5^th World Congress on Neurology and Therapeutics March 14-16, 2016 London, UK

Biography:

Safa Shehab has completed his PhD in Sheffield University. He served in several universities in UK including UMIST, Sheffield, Glasgow and Aberdeen before he joined UAE University. He investigates the neuronal circuitry in the dorsal horn of the spinal cord and the neuronal pathways that are likely to be critical in the production and maintenance of the neuropathic pain after peripheral nerve injury. He is also investigating the mechanism of Deep Brain Stimulation. He has published 48 papers in reputed journals.

Abstract:

Rats develop hyperalgesia and allodynia in the hind paw following L5 spinal nerve ligation and transection as seen in human neuropathic pain. Since the skin of the hind paw of the rat is mainly innervated by L4 and L5 nerves, it is assumed that uninjured L4 nerve would be involved in the development of neuropathic pain. Anatomically, we showed that the unmyelinated primary afferents of L5 spinal nerve did not only terminate in the corresponding L5 spinal segment and rather extended to two spinal segments rostrally and one segment caudally where they intermingle with primary afferents of L4 nerve. Subsequently, we demonstrated up-regulations of NPY, VIP and NK1r and down-regulations of SP, CGRP and IB4 binding following L5 nerve injury not only in the dorsal horn of L5 spinal segment where the injured L5 enters, but also extended from L3-L6 spinal segments. To investigate the potential role of adjacent uninjured L4 nerve in heat hyperalgesia, Phosphorylated Extracellular Regulated Kinase (pERK) was used as a pain marker in response to heat noxious stimuli applied to both hind paws following unilateral L5 nerve injury. The results showed that the number of pERK-immunoreactive neurons was significantly higher in the ipsilateral side of L4 spinal segment, which receives innervation from uninjured L4 nerve, compared with contralateral control side which receives both uninjured L4 and L5 spinal nerves. The data demonstrate the role of uninjured L4 nerve in the development of heat hyperalgesia following L5 nerve injury. Two hypotheses on the production and maintenance of peripheral neuropathic pain will be discussed.

Biography:

David Moore is a Post-doctoral research fellow at the Department of Pain Medicine, St James Hospital, Dublin and the Institute of Neurotherapeutics, Dublin City University.

Abstract:

Neuropathic pain poses a significant burden on the individual and society, because of a lack of effective pharmacological therapies. Interventional pain therapies may be more effective in a select cohort of patients. Neuropathic pain results from a lesion or disease of the somatosensory system. Traditionally neuropathic pain was attributed to dysfunctional activity and hypersensitivity of the neuron. However a maladaptive immune response is increasingly recognized as contributing to the maintenance of chronic neuropathic pain. Glial cell activation and altered peptide biosynthesis are implicated in the maintenance of persistent neuropathic pain. Human data suggests that NGF, VEGF and BDNF play a role here. This neuroimmune process is maintained by cellular and neuropeptide biosynthetic responses which become pathological. Intra-thecal opioids and steroids are associated with alterations in cell signaling and the levels of inflammatory mediators at the neuroimmune interface in humans in vivo. Markers of glial and immune cell activity, up-regulated in neuropathic pain states, are down-regulated in spinal cord stimulator patients. Pulsed radiofrequency of the dorsal root ganglion in patients with radicular pain alters CSF lymphocyte subsets and peptide concentrations

Biography:

Hui-Chieh Lee completed his MD from the National Defense Medical University in 1978 and Undersea Medical Officer Training in Groton USA, in 1979. He had served as the Chief , Dept. of Diving Medicine, Zuoying Naval General Hospital, Taiwan for 10 years and became the President of Hyperbaric and Undersea Medical Association, R.O.C. from 2008 to 2012. Currently, he is the Executive Director of Asian-Pacific Undersea and Hyperbaric Medical Society. He has published 30 papers in the Chinese and International Journal.

Abstract:

Neurological decompression sickness (DCS) is a rare condition that commonly leads to spinal cord injury. We report the case of a 30-year-old man who developed left-sided weakness and numbness after diving to a maximum depth of 15 m with a total dive time of 205 min (10 repetitive dives). To the best of our knowledge, only six cases diagnosed as Brown-Séquard syndrome caused by DCS have been reported in the literature. Divers should be aware of the risk factors of DCS before diving and clinicians should make the diagnosis of spinal cord DCS based primarily on clinical symptoms, not on magnetic resonance imaging findings.

Biography:

Mirjana Djukic has completed her PhD in 2001 at the Faculty of Pharmacy at the University of Belgrade. She became a full Professor of Toxicology in 2012. Her research interest has focused on free radicals-mediated mechanism pathways of drugs/poisonings. Accordingly, on oxidative stress-related topics she introduced an optional subject in the faculty study program (2008); wrote (author and editor) two books; published/presented cc 190 papers and has been reviewing articles to reputable journals. She spent two years in the Center for Free Radical and Antioxidant Health (Prof. Valerian Kagan lab) at the University Pittsburgh, USA (2002/3, 2010/11).

