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1.
Am J Cardiol ; 179: 102-109, 2022 09 15.
Artigo em Inglês | MEDLINE | ID: mdl-35843735

RESUMO

We aimed to determine absolute and relative risks of either symptomatic or asymptomatic SARS-CoV-2 infection for late cardiovascular (CV) events and all-cause mortality. We conducted a retrospective double cohort study of patients with either symptomatic or asymptomatic SARS-CoV-2 infection (COVID-19+ cohort) and its documented absence (COVID-19- cohort). The study investigators drew a simple random sample of records from all patients under the Oregon Health & Science University Healthcare (n = 65,585), with available COVID-19 test results, performed March 1, 2020 to September 13, 2020. Exclusion criteria were age <18 years and no established Oregon Health & Science University care. The primary outcome was a composite of CV morbidity and mortality. All-cause mortality was the secondary outcome. The study population included 1,355 patients (mean age 48.7 ± 20.5 years; 770 women [57%], 977 White non-Hispanic [72%]; 1,072 ensured [79%]; 563 with CV disease history [42%]). During a median 6 months at risk, the primary composite outcome was observed in 38 of 319 patients who were COVID-19+ (12%) and 65 of 1,036 patients who were COVID-19- (6%). In the Cox regression, adjusted for demographics, health insurance, and reason for COVID-19 testing, SARS-CoV-2 infection was associated with the risk for primary composite outcome (hazard ratio 1.71, 95% confidence interval 1.06 to 2.78, p = 0.029). Inverse probability-weighted estimation, conditioned for 31 covariates, showed that for every patient who was COVID-19+, the average time to all-cause death was 65.5 days less than when all these patients were COVID-19-: average treatment effect on the treated -65.5 (95% confidence interval -125.4 to -5.61) days, p = 0.032. In conclusion, either symptomatic or asymptomatic SARS-CoV-2 infection is associated with an increased risk for late CV outcomes and has a causal effect on all-cause mortality in a late post-COVID-19 period.


Assuntos
COVID-19 , Doenças Cardiovasculares , Adolescente , Adulto , Idoso , Teste para COVID-19 , Estudos de Coortes , Feminino , Humanos , Pessoa de Meia-Idade , Estudos Retrospectivos , SARS-CoV-2
3.
J Asthma ; 58(3): 293-298, 2021 03.
Artigo em Inglês | MEDLINE | ID: mdl-31858858

RESUMO

OBJECTIVE: To evaluate the impact of crop burning on the prevalence of asthma and COPD emergency department (ED) treatments in a rural Arkansas county. METHODS: Administrative datasets listing ED treatments for asthma and COPD obtained from the Arkansas Hospital Discharge Dataset System for the calendar years 2014-2016 were used in this semi-ecological study. Primary diagnosis codes (ICD-9: 490-496 and ICD-10: J40-J47) were used to identify patients who were diagnosed with asthma and COPD. Patients with a reported county of residence in Craighead County were determined as case county residents and those in Sebastian County were control county residents. Month of visit was used to determine seasonal variation. PM 2.5 air quality data were obtained from the EPA AQS Data Mart. RESULTS: Between 2014 through 2016, there were a combined total of 2,536 ED treatments due to asthma and 8,530 due to COPD in Craighead and Sebastian counties. The odds of being treated in the ED during the fall months for asthma and COPD are associated with a 20.9% increase and 16.9% increase respectively in Craighead County as compared to Sebastian Country after adjusting for potential confounders (p = 0.04, p = 0.003). PM 2.5 concentrations were higher in Craighead County than Sebastian County during the fall season (p = 0.005). CONCLUSION: Fall ED treatments for asthma and COPD were higher in Craighead County, Arkansas compared to Sebastian County, Arkansas for the years 2014-2016. PM 2.5 levels were also higher in Craighead County in the fall during these years. These differences may be attributable to crop burning.​.


Assuntos
Agricultura , Asma/epidemiologia , Serviço Hospitalar de Emergência/estatística & dados numéricos , Incêndios/estatística & dados numéricos , Doença Pulmonar Obstrutiva Crônica/epidemiologia , Adolescente , Adulto , Idoso , Poluição do Ar , Arkansas/epidemiologia , Criança , Pré-Escolar , Feminino , Humanos , Lactente , Masculino , Pessoa de Meia-Idade , Prevalência , Grupos Raciais , População Rural , Estações do Ano , Adulto Jovem
4.
South Med J ; 112(4): 210-214, 2019 04.
Artigo em Inglês | MEDLINE | ID: mdl-30943538

