Increased expression of matrix metalloproteinase-9 in patients with temporal lobe epilepsy

Aim: The molecular mechanism of epileptogenesis in temporal lobe epilepsy is still unclear. Experimental studies have suggested that matrix metalloproteinases have important roles in this process, but human studies are limited. The aim of this study was to assess the expression of MMP-9, MMP-2 and their tissue inhibitors (TIMP-1 and TIMP-2) in patients with temporal lobe epilepsy with hippocampal sclerosis (TLE-HS). Material and Methods: The tissue samples from temporal neocortex and hippocampus were obtained from patients with temporal lobe epilepsy with hippocampal sclerosis who had undergone anterior temporal lobectomy for recurrent medically resistant seizures. Immunohistochemical methods were used to determine the expression of MMP-9, MMP-2 and their tissue inhibitors. Tissue samples were also analyzed with transmission electron microscopy. Results: The immunoreactivity for MMP-9 both in hippocampal and temporal neocortical neurons was stronger than that of MMP-2. Additionally, there was a mild reaction for its tissue inhibitor TIMP-1 as with TIMP-2. The TEM analysis of the hippocampus revealed that there was apparent ultra-structural damage on the pericarya and neuropil of some neurons. There was obvious damage in the mitochondria and the nuclear membrane. Conclusion: The preliminary results of this study revealed that MMP-9 may have a role in patients with drug resistant TLE-HS

Angiogenesis in neurological disorders: A review

Angiogenesis, recruitment of new blood vessels, is an essential component of the metastatic pathway. These vessels provide the principal route by which tumor cells exit the primary tumor site and enter the circulation. For many tumors, the vascular density can provide a prognostic indicator of metastatic potential, with the highly vascular primary tumors having a higher incidence of metastasis than poorly vascular tumors. The discovery and characterization of tumor-derived angiogenesis modulators greatly contributed to our understanding of how tumors regulate angiogenesis. However, although angiogenesis appears to be a rate-limiting event in tumor growth and metastatic dissemination, a direct connection between the induction of angiogenesis and the progression to tumor malignancy is less well understood. In this review, we discuss the observations concerning the modulation of angiogenesis and their implications in various neurological disorders, as well as their potential impact on cancer therapy. © W. S. Maney & Son Ltd 2012

Effects of excess vitamin B6 intake on serum lipid profile and cerebral cortex in rats

Aim: The present study was undertaken to investigate the effects of dietary excess of vitamin B6 on certain blood parameters [serum total cholesterol, high density lipoprotein (HDL) cholesterol and total lipid] and the cerebral cortex. Materials and Methods: A total of 36 albino rats were included in the study. Saline solution was administered to control groups (CG-10, n = 6 for 10 days; CG-15, n = 6 for 15 days; CG-20, n = 6 for 20 days). The experimental groups (EG-10, n = 6; EG-15, n = 6; EG-20, n = 6) received 5 mg/kg vitamin B6 daily for 10 days, 15 days and 20 days, respectively. Serum total cholesterol, HDL cholesterol and total lipid levels were measured and compared in CGs and EGs. The cerebral cortex tissue samples were examined by electron microscopy. Results: The total serum cholesterol levels were significantly lower (P < 0.05) although serum HDL levels were significantly higher (P < 0.01) in all EGs. Total serum lipid levels were higher in EG-15 and EG-20 groups than in CGs. The structural degenerations in the perikaryon and neuropil were found prominent in EG-15 and EG-20 groups but not in EG-10. Marked damage in the neuronal and neuropilic structure was observed in rats who received long-term high doses of vitamin B6. Based on these results, a relationship between cerebral cortex damage and serum total lipid and HDL levels in the EG-15 and EG-20 groups is suggested. Conclusions: Dietary excess of vitamin B6 intake reduces serum total cholesterol levels, but not serum HDL and total lipid levels, and also causes cerebral cortex damage in long-term treatment. Thus, a careful diet plan and monitoring of vitamin B 6 dose are recommended in patients who are supplemented with this vitamin. © TÜBİTAK

Influence of Tribulus terrestris extract on lipid profile and endothelial structure in developing atherosclerotic lesions in the aorta of rabbits on a high-cholesterol diet

