tbuckley/cabot-search huggingface dataset:
Income or Job Loss and Psychological Distress During the COVID-19 Pandemic
Authors: Grace V. Ringlein, Catherine K. Ettman, Elizabeth A. Stuart
Journal: JAMA Network Open (2024)

Importance Given the expiration of expanded unemployment and other benefits during the COVID-19 pandemic, it is important to understand the association between pandemic income or job loss and long-term implications on mental health. Objective To evaluate the association between income or job loss due to the COVID-19 pandemic and later psychological distress. Design, Setting, and Participants This cohort study used 5 waves of nationally representative, longitudinal survey data (September 16, 2019, through September 18, 2022) from the Pew Research Center’s American Trends Panel. Doubly robust propensity score–weighted quasi-Poisson models were used to estimate the association of self or household income or job loss during the early phase of the COVID-19 pandemic with later psychological distress, while controlling for pre–income loss characteristics (demographics, finances, and psychological distress). The study sample comprised US working-age adults (aged 18-64 years) who had not experienced income or job loss due to the COVID-19 pandemic by March 24, 2020. Exposure Participant-reported self or household income or job loss (ie, reduced hours or demand for work) due to the COVID19 pandemic between March 24, 2020, and August 16, 2020. Main Outcome and Measures Psychological distress was measured using a composite scale of 0 to 15 based on participants’ reported frequency of feeling depressed, on edge, sleepless, lonely, and hopeless in the past week in March 2020, February 2021, and September 2022. Results Of 1392 working-age adults (survey weighted 52.7% male and 47.7% aged 30-49 years) who had not reported income or job loss before March 24, 2020, a survey weighted 35.7% reported job or income loss between March 24 and August 16, 2020. Early-phase pandemic income or job loss was associated with higher distress in February 2021 (estimated ratio, 1.09; 95% CI, 1.01-1.18; P = .03) and September 2022 (estimated ratio, 1.11; 95% CI, 1.02-1.22; P = .02) among participants who experienced job or income loss between March 24 and August 16, 2020, compared with the propensity score–weighted mean in the group who did not experience income loss. Conclusions and Relevance These small but significant within-person associations between early-phase pandemic household income or job loss and psychological distress up to 29 months later suggest that policies are needed to support people with income or job loss to help mitigate the long-term adverse mental health outcomes of economic disruption.
Self-Managed Abortion Attempts Before vs After Changes in Federal Abortion Protections in the US
Authors: Lauren Ralph, Rosalyn Schroeder, Shelly Kaller, Daniel Grossman, M. Antonia Biggs
Journal: JAMA Network Open (2024)

