Gender disparities in symptomology of COVID-19 among adults in Arkansas.

Only a few studies and reports assessing the natural history and symptomatology for COVID-19 by gender have been reported in literature to date. Thus, the objective of this study was to examine patterns in symptomology of COVID-19 by gender among a diverse adult population in Arkansas. Data on COVID-19 symptoms was collected at day of testing, 7th day and 14th day among participants at UAMS mobile testing units throughout the state of Arkansas. Diagnosis for SARS-CoV-2 infection was confirmed via nasopharyngeal swab and RT-PCR methods. Data analysis was conducted using Chi-square test and Poisson regression to assess the differences in characteristics by gender. A total of 60,648 community members and patients of Arkansas received RT-PCR testing. Among adults testing positive, we observed a statistically significant difference for fever (p < 0.001) and chills (p = 0.04). Males were more likely to report having a fever (22.6% vs. 17.1%; p < 0.001) and chills (14.9% vs. 12.6%; p = 0.04) compared to females. Among adults testing negative, females were more likely to report each symptom than males. To conclude, we observed a greater prevalence of certain symptoms such as fever and chills among men testing positive for COVID-19, compared to women during the time of testing. These differences elucidate the important issue of rapidly emerging health disparities during the COVID-19 pandemic.

Intellectual disabilities and autism among children with congenital heart defects, Western Australia, 1983-2010.

BACKGROUND: Children with congenital heart defects (CHDs) are at higher risk of developing an intellectual disability. However, severity of intellectual disabilities among this group of children are largely unknown. Our objective was to determine the risk of intellectual disability (ID), ID severity, and autism among children with CHDs. METHODS: We conducted a retrospective cohort study of singleton live births in Western Australia (n = 20,592) between 1983 and 2010. Children with CHDs were identified from the Western Australian Register for Developmental Anomalies (n = 6563) and infants without CHDs were randomly selected from state birth records (n = 14,029). Children diagnosed with ID before 18 years were identified by linkage to statewide Intellectual Disability Exploring Answers database. Odds ratios (OR) and 95% confidence intervals (CI) were calculated from logistic regression models for all CHDs combined and by CHD severity adjusting for potential confounders. RESULTS: Of 20,592 children, 466 (7.1%) with CHDs and 187 (1.3%) without CHDs had an ID. Compared to children without CHDs, children with any CHD had 5.26 times (95% CI 4.42, 6.26) the odds of having an ID and 4.76 times (95% CI 3.98, 5.70) the odds of having mild/moderate ID. Children with any CHD had 1.76 times the odds of having autism (95% CI 1.07, 2.88), and 3.27 times the odds of having an unknown cause of ID (95% CI 2.65, 4.05) compared to children without CHD. The risk of having autism (aOR 3.23, 95% CI 1.11, 9.38), and unknown cause of ID (aOR 3.45, 95% CI 2.09, 5.70) was greatest for children with mild CHD. CONCLUSIONS: Children with CHDs were more likely to have an ID or autism. Future research should elucidate underlying etiology of ID in children with CHDs.

Analysis of COVID-19 Pandemic on Supplement Usage and Its Combination with Self-Medication within the State of Arkansas.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a novel coronavirus responsible for the COVID-19 pandemic that can lead to severe respiratory distress requiring hospitalization and can be fatal. Media have reported that various dietary supplements (DS) or their combination with different medications can prevent infection or decrease disease severity. Here, we analyzed data collected from 15,830 patient follow-up telephone interviews from the University of Arkansas for Medical Sciences COVID-19 testing sites from March 15 to August 1, 2020. Within the REDCap database, we recorded patient demographics and DS and medication use. In total, data on DS and medication use was available for 8,150 study participants, of whom 21.9% and 4.1% reported using DS or medications, respectively, to either prevent or treat COVID-19. The majority of respondents were female (64%) and non-Hispanic whites (44.5%). Most individuals (64.5%) who took DS were younger than 50 years of age. Products such as vitamin C (1,013, 33.2%), multivitamins (722, 23.6%), and vitamin D (294, 9.6%) were the most commonly used DS among the responders. Analysis of the DS use and symptom scores association did not provide a strong evidence of beneficial health effects of DS. The results of this study demonstrate that a significantly higher proportion of study participants considered usage of DS to mitigate or prevent COVID-19-related symptoms compared to those who preferred medications. However, lack of observable health benefits associated with ingestion of DS suggests that more rigorous research is needed to substantiate the label claims.

Prevalence and Clustering of Congenital Heart Defects Among Boys With Hypospadias.

