Objective To evaluate the influence of patellar resurfacing and non-patellar resurfacing on the effect of total knee arthroplasty to provide the evidence-based basis for selecting the clinical treatment scheme.Methods The clinical randomized controlled trials(RCT)on the whether having patellar replacement in total knee arthroplasty were retrieved from the databases of Pubmed,Cochrane,Medline,Embase,CNKI and WanFang data.The screening was independently performed by two researchers according to the including and excluding criterion.The related data were extracted.The reoperation rate,knee joint pain score and knee joint score served as the measurement criteria.The RevMan 5.2 software was adopted to conduct the meta analysis.Results Fifteen literatures were included to analyze,involving 1 788 patients,among them 871 cases were in the patellar resurfacing group and 917 case sin the non-patellar resurfacing group.The reoperation rate in the patellar resurfacing group was significantly lower than that in the non-patellar resurfacing group(RR=0.50,95 ％CI:0.33-0.76;P =0.001),moreover the knee joint function was significantly improved(WMD=3.04,95％CI:0.41-5.67;P=0.02).However,the anterior knee joint pain(WMD=0.96,95％CI:-0.85-2.76;P=0.30)and knee joint score(RR=0.81,95 ％ CI:0.50-1.32;P =0.41) had no statistical difference between the two operation modes.Conclusion Conducting patellar resurfacing in total knee arthroplasty can reduce the reoperation risk and improves the postoperative knee joint function,but does not improve postoperative knee joint pain score and knee joint score

Objective To assess the relationship between the Chlamydia pneumonia(CPn)infection and coronary heart disease(CHD).Methods Blood samples from 200 CHD patients and 100 heathy controls were col-lected,and Cpn IgM and Cpn IgG were tested by ELISA.Results The Cpn IgM were found in 113 cases (56.5%) and in 24 controls(24.0%).The Cpn IgG positive cases were in 145(72.5%) patients and in 43 controls (43.0%).The positive rate of Cpn IgM and Cpn IgG in CHD group Was higher than that in control group(P<0.05).Conclusion:CPn positive rate is higher in CHD group than that in control group.Cpn is closely related to the pathogenesis of CHD.

In this study, DNAzymes against cyclin D1 (cyclin D1-DRz) were designed according to the secondary structure of cyclin D1 mRNA which was computed with RNAdraw and Mfold. Cyclin D1-DRz were transfected into tumor cell line u251 and HeLa by oligofectamine. The expression of cyclin D1 was detected by RT-PCR. It was shown that the expression of cyclin D1 gene was suppressed obviously, and the expressions of other cell-cycle related genes such as cyclin E1, cyclin A1 and cyclin B1 were also declined. The cell cycle analysis of tumor cells tansfected with cyclin D1-DRz revealed an arrestment in the G0/G1 phase. In conclusion, the approach is effective and feasible for designing DNAzyme. Cyclin D1-DRz is useful for interfering with the cell cycle procession of tumor cells.
Base Sequence ; Cell Cycle ; drug effects ; Cyclin D1 ; antagonists & inhibitors ; genetics ; metabolism ; DNA, Catalytic ; genetics ; metabolism ; pharmacology ; HeLa Cells ; Humans ; Molecular Sequence Data ; RNA, Messenger ; genetics ; metabolism ; Transfection

Objective: To construct the recombinant adenoviral containing fructose 1, 6-biphosphatase 1 (FBP1), and to investigate whether FBP1 has effect on autophagy and proliferation in liver cancer cells (HepG2). Methods: FBP1 cDNA sequence was amplified by PCR and cloned in adenovirus vector pAdTrack-TO4, and then recombinant adenovirus plasmid pAdTrack-FBP1 was constructed. The recombinant adenovirus plasmid was transfected into HEK293 cells by Lipofectamine 3000. High-titer of recombinant adenovirus AdFBP1 was obtained by packaging and amplification. HepG2 cells were infected with recombinant adenovirus AdFBP1, and the Mock and AdGFP group were set at the same time. Western blot and confocal laser scanning microscopy were used to observe the effect of FBP1 on the level of autophagy in hepatocellular carcinoma cells, and the effect of FBP1on the proliferation was observed by MTS and colony formation assay. A t-test and one-way ANOVA were used to compare the mean between group. Results: A high-titer recombinant adenovirus FBP1 was successfully constructed. Western blot and confocal laser scanning microscopy showed that the level of autophagy in AdFBP1 group was significantly lower than that in AdGFP group. Western blot results showed that LC3-II protein expression level in AdGFP was 1.10 ± 0.10 and 0.30 ± 0.01 in AdFBP1 group, F = 90.36, P < 0.01. Confocal laser scanning microscopy analysis showed that the average number of autophages in AdGFP was 28.33 ± 1.53 and 12.33 ± 1.53 in AdFBP1group, F = 97.40, P < 0.01. In addition, the results of colony formation assay and MTS assay showed that the proliferation of liver cancer cells in the AdFBP1 group was significantly inhibited compared with the AdGFP group. The results of colony formation showed that the cell clones in the AdGFP group was 65.66 ± 2.57 and 34.00 ± 2.00 in AdFBP1 group, F = 141.50, P < 0.01. MTS results showed that the absorbance of AdGFP group at 96h was 39.13 ± 2.21 and 30.61 ± 3.33 in AdFBP1 group, F = 7.80, P < 0.05. Conclusion FBP1 inhibited the autophagy and proliferation in liver cancer cells (HepG2).