Importance With decreasing access to facility-based abortion in the US, an increase in self-managed abortion (SMA) using various methods is anticipated. To date, no studies have examined changes in SMA in the shifting policy landscape. Objective To estimate changes in SMA prevalence among the general US population from before to after the Supreme Court’s June 2022 decision overturning federal abortion protections. Design, Setting, and Participants Serial cross-sectional surveys were administered throughout the US from December 10, 2021, to January 11, 2022, and June 14 to July 7, 2023. Participants included online panel members assigned female sex at birth, ages 18 to 49 years (or ages 15-17 years if a household member), who were English- or Spanish-speaking. Exposure Year of the survey (2021-2022 vs 2023). Main Outcome and Measures Participants were asked whether they had “ever taken or done something on their own, without medical assistance, to try to end a pregnancy” and, if so, details of their experience. Changes in the weighted SMA prevalence between survey years were examined, factors associated with SMA experience were identified, and projected lifetime SMA prevalence was calculated using discrete-time event history models, accounting for abortion underreporting. Results Median age of the participants was 32.5 (IQR, 25-41) years in 2021-2022 (n = 7016) and 32.0 (IQR, 24-40) in 2023 (n = 7148). Across both years, approximately 14% were non-Hispanic Black, 21% were Hispanic, and 54% were non-Hispanic White. The weighted adjusted proportion that ever attempted SMA was 2.4% (95% CI, 1.9%-3.0%) in 2021-2022 and 3.4% (95% CI, 2.8%-4.0%) in 2023—an increase of 1.0% (95% CI, 0.2%-1.7%; P = .03). Projected lifetime SMA prevalence accounting for abortion underreporting was 10.7% (95% CI, 8.6%-12.8%). In adjusted analyses, SMA experience was higher among non-Hispanic Black (4.3%; 95% CI, 2.8%-5.8%) vs other racial and ethnic (2.7%; 95% CI, 2.2%-3.1%) groups ( P = .04) and sexual and gender minority (5.0%; 95% CI, 3.4%-6.6%) vs heterosexual or cisgender (2.5%; 95% CI, 2.0%-2.9%) participants ( P &amp;amp;lt; .001). Approximately 4 in 10 (45.3% in 2021 and 39.0% in 2023) SMA attempts occurred before age 20 years. The methods used included herbs (29.8% [2021-2022] vs 25.9% [2023]), physical methods (28.6% [2021-2022] vs 29.7% [2023]), or alcohol or other substances (17.9% [2021-2022] vs 18.6% [2023]). Few participants (7.1% [2021-2022] vs 4.7% [2023]) sought emergency care for a complication. Conclusions and Relevance In this serial nationally representative survey study, increased SMA was observed following the loss of federal abortion protections. The findings revealed increased SMA use among marginalized groups, most often with ineffective methods. These findings suggest the need to expand access to alternative models of safe and effective abortion care and ensure those seeking health care post-SMA do not face legal risks.
Visual Impairment, Eye Conditions, and Diagnoses of Neurodegeneration and Dementia
Authors: Erin L. Ferguson, Mary Thoma, Peter T. Buto, Jingxuan Wang, M. Maria Glymour, Thomas J. Hoffmann, Hélène Choquet, Shea J. Andrews, Kristine Yaffe, Kaitlin Casaletto, Willa D. Brenowitz
Journal: JAMA Network Open (2024)

Importance Vision and eye conditions are associated with increased risk for Alzheimer disease and related dementias (ADRDs), but the nature of the association and the underlying biological pathways remain unclear. If causal, vision would be an important modifiable risk factor with viable population-level interventions. Objective To evaluate potentially causal associations between visual acuity, eye conditions (specifically cataracts and myopia), neuroimaging outcomes, and ADRDs. Design, Setting, and Participants A cohort and 2-sample bidirectional mendelian randomization (MR) study was conducted using UK Biobank participants and summary statistics from previously published genome-wide association studies on cataract, myopia, and AD. The participants included in the analysis were aged 55 to 70 years without dementia at baseline (calendar years 2006 to 2010), underwent genotyping, and reported on eye conditions; a subset completed visual acuity examinations (n = 69 852-71 429) or brain imaging (n = 36 591-36 855). Data were analyzed from August 15, 2022, through November 28, 2023. Exposure Self-reported cataracts, visual acuity, and myopia measured by refraction error. Main Outcomes and Measures ADRD, AD, and vascular dementia were identified from electronic medical records. Total and regional brain volumes were determined using magnetic resonance imaging. Results The sample included 304 953 participants (mean [SD] age, 62.1 (4.1) years; 163 825 women [53.72%]); 14 295 (4.69%) had cataracts and 2754 (3.86%) had worse than 20/40 vision. Cataracts (hazard ratio [HR], 1.18; 95% CI, 1.07-1.29) and myopia (HR, 1.35; 95% CI, 1.06-1.70) were associated with a higher hazard of ADRD. In MR analyses to estimate potential causal effects, cataracts were associated with increased risk of vascular dementia (inverse variance-weighted odds ratio [OR], 1.92; 95% CI, 1.26-2.92) but were not associated with increased dementia (OR, 1.21; 95% CI, 0.98-1.50). There were no associations between myopia and dementia. In MR for potential reverse causality, AD was not associated with cataracts (inverse variance–weighted OR, 0.99; 95% CI, 0.96-1.01). Genetic risk for cataracts was associated with smaller total brain (β = −597.43 mm 3 ; 95% CI, −1077.87 to −117.00 mm 3 ) and gray matter (β = −375.17 mm 3 ; 95% CI, −680.10 to −70.24 mm 3 ) volumes, but not other brain regions. Conclusions and Relevance In this cohort and MR study of UK Biobank participants, cataracts were associated with increased risk of dementia, especially vascular dementia, and reduced total brain volumes. These findings lend further support to the hypothesis that cataract extraction may reduce the risk for dementia.
Suicide in US Preteens Aged 8 to 12 Years, 2001 to 2022
Authors: Donna A. Ruch, Lisa M. Horowitz, Jennifer L. Hughes, Katherine Sarkisian, Joan L. Luby, Cynthia A. Fontanella, Jeffrey A. Bridge
Journal: JAMA Network Open (2024)