Abstract:

Paraquat (PQ) neurotoxicity has not thoroughly investigated. Redox metabolism of PQ2+, results in superoxide anion radical (O2•ï€­) formation. Consequent free radical reactions escalate due to stable resonance radical structure (PQ•+). The OS/NS-associated neurotoxic pathways of PQ were investigated in striatum of Wistar rats after single intra-striatal administration of PQ+ and applied pretreatments, including: N-nitro-L-arginine-methyl ester (L-NAME); 2-amino-5-phosphonovaleric acid (APV); glutathione reductase (GR) and naloxone. Reversible Parkinson’s disease symptoms were observed in PQ group. Contrary to PQ, APV+PQ and GR+PQ groups, initially high O2•ï€­ reached the normal values in L-name+PQ and naloxone+PQ groups, on 7thday. Superoxide dismutase (SOD) activity declined in L-name+PQ, naloxone+PQ and APV+PQ groups. Initially low SOD activity reached normal values on 7th day in Pq and GR+PQ groups. Lipid peroxidation was the highest in PQ, L-name+PQ and GR+PQ groups. Glutathione (GSH) depletion was considerable in L-name, APV and naloxone pretreated rats across the time. Increased GSH values were achieved in PQ and GR+PQ group on the 7th day. Glutathione peroxidase (GPx) activity was inhibited by GR (within 24 hours) and naloxone; elevated GPx activity declined with the time in APV+PQ and L-name+PQ; while it was high in PQ group until the 7th day. In conclusion, inhibitors of NO-synthase, N-methyl-D-aspartate (NMDA) and opioid receptors, reduced SOD and GPx activities and depleted GSH. Rise of O2•ï€­ occurred in APV and GR pretreated groups (twice higher than in PQ group), on 7th day, although APV did not influence LPO.

Biography:

Abstract:

Dietary omega-3 fatty acids have been recognized to improve brain cognitive function. Deficiency leads to dysfunctional zinc metabolism associated with learning and memory impairment. The objective of this study is to explore the effect of short-term dietary omega-3 fatty acids on hippocampus gene expression at the molecular level in relation to spatial recognition memory in mice. A total of 24 male BALB/c mice were randomly divided into four groups and fed a standard pellet as a control group (CTL, n=6), standard pellet added with 10% (w/w) fish oil (FO, n=6), 10% (w/w) soybean oil (SO, n=6) and 10% (w/w) butter (BT, n=6). After 3 weeks on the treatment diets, spatial-recognition memory was tested on a Y-maze. The hippocampus gene expression was determined using a real-time PCR. The results showed that 3 weeks of dietary omega-3 fatty acid supplementation improved cognitive performance along with the up-regulation of α-synuclein, calmodulin and transthyretin genes expression. In addition, dietary omega-3 fatty acid deficiency increased the level of ZnT3 gene and subsequently reduced cognitive performance in mice. These results indicate that the increased the ZnT3 levels caused by the deficiency of omega-3 fatty acids produced an abnormal zinc metabolism that in turn impaired the brain cognitive performance in mice.

Biography:

Abstract:

Dietary omega-3 fatty acids have been recognized to improve brain cognitive function. Deficiency leads to dysfunctional zinc metabolism associated with learning and memory impairment. The objective of this study is to explore the effect of short-term dietary omega-3 fatty acids on hippocampus gene expression at the molecular level in relation to spatial recognition memory in mice. A total of 24 male BALB/c mice were randomly divided into four groups and fed a standard pellet as a control group (CTL, n=6), standard pellet added with 10% (w/w) fish oil (FO, n=6), 10% (w/w) soybean oil (SO, n=6) and 10% (w/w) butter (BT, n=6). After 3 weeks on the treatment diets, spatial-recognition memory was tested on a Y-maze. The hippocampus gene expression was determined using a real-time PCR. The results showed that 3 weeks of dietary omega-3 fatty acid supplementation improved cognitive performance along with the up-regulation of α-synuclein, calmodulin and transthyretin genes expression. In addition, dietary omega-3 fatty acid deficiency increased the level of ZnT3 gene and subsequently reduced cognitive performance in mice. These results indicate that the increased the ZnT3 levels caused by the deficiency of omega-3 fatty acids produced an abnormal zinc metabolism that in turn impaired the brain cognitive performance in mice.

