ObjectiveThis study is designed to investigate the relationship between STR polymorphism in HO-1 gene promoter and susceptibility of CAD,in order to provide a new strategy for prevention and treatment of CAD by using HO-1.Methods200 patients who were diagnosed as CAD by coronary angiography were selected in this study.100 subjects without evidence of CAD under coronary angiography with their sex and age similar to CAD patients were selected as controls.Genotyping was performed using polymerase chain reaction followed by capillary electrophoresis automated DNA sequencer.Each size of the (GT) n repeat was calculated using the GeneMapper Analysis software.ResultsA (GT)n polymorphism was found in the HO-1 gene promoter with n =16 ～39.Subjects with n≤29 expressed much more HO-1 protein than those with n ＞29( P ＜0.01 ).The alleles were then classified into two subgroups,S'allele (n 29 ) and L'allele (n ＞29),the subjects were then classified as having an S/S,S/L,or L/L genotype.Subjects with the L allele ( L/L + L/S genotypes) had more chance to get CAD than those with S/S genotype ( adjusted OR =1.83,95 ％ CI =1.04 - 3.24).Stratified analysis further showed that L allele ( L/L + L/S genotypes) was susceptive to CAD in patients who smoke (adjusted OR =2.59,95％ CI =1.16 -5.80).ConclusionsThe (GT)n polymorphism in HO-1 gene promoter is related to susceptibility to CAD,especially in those patients who smoke.

China ; epidemiology ; Heat Stroke ; epidemiology ; Humans

Objective To investigate whether nestin-positive cells can be isolated from human fetal pancreases and cultured in vitro for passages. Methods The islet-like cell clusters (ICCs) were isolated from pancreases of induced human fetuses at 16, 18, 20 gestational weeks and cultured subsequently. Immunohistochemical staining and reverse transcription-polymerase chain reaction (RT-PCR) were used to detect the expression of the nestin, pancreatic and duodenal homeobox gene-1 (PDX-1/IPF-1), islet endocrine hormone insulin and glucagon. Results Nestin-positive cells, which may further transform into sphere cell clusters that include PDX-1, insulin and glucagon expressing cells, as well as nestin-positive cells, were isolated from the ICCs in vitro and cultured with several passages. Conclusions The nestin-positive cells can be isolated from fetal pancreases, and may have the capability to proliferate and differentiate into islet endocrine cells.

Objective To explore the effect of Xiao Ban Xu, a compound Chinese traditional medicinal prescription, on the expression of collagenⅠand Ⅲ of keloid fibroblasts in vitro. Methods Six samples of keloid fibroblasts (KFB) and 6 samples of normal fibroblasts (NFB) entered the study as experimental and control groups, respectively. With the application of Xiao Ban Xu (10?g/ml), the fibroblast culture system and the ABC immunocytochemical staining method were used to investigate the expression of collagenⅠand Ⅲ of KFB and NFB. Results The density of the staining of collagenⅠand Ⅲ in the experimental group was much higher than that in the control group, with (7675 4?825 5 vs 2305 2?320 4 and 10595 2?1311 5 vs 2434 8?356 9; t =13 37 and 12 66, P =0 00004 and 0 00005) or without (11113 1?1304 9 vs 3519 6?236 0 and 11157 7?1300 3 vs 2626 5?426 3; t =14 42 and 13 47, P =0 00003 and 0 00004) the addition of Xiao Ban Xu. Compared with blank control group, the density of the staining of collagenⅠand Ⅲ was degenerated greatly in the experimental group after 48 hours of application of Xiao Ban Xu (7675 4?825 5 vs 11113 1?1304 9 and 10595 2?1311 5 vs 11157 7?1300 3; t =10 31 and 4 68, P =0 0001 and 0 0054). Furthermore, the inhibition ratios of collagenⅠwas 30 7%, and the one of collagen Ⅲ 5 1%, in the experimental group. Conclusions The expression of collagenⅠand Ⅲ of keloid fibroblasts in vitro may be significantly more intensive than the one of normal skin fibroblasts. It seems that the expression of collagenⅠand Ⅲ, especially collagenⅠ, in keloid fibroblasts and normal skin fibroblasts in vitro may be suppressed greatly by the application of Xiao Ban Xu.

