Objective To study the expressions of TGF-?1 and p21WAF1 in middle ear cholesteatoma and discuses their effects on cholesteatoma.Methods The expressions of TGF-?1 and p21WAF1 were determined by immunohistochemical S-P technology and computer image analysis in 20 specimens of cholesteatoma epithelium and 10 specimens of normal external canal skin.Results ① p21WAF1 and TGF-?1 could be detected in middle ear cholesteatoma and in normal ear canal skin.p21WAF1 was located at karyon,taking on yellow-brown pellet;TGF-?1 was located at cytoplasmic,taking on yellow-brown pellet.②The p21WAF1 positive rate in middle ear cholesteatoma was 65%;and there were almost no positive cells in normal external ear canal skin.p21WAF1 positive cells were detected in each layers,its LI was 28.9%?6.7%.Compared with normal ear canal skin,the expression level of p21WAF1 in middle ear cholesteatoma epithelium was higher than that in normal ear canal skin(P

AIM: To study the molecular mechanism of reproduction dysfunction in pubertal diabetic rat, the level of 5?-reductase (type 2) mRNA in testis, epididymis and prostate in diabetic rat was detected. METHODS: The gene expression of 5?-reductase (type 2) was detected by Northern blot. RESULTS: In the caput of the epididymis, the expression of 5?-reductase (type 2) mRNA of D and ID groups was less than that of C group. CONCLUSION: The decreased expression of 5?-reductase (type 2) results in the decreased production of dihydrotestosterone, which influences the development and function of reproduction system in pubertal rats. [

BACKGROUND:Ca2+expression in astrocytes has been found to be closely related to cognitive function,and the Ca2+signaling pathway regulated by inositol 1,4,5-trisphosphate receptors(IP3R2)and ryanodine receptor(RYR)2 receptors has become a hot spot in the study of cognitive disorder-related diseases. OBJECTIVE:To investigate the expression of Ca2+signals mediated by IP3R2 and RYR2 in hippocampal astrocytes in animal models of delayed encephalopathy after acute carbon monoxide poisoning,and to explore the possible pathogenesis of delayed encephalopathy after acute carbon monoxide poisoning. METHODS:C57BL mice with qualified cognitive function were selected by Morris water maze experiment and randomly divided into control group and experimental group.An animal model of delayed encephalopathy after acute carbon monoxide poisoning was established by static carbon monoxide inhalation in the experimental group,and the same amount of air was inhaled in the control group.Behavioral and neuronal changes,astrocyte specific marker glial fibrillary acidic protein,IP3R2,RYR2 receptor and Ca2+concentration in astrocytes of the two groups were detected using Morris water maze,hematoxylin-eosin staining,western blot,immunofluorescence double labeling and Ca2+fluorescence probe at 21 days after modeling. RESULTS AND CONCLUSION:In the Morris water maze,the escape latency of the experimental group was significantly longer than that of the control group(P<0.05).Hematoxylin-eosin staining results showed that in the experimental group,the number of hippocampal pyramidal cells decreased,the cell structure was disordered,and the nucleus was broken and dissolved.Immunofluorescence results showed that IP3R2 and RYR2 were co-expressed with glial fibrillary acidic protein in the hippocampus,and the expressions of IP3R2,RYR2 and glial fibrillary acidic protein were up-regulated in the hippocampus of the experimental group(P<0.05).Western blot analysis showed that the expressions of IP3R2,RYR2,and glial fibrillary acidic protein in the hippocampus of the experimental group were increased(P<0.05).Ca2+concentration in hippocampal astrocytes increased significantly in the experimental group(P<0.05).To conclude,astrocytes may affect Ca2+signals by mediating IP3R2 and RYR2 receptors,then impair the cognitive function of mice with carbon monoxide poisoning,and eventually lead to delayed encephalopathy after acute carbon monoxide poisoning.