Biography:

Abstract:

Deafness is the most frequent sensory deficit in humans. The etiology is genetic in about half of the cases worldwide. The most frequent cause of non-syndromic autosomal recessive deafness is an altered connex in 26-protein, a communicating gap junction protein encoded by the gene GJB2. Previous studies included Sudanese and Kenyan patients suggested other causes for hearing impairment other than GJB2. Two Sudanese patients with a prelingual, profound, sensorineural, bilateral, non-syndromic hearing loss were screened for GJB2 using DNA extracted from blood which was followed by PCR and sequencing. The patients had different frame shift mutations that were unreported before

Biography:

Nkemamaka Okonkwo is a Junior Doctor embarking on her Core Medical Training (CMT) in NHS England. She completed her Foundation Training in various trusts across London's North East Thames Deanery and Wales Deanery. Prior to the this, she led student committee projects in conjunction with the Wales 1000 Lives Campaign and the Institute for Healthcare Improvement (IHI) where she is an accredited leader. She supported and pioneered work on issues related to quality improvement and assurance, patient safety and use of retrospective measurement data, real-time monitoring and patient stories to drive overall healthcare improvement.She obtained her medical degree from Cardiff University, an intercalated BSc from Leicester University and is currently studying for an MSc in International Health Management from Imperial College London, where she chairs the BioPharma and Healthcare society.

Abstract:

Background: Temporal artery biopsies (TAB) are often performed in suspected cases of sight-threatening arteritis. The results of which often do little to change clinical management. While the American College of Rheumatology (ACR) formed a clinical classification criterion in 1990 for diagnosing GCA to ensure early steroid therapy was commences, they acknowledge TAB should aim in establishing a definitive diagnosis Aims: The audit aimed to assess if TABs were performed in accordance with the national ACR guideline and whether their results altered course of treatment in suspected GCA. Method: A retrospective audit of all patients undergoing TAB at a single DGH between 2010 and 2014, identified from the histopathology database. Main outcome measures included clinical profile and biochemical criteria associated with positive histology; proportion of negative histology patients who were commenced on steroid therapy; Length of TAB’ relationship between ACR score and TAB result Results: Forty TABs were performed (male: female 1:2, mean age=70.23 years). Three (7.5%) biopsies were histologically positive and 37 (92.5%) were negative. One biopsy was non-arterial. 62.5% of Tabs were performed within the recommended one week of suspected diagnosis. Only 46% of TABs were >1cm. Preoperative steroid therapy was commenced in 80% of patients and a negative histology changed management in 32%. 67.5% had sufficient clinical features to classify GCA and not warrant TAB. Histologically positive TAB patients had higher average age, higher ESR, longer biopsy length and shorter time interval between diagnosis and procedure compared to histologically negative TABs. Conclusion: Raised ESR and higher age may be the most useful diagnostic adjunct of GCA. Many histologically negative TAB individuals were nevertheless clinically diagnosed and managed as GCA. Sub-optimal specimen length may be contributing to lack of diagnostic accuracy. Alternative techniques may be warranted in the near future.

Biography:

Deepa Rani has been working as community health worker and site investigator in Haryana, India for last 3 years. While working in the community, she joined NMP Medical Research Institute and been heading Institute's program as part of lifting the burden compaign, Global Campaign to reduce the burden of headache disorder. She is certified research associate on a multicenteric research study in northern states of India.

Abstract:

Worldwide, headache disorders are among the most common medical conditions.Many people with headache need not experience further pain if the diagnosis and treatment are correct. Most patients do not have correct diagnosis and treatment. This study tested a model for treatment of people with headache disorders at primary health-care level in rural areas of Haryana, India. METHODS: A quasi experimental study with peer education intervention was conducted in selected primary care health clinics. Threee hundred sixty patinets from randomly selected communities of Kaithal, Haryana were assessed through screening questionnaires conducted in pre- and post-intervention periods. Pertinent data on socio-demographic and headache related factors were collected. The statistical packages used for data entry and analysis were epi-info version 3.5.4 and SPSS version 20.0 respectively. RESULTS: When the pre and post intervention data of each group were compared, comprehensive Knowledge of headache (P-Values =0.004) and willingness to go to neurologist for diagnosis and treatment (Pvalue = 0.001) showed significant differences among intervention group during post intervention period. In 68% of patients who completed 12 months' treatment, headache frequency was decreased by at least 60%, and a third of patients were headache free. Medication was well tolerated and reported adverse events were mild; only 36 patients (1%) discontinued medication because of side-effects. CONCLUSION: This study confirmed that this simple protocol was suitable for the treatment of headache disorders in rural areas of India. Physicians and community workers with basic training could diagnose and refere headache patients, with beneficial effects for most patients with treatment.

