Increasing Atmospheric Humidity and CO\u3csub\u3e2\u3c/sub\u3e Concentration Alleviate Forest Mortality Risk

Climate-induced forest mortality is being increasingly observed throughout the globe. Alarmingly, it is expected to exacerbate under climate change due to shifting precipitation patterns and rising air temperature. However, the impact of concomitant changes in atmospheric humidity and CO2 concentration through their influence on stomatal kinetics remains a subject of debate and inquiry. By using a dynamic soil–plant–atmosphere model, mortality risks associated with hydraulic failure and stomatal closure for 13 temperate and tropical forest biomes across the globe are analyzed. The mortality risk is evaluated in response to both individual and combined changes in precipitation amounts and their seasonal distribution, mean air temperature, specific humidity, and atmospheric CO2 concentration. Model results show that the risk is predicted to significantly increase due to changes in precipitation and air temperature regime for the period 2050–2069. However, this increase may largely get alleviated by concurrent increases in atmospheric specific humidity and CO2 concentration. The increase in mortality risk is expected to be higher for needleleaf forests than for broadleaf forests, as a result of disparity in hydraulic traits. These findings will facilitate decisions about intervention and management of different forest types under changing climate

U.S. Emergency Room Department Encounters for Firearm Injuries, 2009-2014

Substantial opportunities exist to prevent recurrent firearm injury. Current models must expand beyond patients presenting at trauma centers with firearm assault injuries. Evidence-based prevention programs – including firearm counseling and safe storage interventions – should be adopted across a broad range of EDs and firearm injuries

Treatment with a neutralizing anti-murine interleukin-17 antibody after the onset of coxsackievirus b3-induced viral myocarditis reduces myocardium inflammation

<p>Abstract</p> <p>Background</p> <p>Recently, some studies indicate that interleukin (IL)-17, known as a T cell (Th17)-derived proinflammatory cytokine, is the major mediator of tissue inflammation in inflammatory and autoimmune diseases. Viral myocarditis (VMC) is a T cell-mediated autoimmune disease, but the role for IL-17 in VMC is not well defined.</p> <p>Results</p> <p>Using IL-17 monoclonal antibody (IL-17mAb)-treated VMC mice, we tested the pathogenic role of IL-17 in the development of VMC. VMC mice were treated with monoclonal rat anti-murine IL-17 antibody (anti-IL-17) or rat IgG_2Aisotype control or phosphate-buffered solution 3 days after Coxsackievirus B3 (CVB3) injection. Normal mice without any manipulation were taken as normal control. The survival rates of mice were monitored and heart pathology was examined histologically. IL-17, IL-6, and TNF-α mRNA of the myocardium were assessed by semi-quantitative RT-PCR. Systemic IL-17, IL-6, and TNF-α level were measured by enzyme-linked immunosorbent assay, and local myocardium IL-17 expression was analyzed using immunohistochemical staining. Flow cytometric analysis was used to evaluate the frequencies of Th17 subsets in CD4⁺T cells. Results showed that neutralization of IL-17 with anti-IL-17 can ameliorate clinical symptoms, defer disease course, decrease serum IL-17 level, without declining the IL-17, IL-6 and TNF-α mRNA transcript level and serum IL-6, TNF-α level. The differentiation and proliferation of the Th17 cells were unchanged.</p> <p>Conclusions</p> <p>Our data suggest that IL-17 is crucially involved in the pathogenesis of murine VMC, IL-17 inhibition might ameliorate the myocardium inflammation after the onset of VMC.</p

Restraint use and risky driving behaviors across drug types and drug and alcohol combinations for drivers involved in a fatal motor vehicle collision on U.S. roadways

