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Objective To investigate the prevalence and pattern of androgenetic alopecia (AGA) in Shanghai through a community-based survey. Methods A cluster sampling survey was done among the residents in Beixinjing Community, Changning District, Shanghai. All the subjects were asked to fill a questionnaire to provide their general information, including sex, age, native place, physical status, life habit, family history, etc. The diagnosis of AGA was made by dermatologists. To determine the pattern of hair loss,Norwood-Hamilton classification system and Ludwig classification system were used for male AGA and female AGA, respectively. All the data were statistically analyzed by EpiData and SPSS11.5 software. Results Totally, 7056 subjects completed the questionnaire, including 3519 males and 3537 females, and the response rate was 72.5%. AGA was diagnosed in 809 patients, consisting of 701 males aging from 19 to 91 years (mean 64.16±11.9 years) and 108 females aging from 35 to 91 years (mean 70.46±18.89 years). The standardized prevalence (SP) was 9.47% in total, 15.73% in males and 2.73% in females; the difference was significant between males and females (χ2=356.00, P<0.001). A family history of AGA was observed in 52.7% of all subjects including 391 (55.78%) males and 35 (32.41%) females. Type Ⅲ vertex involvement was the most common type in men aging from 20 to 70 years old, and type Ⅵ in those over 70 years old. Grade Ⅰ and Ⅱ predominated in female AGA. Conclusions The results of this survey indicate that the prevalence of AGA is remarkably higher in men than that in women. Furthermore, the prevalence is steadily increased with advancing age in Shanghai.
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BACKGROUND: Previous studies have demonstrated that the responses of myocardium to short periods of ischemia/reperfusion are associated with changes in the expressions of a variety of genes. However, the characteristics of these changes are unknown.OBJECTIVE: To clone and analyze a stress-inducible gene characteristics in order to study the molecular mechanism of myocardium to short periods of ischemia/reperfusion damage.DESIGN: A controlled animal study.SETTING: Department of Hematology, Xiangya Hospital of Central South University.MATERIALS: Sixteen castrated male German Landrace-type domestic porcines, weighing between 21 and 39 kg, were provided by the laboratory of Department of Experimental of Cardiology at Bad Nauheim in Germany. The porcines were randomly divided into two groups ischemia/reperfusion group (n =14) and control group (n =2). The porcines in the ischemia/reperfusion group were observed at 0, 30 and 90 minutes of reperfusion after reocclusion, and ischemia and non-ischemia myocardial tissues were harvested from each pocrine.METHODS: The experiments were performed in the laboratory of Department of Experimental Cardiology of Max-Planck Institute for Physiological and Clinical Research at Bad Nauheim in Germany and the Department of Hematology, Xiangya Hospital of Central South University from July in 1998 to May in 2007. All the animals were anesthetized and thoracotomized. Following 30 minutes of stabilization, the left anterior descending coronary artery (LAD) was occluded for 10 minutes followed by 30-minute reperfusion and then another 10-minute reocclusion. The porcines were killed immediately at corresponding time points. The sham-operated animals were killed without occlusion. Experimental tissue was removed from the LAD area and control tissue from the region of the left circumflex coronary artery area. Firstly, a porcine heart cDNA library was screened, DNA and deduced amino acid sequences were then analyzed. Meanwhile, short periods of myocardium ischemia/reperfusion was performed by occluding porcine LAD followed by reperfusion as mentioned above, and total RNAs isolated from myocardium or a variety of other tissues were used for Northern blotting. Quantitation of mRNA levels was accomplished by using a PhosphorImager and Image Quant software, the ration of mRNA/18S rRNA was suggested as the level of gene expression.MAIN OUTCOME MEASURES: ① DNA and amino acid sequences analysis of the cloned gene; ② Analysis of the cloned gene expression.RESULTS: All the 16 porcines were involved in the final analysis of results. After screening, a cDNA fragment with 3 461 base pairs was obtained. DNA sequencing and searching revealed that this cDNA shared 86% identity to human structural maintenance of chromosome 6 gene (hSMC6), and 84% identity to Mus musculus SMC6 (mSMC6). Furthermore, a largest polypeptide deduced from this cDNA contained 1007 amino acid residues, and protein homology searching indicated that the predicted polypeptide carried 92% and 89% identity to hSMC6 or mSMC6 protein respectively. Thus, the cloned cDNA was referred to as a porcine homology gene to hSMC6 (pSMC6). The results of Northern blotting showed that the expression of the pSMC6 mRNA in ischemia/reperfusion myocardium was increased, and its mRNA existed in all organs tested. CONCLUSION: A stress-inducible gene of pSMC6 from porcine myocardium has been cloned, which is high homology to hSMC6 gene, and the pSMC6 or along with other molecules is possible involved in the early repair of myocardium to DNA damage caused by ischemia/reperfusion in the porcine heart.