Biography:

Abstract:

The problems of development of infants‘ brain are known to be complex and urgent because the success of solving these problems increases quality of life in childhood and adolescence. One of these problems is epileptic encephalopathy (EE) in infants. There is a wide variety of this syndrome, what makes the diagnostics very difficult (West, Lennox-Gastaut syndrome (LGS) etc.). The main role in establishing of diagnosis plays EEG with video monitoring that shows hypsarrhytmia of the waves. However, the clinical course in combination with hi-tech examination are strongly recommended. The aim of investigation was optimization of methods of treatment of pharmacological resistant forms of epilepsy that can be illustrated by the case of the two-year boy with symptomatic Lennox-Gastaut syndrome. Materials and methods: The diagnosis was based on the routine examination and clinical manifestations (seizures, appeared with different periodicity). The child was ill since birth and treated with different combinations of antiepileptic drugs (AED). The treatment was unsuccessful, what forced us to find another approach. Tablets of hydrocortisone were prescribed in the start dose of 1.0 mg per 1 kg of body weight (according to professor Olivier Dulac’s scheme), followed by decreasing of dose up to 2 mg. The treatment was carried out during five months. EEG with video monitoring was carried out during 8 hours in active and passive wake, night sleeping and after awaking. Results: First EEG examination provided, when child was 1 year old, showed “sharp slow wave”, “spike-, polyspike-and-waves” complexes in the right parieto-temporal area. In the left one were registered “sharp slow wave” and “spike-and-wave” complexes with reverse of phase under the electrodes P3 and T5. Physiological patterns of sleeping were weakly manifested and periodically were substituted by epileptiform activity. In the middle of therapeutic course the child became seizure-free and considerable more active and some life skills developed. During the one-year follow-up period was not revealed any seizures, though the child did not take AED or hormones. EEG registered just single complexes “sharp slow wave” with amplitude up to 100mcV in left temporal area of the brain with reverse of phase under the electrodes T3, T5. There were not any pathological movements during the sleeping. As result of a treatment was also observed obvious development of child’s brain, which was manifested in physical and mental activity. Conclusion: Thus, we can conclude that early beginning of individually selected therapy in infants with EE and LGS gives the possibility for the normal development of their brain that may be seen in the normalization of physical and mental development.

Biography:

Dr Syed Mohammad Abbas Zaidi completed BUMS and MD (Unani) from Hamdard University, New Delhi. Currently he is working as Assistant Professor at H.S.Z.H. Govt. Unani Medical College, Bhopal. He has published 17 papers in various International/National journals, presented 5 papers abroad (USA, Iran, Malaysia, Japan and Srilanka), many papers in various national conferences across the country and got best paper award in Malaysia in 2011. He has 3 patents and is Associate member of Japan Neuroscience Society, member of editorial board of Indian Journal of Unani Medicine, referee of 3 international journals and member of ethical Committee, Clinical Research Unit, CCRUM, Bhopal.

Abstract:

Delphinium denudatum Wall. (Ranunculaceae) is an indigenous medicinal herb popularly known as ‘Jadwar’ widely used in traditional Unani system of medicine for the treatment of a variety of human ailments including epilepsy. In order to increase the bioavailability, the nanophytosome of the Delphinium denudatum root aqueous fraction (DNP) was prepared, characterized and evaluated. The phospholipid complex of the obtained aqueous fraction (AF) was prepared with Phospholipon 90H. The size of nanophytosomes was determined by dynamic light scattering. HPTLC fingerprinting of the AF was also performed. PTZ and ICES models were used to evaluate the anticonvulsant activity while Rotarod test, Elevated Plus maze test, and Forced swimming test were used to evaluate other neuropharmacological effects at dose level of 400mg/kg and 800mg/kg p.o. The particle size of the prepared DNP was around 500 nm. The DNP exerted significant anticonvulsant activity as compared to control, aqueous fraction and placebo treated groups (p<0.001). The DNP significantly increased the threshold current and decreased the mortality percentage against electroshock at all the doses as compared to control, conventional extract and placebo treated groups. However, there was a significant dose dependent reduction in the recovery period following the convulsions (p<0.001). DNP also exhibited anxiolytic and antidepressant activity in a dose dependent manner. Furthermore, DNP did not cause any evidence of neurotoxicity till dose of 2000 mg/kg p.o. It can be hypothesized that DNP may have better access to the brain as evidenced by its improved efficacy than pure aqueous fraction.

Biography:

Mirjana Djukic has completed her PhD in 2001 at the Faculty of Pharmacy at the University of Belgrade. She became a full professor of Toxicology in 2012. Her research interest has focused on free radicals-mediated mechanism pathways of drugs/poisonings. Accordingly, on oxidative stress-related topics she introduced an optional subject in the faculty study program (2008); wrote (author and editor) two books; published/presented cc 190 papers and has been reviewing articles to reputable journals. She spent two years in the Center for Free Radical and Antioxidant Health (prof. Valerian Kagan lab) at the University Pittsburgh, USA (2002/3, 2010/11).

