Epilepsy is one of most frequent neurologic health problem, affecting nearly 1% of world population. It is a chronic disorder characterized by recurrent, sudden, unprovoked seizures of cerebral origin with motor, sensory, autonomic disturbance with or without conscious loss. There is up to 25 % of resistant subgroup of epileptic patients where pharmacologic antiepileptic therapies are insufficient. VNS is an approach for specific resistant epileptic cases when epileptic surgery can’t be feasible. Th e idea of a link in between epilepsy and immune system is present at for the last 30 years. Immunologic alterations in epileptic patients, some favorable responses of resistant epileptic syndromes to immunomodulatory treatment and association of certain obvious immune – mediated diseases with epilepsy all support this link. Th e presence of autoimmune epilepsy and responsive states of some epileptic syndrome for immunotherapy encourage this hypothesis.Pro-infl ammatory cytokines such as IL-1β, IL-2, IL-6 and TNF-α have a correlation in seizure. Besides, there is association between epilepsy and certain autoimmune diseases. Therefore, some antibodies (such as; GluR3, Phospholipid, cardiolipin, β2- Glycoprotein I, nuclear, Haemocyanin, antiprothrombin and GAD) are all important in autoimmune epilepsies. CSF findings (Oligoclonal bands, elevated IgG Index) and venous blood fi ndings (Ig G, M, A, D, E) are other evidences for association of epilepsy and/or immunology. From July 2012 to January 2015, totally 5 pharmaco-resistant epileptic patients are studies on behalf of this ideas. These selected patients are important because of that all of them are VNS patients. All patients were evaluated with aforementioned cytokines,immunoglobulin and some specific antibodies just pre – implantation and 6 mo / 1 y post – implantations. Interestingly the most specific findings are correlated with cytokines rather than Ab’s able to be studied. Most of blood immunoglobulin is not changed in times. But the striking changes belong to IL-1β decrement and IL-6 signifi cant decrement in serum concentration with elongation of time. For the last years, the pro-convulsive and neuro-protective roles of cytokines have an increasing importance in epilepsy. Desperate group of patient with epilepsy rely upon new era approaches such as VNS. Th e exact curative role of this vagal stimulation is still dilemma; but in resistant epilepsy especially good selected patients VNS is gaining an increasing appreciation with a % 50 improvement in seizure frequency and impact. With this study, an untouched aspect of Vagal Nerve Stimulation is tried to be displayed. so that, in passing time period, the cytokine levels of patients start to improve. This may indicate that vagal stimulation may play a role in neuro-immunity of resistant epileptic patients. Since our sampling patient group is so small, there should be more investigation on “the role of VNS in immunology of resistant epilepsy”.

Background: Sporadic Creutzfeldt-Jakob disease (sCJD) is a progressive and fatal disease of the central nervous system. Th e concurrency of herpes simplex virus (HSV) encephalitis who unresponsive to acyclovir and sCJD cases have been reported before (1, 2). In the light of this knowledge, we investigated the HSV antibodies in sJCD cases. Also, we aimed to illustrate the clinical prognosis of these cases.
Case Report: Four patients (ages between 61-77 years, male/female ratio:1/3 ) were admitted with acute changes in mental status and speech disturbances. They developed a rapidly progressive dementia characterised by personality change and myoclonus. Brain magnetic resonance imaging studies showed ribbon sign in the occipital lobe in two cases, increased signal in the basal ganglia in one case and no findings in the other case. Serial electroencephalography recordings showed typical periodic sharp wave complexes. Analysis of cerebrospinal fl uid (CSF) immunoassay of the patients were positive for 14-3-3 protein. HSV IgG antibody specifi city index (ASI) were found higher than 1,3 in 2 patients (range: 0.7-1.3). Also, protein levelswere found 2 folds more (mean:130mg/dl) in HSV plus cases. Th ere is no other differences in CSF fi ndings. The patients who have higher HSV IgG ASI level, died within 3 months after initial symptoms were appeared. The other two patients survived approximately 18 months aft er the diagnosis.
Discussion: There is no clear consensus on the relationship between sCJD and HSV encephalitis since first description by Hsich et al. in 1996 (3). HSV encephalitis and sCJD may stimulate occurence of each other or they might worsen their course by the neuroimmunological mechanisms. Detailed researches are needed including postmortem studies.

