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The SARS-CoV-2 variant of concern, omicron, appears to be less severe than delta. We aim to quantify the differences in symptom prevalence, risk of hospital admission, and symptom duration among the vaccinated population. In this prospective longitudinal observational study, we collected data from participants who were self-reporting test results and symptoms in the ZOE COVID app (previously known as the COVID Symptoms Study App). Eligible participants were aged 16–99 years, based in the UK, with a body-mass index between 15 and 55 kg/m2, had received at least two doses of any SARS-CoV-2 vaccine, were symptomatic, and logged a positive symptomatic PCR or lateral flow result for SARS-CoV-2 during the study period. The primary outcome was the likelihood of developing a given symptom (of the 32 monitored in the app) or hospital admission within 7 days before or after the positive test in participants infected during omicron prevalence compared with those infected during delta prevalence. Between June 1, 2021, and Jan 17, 2022, we identified 63 002 participants who tested positive for SARS-CoV-2 and reported symptoms in the ZOE app. These patients were matched 1:1 for age, sex, and vaccination dose, across two periods (June 1 to Nov 27, 2021, delta prevalent at >70%; n=4990, and Dec 20, 2021, to Jan 17, 2022, omicron prevalent at >70%; n=4990). Loss of smell was less common in participants infected during omicron prevalence than during delta prevalence (16·7% vs 52·7%, odds ratio [OR] 0·17; 95% CI 0·16–0·19, p<0·001). Sore throat was more common during omicron prevalence than during delta prevalence (70·5% vs 60·8%, 1·55; 1·43–1·69, p<0·001). There was a lower rate of hospital admission during omicron prevalence than during delta prevalence (1·9% vs 2·6%, OR 0·75; 95% CI 0·57–0·98, p=0·03). The prevalence of symptoms that characterise an omicron infection differs from those of the delta SARS-CoV-2 variant, apparently with less involvement of the lower respiratory tract and reduced probability of hospital admission. Our data indicate a shorter period of illness and potentially of infectiousness which should impact work–health policies and public health advice. Wellcome Trust, ZOE, National Institute for Health Research, Chronic Disease Research Foundation, National Institutes of Health, and Medical Research Council

Racial/ethnic minorities have been disproportionately impacted by COVID-19. The effects of COVID-19 on the long-term mental health of minorities remains unclear. To evaluate differences in odds of screening positive for depression and anxiety among various racial and ethnic groups during the latter phase of the COVID-19 pandemic, we performed a cross-sectional analysis of 691,473 participants nested within the prospective smartphone-based COVID Symptom Study in the United States (U.S.) and United Kingdom (U.K). from February 23, 2021 to June 9, 2021. In the U.S. ( n =57,187), compared to White participants, the multivariable odds ratios (ORs) for screening positive for depression were 1·16 (95% CI: 1·02 to 1·31) for Black, 1·23 (1·11 to 1·36) for Hispanic, and 1·15 (1·02 to 1·30) for Asian participants, and 1·34 (1·13 to 1·59) for participants reporting more than one race/other even after accounting for personal factors such as prior history of a mental health disorder, COVID-19 infection status, and surrounding lockdown stringency. Rates of screening positive for anxiety were comparable. In the U.K. ( n =643,286), racial/ethnic minorities had similarly elevated rates of positive screening for depression and anxiety. These disparities were not fully explained by changes in leisure time activities. Racial/ethnic minorities bore a disproportionate mental health burden during the COVID-19 pandemic. These differences will need to be considered as health care systems transition from prioritizing infection control to mitigating long-term consequences.

