Estimates of Crowd-Out from a Public Health Insurance Expansion Using Administrative Data

We use a combination of administrative and survey data to estimate the fraction of individuals newly enrolled in public health coverage (Wisconsin’s combined Medicaid and CHIP program) that had access to private, employer-sponsored health insurance at the time of their enrollment and the fraction that dropped this coverage. We estimate that after expansion of eligibility for public coverage, approximately 20% of new enrollees had access to private health insurance at the time of enrollment and that only 8% dropped this coverage (with the remaining 12% having both private and public coverage). We also identify an “upper bound” estimate, which suggests that the percentage of new enrollees with private insurance coverage at the time of enrollment is, at most, 27%. These estimates of crowd-out are relatively low compared with estimates from the literature based on Medicaid and CHIP expansions, although based both on different data and on a different method.

Global burden of 288 causes of death and life expectancy decomposition in 204 countries and territories and 811 subnational locations, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021

BACKGROUND Regular, detailed reporting on population health by underlying cause of death is fundamental for public health decision making. Cause-specific estimates of mortality and the subsequent effects on life expectancy worldwide are valuable metrics to gauge progress in reducing mortality rates. These estimates are particularly important following large-scale mortality spikes, such as the COVID-19 pandemic. When systematically analysed, mortality rates and life expectancy allow comparisons of the consequences of causes of death globally and over time, providing a nuanced understanding of the effect of these causes on global populations. METHODS The Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2021 cause-of-death analysis estimated mortality and years of life lost (YLLs) from 288 causes of death by age-sex-location-year in 204 countries and territories and 811 subnational locations for each year from 1990 until 2021. The analysis used 56 604 data sources, including data from vital registration and verbal autopsy as well as surveys, censuses, surveillance systems, and cancer registries, among others. As with previous GBD rounds, cause-specific death rates for most causes were estimated using the Cause of Death Ensemble model-a modelling tool developed for GBD to assess the out-of-sample predictive validity of different statistical models and covariate permutations and combine those results to produce cause-specific mortality estimates-with alternative strategies adapted to model causes with insufficient data, substantial changes in reporting over the study period, or unusual epidemiology. YLLs were computed as the product of the number of deaths for each cause-age-sex-location-year and the standard life expectancy at each age. As part of the modelling process, uncertainty intervals (UIs) were generated using the 2·5th and 97·5th percentiles from a 1000-draw distribution for each metric. We decomposed life expectancy by cause of death, location, and year to show cause-specific effects on life expectancy from 1990 to 2021. We also used the coefficient of variation and the fraction of population affected by 90% of deaths to highlight concentrations of mortality. Findings are reported in counts and age-standardised rates. Methodological improvements for cause-of-death estimates in GBD 2021 include the expansion of under-5-years age group to include four new age groups, enhanced methods to account for stochastic variation of sparse data, and the inclusion of COVID-19 and other pandemic-related mortality-which includes excess mortality associated with the pandemic, excluding COVID-19, lower respiratory infections, measles, malaria, and pertussis. For this analysis, 199 new country-years of vital registration cause-of-death data, 5 country-years of surveillance data, 21 country-years of verbal autopsy data, and 94 country-years of other data types were added to those used in previous GBD rounds. FINDINGS The leading causes of age-standardised deaths globally were the same in 2019 as they were in 1990; in descending order, these were, ischaemic heart disease, stroke, chronic obstructive pulmonary disease, and lower respiratory infections. In 2021, however, COVID-19 replaced stroke as the second-leading age-standardised cause of death, with 94·0 deaths (95% UI 89·2-100·0) per 100 000 population. The COVID-19 pandemic shifted the rankings of the leading five causes, lowering stroke to the third-leading and chronic obstructive pulmonary disease to the fourth-leading position. In 2021, the highest age-standardised death rates from COVID-19 occurred in sub-Saharan Africa (271·0 deaths [250·1-290·7] per 100 000 population) and Latin America and the Caribbean (195·4 deaths [182·1-211·4] per 100 000 population). The lowest age-standardised death rates from COVID-19 were in the high-income super-region (48·1 deaths [47·4-48·8] per 100 000 population) and southeast Asia, east Asia, and Oceania (23·2 deaths [16·3-37·2] per 100 000 population). Globally, life expectancy steadily improved between 1990 and 2019 for 18 of the 22 investigated causes. Decomposition of global and regional life expectancy showed the positive effect that reductions in deaths from enteric infections, lower respiratory infections, stroke, and neonatal deaths, among others have contributed to improved survival over the study period. However, a net reduction of 1·6 years occurred in global life expectancy between 2019 and 2021, primarily due to increased death rates from COVID-19 and other pandemic-related mortality. Life expectancy was highly variable between super-regions over the study period, with southeast Asia, east Asia, and Oceania gaining 8·3 years (6·7-9·9) overall, while having the smallest reduction in life expectancy due to COVID-19 (0·4 years). The largest reduction in life expectancy due to COVID-19 occurred in Latin America and the Caribbean (3·6 years). Additionally, 53 of the 288 causes of death were highly concentrated in locations with less than 50% of the global population as of 2021, and these causes of death became progressively more concentrated since 1990, when only 44 causes showed this pattern. The concentration phenomenon is discussed heuristically with respect to enteric and lower respiratory infections, malaria, HIV/AIDS, neonatal disorders, tuberculosis, and measles. INTERPRETATION Long-standing gains in life expectancy and reductions in many of the leading causes of death have been disrupted by the COVID-19 pandemic, the adverse effects of which were spread unevenly among populations. Despite the pandemic, there has been continued progress in combatting several notable causes of death, leading to improved global life expectancy over the study period. Each of the seven GBD super-regions showed an overall improvement from 1990 and 2021, obscuring the negative effect in the years of the pandemic. Additionally, our findings regarding regional variation in causes of death driving increases in life expectancy hold clear policy utility. Analyses of shifting mortality trends reveal that several causes, once widespread globally, are now increasingly concentrated geographically. These changes in mortality concentration, alongside further investigation of changing risks, interventions, and relevant policy, present an important opportunity to deepen our understanding of mortality-reduction strategies. Examining patterns in mortality concentration might reveal areas where successful public health interventions have been implemented. Translating these successes to locations where certain causes of death remain entrenched can inform policies that work to improve life expectancy for people everywhere. FUNDING Bill & Melinda Gates Foundation