Importance: Hypospadias is a common birth defect of the male urinary tract that may be isolated or may co-occur with other structural malformations, including congenital heart defects (CHDs). The risk for co-occurring CHDs among boys with hypospadias remains unknown, which limits screening and genetic testing strategies. Objective: To characterize the risk of major CHDs among boys born with hypospadias. Design, Setting, and Participants: This retrospective cohort study used data from population-based birth defect surveillance programs on all male infants born in 11 US states from January 1, 1995, to December 31, 2014. Statistical analysis was performed from September 2, 2020, to March 25, 2022. Exposure: Hypospadias. Main Outcomes and Measures: Demographic and diagnostic data were obtained from 2 active state-based birth defect surveillance programs for primary analyses, the Texas Birth Defects Registry and the Arkansas Reproductive Health Monitoring System, with validation among 9 additional states in the National Birth Defects Prevention Network (NBDPN). Birth defect diagnoses were identified using the British Pediatric Association coding for hypospadias (exposure) and major CHDs (primary outcomes). Maternal covariates and birth year were also abstracted from the vital records. Poisson regression was used to estimate adjusted prevalence ratios and 95% CIs for major CHDs within Texas and Arkansas and combined using inverse variance-weighted meta-analysis. Findings were validated using the NBDPN. Results: Among 3.7 million pregnancies in Texas and Arkansas, 1485 boys had hypospadias and a co-occurring CHD. Boys with hypospadias were 5.8 times (95% CI, 5.5-6.1) more likely to have a co-occurring CHD compared with boys without hypospadias. Associations were observed for every specific CHD analyzed among boys with hypospadias, occurred outside of chromosomal anomalies, and were validated in the NBDPN. An estimated 7.024% (95% CI, 7.020%-7.028%) of boys with hypospadias in Texas and 5.503% (95% CI, 5.495%-5.511%) of boys with hypospadias in Arkansas have a co-occurring CHD. In addition, hypospadias severity and maternal race and ethnicity were independently associated with the likelihood for hypospadias to co-occur with a CHD; boys in Texas with third-degree (ie, more severe) hypospadias were 2.7 times (95% CI, 2.2-3.4) more likely than boys with first-degree hypospadias to have a co-occurring CHD, with consistent estimates in Arkansas (odds ratio, 2.7; 95% CI, 1.4-5.3), and boys with hypospadias born to Hispanic mothers in Texas were 1.5 times (95% CI, 1.3-1.8) more likely to have a co-occurring CHD than boys with hypospadias born to non-Hispanic White mothers. Conclusions and Relevance: In this cohort study, boys with hypospadias had a higher prevalence of CHDs than boys without hypospadias. These findings support the need for consideration of additional CHD screening programs for boys born with hypospadias.

Racial disparities in symptomatology and outcomes of COVID-19 among adults of Arkansas.

Few reports have suggested that non-Hispanic (NH) blacks may present with different symptoms for COVID-19 than NH-whites. The objective of this study was to investigate patterns in symptomatology and COVID-19 outcomes by race/ethnicity among adults in Arkansas. Data on COVID-19 symptoms were collected on day of testing, 7th and 14th day among participants at UAMS mobile testing units throughout the state of Arkansas. Diagnosis for SARS-CoV-2 infection was confirmed via nasopharyngeal swab and RT-PCR methods. Data analysis was conducted using Chi-square test and Poisson regression to assess the differences in characteristics by race/ethnicity. A total of 60,648 individuals were RT-PCR tested from March 29, 2020 through October 7, 2020. Among adults testing positive, except shortness of breath, Hispanics were more likely to report all symptoms than NH-whites or NH-blacks. NH-whites were more likely to report fever (19.6% vs. 16.6%), cough (27.5% vs. 26.1%), shortness of breath (13.6% vs. 9.6%), sore throat (16.7% vs. 10.7%), chills (12.5% vs. 11.8%), muscle pain (15.6% vs. 12.4%), and headache (20.3% vs. 17.8%). NH-blacks were more likely to report loss of taste/smell (10.9% vs. 10.6%). To conclude, we found differences in COVID-19 symptoms by race/ethnicity, with NH-blacks and Hispanics more often affected with specific or all symptoms, compared to NH-whites. Due to the cross-sectional study design, these findings do not necessarily reflect biological differences by race/ethnicity; however, they suggest that certain race/ethnicities may have underlying differences in health status that impact COVID-19 outcomes.

Erratum: Electronic cigarette use and its association with asthma, chronic obstructive pulmonary disease (COPD) and asthma-COPD overlap syndrome among never cigarette smokers.

