ObjectsTo investigate the potential clinical significance between blood lipid levels and lower extremity deep venous thrombosis (LEDVT). Methods: This cohort study included 500 participants, contains 246 patients with LEDVT and 254 patients without LEDVT. The characteristics including age, sex, body mass index (BMI), disease course, ill position, smoking history, history of current illness, drug administration were collected. And blood lipid levels and other clinical parameters including triglyceride (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), apolipoprotein A1 (ApoA1), apolipoprotein B (ApoB), activated partial thromboplastin time (APTT), thromboplastin time (TT), prothrombin time (PT), and fibrinogen (FIB), neutrophils (NEUT), platelet (PLT), lymphocyte count (LY) were observed. Univariate and multivariate logistic regression analyses were applied. In the present study we particularly focused on the potential associations between blood lipid levels and LEDVT. Results: The risk of LEDVT in participants with HDL-C levels of 0.965 to 1.14 mmol/L, 1.14 to 1.36 mmol/L, and >1.36 mmol/L were 0.366, 0.183, 0.203 times than in controls (<0.965 mmol/L), respectively. Compared to individuals with ApoA1 1.38 mmol/L were related to a decreased risk of LEDVT. The risk of LEDVT in patients with TG levels of 0.985 to 1.37 mmol/L, 1.37 to 1.91 mmol/L, and >1.91 mmol/L were 2.243, 2.224, and 2.540 times higher than that of those with TG <0.985 mmol/L, respectively. The risk of LEDVT in subjects with 4.57< TC <5.17 mmol/L was 0.471-fold than that of those with TC <3.97 mmol/L. Conclusion: The present study indicates that higher levesl of HDL-C and ApoA1 could be associated with a decreased risk of LEDVT, while higher TG levels might be associated with an increased risk of LEDVT. In addition, within the normal range, high TC levels were associated with decreased risk of LEDVT. These findings may help clinicals to identify early and treat those patients with a high-risk of LEDVT at proper time, which could improve patients’ life quality.

Background: For low risk patients undergoing median sternotomies, no midterm follow-up studies involving sternal healing have been conducted. In this study we evaluated sternal healing in low risk patients by chest CT scan and the risk factors associated with poor healing were analyzed. Methods: Patients who underwent sternal median incision heart surgery from September 2014 to March 2015 were recruited. The clinical information of these patients during hospitalization was collected, and the CT scan data were submitted to the two chief physicians of the Radiology Department for radiographical sternal healing score determination. Based on the method of wound closure, the patients were divided into sternum plate (Plates) and wire groups (Wires). Results: Forty-four patients were recruited. The mean CT examination time was 17.27 ± 2.30 months postoperatively. Twenty-nine (65.9%) patients met the criteria for radiographic sternal healing. Three segments, including the aortopulmonary window, the main pulmonary artery, and the aortic root, had healed less in comparison to the manubrium segment. Compared to patients in whom 6–7 metal wires were used for sternal closure, healing of the lower sternum was worse in patients in whom five wires were used, but the difference in healing was not statistically significant. Univariate analysis of sternal healing showed that patient age was a risk factor for sternal non-healing. When the patient age was > 45 years, the predicted risk of radiographic sternal non-union was 1.833 (95% CI: 1.343–2.503). Conclusions: At the mid-term follow-up, 65.9% of patients undergoing median sternotomies demonstrated radiographic sternal healing. Age, but not closure device, was a risk factor for sternal non-healing in low risk patients. Use of more wires had a positive impact on sternal healing. Trial registration: researchregistry4918, registered 28 May 2019, retrospectively registered.

Hepatic injury induced by ischemia and reperfusion (HIRI) is a major clinical problem after liver resection or transplantation. The polarization of macrophages plays an important role in regulating the severity of hepatic ischemia/reperfusion injury. Recent evidence had indicated that the ischemia induces an acidic microenvironment by causing increased anaerobic glycolysis and accumulation of lactic acid. We hypothesize that the acidic microenvironment might cause the imbalance of intrahepatic immunity which aggravated HIRI. The hepatic ischemia/reperfusion injury model was established to investigate the effect of the acidic microenvironment to liver injury. Liposomes were used to deplete macrophages in vivo. Macrophages were cultured under low pH conditions to analyze the polarization of macrophages in vitro. Activation of the PPAR-γ signal was determined by Western blot. PPAR-γ agonist GW1929 was administrated to functionally test the role of PPAR-γ in regulating macrophage-mediated effects in the acidic microenvironment during HIRI. We demonstrate that acidic microenvironment aggravated HIRI while NaHCO₃ reduced liver injury through neutralizing the acid, besides, liposome abolished the protective ability of NaHCO₃ through depleting the macrophages. In vivo and vitro experiment showed that acidic microenvironment markedly promoted M1 polarization but inhibited M2 polarization of macrophage. Furthermore, the mechanistic study proved that the PPAR-γ signal was suppressed during the polarization of macrophages under pH = 6.5 culture media. The addition of PPAR-γ agonist GW1929 inhibited M1 polarization under acidic environment and reduced HIRI. Our results indicate that acidic microenvironment is a key regulator in HIRI which promoted M1 polarization of macrophages through regulating PPAR-γ. Conversely, PPAR-γ activation reduced liver injury, which provides a novel therapeutic concept to prevent HIRI.