Miracle-dz/UniFAR-FTUs huggingface dataset:
Lipopolysaccharide, Tumor Necrosis Factor Alpha, or Interleukin-1β Triggers Reactivation of Latent Cytomegalovirus in Immunocompetent Mice

ABSTRACT We have previously shown that cytomegalovirus (CMV) can reactivate in lungs of nonimmunosuppressed patients during critical illness. Our recent work has shown that polymicrobial bacterial sepsis can trigger reactivation of latent murine CMV (MCMV). We hypothesize that MCMV reactivation following bacterial sepsis may be caused by inflammatory mediators. To test this hypothesis, BALB/c mice latently infected with Smith strain MCMV received sublethal intraperitoneal doses of lipopolysaccharide (LPS), tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), or saline. Lung tissue homogenates were evaluated for viral reactivation 3 weeks after mediator injection. Because LPS is known to signal via Toll-like receptor 4 (TLR-4) in mice, further studies blocking this signaling mechanism were performed using monoclonal MTS510. Finally, mice were tested with intravenous TNF-α to determine whether this would cause reactivation. All mice receiving sublethal intraperitoneal doses of LPS, TNF-α, or IL-1β had pulmonary reactivation of latent MCMV 3 weeks following injection, and LPS caused MCMV reactivation with kinetics similar to those for sepsis. When TLR-4 signaling was blocked, exogenous LPS did not reactivate latent MCMV. Intravenous TNF-α administration at near-lethal doses did not reactivate MCMV. Exogenous intraperitoneal LPS, TNF-α, and IL-1β are all capable of reactivating CMV from latency in lungs of previously healthy mice. LPS reactivation of MCMV appears dependent on TLR-4 signaling. Interestingly, intravenous TNF-α did not trigger reactivation, suggesting possible mechanistic differences that are discussed. We conclude that inflammatory disease states besides sepsis may be capable of reactivating CMV from latency.
Epigallocatechin Gallate Attenuates Hip Fracture-Induced Acute Lung Injury by Limiting Mitochondrial DNA (mtDNA) Release

Background The aim of this study was to assess the protective effects and explore the mechanism of epigallocatechin gallate (EGCG) in hip fracture-induced acute lung injury. Material/Methods Thirty male Sprague-Dawley (SD) rats were randomly divided into the control group, hip fracture group, and hip fracture + EGCG (10 mg/Kg) group. After 24 h, blood samples, bronchoalveolar lavage fluid (BALF), and lung tissue were collected. Serum mitochondrial DNA (mtDNA) was measured by RT-PCR and BALF was used to perform cytological analysis and enzyme-linked immunosorbent assay (ELISA) assay. Lung tissue was used to evaluate the injury level. Results EGCG significantly reduced the hip fracture-induced high level of serum mtDNA (p<0.05). HE staining showed protective effects of EGCG. Lower lung injury score and wet/dry ratio were identified in the hip fracture + EGCG group than in the hip fracture group (p<0.05). We found significantly lower levels of infiltration of inflammatory cells and production of inflammatory cytokines in the BALF of the hip fracture + EGCG group than in the hip fracture group (p<0.05). Conclusions Our study found that EGCG had protective effects on hip fracture-induced acute lung injury and suggests that EGCG exerts its protective effects through limiting the release of mtDNA. Our results provide a novel pharmacological agent to attenuate hip fracture-induced acute lung injury, as well as a potential theory to better explain the anti-inflammatory property of EGCG.
Establishing a recovery orientation in mental health services: Evaluating the Recovery Self-Assessment (RSA) in a Swedish context.