[This corrects the article DOI: 10.18332/tid/142579.].

Electronic cigarette use and its association with asthma, chronic obstructive pulmonary disease (COPD) and asthma-COPD overlap syndrome among never cigarette smokers.

INTRODUCTION: Although smoking is a strong risk factor for lung diseases including asthma, COPD, and asthma-COPD overlap syndrome (ACOS), studies are needed to examine the association between e-cigarettes and asthma, COPD, and ACOS. This study evaluated the association between e-cigarette use and self-reported diagnosis of asthma, COPD, and ACOS using a large nationally representative sample of adults aged ≥18 years in the United States. METHODS: Cross-sectional data from the Behavioral Risk Factor Surveillance System (BRFSS) from 2016 to 2018 were used to examine self-reported information on current e-cigarette use, demographic variables, and asthma and COPD status among never cigarette smokers (n=8736). Asthma and COPD were measured by self-reported diagnosis, and respondents who reported having both diagnoses were then classified as having ACOS. Of the 469077 never cigarette smokers, 4368 non-e-cigarette users were 1:1 propensity score-matched to e-cigarette users on age, sex, race/ethnicity and education level. We used multinomial logistic regression to examine association between current e-cigarette use and self-report asthma, COPD, and ACOS while controlling for marital status and employment in addition to matching variables. RESULTS: Compared with never e-cigarette users, e-cigarette users had increased odds of self-reported ACOS (OR=2.27; 95% CI: 2.23-2.31), asthma (OR=1.26; 95% CI: 1.25-1.27) and COPD (OR=1.44; 95% CI: 1.42-1.46). CONCLUSIONS: Our findings suggest that e-cigarette use is associated with an increased odds of self-reported asthma, COPD, and ACOS among never combustible cigarette smokers. BRFSS provides cross-sectional survey data, therefore a causal relationship between e-cigarette use and the three lung diseases cannot be evaluated. Future longitudinal studies are needed to validate these findings.

Electronic cigarette use and its association with asthma, chronic obstructive pulmonary disease (COPD) and asthma-COPD overlap syndrome among never cigarette smokers.

INTRODUCTION: Although smoking is a strong risk factor for lung diseases including asthma, COPD, and asthma-COPD overlap syndrome (ACOS), studies are needed to examine the association between e-cigarettes and asthma, COPD, and ACOS. This study evaluated the association between e-cigarette use and self-reported diagnosis of asthma, COPD, and ACOS using a large nationally representative sample of adults aged ≥18 years in the United States. METHODS: Cross-sectional data from the Behavioral Risk Factor Surveillance System (BRFSS) from 2016 to 2018 was used to examine self-reported information on current e-cigarette use, demographic variables, and asthma and COPD status among never cigarette smokers (n=8736). Asthma and COPD were measured by self-reported diagnosis, and respondents who reported having both diagnoses were then classified as having ACOS. Of the 46079 never cigarette smokers, 4368 non-e-cigarette smokers were 1:1 propensity score-matched to e-cigarette smokers on age, sex, race/ethnicity and education level. We used multinomial logistic regression to examine association between current e-cigarette use and self-report asthma, COPD, and ACOS while controlling for marital status and employment in addition to matching variables. RESULTS: Compared with never e-cigarette smokers, e-cigarette smokers had increased odds of self-reported ACOS (OR=2.27; 95% CI: 2.23-2.31), asthma (OR=1.26; 95% CI: 1.25-1.27) and COPD (OR=1.44; 95% CI: 1.42-1.46). CONCLUSIONS: Data from this large nationally representative sample suggest that e-cigarette use is associated with increased odds of self-reported asthma, COPD, and ACOS among never combustible cigarette smokers. The odds of ACOS were twice as high among e-cigarette users compared with never smokers of conventional cigarettes. The findings from this study suggest the need to further investigate the long-term and short-term health effects of e-cigarette use, since the age of those at risk in our study was 18-24 years.

Paternal genetic variants and risk of obstructive heart defects: A parent-of-origin approach.

