Objective: To investigate the health-seeking delay in tuberculosis among school students in Yining City, Xinjiang Uygur Autonomous Region from 2009 to 2020, and analyze the influencing factors, so as to provide the evidence for reducing the health-seeking delay in tuberculosis among students in Yining City. Methods: The demographic features and diagnosis of students with tuberculosis in Yining City from 2009 to 2020 were retrieved from the Tuberculosis Management Information System of the Chinese Disease Control and Prevention Information System, and the factors affecting the health-seeking delay in tuberculosis were identified using the multivariable logistic regression analysis. Results: A total of 443 students with tuberculosis were reported in Yining City from 2009 to 2020, including 209 boys and 234 girls, with a male/female ratio of 1∶1.12. There were 29 primary school students ( 6.55% ), 81 junior high school students ( 18.28% ), 187 high school students ( 42.21% ) and 146 college students ( 32.96% ) reporting tuberculosis, and 394 cases ( 88.94% ) had locally registered residence. There were 287 students with health-seeking delay in tuberculosis ( 64.79% ), and the median duration of health-seeking delay was 35 ( interquartile range, 33 ) days. Multivariable logistic regression analysis showed that registered residence ( local, OR=1.899, 95%CI: 1.004-3.591 ) and origin of tuberculosis patients ( clinical consultation, OR=3.448, 95%CI: 1.755-6.775; recommendation for symptoms, OR=3.215, 95%CI: 1.161-8.900; tracking, OR=2.415, 95%CI: 1.269-4.596 ) and diagnostic results ( positive sputum smears, OR=3.081, 95%CI: 1.710-5.551 ) statistically correlated with health-seeking delay among students with tuberculosis. Conclusions The proportion of health-seeking delay in tuberculosis was high among students in Yining City from 2009 to 2020; registered residence, origin of tuberculosis patients and diagnostic results were associated.

Objective To investigate the correlation between ATP-binding cassette transporter A1 (ABCA1) R219K polymorphism and ischemic stroke in Chinese populations.Methods The case control studies of the correlation between Chinese ABCA1 R219K polymorphism and ischemic stroke published before May 2013 were collected using comprehensive literature search.The Stata 11.0 software was used to conduct metaanalysis.Odds ratio (OR) and its 95％ confidence interval (CI) was used to evaluate the strength of association between the gene polymorphism and ischemic stroke.Results A total of 10 studies met the criteria and were included in the analysis,including 1 619 patients in the patient group and 1907 in the control group.The selected literature had no obvious bias.Meta-analysis showed that the risk of ischemic stroke in patients carrying RK + KK genotype significantly decreased 8％ (OR 0.92,95％ CI 0.88-0.96; P =0.000)compared to those carrying RR genotype.The risk of ischemic stroke in patients carrying KK genotype significantly decreased 36％ compared to those carrying RR genotype (OR 0.64,95％ CI 0.44-0.94; P =0.02).The risk of ischemic stroke in patients carrying RK genotype significantly decreased 19％ compared to those carrying RR genotype (OR 0.81,95％ CI 0.69-0.95; P =0.009).The risk of ischemic stroke in patients carrying K allele significantly decreased 17％ compared to those carrying R allele (0R 0.83,95％ CI 0.69-0.99; P =0.036).Conclusions ABCA1 R219K polymorphism is associated with the susceptibility of ischemic stroke in Chinese.K allele may be a genetic protective factor for ischemic stroke in Chinese populations.

Objective To construct transgenic mice tissue-specifically co-expressing human DAF/CD59 in the vascular endothelia and to investigate the ability to protect against human comple- ment-mediated attack.Methods Transgenic mice were generated by co-microinjection of hDAF/CD59 expression constructs driven by the human intercellular adhesion molecule-2(ICAM-2)promoter.PCR and Southern blot of genomic DNA were used to assess the presence of hDAF/CD59 in the genome of the founders,and the expression at protein level was measured by flow cytometry.Immunohistochemis- try was used to detect the distribution of hDAF/CD59.An ex vivo perfusion model was used to com- pare hearts from these hDAF/CD59 transgenic mice with hDAF hearts.Results After microinjection of genes,11 of 135 mice born were shown to be double-transgenic,and human DAF/CD59 were ex- pressed on the surface of leucocytes in 6 of the 11 DAF/CD59-integrated mice.Expression levels of 6 founders ranged from 80% to 95% of that in human leucocytes.Human DAF/CD59 were strongly expressed in the vascular endothelia of heart,kidney,with little or no positive staining observed in non- endothelial cells.Compared to hDAF hearts that maintained approximately 20% maximum work during perfusion with 20% human plasma,these endothelial-specific hDAF/CD59 hearts were further protected with work maintained at 40% of the maximum level during 60 min.Conclusion The intro- duced hDAF/CD59 genes have been integrated and specifically expressed in the vascular endothelia. The endothelial co-expression of hDAF/CD59 can provide greater protection against human complement-mediated attack than the expression of hDAF alone.