OBJECTIVE Although there has been an emphasis on developing knowledge regarding recovery in Sweden, it is unclear to what extent this has been translated into a recovery orientation in the provision of mental health services. Instruments, which present the components of recovery as measurable dimensions of change, may provide a framework for program development. Involving users is an essential factor in the utilization of such tools. The purpose of this study was to evaluate the psychometric properties of the Recovery Self-Assessment (RSA) measure and its potential for being utilized in a Swedish context. METHODS The sample consisted of 78 participants from 6 community mental health services targeting people with serious mental illnesses in a municipality in Sweden. They completed the RSA at the study baseline and two weeks later. User panels participated in the translation and administration of the RSA and the reporting of results. RESULTS The Swedish version of the RSA had good face and content validity, satisfactory internal consistency, and a moderate to good level of stability in test-retest reliability. The user panels contributed to establishing validity and as collaborators in the study. CONCLUSIONS AND IMPLICATIONS FOR PRACTICE Establishing the RSA as a valid and reliable instrument with which to focus on the recovery orientation of services is a first step in beginning to study the types of interventions that may effect and contribute to recovery oriented practice in Sweden.
A Non-Paradoxical Interpretation of the Gibson Paradox

In this study, we show how, to yield the real cost of borrowing, the price level can be combined with the nominal interest rate in a monetary regime where the level of prices is trend stationary. We show that the price level then conveys intertemporal information in a way similar to nominal interest rates. We estimate real interest rate series for the gold-standard period in the United Kingdom under the assumption the agents expect the price level to come back to its long-run equilibrium value. The positive correlation between the price level and the nominal interest rate-known as the Gibson paradox and far from being paradoxical-helps explain why the nominal interest rate was so stable in a period characterized by numerous wars and important gold discoveries. The new real interest rate series provides the opportunity to re-examine Barro's (1987) finding on the effect of temporary military spending on interest rates. It also relaxes the assumption that the nominal long-term interest rate is also the expected real rate.
Coaching for character : reclaiming the principles of sportsmanship

"Coaching for Character" provides coaches with a valuable tool to help them understand the basic principles of sportsmanship, the justification of these principles, and how to teach their players to understand and apply them. By applying the understanding of sportsmanship explained in the book, coaches will create more disciplined and coachable individual athletes and teams. And, more important, they will help young athletes develop the character and perspective that will serve them well throughout their lives.Combining years of coaching and teaching experience, Clifford and Feezell provide clear guidelines to help coaches teach their players respect for- opponents, - teammates and team, - officials, - coaches, and - the rules and traditions of the game.With proper respect, athletes are more likely to compete fairly and fully, to sacrifice in order to achieve individual and team goals, and to develop attitudes that make them enjoyable to coach.Coaches' responsibilities as models and educators are brought to life through real situations that confront them on and off the field. The authors provide numerous questions that help readers to become more reflective about sport. The book also urges coaches and athletes to strive for a healthy balance between the playful side of sport and the seriousness of competition.By using "Coaching for Character"'s special suggestions for teaching sportsmanship, coaches will find new ways to reach their athletes--without preaching or sacrificing practice time that could be spent on developing the physical skills, conditioning, and mental strategies that are also essential to athletic success.Clifford and Feezell demonstrate that sportsmanship doesn't get in the way of genuine competition--that a commitment to sportmanship comes from an understanding of the nature of competition.
Activation of the E3 ligase function of the BRCA1/BARD1 complex by polyubiquitin chains

Loss of the tumour suppressor BRCA1 results in profound chromosomal instability. The fundamental defect underlying this catastrophic phenotype is not yet known. In vivo, BRCA1 forms a heterodimeric complex with BARD1. Both proteins contain an N‐terminal zinc RING‐finger domain which confers E3 ubiquitin ligase activity. We have isolated full‐length human BRCA1/BARD1 complex and have shown that it has a dual E3 ubiquitin ligase activity. First, it mediates the monoubiquitylation of nucleosome core histones in vitro, including the variant histone H2AX that co‐localizes with BRCA1 at sites of DNA damage. Secondly, BRCA1/BARD1 catalyses the formation of multiple polyubiquitin chains on itself. Remarkably, this auto‐polyubiquitylation potentiates the E3 ubiquitin ligase activity of the BRCA1/BARD1 complex >20‐fold. Even though BRCA1 has been reported to associate with a C‐terminal ubiquitin hydrolase, BAP1, this enzyme does not appear to function in the deubiquitylation of the BRCA1/BARD1 complex.
Induction of Paclitaxel Resistance by ERα Mediated Prohibitin Mitochondrial-Nuclear Shuttling

