Objective To isolate and culture the hair follicle Bulge cells of rats and study their morphological, immunological characteristics. Methods Hair follicle Bulge obtained by micromanipulation and enzyme digestion was cultured in intro. The morphological features and numbers of Bulge cells were identified and counted with light microscopy. Immunocytochemical staining was used to detect expressing of K19 and ?_ 1integrin in cultured cells. Results Bulge cells after enzyme digestion pasted rapidly. Cells were small and round, paving stone-shape, and had a large ratio of nuclear to cytoplasm. The characteristics suggested a primitive morphologic feature. Cells growth well and could maintain low differentiation and higher reproductive activity, they co-expressing K19 and ?_ 1integrin, immunofluorescence staining showed the cells expressed ?6-integrin strongly, weakly or no expressing CD71. Conclusion This culture system can amplify a lot of pure hair follicle Bulge cells in short time. We successfully isolate and culture the hair follicle Bulge cells of rats in intro and can keeping its property for a long time.

Objective To establish a method for the cultivation of hain follicle outer root sheath (ORS) cells of murine vibrissa and to study their expression of uPA/uPAR. Methods The ORS cells of murine vibrissa were cultured by combination of enzyme digestion and tissue culture with the feeder layer of dermal sheath cells of the hair follicle. The cells and their uPA/uPAR expression were identified by immunocytochemistry (ICC). Results The feeder layer of DS was suitable for the culture of ORS cells. ORS cells expressed uPA/uPAR protein. Conclusion The DS of hair follicle is a better feeder layer for the growth of ORS cells. ORS cells have the ability to migrate and proliferate.

Objective To investigate the feasibility of the transdifferentiation of hair follicle bulge cells into corneal epithelial cells in vitro. Methods The hair follicle bulge cells from 7- to 8-day SD rats were isolated and cultured in vitro, then co-cultured with rabbit corneal limbal stroma in transwell-cultured system. The differentiation and development of hair follicle bulge cells were observed, and immunocytochemical staining were used to detect expression of K19 and K12 in hair follicle bulge cells. Results The cultured bulge cells possesed high proliferation and low differentiation, co-expressed K19 and ?_ 1 integrin, but part of them expressed K12 after 2-week co-culture with rabbit corneal limbal stroma in transwell-cultured system. Conclusion Rat hair follicle bulge cells could transdifferentiate into corneal epithelial cells induced by corneal limbal stroma in vitro.

ObjectiveTo explore the morbidity rate of deviation of nasal septum about personnels who take part in physical examination in the enterprise and facilities of Qinhuangdao,and clinic symptom.MethodsTransverse questionnaire investigation and normal physical examination were adopted.2604 personnels who take part in physical examination were choiced.ResultsMorbidity rate of deviation of nasal septum was 17.6％.The rate of men' s exceeds that of women' s.ConclusionMorbidity rate of deviation of nasal septum was rather high,clinic symptom of snuffle was primary.

Objective To construct the eukaryotic expression plasmid of pEGFPC1uPAR gene and explore the effect on the proliferation and invasion ability of Pam 212 cells. Methods The human uPAR cDNA was cloned by PCR, and inserted into the eukaryotic expression plasmid pEGFPC1. After identification of sequencing, the reconstructive plasmid was transformed transiently into Pam 212 cells, then the cell growth and the invasion ability were evaluated. Results The reconstructive plasmid of pEGFPC1uPAR was validated by sequencing. The reconstructive plasmid can promote the growth of Pam 212 cells and enhance the invasion ability. Conclusion The pEGFPC1uPAR plasmid was constructed successfully and uPAR was confirmed to promote the growth and the invasion ability of Pam 212 cells, which lay the foundation for further studies of uPAR in vivo.

Objective　To investigate the effect of T-2 toxin on apoptosis of chondrocytes.Methods　Chondrocytes which were obtained from aborted fetal were cultured in vitro.Four days later,these chondrocytes were exposed to T-2 toxin in different concetrations for 16 hours.According to the concentratio ns,five experimental groups were divided:0,5,10,20,40 μg/L.Then TUNEL staining and Flowcytometry were used to detect the apoptosis of chondrocytes qualitativel y and quantitatively,the effect of T-2 toxin on proliferation of chondrocytes were also observed.Results　After being exposed to T-2 toxin,the body of chondrocytes shrinked obviously and there was a dose-dependent relationship bet ween the toxin concentration and the degree of shrink.The concentration of T-2 toxin changed from 0 μg/L to 10 ng/ml,the number of apoptosis increased.Conclusions　 T-2 toxin can inhibit the proliferation of chondroyte significantly in a dose-depenent manner. T-2 toxin can induce the apoptosis of chondrocyte and the numbers of apoptosis is proportionate to the concentration of T-2 toxin in particular range.

Objective To study the effects of rehabilitation(RT)on cardiac function in cerebral infarct (CIF)patients with cardiac insufficiency(CIS).Methods Fifty-nine CIF patients with CIS were randomly divid- ed into a treatment group(T group,n=29)and a control group(n=30),and all patients were treated with routine pharmacotherapy for 2 months.In addition,RT was administrated in the T group at the same time.The grading of the New York Heart Association(NYHA)and the changes in cardiac function associated index were observed in both groups before and after treatment.Results Compared with the control group,NYHA grades,left ventricle ejection fraction(LVEF),the levels of brain natriuretic peptide(BNP)in the blood plasma,and the 6min walking range of the T group patients were all significantly improved after treatment(P＜0.05).Conclusion RT can improve car- diac function in CIF patients with CIS.