OBJECTIVETo explore the therapeutic effects of arthroscopy for post-traumatic chronic wrist pain.

METHODSFrom February 2007 to June 2010, 12 patients with post-traumatic chronic wrist pain treated with arthroscopy were reviewed. Among the patients, 9 patients were male and 3 patients were female, ranging in age from 19 to 47 years, with a mean of 35.6 years. After physical examinations or MR abnormal findings, all the patients underwent wrist arthroscopic examination and treatment. Eight patients with tear in the central area of the triangular fibrocartilage complex (TFCC) underwent endoscopic partial resection. Two patients with relaxation of inter-carpal ligament after injury underwent radiofrequency shrinkage. One patient with distal radioulnar joint instability was treated with Kirschner fixation through distal radius and ulna in the neutral forearm rotation after clean-up of wrist joint, and also fixed with long arm cast immobilization for 6 weeks. One patient with ulnar impaction syndrome was treated with wrist clean, border modeling of triangular cartilage plate, partial resection of distal ulna.

RESULTSAll the patients were followed up with an average duration of 10 months. Modified Mayo wrist score were evaluated from preoperative mean of (51.67 +/- 15.27) ( 25 to 75 scores) to postoperative mean of (77.92 +/- 10.54) (65 to 95 scores). Eleven patients recovered to normal work.

CONCLUSIONArthroscopy is an effective method for patients with post-traumatic chronic wrist pain which can diagnosis and cure the injuries under arthroscopy.

Adult ; Arthroscopy ; methods ; Female ; Humans ; Male ; Middle Aged ; Pain ; surgery ; Wrist Injuries ; pathology ; surgery ; Wrist Joint ; pathology ; surgery ; Young Adult

OBJECTIVETo investigate the expression of prostate cancer antigen-1 (PCA-1) in different prostate tissues and analyze its correlation with the clinical parameters of prostate cancer (PCa).

METHODSThe expression of PCA-1 mRNA was detected by RT-PCR in the samples from 45 cases of PCa with various clinico-pathologic characteristics, 30 cases of high-grade prostatic intraepithelial neoplasia (HG-PIN), 43 cases of BPH and 39 cases of other carcinoma tissues. The correlation of PCA-1 mRNA expression with the clinical parameters of PCa was statistically analyzed and the PCA-1 expression was examined in different samples by immunohistochemistry.

RESULTSThe positive expression rate of PCA-1 mRNA was 88.9% and 60.0% and that of PCA-1 protein was 84.4% and 50.0% in the patients with PCa and HG-PIN, respectively. PCA-1 mRNA and PCA-1 proteins were not expressed in the BPH and other carcinoma tissues. The expression of PCA-1 mRNA was unrelated with the clinical parameters of PCa (P > 0.05).

CONCLUSIONIt is suggested that PCA-1 is a PCa-specific gene and its expression is unrelated to the clinical parameters of PCa. It might serve as a specific biomarker for the early diagnosis of PCa.

Aged ; Aged, 80 and over ; Gene Expression Regulation, Neoplastic ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Prostate-Specific Antigen ; biosynthesis ; genetics ; Prostatic Neoplasms ; genetics ; metabolism ; pathology ; RNA, Messenger ; genetics ; metabolism ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVETo evaluate the anticancer effects of exogenous human WT-PTEN overexpression on bladder transitional carcinoma cell line EJ.

METHODSThe plasmid containing WT-PTEN or mutant PTEN was separately transfected into bladder transitional carcinoma cell line EJ, and the protein expression of PTEN in the EJ cells was detected by Western blot. Cell morphological changes were observed under the inverted microscope and transmission electron microscope. MTT test was used to assess the effect of PTEN on proliferation and anticancer effects for mitomycin and theraubicin. The change of bcl-2 expression in the cells was measured by Western blot. The empty plasmid was used as control.