Paclitaxel is a drug within one of the most promising classes of anticancer agents. Unfortunately, clinical success of this drug has been limited by the insurgence of cellular resistance. To address this, Paclitaxel resistance was modeled in an in vitro system using estrogen treated prostate cancer cells. This study demonstrates that emerging resistance to clinically relevant doses of Paclitaxel is associated with 17-β-estradiol (E2) treatment in PC-3 cells, but not in LNCaP cells. We found that small interfering RNA mediated knockdown of ERα lead to a decrease in E2 induced Paclitaxel resistance in androgen-independent cells. We also showed that ERα mediated the effects of estrogen, thereby suppressing androgen-independent cell proliferation and mediating Paclitaxel resistance. Furthermore, E2 promoted Prohibitin (PHB) mitochondrial-nucleus translocation via directly mediation of ERα, leading to an inhibition of cellular proliferation by PHB. Additionally, restoration of Paclitaxel sensitivity by ERα knockdown could be overcome by PHB overexpression and, conversely, PHB knockdown decreased E2 induced Paclitaxel resistance. These findings demonstrate that PHB lies downstream of ERα and mediates estrogen-dependent Paclitaxel resistance signaling cascades.
Obesity indices are predictive of elevated C-reactive protein in long-haul truck drivers.

BACKGROUND Obesity rates in long-haul truck drivers have been shown to be significantly higher than the general population. We hypothesized that commercial drivers with the highest levels of general obesity and abdominal adiposity would have higher concentrations of high sensitivity C-reactive protein (CRP), a marker of inflammation. METHODS Survey and anthropometric data were collected from 262 commercial drivers. Weight, circumference measures, and blood analysis for CRP (N = 115) were conducted and compared to National Health and Nutrition Examination Survey (NHANES) data. CRP values were non-normally distributed and logarithmically transformed for statistical analyses. RESULTS BMI, waist circumference, sagittal abdominal diameter, and CRP were significantly higher than in the general population. Anthropometric indices that included height (BMI, waist-to-height ratio, and sagittal diameter-to-height ratio), were most predictive of CRP values. CONCLUSIONS Abdominal obesity is prevalent in commercial vehicle drivers and is an important indicator of the presence of inflammation in this population. Am. J. Ind. Med. 59:665-675, 2016. © 2016 Wiley Periodicals, Inc.
Computer-Aided Writing in French as a Foreign Language: A Qualitative and Quantitative Look at

Currently little documentation exists on the writing strategies and habits of foreign language (FL) writers. This study was designed to observe, as unobtrusively as possible, the revision strategies of 5 students of French enrolled in a 1-semester intensive intermediate college French course. The participants completed a two-part writing task with the aid of the software program Systeme-D (Noblitt, Sola, & Pet, 1987, 1992). Of considerable interest is the program’s keystroke tracking device, which records the lexical, grammatical, and thematic information that students access while writing. Analysis of the compositions, computer records, videotapes of writing sessions, and student responses to postwriting questionnaires provide a detailed picture of how and when the students revised in real time—with minimal impact on the writing process itself. Results showed that both the self-reported good writers and poor writers engaged in the process of revising and that, as expected, surface-level changes far outnumbered the changes to content. These findings suggest that linguistic concerns and lack of explicit instruction on revision and computer strategies impede the reviewing and reworking of texts.
Parental counseling in trisomy 18: Novel insights in prenatal features and postnatal survival

Data on the outcome of trisomy T18 (T18) when diagnosed during pregnancy are lacking. We performed a retrospective study of pregnancies complicated by T18 diagnosed at our center and a literature search for publications on the topic, with pooled estimates of survival rates at different gestational and post‐natal ages. In our series, all the 60 patients included in the analysis had prenatally detected ultrasound anomalies, which were evidenced in the first trimester or at the second trimester scan in 73% of cases. In the continued pregnancies, ultrasound findings did not correlate with prenatal or post‐natal outcome. A meta‐analysis of available literature and our data showed that 48% [37–60%] of fetuses were live born, and among these 39% [11–72%] survived beyond 48 hr and 11% [3–21%] beyond 1 month. Our results confirm that prenatal ultrasound has high sensitivity in detection of T18 but is not predictive of the outcome of the continued pregnancies. The data on survival support that T18, even when antenatally diagnosed, cannot be considered as a uniformly lethal syndrome. © 2015 Wiley Periodicals, Inc.
Role of Heparanase on Hepatic Uptake of Intestinal Derived Lipoprotein and Fatty Streak Formation in Mice

