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Prior studies have documented the pattern of decreased state funding for higher education in periods of economic contraction (i.e., the balance wheel phenomenon). This qualitative case study examines how policymakers in California and Texas made decisions about funding higher education at the onset of the COVID-19 pandemic, when policymakers faced an economic downturn. Data comprise 28 interviews with key state actors and 69 documents. The analysis expands prior understandings of how state policymakers make budgeting decisions that affect higher education by exploring how they perceive certain target populations as deserving or undeserving of state support. The study also sheds light on the tenuous relationship between policymakers' views of higher education and their funding decisions.

During economic recessions, state funding for higher education contracts (Delaney & Doyle, 2011; Hovey, 1999; SHEEO, 2022). Despite this reality, public higher education officials need to offer insights and explanations to state legislators about the current status of their institutions and their needs when discussing their budget requests. We use a multiple case-study design, framed by the narrative policy framework, to examine how campus officials in California and Texas justify their budget requests to the state legislature during the COVID-19 pandemic. Drawing on 131 h of transcribed legislative budget meetings and 62 documents, our findings suggest that higher education leaders emphasize the economic functions of higher education and center their ability to successfully manage during these uncertain and difficult times by highlighting improved or stable accountability measures such as enrollment, persistence, graduation, and job placement rates. During these budget requests, there are commonalities between the states regarding the structure, justifications, and narrative strategies used. However, higher education leaders evoked different narrative objects depending on the perceived values, beliefs, and norms of their state legislators.

Objective: The purpose of this study was to examine patterns of concurrent cannabis and other substance use and their differential associations with cannabis-related problems and academic outcomes in college students. Participants: Participants were undergraduate students (N = 263; M age = 19.1 years; 61.2% female) who were eligible if they used cannabis at least 3 days in the past month (M = 10.1 days). Method: Substance use, academic-related outcomes, and measures of Cannabis Use Disorder (CUD) severity and problems were obtained in an online survey. Results: The five groups evaluated were cannabis-only users (5.3%), cannabis and alcohol (47.1%), cannabis, alcohol and cigarettes (16.7%), cannabis, alcohol and other substances (14.8%), or all-substances (16%). Cannabis-only and all-substance users reported using cannabis most frequently (ps [less than or equal to] 0.034), but only the latter reported greater CUD severity, problems, and poorer academic outcomes. Discussion: College student polysubstance users may be at increased risk for poorer outcomes compared to cannabis-only users and other groups.

Access to financial aid is crucial in ensuring that students can afford college. Students must file the FAFSA to access federal financial aid and usually the FAFSA is also required for state and institutional aid (U.S. Department of Education, n.d). Prior research has shown, however, that the FAFSA is complicated and burdensome to complete and often acts as a barrier instead of an entry point to college (Bettinger et al., 2012; Bird & Castleman, 2016; Dynarski & Scott-Clayton, 2006, 2008; Dynarski et al., 2013). Given these barriers in accessing aid, some high schools employ college advisers or other school staff to assist students in the financial aid process (Civic Enterprises, 2011; Dunlop Velez, 2016). This single case study explores how College Advising Corps (CAC) advisers perceived their role in the financial aid process and how they discuss college expenses, financial aid, and debt with students. Guided by social capital theory (Coleman, 1988) and administrative burden framework (Herd & Moynihan, 2018), we find that CAC advisers, in their role as a social capital resource, experience learning, psychological, and compliance costs when assisting students to navigate the financial aid bureaucracy. They employ different strategies to overcome, manage, and cope with these costs.

