ABSTRACT
Intracranial aneurysm is an abnormal bulging of intracranial artery wall. Its rupture can lead to subarachnoid hemorrhage. About 50% of patients with aneurysmal subarachnoid hemorrhage will die or have poor outcomes. At present, intracranial aneurysm is considered as a complex disease associated with genetic and environmental factors. Although the etiology of intracranial aneurysm is not completely clear, a lot of evidence has shown that the genetic factor plays an important role in the processes of its occurrence, development and rupture. This article reviews the advances in gene linkage research, genome wide association studies, and gene expression research in intracranial aneurysm in recent years.
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Objective To explore the role and expression of cell apoptosis regulatory genes in patients with temporal lobe epilepsy characterized by hippocampus sclerosis.Methods The experimental specimens were obtained from 15 patients with temporal lobe epilepsy (epilepsy group) and 6 control samples (control group) were obtained from temporal lobe excision of brain trauma decompression,investigated neuron apoptosis by HE stain,TdT-mediated dUTP-biotin nick end labeling (TUNEL) method,and determined the expression of bcl-2,bax and caspase-3 by immunohistochemistry.Results The evidence of neuron apoptosis was not found by HE stain in both control group and epilepsy group.Positive cells was not found in control group,but was obviously observed in epilepsy group by TUNEL staining [(4.39 ± 2.04) numbers/100].Unlike that in normal adult brain,bcl-2 immunoreactivity was obviously observed in some neurons in epilepsy group[(6.72 ± 3.36) numbers/100] (P ＜ 0.01).Compared with control group,bax protein in epilepsy group was mild expression (P ＞ 0.05).Two cases in control group were detected the expression of caspase-3 protein,and caspase-3 significantly increased in epilepsy group [(1.07 ± 0.43),(9.54 ± 3.68) numbers/100] (P ＜ 0.01).Conclusions Neuron apoptosis is an important cause of hippocampal sclerosis of human epilepsy.bcl-2 and caspase-3 may play an important role in this process.
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Objective To investigate the relationship of programmed cell death 4(PDCD4) with the invasion of astrocytic glio-mas .Methods Using the immunohistochemical method to detect the expression of PDCD4 in astrocytic gliomas in different grades . Measuring the peritumoral low-density area on MRI scan ,then compared with the results of immunohistochemical expression .Re-sults The downregulation of PDCD4 was with the increasing of the malignant grade of astrocytic gliomas .The tumor grade malig-nancy was positively correlated with the grade of the peritumoral low-density area on MRI scan(P<0 .05) ,while the expression of PDCD4 was negatively correlated with the grade of astrocytic gliomas (P<0 .01) .Conclusion PDCD4 might serve as one of the in-dicators of invasion and malignant phenotype for astrocytic gliomas .
ABSTRACT
This article reviews the roles of the volume embolization ratio in the assessment of the efficacy of intracrainal aneurysm embolization, particularly the stability, complications, pathological healing after the embolization, as well as the volume embolization ratio and morphological characteristics of aneurysms, including the relationship between the size of aneurysm, the size of aneurysmal neck and the aneurysm rupture.
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<p><b>OBJECTIVE</b>To assess the role of oxidative metabolism and nitric oxide synthesis for elucidating their pathophysiological mechanisms in a Tibetan patient with essential hypertension.</p><p><b>METHODS</b>The serum levels of total superoxide dismutase (T-SOD), malondialdehyde (MDA), total antioxidant capacity (T-AOC), nitric oxide (NO) and nitric oxide synthase (NOS) were assayed in sixty native Tibetans (thirty hypertensive patients and thirty healthy volunteers as control).</p><p><b>RESULTS</b>The levels of T-SOD, T-AOC, NO and NOS were significantly lower in the patient group than in the control group (P < 0.01); MDA was significantly higher in the patient group than in the control group (P < 0.01). The level of MDA had a strong negative correlation with T-SOD, T-AOC, NO and NOS (r = -0.82, -0.76, -0.79, -0.73, respectively, P < 0.001 for all).</p><p><b>CONCLUSION</b>Tibetan patients with essential hypertension (EH) may have underlying oxidative metabolism dysfunction and depressed NO synthesis, both responsible for the hypertensive process.</p>