Background There is limited research on rural–urban disparities in U.S. life expectancy. Purpose This study examined trends in rural–urban disparities in life expectancy at birth in the U.S. between ...1969 and 2009. Methods The 1969–2009 U.S. county-level mortality data linked to a rural–urban continuum measure were analyzed. Life expectancies were calculated by age, gender, and race for 3-year time periods between 1969 and 2004 and for 2005–2009 using standard life-table methodology. Differences in life expectancy were decomposed by age and cause of death. Results Life expectancy was inversely related to levels of rurality. In 2005–2009, those in large metropolitan areas had a life expectancy of 79.1 years, compared with 76.9 years in small urban towns and 76.7 years in rural areas. When stratified by gender, race, and income, life expectancy ranged from 67.7 years among poor black men in nonmetropolitan areas to 89.6 among poor Asian/Pacific Islander women in metropolitan areas. Rural–urban disparities widened over time. In 1969–1971, life expectancy was 0.4 years longer in metropolitan than in nonmetropolitan areas (70.9 vs 70.5 years). By 2005–2009, the life expectancy difference had increased to 2.0 years (78.8 vs 76.8 years). The rural poor and rural blacks currently experience survival probabilities that urban rich and urban whites enjoyed 4 decades earlier. Causes of death contributing most to the increasing rural–urban disparity and lower life expectancy in rural areas include heart disease, unintentional injuries, COPD, lung cancer, stroke, suicide, and diabetes. Conclusions Between 1969 and 2009, residents in metropolitan areas experienced larger gains in life expectancy than those in nonmetropolitan areas, contributing to the widening gap.
We analyzed socioeconomic and racial/ethnic disparities in US mortality, incidence, and survival rates from all-cancers combined and major cancers from 1950 to 2014. Census-based deprivation indices ...were linked to national mortality and cancer data for area-based socioeconomic patterns in mortality, incidence, and survival. The National Longitudinal Mortality Study was used to analyze individual-level socioeconomic and racial/ethnic patterns in mortality. Rates, risk-ratios, least squares, log-linear, and Cox regression were used to examine trends and differentials. Socioeconomic patterns in all-cancer, lung, and colorectal cancer mortality changed dramatically over time. Individuals in more deprived areas or lower education and income groups had higher mortality and incidence rates than their more affluent counterparts, with excess risk being particularly marked for lung, colorectal, cervical, stomach, and liver cancer. Education and income inequalities in mortality from all-cancers, lung, prostate, and cervical cancer increased during 1979–2011. Socioeconomic inequalities in cancer mortality widened as mortality in lower socioeconomic groups/areas declined more slowly. Mortality was higher among Blacks and lower among Asian/Pacific Islanders and Hispanics than Whites. Cancer patient survival was significantly lower in more deprived neighborhoods and among most ethnic-minority groups. Cancer mortality and incidence disparities may reflect inequalities in smoking, obesity, physical inactivity, diet, alcohol use, screening, and treatment.
The present study offers a novel approach in measuring Household Energy Poverty Index (HEPI) using National Sample Survey unit level data, employing a robust set of 15 key energy indicators ...representing multiple dimensions of energy and assigning weights by using principal component analysis (PCA). Grouping households into four different categories such as ‘least energy poor’, ‘less energy poor’, ‘more energy poor’ and ‘most energy poor’, it emerges from the study that more than 1/4th of total households in the country, falls under ‘most energy poor’ category, and 65% households in the country are in the ‘more and most energy poor’ groups implying the wide-scale prevalence of energy poverty in the country. In addition, analysis based on geographical spread of energy poverty reveals that eastern states and north-eastern states are more vulnerable in terms of energy poverty, hence requires strategic policy actions at all layers of governance. The HEPI can form a rigorous analytical basis for energy policy making in India – both the federal scale as well as at the state level.
•HEPI is constructed for India using multi-dimensional energy poverty framework.•15 key energy indicators are used for constructing HEPI.•Results indicate 65% households suffer from some form of energy poverty.
: Research has shown worsening physical and mental health outcomes during the COVID-19 pandemic. Trends in general and mental health inequalities during the pandemic in the US have not been analyzed ...in detail.
: Using Census Bureau's nationally representative pooled Household Pulse Survey (HPS) from April 2020 to May 2021 (N = 1,144,405), we examined monthly trends and disparities in health status by race/ethnicity and socioeconomic status (SES). Logistic regression models and disparity indices were used to analyze trends and inequalities.
