Site-specific mortality in native joint septic arthritis: a national population study.

OBJECTIVE: This national cohort study investigated the incidence, site-specific mortality and prognostic factors of native septic arthritis (SA). METHODS: Tapping Taiwan's National Health Insurance Research Database, we identified inpatients with newly diagnosed SA between 1998 and 2012. They were categorized by site of infection and followed to calculate 30-day, 90-day and 1-year mortality. Predictors of mortality were calculated using Cox models. RESULTS: A total of 31 491 patients were identified as having SA, the most common site of infection being the knee (50.1%), followed by the hip (14.4%), other sites (26.8%), the shoulder (5.5%) and multiple sites (1.2%). Knee joint involvement was the most common site for all subgroups. Incidence increased from 9.8/105 in 1998 to 13.3/105 in 2012. The 30-day, 90-day and 1-year mortality rates were 4.3, 8.6 and 16.4% respectively. Predictors for mortality were hip infection, shoulder infection, multiple-site infection, being male, age ≥65 years old and comorbidities. We derived a mortality scoring model over age/SA site/comorbidity, and age ≥65 years old had the greatest risk contribution to mortality. No matter whether 1-month, 3-month or 1-year mortality was being considered, patients with the higher risk scores had the higher mortality rates (P < 0.0001). CONCLUSION: SA is an emerging infectious disease with a rising incidence, long duration of hospital stay and high mortality rate. The most common affected joint was knee for all subgroups. Patients aged ≥65 years old had a high SA incidence and the greatest risk contribution.

Maslinic acid protects against obesity-induced nonalcoholic fatty liver disease in mice through regulation of the Sirt1/AMPK signaling pathway.

Maslinic acid is a pentacyclic triterpenoid that is distributed in the peel of olives. Previous studies found that maslinic acid inhibited inflammatory response and antioxidant effects. We investigated whether maslinic acid ameliorates nonalcoholic fatty liver disease in mice with high-fat-diet (HFD)-induced obesity and evaluated the regulation of lipogenesis in hepatocytes. Male C57BL/6 mice fed a normal diet or HFD (60% fat, w/w) were tested for 16 wk. After the fourth week, mice were injected intraperitoneally with maslinic acid for 12 wk. In another experiment, HepG2 cells were treated with oleic acid to induce lipid accumulation or maslinic acid to evaluate lipogenesis. Maslinic acid significantly reduced body weight compared with HFD-fed mice. Maslinic acid reduced liver weight and liver lipid accumulation and improved hepatocyte steatosis. Furthermore, serum glucose, leptin, and free fatty acid concentrations significantly reduced, but the serum adiponectin concentration was higher, in the maslinic acid group than in the HFD group. In liver tissue, maslinic acid suppressed transcription factors involved in lipogenesis and increased adipose triglyceride lipase. In vitro, maslinic acid decreased lipogenesis by activating AMPK. These findings suggest that maslinic acid acts against hepatic steatosis by regulating enzyme activity involved in lipogenesis, lipolysis, and fatty acid oxidation in the liver.-Liou, C.-J., Dai, Y.-W., Wang, C.-L., Fang, L.-W., Huang, W.-C. Maslinic acid protects against obesity-induced nonalcoholic fatty liver disease in mice through regulation of the Sirt1/AMPK signaling pathway.

Fisetin Protects Against Hepatic Steatosis Through Regulation of the Sirt1/AMPK and Fatty Acid ß-Oxidation Signaling Pathway in High-Fat Diet-Induced Obese Mice.

BACKGROUND/AIMS: Fisetin is a naturally abundant flavonoid isolated from various fruits and vegetables that was recently identified to have potential biological functions in improving allergic airway inflammation, as well as anti-oxidative and anti-tumor properties. Fisetin has also been demonstrated to have anti-obesity properties in mice. However, the effect of fisetin on nonalcoholic fatty liver disease (NAFLD) is still elusive. Thus, the present study evaluated whether fisetin improves hepatic steatosis in high-fat diet (HFD)-induced obese mice and regulates lipid metabolism of FL83B hepatocytes in vitro. METHODS: NAFLD was induced by HFD in male C57BL/6 mice. The mice were then injected intraperitoneally with fisetin for 10 weeks. In another experiment, FL83B cells were challenged with oleic acid to induce lipid accumulation and treated with various concentrations of fisetin. RESULTS: NAFLD mice treated with fisetin had decreased body weight and epididymal adipose tissue weight compared to NAFLD mice. Fisetin treatment also reduced liver lipid droplet and hepatocyte steatosis, alleviated serum free fatty acid, and leptin concentrations, significantly decreased fatty acid synthase, and significantly increased phosphorylation of AMPKα and the production of sirt-1 and carnitine palmitoyltransferase I in the liver tissue. In vitro, fisetin decreased lipid accumulation and increased lipolysis and ß-oxidation in hepatocytes. CONCLUSION: This study suggests that fisetin is a potential novel treatment for alleviating hepatic lipid metabolism and improving NAFLD in mice via activation of the sirt1/AMPK and ß-oxidation pathway.

