BACKGROUND:The hidden blood loss, accounted for a fairly large proportion of perioperative blood loss in total hip replacement, can seriously affect the recovery of postoperative joint function, but the specific influential factors and mechanisms remain unknown at present. OBJECTIVE:To evaluate the relative influential factors for hidden blood loss after primary total hip arthroplasty by the blood loss condition, and to analyze the association between hidden blood loss and prognosis. METHODS:Clinical data of 110 patients who underwent primary total hip arthroplasty in the Liuzhou Worker’s Hospital between April 2011 and April 2013 were retrospectively analyzed. The hidden blood loss was calculated according to Ward and Gross formula. The effects of patient’s gender, age, body mass index, type of prosthesis, presence of internal diseases, and different causes of a disease on hidden blood loss after arthroplasty were analyzed. The patients were divided into the high blood loss group (≥ 480 mL) and the low blood loss group (<480 mL) according to the hidden blood loss. Al the patients were fol owed up for 1 year. The Harris hip score system was used to assess the recovery of hip joint function between the two groups. The correlation between hidden blood loss and the recovery of joint function was analyzed using Pearson’s correlation analysis RESULTS AND CONCLUSION:The total blood loss of primary total hip arthroplasty was (1 340±367) mL, and the hidden blood loss was (748±324) mL, and the percentage of hidden blood loss was 53.7%. The type of prosthesis, presence of internal diseases, and different causes of a disease were significantly associated with hidden blood loss after total hip arthroplasty (P<0.05). Gender, age, body mass index, and operation time were not significantly associated with hidden blood loss after total hip arthroplasty (P>0.05). The hidden blood loss was correlated with postoperative functional recovery (P=0.046). Results indicated that type of prosthesis, presence of internal diseases, and different causes of a disease are main influential factors for hidden blood loss after total hip arthroplasty. The hidden blood loss has some influence on the recovery of postoperative joint function.

BACKGROUND:Our prior experiments have confirmed that 10 μmol/L oxytocin can induce transformation of bone marrow mesenchymal stem cels into myocardial cels. OBJECTIVE: To investigate the effects of Ginsenoside Rh2 on oxytocin-induced transformation of bone marrow mesenchymal stem cels into myocardial cels. METHODS:Rat bone marrow mesenchymal stem cels were isolated by differential adherence method. These isolated cels were randomly divided into five groups. In the blank control group, cels were routinely cultured. In the oxytocin group, cels were cultured with 10 μmol/L oxytocin for 2 consecutive weeks. In the Ginsenoside Rh2 low-, middle-, and high-dose groups, cels were treated with 0.5, 1, 2 μmol/L Ginsenoside Rh2respectively for 24 hours and then with oxytocin for additional 2 consecutive weeks. RESULTS AND CONCLUSION: Optical microscopy showed that compared to the blank control group, some cels in the oxytocin group exhibited an increased soma and some cels grew in clusters and the cel clusters enlarged with the increase in Ginsenoside Rh2 dose. Immunocytochemical staining and western blot analysis showed that cardiac Troponin T and connexin 43 protein expression in the oxytocin, Ginsenoside Rh2 low-, middle-, and high-dose groups were significantly greater than in the blank control group (P < 0.05), and cardiac Troponin T and connexin 43 protein expression in the Ginsenoside Rh2 groups was increased with the increase in Ginsenoside Rh2 dose and was significantly higher than that in the oxytocin group (P < 0.05). Confocal laser scanning microscopy showed that the relative fluorescence intensity of free calcium in the bone marrow mesenchymal stem cels in the oxytocin group was significantly increased after induction by oxytocin for 2 weeks (P < 0.05), while the relative fluorescence intensity in the Ginsenoside Rh2 groups was significantly higher than that in the Ginsenoside Rh2 groups and was positively correlated with the dose of Ginsenoside Rh2. These findings suggest that Ginsenoside Rh2 can obviously promote oxytocin-induced transformation of bone marrow mesenchymal stem cels into myocardial celsin vitro.

Background Hyperuricemia is frequently present in patients with heart failure. Many pathological conditions, such as tissue ischemia, renal function impairment, cardiac function impairment, metabolic syndrome, and inflammatory status, may impact uric acid (UA) metabolism. This study was to assess their potential relations to UA metabolism in heart failure. Methods We retrospectively assessed clinical characteristics, echocardiological, renal, metabolic and inflammatory variables selected on the basis of previous evidence of their involvement in cardiovascular diseases and UA metabolism in a large cohort of randomly selected adults with congestive heart failure (n = 553). By clustering of indices, those variables were explored using factor analysis. Results In factor analysis, serum uric acid (SUA) formed part of a principal cluster of renal functional variables which included serum creatinine (SCr) and blood urea nitrogen (BUN). Univariate correlation coefficients between variables of patients with congestive heart failure showed that the strongest correlations for SUA were with BUN (r = 0.48, P < 0.001) and SCr (r = 0.47, P < 0.001). Conclusions There was an inverse relationship between SUA levels and measures of renal function in patients with congestive heart failure. The strong correlation between SUA and SCr and BUN levels suggests that elevated SUA concentrations reflect an impairment of renal function in heart failure.

BackgroundThe relationship between lipids and coronary artery disease has been well established. However, this is not the case between lipids and heart failure. Ironically, high lipid levels are associated with better outcomes in heart failure, but the mechan-isms underlying the phenomenon are not fully understood. This study was performed to test the hypothesis that reduced intestinal lipid absorption due to venous congestion may lead to low lipid levels.MethodsWe collected data of clinical characteristics, echocardio-graph, and lipid profile in 442 unselected patients with congestive heart failure. Correlations between lipid levels[including total cho-lesterol(TCL), high-density lipoprotein cholesterol(HDL-C), low-density lipoprotein cholesterol(LDL-C), and triglycerides(TG)]and right ventricle end diastolic diameter (RVEDD), left ventricle end diastolic diameter (LVEDD), right atrium diameter (RA), left atrium diameter (LA), or left ventricle ejection fraction (LVEF) were analyzed using Pearson correlation and partial correlation. RVEDD, LVEDD, RA, and LA were indexed to the body surface area.ResultsThere was a significantly inverse correlation between TCL le-vels and RVEDD (r=-0.34,P<0.001) and RA (r=-0.36,P<0.001). Other lipids such as LDL-C, HDL-C, and TG had asimilar inverse correlation with RVEDD and RA. All these correlations remained unchanged after adjusting for age, gender, smoking status, physical activity levels, comorbidities, and medication use.ConclusionsLipid levels were inversely correlated to RVEDD in patients with congestive heart failure; however, because this was an observational study, further investigation is needed to verify our results as wellas identify a causal relationship, if any.