This cross-sectional study investigates characteristics and trends in suicide rates among US preteens using national mortality data from 2001 to 2022.
Visual Deficit Related to Cataracts—A Potential Modifiable Risk Factor for Vascular Dementia
Authors: Miren Altuna
Journal: JAMA Network Open (2024)

Erin L. Ferguson, MPH; Mary Thoma, MPH; Peter T. Buto, MPH; Jingxuan Wang, MPhil; M. Maria Glymour, ScD; Thomas J. Hoffmann, PhD; Hélène Choquet, PhD; Shea J. Andrews, PhD; Kristine Yaffe, MD; Kaitlin Casaletto, PhD; Willa D. Brenowitz, PhD, MPH
Biomarker profiles associated with reverse ventricular remodelling in patients with heart failure and a reduced ejection fraction: Insights from the echocardiographic substudy of the <scp>VICTORIA</scp> trial
Authors: Jasper Tromp, Carolyn S.P. Lam, Wendimagegn Alemayehu, Christopher R. de Filippi, Vojtěch Melenovský, Karen Sliwa, Yuri Lopatin, Juan Luis Arango, M. Cecilia Bahit, Lothar Roessig, Christopher M. O'Connor, Palak Shah, Cynthia M. Westerhout, Adriaan A. Voors, Burkert Pieske, Paul W. Armstrong
Journal: European Journal of Heart Failure (2024)

Abstract Aims Reverse ventricular remodelling, defined as a decrease in left ventricular end‐systolic volume indexed to body surface area (LVESVI) or an increase in left ventricular ejection fraction (LVEF), is associated with improved clinical outcomes in patients with heart failure with reduced ejection fraction (HFrEF). However, the underlying pathophysiological mechanisms remain unclear. Methods and results We evaluated paired core‐lab assessed echocardiograms and measurements of 92 biomarkers at baseline and 8 months thereafter in 419 participants with HFrEF. Reverse ventricular remodelling was defined as a &gt;5% LVEF increase or &gt;15% LVESVI relative decrease between baseline and 8 months. We evaluated the association between baseline biomarkers and their changes with reverse ventricular remodelling in the prospectively randomized controlled VICTORIA (Vericiguat Global Study in Subjects With Heart Failure With Reduced Ejection Fraction) trial. Of 419 patients (median age 66 [interquartile range 57–74] years, 27.4% women), 206 (49.2%) had reverse ventricular remodelling (either a 5% LVEF increase or a 15% LVESVI decrease). There were no differences in baseline biomarker concentrations between patients with versus those without reverse ventricular remodelling on follow‐up. However, in patients with reverse ventricular remodelling there were significant decreases in biomarkers relating to inflammation and cardiac metabolism; particularly the tumour necrosis factor superfamily member 13B (ratio 0.82, 95% confidence interval [CI] 0.77–0.88), growth differentiation factor‐15 (ratio 0.74, 95% CI 0.66–0.84), and insulin‐like growth factor binding protein 7 (ratio 0.80, 95% CI 0.73–0.88). Conclusions Reverse ventricular remodelling in patients with HFrEF is associated with a decrease of biomarkers related to inflammation and cardiac metabolism.
Prognostic implications of genotype findings in non‐ischaemic dilated cardiomyopathy: A network meta‐analysis
Authors: Vasileios Anastasiou, Andreas S. Papazoglou, Thomas Gossios, Thomas Zegkos, Stylianos Daios, Dimitrios V. Moysidis, Ourania Koutsiouroumpa, Despoina Parcharidou, Georgios Tziomalos, Sotiris Katranas, Pavlos Rouskas, Matthaios Didagelos, Theodoros Karamitsos, Antonios Ziakas, William J. McKenna, Vasileios Kamperidis, Georgios K. Efthimiadis
Journal: European Journal of Heart Failure (2024)