Background Heparanase modulates the level of heparan sulfate proteoglycans (HSPGs) which have an important role in multiple cellular processes. Recent studies indicate that HSPGs have an important function in hepatic lipoprotein handling and processes involving removal of lipoprotein particles. Principal Findings To determine the effects of decreased HSPGs chain length on lipoprotein metabolism and atherosclerosis, transgenic mice over-expressing the human heparanase gene were studied. Hepatic lipid uptake in hpa-Tg mice were evaluated by giving transgenic mice oral fat loads and labeled retinol. Sections of aorta from mice over-expressing heparanase (hpa-Tg) and controls (C57/BL6) fed an atherogenic diet were examined for evidence of atherosclerosis. Heparanase over-expression results in reduced hepatic clearance of postprandial lipoproteins and higher levels of fasting and postprandial serum triglycerides. Heparanase over-expression also induces formation of fatty streaks in the aorta. The mean lesion cross-sectional area in heparanase over-expressing mice was almost 6 times higher when compared to control mice (23,984 µm2±5,922 vs. 4,189 µm2±1,130, p<0.001). Conclusions Over-expression of heparanase demonstrates the importance of HSPGs for the uptake of intestinal derived lipoproteins and its role in the formation of fatty streaks.
Effect of D‐glucose on nitric oxide release from glomerular endothelial cells

Altered glomerular production of nitric oxide (NO) may be involved in hyperfiltration in early diabetic nephropathy. However little is known as to the role of glomerular endothelial cells (GECs) in diabetic hyperfiltration and their ability to release NO in response to hyperglycemia.
AIS Electronic

Electronic Knowledge Repository (EKR) is one of the most commonly deployed knowledge management technologies, yet its success is hindered by employees’ underutilization and further complicated when implemented in the multinational context. To address these challenges, we propose a research model by conceptualizing employees’ knowledge seeking via EKR as a survival-centric behavior, identifying the technology acceptance model as the individual-level explanation for EKR use
P2Y2 Receptor Activation Regulates the Expression of Acetylcholinesterase and Acetylcholine Receptor Genes at Vertebrate Neuromuscular Junctions

At the vertebrate neuromuscular junction (nmj), ATP is known to be coreleased with acetylcholine from the synaptic vesicles. We have previously shown that the P2Y1 receptor is localized at the nmj. Here, we extend the findings to show that another nucleotide receptor, P2Y2, is also localized there and with P2Y1 jointly mediates trophic responses to ATP. The P2Y2 receptor mRNA in rat muscle increased during development and peaked in adulthood. The P2Y2 receptor protein was shown to become restricted to the nmjs during embryonic development, in chick and in rat. In both rat and chick myotubes, P2Y1 and P2Y2 are expressed, increasing with differentiation, but P2Y4 is absent. The P2Y2 agonist UTP stimulated there inositol trisphosphate production and phosphorylation of extracellular signal-regulated kinases, in a dose-dependent manner. These UTP-induced responses were insensitive to the P2Y1-specific antagonist MRS 2179 (2′-deoxy-N6-methyl adenosine 3′,5′-diphosphate diammonium salt). In differentiated myotubes, P2Y2 activation induced expression of acetylcholinesterase (AChE) protein (but not control α-tubulin). This was shown to arise from AChE promoter activation, mediated by activation of the transcription factor Elk-1. Two Elk-1-responsive elements, located in intron-1 of the AChE promoter, were found by mutation to act in this gene activation initiated at the P2Y2 receptor and also in that initiated at the P2Y1 receptor. Furthermore, the promoters of different acetylcholine receptor subunits were also stimulated by application of UTP to myotubes. These results indicate that ATP regulates postsynaptic gene expressions via a common pathway triggered by the activation of P2Y1 and P2Y2 receptors at the nmjs.
Warfarin in Systemic Sclerosis-associated and Idiopathic Pulmonary Arterial Hypertension. A Bayesian Approach to Evaluating Treatment for Uncommon Disease

