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We estimate the prevalence and characteristics of violent hate crime victimization of lesbian, gay, bisexual, and transgender (LGBT) people in the United States, and we compare them to non-LGBT hate crime victims and to LGBT victims of violent non-hate crime. We analyze pooled 2017-2019 data from the National Crime Victimization Survey ( n persons = 553, 925; n incidents = 32, 470), the first nationally representative and comprehensive survey on crime that allows identification of LGBT persons aged 16 or older. Descriptive and bivariate analysis show that LGBT people experienced 6.6 violent hate crime victimizations per 1,000 persons compared with non-LGBT people’s 0.6 per 1,000 persons (odds ratio = 8.30, 95% confidence interval = 1.94, 14.65). LGBT people were more likely to be hate crime victims of sexual orientation or gender bias crime and less likely to be victims of race or ethnicity bias crimes compared to non-LGBT hate crime victims. Compared to non-LGBT victims, LGBT victims of hate crime were more likely to be younger, have a relationship with their assailant, and have an assailant who is white. Compared to LGBT victims of non-hate violence, more LGBT hate crime victims reported experiencing problems in their social lives, negative emotional responses, and physical symptoms of distress. Our findings affirm claims that hate crimes have adverse physical and psychological effects on victims and highlight the need to ensure that LGBT persons who experience hate crime get necessary support and services in the aftermath of the crime.

The p53 family of transcription factors is essential to counteract tumour formation and progression. Although previously this was exclusively associated with the ability of the p53 family to induce cell cycle arrest and apoptosis, an increasing number of reports have now indisputably demonstrated that the tumour suppressive functions of the p53 family members also rely on their ability to control and regulate cellular metabolism and maintain cellular oxidative homeostasis. Here, we review how each p53 family member, including p63 and p73, controls metabolic pathways in physiological conditions, and how these mechanisms could be exploited to provide anticancer therapeutic opportunities.

Membrane fusion triggered by Ca 2+ is orchestrated by a conserved set of proteins to mediate synaptic neurotransmitter release, mucin secretion and other regulated exocytic processes 1 – 4 . For neurotransmitter release, the Ca 2+ sensitivity is introduced by interactions between the Ca 2+ sensor synaptotagmin and the SNARE complex 5 , and sequence conservation and functional studies suggest that this mechanism is also conserved for mucin secretion 6 . Disruption of Ca 2+ -triggered membrane fusion by a pharmacological agent would have therapeutic value for mucus hypersecretion as it is the major cause of airway obstruction in the pathophysiology of respiratory viral infection, asthma, chronic obstructive pulmonary disease and cystic fibrosis 7 – 11 . Here we designed a hydrocarbon-stapled peptide that specifically disrupts Ca 2+ -triggered membrane fusion by interfering with the so-called primary interface between the neuronal SNARE complex and the Ca 2+ -binding C2B domain of synaptotagmin-1. In reconstituted systems with these neuronal synaptic proteins or with their airway homologues syntaxin-3, SNAP-23, VAMP8, synaptotagmin-2, along with Munc13-2 and Munc18-2, the stapled peptide strongly suppressed Ca 2+ -triggered fusion at physiological Ca 2+ concentrations. Conjugation of cell-penetrating peptides to the stapled peptide resulted in efficient delivery into cultured human airway epithelial cells and mouse airway epithelium, where it markedly and specifically reduced stimulated mucin secretion in both systems, and substantially attenuated mucus occlusion of mouse airways. Taken together, peptides that disrupt Ca 2+ -triggered membrane fusion may enable the therapeutic modulation of mucin secretory pathways. Peptides that disrupt Ca 2+ -triggered membrane fusion may enable the therapeutic modulation of mucin secretory pathways.

We give a new proof of the fact that the solutions of the stochastic heat equation, started with nonnegative initial conditions, are strictly positive at positive times. The proof uses concentration of measure arguments for discrete directed polymers in Gaussian environments, originated in M. Talagrand's work on spin glasses and brought to directed polymers by Ph. Carmona and Y. Hu. We also get slightly improved bounds on the lower tail of the solutions of the stochastic heat equation started with a delta initial condition.

