Adamsswanson4315

There were no significant differences in the traits between OVS and OSA subjects, although OVS subjects potentially tolerated a lower ventilation before arousal (i.e., harder to wake; p = .06). Worsened lung function was significantly associated with worsened upper airway response and more unstable breathing (p  less then  .05 for all). Consistent differences in key OSA traits were not observed between OVS and OSA alone. However, worse lung function does appear to exert an influence on several OSA traits. These findings indicate that a diagnosis of OVS should not generally influence the approach to OSA, but that lung function might be considered if utilizing OSA trait-specific treatment. © 2020 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.OBJECTIVE This study aimed to provide updated lifetime prevalence estimates of eating disorders, specifically bulimia nervosa (BN) and binge eating disorder (BED) and investigate changes over time in lifetime prevalence by age. METHOD Two thousand nine hundred seventy-seven participants from South Australia were interviewed in the Health Omnibus Survey. DSM-5 criteria were used for current and broad (in accord with the International Statistical Classification of Diseases and Related Health Problems-11 [ICD-11]) criteria for lifetime prevalence of BED. RESULTS This study found that the lifetime prevalence of BN was 1.21% (95% CI [0.87, 1.67]) and 2.59% (95% CI [2.07, 3.22]) for males and females, respectively, and that lifetime prevalence for BED-broad was 0.74% (95% CI [0.49, 1.11]) and 1.85% (95% CI [1.42, 2.40]) for males and females, respectively, which is higher than reported in previous research. Current prevalence (past 3 months) of BN was 0.40% (95% CI [0.23, 0.70]) and 0.81% (95% CI [0.54, 1.20]) for males and females, respectively, and current prevalence for BED was found to be 0.03 (95% CI [0.01, 0.04]) and 0.20% (95% CI [0.09, 0.44]) for males and females, respectively. CONCLUSIONS The current study confirmed the moderate community prevalence of BN and BED. BED was found to be less prevalent than BN in the present study, and a significant lifetime prevalence by age effect was found for both. Lifetime prevalence by age indicated that past increases in prevalence may be waning in this century and that overall BN and BED are not increasing in Australia. © 2020 John Wiley & Sons, Ltd and Eating Disorders Association.In the present study, we hypothesized that habitual cigarette smoking attenuates endothelial function in the cerebral circulation as well as that of the peripheral circulation in young adults. To test this hypothesis, we measured cerebrovascular and peripheral flow-mediated dilation (FMD) in young smokers and nonsmokers in the present study. Ten healthy nonsmokers and 10 smokers participated in the study. We measured blood velocity and diameter in the brachial artery and internal carotid artery (ICA) using Doppler ultrasound. We identified shear-mediated dilation in the brachial artery and ICA by the percentage change in peak diameter during hyperemia stimulation (reactive hyperemia and hypercapnia). We measured the baseline diameter and the shear rate area under the curve from the onset of hyperemia to peak dilation in the brachial artery and ICA, finding the measurements of the smokers and those of the nonsmokers did not differ (p > .05). In contrast to brachial FMD (5.07 ± 1.79% vs. 7.92 ± 3.01%; smokers vs. nonsmokers, p = .019), FMD in the ICA was not attenuated in the smokers compared with that of the nonsmokers (5.46 ± 2.32% vs. 4.57 ± 2.70%; p = .442). These findings indicate that in young healthy smokers, cerebral endothelial function was preserved, and the response of cerebral endothelial function to smoking was different from that of peripheral vasculature. © 2020 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.RATIONALE Orientin and isoorientin are C-glycosidic flavonoids, considered as markers of some plant species as Passiflora edulis var. flavicarpa Degener and reported in the literature to have pharmacological properties. In order to evaluate and characterize the in vitro metabolism of flavonoids, phase I biotransformation reactions were simulated using Salen complexes. METHODS These flavonoids were oxidized separately in biomimetic reaction in different proportions, using one oxidant, m-chloroperbenzoic acid (m-CPBA) or iodozylbenzen (PhIO), and one catalyst, the Jacobsen catalyst or [Mn(3-MeOSalen)Cl]. The [Mn(3-MeOSalen)Cl] was synthesized and characterized by spectrometric techniques. The oxidation potentials of the catalysts were compared. All reactions were monitored and analyzed by UPLC-DAD and HPLC/MS/MS. RESULTS The analysis by UPLC-DAD and HPLC/MS/MS showed that isoorientin produces more products than orientin and that the [Mn(3-MeOSalen)CI] produces more products than the Jacobsen catalyst. In addition, the [Mn(3-MeOSalen)CI] catalyst, which has a higher oxidation potential, formed products with an addition of one or two atoms of oxygen, while the Jacobsen catalyst formed compounds with only one added oxygen atom. The products with the addition of one oxygen were mainly epoxides, while those with two added oxygens formed an epoxide in the C-ring and incorporated the other oxygen into the glycosidic moiety. CONCLUSIONS The formation of epoxides is common in biomimetic reactions and they may represent a safety risk in medicinal products due to their high reactivity. This study may serve as a basis for subsequent pharmacological and toxicological studies that