Adolescent ; Heart Valve Diseases ; etiology ; Heart Valves ; pathology ; Humans ; Lupus Erythematosus, Systemic ; complications ; pathology ; Male

180,anti-ds-DNA,anti-Sm and lower C3,are high risk factors in the development of LN.The manifestations were various and misdiagnosis at the early stage was not uncommon.

Hypoxia occurs in chronic and acute vascular diseases and tumor formation. The ability of tumor cells to maintain a balance between an adaptation to hypoxia and cell death is regulated by a family of transcription factors called hypoxia-inducible factor 1 (HIF-1). Tumor hypoxia mediated by HIF-1 would facilitate the likelihood of resistance to chemotherapy and radiotherapy, proliferation, metastasis and the invasive potential; all of which culminate in a decrease in patient survival. And HIF-1 alpha subunit decides the activity of HIF-1, which is regulated by oxygen. So understanding the role of HIF in signal pathway, drug resistance mechanism and its feature is crucial for developing novel anticancer therapies. In recent years, more attentions have focused on HIF-1 alpha inhibitors. It is expected that development of more potent and selective HIF inhibitors will provide an effective treatment of cancer and other HIF-related diseases. So we will focus on the biological characteristics and mechanism of HIF-1 to review currently studied HIF-1 inhibitors.
Cell Death ; Humans ; Hypoxia-Inducible Factor 1 ; antagonists & inhibitors ; metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit ; antagonists & inhibitors ; metabolism ; Neoplasms ; drug therapy ; Oxygen ; metabolism ; Signal Transduction

Humans ; Telomere ; metabolism ; Telomere-Binding Proteins ; metabolism

Animals ; Brain Injuries ; drug therapy ; Gynostemma ; Learning ; drug effects ; Memory ; drug effects ; Phytotherapy ; Saponins ; pharmacology ; therapeutic use

BACKGROUND:It has been recently indicated that nervous factors are able to adjust and dominate bone fracture healing. Type Ⅰ collagen is a major factor to promote the differentiation of osteoblasts and enhance the adhesion of osteoblasts; while, it is also a matrix protein for composing bone framework. Type Ⅱ collagen is derived from chondrocytes. OBJECTIVE: To study changing law of type Ⅰ and Ⅱ collagen expression during denervated bone fracture healing. DESIGN, TIME AND SETTING: Randomized controlled anima study was performed at the Animal Laboratory and Cell Biology Laboratory, the Second Military Medical University of Chinese PLA between May and December 2005. MATERIALS: Forty 3-month-year healthy male SD rats were randomly divided into fracture group (tibial fracture alone) and combination group (spinal cord injury combined with tibial fracture), with 20 rats at each group. METHODS: A φ 0.8 mm Kirschner wire was inserted into anterior border of left tibial plateau to establish tibial fracture models in the fracture group. A 0.3-cm spinal cord transection was cut at T10 segment to establish tibial fracture models with entire spinal cord injury. MAIN OUTCOME MEASRUES: Type Ⅰ and Ⅱ collagen protein expressions of callus were detected using Western blot technique in week 1, 2, 4, and 5 post-injury. RESULTS: One week after injury, type Ⅰ and Ⅱ collagen was represented in callus in the two groups, while the expressions in the combination group were significantly higher than fracture group (P<0.05); two weeks after injury, type Ⅱ collagen expression reached at the peak in the combination group, and the expression was significantly higher than the fracture group (P<0.05); four weeks after injury, type Ⅰ collagen expression reached at the peak in the fracture group, and the expression was significantly higher than the combination group (P<0.05), while type Ⅱ collagen still highly expressed in the combination group; five weeks after injury, type Ⅰ and Ⅱ collagen expressions were decreased in the two groups. CONCLUSION: Secretory law of type Ⅰ and Ⅱ collagen during denervated bone fracture healing is similar to normal bone fracture healing; however, the differences at time points, in particular expression at peak, are remarkable between them.

