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l interventions alone, and these interventions may be capable of supporting long-term behavior change. OBJECTIVE To identify the effect of acute and multiple concussions on gait initiation performance. DESIGN Cohort Study SETTING University Research Center PARTICIPANTS A population based sample of 45 participants divided into three groups No Prior Concussion, >3 Prior Concussions, and Acute Concussion. The Acute Concussion participants were assessed within 24 hours of their concussion. Participants were matched based on 1) sport, 2) position, and 3) anthropometric measures. INTERVENTIONS Participants were tested on a single occasion and performed five trials of gait initiation on four force plates. The No Prior Concussion and >3 Prior Concussion groups were tested out of their primary athletic season. MAIN OUTCOME MEASURES The dependent variables were the posterior and lateral displacement and velocity of the center of pressure (COP) during the anticipatory postural adjustment phase and initial step kinematics (step length and step velocity). Comparisons between groups used a One-Way ANOVA with Tukey Post-Hoc n is warranted. Chronic airway inflammatory diseases are characterized by persistent proinflammatory responses in the respiratory tract. Although, several treatment strategies are currently available, lifelong therapy is necessary for most of these diseases. In recent years, phytophenols, namely, flavonoids, derived from fruits and vegetables have been gaining tremendous interest and have been extensively studied due to their low toxicological profile. Naringenin is a bioflavonoid abundantly found in citrus fruits. This substance has shown notable therapeutic potential in various diseases due to its promising diverse biological activities. In this review, we have attempted to review the published studies from the available literature, discussing the molecular level mechanisms of naringenin in different experimental models of airway inflammatory diseases including asthma, chronic obstructive pulmonary disease (COPD), lung cancer, pulmonary fibrosis and cystic fibrosis. NVPBSK805 Current evidences have proposed that the anti-inflammatory properties of naringenin play a major role in ameliorating inflammatory disease states. In addition, naringenin also possesses several other biological properties. Despite the proposed mechanisms suggesting remarkable therapeutic benefits, the clinical use of naringenin is, however, hampered by its low solubility and bioavailability. Furthermore, this review also discusses on the studies that utilise nanocarriers as a drug delivery system to address the issue of poor solubility. Increased O-Linked β-N-acetylglucosamine (O-GlcNAc) is observed in several pathologies, and unbalanced O-GlcNAcylation levels favor endothelial dysfunction. Whether augmented O-GlcNAc impacts the uterine artery (UA) function and how it affects the UA during pregnancy remains to be elucidated. We hypothesized that glucosamine treatment increases O-GlcNAc, leading to uterine artery dysfunction and this effect is prevented by pregnancy. Pregnant (P) and non-pregnant (NP) Wistar rats were treated with glucosamine (300 mg/kg; i.p.) for 21 days. Concentration response-curves (CRC) to acetylcholine (in the presence or absence of L-NAME) and sodium nitroprusside were performed in UAs. In NP rats, glucosamine treatment increased O-GlcNAc expression in UAs accompanied by decreased endothelium-dependent relaxation, which was abolished by L-NAME. Endothelial nitric oxide synthase (eNOS) activity and total Akt expression were decreased by glucosamine-treatment in NP rats. Further, NP rats treated with glucosamine displayed increased glycogen synthase kinase 3 beta (GSK3β) activation and O-GlcNAc-transferase (OGT) expression in the UA. P rats treated with glucosamine displayed decreased O-GlcNAc in UAs and it was accompanied by improved relaxation to acetylcholine, whereas eNOS and GSK3β activity and total Akt and OGT expression were unchanged. Sodium nitroprusside-induced relaxation was not changed in all groups, indicating that glucosamine treatment led to endothelial dysfunction in NP rats. The underlying mechanism is, at least in part, dependent on Akt/GSK3β/OGT modulation. We speculate that during pregnancy, hormonal alterations play a protective role in preventing O-GlcNAcylation-induced endothelial dysfunction in the UAs. This study aimed to investigate the effects of paeonol (Pae) on lipid metabolism in palmitic acid (PA)-induced injury of HepG2, and to evaluate the protective mechanisms. Lipid metabolism dysfunction of HepG2 cells was produced by administration of palmitic acid (PA). The cells were pretreated with different concentrations of Pae. MTT method was used to detect the cell survival; lipid metabolism was evaluated based on total cholesterol (TC), triglycerides (TG); Western blotting was used to detect the expression of Sirtuin 1 (SIRT1), autophagy related 14 (ATG14), microtubule-associated protein 1A/1B-light chain 3 (LC3) and p62 proteins; immunoprecipitation was used to detect the expression of acetylated FoxO1. After treatment for 24 h, the inhibitory concentration 50 (IC50) of PA in HepG2 cells was about 566.8 μM. Pae at the concentration range from 7.5 to 30 μM did not affect cell viability. Thus, 500 μM PA was used to model metabolism dysfunction and Pae at the concentration range was selected to investigate the protective effect. Compared with the normal control group, the cell survival rate decreased, the number of lipid droplets, and TC and TG levels increased in the model group. Compared with model group, the