Neuroblastoma (NB) is a pediatric tumor of the sympathetic nervous system. Survival remains poor for the almost 40 % of patients with high-risk NB. Targeted therapy options for high-risk NB are limited and single compound strategies often fail due to escape mechanisms, driven either by tumor heterogeneity or adaptive (epigenetic) responses or mutations. Novel NB therapeutic approaches rely increasingly on biomarker selected cohorts for phase I/II clinical trials. Parallel intensive research programs are needed to identify novel therapeutic vulnerabilities or drug targeting strategies and to further inform clinical trials and prioritize potent, less toxic combinations. While several effective chemotherapies work by increasing replication stress in cancer cells, recently, newer putatively less toxic small molecule-based approaches that directly target DNA damage response (DDR) pathway components such as ATR, CHK1 and PARP inhibitors are being evaluated in early phase trials for many cancers. NB sequencing studies have identified recurrent alterations (copy number and mutations) in many of these genes encoding critical DDR pathway proteins suggesting susceptibility to specific classes of DDR-targeting therapies. In this review, we summarize current data supporting the roles of DDR and replicative stress addiction in NB, including genetic alterations which impact DDR signaling pathways. Finally, we review the mechanisms, pre-clinical evidence and ongoing trials for drugs that target DDR-deficient and/or replication addicted NB.

Background Seven million lesbian, gay, and bisexual (LGB) adults will be aged >50 years by 2030; assessing and addressing their risk for cardiovascular disease is critical. Methods and Results We analyzed a nationwide cohort using the Veterans Health Administration data. Sexual orientation (SO) was classified via a validated natural language processing algorithm. Prevalent atherosclerotic cardiovascular disease (ASCVD) (history of acute myocardial infarction, ischemic stroke, or revascularization) was identified via International Classification of Diseases, Ninth and Tenth Revision (ICD‐9 and ICD‐10) codes. The index date was the date of the first primary care appointment on or after October 1, 2009. We ascertained covariates and prevalent ASCVD in the year following the index date; the baseline date was 1 year after the index date. We calculated sample statistics by sex and SO and used logistic regression analyses to assess associations between SO and prevalent ASCVD. Of 1 102 193 veterans with natural language processing‐defined SO data, 170 861 were classified as LGB. Prevalent ASCVD was present among 25 031 (4105 LGB). Adjusting for age, sex, race, and Hispanic ethnicity, LGB veterans had 1.24 [1.19–1.28] greater odds of prevalent ASCVD versus non‐LGB identified veterans. This association remained significant upon additional adjustment for the ASCVD risk factors substance use, anxiety, and depression (odds ratio [OR],1.17 [95% CI, 1.13–1.21]). Among a subset with self‐reported SO, findings were consistent (OR, 1.53 [95% CI, 1.20–1.95]). Conclusions This is one of the first studies to examine cardiovascular risk factors and disease of the veteran population stratified by natural language processing‐defined SO. Future research must explore psychological, behavioral, and physiological mechanisms that result in poorer cardiovascular health among LGB veterans.

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Abstract Background Understanding factors associated with opioid dispensing in cancer patients is important for developing tailored guidelines and ensuring equitable access to pain management. We examined patterns and predictors of opioid dispensing among older cancer patients from 2008 to 2015. Methods We analyzed data from the Surveillance, Epidemiology, and End Results (SEER) database linked to Medicare claims. We included the most common cancer types among patients aged 66–95 years. Opioids dispensed within 30 days before and 120 days after cancer diagnosis were assessed. We used logistic regression models to examine trends, adjusted odds ratios (aORs), and 95% confidence intervals (CIs) for opioid dispensing, considering patient demographics, geography, cancer stage, comorbidities, and treatment options. Models were stratified by sex. Results A total of 211,759 cancer patients aged 66–95 years were included in the study. For cancers combined, non‐Hispanic Black men had a significantly lower odds of receiving opioids during the 120 days post‐diagnosis (aOR = 0.89, 95% CI = 0.84–0.94) compared to non‐Hispanic White men. Factors such as pre‐diagnosis opioid dispensing, age, geography, cancer stage, comorbidities, and type of cancer treatment were associated with opioid dispensing during the 120 days post‐diagnosis. Surgery had the strongest association, with men undergoing surgery being 4.4 times more likely to receive opioids within 120 days post‐diagnosis (aOR = 4.41, 95% CI = 4.23–4.60), while women had an odds ratio of 2.72 (95% CI = 2.62–2.83). Chemotherapy and radiotherapy were also positively associated with opioid dispensing, with less pronounced estimates. Conclusions We observed significant variations in opioid dispensing among cancer patients aged 66‐95 years across cancer types and demographic and clinical factors.