Previous research on risk factors for obstructive heart defects (OHDs) focused on maternal and infant genetic variants, prenatal environmental exposures, and their potential interaction effects. Less is known about the role of paternal genetic variants or environmental exposures and risk of OHDs. We examined parent-of-origin effects in transmission of alleles in the folate, homocysteine, or transsulfuration pathway genes on OHD occurrence in offspring. We used data on 569 families of liveborn infants with OHDs born between October 1997 and August 2008 from the National Birth Defects Prevention Study to conduct a family-based case-only study. Maternal, paternal, and infant DNA were genotyped using an Illumina Golden Gate custom single nucleotide polymorphism (SNP) panel. Relative risks (RR), 95% confidence interval (CI), and likelihood ratio tests from log-linear models were used to estimate the parent-of-origin effect of 877 SNPs in 60 candidate genes in the folate, homocysteine, and transsulfuration pathways on the risk of OHDs. Bonferroni correction was applied for multiple testing. We identified 3 SNPs in the transsulfuration pathway and 1 SNP in the folate pathway that were statistically significant after Bonferroni correction. Among infants who inherited paternally-derived copies of the G allele for rs6812588 in the RFC1 gene, the G allele for rs1762430 in the MGMT gene, and the A allele for rs9296695 and rs4712023 in the GSTA3 gene, RRs for OHD were 0.11 (95% CI: 0.04, 0.29, P = 9.16x10-7), 0.30 (95% CI: 0.17, 0.53, P = 9.80x10-6), 0.34 (95% CI: 0.20, 0.57, P = 2.28x10-5), and 0.34 (95% CI: 0.20, 0.58, P = 3.77x10-5), respectively, compared to infants who inherited maternally-derived copies of the same alleles. We observed statistically significant decreased risk of OHDs among infants who inherited paternal gene variants involved in folate and transsulfuration pathways.

Genome-wide tracts of homozygosity and exome analyses reveal repetitive elements with Barrets esophagus/esophageal adenocarcinoma risk.

BACKGROUND: Barrett's esophagus (BE) is most commonly seen as the condition in which the normal squamous epithelium lining of the esophagus is replaced by goblet cells. Many studies show that BE is a predisposing factor for the development of esophageal adenocarcinoma (EAC), a particularly lethal cancer. The use of single nucleotide polymorphisms (SNPs) to map BE/EAC genes has previously provided insufficient genetic information to fully characterize the heterogeneous nature of the disease. We therefore hypothesize that rigorous interrogation of other types of genomic changes, e.g. tracts of homozygosity (TOH), repetitive elements, and insertion/deletions, may provide a comprehensive understanding of the development of BE/EAC. RESULTS: First, we used a case-control framework to identify TOHs by using SNPs and tested for association with BE/EAC. Second, we used a case only approach on a validation series of eight samples subjected to exome sequencing to identify repeat elements and insertion/deletions. Third, insertion/deletions and repeat elements identified in the exomes were then mapped onto genes in the significant TOH regions. Overall, 24 TOH regions were significantly differentially represented among cases, as compared to controls (adjusted-P = 0.002-0.039). Interestingly, four BE/EAC-associated genes within the TOH regions consistently showed insertions and deletions that overlapped across eight exomes. Predictive functional analysis identified NOTCH, WNT, and G-protein inflammation pathways that affect BE and EAC. CONCLUSIONS: The integration of common TOHs (cTOHs) with repetitive elements, insertions, and deletions within exomes can help functionally prioritize factors contributing to low to moderate penetrance predisposition to BE/EAC.

PARP1 Is Up-Regulated in Non-small Cell Lung Cancer Tissues in the Presence of the Cyanobacterial Toxin Microcystin.

Non-small cell lung cancer (NSCLC) is the major form of lung cancer, with adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC) being its major subtypes. Smoking alone cannot completely explain the lung cancer etiology. We hypothesize that altered lung microbiome and chronic inflammatory insults in lung tissues contribute to carcinogenesis. Here we explore the microbiome composition of LUAD samples, compared to LUSC and normal samples. Extraction of microbiome DNA in formalin-fixed, paraffin-embedded (FFPE) lung tumor and normal adjacent tissues was meticulously performed. The 16S rRNA product from extracted microbiota was subjected to microbiome amplicon sequencing. To assess the contribution of the host genome, CD36 expression levels were analyzed then integrated with altered NSCLC subtype-specific microbe sequence data. Surprisingly phylum Cyanobacteria was consistently observed in LUAD samples. Across the NSCLC subtypes, differential abundance across four phyla (Proteobacteria, Bacteroidetes, Actinobacteria, and Firmicutes) was identified based on the univariate analysis (p-value < 6.4e-4 to 3.2e-2). In silico metagenomic and pathway analyses show that presence of microcystin correlates with reduced CD36 and increased PARP1 levels. This was confirmed in microcystin challenged NSCLC (A427) cell lines and Cyanobacteria positive LUAD tissues. Controlling the influx of Cyanobacteria-like particles or microcystin and the inhibition of PARP1 can provide a potential targeted therapy and prevention of inflammation-associated lung carcinogenesis.