Abstract Aims Evidence on the relative impact of diverse genetic backgrounds associated with non‐ischaemic dilated cardiomyopathy (DCM) remains contradictory. This study sought to synthesize the available data regarding long‐term outcomes of different gene groups in DCM. Methods and results Electronic databases were systematically screened to identify studies reporting prognostic data on pre‐specified gene groups. Those included pathogenic/likely pathogenic (P/LP) variants, truncating titin variants (TTNtv), lamin A/C variants (LMNA), and desmosomal proteins. Outcomes were divided into composite adverse events (CAEs), malignant ventricular arrhythmic events (MVAEs) and heart failure events (HFEs). A total of 26 studies ( n = 7255) were included in the meta‐analysis and 6791 patients with genotyped DCM were analysed. Patients with P/LP variants had a higher risk for CAEs (odds ratio [OR] 2.10, 95% confidence interval [CI] 1.67–2.65), MVAEs (OR 1.86, 95% CI 1.52–2.26), and HFEs (OR 2.01, 95% CI 1.08–3.73) than genotype‐negative patients. The presence of TTNtv was linked to a higher risk for CAEs (OR 1.78, 95% CI 1.20–2.63), but not MVAEs or HFEs. LMNA and desmosomal groups suffered a higher risk for CAEs, MVAEs, and HFEs compared to non‐LMNA and non‐desmosomal groups, respectively. When genes were indirectly compared, the presence of LMNA resulted in a more detrimental effect that TTNtv, with respect to all composite outcomes but no significant difference was found between LMNA and desmosomal genes. Desmosomal genes harboured a higher risk for MVAEs compared to TTNtv. Conclusions Different genetic substrates associated with DCM result in divergent natural histories. Routine utilization of genetic testing should be employed to refine risk stratification and inform therapeutic strategies in DCM.
Youth Suicide, Mental Health, and Firearm Access—Time to Focus on Upstream Prevention
Authors: Lisa M. Horowitz, John V. Campo, Jeffrey A. Bridge
Journal: JAMA Network Open (2024)

Sofia Chaudhary, MD; Jennifer A. Hoffmann, MD, MS; Christian D. Pulcini, MD, MEd, MPH; Mark Zamani, MS; Matt Hall, PhD; Kristyn N. Jeffries, MD; Rachel Myers, MSCE; Joel Fein, MD, MPH; Bonnie T. Zima, MD, MPH; Peter F. Ehrlich, MD, MSc; Elizabeth R. Alpern, MD, MSCE; Stephen Hargarten, MD, MPH; Karen M. Sheehan, MD, MPH; Eric W. Fleegler, MD, MPH; Monika K. Goyal, MD, MSCE; Children's Hospital Association Research in Gun Related Events (CHARGE) Collaborative
Building an Evidence Base for Deprescribing in the Setting of Polypharmacy
Authors: Michelle C. Odden
Journal: JAMA Network Open (2024)

