Explore the vast range of titles available.

BackgroundBariatric surgery (BS) is an increasingly common treatment for morbid obesity that has the potential to effect bone and mineral metabolism. The effect of prior BS on spine surgery outcomes has not been well established. The aim of this study was to assess differences in complication rates following spinal surgery for patients with and without a history of BS.MethodsRetrospective analysis of the prospectively collected New York State Inpatient Database (NYSID) years 2004–2013. BS patients and morbidly obese patients (non-BS) were divided into cervical and thoracolumbar surgical groups and propensity score matched for age, gender, and invasiveness and complications compared.ResultsOne thousand nine hundred thirty-nine spine surgery patients with a history of BS were compared to 1625 non-BS spine surgery patients. The average time from bariatric surgery to spine surgery is 2.95 years. After propensity score matching, 740 BS patients were compared to 740 non-BS patients undergoing thoracolumbar surgery, with similar comorbidity rates. The overall complication rate for BS thoracolumbar patients was lower than non-BS (45.8% vs 58.1%, P < 0.001), with lower rates of device-related (6.1% vs 23.2%, P < 0.001), DVT (1.2% vs 2.7%, P = 0.039), and hematomas (1.5% vs 4.5%, P < 0.001). Neurologic complications were similar between BS patients and non-BS patients (2.3% vs 2.7%, P = 0.62). For patients undergoing cervical spine surgery, BS patients experienced lower rates of bowel issues, device-related, and overall complication than non-BS patients (P < 0.05).ConclusionsBariatric surgery patients undergoing spine surgery experience lower overall complication rates than morbidly obese patients. This study warrants further investigation into these populations to mitigate risks associated with spine surgery for bariatric patients.

The AHRQ (Agency for Healthcare Research and Quality) has requested the correction of the result Tables 1–3 of this study: All stated numbers below 10 shall be modified to read “<10” instead.

Mitigation of greenhouse gas emissions often reduces co-emitted air pollutants, with advantages for human health. Avoided mortality from air pollution, a co-benefit of CO 2 abatement, is estimated under global climate change mitigation scenarios to be in the range of US$50–US$380 per tonne of CO 2 . This exceeds the projected mitigation costs for 2030 and 2050, and is within the lower range of costs expected in 2100. Actions to reduce greenhouse gas (GHG) emissions often reduce co-emitted air pollutants, bringing co-benefits for air quality and human health. Past studies 1 , 2 , 3 , 4 , 5 , 6 typically evaluated near-term and local co-benefits, neglecting the long-range transport of air pollutants 7 , 8 , 9 , long-term demographic changes, and the influence of climate change on air quality 10 , 11 , 12 . Here we simulate the co-benefits of global GHG reductions on air quality and human health using a global atmospheric model and consistent future scenarios, via two mechanisms: reducing co-emitted air pollutants, and slowing climate change and its effect on air quality. We use new relationships between chronic mortality and exposure to fine particulate matter 13 and ozone 14 , global modelling methods 15 and new future scenarios 16 . Relative to a reference scenario, global GHG mitigation avoids 0.5±0.2, 1.3±0.5 and 2.2±0.8 million premature deaths in 2030, 2050 and 2100. Global average marginal co-benefits of avoided mortality are US$50–380 per tonne of CO 2 , which exceed previous estimates, exceed marginal abatement costs in 2030 and 2050, and are within the low range of costs in 2100. East Asian co-benefits are 10–70 times the marginal cost in 2030. Air quality and health co-benefits, especially as they are mainly local and near-term, provide strong additional motivation for transitioning to a low-carbon future.

Background: Ground-level concentrations of ozone (O₃) and fine particulate matter [≤ 2.5 μm in aerodynamic diameter (PM2.5)] have increased since preindustrial times in urban and rural regions and are associated with cardiovascular and respiratory mortality. Objectives: We estimated the global burden of mortality due to O₃ and PM2.5 from anthropogenic emissions using global atmospheric chemical transport model simulations of preindustrial and present-day (2000) concentrations to derive exposure estimates. Methods: Attributable mortalities were estimated using health impact functions based on long-term relative risk estimates for O₃ and PM2.5 from the epidemiology literature. Using simulated concentrations rather than previous methods based on measurements allows the inclusion of rural areas where measurements are often unavailable and avoids making assumptions for background air pollution. Results: Anthropogenic O₃ was associated with an estimated 0.7 ± 0.3 million respiratory mortalities (6.3 ± 3.0 million years of life lost) annually. Anthropogenic PM2.5 was associated with 3.5 ± 0.9 million cardiopulmonary and 220,000 ± 80,000 lung cancer mortalities (30 ± 7.6 million years of life lost) annually. Mortality estimates were reduced approximately 30% when we assumed low-concentration thresholds of 33.3 ppb for O₃ and 5.8 μg/m³ for PM2.5. These estimates were sensitive to concentration thresholds and concentration—mortality relationships, often by > 50%. Conclusions: Anthropogenic O₃ and PM2.5 contribute substantially to global premature mortality. PM2.5 mortality estimates are about 50% higher than previous measurement-based estimates based on common assumptions, mainly because of methodologic differences. Specifically, we included rural populations, suggesting higher estimates; however, the coarse resolution of the global atmospheric model may underestimate urban PM2.5 exposures.

