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Objective To investigate the effect of fluvastatin on the expressions of caspase-12,CCAAT/enhancer-binding protein homologous protein(CHOP), and c-Jun N-terminal kinases (JNK) in ischemia-reperfusion brain injury in rats.Methods Forty two rats were randomly divided into sham operation group (6 rats), ischemia-reperfusion (I/R) group (18 rats), and fluvastatin (Flu) group (18 rats).The rats of I/R and Flu groups were molded by modified Longa intraluminal thread, then put to death at 2 h occlusion and 24 h reperfusion point.Expressions of caspase-12, CHOP, and JNK were detected with immunohistochemistry and Western blot.Results Immunohistochemistry and Western blot showed that the expressions of caspase-12, CHOP, and JNK were increased at 24 h reperfusion.Compared to I/R group, the expressions of caspase-12 and CHOP in Flu group were decreased significantly (all P ＜0.01);and the expression of JNK had no difference between I/R and Flu groups(P ＞ 0.05).Conclusions The increased expression of caspase-12, CHOP, and JNK showed that endoplasmic reticulum stress was involved in the pathological process of ischemia-reperfusion brain injury.Fluvastatin could inhibit the expression of caspase12 and CHOP, and could delete endoplasmic reticulum stress (ERS) in ischemia-reperfusion brain injury.
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Objective To investigate the changes of cerebrovascular reserve capacity (CVR) in patients with ischemic white matter lesions (WML). Methods 126 patients with WML were divided into mild lesion, moderate lesion, severe WML groups and a normal control group by brain MRI. Blood pressure, blood sugar, blood fat were measured and past medical histories were recorded in details. All the patients were routinely examined using TCD to evaluate CVR. Hypercapnia was induced by inhaling the CO2 they breathed themselves and hypocapnia was done by voluntary hyperventilation. Results Age, hypertension, diabetes mellitus and Apo-A were the independent risk factors for WML. Compared with the controls , CVR decreased significantly in the severe and moderate WML groups (P < 0.05). The extent of WML negatively correlated to the cerebrovascular reserve capacity (rs = -0.273, -0.392). Conclusions Age, hypertension, diabetes mellitus and Apo-A are the independent risk factors for WML. CVR is significantly decreased in the WML.
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Objective To assess cerebrovascular reserve capacity in patients with obstructive sleep apnea-hypopnea syndrome(OSAHS).Methods One hundred and fourteen patients with OSAHS and 43 normal persons were enrolled in this study.The patients were divided into mild,moderate,severe according to apnea hypopnea index (AHI) and LSaO2 (lowest arterial oxygen saturation).All the patients and normal persons were routinely examined using transcranial Doppler (TCD) and end-tidal carbon dioxide partial pressure(ETCO2) to evaluate cerebrovascular reserve.Hypercapnia was induced by inhaling the CO2 which produced by the patients themselves,and hypocapnia was elicited by voluntary hyperventilation.Results CVR in the severe and moderate OSAHS were significantly lower than that in the control group [ (1.80 ± 1.34) ％/mm Hg and (1.43 ±1.05)％/mm Hg vs (2.93 ±0.93)％/mm Hg,P ＜0.05] when patients in the condition of hypocapnia.And there was no significant difference on CRV between the mild OSAHS group and control group [ (2.53 ±1.83 ) ％/mm Hg vs ( 2.93 ± 0.93 ) ％/mm Hg,P ＞ 0.05 ].When patients in the condition of Hypercapnia,CRV in the severe and moderate OSAHS were also significantly lower than that in the control group [ ( 1.83 ±1.32) ％/mm Hg and (1.08 ± 1.00)％/mm Hg vs (3.32 ± 1.53)％/mm Hg,P ＜ 0.05),AHI was negatively correlated with the cerebrovascular reserve at the condition of hypercapnia and hypocapnia (r=-0.665,-0.721; P ＜ 0.05 ).Conclusion Inhaling CO2 is a effective method for assessing CVR.Cerebrovascular reserve capacity is associated with AHI.Reduced CVR causes hemodynamics change being severe hypoxia in the moderate and severe OSAHS.
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Objective To investigate the clinical features and the gene mutation of patients with spinocerebellar ataxia type3 and type7.Methods The trinucleotide repeat mutations were detected by polymerase chain reaction (PCR),agarose gel electrophoresis method,and DNA sequencing in 13 patients,4 related members and 4 common members from 3 spinocerebellar ataxia families.Results Among the 13 patients,four patients had SCA3/MJD(CAG) n expansion mutation(n = 65 ～ 74),nine patients had SCA7 allele expansion for 40 ～ 52 times.Patients with type 3 or 7 showed significant difference in nervous system injury.Conclusion The difference of clinical feature might be used in diagnosis of SCA3/MJD and SCA7,but genotype determination would be the only method of definite diagnosis.
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Objective To observe the changes of PECAM-1,Bcl-2 and Bax expressed by ischemic cerebrum of adult rats after focal cerebral ischemia. Methods Middle cerebral artery occlusion (MCAO) models were made by operation with Longa suture method in Wistar rats. The expression levels of PECAM-1,Bcl-2 and Bax at the 6th,12th,18th,24th,48th,72nd hour after MCAO were detected by immunohistochemistry staining. Results The expression levels of PECAM-1,Bcl-2 and Bax in cerebrum were significantly increased after MCAO. The expression levels of Bcl-2 we、re up to the peak at the 12th hour after MCAO, while the levels of Bax and PECAM-1 were up to the peak at the 24th and 48th hour after MCAO. At the 72nd hour after MCAO, the expression levels of PECAM.1.Bcl-2 and Bax were still higher than that in the control group(all P＜0.001).Conclusions PECAM-1,Bcl-2 and Bax participate in the different pathological stages of focal cerebral ischemia.