Background While driving impaired is a well-recognized risk factor for motor vehicle (MV) crash, recent trends in recreational drug use and abuse may pose increased threats to occupant safety. This study examines mechanisms through which drug and/or alcohol combinations contribute to fatal MV crash. Methods The Fatality Analysis Reporting System (FARS) for 2008–2013 was used to examine drugs, alcohol, driver restraint use, driver violations/errors and other behaviors of drivers of passenger vehicles who were tested for both alcohol and drugs (n = 79,932). Statistical analysis was based on Chi-square tests and multivariable logistic regression. Associations of restraint use and other outcomes with alcohol and drug use were measured by estimated odds ratios (ORs) and 95 % confidence intervals (95 % CIs). Results More than half (54.8 %) of the study population were positive for drugs or alcohol at the time of crash. Approximately half of drivers were belted, but this varied from 67.1 % (unimpaired) to 33.0 % (drugs plus alcohol). Compared to the unimpaired, the odds of a driver being unbelted varied: alcohol and cannabis (OR 3.70, 95 % CI 3.44–3.97), alcohol only (3.50,3.36–3.65), stimulants (2.13,1.91–2.38), depressants (2.09,1.89–2.31), narcotics (1.84,1.67–2.02) and cannabis only (1.55,1.43–1.67). Compared to belted drivers, unbelted drivers were over 4 times more likely to die. Driving violations varied across drug/drug alcohol combinations. Speed-related violations were higher for drivers positive for stimulants, alcohol, cannabis, and cannabis plus alcohol, with a more than two fold increase for alcohol and cannabis (2.36, 2.05, 2.71). Conclusions Mechanisms through which drugs, alcohol and substance combinations produce increased risks to occupant safety include lowered restraint use and increases in risky driving behaviors, including speeding, lane, passing, turning and signal/sign violations

Restraint use and risky driving behaviors across drug types and drug and alcohol combinations for drivers involved in a fatal motor vehicle collision on U.S. roadways

Background While driving impaired is a well-recognized risk factor for motor vehicle (MV) crash, recent trends in recreational drug use and abuse may pose increased threats to occupant safety. This study examines mechanisms through which drug and/or alcohol combinations contribute to fatal MV crash. Methods The Fatality Analysis Reporting System (FARS) for 2008–2013 was used to examine drugs, alcohol, driver restraint use, driver violations/errors and other behaviors of drivers of passenger vehicles who were tested for both alcohol and drugs (n = 79,932). Statistical analysis was based on Chi-square tests and multivariable logistic regression. Associations of restraint use and other outcomes with alcohol and drug use were measured by estimated odds ratios (ORs) and 95 % confidence intervals (95 % CIs). Results More than half (54.8 %) of the study population were positive for drugs or alcohol at the time of crash. Approximately half of drivers were belted, but this varied from 67.1 % (unimpaired) to 33.0 % (drugs plus alcohol). Compared to the unimpaired, the odds of a driver being unbelted varied: alcohol and cannabis (OR 3.70, 95 % CI 3.44–3.97), alcohol only (3.50,3.36–3.65), stimulants (2.13,1.91–2.38), depressants (2.09,1.89–2.31), narcotics (1.84,1.67–2.02) and cannabis only (1.55,1.43–1.67). Compared to belted drivers, unbelted drivers were over 4 times more likely to die. Driving violations varied across drug/drug alcohol combinations. Speed-related violations were higher for drivers positive for stimulants, alcohol, cannabis, and cannabis plus alcohol, with a more than two fold increase for alcohol and cannabis (2.36, 2.05, 2.71). Conclusions Mechanisms through which drugs, alcohol and substance combinations produce increased risks to occupant safety include lowered restraint use and increases in risky driving behaviors, including speeding, lane, passing, turning and signal/sign violations

Distinct different expression of Th17 and Th9 cells in coxsackie virus B3-induced mice viral myocarditis

<p>Abstract</p> <p>Background</p> <p>Recently, a new subset of CD4⁺T helper(Th) cell that predominantly secret cytokine interleukin-9(IL-9) is identified, termed Th9 cell. It has been reported to participate in tissue inflammation and autoimmune responses, and induce disease which differed from Th17 cells. Th17 cells have been shown to play a critical role in viral myocarditis (VMC), but whether Th9 cells are involved in the pathogenesis of VMC remains unclear.</p> <p>Results</p> <p>BALB/c mice were intraperitoneally (i.p) injected with coxsackie virus B3(CVB3) for establishing VMC models. Control mice were treated with phosphate-buffered saline i.p. On day 0,7,14,21,28,35,42 after injection, myocardial histopathological changes were evaluated by hematoxylin-eosin staining. Splenic Th17 and Th9 cells subsets were analyzed by flow cytometry. And cardiac IL-17, IL-9 mRNA were measured by semi-quantitative reverse transcription-PCR and nested PCR, respectively. Results showed the levels of Th17 cells and IL-17 mRNA obviously increased in VMC mice on 7 day after infection, peaked on day 28, and highly persisted to at least day 42 (p < 0.05). While the frequencies of Th9 cells and IL-9 mRNA showed no significant difference between VMC and control group throughout the course of the experiment(p > 0.05).</p> <p>Conclusions</p> <p>It was differentiated Th17 but not Th9 cells significantly elevated in the development of CVB3-induced VMC. The microenvironment of VMC seemed to contribute to the differentiation and proliferation of Th17 rather than Th9 cells. Our preliminary data implied Th9 cells could not protect against VMC nor promote the disease.</p