There are well-established disparities in cancer incidence and outcomes by race/ethnicity that result from the interplay between structural, socioeconomic, socio-environmental, behavioural and biological factors. However, large research studies designed to investigate factors contributing to cancer aetiology and progression have mainly focused on populations of European origin. The limitations in clinicopathological and genetic data, as well as the reduced availability of biospecimens from diverse populations, contribute to the knowledge gap and have the potential to widen cancer health disparities. In this review, we summarise reported disparities and associated factors in the United States of America (USA) for the most common cancers (breast, prostate, lung and colon), and for a subset of other cancers that highlight the complexity of disparities (gastric, liver, pancreas and leukaemia). We focus on populations commonly identified and referred to as racial/ethnic minorities in the USA—African Americans/Blacks, American Indians and Alaska Natives, Asians, Native Hawaiians/other Pacific Islanders and Hispanics/Latinos. We conclude that even though substantial progress has been made in understanding the factors underlying cancer health disparities, marked inequities persist. Additional efforts are needed to include participants from diverse populations in the research of cancer aetiology, biology and treatment. Furthermore, to eliminate cancer health disparities, it will be necessary to facilitate access to, and utilisation of, health services to all individuals, and to address structural inequities, including racism, that disproportionally affect racial/ethnic minorities in the USA.

In this placebo-controlled trial involving patients with recently diagnosed adenomas, daily supplementation with vitamin D 3 (1000 IU), calcium (1200 mg), or both did not reduce the risk of recurrent colorectal adenomas over 3 to 5 years. Vitamin D, an essential nutrient that is important for bone mineralization and calcium homeostasis, 1 also has effects beyond bone and calcium. Many studies have shown it to be antineoplastic, particularly in the colorectum. In in vitro studies, vitamin D and its analogues have been shown to inhibit proliferation, induce differentiation, inhibit angiogenesis, and promote apoptosis in epithelial tissues. 2 , 3 High vitamin D intake inhibits experimental carcinogenesis, 2 , 3 even in animals that are vitamin D–replete. 4 Observational studies of vitamin D intake 5 – 7 and serum levels of 25-hydroxyvitamin D 8 – 10 have shown inverse associations between these measures and the risk of colorectal . . .

Constipation, a low fiber diet, sedentary lifestyle and gravidity are commonly assumed to increase the risk of hemorrhoids. However, evidence regarding these factors is limited. We examined the association between commonly cited risk factors and the prevalence of hemorrhoids. We performed a cross sectional study of participants who underwent a colonoscopy in a colorectal adenoma prevention trial and who had a detailed assessment of bowel habits, diet and activity. The presence of hemorrhoids was extracted from the subjects' colonoscopy reports. We used logistic regression to estimate odds ratios and 95% confidence intervals while adjusting for age and sex. The study included 2,813 participants. Of these, 1,074 had hemorrhoids recorded. Constipation was associated with an increased prevalence of hemorrhoids (OR 1.43, 95% CI 1.11, 1.86). Of the fiber subtypes, high grain fiber intake was associated with a reduced risk (OR for quartile 4 versus quartile 1 = 0.78, 95% CI 0.62, 0.98). We found no association when comparing gravid and nulligravida women (OR 0.93, 95% CI 0.62-1.40). Sedentary behavior was associated with a reduced risk (OR 0.80, 95% CI 0.65-0.98), but not physical activity (OR 0.83, 95% CI 0.66-1.03). Neither being overweight nor obese was associated with the presence of hemorrhoids (OR 0.89, 95% CI 0.72-1.09 and OR 0.86, 95% CI 0.70-1.06). Constipation is associated with an increased risk of hemorrhoids. Gravidity and physical activity do not appear to be associated. High grain fiber intake and sedentary behavior are associated with a decreased risk of hemorrhoids.

