Objective To study the effects ofautologous bone marrow mononuclear cells (BMMCs)transplantation during coronary artery bypass gafting (CABG) on myocardial infarct size. Methods Forty myocardial infarction patients diagnosed by coronary angiography (CAG) and SPECT and confirmed at surgery were enrolled and randomly assigned CABG alone (group Ⅰ) or CABG with intramyocardial or intracoronary injection of autologous BMMCs (group Ⅱ), 20 cases in each group. Baseline and followed up evaluations included SPECT and NYHA-FC before and after 6 months operation, recorded the major adverse cardiac events (MACE) at the same time. The number of autologous BMMCs injected was (6.84 ± 2.88) ×107 in group Ⅱ. Results There was no procedure-related complication during 6 months followed up in all patients. After 6 months operation,left ventricular ejection fraction in group Ⅱ was significantly higher than that in group Ⅰ [(57.40 ±5.21)% vs. (50.75 ±5.88)%,t =3.79,P＜0.05],NYHA-FC in group Ⅱ was significantly improved than that in group Ⅰ [(1.30 ± 0.47) grades vs. (1.85 ± 0.59) grades, t = 3.27, P ＜0.05],SPECT showed myocardial infarct size in group Ⅱ was significantly lower than that in group Ⅰ[(14.57 ±5.20)% vs. (20.45 ±5.18)% ,P ＜0.05]. Conclusion Autologous BMMCs transplantation during CABG is safe and feasible, which can reduce the myocardial infarct size in patients with myocardial infarction.

Objectives:To examine whether lipopolysaccharide (LPS) induced apoptosis correlates with TNF ? release by type Ⅱ alveolar epithelial cells (AEC Ⅱ), whether TNF ? knockout (TNF KO) abrogates the induction of apoptosis by LPS and whether TNF ? is sufficient to induce apoptosis in this cell type. Methods:AEC Ⅱ was isolated from wild type mice and TNF KO mice. Cells were stimulated with LPS or recombinant murine TNF ? for 24 h. TNF ? in culture supernatant was determined by ELISA following LPS stimulation. Apoptosis was determined by the TUNEL assay after treatment with either LPS or TNF ?. Results:LPS induced apoptosis in wild type AEC Ⅱ in a concentration dependent manner. LPS induced AEC Ⅱ apoptosis was accompanied by a 11 fold increase from (0.073?0.065) ng/ml in controls to( 0.94?0.14)ng/ml in 50 ?g/ml of LPS( P

OBJECTIVETo examine whether lipopolysaccharide (LPS)-induced apoptosis correlates with TNF-alpha release by type II alveolar epithelial cells (AEC II), whether TNF-alpha knockout (TNF KO) abrogates the induction of apoptosis by LPS and whether TNF-alpha is sufficient to induce apoptosis in this cell type.

METHODSAEC II were isolated from wild type mice and TNF KO mice. Cells were stimulated with LPS or recombinant murine TNF-alpha for 24 h. TNF-alpha in culture supernatant was determined by ELISA following LPS stimulation. Apoptosis was determined by the terminal deoxynucleotidyl transferase end-labeling (TUNEL) assay after treatment with either LPS or TNF-alpha.

RESULTSLPS induced apoptosis in wild type AEC II in a concentration-dependent manner. LPS-induced AEC II apoptosis was accompanied by an 11-fold increase (from 0.073 +/- 0.065 ng/ml in control to 0.94 +/- 0.14 ng/ml in 50 micro g/ml of LPS, P < 0.01) in TNF-alpha release. However, increasing concentrations (5 or 25 ng/ml) of recombinant murine TNF-alpha failed to induce AEC II apoptosis. In addition, apoptosis did occur in AEC II isolated from TNF KO mice following LPS stimulation.

CONCLUSIONSThis study confirms that LPS induces TNF-alpha release and apoptosis in murine AEC II in vitro. Exogenous TNF-alpha failed to induce AEC II apoptosis, and apoptosis occurred following LPS stimulation in cells lacking the ability to produce TNF-alpha. Taken together, these results suggest that LPS-induced AEC II apoptosis occurs by a TNF-alpha-independent mechanism.