Abstract Pancreatic acinar cell carcinoma (PACC) is a rare form of pancreatic cancer that commonly harbors targetable alterations, including activating fusions in the MAPK pathway and loss-of-function (LOF) alterations in DNA damage response/homologous recombination DNA repair-related genes. Here, we describe a patient with PACC harboring both somatic biallelic LOF of NBN and an activating NTRK1 fusion. Upon disease progression following 13 months of treatment with folinic acid, fluorouracil, irinotecan, and oxaliplatin (FOLFIRINOX), genomic analysis of a metastatic liver biopsy revealed the emergence of a novel reversion mutation restoring the reading frame of NBN. To our knowledge, genomic reversion of NBN has not been previously reported as a resistance mechanism in any tumor type. The patient was treated with, but did not respond to, targeted treatment with a selective NTRK inhibitor. This case highlights the complex but highly actionable genomic landscape of PACC and underlines the value of genomic profiling of rare tumor types such as PACC.

ImportanceUnderstanding the causes of infant mortality shapes public health, surveillance, and research investments. However, the association of single-locus (mendelian) genetic diseases with infant mortality is poorly understood.ObjectiveTo determine the association of genetic diseases with infant mortality.Design, setting, and participantsThis cohort study was conducted at a large pediatric hospital system in San Diego County (California) and included 546 infants (112 infant deaths [20.5%] and 434 infants [79.5%] with acute illness who survived; age, 0 to 1 year) who underwent diagnostic whole-genome sequencing (WGS) between January 2015 and December 2020. Data analysis was conducted between 2015 and 2022.ExposureInfants underwent WGS either premortem or postmortem with semiautomated phenotyping and diagnostic interpretation.Main outcomes and measuresProportion of infant deaths associated with single-locus genetic diseases.ResultsAmong 112 infant deaths (54 girls [48.2%]; 8 [7.1%] African American or Black, 1 [0.9%] American Indian or Alaska Native, 8 [7.1%] Asian, 48 [42.9%] Hispanic, 1 [0.9%] Native Hawaiian or Pacific Islander, and 34 [30.4%] White infants) in San Diego County between 2015 and 2020, single-locus genetic diseases were the most common identifiable cause of infant mortality, with 47 genetic diseases identified in 46 infants (41%). Thirty-nine (83%) of these diseases had been previously reported to be associated with childhood mortality. Twenty-eight death certificates (62%) for 45 of the 46 infants did not mention a genetic etiology. Treatments that can improve outcomes were available for 14 (30%) of the genetic diseases. In 5 of 7 infants in whom genetic diseases were identified postmortem, death might have been avoided had rapid, diagnostic WGS been performed at time of symptom onset or regional intensive care unit admission.Conclusions and relevanceIn this cohort study of 112 infant deaths, the association of genetic diseases with infant mortality was higher than previously recognized. Strategies to increase neonatal diagnosis of genetic diseases and immediately implement treatment may decrease infant mortality. Additional study is required to explore the generalizability of these findings and measure reduction in infant mortality.

Summary:. Autologous breast reconstruction with a deep inferior epigastric artery perforator (DIEP) flap is an excellent option for many patients proceeding with mastectomy for surgical management of their breast cancer. As microsurgical techniques and results improve and ensure consistent flap survival, optimizing aesthetic outcomes may become a primary focus. This article outlines 20 tips that can improve aesthetic results in DIEP flap breast reconstruction, based on our senior author’s 8-year career in microsurgical breast reconstruction, with an emphasis on enhanced cosmesis. We highlight tips on preoperative planning, intraoperative, and revision stages of the reconstruction and provide a schematic for integrating the tips into a reader’s microsurgical breast reconstruction practice.