Abstract:

Paraquat (PQ) neurotoxicity has not thoroughly investigated. Red-ox metabolism of PQ2+ results in superoxide anion radical (O2•) formation. Consequent free radical reactions escalate due to stable resonance radical structure (PQ•+). The OS/NS-associated neurotoxic pathways of PQ were investigated in striatum of Wistar rats after single intrastriatal administration of PQ+ and applied pretreatments, including: N-nitro-L-arginine-methyl ester (L-NAME); 2-amino-5-phosphonovaleric acid (APV); glutathione reductase (GR); and naloxone. Reversible Parkinson’s disease symptoms were observed in PQ group. Contrary to PQ, APV+PQ and GR+PQ groups, initially high O2• reached the normal values in L-name+PQ and naloxone+PQ groups, on 7th day. Superoxide dismutase (SOD) activity declined in L-name+PQ, naloxone+PQ and APV+PQ groups. Initially low SOD activity reached normal values on 7th day in Pq and GR+PQ groups. Lipid peroxidation was the highest in PQ, L-name+PQ and GR+PQ groups. Glutathione (GSH) depletion was considerable in L-name, APV and naloxone pretreated rats across the time. Increased GSH values were achieved in PQ and GR+PQ group on the 7th day. Glutathione peroxidase (GPx) activity was inhibited by GR (within 24 hours) and naloxone; elevated GPx activity declined with the time in APV+PQ and L-name+PQ; while it was high in PQ group until the 7th day. In conclusion, inhibitors of NO-synthase, N-methyl-D-aspartate (NMDA) and opioid receptors, reduced SOD and GPx activities and depleted GSH. Rise of O2• occurred in APV and GR pretreated groups (twice higher than in PQ group), on 7th day, although APV did not influence LPO.

Biography:

Professor Geoffrey Burnstock completed his PhD at King's College and University College London. He was head of the Department of Zoology, Melbourne University (1964-1975) before moving to London to head the Department of Anatomy and Developmental Biology, UCL until 1997. He is currently President of the Autonomic Neuroscience Centre, University College Medical School, UK. He is a Fellow of the Australian Academy of Sciences (1971), Royal Society (1986) and Academy of Medical Sciences (1998). He was awarded the Royal Society Gold Medal (2000) and has over 1520 publications and an h-index of 135.

Abstract:

The concept of purinergic neurotransmission (i.e. neurally released ATP acting as an extracellular signalling molecule) was proposed in 1972(Burnstock, 1972). Later it was recognised as a cotransmitter in most, if not all, nerves in the peripheral and central nervous systems, acting on post- and also pre-junctional membranes, at autonomic neuroeffector junctions and ganglionic and central synapses. ATP and its breakdown product adenosine also act as trophic factors during development and regeneration. Brief background information is given about ATP storage, release and ectoenzymatic breakdown. Purines and pyrimidines have key roles in neurotransmission and neuromodulation, with their effects being mediated by P1 (adenosine), P2X ion channel and P2Y G protein-coupled receptors. There is coverage of neuron-glia interactions and of purinergic neuroeffector transmission to non-muscular cells. Purinergic mechanisms and specific receptor subtypes have been shown to be involved in pathological conditions, including brain trauma and ischaemia, epilepsy, visceral and neuropathic pain, neurodegenerative diseases associated with neuroimmune and neuroinflammatory reactions, as well as neuropsychiatric diseases, including depression, anxiety and schizophrenia (see Burnstock, 2007). Specific purinergic receptor subtypes, notably A2A, P2X4 and P2X7 are being explored as therapeutic targets for the treatment of these conditions.

Biography:

Abstract:

The Biology of Neurodegeneration program evolved from our laboratory studying the basic biology of neuronal cytoskeletal protein phosphorylation during development and normal function in the adult. To understand the molecular basis of neurodegeneration our major focus has been to study the regulation of compartment-specific patterns of cytoskeletal protein phosphorylation in neuronal perikarya and axons. We have demonstrated that phosphorylation of the numerous acceptor sites on such proteins as Tau and neurofilament are tightly and topographically regulated and generally confined to the axonal compartment under physiological conditions. However, during neuronal insults, it is deregulated induces neuropathology. During our course of studies to understand the biology of this regulation we identified cyclin dependent kinase5 (Cdk5); a neuron specific kinase involved in the nervous system development, function and survival. It was recognized that in neurodegenerative disorders such as Alzheimer’s disease (AD), Parkinson’s (PD) and Amyotrophic lateral sclerosis (ALS) the pathology was characterized by aberrant and hyper activation of Cdk5 and accumulation of aberrantly hyper phosphorylated cytoskeletal proteins in cell bodies, suggesting that topographic regulation had been compromised. This led inevitably into studies of neurodegeneration in cell culture and model mice with emphasis on Cdk5, that targets numerous neuronal proteins including cytoskeletal protein regulation by phosphorylation, which when deregulated, is responsible for the pathology seen in neurodegenerative diseases. In cell systems, neuronal stress leads to deregulated kinases. Recently we have discovered peptides derived from, p35, and a neuron specific activator of Cdk5, which rescue cells in vitro from stress induced pathology. The questions currently being investigated are (1) how is cytoskeletal protein phosphorylation topographically regulated in neurons? (2) What factors are responsible for the deregulation of Cdk5 in neurons? (3) Can mouse models of AD, PD and ALS be treated therapeutically with peptides that inhibit deregulated Cdk5?