Agreement Between Automated and Human Measurements of Heart Rate in Patients With Atrial Fibrillation.

BACKGROUND: The accuracy of heart rate (HR) measurement by automated blood pressure monitors in patients with atrial fibrillation (AF) remains unclear. The authors investigate the agreement between HR measurements by 2 automated devices and human counting in patients with AF. METHODS: In 47 patients with persistent AF, HR was recorded using 2 automated blood pressure monitors: Omron M5-I and Microlife BPA100 Plus. Human counting of HR by a stethoscope was used as the reference. For each method, 3 readings were made and the mean was calculated for comparison. In addition to Wilcoxon signed rank test, the correlation between HR measurements by automated devices and human counting was determined using Spearman's rank correlation coefficient (r), and the agreement between HR measurements by both devices and human counting was validated by the Bland-Altman plot and intraclass correlation coefficient (ICC). RESULTS: Overall, we found no significant difference in HR measurements between devices and human counting (Omron vs human counting, 81.1 ± 11.1 vs 80.2 ± 10.8 beats per minute [bpm]; P = .21, r = 0.911; ICC, 0.954; Microlife vs human counting, 81.3 ± 10.8 vs 80.2 ± 10.8 bpm; P = .22, r = 0.842; ICC, 0.912). However, in patients with HR greater than 80 bpm, the HR measured by the Microlife device was significantly higher than that measured by human counting (91.1 ± 5.2 vs 87.1 ± 8.6 bpm, P = .034). CONCLUSION: There was a high agreement between HR measurements by 2 automated devices and human counting, but the Microlife device may overestimate HR in AF patients with HR greater than 80 bpm.

Deficiency of Endothelial Progenitor Cells Associates with Graft Thrombosis in Patients Undergoing Endovascular Therapy of Dysfunctional Dialysis Grafts.

BACKGROUND: The deficiency of endothelial progenitor cells has been demonstrated to be associated with cardiovascular events in patients undergoing dialysis. However, their correlation with dialysis graft outcomes remains unknown. The objective of this study was to investigate the relationship between circulating endothelial progenitor cells and dialysis graft outcomes. METHODS: After excluding 14 patients with acute coronary syndrome, decompensated heart failure or graft thrombosis in the prior three months, a total of 120 patients undergoing dialysis who underwent endovascular therapy of dysfunctional dialysis grafts were prospectively enrolled. Blood was sampled from study subjects in the morning of a mid-week non-dialysis day. Surface makers of CD34, KDR, and CD133 were used in combination to determine the number of circulating endothelial progenitor cells. All participants were prospectively followed until June 2013. RESULTS: The median follow-up duration was 13 months, within which 62 patients experienced at least one episode of graft thrombosis. Patients with graft thrombosis had lower CD34+KDR+ cell counts compared with patients without graft thrombosis (median 4.5 vs. 8 per 105 mononuclear cells, p = 0.02). Kaplan-Meier analysis demonstrated thrombosis-free survival was lower in the low CD34+KDR+ cell count group (30%) than in the high CD34+KDR+ cell count group (61%; p = 0.007). Univariate analysis showed diabetes, high sensitive C-reactive protein, lesion length and CD34+KDR+ cell counts associated with graft thrombosis. Multivariate analyses confirmed an independent association between low CD34+KDR+ cell counts and graft thrombosis (hazard ratio, 2.52; confidence interval, 1.43-4.44; p = 0.001). CONCLUSIONS: Our study demonstrated an independent association between low circulating endothelial progenitor cell counts and dialysis graft thrombosis.

A micromechanical study on the effects of precipitation on the mechanical properties of CoCrFeMnNi high entropy alloys with various annealing temperatures.

The CoCrFeMnNi high entropy alloys remain an active field over a decade owing to its excellent mechanical properties. However, the application of CoCrFeMnNi is limited because of the relatively low tensile strength. Here we proposed a micromechanical model which adopted from the theory of dislocation density to investigate the strengthening mechanisms of precipitation of chromium-rich non-equiatomic CoCrFeMnNi alloy. The microstructures of CoCrFeMnNi were obtained directly from SEM-BSE images with different annealing temperatures. The proposed framework is validated by comparing simulations with experiments of uniaxial tensile tests on the CoCrFeMnNi alloys under different annealing temperatures. The stress-strain curves indicate that the precipitate has greater influence on post-yield hardening than the initial yielding strength. In addition, we identified that the particle distribution, controlled by the average size of the particle and the volume fraction of precipitation, can significantly enhance the strengthening effect. The numerical results indicate that HEAs with a precipitate distribution closer to a normal distribution and with smaller average size will tend to have higher strength and ductility.

The impact of door-to-electrocardiogram time on door-to-balloon time after achieving the guideline-recommended target rate.