National Variation in Opioid Prescribing and Risk of Prolonged Use for Opioid-Naive Patients Treated in the Emergency Department for Ankle Sprains

Between 2011 and 2015, nearly one in four patients with ankle sprains were prescribed opioids in the emergency department. The overall prescribing rate declined during the study period, but varied significantly by state, ranging from 2.8% in North Dakota to 40% in Arkansas. Patients prescribed the largest amounts of opioid were nearly five times more likely to transition to continued use as those prescribed lesser amounts

HIV-1 Transactivator Protein Induces ZO-1 and Neprilysin Dysfunction in Brain Endothelial Cells via the Ras Signaling Pathway

Amyloid beta (Aβ) deposition is increased in human immunodeficiency virus-1- (HIV-1-) infected brain, but the mechanisms are not fully understood. The aim of the present study was to evaluate the role of Ras signaling in HIV-1 transactivator protein- (Tat-) induced Aβ accumulation in human cerebral microvascular endothelial cells (HBEC-5i). Cell viability assay showed that 1 μg/mL Tat and 20 μmol/L of the Ras inhibitor farnesylthiosalicylic acid (FTS) had no significant effect on HBEC-5i cell viability after 24 h exposure. Exposure to Tat decreased protein and mRNA levels of zonula occludens- (ZO-) 1 and Aβ-degrading enzyme neprilysin (NEP) in HBEC-5i cells as determined by western blotting and quantitative real-time polymerase chain reaction. Exposure to Tat also increased transendothelial transfer of Aβ and intracellular reactive oxygen species (ROS) levels; however, these effects were attenuated by FTS. Collectively, these results suggest that the Ras signaling pathway is involved in HIV-1 Tat-induced changes in ZO-1 and NEP, as well as Aβ deposition in HBEC-5i cells. FTS partially protects blood-brain barrier (BBB) integrity and inhibits Aβ accumulation

Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study

Funder: European Society of Intensive Care Medicine; doi: http://dx.doi.org/10.13039/501100013347Funder: Flemish Society for Critical Care NursesAbstract: Purpose: Intensive care unit (ICU) patients are particularly susceptible to developing pressure injuries. Epidemiologic data is however unavailable. We aimed to provide an international picture of the extent of pressure injuries and factors associated with ICU-acquired pressure injuries in adult ICU patients. Methods: International 1-day point-prevalence study; follow-up for outcome assessment until hospital discharge (maximum 12 weeks). Factors associated with ICU-acquired pressure injury and hospital mortality were assessed by generalised linear mixed-effects regression analysis. Results: Data from 13,254 patients in 1117 ICUs (90 countries) revealed 6747 pressure injuries; 3997 (59.2%) were ICU-acquired. Overall prevalence was 26.6% (95% confidence interval [CI] 25.9–27.3). ICU-acquired prevalence was 16.2% (95% CI 15.6–16.8). Sacrum (37%) and heels (19.5%) were most affected. Factors independently associated with ICU-acquired pressure injuries were older age, male sex, being underweight, emergency surgery, higher Simplified Acute Physiology Score II, Braden score 3 days, comorbidities (chronic obstructive pulmonary disease, immunodeficiency), organ support (renal replacement, mechanical ventilation on ICU admission), and being in a low or lower-middle income-economy. Gradually increasing associations with mortality were identified for increasing severity of pressure injury: stage I (odds ratio [OR] 1.5; 95% CI 1.2–1.8), stage II (OR 1.6; 95% CI 1.4–1.9), and stage III or worse (OR 2.8; 95% CI 2.3–3.3). Conclusion: Pressure injuries are common in adult ICU patients. ICU-acquired pressure injuries are associated with mainly intrinsic factors and mortality. Optimal care standards, increased awareness, appropriate resource allocation, and further research into optimal prevention are pivotal to tackle this important patient safety threat