Biography:

Prof. G. Nagesh Babu completed his PhD at the age of 25 years from University of Hyderabad, India. He did his postdoctoral studies from University of Connecticut and University of Arkansas in USA. He also held research positions in Nagoya University, Japan, University of Wisconsin, Madison, USA and University of Porto, Portugal. Currently he is working as a Professor in the Department of Neurology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, India. He has published more than 35 papers in reputed journals and has been serving as an editorial board member of International Journal of Neuroscience and Psychiatry.

Abstract:

It is well known that the neurotoxicity effects of Glutamate (L-Glu) involve the activation of glutamate receptors. However, during periods of cerebral ischemia there is also an activation of the Kyneurinine (KYN) pathway of tryptophan metabolism, which generates the NMDA receptor-glycine site antagonist Kyneurinic Acid (KYNA). We studied the effects of pretreatment of peripheral KYN on acute-L-Glu-induced neurotoxicity. NMDA receptors are supposed to play a crucial role in Glutamate (L-Glu) neurotoxicity.To evaluate the effects of the astrocyte-derived tryptophan metabolite KYNA, on L-Glu neurotoxicity, adult male rats were pretreated with KYN which is a precursor of KYNA, at a dose of 30 mg or 300 mg/kg bw i.p., 2 h before administration of a stereotactic L-Glu bolus (1µmole/1µl) administration into the cerebral cortex. Key oxidant and anti-oxidant parameters were estimated in both brain homogenates and isolated cortical neurons. To obtain individual neurons, finely chopped cerebral cortex tissue was treated with dispase (1000 protease units/ml) for 45 min at 370C. Viability test was done by trypan blue and 90% viable population of neurons was obtained. Acute L-Glu administration increased the rate of lipid peroxidation, nitric oxide and decreased key antioxidant parameters such as SOD, catalase, total glutathione and glutathione reductase in brain homogenates. In isolated cortical neurons, we observed increased levels of reactive oxygen species, calcium along with decreased mitochondrial membrane potential. Peripheral loading of 30 mg/kg dose of KYN had no protective effects on L-Glu induced neurotoxicity, but a dose of 300 mg/kg dose prevented the toxic effects following intracortical L-Glu.

Biography:

Mr. A. K. Srivastava is working in the Department of Pharmaceutics, IIT-BHU as an Associate Professor, of Pharmaceutics. He did his B. Pharm and M. Pharm degree from the Department of Pharmaceutics, IIT-BHU, Varanasi. Before joining the academics in the department he has served in Pharma Industry in production. Mr.Srivastava has vast experience of teaching and research. He has more than 30 year of teaching experience. Mr. Srivastava has guided about 80 research Scholars for M. Pharm degree including 3 Ph. D scholars. He has about 35 research papers in national and international research journals of repute. Mr. A. K Srivastava is recipient of Indian Drug Manufacturer Association, Mumbai (IDMA) gold medal as well as gold medallist in B. Pharm and M. Pharm degree course. Besides, he is involved actively in university administration in various capacities. Area of research of Mr.Srivastava is towards oral Drug Delivery under advance drug delivery system.

Abstract:

Development of an effective formulation for Antitubercular Drug (Rifabutin) involves careful optimization of a number of excipient and process variables. Some times the number of variables are so large that even the most efficient optimized designs require a very large number of trials which put stress on costs as well as time. A creative and Hybrid combination of number of design methods leads to a smaller number of trials. This study was aimed at the development of Nano Structured Lipid Carriers (NLCs) by using a combination of different optimization methods. We were screened using for full factorial design for their effects on formulation characteristics like particle size, entrapment efficiency, Zeta Potential, PDI. Few were found to have in-significant effects on the formulation parameters and hence were screened out. Out of the remaining variables it was found that some of these have significant effects on the size of the particles while the other had a higher influence on the entrapment efficiency and other responses. The screened variables were optimized for their effect on size using the Taguchi orthogonal array. The optimized values of the surfactants and lipids were kept constant for the next stage, where the sonication time, phase ratio, and drug: lipid ratio were varied using the Box–Behnken design and response surface method to optimize the entrapment efficiency. Finally, by performing only less number of trials, few variable were optimised for the development of Nano Lipid Carrier for Rifabutin.

Biography:

Dr David Moore is a post-doctoral research fellow at the Department of Pain Medicine, St James Hospital, Dublin and the Institute of Neurotherapeutics, Dublin City University. Dr Connail McCrory is Dean of the Faculty of Pain Medicine Ireland. He is a Primary Investigator at Trinity College Institute of Neuroscience and the Institute of Neurotherapeutics, Dublin City University. He is Senior Lecturer in the School of Medicine, Trinity College Dublin and Director of Pain Medicine St James Hospital Dublin.

