past President; rejuvenated IASP taxonomists; (the AMA always agreed)… and now, the E.N.S.? Why? CRPS-I hypothesis (former “RSD” and “SMP) features: there is no structural pathology; no diagnostic test; the “objective signs” are non-specific, often reflect disuse or self-infliction; and some are willful behaviors. Pain experts admit: “for diagnosis we don’t use Evidence… we use our Default Criterion #4…” Because such perversion of the Falsifiability Principle, allowing Scientific diagnosis (Popper), is unfalsifiable (alternative diagnoses not eliminated), it cannot be proven false… it is pseudoscience. The Default position, one that cannot be proven false, also fits the Null Hypothesis which can never be proven correct: the data can only reject… or fail to reject it (Fisher). Items to be presented: • Symptoms, signs and laboratory in “RSD/CRPS”. • S.W. Mitchell excludes the “great sympathetic” from “Causalgia”. • The invention of “RSD” by Evans. • R.Verdugo exposes placebo in faulty “diagnostic sympathetic blocks”: SMP and RSD die. • M.Campero rules out sympathetic activation of C nociceptors in CRPS (microneurography). • Abnormal human nerves as impulse generators’ science. • Neurologists sort true versus Pseudoneurological displays… which are Psychogenic. • “CRPS-I” nick-“diagnosis” by non-neurologists, of pseudoneurological patients: iatrogenic harm. • “Hysterical” versus malingered “CRPS” • What is wrong with the Budapests. This lecture outline will survey sensation, receptor to brain, where Psyche lives.

Biography:

Frederic Haesebaert has completed his MD in 2010, and his PhD in 2013 at the age of 33 years from Lyon University. He is now the head of a department of neuromodulation in psychiatry dedicated to treatment resistant pathologies, in Lyon, and also a reseacher investigating the mechanisms of action of Non Invasive Brain Stimulations (NIBS) in psychiatric populations. He has published more than 10 papers in reputed journals and is the author of book chapters and confrences in this field of psychiatry and neuromodulation .

Abstract:

Auditory hallucinations (AH) are common and disabling symptoms of schizophrenia. Despite prescriptions including adequate pharmacological treatments, about 25% of patients still experience refractory AH symptoms. This epidemiological fact supports the urge need of understanding AH and developping new treatement strategies. Indeed, the pathophysiology of AH is complex and still partially unelucidated. In clinical terms AH correspond to "true" auditory perception in the absence of an auditive stimulus. In a neuropsychological perspective, they are commonly related to a lack of cognitive control over the hearing function. This lack of control leads to perception of self-generated events misattributed to someone else. We present here key findings on brain networks supporting hearing and speech perception involved in the pathogenesis of AH symptoms, drawing perspectives for new treatements. Indeed, our team’s research includes studies at the clinical, neuropsychological and neurophysiological level highliting the role of fronto temporal networks in AH generation. First we will briefly review data of the literature assessing the involvement of temporal and frontal lobes in AH and their pathological interactions with other brain structures in schizophrenic patients with AH. Then we will show how transcranial current brain stimulations (tCS) of fronto temporal network can induce a clinical reduction of AH. Finally we will focus on the mechanisms of action of AH improvement with tCS, investigating biological markers of response.

Biography:

Sedra Mohammadi is pursuing her Medicine from the Urmia University of Medical Science. She is a Member of Student Research Committee of Urmia University of Medical Science since 2014. She has published 2 papers in journals and has been serving as a Redactor of Scientific Journal of Student Research Committee.

Abstract:

Introduction & Aim: A febrile seizure is a neurological disorder that occurs following an infection that results in a rapid rise in body temperature. It commonly affects 3–5% of children between the ages of 3 months and 5 years. There is evidence suggesting that neurological disorders can be exacerbated in an offspring that was exposed to stress prenatally. This study aimed to investigate severity of febrile seizures in prenatally stressed offspring.

Method: In the current study, 158 children under 2 years old with febrile seizure were selected. Information about convulsion including seizure lasting, recurrence of seizure, age of first seizure and type of febrile seizure (simple or complex) were obtained. Questionnaire to evaluate the perceived stress and exposure to major stress during pregnancy was completed.

Results: This finding showed that both high score of perceived stress and exposure to major stress during pregnancy significantly increased seizure lasting and seizure intensity. Exposure to prenatal stress did not have any significant effects on recurrences of febrile seizure and on age of onset of first febrile seizure. Also, appearance of complex febrile seizure was significantly higher in children born from mothers with major-stress exposure compared to unexposed one.

Conclusion: This study indicated that there is a significant positive relationship between both higher perceived stress score and exposure to major stresses during pregnancy with seizure parameters in offspring.