影響高科技研發人員過度工作因素及工作類型之探討

本研究旨在以Spence和Robbins（1992）工作狂熱建構中的內在驅迫因素和工作樂趣因素為基礎，並加入外在驅迫因素，來探討高科技研發人員過度工作的不同因素對於工作時數以及健康生活工作等層面變項的預測力或關聯性，最後由因素劃分出過度工作者類型，並比較不同類型過度工作者的差異性。本研究採問卷調查法，以249位台灣北部地區的高科技研發人員為樣本以及52位高科技行政人員為工作時數的對照組。研究結果發現：（1）研發人員與全國製造業工作者及高科技行政人員相較下，有顯著的過度工作現象。（2）外在驅迫因素意指源自專業工作環境而迫使個體長時數工作的各影響因素。針對研發人員，包括工作負荷過重、產業特性、組織文化酬賞等外在驅迫因素，以及內在驅迫因素，皆對過度工作具有顯著的預測力。而外在驅迫因素對研發人員過度工作的相對預測力高於內在因素。（3）對於健康生活工作三層面的影響性而言，內在因素中的內在驅迫有廣泛不利於三層面的顯著影響性而屬於健康生活工作的危險因子，內在因素中的工作樂趣則相對地於三層面皆有顯著助益而在三層面居於保護因子的角色；外在驅迫因素中的工作負荷過重，對於生活層面有顯著的不良影響，但對健康和工作沒有顯著影響。（4）辨識出三類型的過度工作研發人員，其中內在驅迫高工作樂趣低的「被驅迫狂」在各層面皆有最不利的行為表現，屬於積極的健康定義下的高危險群，內在驅迫高工作樂趣高的「幹勁狂」則較「被驅迫狂」有顯著較高的生活滿足，內在驅迫普通而工作樂趣高的「幹勁者」雖然長時數工作，但各層面狀況反而有優於全體研發人員平均值的傾向。最後，本研究針對上述研究結果做更深層的探討，並說明在個人層次和組織層次實務上的意涵。Two internal factors, “driveness” and “enjoyment of work” from the workaholism model of Spence and Robbins (1992), and “external force” factors were adopted to investigate the phenomenon of excessive work (defined as long hours of working) in the population of high-tech R&D professionals. The purpose of this study is to clarify the effects of these factors on high-tech R&D professionals’ working habits, as well as on their health and life styles. These factors were used to categorize high-tech R&D professionals further. The results showed (1) R&D professionals worked significantly longer hours than high-tech administrative staff and workers in manufacturing industry. (2) “Work overload”, one external force factor, compared to other factors, predicted best to R&D professionals’ hours of working. Moreover, the amount of variance explained by the external force factors was relatively larger than the internal factors. (3) Driveness was constantly found to be a risk factor for one’s holistic health, whereas the enjoyment of work was found to be a protective factor. The third factor, work overload, influenced one’s health only on one’s social life. (4) Three types of overworkers were identified: the nonenthusiastic workaholics (NWs), the enthusiastic workaholics (EWs), and the enthusiasts (Es). Among these overworkers, the NWs acted most consistently with the indicators of unhealthiness, showing that the NWs may be most vulnerable to health complaints, unsatisfied social life, and inefficient work habits. The EWs, though acted similarly as the NWs, were not as extreme as the NWs and had higher life-satisfaction than the NWs. As for Es, who also worked long hours, their health complains were the least of all workers and they had relatively healthy life styles than the other two kinds of workers. Implications of the internal and external factors on the high-tech R&D professionals, as well as the typology of the overworkers, were discussed

Does the Gender Composition of Sibships Affect Women's Educational Attainment?