Abstract:

Neuropathic pain poses a significant burden on the individual and society, because of a lack of effective pharmacological therapies. Interventional pain therapies may be more effective in a select cohort of patients. Neuropathic pain results from a lesion or disease of the somatosensory system. Traditionally neuropathic pain was attributed to dysfunctional activity and hypersensitivity of the neuron. However a maladaptive immune response is increasingly recognised as contributing to the maintenance of chronic neuroapthic pain (1). Glial cell activation and altered peptide biosynthesis are implicated in the maintence of persistent neuropathic pain. Human data suggests that NGF, VEGF and BDNF play a role here. This neuroimmune process is maitained by cellular and neuropeptide biosynthetic responses which become pathological. Intrathecal opioids and steroids are associated with alterations in cell signalling and the levels of inflammatory mediators at the neuroimmune interface in humans in vivo (2,3). Markers of glial and immune cell activity, up-regulated in neuropathic pain states, are down-regulated in spinal cord stimulator patients (4). Pulsed radiofrequency of the dorsal root ganglion in patients with radicular pain alters CSF lymphocyte subsets and peptide comcentrations (unpublished data).

Biography:

Fabián Nishida, 30 years old, completed his PhD degree in 2014 at the School of Veterinary Sciences, National University of La Plata. He is now doing his posdoc training. His area of expertise is focused on studies of sensory and motor behaviour, histomorphometry and statistical analysis. Publihed several articles in international journals and participated as a lecturer in several training courses of image analysis and immunohistochemistry. He received some grants for young researchers, as well as honours and prices for his research work. He is now forming three PhD students.

Abstract:

Kainic acid (KA) is an analogue of the neurotransmitter glutamate and causes extensive neuronal network damage and early irreversible loss of neuronal activity. The present work was aimed at evaluating motor and sensory performance of rats and analysing morphometric parameters and immunohistochemical reactivity of spinal cord neurons after intraparenchymal KA injection. Animals were injected either with 0.75 mM, 1 mM or 1.25 mM of KA at the C5 segment of the cervical spinal cord. Motor and sensory performance were evaluated at days 0, 1, 2, 3 and 7 post-injection (pi) and compared with those of saline-treated and non-operated animals. Three animals were euthanized at each time point. All KA-treated animals showed a significant impairment at the motor and sensory tests for the ipsilateral forelimb in a concentration-dependent manner in comparison to control groups. Neuronal cell count showed a significant loss of neurons at C4, C5 and C6 cervical segment when compared with those of saline-treated and non-operated animals. The contralateral side of the cervical segments in KA-treated rats remained unchanged. Immunohistochemical technique showed a similar immunoreactivity pattern with those observed in brains of Alzheimer´s diseases patients. Some improvement at the motor and sensory tests was observed in animals injected with 0.75 mM and 1 mM KA. Moreover, a mild increase in the neuronal count at the damaged segments was also recorded. Functional improvements registered in the motor and sensory tests by day 7 pi may be a consequence of a neuron repairing mechanism triggered soon after the KA excitotoxic effect.

Biography:

Abstract:

Background: Temporal artery biopsies (TAB) are often performed in suspected cases of sight-threatening arteritis. The results of which often do little to change clinical management. While the American College of Rheumatology (ACR) formed a clinical classification criterion in 1990 for diagnosing GCA to ensure early steroid therapy was commences, they acknowledge TAB should ain in establishing a definitive diagnosis Aims: The audit aimed to assess if TABs were performed in accordance with the national ACR guideline and whether their results altered course of treatment in suspected GCA. Method: A retrospective audit of all patients undergoing TAB at a single DGH between 2010 and 2014, identified from the hostopathology database. Main outcome measures included clinical profile and biochemical criteria associated with positive histology; proportion of negative histology patients who were commenced on steroid therapy; Length of TAB’ relationship between ACR score and TAB result Results: Forty TABs were performed (male:female 1:2, mean age =70.23 years). Three (7.5%) biopsies were histologically positive and 37 (92.5%) were negative. One biopsy was non-arterial. 62.5% of Tabs were performed within the recommended one week of suspected diagnosis. Only 46% of TABs were >1cm. Preoperative steroid therapy was commenced in 80% of patients and a negative histology changed management in 32%. 67.5% had sufficient clinical features to classify GCA and not warrant TAB. Histologically positive TAB patients had higher average age, higher ESR, longer biopsy length and shorter time interval between diagnosis and procedure compared to histologically negative TABs. Conclusion: Raised ESR and higher age may be the most useful diagnostic adjunct of GCA. Many histologically negative TAB individuals were nevertheless clinically diagnosed and managed as GCA. Sub-optimal specimen length may be contributing to lack of diagnostic accuracy. Alternative techniques may be warranted in the near future.