Animals ; Apoptosis ; drug effects ; Cells, Cultured ; Epithelial Cells ; drug effects ; Lipopolysaccharides ; pharmacology ; Mice ; Mice, Inbred C57BL ; Pulmonary Alveoli ; cytology ; drug effects ; Tumor Necrosis Factor-alpha ; pharmacology

Objective:To explore the relationship between the triglyceride glucose (TyG) index and impairment of renal function in community-dwelling middle-aged and elderly population.Methods:A total of 4 988 residents aged ≥45 years undergoing health check-up in Yongshun Health Service Center from January 2016 to December 2021 were enrolled and followed up. According to the quartile of the baseline TyG index, all subjects were divided into Q1, Q2, Q3 and Q4 groups. The medical history, physical examination and laboratory test results were documented. Participants were followed up through regular health check-up until March 31, 2023. The outcomes were rapid decline of estimated glomerular filtration rate (eGFR) (a loss in eGFR>3 ml·min -1·1.73 m -2 per year) and the new-onset of chronic kidney disease (CKD) during the follow-up period. Linear regression model, multivariate logistic regression model, restricted cubic spline fitting logistic regression model and ROC curve analysis were used to analyze the association between the TyG index and the impairment of renal function. Results:Among 4 988 residents, 1 396 (28.0%) were males and the age was (59.76±6.28) years. There were 1 247 participants in Q1, Q2, Q3 and Q4 groups, respectively. After 56 months of follow-up, the incidence of rapid eGFR decline and new-onset CKD was 21.9% (1 294/4 988) and 4.0% (200/4 988), respectively. Multivariate logistic regression model analysis showed that TyG index was correlated positively with rapid eGFR decline and new-onset of CKD ( OR=1.34, 95%CI: 1.17-1.52, P<0.001, and OR=1.57, 95%CI:1.19-2.06, P=0.001). Taking group Q1 as a reference, higher levels of TyG index ( Q2, Q3 and Q4 groups) was an independent risk factor for rapid eGFR decline ( P<0.05), which has a dose-response relationship (for trend P=0.002). Compared with the lowest quartile, the adjusted OR of new-onset CKD in the highest quartile was 1.85 ( 95%CI:1.13-3.03, P=0.014). The results of restricted cubic spline fitting logistic regression analysis showed a linear association between TyG index and both outcomes (both P>0.05). The area under ROC curve ( AUC) of the TyG index for predicting the two adverse outcomes were 0.536 ( 95%CI: 0.516-0.556, P<0.001) and 0.588 ( 95%CI:0.548-0.627, P<0.001), respectively. Conclusion:The elevated levels of TyG index may be used as an independent predictor of rapid eGFR decline and new-onset CKD.

Objective:To investigate the association between plasma uric acid and hypertension and the gender difference in community-dwelling middle-aged and elderly population.Methods:A community-based cross-sectional study was conducted in Beijing Tongzhou Yongshun Community Health Service Center from June to December 2021, among residents aged 45 years or older selected by cluster sampling method. According to plasma uric acid (UA) level in quartiles, the subjects were divided into 4 groups; and stratified by gender, the subjects were further divided into subgroups. Multivariate logistic regression model was used to analyze the related factors of hypertension, and restricted cubic spline fitting logistic regression model was used to analyze the nonlinear association between uric acid and hypertension and the cut-off values of uric acid.Results:A total of 6 229 residents with the age of (63.2±7.3) years were enrolled in the study. In 1 874 male participants (30.1%), 946 participants (50.5%) had hypertension, and the uric acid level was 359 (309, 418)μmol/L; in 4 355 female participants (69.9%), 2 003 participants (46.0%) had hypertension, and the uric acid level was 306 (261, 359)μmol/L. Multivariate logistic regression analysis showed that after adjusting for factors that were statistically significant in univariate analyses or potentially clinically relevant (including age, body mass index, diabetes mellitus, coronary heart disease, cerebrovascular disease, albumin, estimated glomerular filtration rate, and cholesterol), uric acid was independently associated with hypertension ( P<0.001), for total participants the risk of hypertension in Q4 group was 1.33 times of that in Q1 group ( OR=1.33,95% CI 1.13-1.56, P=0.001); while for females the risk of hypertension in Q4 group was 1.38 times of that in Q1 group ( OR=1.38,95% CI 1.13-1.68, P=0.002), but no significant association was observed for males ( P>0.05). The results of restricted cubic spline fitting logistic regression analysis showed that there was a linear association between uric acid level and hypertension in the total population and males, and the risk of hypertension increased with uric acid level ( P<0.001 for the total population, P=0.016 for male). However, there was a non-linear association in females. When uric acid>307 μmol/L in females, the risk of hypertension increased significantly as the level of uric acid increased ( P<0.001). Conclusions:Uric acid level was independently associated with hypertension in the community-dwelling middle-aged and elderly population, and there was a gender difference in the correlation. The association was nonlinear in females and the cut-off value of uric acid in females was 307 μmol/L.