Project description:This clinical trial studies disparities involving colorectal cancer prevention and screening in Black and underserved communities in the Phoenix metropolitan area. The Black community is disproportionately impacted by colorectal cancer, with the highest rate of any racial/ethnic group in the United States. There are complex reasons behind these disparities, largely related to socioeconomic factors and healthcare access. Providing access to free, home-based fecal immunochemical testing (FIT), colorectal screening education, and appropriate follow-up to predominantly Black community-based organizations and underserved communities may help to close this gap.
Project description:Renal transplantation is the preferred treatment of end stage renal disease, but allograft survival is limited by development of interstitial fibrosis and tubular atrophy in response to various stimuli. Much effort has been put into identifying new protein markers of fibrosis to support the diagnosis. In present work, we performed an in-depth quantitative proteomics analysis of allograft biopsies from 31 prevalent renal transplant patients and identified correlated the quantified proteins with the volume fraction of fibrosis as determined by a morphometric method. Linear regression analysis identified four proteins that were highly associated with the degree of interstitial fibrosis, namely Coagulation Factor XIII A chain (estimate 18.7, adjusted p<0.03), Uridine Phosphorylase 1 (estimate 19.4, adjusted p<0.001), Actin-related protein 2/3 subunit 2 (estimate 34.2, adjusted p<0.05) and Cytochrome C Oxidase Assembly Factor 6 homolog (estimate -44.9, adjusted p<0.002) even after multiple testing. Proteins that were negatively associated with fibrosis (p < 0.005) were primarily related to normal metabolic processes and respiration, whereas proteins that were positively associated with fibrosis (p < 0.005) were involved in catabolic processes, cytoskeleton organization and immune response. The identified proteins may be candidates for further validation with regards to renal fibrosis. The results support the notion that cytoskeleton organization and immune responses are prevalent processes in renal allograft fibrosis.
Project description:Diabetic kidney disease (DKD) appears heritable, suggesting genetic factors influence disease susceptibility. In our study, genes were mapped mediating early renal hypertrophic in response to diabetes. A survey of murine strains (N=15) was conducted to identify variation in kidney hypertrophy following diabetes induction. Mice with greater FVB/N and less C57BL/6 renal hypertrophy were crossed and diabetic F2 generation mice (n=534) were characterised. To confirm loci responsible for the renal hypertrophic response, diabetic congenic mice were generated by backcrossing FVB/N mice that conferred greater or C57BL/6 conferring lower risk into the reciprocal strain mice. Kidney weights of (FVB/N x C57BL/6) F2 diabetic mice were broadly distributed. Quantitative trait locus (QTL) analysis revealed that diabetic mice with kidney weights in the upper quartile shared alleles on chromosomes 6 and 12, with the FVB/N allele on chromosome 6 conferring greater susceptibility. On chromosome 12, C57BL/6 homozygotes were more significantly represented (LOD=3.8) conferring less susceptibility. The diabetic B6.Drc1/2f congenic strain developed kidney damage, while the reciprocal congenic, with FVB.Drc1/2b strain were protected. Microarray analysis identified differentially expressed genes between diabetic C57BL/6 and FVB/N mice. QTL mapping for early renal responses to diabetes identified two loci syntenic with regions identified for human diabetic kidney disease. Providing a new resource to study DKD.