OBJECTIVE: To explore the inhibitory role of spermatogenesis-associated gene 12 (SPATA12) on tumor cell proliferation and its possible mechanism. METHODS: The expression pattern of SPATA12 in testicular tumors was investigated by in situ hybridization analysis using tissue microarrays. The effects of SPATA12 on tumor cell proliferation and colony formation was detected by 3-(4.5-dimethylthiazol-2- yl)-2,5-diphenyl tetrazolium bromide (MTT) assay and colonyforming assays, respectively. The changes of expression level of cell cycle genes in tumor cells were detected by reverse transcription polymerase chain reaction(RTPCR). RESULTS: In situ hybridization analysis showed that the SPATA12 was highly expressed in normal adult testis, but lacking in testicular tumors such as seminoma. MTT assay and colony-forming assay indicated that the exogenous expression of SPATA12 could suppress both tumor cell proliferation and colony formation. RT-PCR showed that the expression of cyclin A1 gene was markedly suppressed and the level of cyclin D1 was somewhat reduced following SPATA12 transfection. However, no obvious changes were observed in mRNA expression of cyclin B1 or cyclin E1 after SPATA12 transfection. CONCLUSION SPATA12 could be an inhibitor during the development of tumor via regulation of cell cycle genes.
Cell Line, Tumor ; Cell Proliferation ; Genes, Tumor Suppressor ; Genes, cdc ; HeLa Cells ; Homeodomain Proteins ; genetics ; metabolism ; Humans ; Male ; Testicular Neoplasms ; genetics ; pathology ; Transfection

Objective:To examine the heritability of body mass index (BMI) and coronary heart disease (CHD), and to explore whether genetic factors can explain their correlation.Methods:Participants were from 11 provinces/municipalities reqistered in the Chinese National Twin Registry (CNTR) from 2010 to 2018. Participants data were collected from face-to-face questionnaire survey. Bivariate structure equation model was used to estimate the heritability and the genetic correlation of BMI and CHD.Results:A total of 20 340 pairs of same-sex twins aged ≥25 years were included in this study. After adjusting for age and gender, the heritability of BMI and CHD was 0.52 (95% CI: 0.49-0.55) and 0.76 (95% CI: 0.69-0.81), respectively. Further, a genetic correlation was identified between BMI and CHD ( rA=0.10, 95% CI:0.02-0.17). Conclusion:In Chinese adult twin population, BMI and CHD are affected by genetic factors, and their correlation can be attributed to the common genetic basis.

Background::Exercise, as the cornerstone of pulmonary rehabilitation, is recommended to chronic obstructive pulmonary disease (COPD) patients. The underlying molecular basis and metabolic process were not fully elucidated.Methods::Sprague-Dawley rats were classified into five groups: non-COPD/rest ( n = 8), non-COPD/exercise ( n = 7), COPD/rest ( n = 7), COPD/medium exercise ( n = 10), and COPD/intensive exercise ( n = 10). COPD animals were exposed to cigarette smoke and lipopolysaccharide instillation for 90 days, while the non-COPD control animals were exposed to room air. Non-COPD/exercise and COPD/medium exercise animals were trained on a treadmill at a decline of 5° and a speed of 15 m/min while animals in the COPD/intensive exercise group were trained at a decline of 5° and a speed of 18 m/min. After eight weeks of exercise/rest, we used ultrasonography, immunohistochemistry, transmission electron microscopy, oxidative capacity of mitochondria, airflow-assisted desorption electrospray ionization-mass spectrometry imaging (AFADESI-MSI), and transcriptomics analyses to assess rectal femoris (RF). Results::At the end of 90 days, COPD rats’ weight gain was smaller than control by 59.48 ± 15.33 g ( P = 0.0005). The oxidative muscle fibers proportion was lower ( P < 0.0001). At the end of additional eight weeks of exercise/rest, compared to COPD/rest, COPD/medium exercise group showed advantages in weight gain, femoral artery peak flow velocity (Δ58.22 mm/s, 95% CI: 13.85-102.60 mm/s, P = 0.0104), RF diameters (Δ0.16 mm, 95% CI: 0.04-0.28 mm, P = 0.0093), myofibrils diameter (Δ0.06 μm, 95% CI: 0.02-0.10 μm, P = 0.006), oxidative muscle fiber percentage (Δ4.84%, 95% CI: 0.15-9.53%, P = 0.0434), mitochondria oxidative phosphorylate capacity ( P < 0.0001). Biomolecules spatial distribution in situ and bioinformatic analyses of transcriptomics suggested COPD-related alteration in metabolites and gene expression, which can be impacted by exercise. Conclusion::COPD rat model had multi-level structure and function impairment, which can be mitigated by exercise.

Objective:To examine the heritability of body mass index (BMI) and coronary heart disease (CHD), and to explore whether genetic factors can explain their correlation.Methods:Participants were from 11 provinces/municipalities reqistered in the Chinese National Twin Registry (CNTR) from 2010 to 2018. Participants data were collected from face-to-face questionnaire survey. Bivariate structure equation model was used to estimate the heritability and the genetic correlation of BMI and CHD.Results:A total of 20 340 pairs of same-sex twins aged ≥25 years were included in this study. After adjusting for age and gender, the heritability of BMI and CHD was 0.52 (95% CI: 0.49-0.55) and 0.76 (95% CI: 0.69-0.81), respectively. Further, a genetic correlation was identified between BMI and CHD ( rA=0.10, 95% CI:0.02-0.17). Conclusion:In Chinese adult twin population, BMI and CHD are affected by genetic factors, and their correlation can be attributed to the common genetic basis.