Retinopathy of prematurity is a leading cause of preventable childhood vision loss, and infants remain at risk of long-term ocular complications even after ROP screening concludes. However, adherence to recommended pediatric ophthalmology follow-up after ROP screening completion is not well characterized. This study aimed to evaluate adherence to pediatric ophthalmology follow-up visits after completion of ROP screening and identify factors associated with loss to follow-up in a tertiary care setting. We performed a retrospective chart review of premature infants eligible for ROP screening at a single urban academic center between January 2018 and December 2021. All infants were screened by a single vitreoretinal specialist, with pediatric ophthalmology follow-up recommended at the time of ROP clearance within 4 to 6 months. The primary outcome was a documented follow-up visit with pediatric ophthalmology. Demographic, perinatal, and ROP-related factors were compared between those who did and did not follow up, using univariate and multivariate logistic regression analyses. Of 475 eligible infants, 223 (46.9%) completed at least one pediatric ophthalmology follow-up appointment. In multivariate analysis, outpatient discharge from ROP care (OR 0.66, 95% CI 0.45-0.97, p = 0.035) and higher gestational age (OR 0.92, 95% CI 0.84-1.00, p = 0.041) were significantly associated with lower adherence to follow-up. Timing of follow-up (pre-COVID-19 vs COVID-19 era), insurance status, race, ethnicity, number of comorbidities, and distance to the clinic were not significantly associated with follow-up adherence. Fewer than half of infants completed their recommended pediatric ophthalmology follow-up appointments after ROP screening completion. Lower adherence among infants discharged from outpatient ROP care and those born at higher gestational ages highlights a critical care transition from ROP screening to pediatric ophthalmology. Interventions such as scheduling follow-up appointments prior to discharge and improving caregiver education may enhance continuity of care and reduce preventable vision loss in this vulnerable population.

BACKGROUNDFrom March 2, 2020, to April 12, 2020, New York City (NYC) experienced exponential growth of the COVID-19 pandemic due to novel coronavirus (SARS-CoV-2). Little is known regarding how physicians have been affected. We aimed to characterize the COVID-19 impact on NYC resident physicians.METHODSIRB-exempt and expedited cross-sectional analysis through survey to NYC residency program directors April 3-12, 2020, encompassing events from March 2, 2020, to April 12, 2020.RESULTSFrom an estimated 340 residency programs around NYC, recruitment yielded 91 responses, representing 24 specialties and 2306 residents. In 45.1% of programs, at least 1 resident with confirmed COVID-19 was reported. One hundred one resident physicians were confirmed COVID-19-positive, with an additional 163 residents presumed positive for COVID-19 based on symptoms but awaiting or unable to obtain testing. Two COVID-19-positive residents were hospitalized, with 1 in intensive care. Among specialties with more than 100 residents represented, negative binomial regression indicated that infection risk differed by specialty (P = 0.039). In 80% of programs, quarantining a resident was reported. Ninety of 91 programs reported reuse or extended mask use, and 43 programs reported that personal protective equipment (PPE) was suboptimal. Sixty-five programs (74.7%) redeployed residents elsewhere to support COVID-19 efforts.CONCLUSIONMany resident physicians around NYC have been affected by COVID-19 through direct infection, quarantine, or redeployment. Lack of access to testing and concern regarding suboptimal PPE are common among residency programs. Infection risk may differ by specialty.FUNDINGNational Eye Institute Core Grant P30EY019007; Research to Prevent Blindness Unrestricted Grant; Parker Family Chair; University of Pennsylvania.

Retinopathy of prematurity (ROP) is a disorder affecting low birthweight, preterm neonates. In the preterm eye, the retina is not fully developed and neovascularization may occur at the margin between the developed vascular retina and undeveloped avascular retina. Without timely treatment by laser or intravitreal anti-vascular endothelial growth factor (VEGF) therapy, this can lead to tractional retinal detachment and blindness. Visualization of the retina in regular examinations by indirect ophthalmoscopy is hence the current standard of care, but the exams are stressful and interpretation of images is subjective. The upregulation of VEGF in ROP would suggest an increase in ocular blood flow. In this report, we evaluate the potential of ultrafast plane-wave Doppler ultrasound (PWU) to detect increased flow velocities in the orbital vessels supplying the eye in a gentle exam with objective findings. We imaged both eyes of 50 low-birthweight preterm neonates using 18 MHz PWU. Flow velocity in the central retinal artery (CRA) and vein (CRV), and the short posterior ciliary arteries were determined and values at each ROP Stage compared. We found significantly increased velocities in the CRA and CRV in Stage 3 ROP eyes, where intervention would be considered. We compared multivariate models for identifying Stage 3 eyes comprised solely of clinical factors, solely of Doppler parameters, and clinical plus Doppler parameters. The respective models provided areas under their respective ROC curves of 0.760, 0.812, and 0.904. PWU Doppler represents a gentle, objective means for identifying neonates at risk for ROP that could complement ophthalmoscopy.