Preterm birth, defined as birth at <37 weeks of gestation, is the leading cause of neonatal death globally and the second leading cause of infant mortality in the United States. There is mounting evidence that COVID-19 infection during pregnancy is associated with an increased risk of preterm birth; however, data remain limited by trimester of infection. The ability to study COVID-19 infection during the earlier stages of pregnancy has been limited by available sources of data. The objective of this study was to use self-reports in large-scale social media data to assess the association between the trimester of COVID-19 infection and preterm birth. In this retrospective cohort study, we used natural language processing and machine learning, followed by manual validation, to identify self-reports of pregnancy on Twitter and to search these users' collection of publicly available tweets for self-reports of COVID-19 infection during pregnancy and, subsequently, a preterm birth or term birth outcome. Among the users who reported their pregnancy on Twitter, we also identified a 1:1 age-matched control group, consisting of users with a due date before January 1, 2020-that is, without COVID-19 infection during pregnancy. We calculated the odds ratios (ORs) with 95% CIs to compare the frequency of preterm birth for pregnancies with and without COVID-19 infection and by the timing of infection: first trimester (1-13 weeks), second trimester (14-27 weeks), or third trimester (28-36 weeks). Through August 2022, we identified 298 Twitter users who reported COVID-19 infection during pregnancy, a preterm birth or term birth outcome, and maternal age: 94 (31.5%) with first-trimester infection, 110 (36.9%) with second-trimester infection, and 95 (31.9%) with third-trimester infection. In total, 26 (8.8%) of these 298 users reported preterm birth: 8 (8.5%) with first-trimester infection, 7 (6.4%) with second-trimester infection, and 12 (12.6%) with third-trimester infection. In the 1:1 age-matched control group, 13 (4.4%) of the 298 users reported preterm birth. Overall, the odds of preterm birth were significantly higher for pregnancies with COVID-19 infection compared to those without (OR 2.08, 95% CI 1.06-4.28; P=.046). In particular, the odds of preterm birth were significantly higher for pregnancies with COVID-19 infection during the third trimester (OR 3.16, 95% CI 1.36-7.29; P=.007). The odds of preterm birth were not significantly higher for pregnancies with COVID-19 infection during the first trimester (OR 2.05, 95% CI 0.78-5.08; P=.12) or second trimester (OR 1.50, 95% CI 0.54-3.82; P=.44) compared to those without infection. Based on self-reports in large-scale social media data, the results of our study suggest that COVID-19 infection particularly during the third trimester is associated with higher odds of preterm birth.

This study examines the value of risk stratification by documented diagnosis of diabetes and objectively measured height and weight (BMI) in COVID-19 severity and mortality in a large sample of patients in an urban hospital located in Southern California. Data from a retrospective cohort study of COVID-19 patients treated at Cedars-Sinai Medical Center between March 8, 2020, and January 25, 2021, was analyzed. Sociodemographic characteristics and pre-existing conditions were extracted from electronic medical records. Univariable and multivariable logistic regression models identified associated risk factors, and a regression causal mediation analysis examined the role of diabetes in the association between obesity and illness severity. All analyses were stratified by age (<65 and ≥65). Among individuals <65yo, diabetes accounted for 19-30% of the associations between obesity and COVID-19 illness severity. Among patients ≥65yo, having a BMI <18.5 was a risk factor for mortality regardless of diabetes history. Our findings have clinical implications in documenting which patients may be at elevated risk for adverse outcomes. More in-depth prospective studies are needed to capture how glycemic regulation may influence prognosis.

Background Gallbladder disease (GBD) is a highly prevalent condition; however, little is known about potential differences in risk factors by sex and ethnicity/race. Our aim was to evaluate dietary, reproductive and obesity-related factors and GBD in multiethnic populations. Methods We performed a prospective analysis from the Multiethnic Cohort study who self-identified as non-Hispanic White ( n  = 32,103), African American ( n  = 30,209), Japanese ( n  = 35,987), Native Hawaiian ( n  = 6942) and Latino ( n  = 39,168). GBD cases were identified using Medicare and California hospital discharge files (1993–2012) and self-completed questionnaires. We used exposure information on the baseline questionnaire to identify exposures of interest. Associations were estimated by hazard ratios and 95% confidence intervals using Cox models adjusted for confounders. Result After a median 10.7 years of follow-up, there were 13,437 GBD cases. BMI over 25 kg/m 2 , diabetes, past and current smoking, red meat consumption, saturated fat and cholesterol were significant risk factors across ethnic/racial populations (p-trends < 0.01). Protective factors included vigorous physical activity, alcohol use, fruits, vegetables and foods rich in dietary fiber (p-trends < 0.01). Carbohydrates were inversely associated with GBD risk only among women and Latinos born in South America/Mexico (p-trend < 0.003). Parity was a significant risk factor among women; post-menopausal hormones use was only associated with an increased risk among White women (estrogen-only: HR = 1.24; 95% CI = 1.07–1.43 and estrogen + progesterone: HR = 1.23; 95% CI = 1.06–1.42). Conclusion Overall, dietary, reproductive and obesity-related factors are strong risk factors for GBD affecting men and women of different ethnicities/races; however some risk factors appear stronger in women and certain ethnic groups.