RESULTSWestern blot analysis showed that EJ cells expressed high level of PTEN protein after transfection with WT-PTEN or mutant PTEN plasmid. Abnormal morphological changes of the cells were observed in WT-PTEN transfected groups. The growth of EJ cells treated with WT-PTEN was significantly inhibited by 40.1% and anticancer effects were enhanced by mitomycin and theraubicin, but the cells transfected with mutant PTEN plasmid did not show such similar biological behavior.

CONCLUSIONWT-PTEN gene transfection can suppress the in vitro growth and induce apoptosis of bladder transitional carcinoma cell line EJ cells. Mutant PTEN does not show similar biological behavior. Overexpression of WT-PTEN inhibits cancer cell proliferation by down-regulating bcl-2 expression in the cells.

Antibiotics, Antineoplastic ; pharmacology ; Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Blotting, Western ; Carcinoma, Transitional Cell ; genetics ; metabolism ; pathology ; Cell Line, Tumor ; Cell Proliferation ; Doxorubicin ; analogs & derivatives ; pharmacology ; Green Fluorescent Proteins ; genetics ; metabolism ; Humans ; Microscopy, Electron, Transmission ; Mitomycin ; pharmacology ; Mutation ; PTEN Phosphohydrolase ; genetics ; metabolism ; physiology ; Plasmids ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Recombinant Fusion Proteins ; genetics ; metabolism ; physiology ; Transfection ; Urinary Bladder Neoplasms ; genetics ; metabolism ; pathology

OBJECTIVETo investigate the inhibitory effects of antisense TGF beta1 on proliferation of human bladder transitional cell carcinoma in vitro and in vivo.

METHODSHuman bladder carcinoma cell line EJ was transfected with pRevT beta-AS, a replication defective retroviral vector carried antisense TGF beta1 fragment. The growth of the transfected cells was observed in vitro and in vivo. TGF beta1 mRNA expression and protein expression were detected by RT-PCR and ELISA. The proliferative activity was evaluated by immunohistochemistry method. The ultrastructure of cells was observed by image analysis system and electron microscopy. Cell cycle was determined by flow cytometry.

RESULTSThe expression of TGF beta1 mRNA and protein in EJ cells was inhibited by pRevT beta-AS, G(1) to S transition was restrained in cell cycle and cell proliferation decreased in vitro. The tumorigenesis and growth of EJ cells and DNA heteroploidy were reduced by antisense TGF beta1 in vivo.

CONCLUSIONTGF beta1 plays a role in vitro proliferation and in vivo growth of bladder transitional cell carcinoma.

Animals ; Cell Division ; drug effects ; Cell Line, Tumor ; Female ; Humans ; Mice ; Mice, SCID ; RNA, Antisense ; therapeutic use ; Transforming Growth Factor beta ; antagonists & inhibitors ; genetics ; Transforming Growth Factor beta1 ; Urinary Bladder Neoplasms ; drug therapy ; pathology

OBJECTIVETo construct a recombinant human CD59 gene containing intercellular adhesion molecule-2 promoter for high level endothelial-specific expression in xenotransplantation.

METHODSICAM-2 promotor fragment and CD59-intron 1 fragment were produced by PCR from the human blood genome, and then clone these fragments into a pcDNA3-CD59 eukaryotic expression vector which was followed by digestion with the specific restricted endonuclease (for example: EcoRI, Hind III). The ICAM-2 promoter and CD59-intron 1 fragments were identified by PCR, and sequencing. The recombinant was then transfected into pig aorta endothelial cells with Lipofection, and the expression was measured by flow cytometer.

RESULTSProducts of the sequences measured were in accord with the frames of the gene bank. The expression of the protein of this recombinant was positive.

CONCLUSIONThe CD59 recombinant gene is constructed successfully, providing a basis for transgenic research.

Animals ; Antigens, CD ; genetics ; CD59 Antigens ; biosynthesis ; genetics ; Cell Adhesion Molecules ; genetics ; Cloning, Molecular ; Endothelium, Vascular ; cytology ; metabolism ; Eukaryotic Cells ; metabolism ; Gene Expression Regulation ; Humans ; Promoter Regions, Genetic ; Recombinant Proteins ; biosynthesis ; genetics ; Swine ; Transfection ; Transplantation, Heterologous

AIMTo investigate the effect of androgen on the proliferation, differentiation and regression of canine prostatic stromal cells in vivo and human stromal cells in vitro.