ObjectiveTo explore the diagnosis and prognosis value of clinical pneumonic infection score (CPIS) in patients with stroke-associated pneumonia (SAP).MethodsOne hundred and fifty stroke patients were evaluated and analyzed by CPIS.SAP was regarded as gold standard,and sensitivity,specificity,diagnose accordance rate,positive predictive value and negative predictive value were calculated.Results Thirty-nine patients had SAP and 111 patients did not have SAP by CPIS,and the incidence of SAP was 22.0％ (33/150).CPIS diagnostic sensitivity was 84.8％ (28/33),specificity was 90.6％ ( 106/117 ),positive predictive value was 71.8％ (28/39),negative predictive value was 95.5％ (106/111),and diagnose accordance rate was 89.3％(134/150).The patients of SAP were divided into good prognosis (28 cases) and bad prognosis (5 cases),and the CPIS was significantly lower in patients of good prognosis 7 days after SAP than that in patients of bad prognosis[(4.21 ± 2.23) scores vs. (6.05 ±2.32) scores,P ＜0.05].ConclusionsNot only CPIS has higher diagnosis rate in SAP incidence,but also has good judgment to prognosis.It is worthy of clinical application.

Objective To observe the effect of rosuvastatin calcium on lipid,vascular endothelial growth factor (VEGF),nitric oxide (NO),tumor necrosis factor (TNF)-α and interleukin (IL)-1 in hyperlipidemia patients.Methods One hundred and twenty-seven hyperlipidemia patients were randomly divided into two groups.Patients in the study group included 72 patients which were given rosuvastatin calcium 10 mg and enteric-coated aspirin 100 mg,orally,once a day for 8 weeks.The control group included 55 patients which were only given enteric-coated aspirin 100 mg,orally,once a day for 8 weeks.The change of lipid,VEGF,NO,TNF-α and IL-1 was observed before and after treatment.Results Before treatment,the level of total cholesterol(TC),triglyceride (TG),low density lipoprotein-cholesterol (LDL-C),high density lipoprotein-cholesterol (HDL-C),VEGF,NO,TNF-α and IL-1 in two groups had no significant difference (P ＞ 0.05).After treatment,the level of TC,TG,LDL-C,TNF-α and IL-1 in study group were significantly lower than those in control group [(4.410 ± 0.688) mmol/L vs.(6.491 ± 0.744) mmol/L,(1.762 ± 0.834) mmol/L vs.(2.632 ± 0.792) mmol/L,(2.256 ± 0.347) mmol/L vs.(4.544 ± 0.493) mmol/L,(41.14 ± 5.41) ng/L vs.(71.34 ± 6.76) ng/L,(0.22 ± 0.18) μ g/L vs.(0.42 ± 0.23) μ g/L] (P ＜ 0.05).The level of HDL-C,VEGF and NO in study group were significantly higer than those in control group [(1.807 ± 0.730) mmol/L vs.(1.432 ± 0.514) mmol/L,(564.86 ± 120.02) ng/L vs.(451.23 ± 100.72) ng/L,(42.39 ± 6.71) μ mol/L vs.(33.65 ± 6.24) μ mol/L](P＜ 0.05).No adverse reaction occurred in two groups.Conclusions Rosuvastatin calcium can obviously decrease the level of lipid,elevate the expression of VEGF and NO,and reduce the expression of TNF-α and IL-1.Rosuvastatin calcium can improve vascular endothelial function obviously in hyperlipidemia patients.

Objective To investigate the effect of gastrodin on rat vascular smooth muscle cell (VSMC) migration induced by platelet-derived growth factor-BB (PDGF-BB) and its possible mechanisms.Methods Enzyme digestion method wasused to obtain rataorticVSMCs and be purified bypassage.Immunofluorescence staining was used to identify VSMC marker proteins.A PDGF-BB induced cell migration model was established.Transwell chamber assay was used to evaluate the effect of gastrodin on PDGF-BB induced VSMC migration.Western blots were performed to detect the phosphohorylation levels of c-jun N-terminal kinase (JNK).Results The purity of primary cultured VSMC was more than 99％.The VSMC migrated number in the PDGF-BB group was 85.2 ± 3.486 per field.It was significantly more than 42.5 ± 1.927 per field in the control group (t =9.981,P＜0.001),and gastrodin was enable to make PDGF-BB induced the number of VSMC migration significantly reduce to 71.3 ± 1.783 per filed (t=3.550,P =0.002).Western blots analysis showed that gastrodin inhibited PDGF-BB induced JNK phosphorylation (0.190 ± 0.015 vs.0.190 ± 0.015; t =14.548,P =0.000).Conclusions Gastrodin inhibits PDGF-BB induced VSMC migration,its mechanisms may be associated with the inhibition of the JNK signaling pathway activation.