ABSTRACT
@#Numerous studies and meta-analyses have been conducted on the role of infectious agents in susceptibility to multiple sclerosis (MS). In this study we aimed to investigate the role of varicella zoster virus (VZV) in susceptibility to MS as an individual participant data (IPD) meta-analysis. After screening and applying eligibility criteria 19 studies were imported for qualitative systematic review and 11 studies were imported for meta-analysis as different subgroups. No significant result was obtained for association of VZV IgG seropositivity with susceptibility to MS. Positive history of VZV infection was significantly associated with susceptibility to MS. Synthesis of IPD showed that presence of VZV DNA was associated with MS(P<0.001) both in peripheral blood mononuclear cells (OR= 22.40 [5.85-85.71]) and in cerebrospinal fluid (OR= 14.42 [5.29-39.29]). In general VZV can be a risk factor for MS; but since VZV infection history is highly prevalent in populations without vaccination and on the other hand MS has low prevalence, this association should not be used as a prognostic or predictive value. The exact mechanism should be investigated in future.
ABSTRACT
Introduction: Transforming Growth Factor-Beta 1 [TGF-beta1] is a pleiotropic cytokine with potent anti-inflammatory property, which has been considered as an essential risk factor in the inflammatory process of Ischemic Stroke [IS], by involving in the pathophysiological progression of hypertension, atherosclerosis, and lipid metabolisms. -509C/T TGF-beta1 gene polymorphism has been found to be associated with the risk of IS. The aim of this meta-analysis was to provide a relatively comprehensive account of the relation between -509C/T gene polymorphisms of TGF-beta1 and susceptibility to IS
Methods: Male Wistar rats were divided into sham [receiving phosphate buffered saline within dorsal hippocampus], pilocarpine [epileptic model of TLE], single injection BDNF [epileptic rats which received single high dose of BDBF within dorsal hippocampus], and multiple injections BDNF [epileptic rats which received BDNF in days 10, 11, 12, and 13 after induction of TLE] groups. Their electrocorticogram was recorded and amplitude, frequency, and duration of spikes were evaluated
Results: Amplitude and frequency of epileptiform burst discharges were significantly decreased in animals treated with BDNF compared to pilocarpine group
Conclusion: Our findings suggested that BDNF may modulate the epileptic activity in the animal model of TLE. In addition, it may have therapeutic effect for epilepsy. More studies are necessary to clarify the exact mechanisms of BDNF effects