Obesity is one of the dramatic health issues affecting developed and developing nations, and exercise is a well-established intervention strategy. While exercise-by-genotype interactions have been shown in humans, overall little is known. Using the natural negative geotaxis of Drosophila melanogaster, an important model organism for the study of genetic interactions, a novel exercise machine, the TreadWheel, can be used to shed light on this interaction. The mechanism for inducing exercise with the TreadWheel is inherently gentle, thus minimizing possible confounding effects of other stressors. Using this machine, we were able to assess large cohorts of adult flies from eight genetic lines for their response to exercise after one week of training. We measured their triglyceride, glycerol, protein, glycogen, glucose content, and body weight, as well as their climbing ability and feeding behavior in response to exercise. Exercised flies showed decreased stored triglycerides, glycogen, and body weight, and increased stored protein and climbing ability. In addition to demonstrating an overall effect of TreadWheel exercise on flies, we found significant interactions of exercise with genotype, sex, or genotype-by-sex effects for most of the measured phenotypes. We also observed interaction effects between exercise, genotype, and tissue (abdomen or thorax) for metabolite profiles, and those differences can be partially linked to innate differences in the flies' persistence in maintaining activity during exercise bouts. In addition, we assessed gene expression levels for a panel of 13 genes known to be associated with respiratory fitness and found that many responded to exercise. With this study, we have established the TreadWheel as a useful tool to study the effect of exercise in flies, shown significant genotype-specific and sex-specific impacts of exercise, and have laid the ground work for more extensive studies of how genetics, sex, environment, and aging interact with exercise to influence metabolic fitness in Drosophila.
Objectives: To characterize the impact of obesity on disease severity in patients with coronavirus disease 2019. Design: This was a retrospective cohort study designed to evaluate the association between body mass index and risk of severe disease in patients with coronavirus disease 2019. Data were abstracted from the electronic health record. The primary endpoint was a composite of intubation or death. Setting: Two hospitals in Massachusetts (one quaternary referral center and one affiliated community hospital). Patients: Consecutive patients hospitalized with confirmed coronavirus disease 2019 admitted between March 13, 2020, and April 3, 2020. Interventions: None. Measurements and Main Results: A total of 305 patients were included in this study. We stratified patients by body mass index category: < 25 kg/m 2 (54 patients, 18%), ≥ 25 kg/m 2 to < 30 kg/m 2 (124 patients, 41%), ≥ 30 kg/m 2 to < 35 kg/m 2 (58 patients, 19%), and ≥ 35 kg/m 2 (69 patients, 23%). In total, 128 patients (42%) had a primary endpoint (119 patients [39%] were intubated and nine died [3%] without intubation). Sixty-five patients (51%) with body mass index greater than or equal to 30 kg/m 2 were intubated or died. Adjusted Cox models demonstrated that body mass index greater than or equal to 30 kg/m 2 was associated with a 2.3-fold increased risk of intubation or death (95% CI, 1.2–4.3) compared with individuals with body mass index less than 25 kg/m 2 . Diabetes was also independently associated with risk of intubation or death (hazard ratio, 1.8; 95% CI, 1.2–2.7). Fifty-six out of 127 patients (44%) with body mass index greater than or equal to 30 kg/m 2 had diabetes, and the combination of both diabetes and body mass index greater than or equal to 30 kg/m 2 was associated with a 4.5-fold increased risk of intubation or death (95% CI, 2.0–10.2) compared with patients without diabetes and body mass index less than 25 kg/m 2 . Conclusions: Among consecutive patients hospitalized with coronavirus disease 2019, obesity was an independent risk factor for intubation or death.
and the loss of hypoxic pulmonary vasoconstriction play a pivotal role in the pathophysiology of coronavirus disease 2019 (COVID-19) respiratory distress. 1,2 Dihydropyridine calcium channel blockers (CCBs), frequently prescribed first-line antihypertensive agents, have the potential to disrupt hypoxic pulmonary vasoconstriction 3 and worsen V_/Q_ mismatch that leads to profound hypoxemia in patients with pulmonary disease. 4 We hypothesized that CCBs would be associated with worse respiratory failure in patients with COVID-19. MethodsAmong 444 consecutively hospitalized patients with confirmed COVID-19 (admitted between March 13 and April 7, 2020, at a quaternary referral center and an affiliated community hospital in Massachusetts), 245 patients had hypertension and were included in the analysis. Data elements were abstracted retrospectively from the electronic health record by trained study personnel who followed standardized protocol. The study was approved by the Partners Healthcare Institutional Review Board with a waiver of informed consent.Dihydropyridine CCB exposure status was based on confirmed home medication list at the time of hospital admission. The primary end point was a composite of intubation or death modeled as a time-to-event analysis. 5 For patients who died after intubation, the time of intubation was considered time of primary end point as with previous studies. 5 Cox models were used to evaluate the association between CCBs and the primary end point. Models were adjusted for age, sex, race/ethnicity, BMI, diabetes mellitus, coronary artery disease, heart failure, pulmonary hypertension, chronic kidney disease, asthma/COPD, peripheral arterial disease, Charlson Comorbidity Index, and the following medications: angiotensinconverting enzyme inhibitor/angiotensin receptor blocker, thiazide diuretic, loop diuretic, beta blocker, aspirin, and statin. To further account for potential confounding, an additional analysis was performed with propensity score matching. The propensity score for CCB use was estimated with a logistic regression model that incorporated the same covariates used in the multivariable Cox model.
Introduction: The role of cardiac biomarkers in patients after out-of-hospital cardiac arrest (OHCA) has been subject to recent research due to myocardial stress and injury associated with cardiac arrest. However, it remains unclear to what extent NT-proBNP can be used as a prognostic tool after OHCA. Hypothesis: Baseline NT-proBNP is an independent predictor of mortality in patients after OHCA. Methods: Multicenter retrospective observational cohort study including non-traumatic OHCA patients presenting from 2/1/2017 to 4/1/2019. Relationship between NT-proBNP quartiles and mortality was assessed through unadjusted and adjusted (age, gender, presenting rhythm) analyses with logistic regression. Results: Baseline NT-proBNP values were obtained for 283 patients on presentation after OHCA with median 965 pg/mL (IQR 157-3550). Levels did not differ by arrest etiology (cardiac vs noncardiac) or presenting rhythm. NT-proBNP levels correlated with age (r = 0.44, p<0.0001), but not with lactate, CPR duration, or intra-arrest epinephrine. Overall in-hospital mortality was 68% (196/283). Mortality increased in a stepwise fashion among patients in increasing quartiles of NT-proBNP level (Figure). Mortality rate in Q1: 59% ( 42/71), Q2: 61% (43/70), Q3: 75% (54/72), Q4: 77% (54/70). Odds Ratios (OR) vs Q1 as reference: Q2 OR 1.10 [95% CI 0.56-2.17] p= 0.48; Q3 OR 2.08 [95% CI 1.01-4.17] p= 0.045; Q4 OR 2.33 [95% CI 1.11-4.76] p=0. 023. After adjusting for age, gender, and shockable rhythm there remained a stepwise relationship between higher mortality with increasing NT-proBNP quartile (Q2 OR 1.30 [95% CI 0.61-2.78] p= 0.78; Q3 OR 2.33 [95% CI 1.05-5.26] p= 0.038; Q4 OR 2.50 [95% CI 1.05-5.88] p= 0.039). Conclusion: In this multicenter cohort of patients with shockable and nonshockable OHCA, increased levels of NT-proBNP were predictive of an increased risk of in-hospital mortality even after adjustment for age, gender, and presenting rhythm.
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