Objective: To observe the effects of interferon-induced protein 204 (p204) over-expression on apoptosis, proliferation and migration of aortic vascular adventitial ifbroblast (VAFs) in experimental rats.
Methods: Our research included in 3 groups: Iif204-Lv group, in whichVAFs were infected by Iif204-recombined lentivirus, Con-Lv group, in which VAFs carried the empty vector without virus, Blank control group, in which VAFs were untreated. VAFs proliferation was examined by MTT method, cell apoptosis was measured by lfow cytometry and the migration was detected by scratching assay and transwell chamber method. The mRNA and protein expressions of p204, p53 and p21were evaluated by real-time q RT-PCR and Western blot analysis respectively.
Results: Compared with Con-Lv and Blank control groups, Iif204-Lv group had decreased VAFs proliferation (by OD value) at 48 hours: (0.53 ± 0.05) vs (0.66±0.03) and (0.63 ± 0.06), at 72 hours: (0.89 ± 0.06) vs (1.02 ± 0.06) and (1.01 ± 0.07); distance of cell migration (by pixel): (61.00 ± 1.83) vs (74.50 ± 6.25) and (75.50 ± 7.85); number of cell migration: (61.75 ± 10.69) vs (155.25 ± 10.21) and (153.75 ± 9.40), allP<0.05. VAFs apoptosis rates were similar among different groups. Compared with Con-Lv and Blank control groups, Ifi204-Lv group presented up-regulated mRNA expressions of p204 (3.45 ± 0.15) vs (2.09 ± 0.10) and (2.06 ± 0.09); p53 (3.41 ± 0.09) vs (2.06 ± 0.07) and (2.10 ± 0.06); p21 (3.01 ± 0.08) vs (2.05 ± 0.06) and (2.11 ± 0.08), allP<0.05.
Conclusion: p204 over-expression inhibits VAFs proliferation and migration which might be partly related to the activation of p53 and p21 expression in experimental rats.

0.05).Conclusions:The integrated medicine can regulate monoamine neurotransmitter to some extent.

BackgroundHigh myopia is one of leading causes of blindness,so far the pathogenesis remains unclear.Two single-nucleotide polymorphisms (SNPs) of rs6885224 and rs12716080 in CTNND2 gene were recently found to be associated with high myopia in Singaporean Chinese.But whether these SNPs are related with the pathogenesis of high myopia in Han Chinese is worth studying,Objective This study was to investigate the relationship between the genetic variations of the CTNND2 gene and high myopia in Han Chinese.MethodsA case-controlled association study was designed.Nine hundred and thirty-three individuals with high myopia and 1227age- and gender-matched normal subjects were included in this study.The 5 ml of periphery blood was obtained from all subjects for the extraction of genomic DNA.The target DNA was amplified using PCR and purified by the SNaPshot method.Four SNPs rs12716080,rs917012,rs6885224 and rs16901340 in the CTNND2 gene were genotyped.This study was approved by the Ethic Committee of Sichuan Provincial People Hospital.Written informed consent was obtained from each subject before his/her enrollment.Results The frequencies of the genotypes rs6885224,rs12716080,rs917012,rs16901340 SNPs were in Hardy-Weinberg equilibrium (HWE) ( P=0.181,0.085,0.732,0.313,0.264,0.663,0.084,0.196).There were no significant differences in genotypes frequency distribution ( in turn P =0.654,0.406,0.828,0.403 ) and allele frequency distribution of the CTNND2 gene ( in turn P =0.377,0.209,0.743,0.198) between the high myopia group and normal control group.The haplotypes (TA and GA)frequencies of rs12716080 and rs917012 in the high myopia group were significantly different from those of the normal control group(TA:0.784 vs.0.719;GA:0.087 vs.0.136) (x2 =6.115,P=0.013 ;x2 =6.634,P=0.010),but those of GG were similar between the high myopia group and normal control group ( 0.123 vs.0.143,x2 =0.889,P =0.346). ConclusionsThe SNPs rs12716080,rs917012,rs6885224 and rs16901340 in CTNND2 gene were not responsible for high myopia,however,the haplotypes of rs12716080 and rs917012 are susceptible for high myopia in Han Chinese.

Objective: To study the impact of interferon-inducible protein 16 (IFI16) inhibition on apoptosis of human aortic adventitial fibroblasts (HAAFs). Methods: Our research included 3 groups: ① IFI16-siRNA group, specific small interference RNAs (siRNAs) of IFI16 were transfected into HAAFs in vitro to make IFI16 gene silence, ②Con-siRNA group, non-specific siRNAs were transfected into HAAFs as negative control and ③Untreated HAAFs group, blank control. HAAFs cell cycle and apoptosis rate were examined by flow cytometry, IFI16 mRNA expression was measured by real time qRT-PCR, protein expressions of IFI16, p53, p21, Bax and Bcl-2 were detected by Western blot analysis. Results: Compared with Con-siRNA group and Untreated HAAFs group, IFI16-siRNA group showed decreased apoptosis rate of HAAFs (3.33±0.41) % vs (7.42±1.51) % and (6.49±1.10) %, P<0.05, reduced ratio of G0/G1 phase cells (56.64 ± 4.77 ) % vs (69.67±3.54) % and (68.29±4.14) %, P<0.05, while increased ratio of S phase cells (25.23±5.19)% vs (13.76±2.07) % and (14.04±3.00) %, P<0.05. Meanwhile, IFI16-siRNA group presented down-regulated IFI16 mRNA and protein expressions, decreased protein levels of p53, p21, Bax and increased protein level of Bcl-2, all P<0.05. Conclusion: Inhibited IFI16 expression could decrease HAAFs apoptosis, promote cell cycle transition from G1 to S phase which might be related to the suppression of p53/p21 signaling pathway and regulation of Bax/Bcl-2 expression.