The impact of detoxifying and repair gene polymorphisms on oxidative stress in ischemic stroke.

Stroke is a multifactorial disease caused by the combination of certain risk factors and genetic factors. There are possible risk factors having important role in the pathogenesis of stroke. The most important environmental factors are cigarette smoking and oxidative stress which have different sources. GST (M1, T1, P1) have major roles in detoxification of the products of oxidative stress and they are polymorphic. DNA damages can also be repaired by repair enzymes such as OGG1 and XRCC1 which are highly polymorphic and have pivotal roles in repair systems. In the present study, we investigated that polymorphisms in genes involved in detoxification and DNA-repair pathways might modify the individual's risk for ischemic stroke. Furthermore, the products of oxidative stress and antioxidant capacity were measured and the impact of gene polymorphism on them was evaluated. Our data showed that OGG1 Ser326Cys and XRCC1 Arg399Gln gene polymorphisms had impacts on the development of stroke.

Hypoxic Corpus Callosum Lesion after Cardiac Arrest with Good Prognosis.

Hypoxic ischemic damage of the corpus callosum after cardiac arrest is a rare condition. Lesions of the splenium of the corpus callosum after hypoxia are bilateral and lead to poor prognosis. Herein, we present a case with good prognosis after cardiac arrest with bilateral lesions of the splenium of corpus callosum.

Acute-Phase Stroke Outcome and Lipids.

Objectives: The aim of the study is to investigate the relationship of lipid subgroups with short-term mortality in acute stroke (AS). Methods: This retrospective study included 698 patients with AS who presented within 24 h of symptom onset. A hemogram from peripheral venous blood samples was taken at admission. Total cholesterol (TC), triglyceride (TG), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), TC/HDL-C rate, and TG/HDL-C rate were recorded. Duration of follow-up was defined as 30 days. Results: 64 out of 698 patients died during the follow-up period. The mean TG, TG/HDL-C, and TC/HDL-C levels were significantly lower in the mortality group than the survival group. In the receiver operating characteristic (ROC) analysis, the cutoff values and area under the curve of the TG, TG/HDL-C, TC, and TC/HDL-C levels for short-term stroke mortality are as follows ([100.2 mg/dL, 0.648]; [2.52, 0.650]; [170.50 mg/dL, 0.598]; and [4.32, 0.640], respectively). In the Cox regression model, only TG and TG/HDL-C, according to their ROC cutoff values, were independent variables as short-term mortality predictors (TG ≤100.2 mg/dL, HR:2.413 , 95% CI: 1.345-4.327, P:0.004); (TG/HDL ≤2.56, HR: 2.720, 95% CI: 1.389-5.359, P:0.003, respectively). Conclusion: Dyslipidemia is a well-known as a risk factor of stroke. However, this study focused on the estimation that lower TG and TG/HDL-C levels at the time of hospital admission might be predictors of short-term mortality within a month of AS attack, which is a different subject from long term risk factors of stroke. Serum TG level may be a better indicator for mortality in the acute hypercatabolic trauma such as stroke.

Forced normalization: An overlooked entity in epileptic patients.

The "forced normalization" phenomenon is characterized by acute/subacute onset of psychotic symptoms in the early post-ictal period with dramatic improvement of electrophysiological epileptiform activity. A 56 years old female with going on personality changes, maladaptive behaviours and a mild cognitive impairment since last seizure which was forty-five days ago has been admitted. An evident increase was observed in her maladaptive behaviours with the use of levetiracetam. She began describing visual hallucinations and déjàvu. Control EEG performed 24h after the seizure was completely normal. Levetiracetam therapy was replaced with phenytoin. Quetiapine therapy was also administered. Psychotic symptoms disappeared.

The association of IL-18 gene promoter polymorphisms and the levels of serum IL-18 on the risk of multiple sclerosis.

OBJECTIVES: Multiple sclerosis is an inflammatory condition of the central nervous system whose etiology is influenced by immunologic, genetic, and environmental factors. Aim of the present study was to determine if any relation exists between IL-18 -137C/G and -607C/A gene promoter polymorphisms on the individual susceptibility of multiple sclerosis and also to investigate the possible effect of IL-18 activity regarding this kind of polymorphism and MS. PATIENTS AND METHODS: 113 patients with clinically definite MS and 135 ethnically-matched controls were participated in this study. IL-18 -137C/G and -607C/A gene promoter polymorphisms were analyzed by Sequence Specific Polymerase Chain Reaction (SS-PCR), while levels of serum IL-18 were measured by Enzyme Linked Immunoassay Assay (ELISA) in patients with MS and healthy controls. RESULTS: Our results showed that the IL-18 -607AA genotype indicated 6 times higher risk in the development of MS (OR=6.883; 3.17-14.96; p<0.001). According to our findings, smoking seems to be an important confounding factor in MS patients with carrying IL-18 -607 AA and CA+AA genotypes. However, no meaningful association was found with IL-18 -137C/G gene promoter polymorphism. CONCLUSION: In conclusion, we suggest that IL-18 -607C/A gene promoter polymorphism is a major genetic factor for determining individual susceptibility to MS, where smoking status also increases the risk of MS.