Culturally Responsive Academic Advisement

Abstract African American and Latino males are not only underrepresented in graduate schools, but demonstrate a lower rate of completion than their female and White counterparts nationally. This sequential explanatory study was undertaken to positively impact the academic achievement of African American and Latino males enrolled in a graduate school of education in the north eastern United States. A culturally responsive academic advisement model was implemented with the intended goal of 85% - 90% of African American and Latino males perceiving the advisement positively and meeting academic achievement benchmarks. The study resulted in both Latino and African American males meeting academic benchmarks and benchmarks that were set for positive perception of culturally responsive academic advisement. The results of the study positions colleges and universities to use cultural responsive academic advisement to support the achievement of African American and Latino males at institutions of higher education. Helping African American and Latino males earn post baccalaureate degrees can significantly impact their future earning potential and overall quality of life

Health services use for ambulatory care sensitive conditions in the developing country of Barbados

Objective: This research examined hospitalization for ambulatory care sensitive conditions (ACSH) for the population of Barbados during 2003-2008. I examined differences in ACSH rates for females and males at the parish and population levels over the six year period. This study compared hospitalization rates across years and geographic locations for the six most prevalent ambulatory care sensitive conditions in the adult population, ages 20 and over, and for five individual ambulatory care sensitive conditions in the population ages 19 years and younger. I also compared ACSH rates in Barbados to published rates for other developed and developing countries. Methods: ACSHs were identified using data from the Queen Elizabeth Hospital in Barbados for 2003-2008. For the adult population, ages 20 and over, International Classification of Diseases, Tenth Revision Australian Modification (ICD-10-AM) codes and categories were used to identify ACSH rates based on the codes used to define potentially avoidable hospitalizations by the Victorian Government Department of Human Services (VGDHS, 2004), codes that are used by the government of Australia that have been validated through extensive research and publication. The United States Agency for Healthcare Research and Quality (AHRQ) area level pediatric quality indicators (PDIs) were used to identify ACSHs for the population ages 19 years and younger, using an ICD-10 cross-walk developed for this research. Cross-sectional and time series analyses of ACSH rates were performed for the period 2003-2008. Poisson analysis estimated relative rates and provided 95% confidence intervals and p-values, enabling comparisons of differences in hospitalization rates between women and men, among years of the study, and across parishes. Results: For the adult population, the gender analysis showed that women age 50+ had the highest percent of hospitalizations that were ACSH, nearly half of all hospitalizations (47.4%). Across years studied, the highest ACSH population-based rates were observed for men age 50+ (31.36 per 1000). Considerable variation in ACSH rates was observed among parishes for both men and women for all age groups. The analysis by gender found that, compared with men, women ages 20-49 had higher rates of hospitalization across the study period 2003-2008 and for each year. For women and men ages 50+, ACSH rates were higher for men than for women. For men and women ages 20-49 years, those who lived in St. Michael had the highest rates of ACSH of the eleven parishes. Among adults ages 20-49 and 50+, the top six ambulatory care sensitive conditions were influenza and pneumonia, congestive heart failure, diabetes, angina, dehydration, and hypertension. Among all ACSHs, the rate of hospitalization for influenza and pneumonia was highest for both women and men ages 20-49 and 50+. In the age 19 and younger population, ACSH rates differed considerably for girls and boys, and were generally higher for boys than girls across parishes and across the years 2003-2008. The most prevalent ACSH in the 19 and younger group was asthma. Trends for ACSH rates in Barbados were consistent with countries such as Taiwan and Australia, with considerable variability across the study years; however, there was notable evidence that ACSH rates may have increased considerably in the latter study years. Discussion: There were significant differences in ACSH rates across the parishes in Barbados for females and males. The substantial variation in ACSH rates among parishes suggests evidence of potential problems in access to primary care, particularly for residents of St. Michael, and the adult populations in St. Thomas, St. Andrew, and St. James. This study provides relevant base line informationaboutACSHratesandsuggeststheneedforfutureresearchinthisarea. Itis possible that the higher ACSH rates in these parishes are attributable to area factors other than primary care, factors such as disease prevalence or differences in education; further research should investigate this possibility