Objective To investigate the expression of nestin in keloid and hypertrophic scarring.Methods Samples were obtained from patients with normal skin(n=8),flat scars(n=7),keloids(n=8) and hypertrophic scars(n=8),respectively.Immunohistochemistry staining was used to measure the nestin expression in above samples.Nestin positive cells were counted to evaluate the expression levels.Results ①Nestin expression was detected in basal cells,prickle cells,sweat glands,hair follicles,sebaceous glands,and vascular endothelial cells in 8 samples of normal skin,and in fibroblasts in 7 of them.Nestin was also positively expressed in abovementioned cells or skin appendages in samples of flat scars,keloids and hypertrophic scars.②Nestin positive cell counts(epidermic cells,fibroblasts,and vascular endothelial cells) in keloids and hypertrophic scars were significantly higher than those in normal skin and flat scars(P0.05).Conclusions The increased expression of nestin in epidermic cells,fibroblasts,and vascular endothelial cells in keloid and hypertrophic scarring supports a possible role of nestin as fibrosis inducing factors in keloids and hypertrophic scars.

Objective To investigate the expression of nestin in fibroblasts of adult human dermis.Methods A total of 6 samples of normal human skin were collected.Immunohistochemistry and immunocytochemistry staining were used to detect the nestin expression in adult human dermis and in cultured fibroblasts of different passages(3rd,5th,7th,10th,and 12th passages,respectively) in vitro.Nestin positive cells were counted to evaluate the expression quantity and intensity.Results There were 103.3?67.4 fibroblasts per square millimeter(mm~2) of adult human dermis,and the nestin positive fibroblasts accounted for(9.5?3.0)% of total amount.The amount of nestin positive fibroblasts in vitro was obviously higher than that in vivo.Significant difference was observed in the amount of nestin expression among different passages(P

Objective To discuss the effect of small needle knife therapy on collagensⅠ and Ⅲ in the hypertrophic scar tissues that was subcutaneously transplanted into nude mice. Methods Six samples of human hypertrophic scar tissues without cuticle were subcutaneously transplanted into the back of 24 nude mice to create the animal models of hypertrophic scar. Ten days after of the operation,the mice were divided into control,0.1 mg/ml triamcinolone,0.2 mg/ml triamcinolone,and small needle-knife groups with 6 mice in each. Specimens of the scar tissues were collected in 14 days for immunohistochemistry to detect the collagen Ⅰ and Ⅲ. Results In all the groups,collagens Ⅰand Ⅲ distributed extensively in the cytoplasm of fibroblast and tissues. Image analysis showed that the concentration of collagens Ⅰand Ⅲ in 0.1 mg/ml and 0.2 mg/ml triamcinolone groups were significantly lower than those in the control (0.09?0.03,0.11?0.05 and 0.12?0.02,0.11?0.01 vs. 0.17?0.04,0.19?0.03,P0.05). Conclusions Small needle-knife therapy can reduce the concentration of collagens Ⅰand Ⅲ in transplanted hypertrophic scar tissues in nude mice.

Objective To examine the expression of p44/42 mitogen -activated protein kinase (p44/42MAPK) and Phospho-p44/42MAPK in cicatrix (hy pertropic scars and keloids) and to aim at exploring the role of activated p44/ 42 MAPK pathway in development of cicatrix. Methods In or der to analyse the differences, 10 samples of normal skin (NS), hypertropic scar s (HS) and keloids (K) were collected, and then the extracted cytoplasmic protei ns from each tissue were examined by Western blotting for p44/42 MAPK and Phosph o p44/42MAPK and immunohistochemical staining with specific antibodies was emplo yed to determine that in fibroblasts of K, HS and NS. Results There was no evident difference of p44/42MAPK in the tissues and fibroblas ts between cicatrix and NS, but Phospho-p44/42MAPK was obviously higher in cica trix than that in NS. In cicatrix, there was no evident difference of p44/42MAPK in tissues between HS and K, while in fibroblasts, Phospho-p44/42MAPK in K was much higher than in HS. Conclusion Activation of p44/42MA PK pathways involves in formation of cicatrix.

Objective To explore the mechanism of inhibitory effect of dimethyl sulfoxide (DMSO) on the hyperplasia of the fibrous capsule around the tissue expander. Methods The experimental model was established in rats as follows: after implanting the expander on the back of rats, 30 % DMSO or normal saline was injected into the expander. The former was classified as experimental group, and the latter as control group. The cystic wall was resected after the skin and soft tissues were expanded. In situ hybridization and the immunohistochemical staining were used to determine the expression of typesⅠand Ⅲ of collagen and procollagen mRNA in the cystic walls. Results It was found that both the typeⅠand Ⅲ of collagen content and the expressing quantity of mRNA of procollagen in the cystic wall of the experimental group were less than those of control group. Conclusion The results imply that the mechanism that DMSO inhibits the expression of typesⅠand Ⅲ of collagen in the fibrous cystic wall may be achieved through down-regulating the genetic expression of procollagen in the fibroblasts.