Kenya Ie, MD, MPH, PhD; Masanori Hirose, MD, PhD; Tsubasa Sakai, MD; Iori Motohashi, MD, MPH; Mari Aihara, MD; Takuya Otsuki, MD, PhD; Ayako Tsuboya, PharmD, PhD; Hiroshi Matsumoto, PharmD; Hikari Hashi, PharmD; Eisuke Inoue, PhD; Masaki Takahashi, MSc; Eiko Komiya, PharmD; Yuka Itoh, PharmD; Reiko Machino, PharmD; Tomoya Tsuchida, MD, PhD; Steven M. Albert, PhD; Yoshiyuki Ohira, MD, PhD; Chiaki Okuse, MD, PhD
Self-Managed Abortion and Criminalization in the Post-<i>Dobbs</i> US
Authors: Caitlin Gerdts, Kylee Sunderlin, Nancy Cárdenas-Peña
Journal: JAMA Network Open (2024)

Lauren Ralph, PhD; Rosalyn Schroeder, MSc; Shelly Kaller, MPH; Daniel Grossman, MD; M. Antonia Biggs, PhD
Lysosomal-Associated Protein Transmembrane 5, Tubular Senescence, and Progression of CKD
Authors: Xiaohan Liu, Ping Zhan, Yang Zhang, Huiying Jin, Youzhao Wang, Yujie Yang, Ziying Wang, Xiaojie Wang, Qianqian Xu, Junhui Zhen, Rong Sun, Jinpeng Sun, Min Liu, Fan Yi
Journal: Journal of the American Society of Nephrology (2024)

Key Points Lysosomal-associated protein transmembrane 5 (LAPTM5) is increased in tubular epithelial cells in CKD. Conditional knockout of Laptm5 in tubules attenuates kidney fibrosis in mice with CKD. LAPTM5 contributes to tubular senescence by inhibiting WWP2-mediated ubiquitination of notch1 intracellular domain. Background Tubular senescence is a major determinant of CKD, and identification of potential therapeutic targets involved in senescent tubular epithelial cells has clinical importance. Lysosomal-associated protein transmembrane 5 (LAPTM5) is a key molecule related to T- and B-cell receptor expression and inflammation. However, the expression pattern of LAPTM5 in the kidney and the contribution of LAPTM5 to the development of CKD are unknown. Methods Laptm5 −/− mice and tubule specific– Laptm5 knockout mice were used to examine the role of LAPTM5 in tubular senescence by establishing different experimental mouse CKD models. Results LAPTM5 expression was significantly induced in the kidney, especially in proximal tubules and distal convoluted tubules, from mice with aristolochic acid nephropathy, bilateral ischemia/reperfusion injury–induced CKD, or unilateral ureter obstruction. Tubule-specific deletion of Laptm5 inhibited senescence of tubular epithelial cells and alleviated tubulointerstitial fibrosis in aged mice. Moreover, Laptm5 deficiency ameliorated kidney injury and tubular senescence in mice with CKD. Mechanistically, LAPTM5 inhibited ubiquitination of notch1 intracellular domain by mediating WWP2 lysosomal degradation and then leading to cellular senescence in tubular epithelial cells. We also observed a higher expression of LAPTM5 in tubules from patients with CKD, and the level of LAPTM5 was correlated with kidney fibrosis and tubular senescence in people with CKD. Conclusions LAPTM5 contributed to tubular senescence by regulating the WWP2/notch1 intracellular domain signaling pathway and exacerbated kidney injury during the progression of CKD.
Single-nucleus transcriptomics identifies separate classes of UCP1 and futile cycle adipocytes
Authors: Tongtong Wang, Anand Kumar Sharma, Chunyan Wu, Claudia Irene Maushart, Adhideb Ghosh, Wu Yang, Patrik Stefanicka, Zuzana Kovanicova, Jozef Ukropec, Jing Zhang, Myrtha Arnold, Manuel Klug, Katrien De Bock, Ulrich Schneider, Cristina Popescu, Bo Zheng, Lianggong Ding, Fen Long, Revati Sumukh Dewal, Caroline Moser, Wenfei Sun, Hua Dong, Martin Takes, Dominique Suelberg, Alexander Mameghani, Antonio Nocito, Christoph Johannes Zech, Alin Chirindel, Damian Wild, Irene A Burger, Michael R Schön, Arne Dietrich, Min Gao, Markus Heine, Yizhi Sun, Ariana Vargas-Castillo, Susanna Søberg, Camilla Scheele, Miroslav Balaz, Matthias Blüher, Matthias Johannes Betz, Bruce M Spiegelman, Christian Wolfrum
Journal: Cell Metabolism (2024)