METHODSTwenty-two dogs, including 15 normal prostate dogs and 7 prostatic hyperplasia dogs, had their serum concentration of testosterone and estrodiol determined by radioimmunoassay before and after castration. The expression of androgen receptor (AR) and estrogen receptor (ER) in the prostate were analysed by immunohistochemistry and semi-quantitative RT-PCR before and after castration. Light microscopy, transmission electron microscopy and TUNEL assay were carried out successively before and after castration to evaluate the prostatic histomorphology. In vitro serum-free cell cultures from human prostatic stroma were established and exposed to dihydrotestosterone (DHT). The proliferation of the cell culture was detected by MTT assay. The expression of TGFbgr, bFGF, AR, and smooth muscle cell (SMC) specific proteins (myosin and/or smoothelin) were detected using immunohistochemistry and RT-PCR. The differentiation from fibroblasts to smooth muscle cells was deduced by measuring the expression of SMC specific proteins.

RESULTSBefore castration, the serum concentrations of testosterone and estrodiol were not statistically different between normal and hyperplasia groups. Following castration, the serum concentration of testosterone decreased rapidly in 2 days, and the concentration of estrodiol had no significant change compared with the pre-castration data. In the prostate, AR was presented in both the epithelial and stromal cells and the AR mRNA level was higher in hyperplasia than in normal prostate tissues (P<0.05). While ER predominantly existed in the prostate stromal cells and the ER mRNA had no difference between the hyperplasia and the normal group. Within the early phase of castration (

CONCLUSIONThe whole prostate gland is an androgen-sensitive organ with both the epithelium and stroma under the control of androgen. Androgen may direct the proliferation, differentiation and regression of stromal cells by regulating the expression of TGFbgr, bFGF, AR and smooth muscle cell specific proteins.

Animals ; Biomarkers ; Cell Differentiation ; drug effects ; physiology ; Cell Division ; drug effects ; physiology ; Cells, Cultured ; Dihydrotestosterone ; pharmacology ; Dogs ; Estradiol ; blood ; Fibroblast Growth Factor 2 ; genetics ; pharmacology ; Gene Expression ; Humans ; Male ; Muscle, Smooth ; cytology ; physiology ; Orchiectomy ; Prostate ; cytology ; physiology ; Prostatic Hyperplasia ; physiopathology ; RNA, Messenger ; analysis ; Receptors, Androgen ; genetics ; Receptors, Estrogen ; genetics ; Stromal Cells ; cytology ; physiology ; Testosterone ; blood ; Transforming Growth Factor beta ; genetics ; pharmacology

Objective To evaluate the effects of small interfering RNA(siRNA)against Ki67 gene on the proliferation and apoptosis of human renal carcinoma cell line 786-0 cells.Methods The human renal carcinoma 786-0 cells were treated with Ki67-siRNA(100 nmol/L).The mRNA expression of Ki67 was detected by RT-PCR.The protein expression of Ki67 was detected by Western blot and immunohisto- chemical technique,respectively.The proliferation of 786-0 cells was detected by MTT assay.The apoptosis of 786-0 cells was detected by TUNEL assay.Results RT-PCR and Western blot analysis showed that the Ki67 mRNA and Ki67 protein expression levels of the 786-0 cells treated with Ki67-siRNA were(37.6?1.9)% and(46.4?0.9)% ,respectively,which were significantly lower than those of controls [(97.3?0.9)% and(95.3?0.9)%,P＜0.01],The Ki67 positive expression rate of 786-0 cells treated with Ki67-siRNA by immunohistochemical technique was 52.5?2.3,which was significantly lower than that of controls(114.5?4.9 ,P＜0.01).The proliferation-inhibiting rate and apoptosis rate of the 786-0 cells trea- ted with Ki67-siRNA were( 63.6?1.6)% and(41.7?0.6)% ,respectively,which were significantly higher than those of controls [(2.8?0.2)% and(10.3?1.4)%,P＜0.01].Conclusions siRNA against Ki67 gene can inhibit the proliferation and induce the apoptosis by blocking Ki67 expression of hu- man renal carcinoma 786-0 cells.The inhibition of Ki67 expression by siRNA may be a promising approach in gene therapy for renal cancer.