Adenomas and serrated lesions represent heterogeneous sets of early precursors in the colorectum with varying malignant potential. They are often distinguished by their histopathologic differences, but little is known about potential differences in regulation of epithelial proliferation and apoptosis. We conducted a protein expression analysis using tissue microarrays of 625 colorectal adenomas and 142 serrated lesions to determine potential differences in regulation of epithelial proliferation and apoptosis. We quantitated proliferation with Ki-67; apoptosis with activated caspase-3 (CASP3); up- and down-regulators of proliferation with cyclin D1, p16INK2, and p21Cip1; and apoptosis regulators with BAX, BCL2, and survivin. Linear mixed effects models and circos diagrams were used to determine relationships among expression and lesion characteristics. Adenomas had a significantly higher CASP-3 labeling index (LI) than serrated lesions, resulting in a lower net growth ratio (Ki-67 LI/activated CASP-3 LI, p-value<0.0001). Cyclin D1 LI, p16 LI and p21 LI were lower in adenomas compared to serrated lesions, while expression of both BCL2 and BAX were higher (p <0.001). Among adenomas, cyclin D1 LI and p16 LI levels increased with greater villous component, and the highest BAX expression was detected in adenomas larger than 2 cm (both p<0.0001). Right-sided adenomas had higher CASP3 LI than left colorectal adenomas (p = 0.008). Significant differences in cyclin D1 LI, p21 LI and survivin LI were also observed across histopathologic subtypes of serrated lesions. Our findings demonstrate different patterns of regulatory protein expression in adenomas than serrated lesions, especially involving apoptosis. ClinicalTrials.gov Identifier: NCT00272324.

Background Bladder cancer (BCa) is a lethal cancer, but early-detection offers an opportunity to improve prognosis. Our objective was to develop a urine-based multi-marker panel for BCa detection across multiple longitudinal cohort studies in a nested case-control study. Methods Longitudinal cohorts included healthy participants enrolled in the Southern Community Cohort Study (SCCS), Singapore Chinese Health Study (SCHS), Shanghai Women/Men Health Study (SWMHS), and Multiethnic Cohort (MEC). We measured the levels of 10 protein biomarkers (A1AT, ANG, APOE, CA9, IL8, MMP9, MMP10, PAI1, SDC1, and VEGF) in spot-voided urine samples using the multiplex immunoassay Oncuria. Single urine specimens collected from 274 participants who would go on to develop BCa in the ensuing 3‒60 months (i.e., cases) were age/sex-matched to 274 cancer-free controls. We used generalized estimating equation models, logistic regression analysis, and random forest algorithms to analyze the data. Results Differences in the individual biomarker levels between cases and controls were noted for ANG at 12 months ( p  = 0.046), APOE at 12 months ( p  < 0.001), MMP10 at 12 months ( p  = 0.009), PAI1 at 12 months ( p  = 0.005), SDC1 at 12 months ( p  = 0.003), 48 months ( p  = 0.029) and 60 months ( p  = 0.002), and VEGF at 12 months ( p  < 0.001). Lastly, the best preliminary model to predict subsequent BCa was IL8, CA9, PAI1, APOE and clinical features which had an AUC of 0.98, accuracy of 0.94 with a sensitivity of 0.88 and specificity of 1.00. Conclusions Additional testing is needed; however preliminary results demonstrate that a multiplex immunoassay may be able to facilitate the early detection of BCa in at-risk patients. Identification of BCa at an early stage may lead to improved patient outcomes. Prevention relevance Using large multinational patient populations, we tested the performance of the Oncuria multiplex assay to accurately predict the risk of developing bladder cancer by simultaneously analyzing the concentrations of 10 protein biomarkers in urine samples.