Introduction: The C-reactive protein (CRP) is an acute phase reactant and a strong inflammatory biomarker. The concentration of CRP increases 1000 fold markedly within 24-72 hour in response to inflammatory events, tissue damage and infections. Therefore the CRP is a well renowned bio-inflammatory marker as an important strong independent predictive tool of cardio vascular disease. The CRP in nature is a pentamer and can dissociate into a monomeric form. Recent studies have proven that mCRP is a stronger pro-inflammatory protein then the pCRP.Introduction: Th e C-reactive protein (CRP) is an acute phase reactant and a strong inflammatory biomarker. Th e concentration of CRP increases 1000 fold markedly within 24-72 hour in response to infl ammatory events, tissue damage and infections. Th erefore the CRP is a well renowned bio-inflammatory marker as an important strong independent predictive tool of cardio vascular disease. Th e CRP in nature is a pentamer and can dissociate into a monomeric form. Recent studies have proven that mCRP is a stronger pro-infl ammatory protein then the pCRP. Materials and Methods: Th e mCRP in-house ELISA was developed using the clone 3H12 and validated in the patients with diff erent inflammatory diseases. Th e mCRP and pCRP were measured using ELISA in 9 age and sex matched pairs of patients with major depression and healthy controls. Results: Th e mCRP levels were higher in patients than controls (p=0.05) whereas no significant diff erence was observed in pCRP. Th is difference was lost when BMI was controlled since patients have higher BMI. Moreover, mCRP levels showed signifi cant association with triglyceride levels in the controls but not in the patients. Conclusion: Our findings raised a question as to whether the mCRP levels can be early predictor in development of metabolic syndrome in the patients.Introduction: Th e C-reactive protein (CRP) is an acute phase reactant and a strong inflammatory biomarker. Th e concentration of CRP increases 1000 fold markedly within 24-72 hour in response to infl ammatory events, tissue damage and infections. Therefore the CRP is a well renowned bio-inflammatory marker as an important strong independent predictive tool of cardio vascular disease. The CRP in nature is a pentamer and can dissociate into a monomeric form. Recent studies have proven that mCRP is a stronger pro-inflammatory protein then the pCRP. Materials and Methods: Th e mCRP in-house ELISA was developed using the clone 3H12 and validated in the patients with diff erent inflammatory diseases. Th e mCRP and pCRP were measured using ELISA in 9 age and sex matched pairs of patients with major depression and healthy controls.Introduction: The C-reactive protein (CRP) is an acute phase reactant and a strong infl ammatory biomarker. Th e concentration of CRP increases 1000 fold markedly within 24-72 hour in response to inflammatory events, tissue damage and infections. Th erefore the CRP is a well renowned bio-infl ammatory marker as an important strong independent predictive tool of cardiovascular disease. The CRP in nature is a pentamer and can dissociate into a monomeric form. Recent studies have proven that mCRP is a stronger pro-infl ammatory protein then the pCRP. Materials and Methods: The mCRP in-house ELISA was developed using the clone 3H12 and validated in the patients with diff erent infl ammatory diseases. The mCRP and pCRP were measured using ELISA in 9 age and sex matched pairs of patients with major depression and healthy controls.Introduction: Th e C-reactive protein (CRP) is an acute phase reactant and a strong infl ammatory biomarker. Th e concentration of CRP increases 1000 fold markedly within 24-72 hour in response to infl ammatory events, tissue damage and infections. Therefore the CRP is a well renowned bio-infl ammatory marker as an important strong independent predictive tool of cardiovascular disease. Th e CRP in nature is a pentamer and can dissociate into a monomeric form. Recent studies have proven that mCRP is a stronger pro-infl ammatory protein then the pCRP. Materials and Methods: Th e mCRP in-house ELISA was developed using the clone 3H12 and validated in the patients with diff erent inflammatory diseases. Th e mCRP and pCRP were measured using ELISA in 9 age and sex matched pairs of patients with major depression and healthy controls.
Results: Th e mCRP levels were higher in patients than controls (p=0.05) whereas no signifi cant diff erence was observed in pCRP. Th is diff erence was lost when BMI was controlled since patients have higher BMI. Moreover, mCRP levels showed signifi cant association with triglyceride levels in the controls but not in the patients. Conclusion: Our fi ndings raised a question as to whether the mCRP levels can be early predictor in development of metabolic syndrome in the patients.
Results: Th e mCRP levels were higher in patients than controls (p=0.05) whereas no signifi cant diff erence was observed in pCRP. Th is diff erence was lost when BMI was controlled since patients have higher BMI. Moreover, mCRP levels showed signifi cant association with triglyceride levels in the controls but not in the patients. Conclusion: Our fi ndings raised a question as to whether the mCRP levels can be early predictor in development of metabolic syndrome in the patients.
Results: The mCRP levels were higher in patients than controls (p=0.05) whereas no signifi cant diff erence was observed in pCRP. Th is diff erence was lost when BMI was controlled since patients have higher BMI. Moreover, mCRP levels showed signifi cant association with triglyceride levels in the controls but not in the patients. Conclusion: Our fi ndings raised a question as to whether the mCRP levels can be early predictor in development of metabolic syndrome in the patients.
Materials and Methods: The mCRP in-house ELISA was developed using the clone 3H12 and validated in the patients with different inflammatory diseases. Th e mCRP and pCRP were measured using ELISA in 9 age and sex matched pairs of patients with major depression and healthy controls.
Results: Th e mCRP levels were higher in patients than controls (p=0.05) whereas no signifi cant difference was observed in pCRP. This difference was lost when BMI was controlled since patients have higher BMI. Moreover, mCRP levels showed significant association with triglyceride levels in the controls but not in the patients. Conclusion: Our findings raised a question as to whether the mCRP levels can be early predictor in development of metabolic syndrome in the patients.