: During the pandemic, the adjusted odds of fair and/or poor health were, respectively, 33%, 157%, 398%, 22% higher for non-Hispanic others, adults with <high school education, those with income <$25,000, and renters, compared to non-Hispanic Whites, those with ≥master's degree, those with incomes ≥$200,000, and homeowners. The adjusted odds of serious depression were, respectively, 49%, 130%, 25% higher for adults with <high school education, with income <$25,000, and renters, compared to their higher-SES counterparts. Disparity indices show increasing trends in racial and/or ethnic and some SES disparities in general and mental health during the pandemic.
: In light of the rising trends and inequalities in physical and mental health, increased policy efforts are needed to reduce health disparities during the ongoing pandemic and beyond.
This study examined trends in rural–urban disparities in all-cause and cause-specific mortality in the USA between 1969 and 2009. A rural–urban continuum measure was linked to county-level mortality ...data. Age-adjusted death rates were calculated by sex, race, cause-of-death, area-poverty, and urbanization level for 13 time periods between 1969 and 2009. Cause-of-death decomposition and log-linear and Poisson regression were used to analyze rural–urban differentials. Mortality rates increased with increasing levels of rurality overall and for non-Hispanic whites, blacks, and American Indians/Alaska Natives. Despite the declining mortality trends, mortality risks for both males and females and for blacks and whites have been increasingly higher in non-metropolitan than metropolitan areas, particularly since 1990. In 2005–2009, mortality rates varied from 391.9 per 100,000 population for Asians/Pacific Islanders in rural areas to 1,063.2 for blacks in small-urban towns. Poverty gradients were steeper in rural areas, which maintained higher mortality than urban areas after adjustment for poverty level. Poor blacks in non-metropolitan areas experienced two to three times higher all-cause and premature mortality risks than affluent blacks and whites in metropolitan areas. Disparities widened over time; excess mortality from all causes combined and from several major causes of death in non-metropolitan areas was greater in 2005–2009 than in 1990–1992. Causes of death contributing most to the increasing rural–urban disparity and higher rural mortality include heart disease, unintentional injuries, COPD, lung cancer, stroke, suicide, diabetes, nephritis, pneumonia/influenza, cirrhosis, and Alzheimer’s disease. Residents in metropolitan areas experienced larger mortality reductions during the past four decades than non-metropolitan residents, contributing to the widening gap.
Lysophosphatidylcholine (LPC) is increasingly recognized as a key marker/factor positively associated with cardiovascular and neurodegenerative diseases. However, findings from recent clinical ...lipidomic studies of LPC have been controversial. A key issue is the complexity of the enzymatic cascade involved in LPC metabolism. Here, we address the coordination of these enzymes and the derangement that may disrupt LPC homeostasis, leading to metabolic disorders. LPC is mainly derived from the turnover of phosphatidylcholine (PC) in the circulation by phospholipase A₂ (PLA₂). In the presence of Acyl-CoA, lysophosphatidylcholine acyltransferase (LPCAT) converts LPC to PC, which rapidly gets recycled by the Lands cycle. However, overexpression or enhanced activity of PLA₂ increases the LPC content in modified low-density lipoprotein (LDL) and oxidized LDL, which play significant roles in the development of atherosclerotic plaques and endothelial dysfunction. The intracellular enzyme LPCAT cannot directly remove LPC from circulation. Hydrolysis of LPC by autotaxin, an enzyme with lysophospholipase D activity, generates lysophosphatidic acid, which is highly associated with cancers. Although enzymes with lysophospholipase A₁ activity could theoretically degrade LPC into harmless metabolites, they have not been found in the circulation. In conclusion, understanding enzyme kinetics and LPC metabolism may help identify novel therapeutic targets in LPC-associated diseases.
Purpose: The aim of this study was to evaluate the efficacy of Orthoptek (Magnocellular Stimulator OMS; Carditek Pvt. Ltd., Bangalore) as a treatment modality for amblyopia and strabismus. Methods: ...Thirty-five patients with amblyopia of any type, reduced vision in one or both eyes with no binocular vision and or poor stereopsis were included in the study. All patients underwent a minimum of 10 sessions of therapy with each session lasting for a cumulative period of 60 min. At the end of the 10th session, patients were evaluated for improvement in visual acuity, stereopsis, Binocular single vision and amount of strabismus, if any. Results: The mean logMAR corrected distance visual acuity improved from 0.31 ± 0.34 and 0.32 ± 0.44 to 0.08 ± 0.12 and 0.07 ± 0.12 posttreatment in the right eye and left eye, respectively. Following therapy, 34 (97%) patients showed improvement in stereopsis, orthophoria was noticed in 28 (80%), and binocular single vision was noted in 33 (94%). All patients were followed up for 1 year with maintenance therapy and none showed any regression. Conclusion: We believe that top-down impulses and the role of the attention area in the parietal cortex have not been studied well enough in the treatment of amblyopia. Our device addresses these issues and corrects the visual deficits in amblyopia. However, the study needs validation of this pilot study from independent centers. The same will be done at some stage
•A blend of recycled fuel and renewable fuel was utilized in diesel engine.•Collective influence of 1-decanol, fuel injection pressure and EGR on engine characteristics were studied.•Best operating ...parameters were determined.
