Assessing Disparities in the Prevalence of Atopic Comorbidities Among Food-Allergic Children.

BACKGROUND: Previous studies have reported that Black children with food allergy (FA) have higher risk of atopic comorbidities than White children. OBJECTIVE: Our study sought to understand if disparities in the prevalence of atopic comorbidities among children with FA are driven by individual and community-level socioeconomic status (SES). METHODS: We analyzed data from a prospective, multicenter cohort investigating the natural history of pediatric atopy: the Food Allergy Outcomes Related to White and African American Racial Differences (FORWARD) study. A validated, multicomponent area deprivation index (ADI) percentile score was tabulated by the census block group for each subject's home address. The association of ADI with atopic comorbidities in FA was assessed via multivariable regression analysis. RESULTS: Of the 700 children in this study, the mean ADI was 37.7 (95% confidence interval: 35.6-39.7). The mean ADI was higher in children with asthma (43.3) compared with those without asthma (31.8), which remained significant after adjusting for race (P < .0001). Children with allergic rhinitis (AR) had a higher mean ADI (39.1) compared with those without (33.4) (P = .008). ADI was associated with secondhand smoking, parents' education, and household income. Black children had a higher risk for asthma after adjusting for ADI and SES-related factors. CONCLUSION: The independent association of ADI with asthma and AR, regardless of race, suggests a role of neighborhood-level socioeconomic deprivation in the development of these conditions among children with FA. Black children with FA remained at higher risk for asthma after adjusting for SES-related variables, which can indicate an independent risk for asthma in these children.

miR-335-5p Targets SDC1 to Regulate the Progression of Breast Cancer.

The objective of the study was to explore the role of SDC1 in breast cancer cells. Our study also investigated the regulatory relationship between SDC1 and the microRNA (miRNA) miR-335-5p as well as the impact of these two genes on the progression of breast cancer. Bioinformatic approaches were employed to analyze the differentially expressed messenger RNAs (mRNAs) and miRNAs (DE-mRNAs and DE-miRNAs) in breast cancer tissue. Then mRNA SC1 was obtained. Differentially downregulated mRNAs were intersected with target miRNAs predicted by databases, and miR-335-5p was determined as the study object. Quantitative reverse transcription polymerase chain reaction was applied to assess the expressions of SDC1 and miR-335-5p in each cell line. Next, Western blot assay was conducted to detect the protein level of SDC1 and dual-luciferase assay was performed to verify the binding relationship between miR-335-5p and SDC1. Finally, we conducted methyl thiazolyl tetrazolium (MTT), colony formation, and Transwell assays and flow cytometry to further investigate the impacts of SDC1 and miR-335-5p on the progression of breast cancer. SDC1 was significantly highly expressed while miR-335-5p was remarkably lowly expressed in human breast cancer. Silencing SDC1 in breast cancer blocked the proliferation, migration and invasion of the cells. In breast cancer, SDC1 was a target gene of miR-335-5p and silencing miR-335-5p notably increased SDC1 expression. Compared with the silence of miR-335-5p, simultaneous silences of miR-335-5p and SDC1 significantly reduced the proliferative, migratory and invasive abilities of breast cancer cells. The result revealed the interaction between miR-335-5p and SDC1 in the progression of breast cancer, which may contribute to the treatments for this cancer.

CD8+ T Lymphocyte Coexpression Genes Correlate with Immune Microenvironment and Overall Survival in Breast Cancer.

PURPOSE: To identify CD8+ T lymphocyte-related coexpressed genes that increase CD8+ T lymphocyte proportions in breast cancer and to elucidate the underlying mechanisms among relevant genes in the tumor microenvironment. METHOD: We obtained breast cancer expression matrix data and patient phenotype following information from TCGA-BRCA FPKM. Tumor purity, immune score, stromal score, and estimate score were calculated using the estimate package in R. The CD8+ T lymphocyte proportions in each breast carcinoma sample were estimated using the CIBERSORT algorithm. The samples with p < 0.05 were considered to be significant and were taken into the weighted gene coexpression network analysis. Based on the CD8+ T lymphocyte proportion and tumor purity, we generated CD8+ T lymphocyte coexpression networks and selected the most CD8+ T lymphocyte-related module as our interested coexpression modules. We constructed a CD8+ T cell model based on the least absolute shrinkage and selection operator method (LASSO) regression model and robust model and evaluate the prediction ability in different subgroups. RESULTS: A breast carcinoma CD8+ T lymphocyte proportion coexpression yellow module was determined. The coexpression genes in the yellow module were determined to increase the CD8+ T lymphocyte proportion levels in breast cancer patients. The yellow module was significantly enriched in the antigen presentation process, cellular response to interferon-gamma, and leukocyte proliferation. Subsequently, we generated CD8+ T cell-related genes lasso regression risk model and robust model, and eight genes were taken into the risk model. The risk score showed significant prognostic ability in various subgroups. Expression levels of proteins, encoded by CD74, were lower in the breast carcinoma samples than in normal tissue, suggesting expression differences at both the mRNA and the protein levels. CONCLUSION: These eight CD8+ T lymphocyte proportion coexpression genes increase CD8+ T lymphocyte in breast cancer by an antigen presentation process. The mechanism might suggest new pathways to improve outcomes in patients who do not benefit from immune therapy.

