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.

The mosquito vector of filariasis malayi and its vectorial capacity was investigated In 5 endemic villages in Leshan Prefecture, Sichuan Province. The results showed that the man-biting rate, numan blood index and vectorial capacity of An. lesteri anthropophagus were 0.7, 5.1 and 10.63 times higher than those of An. sinensis. Besides, the natural infection by microfilaria in An, lesteri anthropophagus was also higher than that in An. sinensis by 5 times.From the above result, the authors concluded that An. lesteri anthropophagus was the main vector for transmitting filariasis malayi in the area under study.

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 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).

Chemical modification of DNA bases in recent years has been one of the hot areas of life science research. DNA methylation is a common epigenetic phenomenon and can change the genetic performance without changing the DNA sequence. Various stress factors can induce the variation of DNA methylation in plants, but the response mechanism is still unknown. In this paper, the progress of DNA methylation in plants was reviewed. In combination with the researchconclusions of our own research group, the DNA methylation variation induced by 7Li ion beam and gamma ray was reported to provide a basis for DNA methylation, which may be involved in the phenotypic plasticity of plants.
DNA Methylation ; Epigenesis, Genetic ; Epigenomics ; Plants ; genetics

Objective To investigate the therapeutic effect of chimeric antigen receptor (CAR) T cells on myocardial infarction (MI) and observe the impact of different administration routes on CAR-T cell cardiac toxicity. Methods Twenty-four SCID Beige immunodeficient mice, which successfully established a myocardial infarction model, were randomly divided into Hank’s balanced salt solution (HBSS) group, CAR-TIM group, CAR-TIV group, and CAR-TIMIV group (n＝6 for each group). In addition, a Sham group (n＝6) was set up. The Sham group, HBSS group, CAR-TIM group, and CAR-TIMIV group were injected with HBSS or CAR-T cells via intramyocardial injection on the 7th day after modeling. The Sham group, HBSS group, CAR-TIV group, and CAR-TIMIV group were injected with HBSS or CAR-T cells via tail vein injection on the 7th day and 14th day after modeling. After 28 days of modeling, the electrical physiological indicators of the mice were observed, and the myocardial tissues were subjected to Masson staining to calculate the area of myocardial infarction. Results Compared with the Sham group, the HBSS group had significant increases in myocardial infarction size and incidence of arrhythmia (P＜0.05). Compared with HBSS group, different routes of CAR-T cell therapy significantly reduced the area of myocardial infarction (all P＜0.05) and significantly increased the incidence of arrhythmia (all P＜0.05). There was no significant difference in the effect of CAR-TIV and CAR-TIM groups on the area of myocardial infarction and the incidence of arrhythmia. Compared with the CAR-TIV group,the area of myocardial infarction significantly reduced in the CAR-TIMIV group (P＜0.05), with no significant difference in the incidence of arrhythmia between the two groups. Conclusions Intravenous and local myocardial injection of CAR-T cells can effectively reduce the myocardial infarction area but increase the incidence of arrhythmia. The mechanism needs further study.

Heart failure with preserved ejection fraction (HFpEF) displays normal or near-normal left ventricular ejection fraction, diastolic dysfunction, cardiac hypertrophy, and poor exercise capacity. Berberine, an isoquinoline alkaloid, possesses cardiovascular benefits. Adult male mice were assigned to chow or high-fat diet with L-NAME ("two-hit" model) for 15 weeks. Diastolic function was assessed using echocardiography and noninvasive Doppler technique. Myocardial morphology, mitochondrial ultrastructure, and cardiomyocyte mechanical properties were evaluated. Proteomics analysis, autophagic flux, and intracellular Ca²⁺ were also assessed in chow and HFpEF mice. The results show exercise intolerance and cardiac diastolic dysfunction in "two-hit"-induced HFpEF model, in which unfavorable geometric changes such as increased cell size, interstitial fibrosis, and mitochondrial swelling occurred in the myocardium. Diastolic dysfunction was indicated by the elevated E value, mitral E/A ratio, and E/e' ratio, decreased e' value and maximal velocity of re-lengthening (-dL/dt), and prolonged re-lengthening in HFpEF mice. The effects of these processes were alleviated by berberine. Moreover, berberine ameliorated autophagic flux, alleviated Drp1 mitochondrial localization, mitochondrial Ca²⁺ overload and fragmentation, and promoted intracellular Ca²⁺ reuptake into sarcoplasmic reticulum by regulating phospholamban and SERCA2a. Finally, berberine alleviated diastolic dysfunction in "two-hit" diet-induced HFpEF model possibly because of the promotion of autophagic flux, inhibition of mitochondrial fragmentation, and cytosolic Ca²⁺ overload.
Male ; Mice ; Animals ; Heart Failure/drug therapy* ; Stroke Volume/physiology* ; Ventricular Function, Left/physiology* ; Berberine/therapeutic use* ; Disease Models, Animal ; Mitochondrial Dynamics ; Myocardium ; Homeostasis