BACKGROUND: Little is known about the components and contributing factors of door-to-balloon time after implementation of Door-to-Balloon Alliance quality-improving (QI) strategies, including the impact of door-to-ECG time on door-to-balloon time. OBJECTIVE: We investigated whether modification of emergency department (ED) triage processes could improve door-to-ECG and door-to-balloon times after implementation of QI strategies. METHODS: This was a retrospective before-and-after study of a prospectively collected database. From June 2014 to October 2014, interventions were implemented in our ED, including a protocol-driven ECG initiation and moving an ECG station and technician to the triage area. The primary outcome was the percentage of patients with ST-elevation myocardial infarction (STEMI) who received ECG within 10 min of arrival; the secondary outcome was the percentage of patients with door-to-balloon times of <90 min from arrival. Patients from the year pre- and post-QI initiative were defined as the control and intervention groups, respectively. RESULTS: Enrollment comprised 214 patients with STEMI: 109 before the intervention and 105 after the intervention. We analyzed the components of the door-to-balloon process and found the door-to-ECG process was the most critical interval of delay (20.8%). Unrecognized symptoms were the most common cause of delay in the door-to-ECG process resulting in a significant impact on the door-to-balloon time. The intervention group had a higher percentage of patients with door-to-ECG times <10 min than did the control group (93.3% vs. 79.8%, p = 0.005), with a corresponding improvement in door-to-balloon times <90 min (91.1% vs. 76.2%, p = 0.007). In subgroup analysis, the intervention benefits occurred only in non-transferred or walk-in patients. After adjustment for possible co-variates, the QI interventions remained a significant contributing factor for achieving the door-to-ECG and door-to-balloon targets. CONCLUSIONS: The modification of ED triage processes through implementation of QI strategies are effective in achieving better door-to-ECG times and thus, achieving door-to-balloon times <90 min. In patients presenting with ambiguous symptoms, improved door-to ECG target achievement rates, through a protocol-driven and multidisciplinary approach allows for earlier identification of STEMI.

Corrigendum to "Ginkgolide C Suppresses Adipogenesis in 3T3-L1 Adipocytes via the AMPK Signaling Pathway".

[This corrects the article DOI: 10.1155/2015/298635.].

Comparison of two pegylated copolymeric micelles and their potential as drug carriers.

The aim of this study was to evaluate the ability of forming micelles from two types of synthesized diblock pegylated amphiphilic copolymers and their potential as a drug carrier. Two lactone monomers, epsilon-caprolactone (CL) and delta-valerolactone (VL), were copolymerized with methoxy poly(ethylene glycol) (MePEG), respectively. The properties of copolymers were investigated and their biocompatibility was tested through an in vitro cytotoxicity study. The influences of the type of lactone monomer (CL and VL) and the feed molar ratios of lactone/MePEG (50/1, 80/1, 160/1) on the performance and release behavior of drug-loaded micelles were investigated. The opening of CL and VL rings by MePEG was efficient, and the pegylation of poly(lactone)s allowed copolymers possessing amphiphilic property and efficiently self-assembled to form micelles with a low critical micelle concentration (CMC) in the range of 10(-7)-10(-8) M. The nano-sized micelles were able to incorporate hydrophobic drug and regulate drug release, and the release of drug was dominated by the hydrophobic poly(lactone) chain length. Although both amphiphilic copolymers exhibited similar controlled release character, the PCL/MePEG micelles possessed lower CMC, higher biocompatibility, and higher drug loading than PVL/MePEG micelles. These suggested that results choosing pegylated PCL as a drug carrier could be better than PVL/MePEG.

Ginkgolide C Suppresses Adipogenesis in 3T3-L1 Adipocytes via the AMPK Signaling Pathway.

Ginkgolide C, isolated from Ginkgo biloba leaves, is a diterpene lactone derivative [corrected] reported to have multiple biological functions, from decreased platelet aggregation to ameliorating Alzheimer disease. The study aim was to evaluate the antiadipogenic effect of ginkgolide C in 3T3-L1 adipocytes. Ginkgolide C was used to treat differentiated 3T3-L1 cells. Cell supernatant was collected to assay glycerol release, and cells were lysed to measure protein and gene expression related to adipogenesis and lipolysis by western blot and real-time PCR, respectively. Ginkgolide C significantly suppressed lipid accumulation in differentiated adipocytes. It also decreased adipogenesis-related transcription factor expression, including peroxisome proliferator-activated receptor and CCAAT/enhancer-binding protein. Furthermore, ginkgolide C enhanced adipose triglyceride lipase and hormone-sensitive lipase production for lipolysis and increased phosphorylation of AMP-activated protein kinase (AMPK), resulting in decreased activity of acetyl-CoA carboxylase for fatty acid synthesis. In coculture with an AMPK inhibitor (compound C), ginkgolide C also improved activation of sirtuin 1 and phosphorylation of AMPK in differentiated 3T3-L1 cells. The results suggest that ginkgolide C is an effective flavone for increasing lipolysis and inhibiting adipogenesis in adipocytes through the activated AMPK pathway.