Black, Male, African Immigrants’ Perceptions of Colorectal Cancer Screening in Baltimore, Maryland

Colorectal cancer (CRC) represents a public health issue that may be prevented using the screening strategy. Black people in Africa represent the population with the lowest risk for CRC. However, in Africa as well as the United States, Black people participate the least in CRC screening. Little is known about the perceptions of CRC and CRC screening in the Black, male, African immigrants residing in Baltimore, Maryland. The low participation in CRC screening in this population was the problem addressed by this dissertation. The purpose of this qualitative study was to explore and describe Black, male, African immigrants’ experience with CRC screening in Baltimore. Two research questions focused on understanding the meaning of CRC and describing the experience with CRC screening in this population. The health belief model served as a conceptual framework. The descriptive phenomenological approach was used using semistructured interviews with 8 participants. Data collected from eligible participants in the population of interest were transcribed and analyzed thematically using Colaizzi’s 7-step strategy. Three key findings from this study included the limited knowledge of CRC, the limited perceived barriers to CRC screening, and the high level of trust in health care providers of the participants. Fear of results and negative cultural beliefs about CRC screening were no barriers to the screening. The recommendations for future studies include the consideration of the female population and the inclusion of participants resident in Baltimore for fewer than 6 months. The implications for a positive social change include the improvement of CRC awareness and physician-patient conversations, as well as the development of policies that can facilitate access to health care

Short Telomeres Compromise β-Cell Signaling and Survival

The genetic factors that underlie the increasing incidence of diabetes with age are poorly understood. We examined whether telomere length, which is inherited and known to shorten with age, plays a role in the age-dependent increased incidence of diabetes. We show that in mice with short telomeres, insulin secretion is impaired and leads to glucose intolerance despite the presence of an intact β-cell mass. In ex vivo studies, short telomeres induced cell-autonomous defects in β-cells including reduced mitochondrial membrane hyperpolarization and Ca2+ influx which limited insulin release. To examine the mechanism, we looked for evidence of apoptosis but found no baseline increase in β-cells with short telomeres. However, there was evidence of all the hallmarks of senescence including slower proliferation of β-cells and accumulation of p16INK4a. Specifically, we identified gene expression changes in pathways which are essential for Ca2+-mediated exocytosis. We also show that telomere length is additive to the damaging effect of endoplasmic reticulum stress which occurs in the late stages of type 2 diabetes. This additive effect manifests as more severe hyperglycemia in Akita mice with short telomeres which had a profound loss of β-cell mass and increased β-cell apoptosis. Our data indicate that short telomeres can affect β-cell metabolism even in the presence of intact β-cell number, thus identifying a novel mechanism of telomere-mediated disease. They implicate telomere length as a determinant of β-cell function and diabetes pathogenesis

BglJ-RcsB Heterodimers Relieve Repression of the Escherichia coli bgl Operon by H-NS

RcsB is the response regulator of the complex Rcs two-component system, which senses perturbations in the outer membrane and peptidoglycan layer. BglJ is a transcriptional regulator whose constitutive expression causes activation of the H-NS- and StpA-repressed bgl (aryl-beta, D-glucoside) operon in Escherichia coli. RcsB and BglJ both belong to the LuxR-type family of transcriptional regulators with a characteristic C-terminal DNA-binding domain. Here, we show that BglJ and RcsB interact and form heterodimers that presumably bind upstream of the bgl promoter, as suggested by mutation of a sequence motif related to the consensus sequence for RcsA-RcsB heterodimers. Heterodimerization of BglJ-RcsB and relief of H-NS-mediated repression of bgl by BglJ-RcsB are apparently independent of RcsB phosphorylation. In addition, we show that LeuO, a pleiotropic LysR-type transcriptional regulator, likewise binds to the bgl upstream regulatory region and relieves repression of bgl independently of BglJ-RcsB. Thus, LeuO can affect bgl directly, as shown here, and indirectly by activating the H-NS-repressed yjjQ-bglJ operon, as shown previously. Taken together, heterodimer formation of RcsB and BglJ expands the role of the Rcs two-component system and the network of regulators affecting the bgl promoter