Abstract Background Hepatocellular carcinoma (HCC) incidence was rising in the United States. Previously, using data collected by the Surveillance, Epidemiology, and End Results (SEER) Program through 2017, we found that overall incidence had begun to decline, although not in Black and American Indian/Alaska Native (AI/AN) populations. Utilizing expanded SEER data encompassing ~50% of the population, we examined secular trends and demographic differences in HCC incidence through 2019. Methods We included cases of HCC diagnosed in adults aged ≥20 years residing in SEER‐22 registry areas. We examined case counts, incidence rates (per 100,000 person‐years), annual percent changes (APCs), and calendar years when APCs changed significantly. Results HCC incidence increased from 5.56 in 2000 to 8.89 in 2009 (APC, 5.17%), then rose more slowly during 2009–2015 (APC, 2.28%). After peaking at 10.03 in 2015, incidence fell to 9.20 in 2019 (APC, −2.26%). In Asian/Pacific Islanders (A/PI), the decline began in 2007 and accelerated in 2015 (APCs: 2007–2015, −1.84%; 2015–2019, −5.80%). In 2014, incidence began to fall in the White (APC: 2014–2019, −1.11%) and Hispanic populations (APC: 2014–2019, −1.72%). In 2016, rates began to fall in Black individuals (APC: 2016–2019, −6.05%). In the AI/AN population, incidence was highest in 2017, although the subsequent decline was not statistically significant. In 2019, population‐specific rates were: White, 6.94; Black, 10.74; A/PI, 12.11; AI/AN, 14.56; Hispanic, 15.48. Conclusion HCC incidence is now decreasing in most US racial/ethnic populations, including among Black individuals. The onset of decline differed among racial/ethnic groups and wide disparities in HCC rates remain.

IntroductionHuman and nonhuman animal research suggests that greater oxytocin (OT) activity is protective against harmful substance use. Most research on this topic is preclinical, with few studies evaluating the association between substance use and individual differences in the human OT system. The present study sought to fill this gap by evaluating the relationship between alcohol use and multiple biological measures of OT activity in an overall low to moderate-drinking sample.MethodAs part of a larger study, generally healthy young (n = 51) and older (n = 53) adults self-reported whether they regularly used alcohol and how much alcohol they consumed per week. Participants also provided blood samples from which peripheral OT, and in an age-heterogeneous subset of participants (n = 56) variation in the oxytocin receptor gene (the OXTR rs53576 polymorphism) and OXTR DNA methylation levels (at cytosine-guanine dinucleotide sites -860, -924, -934), were obtained.ResultsA-allele carriers of the OXTR rs53579 polymorphism were less likely to regularly consume alcohol. Among regular alcohol consumers, number of alcoholic drinks per week was positively associated with peripheral OT in regression models excluding observations of high influence (postdiagnostic models). Number of alcoholic drinks per week was consistently negatively associated with OXTR DNA methylation at site -860; and with OXTR DNA methylation at site -924 in postdiagnostic models.ConclusionsThe significant associations between alcohol use and individual differences in OT activity support the involvement of the OT system in alcohol use, which most likely reflect the role of OT when alcohol use is under control of its rewarding properties and/or the acute impacts of alcohol on the OT system. Additional research with markers of OT activity and alcohol use, particularly longitudinal, is needed to clarify the bidirectional effects of OT and alcohol use in moderate to harmful drinking and dependence.

While many genetic diseases have effective treatments, they frequently progress rapidly to severe morbidity or mortality if those treatments are not implemented immediately. Since front-line physicians frequently lack familiarity with these diseases, timely molecular diagnosis may not improve outcomes. Herein we describe Genome-to-Treatment, an automated, virtual system for genetic disease diagnosis and acute management guidance. Diagnosis is achieved in 13.5 h by expedited whole genome sequencing, with superior analytic performance for structural and copy number variants. An expert panel adjudicated the indications, contraindications, efficacy, and evidence-of-efficacy of 9911 drug, device, dietary, and surgical interventions for 563 severe, childhood, genetic diseases. The 421 (75%) diseases and 1527 (15%) effective interventions retained are integrated with 13 genetic disease information resources and appended to diagnostic reports ( https://gtrx.radygenomiclab.com ). This system provided correct diagnoses in four retrospectively and two prospectively tested infants. The Genome-to-Treatment system facilitates optimal outcomes in children with rapidly progressive genetic diseases.

