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Background Deep sternal wound infection (DSWI) is a rare but serious complication after median sternotomy, and treatment success depends mainly on surgical experience. Traditional treatment methods for DSWI include complete debridement, vacuum sealing drainage wound therapy and sometimes transposition of muscle flap. This study aimed to evaluate the utility of antibiotic-loaded bone cement combined with vacuum sealing drainage on DSWI and explore the effect of this treatment on lung function. Methods Between January 2018 and December 2019, we treated 12 patients suffering a mediastinitis and open thorax using antibiotic-loaded bone cement combined with vacuum sealing drainage. Subsequently, the blood and local concentration of antibiotic were measured. The patient characteristics, pulmonary function, were retrospectively analyzed. Subjects were followed up for 12 months. Results There were no intraoperative deaths. All patients’ healing wounds were first-stage healing without complications and reoperation, the mean hospital stay was 20.2 ± 3.5 days. Local vancomycin concentrations largely exceeded the ones needed for their efficacy while little antibiotic was found in the blood. Pulmonary function testing was improved 2 weeks after the operation. No infection reoccurred in12-month follow-up. Conclusions The antibiotic-loaded bone cement combined with vacuum sealing drainage might be an effective method for the sternal reconstruction of deep sternal wound infection and it can improve the patient's lung function in a short time.

A 67-year-old male presented with sternal dehiscence following open cardiac surgery. Extensive debridement and attempted closure failed, and the wound had since been managed with vacuum-assisted closure therapy, with little progress. We treated him with antibiotic-loaded bone cement to repair the wound defect. After 3 weeks, the wound healed with excellent result. To our knowledge, this is the first report of antibiotic-loaded bone cement for deep sternal wound infection.

MicroRNAs (miRNAs) play critical roles in tumorigenesis and metastasis by negatively regulating gene expression through complementary binding to the 3'-untranslated region of target mRNAs. The role of miRNAs in expression of the tumor suppressor DAB2IP in bladder cancer (BC) remains unknown. The aim of the present study was to identify miRNAs targeting DAB2IP and determine their expression and function in BC. We predicted candidate miRNAs targeting DAB2IP using TargetScan software. Dual-luciferase reporter assays confirmed that miRNA-556-3p directly regulated DAB2IP expression. Quantitative RT-PCR and RNase protection assays showed that endogenous miRNA-556-3p expression was significantly upregulated in clinical samples of BC patients and BC cell lines and western blot analysis indicated that DAB2IP expression in BC tissues and BC cell lines was concurrently downregulated. Gain or loss of function studies showed that upregulation of miRNA-556-3p promoted proliferation, invasion, migration and colony formation of BC cells, whereas downregulation resulted in opposite effects. Importantly, restoration of DAB2IP expression rescued the effects induced by miRNA-556-3p. Overexpression of miRNA-556-3p in BC cells not only decreased DAB2IP expression, but also markedly increased Ras GTPase activity and ERK1/2 phosphorylation level. These findings suggest that DAB2IP is a direct target of miRNA-556-3p, and endogenous miRNA-556-3p expression shows inverse correlation with simultaneous DAB2IP expression in BC tissues and cells. miRNA-556-3p functions as a tumor promoter in tumorigenesis and metastasis of BC by targeting DAB2IP. Moreover, miRNA-556-3p-mediated DAB2IP suppression plays an oncogenic role by partial activation of the Ras-ERK pathway.

Objective. Exploring the use of echo-tracking (ET) for evaluating changes in carotid artery wall elasticity after smoking cessation. Methods. Carotid artery ultrasound examination was performed in 67 male patients before and after smoking cessation treatment, for measurement of intimal media thickness (IMT), and ET measurement of wall elasticity variables, ie, wall stiffness index (β), pressure-strain elastic modulus (Ep), compliance (AC), augmentation index (AI), and local pulse wave velocity (PWVβ). We also measured heart rate (HR), systolic pressure (Ps), diastolic pressure (Pd), total cholesterol (TC), triglyceride level (TG), low-density lipoprotein (LDL), and high-density lipoprotein (HDL). Results. Hyperlipemia and/or arterial hypertension and/or hyperglycemia were absent in 22 (group A1) and 12 (group B1) and present in 19 (group A2) and 14 (group B2) of the patients with successful (group A, n = 41) and unsuccessful (group B, n = 26) treatment, respectively. In the A1 group, there was no significant difference in AI before and after smoking cessation, whereas β, Ep, and PWVβ decreased, and AC increased (p < 0.05). None of these variables changed after smoking cessation in groups A2, B1, and B2. There was no change in IMT in either group. HR decreased and HDL increased in the A1 group, without change in Ps, Pd, TC, TG, and LDL. There was no change in HR, Ps, Pd, TC, TG, LDL, and HDL in groups A2, B1, and B2. Conclusions. ET can be used to evaluate quantitatively the impact of smoking cessation on common carotid artery wall elasticity. © 2012 Wiley Periodicals, Inc. J Clin Ultrasound, 2012