Objective. Warfarin is recommended in systemic sclerosis-associated pulmonary arterial hypertension (SSc-PAH) and idiopathic PAH (IPAH) to improve survival. There is no evidence to support this in SSc-PAH and the evidence in IPAH is conflicting. We evaluated the ability of warfarin to improve survival using 2 large SSc-PAH and IPAH cohorts. Methods. The effect of warfarin on all-cause mortality was evaluated. Bayesian propensity scores (PS) were used to adjust for baseline differences between patients exposed and not exposed to warfarin, and to assemble a matched cohort. Bayesian Cox proportional hazards models were constructed using informative priors based on international PAH expert elicitation. Results. Review of 1138 charts identified 275 patients with SSc-PAH (n = 78; 28% treated with warfarin) and 155 patients with IPAH (n = 91; 59% treated with warfarin). Baseline differences in PAH severity and medications were resolved using PS matching. In the matched cohort of 98 patients with SSc-PAH (49 treated with warfarin), the posterior median hazard ratio (HR) was 1.06 [95% credible interval (CrI) 0.70, 1.63]. In the matched cohort of 66 patients with IPAH (33 treated with warfarin), the posterior median HR was 1.07 (95% CrI 0.57, 1.98). The probability that warfarin improves median survival by 6 months or more is 23.5% in SSc-PAH and 27.7% in IPAH. Conversely, there is a > 70% probability that warfarin provides no significant benefit or is harmful. Conclusion. There is a low probability that warfarin improves survival in SSc-PAH and IPAH. Given the availability of other PAH therapies with demonstrable benefits, there is little reason to use warfarin to improve survival for these patients.
Effect of delay to operation on outcomes in adults with acute appendicitis.

OBJECTIVE To examine the effect of delay from surgical admission to induction of anesthesia on outcomes after appendectomy for acute appendicitis in adults. DESIGN Retrospective cohort study with the principal exposure being time to operation. Regression models yielded probabilities of outcomes adjusted for patient and operative risk factors. SETTING Data were submitted to the American College of Surgeons National Surgical Quality Improvement Program database from January 1, 2005, through December 31, 2008. PATIENTS Patients with acute appendicitis who underwent an appendectomy. MAIN OUTCOME MEASURES Thirty-day overall morbidity and serious morbidity/mortality. RESULTS Of 32,782 patients, 24,647 (75.2%) underwent operations within 6 hours of surgical admission, 4934 (15.1%) underwent operations more than 6 through 12 hours, and 3201 (9.8%) underwent operations more than 12 hours after surgical admission. Differences in operative duration (51, 50, and 55 minutes, respectively; P < .001) were statistically significant but not clinically meaningful. The length of postoperative stay (2.2 days for the >12-hour group vs 1.8 days for the remaining groups; P < .001) was statistically significant but not clinically meaningful. No significant differences were found in adjusted overall morbidity (5.5%, 5.4%, and 6.1%, respectively; P = .33) or serious morbidity/mortality (3.0%, 3.6%, and 3.0%, respectively; P = .17). Duration from surgical admission to induction of anesthesia was not predictive in regression models for overall morbidity or serious morbidity/mortality. CONCLUSIONS In this retrospective study, delay of appendectomy for acute appendicitis in adults does not appear to adversely affect 30-day outcomes. This information can guide the use of potentially limited operative and professional resources allocated for emergency care.
Successful treatment of severe atopic dermatitis in a child and an adult with the T-cell modulator efalizumab.

An 8-year-old white boy presented in January 2003 with a long-standing history of atopic dermatitis, with onset between ages 1 and 2 years, in addition to insulindependent diabetes mellitus diagnosed at age 7 years. During the prior 6 years, he had undergone treatment with a variety of topical corticosteroids, 1% pimecrolimus cream, emollients, and courses of prednisone. Both diseases were poorly controlled. The patient was initially treated with 0.05% diflorasone diacetate ointment, petroleum jelly, and oral cetirizine. In February 2003, 4 mg/kg per day of oral cyclosporine was added to his regimen. This was subsequently increased to 5.6 mg/kg per day in late March and to 6.2 mg/kg per day in late April. In March and May 2003, he received 2 courses of oral cephalexin for flares.