RESUMO

With the increase in participation in endurance events in the general population, patient concern may arise as to whether endurance exercise is safe. Acute but not chronic increases in blood urea nitrogen, creatinine, and urine albumin occur in endurance exercise. Iron-deficiency anemia may be observed in female athletes. Upper respiratory illness is increased in elite athletes but decreased in intense recreational athletes. No convincing evidence of developing osteoarthritis exists. Common gastrointestinal symptoms occur and isolated reports of gastrointestinal bleeding exist. Nevi are increased and the minimal erythematous dose is decreased. Exercising in the presence of air pollution has negative pulmonary effects, but overall, benefit exists. Numerous reports pertain to the cardiovascular system. The risk of cardiac arrest increases during exercise, troponin is elevated after exercise, and a predisposition for atrial fibrillation exists. Ventricular myocardial scar formation as assessed by gadolinium enhancement on magnetic resonance imaging is inconsistently observed, and increased coronary plaque of a more stable variety is reported. Left ventricular compliance is chronically increased and no decrease in longevity is found. Although some concerns exist, endurance exercise is safe.


Assuntos
Treino Aeróbico/estatística & dados numéricos , Exercício Físico/fisiologia , Poluição do Ar , Albuminúria/epidemiologia , Anemia Ferropriva/epidemiologia , Fibrilação Atrial/epidemiologia , Nitrogênio da Ureia Sanguínea , Cicatriz/diagnóstico por imagem , Cicatriz/epidemiologia , Complacência (Medida de Distensibilidade) , Doença da Artéria Coronariana/epidemiologia , Creatinina/sangue , Exposição Ambiental/estatística & dados numéricos , Coração/diagnóstico por imagem , Hemoglobinas/metabolismo , Humanos , Imageamento por Ressonância Magnética , Nevo/epidemiologia , Osteoartrite/epidemiologia , Placa Aterosclerótica/epidemiologia , Infecções Respiratórias/epidemiologia , Troponina/sangue
6.
J Bone Miner Res ; 32(3): 560-574, 2017 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-27714847

RESUMO

Old age and sex steroid deficiency are the two most critical factors for the development of osteoporosis. It remains unknown, however, whether the molecular culprits of the two conditions are similar or distinct. We show herein that at 19.5 months of age-a time by which the age-dependent decline of cortical and cancellous bone mass and cortical porosity were fully manifested in C57BL/6J mice-these animals remained functionally estrogen sufficient. Transgenic mice with conditional expression of mitochondria-targeted catalase-a potent H2 O2 inactivating enzyme-in cells of the myeloid lineage (mitoCAT;LysM-Cre mice) were protected from the loss of cortical, but not cancellous, bone caused by gonadectomy in either sex. Consistent with these findings, in vitro studies with ERα-deficient Prx1+ cells and gonadectomized young adult mice showed that in both sexes decreased ERα signaling in Prx1+ cells leads to an increase in SDF1, a.k.a. CXCL12, an osteoclastogenic cytokine whose effects were abrogated in macrophages from mitoCAT;LysM-Cre mice. In contrast to sex steroid deficiency, the adverse effects of aging on either cortical or cancellous bone were unaffected in mitoCAT;LysM-Cre mice. On the other hand, attenuation of H2 O2 generation in cells of the mesenchymal lineage targeted by Prx1-Cre partially prevented the loss of cortical bone caused by old age. Our results suggest the effects of sex steroid deficiency and aging on the murine skeleton are independent and result from distinct mechanisms. In the former, the prevailing mechanism of the cortical bone loss in both sexes is increased osteoclastogenesis caused by estrogen deficiency; this is likely driven, at least in part, by mesenchymal/stromal cell-derived SDF1. Decreased osteoblastogenesis, owing in part to increased H2 O2, combined with increased osteoclastogenesis caused by aging mechanisms independent of estrogen deficiency, are the prevailing mechanisms of the loss of cortical bone with old age. © 2016 American Society for Bone and Mineral Research.


Assuntos
Envelhecimento/fisiologia , Osso e Ossos/fisiologia , Hormônios Esteroides Gonadais/deficiência , Animais , Fenômenos Biomecânicos , Reabsorção Óssea/patologia , Reabsorção Óssea/fisiopatologia , Calcificação Fisiológica , Osso Esponjoso/fisiologia , Contagem de Células , Linhagem da Célula , Quimiocina CXCL12/metabolismo , Osso Cortical/fisiologia , Receptor alfa de Estrogênio/metabolismo , Estrogênios/metabolismo , Feminino , Hormônios Esteroides Gonadais/metabolismo , Peróxido de Hidrogênio/metabolismo , Masculino , Células-Tronco Mesenquimais/metabolismo , Camundongos Endogâmicos C57BL , Células Mieloides/metabolismo , Osteoclastos/metabolismo , Ovariectomia , Porosidade
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