The aim of this study was to investigate the pleotropic effects of an extract of a traditional herb, Tribulus terrestris (TT), on the lipid profile and vascular endothelium of the abdominal aorta in New Zealand rabbits fed a cholesterol-rich diet. Eighteen rabbits were randomly divided into three groups (n=6 for each). One experimental group (EG-I) was given a cholesterol-rich diet, a second experimental group (EG-II) was treated with TT following a cholesterol-rich diet, and a control group (CG) was fed a standard diet. Blood samples were collected on day 0 and then at weeks 4 and 12 to determine total serum cholesterol (TC), high density lipid-cholesterol (HDL-C), low density lipid-cholesterol (LDL-C) and triglyceride (TG) levels. Tissues were collected from the abdominal aorta for immunohistochemistry and transmission and scanning electron microscopy. In EG-II, the serum lipid profile was significantly lower than that of EG-I at week 12 with a reduction of TC: 65%; LDL-C: 66%; HDL-C: 64%; TG: 55%. Ultrastructural analysis revealed that endothelial damage was more prominent in EG-I compared to EG-II. The ruptured endothelial linings and damaged cellular surfaces increased in EG-I compared to EG-II. Our data indicate that dietary intake of TT can significantly lower serum lipid profiles, decrease endothelial cellular surface damage and rupture and may partially repair the endothelial dysfunction resulting from hyperlipidemia. © 2008 Elsevier GmbH. All rights reserved

Effects of excess vitamin B6 intake on cerebral cortex neurons in rat: An ultrastructural study

The aim of this study was to investigate whether excess of vitamin B6 leads to ultrastructural changes in cerebral cortex of forty-eight healthy albino rats which were included in the study. Saline solution was injected to to the control groups (CG-10, n=12 for 10 days; CG-15, n=12 for 15 days; CG-20, n=12 for 20 days). The three experimental groups (EG-10, n=12; EG-15, n=12; EG-20, n=12) were treated with 5 mg/kg vitamin B6 daily for 10 days (EG-10), 15 days (EG-15) and 20 days (EG-20). Brain tissues were prepared by glutaraldehyde-osmium tetroxide double fixation for ultrastructural analysis. No significant changes were observed in the control groups. The ultrastructural analysis revealed that the numbers of damaged mitochondria, lipofuscin granules and vacuoles were significantly higher in all the experimental groups than in the control groups (p<0.05). However, synaptic density was significantly decreased in the experimental groups as compared to the control groups (p<0.05). The results suggest that the excess of vitamin B6 intake causes damage to the cerebral cortex due to cellular intoxication and decreased synaptic density. Thus, careful attention should be paid to the time and dose of vitamin B6 recommended for patients who are supplemented with this vitamin

The effect of sleep disorders on quality of life in patients with epilepsy: A multicenter study from Turkey

Objective: We aimed to investigate sleep disorders in patients with epilepsy (PWE) and to investigate the effects of sleep disorders on quality of life. Methods: In our multicenter study conducted in Turkey, 1358 PWE were evaluated. The demographic and clinical data of the patients were recorded. The Insomnia Severity Index (ISI), Epworth Sleepiness Scale (ESS), Pittsburgh Sleep Quality Index (PSQI), Beck Depression Inventory (BDI), and Quality of Life in Epilepsy Inventory-10 (QOLIE-10) were administered. Results: The mean age of 1358 patients was 35.92 ± 14.11 (range, 18–89) years. Seven hundred fifty-one (55.30 %) were women. Some 12.7 % of the patients had insomnia (ISI > 14), 9.6 % had excessive daytime sleepiness (ESS > 10), 46.5 % had poor sleep quality (PSQI > 5), and 354 patients (26.1 %) had depressive symptoms (BDI > 16). The mean QOLIE-10 score was 22.82 ± 8.14 (10–48). Resistant epilepsy was evaluated as the parameter with the highest risk affecting quality of life Adjusted odds ratio (AOR = 3.714; 95 % confidence interval (CI): [2.440–5.652] < 0.001)). ISI (AOR = 1.184; 95 % CI: [1.128–1.243]; p < 0.001), ESS (AOR = 1.081; 95 % CI: [1.034–1.130]; p < 0.001), PSQI (AOR = 0.928; 95 % CI: [0.867 – 0.994]; p = 0.034), BDI (AOR = 1.106; 95 % CI: [1.084–1.129]; p < 0.001), epilepsy duration (AOR = 1.023; 95 % CI: [1.004–1.041]; p = 0.014), were determined as factors affecting quality of life. Significance: Sleep disorders are common in PWE and impair their quality of life. Quality of life can be improved by controlling the factors that may cause sleep disorders such as good seizure control, avoiding polypharmacy, and correcting the underlying mood disorders in patients with epilepsy