BackgroundEvidence has increased in recent years regarding the potential for ketamine to serve as a novel treatment option for a range of conditions, particularly depression (unipolar and bipolar). However, research regarding ketamine as a potential therapeutic for Autism Spectrum Disorder (ASD) is lacking, despite high overlap with bipolar depression and theoretical foundations for its use.Case presentationA 29-year-old man with bipolar disorder and Autism Spectrum Disorder, type 2 diabetes, presented with mood swings and suicidal thoughts, and anger outbursts occurring daily. The patient was referred by a psychiatrist due to irritability and outbursts during the previous 5 months. These outbursts were unable to be controlled by the medications prescribed, included yelling and screaming, and the patient was unable to speak with the psychiatrist. The patient underwent ketamine assisted psychotherapy with 6 initial IV infusions of ketamine over a 1 month period followed by 2 booster IV ketamine infusions. Following ketamine treatment, dramatic reductions in outbursts were observed as well as reductions in anxiety, suicidality, and depression scores.ConclusionThis case study adds to the scant literature regarding ketamine treatment for individuals with bipolar disorder and ASD. We did not find ASD to be a contraindication for IV ketamine and ketamine assisted psychotherapy. Reductions in anger outbursts, anxiety, suicidality, and depression suggest ketamine treatment might be tailored to individuals with bipolar disorder and ASD, and additional systematized research is warranted. Although potential mechanisms of action are not clear, these data add to the discussion regarding clinical practice considerations and the potential for ketamine to improve quality of life and associated metrics.

Background People living with HIV have higher sudden cardiac death (SCD) rates compared with the general population. Whether HIV infection is an independent SCD risk factor is unclear. Methods and Results This study evaluated participants from the Veterans Aging Cohort Study, an observational, longitudinal cohort of veterans with and without HIV infection matched 1:2 on age, sex, race/ethnicity, and clinical site. Baseline for this study was a participant's first clinical visit on or after April 1, 2003. Participants were followed through December 31, 2014. Using Cox proportional hazards regression, we assessed whether HIV infection, CD4 cell counts, and/or HIV viral load were associated with World Health Organization (WHO)-defined SCD risk. Among 144 336 participants (30% people living with HIV), the mean (SD) baseline age was 50.0 years (10.6 years), 97% were men, and 47% were of Black race. During follow-up (median, 9.0 years), 3035 SCDs occurred. HIV infection was associated with increased SCD risk (hazard ratio [HR], 1.14; 95% CI, 1.04-1.25), adjusting for possible confounders. In analyses with time-varying CD4 and HIV viral load, people living with HIV with CD4 counts 500 copies/mL (HR, 1.70; 95% CI, 1.46-1.98) had increased SCD risk versus veterans without HIV. In contrast, people living with HIV who had CD4 cell counts >500 cells/mm3 (HR, 1.03; 95% CI, 0.90-1.18) or HIV viral load

BackgroundStudies suggest lower risk of breast cancer in women with HIV versus without HIV. These estimates may be biased by lower life expectancy and younger age distribution of women with HIV. Our analysis evaluated this bias and characterized secular trends in breast cancer among women with HIV initiating antiretroviral therapy. We hypothesized breast cancer risk would increase over time as mortality decreased.SettingWomen with HIV prescribed antiretroviral therapy in the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) from 1997 through 2016.MethodsWe estimated breast cancer hazard (cause-specific hazard ratios) and cumulative incidence accounting for competing risks (subdistribution hazard ratios) to assess changes in breast cancer risk over time. This was assessed overall (1997-2016) and within/across calendar periods. Analyses were adjusted for race/ethnicity and inverse probability weighted for cohort. Cumulative incidence was graphically assessed by calendar period and race/ethnicity.ResultsWe observed 11,587 women during 1997-2016, contributing 63 incident breast cancer diagnoses and 1,353 deaths [73,445 person-years (median follow-up = 4.5 years)]. Breast cancer cumulative incidence was 3.2% for 1997-2016. We observed no secular trends in breast cancer hazard or cumulative incidence. There were annual declines in the hazard and cumulative incidence of death (cause-specific hazard ratios and subdistribution hazard ratios: 0.89, 95% confidence interval: 0.87 to 0.91) which remained within and across calendar periods.ConclusionsThese findings contradict the hypothesis of increasing breast cancer risk with declining mortality over time among women with HIV, suggesting limited impact of changing mortality on breast cancer risk. Additional inquiry is merited as survival improves among women with HIV.