Increased concentrations of ozone and fine particulate matter (PM2.5) since preindustrial times reflect increased emissions, but also contributions of past climate change. Here we use modeled concentrations from an ensemble of chemistry-climate models to estimate the global burden of anthropogenic outdoor air pollution on present-day premature human mortality, and the component of that burden attributable to past climate change. Using simulated concentrations for 2000 and 1850 and concentration-response functions (CRFs), we estimate that, at present, 470 000 (95% confidence interval, 140 000 to 900 000) premature respiratory deaths are associated globally and annually with anthropogenic ozone, and 2.1 (1.3 to 3.0) million deaths with anthropogenic PM2.5-related cardiopulmonary diseases (93%) and lung cancer (7%). These estimates are smaller than ones from previous studies because we use modeled 1850 air pollution rather than a counterfactual low concentration, and because of different emissions. Uncertainty in CRFs contributes more to overall uncertainty than the spread of model results. Mortality attributed to the effects of past climate change on air quality is considerably smaller than the global burden: 1500 (−20 000 to 27 000) deaths yr−1 due to ozone and 2200 (−350 000 to 140 000) due to PM2.5. The small multi-model means are coincidental, as there are larger ranges of results for individual models, reflected in the large uncertainties, with some models suggesting that past climate change has reduced air pollution mortality.

Long-term exposure to ambient ozone (O3) is associated with excess respiratory mortality. Pollution emissions, demographic, and climate changes are expected to drive future ozone-related mortality. Here, we assess global mortality attributable to ozone according to an Intergovernmental Panel on Climate Change (IPCC) Shared Socioeconomic Pathway (SSP) scenario applied in Coupled Model Intercomparison Project Phase 6 (CMIP6) models, projecting a temperature increase of about 3.6 °C by the end of the century. We estimated ozone-related mortality on a global scale up to 2090 following the Global Burden of Disease (GBD) 2019 approach, using bias-corrected simulations from three CMIP6 Earth System Models (ESMs) under the SSP3-7.0 emissions scenario. Based on the three ESMs simulations, global ozone-related mortality by 2090 will amount to 2.79 M [95% CI 0.97 M–5.23 M] to 3.12 M [95% CI 1.11 M–5.75 M] per year, approximately ninefold that of the 327 K [95% CI 103 K–652 K] deaths per year in 2000. Climate change alone may lead to an increase of ozone-related mortality in 2090 between 42 K [95% CI −37 K–122 K] and 217 K [95% CI 68 K–367 K] per year. Population growth and ageing are associated with an increase in global ozone-related mortality by a factor of 5.34, while the increase by ozone trends alone ranges between factors of 1.48 and 1.7. Ambient ozone pollution under the high-emissions SSP3-7.0 scenario is projected to become a significant human health risk factor. Yet, optimizing living conditions and healthcare standards worldwide to the optimal ones today (application of minimum baseline mortality rates) will help mitigate the adverse consequences associated with population growth and ageing, and ozone increases caused by pollution emissions and climate change.

Ground-level ozone and fine particulate matter (PM (sub 2.5)) are associated with premature human mortality; their future concentrations depend on changes in emissions, which dominate the near-term, and on climate change. Previous global studies of the air-quality-related health effects of future climate change used single atmospheric models. However, in related studies, mortality results differ among models. Here we use an ensemble of global chemistry-climate models to show that premature mortality from changes in air pollution attributable to climate change, under the high greenhouse gas scenario RCP (Representative Concentration Pathway) 8.5, is probably positive. We estimate 3,340 (30,300 to 47,100) ozone-related deaths in 2030, relative to 2000 climate, and 43,600 (195,000 to 237,000) in 2100 (14 percent of the increase in global ozone-related mortality). For PM (sub 2.5), we estimate 55,600 (34,300 to 164,000) deaths in 2030 and 215,000 (76,100 to 595,000) in 2100 (countering by 16 percent the global decrease in PM (sub 2.5)-related mortality). Premature mortality attributable to climate change is estimated to be positive in all regions except Africa, and is greatest in India and East Asia. Most individual models yield increased mortality from climate change, but some yield decreases, suggesting caution in interpreting results from a single model. Climate change mitigation is likely to reduce air-pollution-related mortality.