Ionizing radiation (IR)-induced intestinal damage is characterized by a loss of intestinal crypt cells, intestinal barrier disruption and translocation of intestinal microflora resulting in sepsis-mediated lethality. We have shown that mice lacking C/EBPδ display IR-induced intestinal and hematopoietic injury and lethality. The purpose of this study was to investigate whether increased IR-induced inflammatory, oxidative and nitrosative stress promote intestinal injury and sepsis-mediated lethality in Cebpd^−/− mice. We found that irradiated Cebpd^−/− mice show decreased villous height, crypt depth, crypt to villi ratio and expression of the proliferation marker, proliferating cell nuclear antigen, indicative of intestinal injury. Cebpd^−/− mice show increased expression of the pro-inflammatory cytokines (Il-6, Tnf-α) and chemokines (Cxcl1, Mcp-1, Mif-1α) and Nos2 in the intestinal tissues compared to Cebpd^+/+ mice after exposure to TBI. Cebpd^−/− mice show decreased GSH/GSSG ratio, increased S-nitrosoglutathione and 3-nitrotyrosine in the intestine indicative of basal oxidative and nitrosative stress, which was exacerbated by IR. Irradiated Cebpd-deficient mice showed upregulation of Claudin-2 that correlated with increased intestinal permeability, presence of plasma endotoxin and bacterial translocation to the liver. Overall these results uncover a novel role for C/EBPδ in protection against IR-induced intestinal injury by suppressing inflammation and nitrosative stress and underlying sepsis-induced lethality.

Timely receipt of colorectal cancer screening can reduce morbidity and mortality. This is the first known study to adopt Andersen's model of health services use to identify factors associated with colorectal cancer screening among U.S. adults. The data from National Health Interview Survey from 2019 was utilized to conduct the analyses. Multivariable logistic regression was used to separately analyze data from 7,503 age-eligible women and 6,486 age-eligible men. We found similar colorectal cancer screening levels among men (57.7%) and women (57.6%). Factors associated with higher screening odds in women were older age, married/cohabitating with a partner, Black race, >bachelor's degree, having a usual source of care, and personal cancer history. Factors associated with lower odds for women were American Indian/Alaska Native race, living in the United States for ≤10 years, ≤138% federal poverty level (FPL), uninsured or having Medicare, and in fair/poor health. For men, factors associated with higher screening odds were older age, homosexuality, married/cohabitating with a partner, Black race, >high school/general educational development education, having military insurance, having a usual source of care, and personal cancer history. Factors associated with lower odds for men were being a foreign-born U.S. resident, living in the South or Midwest, ≤138% FPL, and being uninsured or having other insurance. Despite lower screening rates in the past, Black adults show a significantly higher likelihood of colorectal cancer screening than White adults; yet, screening disparities remain in certain other groups. Colorectal cancer screening efforts should continue to target groups with lower screening rates to eliminate screening disparities.Significance: Timely receipt of colorectal cancer screening can reduce morbidity and mortality. Identification of populations and domains of factors associated with colorectal cancer screening receipt among men and women can help future interventions to alleviate impeding factors and target screening promotion efforts in populations not adherent with screening guidelines.

The purpose of this study was to describe the thoughts and feelings of individuals expressing concerns about the COVID-19 vaccine. A qualitative descriptive study was conducted in order to examine the thoughts and feelings of participants who are hesitant about the COVID-19 vaccine. Data were collected from 754 participants using an online instrument. Emergent themes included a lack of knowledge about the safety of the COVID-19 vaccine; concerns over the speed of development, testing, and approval of these vaccines; reluctance to be among the first vaccinated; concerns about the motivations of government actors, pharmaceutical companies, and others involved in producing the COVID-19 vaccine; and hesitancy about vaccines generally.

A cross-sectional survey design was used to assess Arkansas parents’/guardians’ intentions to vaccinate their child against COVID-19. Parents/guardians whose oldest child was age 0–11 years (n = 171) or 12–17 years (n = 198) were recruited between 12 July and 30 July 2021 through random digit dialing. Among parents/guardians with an age-eligible child, age 12–17, 19% reported their child had been vaccinated, and 34% reported they would have their child vaccinated right away. Among parents/guardians with a child aged 0–11, 33% of parents/guardians reported they would have their child vaccinated right away. Twenty-eight percent (28%) of parents/guardians whose oldest child was 12–17 and 26% of parents/guardians whose oldest child was 0–11 reported they would only have their child vaccinated if their school required it; otherwise, they would definitely not vaccinate them. For both groups, parents’/guardians’ education, COVID-19 vaccination status, and COVID-19 vaccine hesitancy were significantly associated with intentions to vaccinate their child. More than a third of parents/guardians whose child was eligible for vaccination at the time of the survey reported they intended to have them vaccinated right away; however, they had not vaccinated their child more than two months after approval. This finding raises questions about the remaining barriers constraining some parents/guardians from vaccinating their child.

Antiretrovirals have immensely increased the average life expectancy of HIV-positive patients. However, the incidence of QT interval prolongation and other arrhythmias has also increased. Pubmed and Google Scholar were searched for relevant literature published between 1990 and 2019. HIV-positive patients with high viral load, low CD4 count, chronic inflammation, and autonomic neuropathy can develop QT interval prolongation. Another factor prolonging QT interval includes exposure to the HIV transactivator protein, which inhibits hERG K (+) channels controlling IKr K (+) currents in cardiomyocytes. Protease inhibitors inhibiting the CYP3A4 enzyme can also lead to QT interval prolongation. QT interval prolongation can potentially be exacerbated by opioids, antipsychotics, antibiotics, and antifungals, the adjunct medications often used in HIV-positive patients. Hepatic insufficiency in seropositive patients on antiretrovirals may also increase the risk of QT interval prolongation. Baseline and follow-up EKG in the susceptible population is suggested.

Gamma-tocotrienol (GT3) confers protection against ionizing radiation (IR)-induced injury. However, the molecular targets that underlie the protective functions of GT3 are not yet known. We have reported that mice lacking CCAAT enhancer binding protein delta (Cebpd^−/−) display increased mortality to IR due to injury to the hematopoietic and intestinal tissues and that Cebpd protects from IR-induced oxidative stress and cell death. The purpose of this study was to investigate whether Cebpd mediates the radio protective functions of GT3. We found that GT3-treated Cebpd^−/− mice showed partial recovery of white blood cells compared to GT3-treated Cebpd^+/+ mice at 2 weeks post-IR. GT3-treated Cebpd^−/− mice showed an increased loss of intestinal crypt colonies, which correlated with increased expression of inflammatory cytokines and chemokines, increased levels of oxidized glutathione (GSSG), S-nitrosoglutathione (GSNO) and 3-nitrotyrosine (3-NT) after exposure to IR compared to GT3-treated Cebpd^+/+ mice. Cebpd is induced by IR as well as a combination of IR and GT3 in the intestine. Studies have shown that granulocyte-colony stimulating factor (G-CSF), mediates the radioprotective functions of GT3. Interestingly, we found that IR alone as well as the combination of IR and GT3 caused robust augmentation of plasma G-CSF in both Cebpd^+/+ and Cebpd^−/− mice. These results identify a novel role for Cebpd in GT3-mediated protection against IR-induced injury, in part via modulation of IR-induced inflammation and oxidative/nitrosative stress, which is independent of G-CSF.