Magnolol inhibited proliferation of human malignant melanoma A375-S2 cells. The drug induced oligonucleosomal fragmentation of DNA in A375-S2 cells and increased caspase-3, 8, 9 activities followed by the degradation of caspase-3 substrates, inhibitor of caspase dependent DNase (ICAD) and poly-(ADP-ribose) polymerase (PARP). Pan-caspase inhibitor (z-VADfmk), caspase-3 inhibitor (z-DEVD-fmk), capase-8 inhibitor (z-IETD-fmk), caspase-9 inhibitor (z-LEHD-fmk) and caspase-10 inhibitor (z-AEVD-fmk) inhibited magnolol-induced A375-S2 cell apoptosis. The level of anti-apoptotic mitochondrial protein Bcl-2 was up-regulated while the level of pro-apoptotic protein Bax was down-regulated. Taken together, our results indicate that magnolol induces apoptosis by activation of both mitochondrial and death receptor pathways in A375-S2 cells.

To explore the change patterns, influencing factors and predictors of quality of life for 4 years in patients with Alzheimer's disease (AD).A total of 96 mild-moderate AD patients on combined therapies of medicine and recuperation were enrolled. Their clinical symptoms were graded by mini-mental state examination (MMSE), activity of daily living (ADL), global deterioration scale (GDS), neuropsychiatric inventory (NPI), Hamilton depression scale (HRSD), Hamilton anxiety scale (HAMA) and Pittsburgh sleep quality index (PQSI). And their qualities of life were evaluated by Quality of Life-Alzheimer's Disease (QOL-AD) at baseline and at the end of 1, 2, 3, 4 year.(1) During a 4-year follow-up, the scores of QOL-AD, MMSE, ADL, GDS, NPI, HRSD, HAMA and PQSI decreased markedly compared with baseline [(17.5±1.9), (12±3), (45±9), (5.2±0.8), (31±11), (20±6), (14±6), (14±4) vs (30.5±4.6), (21±4), (34±10), (3.3±0.9), (22±9), (18±6), (11±4), (12±4) respectively, t=25.31, 15.42, -7.16, -14.83, -5.56, -2.94, -4.45, -5.60, all P0.01]. With the deterioration of AD, their qualities of life decreased significantly. (2) Spearman's correlation analysis showed that the scores of 4-year QOL-AD were correlated with the 4-year score changes of MMSE, ADL, GDS (r=0.344, 0.368, 0.213; P=0.002, 0.001, 0.047). (3) Multiple Logistic regression model showed that the baseline scores of NPI and HRSD were strong predictors of loss of quality of life (OR=1.697, 1.269; P=0.000, 0.006). And the area under the curve of receiver operating characteristic (ROC) of NPI and HRSD were 0.918 (95% CI: 0.844-0.991) and 0.878 (95% CI: 0.804-0.953) respectively.With the deterioration of AD, the quality of life decreases significantly and has correlations with the score changes of MMSE, ADL and GDS. High scores of NPI and HRSD are the important predictors for a loss of quality of life in AD patients. Early detection and timely interventions are necessary.

Familial hypercholesterolemia (FH) is an inherited disorder of blood lipid metabolism characterized by high serum low-density lipoprotein cholesterol levels and premature coronary artery disease. In this study, we used a system biology approach to identify co-expressed gene pairs that were potentially involved in the progression of FH and constructed a conserved co-expression network using these genes. A total of 4232 co-expressed relationships were identified and we verified the significance by random permutation. FH patients showed differences in lipoprotein and cholesterol metabolism in circulating monocytes and lymphocytes compared to healthy controls. We hope our study could aid in understanding of FH and could provide the basis for FH biomarker identification.