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Objective To detect the expression of integrin ?5?1 in restenosed human vein grafts.Methods The expression of integrin ?5?1 and ?-smooth muscle actin(?-SMA) in 30 resected restenosed human vein grafts(from Kerfuff clinical hospital of Germany) was detected by confocal immunofluorescence with specific antibodies against ?5?1 and ?-SMA.Images were processed with Silicon Graphics Octane.Results In normal veins,integrin ?5?1 expression was very weak in media smooth muscle cells and in endothelium,and ?-SMA expression was present in media smooth muscle cells.In the restenosed vein grafts,integrin ?5?1 was strongly stained in the media smooth muscle cells and intimal endothelial cells,and moderately in the intimal smooth muscle cells,?-SMA was present in media smooth muscle cells and in the intimal smooth muscle cells.Conclusion Our research reveals that integrin ?5?1 is significantly upregulated in the media smooth muscle cells and intimal endothelial cells in the restenosed human vein grafts,suggesting the participation of integrin ?5?1 in the restenosis formation of human vein grafts.
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The distribution of TrkA and the postnatal development(PD) of TrkA and ChAT-immunoreactive(-IR) neurons andthe relation between them in the basal nucleus of Meynert of rats were studied with immunohistochemical method. The number,mean profile areas and grey degree of TrkA-IR and ChAT-IR neurons were examined with image analyser. The data revealed thatTrkA-IR neurons were localized in the basal forebrain of rats. TrkA immunostaining was present at PDI, but ChAT was not.ChAT immunostaining was present at PD5. Most densely stained TrkA and ChAT neuronal bodies and fibers were present atPD20, the mean grey degrees of TrkA-IR and ChAT-IR neuronal profiles reached its peak. Both TrkA and ChAT neurons beganto cline at PD30 and maintained a relatively higher level in the adult. However, during aging both TrkA and ChAT-IR neuronsatrophy and became smaller than that in the adult. The number of TrkA-IR and ChAT-IR neurons were decreased by 41.38% and 51.61%; the mean profile areas decreased by 15.7% and 12.8%; and the mean grey degrees by 29.9% and 9.9%, respec-tively. The mean profile areas of TrkA-IR and ChAT-IR neurons from PD5 to aged rats were positively correlated. The resultsindicated that the expression of TrkA was earlier than ChAT. The expression of TrkA and ChAT followed a very similar tempo-ral pattern in the basal nucleus of Meynert from PD5 to aged rats, suggesting that TrkA might participate the regulation ofChAT-IR neuronal development, differentiation, maturation, and ageing. The down-regulation of TrkA and ChAT of aged ratsis associated with neuronal atrophy and loss and may contribute to the pronounced vulnerability of these neurons to degenerationin aging animals and Alzheimer's disease.
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By means of cell hybridization in situ with digoxigenin labeled probe, we detected the expression of C-myc protooncogene in peripheral blood mononuclear cells from 31 SLE patients and 10 healthy persons. The results showed that the level of C-myc mRNA in SLE patients was significantly higher than that in normal controls, and the increased level correlated with disease activity. There was also a positive correlation between C-myc mRNA and serum levels of ANA, anti-dsDNA, IgG, C3. Our study indicates that C-myc gene is important for the pathogenesis of SLE.
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Objective To investigate the postnatal developmental rule of TrkA and ChAT\|immunoreactive(ChAT\|ir) neurons and the relationship between TrkA and ChAT\|ir neurons in the horizontal limb of diagonal band(HDB) of rats. Methods Immunohistochemistry technique combined with image analyser were used. Results TrkA and ChAT\|ir neurons localized in the neurons of basal forebrain of rats. TrkA immunostaining was present at postnatal day 1(PD1), but ChAT immunostaining was present at PD5 Most densely stained TrkA and ChAT neuronal bodies and fibers were present at PD20, while the mean grey degrees of TrkA and ChAT\|ir neurons reached to the peak. Both TrkA and ChAT began to decline at PD30 and maintain a relatively higher level in the adult. However, during aging both TrkA and ChAT\|ir neurons atrophied and became smaller than that of adult. The number of TrkA and ChAT\|ir neurons decreased 39 8% and 33 3%;the mean areas 15 7% and 12 8%; the mean grey degree values were 29 9% and 9 9%, respectively. The mean areas, grey degrees and numbers of TrkA and ChAT\|ir neurons from PD5 to aged rats had positive correlation. Conclusion The results indicate that the expression of TrkA was earlier than ChAT. The expression of TrkA and ChAT followed a very similar temporal pattern in HDB from PD5 to aged rats, suggesting that TrkA may participate in the regulation of ChAT\|ir neuronal development, differentiation, maturation and aging. The down\|regulation of TrkA and ChAT of aged rats is associated with neuronal atrophy and loss and may contribute to the pronounced vulnerability of these neurons to degeneration in aging animals and Alzheimer disease.\;