Children were often near the center of public debates about legal marriage recognition for same-sex couples. Obergefell v . Hodges (2015), the case that resulted in legal same-sex marriage recognition, stressed the importance of these children as one of many factors compelling the opinion. Estimates indicated same-sex couples were raising 200,000 children in the United States. Children raised by same-sex couples may be politically socialized in distinct ways compared to children of different-sex couples because lesbians, gay men, and bisexuals tend to hold distinct and progressive political viewpoints on a wide variety of issues. What are the political attitudes of people with same-sex parents? In this exploratory study, we analyze a large, representative survey of first-year college students across the United States; we find few differences between people with same-sex and different-sex parents, and some of those differences may be attributable to households and respondent characteristics. When on the rare occasion a difference exists, we find that people with same-sex female parents are more progressive, but people with same-sex male parents are more conservative. Gender differences also emerged, with some distinctive patterns between males with same-sex parents and females with same-sex parents.

BackgroundThe aims were to compare: (1) baseline weights and weight gain trajectories; (2) sociodemographic, behavioural and health characteristics driving weight gain; and (3) estimated average weight in 20 years’ time, in two cohorts of young women.MethodsData were from 16066 participants in two population-based cohorts of young adult women, born in 1973–78 (“GenX”) and 1989–95 (“millennials”). Weight was reported at baseline (age 18–23 in both cohorts) and 4 years later. High weight gain was defined as >2.5% per year. Data were analysed in 2020.ResultsWomen born in 1989–95 were almost 4 kg heavier at age 18–23 and gained weight over 4 years 1.7 times faster than those born in 1973–78. Prevalence of high weight gain was 34.2% in the 1989–95 cohort and 24% in the 1973–78 cohort. In both cohorts, older age, higher education and high physical activity were associated with lower odds of high weight gain, and more hours in paid work, poorer self-rated health and higher baseline BMI were associated with higher odds of high weight gain. Five factors (outer regional areas, one child, ex or current smoker, high stress and depression) were determinants of high weight gain in the 1989–95 cohort, but not in the 1973–78 cohort. Based on average weight at age 21 and annual percentage weight gain, we estimate that women born in 1989–95 will, on average, be 16.7 kg heavier at age 41 (93.2 kg), than women in the 1973–78 cohort (76.5 kg).ConclusionHigh weight gain was evident in every sociodemographic group in both cohorts but most evident in millennial women with high levels of stress and depression. Without effective weight gain prevention strategies we estimate that more than 50% of the millennial women will be in the obese BMI category in 20 years. This will have serious economic, health and societal consequences.

Prior research has found that experiences with violence in the U.S. differ across individual demographic characteristics, including race, gender, and sexual orientation. However, peer reviewed studies have yet to examine the relationship between the intersections of race, gender, and sexual orientation, victimization risk, and characteristics of victimization. We use data from three years (2017-2019) of the National Crime Victimization Survey, the primary source of information on criminal victimization in the United States, to examine victimization at the intersection of sexual orientation, gender, and race/ethnicity. We test whether non-Hispanic Black, Hispanic, and non-Hispanic White sexual and gender minority (SGM) persons aged 16 or over are victimized at greater rates than their non-SGM counterparts and assess whether there are differences between sexual minority females and males of each racial group. We further document characteristics of victimization such as reporting to the police by SGM status and race or ethnicity. We find that SGMs are disproportionately more likely to be victims of violent crime than non-SGM people, and these disparities are present across the assessed racial and ethnic groups (non-Hispanic Black odds ratio [OR] = 3.3, 90% CI [CI] = 1.36, 5.16; Hispanic OR = 4.5, CI = 2.25, 6.71; non-Hispanic White OR = 4.8, CI = 2.25, 6.71). However, sexual orientation disparities are statistically distinguishable for lesbian or bisexual (LB) non-Hispanic White and Hispanic females but not for non-Hispanic Black LB females. Among LB females, the overall differences in victimization were primarily driven by bisexual respondents. We further find racial and ethnic differences among SGM victims in the likelihood of having the victimization reported to the police, in the utilization of community (non-police) resources, and in other aspects of victimization experiences, such as whether arrests occurred or in the suspicion that the violent incident was a hate crime. Our findings raise indicate a complex picture of how sexual orientation, gender identity, sex, and race and ethnicity interact in victimizations and their characteristics that should be further explored.

