Effects of repetitive transcranial magnetic stimulation on adenosine triphosphate content and microtubule associated protein-2 expression after cerebral ischemia-reperfusion injury in rat brain

Background Repetitive transcranial magnetic stimulation （rTMS） research has mainly been focused on the therapeutic effect of psychiatric disorders and Parkinson＇s disease. A few studies have shown that rTMS might protect against delayed neuronal death induced by transient ischemia, enhance long-term potentiation in ischemic conditions and affect regional brain blood flow and metabolism. The aim of this study was to determine the effects of repetitive transcranial magnetic stimulation （rTMS） on adenosine triphosphate （ATP） content and microtubule associated protein-2 （MAP-2） expression in rat brain after middle cerebral artery occlusion （MCAO）/reperfusion. Methods To study the effects of different timecourses of rTMS on ATP content and MAP-2 expression, 90 rats were randomly divided into three groups （30 rats in each group）. To study the effects of multiple rTMS parameters on ATP content and MAP-2 expression, the rats in each group were further divided into six subgroups （five rats each）. The rats were sacrificed at 1-hour, 24-hour and 48-hour intervals after reperfusion, and the brain tissues were collected for the detection of ATP and MAP-2. Results rTMS could significantly increase ATP content and MAP-2 expression in the left brain following ischemic insult （P 〈0.01） and different rTMS parameters had different effects on the ATP level and the MAP-2 expression in the left striatum. A high-frequency rTMS played an important role in MAP-2 expression and ATP preservation. Conclusions This study revealed that rTMS induced significant increase of ATP content and MAP-2 expression in the injured area of the brain, suggesting that the regulation of both ATP and MAP-2 may be involved in the biological mechanism of the effect of rTMS on neural recovery. Therefore, rTMS may become a potential adjunctive therapy for ischemic cerebrovascular disease.

Correlation between neuronal injury and Caspase-3 after focal ischemia in human hippocampus

Background Cerebral ischemia is a significant clinical problem, and cerebral ischemia usually causes neuron injury such as apoptosis in various brain areas, including hippocampus. Cysteinyl aspartate-specific protease (Caspases) are fundamental factors of apoptotic mechanism. Caspase-3 inhibitors show effect in attenuating brain injury after ischemia. But all the results were from animal models in research laboratories. This study aimed at investigating the correlation between the change of ischemic neuronal injury and Caspase-3 post-ischemia in human hippocampus. Methods We selected and systematized 48 post-mortem specimens from 48 patients, who died of cerebral infarction. Morphological change was firstly analyzed by observing hematoxyline/eosin-staining hippocampal sections. The expression of Caspase-3 was investigated using the methods of in situ hybridization and immunohistochemistry. Terminal deoxynucleotidyl transferase-mediated 2’-deoxyuridine 5’-triphosphate-biotin nick-end labeling (TUNEL) method was used to clarify the involvement of Caspase-3 in neuron death. The loss of MAP 2 (MAP-2) was applied to judging the damaged area and degree of neuronal injury caused by ischemia.Results In the CA1 sector of hippocampus, Caspase-3 immunostaining modestly increased at 8 hours [8.05/high-power field (hpf)], dramatically increased at 24 hours (24.85/hpf), decreased somewhat after 72 hours. Caspase-3 mRNA was detectable at 4 hours (6.75/hpf), reached a maximum at 16 hours (17.60/hpf), faded at 72 hours. TUNEL-positive cells were detectable at 24 hours (10.76/hpf), markedly increased at 48-72 hours. The loss of MAP-2 was obviously detected at 4 hours, progressed significantly between 24 and 72 hours; MAP-2 immunoreactivity was barely detectable at 72 hours. Before 72 hours, the Caspase-3 evolution was related with the upregulation of TUNEL and the loss of MAP-2. The positive correlation between Caspase-3 mRNA and TUNEL was significant at the 0.05 level (correlation coefficient was 0.721); the negative correlation between Caspase-3 mRNA and MAP-2 was significant at the 0.05 level (correlation coefficient is 0.857). In the early stage (before 72 hours), the staining of Caspase-3 mRNA and immunohistochemistry was predominantly present in cytoplasm; the staining of TUNEL was predominantly localized in nucleus. At 4-16 hours, most neurons in hippocampal CA1 areas had relatively normal morphology; at 24-48 hours, neurons showed apoptotic morphology; at 72 hours, most cells showed significantly pathological morphology. Conclusions There exist a time-dependent evolution of neuronal damage after hippocampal ischemia in human brain, which was characterized by its close correspondence to Caspase-3.

Postinfectious encephalitis (21 cases appended)

To report 21 cases of postinfectious encephatitis according to ICD-NA, postinfectious/parainfectious encephalitis is an independent disease Methods Using the uniform criteria provided by The Council of State and Territorial Epidemiologists (CSTE) and Centers for Disease Control and Prevention (CDC), we diagnosed postinfectious encephalitis among patients admitted to The First Hospital of Harbin Medical University and analyzed the characteristics of these cases Results All the patients had histories of preceding infection, and most of them suffered from mental and conscious disorders Adrenocortical hormone was effective Conclusions Postinfectious encephalitis is an independent disease According to this article, about 10% patients with encephalitis admitted to our hospital are postinfectious