Elevated lipid levels in patients with achilles tendon ruptures: a retrospective matching study.

BACKGROUND: Achilles tendon rupture (ATR) can lead to significant disability of patients. However, whether serum lipid levels are associated with ATR is still unclear. This study aimed to examine the difference in lipid levels between patients with and those without ATR. METHODS: Patients who received ATR surgery during January 2017 to December 2017 were categorized into the case group, and those who had physical examinations during the same period without ATR were in the control group. Different matching methods [case-control matching (CCM) and propensity score matching (PSM)] were used to match the cases and controls at a 1:1 ratio. RESULTS: Among a total of 216 pairs of subjects with CCM, cholesterol, triglyceride, and low-density lipoprotein (LDL) levels were significantly higher (all P<0.05) in the case group than in the control group. Among 241 pairs of subjects with PSM, the same results as those with CCM were obtained. Abnormal rates of cholesterol, triglyceride, and LDL levels in the case group were also significantly higher than those in the control group in CCM and PSM (all P<0.05). After adjusting for the factors of height and weight, there were still significant differences in cholesterol, triglyceride, and LDL levels, as well as high-density lipoprotein levels, between the case and control groups (all P<0.05). CONCLUSIONS: Cholesterol, triglyceride, and LDL levels in patients with ATR are higher than those in healthy people. Further studies are required to verify the effect of some components of lipids on Achilles tendon structure.

The correlation between trimethylamine N-oxide, lipoprotein ratios, and conventional lipid parameters in patients with unstable angina pectoris.

PURPOSE: Trimethylamine N-oxide (TMAO) is recently the main risk factor for coronary heart disease (CHD). Plasma lipid levels are conventionally used to predict coronary risk, but the correlation between TMAO and plasma lipid levels in unstable angina pectoris (UAP) was unclear. Our objective was to compare the plasma level of TMAO to lipoprotein ratios and conventional lipid parameters in UAP patients. METHODS: A total of 114 control participants and 184 UAP patients were enrolled. Demographic characteristics were collected. Plasma levels of TMAO and lipid in all patients were measured and analyzed. The receiver operating characteristic analysis (ROC), univariate, and multivariate logistic regression analyses were carried out to examine the relationship between TMAO, lipoprotein ratios, conventional lipid parameters, and UAP. RESULTS: The plasma levels of TMAO were remarkably increased in UAP patients (3.28 ± 1.97 µM) compared with control participants (1.52 ± 0.59 µM, P < 0.01). TMAO was significantly correlated with lipid levels in UAP patients. The ROC, univariate and multivariate logistic regression analysis both showed that the TMAO significantly increased the risk for occurrence of UAP. CONCLUSIONS: Our data indicate that the TMAO is superior to lipoprotein ratios and conventional lipid parameters in predicting occurrence of UAP.

Both FOXO3a and FOXO1 are involved in the HGF-protective pathway against apoptosis in endothelial cells.

Hepatocyte growth factor (HGF) was identified as an endogenous tissue protective agent against apoptosis in many cell types. The mechanism by which HGF protects primary endothelial cells (ECs) has not yet been completely elucidated. FOXO1 and FOXO3a, two members of the FOXO family, are the most abundant FOXO isoforms in mature endothelial cells. In this study, we aimed to explore whether FOXO1 and FOXO3a play similar roles in HGF-mediated protection against apoptosis in mature endothelial cells. Our result showed that HGF prevented ECs from oxidative-stress induced apoptosis in part by inducing the phosphorylation of FOXO proteins. FOXO1 and FOXO3a are equally important in this process by regulating the expression of Bim, PUMA, FasL, and TRAIL.

Platelet-derived microparticles are implicated in remote ischemia conditioning in a rat model of cerebral infarction.

AIM: Remote ischemic preconditioning protects against ischemic organ damage by giving short periods of subcritical ischemia to a remote organ. We tested the hypothesis that remote ischemic conditioning can attenuate cerebral stroke in a rat middle cerebral artery occlusion (MCAO) model by microparticles (MPs). METHODS AND RESULTS: MPs were extracted from healthy rats that underwent hindlimb ischemia-reperfusion preconditioning (RIPC), and were transfused into rats that had undergone MCAO without RIPC. The transfusion resulted in an increase in platelet-derived MPs in blood and reduction in infarction area, confirmed by both 2-3-5-triphenyltetrazolium chloride staining and magnetic resonance imaging, albeit to a lesser degree than RIPC itself. Behavioral tests (modified Neurological Severity Score [mNSS]) were calculated to judge the behavioral change. However, no significant difference was observed after MP transfusion in 24 h or the following consecutive 9 days. CONCLUSIONS: RIPC induces an increase in MPs, and platelet-derived MPs may confer at least part of the remote protective effect against cerebral ischemic-reperfusion injury.