investigate the presence of these compounds as phase I metabolites, and ensure the safe use of plant products containing orientin as a chemical marker. This article is protected by copyright. Gossypol All rights reserved.The immunologic responses that occur early in the acute respiratory distress syndrome (ARDS) elicit immune-mediated damage. The mechanisms underlying the resolution of ARDS, particularly the role of signaling molecules in regulating immune cell kinetics, remain important questions. Th1-mediated responses can contribute to the pathogenesis of acute lung injury (ALI). Interferon-gamma (IFN-γ) orchestrates early inflammatory events, enhancing immune-mediated damage. The current study investigated IFN-γ during resolution in several experimental models of ALI. The absence of IFN-γ resulted in altered kinetics of lymphocyte and macrophage responses, suggesting that IFN-γ present in this microenvironment is influential in ALI resolution. Genetic deficiency of IFN-γ or administering neutralizing IFN-γ antibodies accelerated the pace of resolution. Neutralizing IFN-γ decreased the numbers of interstitial and inflammatory macrophages and increased alveolar macrophage numbers during resolution. Our results underline the complexity of lung injury resolution and provide insight into the effects through which altered IFN-γ concentrations affect immune cell kinetics and the rate of resolution. These findings suggest that therapies that spatially or temporally control IFN-γ signaling may promote ALI resolution. Identifying and elucidating the mechanisms critical to ALI resolution will allow the development of therapeutic approaches to minimize collateral tissue damage without adversely altering the response to injury. © 2020 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.Natural polyphenols are being tested both in preclinical and clinical settings for the treatment of different neurological disorders. The article describes the outcome of three polyphenols, resveratrol, epigallocatechin gallate, and quercetin, in preclinical animal models of epilepsy (both acute and chronic) and epileptogenesis. In theory, the antioxidant and neuroprotective properties of these natural polyphenols might be valuable in the management of acute seizures and the prevention of epileptogenesis. It is fascinating to observe that these polyphenols have a capacity to alter various signaling processes involved in the pathogenesis of epilepsy. The antiepileptic or antiseizure potential with these molecules delivers a mixed outcome. Some studies have demonstrated the usefulness of these molecules in preclinical models of epilepsy; however, contrary to the findings also exist. These molecules have poor bioavailability that may remain as the limiting factor in their clinical effects. The use of nanotechnology and other techniques have been tested to enhance bioavailability and brain penetration. There are no randomized double-blinded clinical studies establishing their antiepileptic effects in humans. It is concluded that more preclinical mechanism-based studies are needed to deliver a more certain picture regarding the use of natural polyphenols in the treatment of epilepsy. © 2020 John Wiley & Sons, Ltd.Phase II clinical trials designed for evaluating a drug's treatment effect can be either single-arm or double-arm. A single-arm design tests the null hypothesis that the response rate of a new drug is lower than a fixed threshold, whereas a double-arm scheme takes a more objective comparison of the response rate between the new treatment and the standard of care through randomization. Although the randomized design is the gold standard for efficacy assessment, various situations may arise where a single-arm pilot study prior to a randomized trial is necessary. To combine the single- and double-arm phases and pool the information together for better decision making, we propose a Single-To-double ARm Transition design (START) with switching hypotheses tests, where the first stage compares the new drug's response rate with a minimum required level and imposes a continuation criterion, and the second stage utilizes randomization to determine the treatment's superiority. We develop a software package in R to calibrate the frequentist error rates and perform simulation studies to assess the trial characteristics. Finally, a metastatic pancreatic cancer trial is used for illustrating the decision rules under the proposed START design. © 2020 John Wiley & Sons Ltd.The liver is the primary metabolic organ involved in the endogenous production of glucose through glycogenolysis and gluconeogenesis. Hepatic glucose production (HGP) is increased via neural-hormonal mechanisms such as increases in catecholamines. To date, the effects of prior exercise training on the hepatic response to epinephrine have not been fully elucidated. To examine the role of epinephrine signaling on indices of HGP in trained mice, male C57BL/6 mice were either subjected to 12 days of voluntary wheel running or remained sedentary. Epinephrine, or vehicle control, was injected intraperitoneally on day 12 prior to sacrifice with blood glucose being measured 15 min postinjection. Epinephrine caused a larger glucose response in sedentary mice and this was paralleled by a greater reduction in liver glycogen in sedentary compared to trained mice. There was a main effect of epinephrine to increase the phosphorylation of protein kinase-A (p-PKA) substrates in the liver, which was driven by increases in the sedentary, but not trained, mice.