ObjectiveTo determine the diurnal variation,moon phase,and seasonal variation in the onset of stroke. MethodsThe time parameters,including the time,the moon phase and the season of the stroke occurrence for 905 in-patients from 1989-2001 were investigated.ResultsThere was a significant difference (D=0.155,P<0.01) for circadian rhythm in the onset of 321 cases with cerebral infarction,and the incidence frequency at dawn was much higher than that at other time,but the difference of the moon phase and seasonal rhythm in the onset of cerebral infarction were not significant(P>0.05).There were not diurnal variation,moon phase and seasonal rhythms in the onset for cerebral haemorrhage(P>0.05).ConclusionsThe cerebral infarction occur more frequently at dawn time.

Humans ; Occupational Diseases ; diagnosis ; Reference Standards

Humans ; Pesticides ; poisoning ; Poisoning ; prevention & control

AIM: To study the apoptotic effect of TNFα on rat pulmonary microvascular endothelial cells (PMVEC) and the influences of Fas, NF-κB in its mechanism. METHODS: Apoptosis of PMVEC was analyzed and quantitated with TUNEL, flow cytometer. The distribution of NF-κB was detected via histoimmunochemical staining in TNF-treated cells and the control. Northern blot was applied to assess the influence of TNF on PMVEC Fas expression. Fas antibody was used to investigate the apoptotic effect of Fas on PMVEC. Activation of caspase-8 was detected with Western blot. Expression of caspase-3 was analyzed with histoimmunochemical staining. RESULTS: After treatment with 5×108 U/L TNF for 24 hours, viable PMVEC significantly diminished. Apoptosis rate was 14.0%±3.1% detected with TUNEL, and 13.1% with flow cytometer. Histoimmunochemical staining showed that NF-κB relocated from cytoplasm to the nuclear. When the cells were co-cultured with TNF and APDC, an NF-κB inhibitor, less cells were viable and more cells were positively stained with TUNEL. Fas expression in PMVEC was elevated treated with TNF. Apoptosis in PMVEC was found aggravated, when the cells were co-cultured with TNF and anti-Fas antibody. The positive rate was 24.1%±1.5% with TUNEL. Increase of caspase-8 activation was manifested by Western blot following TNF stimulation. Caspase-3 expression was found elevated using histoimmunochemical staining. Cell permeable caspase-3 inhibitor significantly ameliorated PMVEC apoptosis induced by TNF. CONCLUSION: 1. Large dose of TNF(5×108 U/L) can induce apoptosis in rat PMVEC. 2. NF-κB has a protective effect on PMVEC apoptosis. 3. TNF up-regulates Fas expression in PMVEC. And the latter takes a part in apoptosis. 4. TNF induced caspase-8 activation in PMVEC, and more caspase-3 was expressed. These may be involved in PMVEC apoptosis induced by TNF.

Accidents, Occupational ; prevention & control ; Humans ; Metals ; poisoning

Acute Disease ; China ; Humans ; Insecticides ; poisoning ; Organophosphate Poisoning ; Poisoning ; prevention & control

AIM:To study the apoptotic effect of TNF? on rat pulmonary microvascular endothelial cells (PMVEC)and the role of Fas, NF-?B in its mechanism. METHODS: Apoptosis of PMVEC was analyzed and quantitated with TUNEL, flow cytometer. Northern blot was applied to assess the influence of TNF? on PMVEC Fas expression. Fas antibody was used to investigate the apoptotic effect of Fas on PMVEC. Activation of caspase-8 was examined by Western blot. Expression of caspase-3 was analyzed with histo-immunochemical staining. RESULTS:Growth curve showed that TNF? suppressed endothelial cell proliferation in a dose-dependent manner. After treatment with 5?10 6 U/L TNF?, apoptotic rate was 14.0%?3.1% detected with TUNEL, and 13.1% with flow cytometer. When the cells were co-cultured with TNF? and APDC, an NF-?B inhibitor, less cells were viable and more cells were positively stained with TUNEL. Fas expression in PMVEC was elevated after TNF? treatment. Co-culturing with Anti-Fas antibody aggravated PMVEC apoptosis. Caspase-8 activity and caspase-3 expression was elevated. Caspase-3 inhibitor significantly ameliorated PMVEC apoptosis. CONCLUSION: Large dose of TNF? (5?10 6 U/L) can induce apoptosis in rat PMVEC. NF-?B has an anti-apoptotic effect in PMVEC. TNF? up-regulates Fas expression in PMVEC, and the latter takes a part in apoptosis. Caspase-8 and caspase-3 are involved in PMVEC apoptosis induced by TNF?.

Acute Disease ; Adolescent ; Child ; Child, Preschool ; Female ; Humans ; Male ; Pancreatitis ; diagnosis ; etiology ; therapy ; Prognosis

Brucellosis ; diagnosis ; therapy ; Female ; Humans ; Malta ; Middle Aged ; Spondylitis ; diagnosis ; therapy

Astragalus Plant ; Cell Differentiation ; drug effects ; Cell Division ; drug effects ; Codonopsis ; Drugs, Chinese Herbal ; pharmacology ; Hematopoietic Stem Cells ; cytology ; drug effects