BackgroundWith the increasing number of genomic sequencing studies, hundreds of genes have been implicated in neurodevelopmental disorders (NDDs). The rate of gene discovery far outpaces our understanding of genotype-phenotype correlations, with clinical characterization remaining a bottleneck for understanding NDDs. Most disease-associated Mendelian genes are members of gene families, and we hypothesize that those with related molecular function share clinical presentations.MethodsWe tested our hypothesis by considering gene families that have multiple members with an enrichment of de novo variants among NDDs, as determined by previous meta-analyses. One of these gene families is the heterogeneous nuclear ribonucleoproteins (hnRNPs), which has 33 members, five of which have been recently identified as NDD genes (HNRNPK, HNRNPU, HNRNPH1, HNRNPH2, and HNRNPR) and two of which have significant enrichment in our previous meta-analysis of probands with NDDs (HNRNPU and SYNCRIP). Utilizing protein homology, mutation analyses, gene expression analyses, and phenotypic characterization, we provide evidence for variation in 12 HNRNP genes as candidates for NDDs. Seven are potentially novel while the remaining genes in the family likely do not significantly contribute to NDD risk.ResultsWe report 119 new NDD cases (64 de novo variants) through sequencing and international collaborations and combined with published clinical case reports. We consider 235 cases with gene-disruptive single-nucleotide variants or indels and 15 cases with small copy number variants. Three hnRNP-encoding genes reach nominal or exome-wide significance for de novo variant enrichment, while nine are candidates for pathogenic mutations. Comparison of HNRNP gene expression shows a pattern consistent with a role in cerebral cortical development with enriched expression among radial glial progenitors. Clinical assessment of probands (n = 188-221) expands the phenotypes associated with HNRNP rare variants, and phenotypes associated with variation in the HNRNP genes distinguishes them as a subgroup of NDDs.ConclusionsOverall, our novel approach of exploiting gene families in NDDs identifies new HNRNP-related disorders, expands the phenotypes of known HNRNP-related disorders, strongly implicates disruption of the hnRNPs as a whole in NDDs, and supports that NDD subtypes likely have shared molecular pathogenesis. To date, this is the first study to identify novel genetic disorders based on the presence of disorders in related genes. We also perform the first phenotypic analyses focusing on related genes. Finally, we show that radial glial expression of these genes is likely critical during neurodevelopment. This is important for diagnostics, as well as developing strategies to best study these genes for the development of therapeutics.

Background Oesophageal cancer is one of the most aggressive cancers. The aim was to describe the disparities in oesophageal cancer incidence and mortality, and county-level factors in the state of Mississippi from 2003 to 2019 by sex, race, and geolocation.Methods This study used data from the Mississippi Cancer Registry, linked to county-level data from the Behavioral Risk Factor Surveillance System, the American Community Survey, and the Institutes for Health Metrics and Evaluation. We estimated age-standardised incidence (crude ASR) and mortality rates (crude AMR), mortality–incidence rate ratio and average annual percent change (AAPC) in rates by sex, race, and geolocation, using the Joinpoint Software V.5.0. We further calculated relative risks for oesophageal cancer using age-adjusted quasi-Poisson regression for each county-level factor including smoking, obesity, college degree completion, unemployment rate and median household income ranking within the state.Results Between 2003 and 2019, a total of 2737 oesophageal cancer cases and 2259 oesophageal cancer deaths occurred in Mississippi. Black men had the greatest reduction in oesophageal cancer incidence and mortality despite high rates (crude ASR2019=10.5, crude AMR2019=7.3 per 100 000; AAPCincidence=−3.7%, p

