No abstract

No abstract

BackgroundHeparin saline (HS) is theoretically superior to normal saline (NS) for maintaining the patency of central venous catheters (CVCs), but the comparative efficacy of them remains controversial. The aim of this systematic review and meta-analysis was to assess the efficacy of NS versus HS in the maintenance of the patency of CVCs in adult patients.MethodsWe searched PubMed, Embase and the Cochrane library databases. Randomized controlled trials (RCTs) evaluating the use of NS vs. HS to maintain the permeability of CVCs among adult patients were included in our meta-analysis. References of relevant papers were reviewed manually. No language restriction was applied. Non-human studies were excluded. Pooled relative risk (RR) was calculated using a Mantel-Haenszel random-effects model. We also performed subgroup analysis examining the effect of the duration of catheter placement on the outcome. All statistical tests were two-sided using a significance level of 0.05.ResultsTen RCTs involving 7875 subjects (with analysis at patient, catheter, lumen and line access level) were included in this meta-analysis. Whether in terms of pooled or local analysis (RR with 95% confidence interval spans 1), NS can be equally, if not more effective, in keeping the CVCs open. Of studies reporting secondary outcomes (maneuver needed, heparin-induced thrombocytopenia, haemorrhage, central venous thrombosis and catheter-related bloodstream infection), heparinised saline was shown not to be superior to non-heparinised solution. Subgroup analysis in patients with short vs long term CVC placement was consistent with the main outcome partly and in particular for maintenance of catheter patency in patients with a long-term placement i.e. >30 days, the RR was 0.97 (n = 6589; 95% CI = 0.76 to 1.23; P = 0.796). However, for patients in whom the catheter was in place for <30 days, the RR was 1.52 (n = 1286; 95% CI = 1.02 to 2.27; P = 0.041).ConclusionsBased on the results of this meta-analysis, HS is not superior to NS in reducing CVCs occlusion. But in the short term, the use of HS is slightly superior to NS for flushing catheters from a statistical point of view.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-016-1585-x) contains supplementary material, which is available to authorized users.

Monosodium iodoacetate (MIA) is an inhibitor of glyceraldehyde-3-phosphate dehydrogenase activity, and causes dosedependent cartilage degradation resembling the pathological changes of human osteoarthritis (OA). In this study, we assessed the apoptosis induced by MIA and clarified the underlying mechanisms using the primary rat chondrocytes. The apoptosis of primary rat chondrocytes was analyzed by flow cytometry. The levels of mitochondrial membrane potential (DCm) were evaluated using fluorescence spectrophotometer. The production of reactive oxygen species (ROS) was determined by fluorescence spectrophotometer. Apoptosis-related protein cytochrome c and procaspase-3 expressions were examined by Western blotting. We found that MIA treatment induces apoptosis in chondrocytes, as confirmed by increases in the percent of apoptotic cells, up-regulation of cytochrome c and caspase-3 protein levels. Treatment with MIA increases ROS production and decreases the levels of DCm. The antioxidant, N-acetylcysteine (NAC), significantly prevented the production of ROS, the reduction of DCm, the release of cytochrome c and the activation of caspase-3. Further, NAC completely protected the cells from MIA-induced apoptosis. Together these observations suggest that the mechanisms of MIA-induced apoptosis are primarily via ROS production and mitochondria-mediated caspase-3 activation in primary rat chondrocytes. Keywords: monosodium iodoacetate; reactive oxygen species; mitochondrial membrane potential; caspase-3; apoptosis Osteoarthritis (OA) is a typical slow and degenerative joint disease. It affects about 80% of individuals of both sexes over the age of 60 and nearly 15% of the total population. OA is characterized by histological changes of the joint including degeneration of articular cartilage, synovitis, remodeling of subchondral bone and sclerosis formation, leading to a gradual loss of articular cartilage. 1 Though the symptoms associated with OA are well documented, the cartilage matrix changes that trigger onset of OA have not yet fully understood. Chondrocytes in OA cartilage demonstrated morphologic changes that are characteristic features of apoptosis. The number of apoptotic chondrocytes is closely correlated with the OA grade. 2 Moreover, chondrocytes play an important role in the OA process in that the progression of OA can be judged by the viability of chondrocytes and their ability to resist apoptosis. 3 Recent studies showed that several different mechanisms may adjust apoptosis of chondrocytes, including the death receptor Fas/CD95-mediated extrinsic pathway, the p53-dependent intrinsic pathway, as well as the ubiquitin-proteasome protein degradation pathway. 4 Chondrocyte apoptosis and apoptotic pathways in the pathology of OA have not yet clearly elucidated, however apoptosis is understood to have prominent role in the OA. This indicates that chondrocyte apoptosis is important to the pathogenesis of OA and mechanism of cell death could be targeted for drug screening and new therapeutic strategie...