Association Between Cancer and Utilization of Traditional Chinese Medicine in U.S. Chinese Women: Findings From the PINE Study.

Objective: To examine U.S. Chinese older women and the association between their cancer screening behaviors and self-reported cancers with Traditional Chinese Medicine (TCM) use across sociodemographic characteristics. Method: Through the Population Study of Chinese Elderly in Chicago (PINE), 1,830 Chinese older women self-reported history of cancer screening, presence of women's cancers, and TCM use according to type. Analyses were performed using multivariate regression models. Results: Chinese older women who underwent breast cancer screening are more likely to use herbal TCM (rate ratio [RR] = 1.15, 95% confidence interval [CI] = [1.03, 1.29]), acupuncture (RR = 1.62, CI = [1.21, 2.15]), massage therapy (RR = 2.05, CI = [1.46, 2.88]), and tai chi (RR = 1.86, CI = [1.28, 2.69]). Those who had cervical cancer screening are more likely to use herbal TCM (RR = 1.32, CI = [1.17, 1.48]), acupuncture (RR = 1.66, CI = [1.27, 2.18]), massage therapy (RR = 1.61, CI = [1.17, 2.21]), tai chi (RR = 1.69, CI = [1.19, 2.40]), and other forms of TCM (RR = 1.36, CI = [1.04, 1.79]). Those with cervical cancer are less likely to use herbal TCM (RR = 0.42, CI = [0.19, 0.93]). Conclusion: Contrary to previous studies, our results suggest that U.S. Chinese older women who have engaged in cancer screening use TCM while those with self-reported cancer did not use TCM at a higher rate. This warrants further research on TCM utilization to identify reasons of use in this population and encourage patient-centered care.

Extrinsic Calcitonin Gene-Related Peptide Inhibits Hyperoxia-Induced Alveolar Epithelial Type II Cells Apoptosis, Oxidative Stress, and Reactive Oxygen Species (ROS) Production by Enhancing Notch 1 and Homocysteine-Induced Endoplasmic Reticulum Protein (HERP) Expression.

BACKGROUND Lung alveolar epithelial type II cells (AEC II) are the most important stem cells in lung tissues, which are critical for wound repair of bronchopulmonary dysplasia (BPD). This study investigated the effects of calcitonin gene-related peptide (CGRP) on AEC II cells exposed to hyperoxia. MATERIAL AND METHODS Neonatal rat AEC II cells were isolated and identified by detecting surfactant protein C (SP-C). Three small interfering RNAs targeting Notch 1 were synthesized and transfected into AEC II. A hyperoxia-exposed AEC II cell injury model was established and was divided into 8 groups. MDA levels and SOD activity were examined using lipid peroxidation assay kits. Apoptosis and reactive oxygen species (ROS) production were evaluated using flow cytometry. Notch 1 mRNA expression was examined using RT-PCR. Homocysteine-induced endoplasmic reticulum protein (HERP) was examined using Western blot analysis. RESULTS CGRP treatment significantly enhanced MDA levels and decreased SOD activity compared to hyperoxia-treated AEC II cells (P<0.05). CGRP treatment significantly inhibited hyperoxia-induced AEC II cell apoptosis, and significantly suppressed hyperoxia-induced ROS production compared to hyperoxia-treated AEC II cells (P<0.05) either undergoing g secretase inhibitor or Notch RNA interference. CGRP significantly triggered Notch 1 mRNA expression and significantly enhanced HERP expression compared to hyperoxia-treated AEC II cells (P<0.05) either undergoing g secretase inhibitor or Notch RNA interference. CONCLUSIONS In AEC II cells, extrinsic peptide CGRP suppressed hyperoxia-induced apoptosis, oxidative stress, and ROS production, which may be triggered by Notch 1 and HERP signaling pathway.