Biography:

Nicoleta Dumitrescu, 2nd year medical student, “Gr. T. Popa” University of Medicine and Pharmacy (UMF), Iasi, Romania, presented papers to several national and international medical congresses and participated to Student Surgical Society Romania workshops. Professor Ion Poeata, MD, PhD, is Vice-president of the Romanian Neurosurgical Society, chief of the Neurosurgical Department “Prof. dr. N. Oblu” Emergency Clinical Hospital, Iasi, coordinator of the Neurosurgical Department, “Gr. T. Popa” UMF Iasi. Luminita Smaranda Iancu, MD, PhD, is Vice-president of the Romanian Microbiology Society, chief of Microbiology Discipline from “Gr. T. Popa” UMF Iasi, and head of Regional Center of Public Health Iasi.

Abstract:

Worldwide are registered annually about 9 million cases of tuberculosis, Romania being the first in the EU, with an incidence of 87 cases /100.000 inhabitants (2013, World Health Organization). Aim: to report a very rare case of a 27 years-old man diagnosed with a cerebral intraventricular tuberculoma, after he had been treated two months for pulmonary tuberculosis with Mycobacterium tuberculosis - negative sputum smear. Case Report: The patient was brought on August 2015 to “Prof. dr. N. Oblu” Emergency Clinical Hospital, Iasi, by his family because of a confusional syndrome, somnolence and sphincter disorders. Cerebral magnetic resonance imaging showed asymmetrical hydrocephalus and a small homogenous enhanced lesion that was located in the lateral right cerebral ventricle and foramen of Monro. A surgical intervention by endoscopic approach was made. A white-yellowish, soft tumor located in the right lateral ventricle and extended into the third ventricle was seen. Cerebrospinal fluid (CSF) examination revealed leukocytes (8 cells/mm3) and intact red blood cells (340 cells/mm3). Histopathological examination of the biopsy showed rare Langhans giant cells, epithelioid histiocytes, and lymphocytes, but no caseous necrosis. A final diagnosis of an early intraventricular tuberculoma was established. The patient's evolution was favorable under the tuberculostatic treatment and corticoids. Conclusions: This case is customized by the acute development of the intraventricular tuberculoma (while the patient had already been treated with tuberculostatic therapy for two months for active pulmonary tuberculosis), low number of white blood cells in CSF, and negative bacterioscopic exam of sputum.

Biography:

Yuanlong Pan completed his BVM from Gansu Agricultural University, P.R. China. Dr. Pan received his PhD in Animal Nutrition from Virginia Tech, USA and PhD in Human Nutrition from UNC-Greensboro, USA. Dr. Pan conducted research in the area of menopause and cognition at Wake Forest University School of Medicine from 1996 to 2000. In 2000, Dr. Pan joined Nestle Purina Research. He has published more than 18 papers, filed 41 patent applications and obtained 10 patents. Recently Dr. Pan won the Academy of Science-St Louis 2016 George Engelmann Interdisciplinary Award for his outstanding achievement in science through collaboration.

Abstract:

Aging has adverse effects on all tissues and organs in humans and animals including dogs and cats. Just like in humans, some of the senior dogs and cats eventually develop cognitive impairment and dementia called cognitive dysfunction syndrome (CDS). Since CDS is not a curable disease, our research has been focused on nutritional solutions that promote healthy brain aging in dogs and cats for the past 15 years. We have developed two solutions to enhance cognitive functions in dogs and cats. The first approach is to address the reduced ability of brain cells to utilize glucose as energy by providing medium chain triglycerides (MCTs), and we have confirmed that MCTs do enhance cognition in aging dogs. The second solution is to minimize known risk factors associated with brain aging. Since there are multiple risk factors, we have developed a nutrient blend and demonstrated its cognition-enhancing benefits in middle-aged and aging cats. In summary, our research shows that optimal nutrition can enhance cognitive functions in healthy aging dogs and cats. What we have learned from pets may be able to facilitate the development of nutritional and therapeutic solutions for people.

Biography:

Abstract:

Aims and Hypothesis: To review the previous case reports on positive anti-NMDAR antibodies that were treated with ECT. Background: It is now well accepted that autoimmune encephalitis can present with a combination of neurological and psychiatric symptoms. Currently, the most widely used therapy for these conditions is prompt plasmapheresis and steroid treatment (and tumour resection if indicated), followed by second line immunosuppression if this fails. Cases: We discuss several case reports, which suggest that ECT plays a role in treatment for some types of autoimmune encephalitis, particularly those in which psychiatric symptoms are especially debilitating and refractory to standard treatment. We present a new case of a 71 year old previously healthy female who presented with depression and anxiety after anti-NMDAR antibodies were isolated, she received plasmapheresis and corticosteroid treatment and then she underwent 8 sessions of ECT and returned to her premorbid state. Discussion: We discuss factors predicting good outcome and possible mechanisms behind the use of ECT in autoimmune encephalitis. Conclusions: Although there are still only a small number of case reports supporting the theory that ECT is effective in treating symptoms of autoimmune encephalitis, it is reasonable to suggest that it should be considered as an alternative or adjunct to standard immunosuppressive therapies.