Hypertension can lead to abnormal left atrial reservoir and conduit functions, and coexisting diabetes can further impair conduit function. 2DSTE-derived strain and strain rate imaging are sensitive methods for evaluating left atrial phasic function.

The chemoprotective effect of hydroxytyrosol (HT) against UVB-induced DNA damage was investigated in a human skin keratinocyte cell line, HaCaT. The comet assay was used to monitor DNA strand breaks. Intracellular reactive oxygen species (ROS) formation was measured by flow cytometry using 2,7-dichlorofluorescein diacetate (DCFH-DA). The levels of oxidatively generated damage to DNA were estimated by immunocytochemistry analysis of 8-hydroxy-2'-deoxyguanosine (8-OHdG). The protein expression of p53 and NF-kappaB was estimated by western blotting. The results showed that HT significantly reduced the DNA strand breaks caused by UVB. It was also found that HT reduced intracellular ROS formation and 8-OHdG level caused by UVB. Furthermore, HT attenuated the expression of p53 and NF-kappaB in a concentration-dependent manner. These results strongly suggest that HT has a significant protective ability against UVB-induced DNA damage and that oxidative stress plays an important part in it.

No abstract

Aim: To compare the efficacy and safety of cemented and uncemented hemiarthroplasty in elderly patients with femoral neck fracture. Materials and methods: We searched PubMed, EMBASE, and Cochrane Library databases for published randomized clinical trials comparing cemented hemiarthroplasty with uncemented hemiarthroplasty in elderly patients with a femoral neck fracture. The search was not limited to language, time, or other factors. The quality of each study was assessed using the revised Jadad scale. Two researchers independently extracted data from all selected studies, including the following base line data: study period, fracture stage, number of patients, male female ratio, average age, and per-protocol (PP) or intent-to-treat (ITT), and the interest outcomes: the mortality at 12 months, operative time, hospital stay, common complications, prosthetic-related complications, blood loss and Harris Hip Score (HHS). Fixed-effects or random-effects models with mean differences and odds ratios were used to pool the continuous and dichotomous variables to determine heterogeneity of the included studies. Results: A total of 8 studies involving 1577 hips (782 uncemented and 795 cemented) were included in this meta-analysis. The meta-analysis is indicated that the operation time of cemented hemiarthroplasty was longer than uncemented hemiarthroplasty and there was statistical significance between two groups (OR = −7.30, 95%CI, −13.13, −1.46; P = .01). However, there was no significant difference between the two methods of fixation in mortality at 12 months (OR = 1.22, 95%CI, 0.94–1.59; P = .14), hospital stay (OR = 0.26, 95%CI, −0.41, 0.93; P = .44), blood loss (OR = −17.94, 95%CI, −65.83, 29.95; P = .46), and HHS score. There were significant differences in the common complications of pulmonary embolism between the two groups, but there were no differences in the other five common complications. The results showed that uncemented hemiarthroplasty could reduce the incidence of pulmonary embolism after operation. Moreover, the outcomes of prosthetic-related complications showed that there were significant differences between the two groups in periprosthetic fracture (OR = 8.32, 95%CI, 3.85–17.98; P < .00001) and prosthetic subsidence and loosening (OR = 5.33, 95%CI, 2.18–13.00; P = .0002). Conclusions: Our study shows that uncemented prosthesis can shorten the operation time and reduce the incidence of pulmonary embolism, but it does not reduce mortality, blood loss, and hospital stay. Most importantly, the incidence of prosthetic-related complications was higher in uncemented patients.