Adipose tissue can recruit catabolic adipocytes that utilize chemical energy to dissipate heat. This process occurs either by uncoupled respiration through uncoupling protein 1 (UCP1) or by utilizing ATP-dependent futile cycles (FCs). However, it remains unclear how these pathways coexist since both processes rely on the mitochondrial membrane potential. Utilizing single-nucleus RNA sequencing to deconvolute the heterogeneity of subcutaneous adipose tissue in mice and humans, we identify at least 2 distinct subpopulations of beige adipocytes: FC-adipocytes and UCP1-beige adipocytes. Importantly, we demonstrate that the FC-adipocyte subpopulation is highly metabolically active and utilizes FCs to dissipate energy, thus contributing to thermogenesis independent of Ucp1. Furthermore, FC-adipocytes are important drivers of systemic energy homeostasis and linked to glucose metabolism and obesity resistance in humans. Taken together, our findings identify a noncanonical thermogenic adipocyte subpopulation, which could be an important regulator of energy homeostasis in mammals.
A human commensal-pathogenic fungus suppresses host immunity via targeting TBK1
Authors: Gang Luo, Jingkai Zhang, Tianxu Wang, Hao Cui, Yukun Bai, Jianchen Luo, Jinqiu Zhang, Mao Zhang, Linyan Di, Yuncong Yuan, Kang Xiong, Xiangtai Yu, Yaling Zhang, Chao Shen, Cheng Zhu, Yong Wang, Chang Su, Yang Lu
Journal: Cell Host & Microbe (2024)
Chromosome 7 gain compensates for chromosome 10 loss in glioma
Authors: Nishanth Ulhas. Nair, Alejandro A. Schaffer, E. Michael. Gertz, Kuoyuan Cheng, Johanna Zerbib, Avinash Das. Sahu, Gil Leor, Eldad D. Shulman, Kenneth D. Aldape, Uri Ben-David, Eytan Ruppin
Journal: Cancer Research (2024)

The co-occurrence of chromosome 10 loss and chromosome 7 gain in gliomas is the most frequent loss-gain co-aneuploidy pair in human cancers. This phenomenon has been investigated since the late 1980s without resolution. Expanding beyond previous gene-centric studies, we investigated the co-occurrence in a genome-wide manner, taking an evolutionary perspective. Mining of large-scale tumor aneuploidy data confirmed the previous finding of a small-scale longitudinal study that the most likely order is chromosome 10 loss, followed by chromosome 7 gain. Extensive analysis of genomic and transcriptomic data from both patients and cell lines revealed that this co-occurrence can be explained by functional rescue interactions that are highly enriched on chromosome 7, which could potentially compensate for any detrimental consequences arising from the loss of chromosome 10. Transcriptomic data from various normal, noncancerous human brain tissues were analyzed to assess which tissues may be most predisposed to tolerate compensation of chromosome 10 loss by chromosome 7 gain. The analysis indicated that the preexisting transcriptomic states in the cortex and frontal cortex, where gliomas arise, are more favorable than other brain regions for compensation by rescuer genes that are active on chromosome 7. Collectively, these findings suggest that the phenomenon of chromosome 10 loss and chromosome 7 gain in gliomas is orchestrated by a complex interaction of many genes residing within these two chromosomes and provide a plausible reason why this co-occurrence happens preferentially in cancers originating in certain regions of the brain. Significance: Increased expression of multiple rescuer genes on the gained chromosome 7 could compensate for the downregulation of several vulnerable genes on the lost chromosome 10, resolving the long-standing mystery of this frequent co-occurrence in gliomas.