I am Priyadharshini Arunachalam M.Sc., ASMB (M.S.), doing my PhD in University Hamburg (Universitätsklinikum Hamburg-Eppendorf) in medical faculty under Department of Neurology. I work as junior scientist in same department. I have published 5 papers as a co-author and my main first author paper is in process. I have expertise inneuroimmunology research for past 4 years, working in cerebral ischemic disease models.

The contribution of neuroinflammation is increasingly recognized as a substantial pathophysiological mechanism after stroke. FTY720 is a potent treatment for primary neuroinflammatory diseases by inhibiting lymphocyte circulation and brain immigration. Infiltrating monocytes and leukocytes are considered major producer of tumor necrosis factor (TNF) TNF can have a neuroprotective role but also has been described as a mediator of brain inflammation. Previous studies using transient focal ischemia models showed a protective eff ect of FTY720 but did only partially characterize the involved pathways. FTY720 treatment resulted in substantial reduction of circulating lymphocytes while monocyte counts were significantly increased. After temporary middle cerebral artery occlusion (tMCAO), the number of fl ow cytometrically analyzed brain invading macrophages signifi cantly increased where as T- and B-lymphocytes were signifi cantly reduced in FTY720 treated mice. Particularly, the number of TNF positive infl ammatory macrophage increased in FTY720 treated mice. Th ere was a signifi cant decrease in infarct volume and behavioral dysfunction on 3d aft er tMCAO between treated and untreated mice. In the present study, we were able to detect increased monocyte population and reduction of lymphocyte brain invasion aft er cerebral ischemia following FTY720 treatment. The neuroprotection with eff ective inclination in the TNF positive macrophages and decreased lymphocyte invasion might attribute to a divergent impact of FTY720 in the brain ischemia. We could identify a new mechanism of FTY720, which is attributable to an increase in monocyte, and microglia derived TNF in cerebral ischemia.

Olanzapine, a commonly used atypical antipsychotic drug, is known to induce diabetes and diabetes-associated heart disease. However, the associated mechanisms are not well elucidated. Olanzapine-caused insulin resistance directly or through obesity could be a reason. However this can’t explain the acute eff ect of olanzapine i.e. hyperglycaemic emergencies (hyperglycaemia, diabetic ketoacidosis, hyperosmolar hyperglycaemic state). We propose that olanzapine-induced direct damage on beta-cells may play a key role in olanzapine-induced diabetes. In this study, we examined the eff ects of olanzapine on beta-cell survival ability and mitochondrial apoptotic pathway. Mouse beta-cell line MIN6 was cultured in DMEM medium containing 4.5 g/L D-glucose, supplemented with 50 μM β-mercaptoethanol, 10% fetal bovine serum and 1% Penicillin -Streptomycin and maintained at 37°C incubator with 5% CO2. Cell viability was detected by MTT assay. Apoptosis was determined by BD PharmingemTM Annexin V apoptosis kit I. Mitochondrial functions were measured by Rhodamine assay and ATP production. Key signalling molecules in mitochondrial apoptotic pathway were detected by Western Blotting. Olanzapine decreased the viability of MIN6 cells in a doseand time-dependent fashion. Th e olanzapine-induced beta-cell damage was also demonstrated by apoptotic assay. Olanzapine reduced rhodamine retention and ATP production, indicating it damaged beta-cell mitochondria. Western blotting showed that olanzapine decreased mitochondrial anti-apoptotic protein Bcl-2 and increased cleaved caspase 3. In conclusion, olanzapine decreases beta-cell function and viability through mitochondrial pathway. Olanzapine-caused beta-cell damage could explain the acute hyperglycaemic emergencies in humans as well as low compensatory ability to secret more insulin in animal experiments.