Plasmodium ovale curtisi (Poc) and Plasmodium ovale wallikeri (Pow) represent distinct non-recombining Plasmodium species that are increasing in prevalence in sub-Saharan Africa. Though they circulate sympatrically, co-infection within human and mosquito hosts has rarely been described. Separate 18S rRNA real-time PCR assays that detect Poc and Pow were modified to allow species determination in parallel under identical cycling conditions. The lower limit of detection was 0.6 plasmid copies/μL (95% CI 0.4-1.6) for Poc and 4.5 plasmid copies/μL (95% CI 2.7-18) for Pow, or 0.1 and 0.8 parasites/μL, respectively, assuming 6 copies of 18s rRNA per genome. However, the assays showed cross-reactivity at concentrations greater than 103 plasmid copies/μL (roughly 200 parasites/μL). Mock mixtures were used to establish criteria for classifying mixed Poc/Pow infections that prevented false-positive detection while maintaining sensitive detection of the minority ovale species down to 100 copies/μL (

Background Hospitalization with community-acquired pneumonia (CAP) is associated with an increased risk of cardiovascular disease (CVD) events in patients uninfected with HIV. We evaluated whether people living with HIV (PLWH) have a higher risk of CVD or mortality than individuals uninfected with HIV following hospitalization with CAP. Methods and Results We analyzed data from the Veterans Aging Cohort Study on US veterans admitted with their first episode of CAP from April 2003 through December 2014. We used Cox regression analyses to determine whether HIV status was associated with incident CVD events and mortality from date of admission through 30 days after discharge (30-day mortality), adjusting for known CVD risk factors. We included 4384 patients (67% [n=2951] PLWH). PLWH admitted with CAP were younger, had less severe CAP, and had fewer CVD risk factors than patients with CAP who were uninfected with HIV. In multivariable-adjusted analyses, CVD risk was similar in PLWH compared with HIV-uninfected (hazard ratio [HR], 0.89; 95% CI, 0.70-1.12), but HIV infection was associated with higher mortality risk (HR, 1.49; 95% CI, 1.16-1.90). In models stratified by HIV status, CAP severity was significantly associated with incident CVD and 30-day mortality in PLWH and patients uninfected with HIV. Conclusions In this study, the risk of CVD events during or after hospitalization for CAP was similar in PLWH and patients uninfected with HIV, after adjusting for known CVD risk factors and CAP severity. HIV infection, however, was associated with increased 30-day mortality after CAP hospitalization in multivariable-adjusted models. PLWH should be included in future studies evaluating mechanisms and prevention of CVD events after CAP.

The global distribution of primary production and consumption by humans (fisheries) is well-documented, but we have no map linking the central ecological process of consumption within food webs to temperature and other ecological drivers. Using standardized assays that span 105° of latitude on four continents, we show that rates of bait consumption by generalist predators in shallow marine ecosystems are tightly linked to both temperature and the composition of consumer assemblages. Unexpectedly, rates of consumption peaked at midlatitudes (25 to 35°) in both Northern and Southern Hemispheres across both seagrass and unvegetated sediment habitats. This pattern contrasts with terrestrial systems, where biotic interactions reportedly weaken away from the equator, but it parallels an emerging pattern of a subtropical peak in marine biodiversity. The higher consumption at midlatitudes was closely related to the type of consumers present, which explained rates of consumption better than consumer density, biomass, species diversity, or habitat. Indeed, the apparent effect of temperature on consumption was mostly driven by temperature-associated turnover in consumer community composition. Our findings reinforce the key influence of climate warming on altered species composition and highlight its implications for the functioning of Earth's ecosystems.