Plastic waste is abundant and its recovery to diesel-like fuel could reduce fossil fuel dependency and the associated risk of environmental pollution. In the present work, diesel-like fuel was produced from low-density polyethylene by catalytic pyrolysis method. Experiments were conducted to study the effect of substituting 10% vol. of 1-decanol in place of waste LDPE oil in D70L30 blend, under the influence of three injection pressures (400 bar, 500 bar, and 600 bar) and three EGR rates (0%, 10%, and 20%) on performance, combustion and emission characteristics of a CRDi engine at its rated power output. For this purpose, a ternary blend was prepared and the results were compared with diesel and D70L30 blend. Results reveal that, the substitution of 1-decanol in place of waste LDPE oil resulted in the shorter ignition delay period. The peak in-cylinder pressure and peak HRR dropped with increasing EGR rate and decreasing injection pressure. D70L20DEC10 injected at 600 bar with 0% and 10% EGR rates delivered 1.02% and 0.5% better BTE than D70L30 blend. NOx decreased by 112% when the EGR was increased from 0% to 20% at 400 bar FIP. It is concluded that the 1-decanol blend injected at 600 bar pressure and a low EGR rate of 10% gave the best possible performance and low emissions.
Circadian clocks are oscillatory systems that schedule daily rhythms of organismal behavior. The ability of the clock to reset its phase in response to external signals is critical for proper ...synchronization with the environment. In the model clock from cyanobacteria, the KaiABC proteins that comprise the core oscillator 1, 2 are directly sensitive to metabolites. Reduced ATP/ADP ratio and oxidized quinones cause clock phase shifts in vitro 3, 4. However, it is unclear what determines the metabolic response of the cell to darkness and thus the magnitude of clock resetting. We show that the cyanobacterial circadian clock generates a rhythm in metabolism that causes cells to accumulate glycogen in anticipation of nightfall. Mutation of the histidine kinase CikA creates an insensitive clock-input phenotype by misregulating clock output genome wide, leading to overaccumulation of glycogen and subsequently high ATP in the dark. Conversely, we show that disruption of glycogen metabolism results in low ATP in the dark and makes the clock hypersensitive to dark pulses. The observed changes in cellular energy are sufficient to recapitulate phase-shifting phenotypes in an in vitro model of the clock. Our results show that clock-input phenotypes can arise from metabolic dysregulation and illustrate a framework for circadian biology where clock outputs feed back through metabolism to control input mechanisms.
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•The circadian clock generates a rhythm in energy-storage metabolism•A mutant with insensitive clock input has a high-energy metabolic state•Disruption of glycogen metabolism makes phase shifts hypersensitive•There is a quantitative correspondence between dark metabolism and phase shifts
Pattanayak et al. show that the circadian rhythm in cyanobacteria is intimately connected to energy-storage metabolism. They show that the mechanisms that reset the clock time depend on the cell’s metabolic preparation for darkness and that mutants with abnormal energy charge in the dark have correspondingly abnormal clock phase shifts.
Purpose This study examines changes between 2003 and 2007 in obesity and overweight prevalence among U.S. children and adolescents 10 to 17 years of age from detailed racial/ethnic and socioeconomic ...groups. Methods The 2003 ( N = 46,707) and 2007 ( N = 44,101) National Survey of Children's Health were used to calculate overweight and obesity prevalence (body mass index BMI ≥85th and ≥95th percentiles, respectively). Logistic regression was used to model odds of obesity. Results In 2007, 16.4% of U.S. children were obese and 31.6% were overweight. From 2003 to 2007, obesity prevalence increased by 10% for all U.S. children but increased by 23%–33% for children in low-education, low-income, and higher unemployment households. Obesity prevalence increased markedly among Hispanic children and children from single-mother households. In 2007, Hispanic, non-Hispanic White, and American Indian children had 3.0–3.8 times higher odds of obesity and overweight than Asian children; children from low-income and low-education households had 3.4–4.3 times higher odds of obesity than children from higher socioeconomic households. The magnitude of racial/ethnic and socioeconomic disparities in obesity and overweight prevalence increased between 2003 and 2007, with substantial social inequalities persisting even after controlling for behavioral factors. Conclusions Social inequalities in obesity and overweight prevalence increased because of more rapid increases in prevalence among children in lower socioeconomic groups.
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