cell survival rate of Pae (7.5, 15, 30 μM) group increased, the number of lipid droplets and content of TC and TG decreased, the ratio of LC3-II/I increased and p62 expression decreased with pretreatment of Pae. Additionally, Pae pretreatment promoted SIRT1 and ATG14 expression, but reduced acetylated FoxO1 levels in PA-treated cells. Most importantly, autophagy inhibitor, as well as SIRT1 inhibitor blocked the effects of Pae on PA-induced cell injury and metabolism dysfunction, respectively. Pae prevents lipid metabolism dysfunction in PA-induced HepG2 injury by promoting SIRT1-FoxO1-ATG14-dependent autophagy. Novel coronavirus disease 2019 (COVID-19) emerged in late December 2019 in Wuhan, China. Since then, COVID-19 has become a pandemic affecting more than 1.5 million people worldwide. Patients with COVID-19 have a wide spectrum of manifestations, one being cytokine release syndrome (CRS) and its fatal correlate, secondary hemophagocytic lymphohistiocytosis (sHLH). Anti-cytokine therapy such as tocilizumab, an IL-6 receptor antagonist, is a potential treatment for COVID-19; however, data regarding the efficacy of this anti-IL-6 therapy are currently lacking. We report two cases of patients who received a diagnosis of COVID-19 complicated by CRS and were treated with tocilizumab. Both patients progressed to sHLH despite treatment with tocilizumab, and one developed viral myocarditis, challenging the safety and clinical usefulness of tocilizumab in the treatment of COVID-19-induced CRS. These cases highlight the need for clinical trials to determine optimal patient selection and timing for the use of tocilizumab during this disease process. Published by Elsevier Inc.BACKGROUND Peak inspiratory flow (PIF) has been proposed as a measure to assess a patient's ability to use dry powder inhalers (DPI). However, robust quality criteria to determine a repeatability limit for measuring PIF are lacking. RESEARCH QUESTIONS What are the repeatability limits for measuring PIF? What is the relationship between PIF measured using the In-Check™ DIAL device at Diskus® (PIFD) and HandiHaler® (PIFHH) resistances? STUDY DESIGN AND METHODS Data from a randomized, controlled, phase 3 trial (study 0149) was used to define repeatability limits for PIF. Additionally, a model to characterize the relationship between PIF measured using the In-Check DIAL device at PIFD and PIFHH was defined using data from two randomized, controlled, phase 3 trials (studies 0128 and 0149). RESULTS In study 0128, the mean values (standard deviation [SD]) for PIF at zero resistance and PIFHH were 84.6 (33.4) and 57.3 (26.1) L/min, respectively. In study 0149, the mean values (SD) for PIFD and PIFHH were 42.4 (11.2) and 29.0 (8.3) L/min, respectively. At the mean level, the mean difference between measurement attempts for PIFD and PIFHH was small, less then 5 L/min and less then 3 L/min, respectively. The repeatability limit was determined as 10 and 5 L/min for PIFD and PIFHH, respectively. Modeling the relationship between PIFD and PIFHH, after controlling for significant covariates demonstrated that a PIFD value of 60 L/min was approximately equivalent to PIFHH of 40 L/min. INTERPRETATIONS This analysis demonstrated that the two highest values of PIF using the In-Check DIAL device among three inspiratory efforts met the repeatability limit. Altogether, these data provide guidance for measuring PIF against the simulated resistance of a specific DPI in clinical practice and research studies. BACKGROUND Obstructive sleep apnea (OSA) conveys worse clinical outcomes in coronary artery disease patients. The STOP-BANG score is a simple tool that evaluates the risk of OSA and can be added to the large number of clinical variables and scores obtained during the management of myocardial infarction (MI) patients. Currently, machine learning (ML) is able to select and integrate numerous variables to optimize prediction tasks. RESEARCH QUESTION Can the integration of STOP-BANG score with clinical data and scores through ML better identify patients who suffered an in-hospital cardiovascular event after acute MI? STUDY DESIGN AND METHODS This is a prospective observational cohort study of 124 acute MI patients in which the STOP-BANG score classified 34 low-(27.4%), 30 intermediate-(24.2%), and 60 high-(48.4%) OSA-risk patients who were followed during hospitalization. ML implemented feature selection and integration across 47 variables (including STOP-BANG score, Killip-class, GRACE score and LVEF) to identift. BACKGROUND Pulmonary gas exchange efficiency, determined by the alveolar-to-arterial PO2 difference (A-aDO2), progressively worsens during exercise at sea-level; this response is further elevated during exercise in hypoxia. Traditionally, pulmonary gas exchange efficiency is assessed through measurements of ventilation and end-tidal gases paired with direct arterial blood gas (ABG) sampling. Since these measures have a number of caveats, particularly invasive blood sampling, the development of new approaches for the non-invasive assessment of pulmonary gas exchange is needed. RESEARCH QUESTION Is a non-invasive method of assessing pulmonary gas exchange valid during rest and exercise in acute hypoxia? STUDY DESIGN and Methods Twenty-five healthy participants (10 female) completed a staged maximal exercise test on a cycle ergometer in a hypoxic chamber (FIO2=0.11). Simultaneous ABGs via a radial arterial catheter and non-invasive gas-exchange measurements (AGM100) were obtained in two-minute intervals. Non-invbe used clinically as a tool during normoxic exercise in patients with pre-existing impairments in gas exchange efficiency.