Data from the Panel Study of Income Dynamics, the November 1989 Current Population Survey, and the National Longitudinal Study of Women suggest that women with sisters may have completed less schooling than women without sisters. This hypothesis follows a long tradition of theories about the effects of sibling number and configuration. There is relatively weak evidence for this hypothesis in the analysis on which the findings are based. Analyses of the effects of sibling gender composition on educational attainment among cohorts of women in the Occupational Changes in a Generation Survey, the Survey of Income and Program Participation, and the National Survey of Families and Households offer no support for this hypothesis or for other related hypotheses about the effects of the gender composition of sibships.

The role of microRNA-30c in the self-renewal and differentiation of C6 glioma cells

Background: Sphere formation, one method for identifying self-renewal ability, has been used to report that cancer stem-like cells exist in rat C6 glioma cells. Recent studies suggested that cancer stem-like cells share the stem cell properties of self-renewal and multipotent ability of neural stem cells and might be regulated by microRNAs (miRNAs). However, the mechanism of miRNA involvement in the sphere formation and neural differentiation abilities of cancer stem-like cells is poorly understood. Results: We found that miRNA-30c could assist in sphere formation of C6 cells under defined conditions in neural stem cell medium DMEM/F12-bFGF-EGF-B27. Moreover, overexpression of miRNA-30c might reduce 3-isobutyl-1-methylxanthine (IBMX)-induced neural differentiation, as the expression of neural markers, especially glial fibrillary acidic protein (GFAP), decreased. Further experiments revealed that miRNA-30c inhibited the IBMX-induced astrocyte differentiation via targeting the upstream genes and inactivating phosphorylation of STAT3 of the JAK-STAT3 pathway. Subsequently, the expression of GFAP was reduced and the number of astrocyte differentiation from C6 cells decreased. Conclusions: Our findings suggest that miRNA-30c could play a regulatory role in self-renewal and neural differentiation in C6 glioma cells

Center for Demography and Ecology University of Wisconsin-Madison Gender, Early Life Circumstances, and Smoking

to the first author. We used SPSS and LIMDEP 7.0 for statistical analysis. We would like to thank John A. Logan, Emily Agree and Bob Hauser for suggestions and comments. The opinions expressed here are of the authors. Please direct comments and questions to Daphne Kuo, Department of Sociology, University of Washington, Box 353340, Seattle, WA 9819

Suppression of Extensive Neurofilament Phosphorylation Rescues α-Internexin/Peripherin-Overexpressing PC12 Cells from Neuronal Cell Death

<div><p>Intermediate filament (IF) overproduction induces abnormal accumulation of neuronal IF, which is a pathological indicator of some neurodegenerative disorders. In our study, α-Internexin- and peripherin-overexpressing PC12 cells (pINT-EGFP and pEGFP-peripherin) were used as models to study neuropathological pathways responsible for neurodegenerative diseases. Microarray data revealed that Cdk5-related genes were downregulated and Cdk5 regulatory subunit-associated protein 3 (GSK-3α and GSK-3β) were upregulated in pINT-EGFP cells. Increased expression of phosphorylated neurofilament and aberrant activation of Cdk5 and GSK-3β were detected in both pEGFP-peripherin and pINT-EGFP cells by Western blotting. In addition, pharmacological approaches to retaining viability of pINT-EGFP and pEGFP-peripherin cells were examined. Treatment with Cdk5 inhibitor and GSK-3β inhibitor significantly suppressed neuronal death. Dynamic changes of disaggregation of EGFP-peripherin and decrease in green fluorescence intensity were observed in pEGFP-peripherin and pINT-EGFP cells by confocal microscopy after GSK-3β inhibitor treatment. We conclude that inhibition of Cdk5 and GSK-3β suppresses neurofilament phosphorylation, slows down the accumulation of neuronal IF in the cytoplasm, and subsequently avoids damages to cell organelles. The results suggest that suppression of extensive neurofilament phosphorylation may be a potential strategy for ameliorating neuron death. The suppression of hyperphosphorylation of neuronal cytoskeletons with kinase inhibitors could be one of potential therapeutic treatments for neurodegenerative diseases.</p> </div