Mucosal damage, barrier breach, inflammation, and iron-deficiency anemia (IDA) typify ulcerative colitis (UC) in humans. The anemia in UC appears to mainly relate to systemic inflammation. The pathogenesis of this ‘anemia of inflammation’ (AI) involves cytokine-mediated transactivation of hepatic Hamp (encoding the iron-regulatory hormone, hepcidin). In AI, high hepcidin represses iron absorption (and iron release from stores), thus lowering serum iron, and restricting iron for erythropoiesis (causing anemia). In less-severe disease states, inflammation may be limited to the intestine, but whether this perturbs iron homeostasis is uncertain. We hypothesized that localized gut inflammation will increase overall iron demand (to support the immune response and tissue repair), and that hepatic Hamp expression will decrease in response, thus derepressing (i.e., enhancing) iron absorption. Accordingly, we developed a rat model of mild, acute colitis, and studied iron absorption and homeostasis. Rats exposed (orally) to DSS (4%) for 7 days had intestinal (but not systemic) inflammation, and biomarker analyses demonstrated that iron utilization was elevated. Iron absorption was enhanced (by 2-3-fold) in DSS-treated, WT rats of both sexes, but unexpectedly, hepatic Hamp expression was not suppressed. Therefore, to gain a better understanding of regulation of iron absorption during acute colitis, Hamp KO rats were used for further experimentation. The severity of DSS-colitis was similar in Hamp KOs as in WT controls. In the KOs, increased iron requirements associated with the physiological response to colitis were satisfied by mobilizing hepatic storage iron, rather than by increasing absorption of enteral iron (as occurred in WT rats). In conclusion then, in both sexes and genotypes of rats, iron absorption was appropriately modulated to match physiological demand for dietary iron during acute intestinal inflammation, but regulatory mechanisms may not involve hepcidin.

Triple negative breast cancers (TNBCs) are known to express low PGR, ESR1, and ERBB2, and high KRT5, KRT14, and KRT17. However, the reasons behind the increased expressions of KRT5, KRT14, KRT17 and decreased expressions of PGR, ESR1, and ERBB2 in TNBCs are not fully understood. Here we show that, expression of chromosome 19 miRNA cluster (C19MC) specifically marks human TNBCs. Low REST and high CEBPB correlate with expression of C19MC, KRT5, KRT14, and KRT17 and enhancers of these genes/cluster are regulated by CEBPB and REST binding sites. The C19MC miRNAs in turn can potentially target REST to offer a positive feedback loop, and might target PGR, ESR1, ERBB2, GATA3, SCUBE2, TFF3 mRNAs to contribute towards TNBC phenotype. Thus our study demonstrates that C19MC miRNA expression marks TNBCs and that C19MC miRNAs and CEBPB might together determine the TNBC marker expression pattern.

BackgroundThere is no identified level of FDG uptake in cardiac sarcoidosis (CS) associated with increased risk of arrhythmias, conduction disease, heart failure, or death. We aim to utilize standardized uptake value (SUV) quantitation and localization to identify patients at increased risk of cardiac events.Methods and ResultsF18-FDG PET/CT with MPI was used in CS diagnosis (N = 67). Mean and max SUV were measured and grouped as basal, mid, and apical disease. Post-scan ventricular tachycardia, AICD placement, complete heart block, pacemaker placement, atrial fibrillation, heart failure, and cardiac-related hospital admissions were recorded (mean follow up 2.98 ± 2 years). Poisson regression analysis revealed that max SUV, mean SUV, as well as mean basal SUV, and LVEF were significantly associated with total cardiac events. Max SUV odds ratio (OR) = 1.068 (95% CI 1.024-1.114, P = 0.002), mean SUV OR = 1.059 (95% CI 1.008-1.113, P = 0.023), mean SUV OR = 1.061 (95% CI 1.012-1.112, P = 0.014), scan LVEF OR = 0.731 (95% CI 0.664-0.805, P < 0.001).ConclusionsSUV at time of CS diagnosis has significant associations with future cardiac events. Patients with higher SUV, particularly in basal segments, are at increased risk of events. Further studies are needed to identify treatment methods utilizing risk stratification of CS.