Transcription factor HNF1β and novel partners affect nephrogenesis

Heterozygous mutations of the tissue-specific transcription factor hepatocyte nuclear factor (HNF)1β, cause maturity onset diabetes of the young (MODY5) and kidney anomalies including agenesis, hypoplasia, dysplasia and cysts. Because of these renal anomalies, HNF1β is classified as a CAKUT (congenital anomalies of the kidney and urinary tract) gene. We searched for human fetal kidney proteins interacting with the N-terminal region of HNF1β using a bacterial two-hybrid system and identified five novel proteins along with the known partner DCoH. The interactions were confirmed for four of these proteins by GST pull-down assays. Overexpression of two proteins, E4F1 and ZFP36L1, in Xenopus embryos interfered with pronephros formation. Further, in situ hybridization showed overlapping expression of HNF1β, E4F1 and ZFP36L1 in the developing pronephros. HNF1β is present largely in the nucleus where it colocalized with E4F1. However, ZFP36L1 was located predominantly in the cytoplasm. A nuclear function for ZFP36L1 was shown as it was able to reduce HNF1β transactivation in a luciferase reporter system. Our studies show novel proteins may cooperate with HNF1β in human metanephric development and propose that E4F1 and ZFP36L1 are CAKUT genes. We searched for mutations in the open reading frame of the ZFP36L1 gene in 58 patients with renal anomalies but found none

Sequencing PDX1 (insulin promoter factor 1) in 1788 UK individuals found 5% had a low frequency coding variant, but these variants are not associated with Type 2 diabetes

OnlineOpen Article. This is a copy of an article published in Diabetic Medicine. This journal is available online at: http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1464-5491Genome-wide association studies have identified >30 common variants associated with Type 2 diabetes (>5% minor allele frequency). These variants have small effects on individual risk and do not account for a large proportion of the heritable component of the disease. Monogenic forms of diabetes are caused by mutations that occur in <1:2000 individuals and follow strict patterns of inheritance. In contrast, the role of low frequency genetic variants (minor allele frequency 0.1-5%) in Type 2 diabetes is not known. The aim of this study was to assess the role of low frequency PDX1 (also called IPF1) variants in Type 2 diabetes

Challenging Perceptions of Disability through Performance Poetry Methods: The "Seen but Seldom Heard" Project.

This paper considers performance poetry as a method to explore lived experiences of disability. We discuss how poetic inquiry used within a participatory arts-based research framework can enable young people to collectively question society’s attitudes and actions towards disability. Poetry will be considered as a means to develop a more accessible and effective arena in which young people with direct experience of disability can be empowered to develop new skills that enable them to tell their own stories. Discussion of how this can challenge audiences to critically reflect upon their own perceptions of disability will also be developed

Biallelic PDX1 (insulin promoter factor 1) mutations causing neonatal diabetes without exocrine pancreatic insufficiency

This is the final version. Available on open access from Wiley via the DOI in this recordAims: Recessive PDX1 (IPF1) mutations are a rare cause of pancreatic agenesis, with three cases reported worldwide. A recent report described two cousins with a homozygous hypomorphic PDX1 mutation causing permanent neonatal diabetes with subclinical exocrine insufficiency. The aim of our study was to investigate the possibility of hypomorphic PDX1 mutations in a large cohort of patients with permanent neonatal diabetes and no reported pancreatic hypoplasia or exocrine insufficiency. Methods: PDX1 was sequenced in 103 probands with isolated permanent neonatal diabetes in whom ABCC8, KCNJ11 and INS mutations had been excluded. Results: Sequencing analysis identified biallelic PDX1 mutations in three of the 103 probands with permanent neonatal diabetes (2.9%). One proband and his affected brother were compound heterozygotes for a frameshift and a novel missense mutation (p.A34fsX191; c.98dupC and p.P87L; c.260C>T). The other two probands were homozygous for novel PDX1 missense mutations (p.A152G; c.455C>G and p.R176Q; c.527G>A). Both mutations affect highly conserved residues located within the homeobox domain. None of the four cases showed any evidence of exocrine pancreatic insufficiency, either clinically, or, where data were available, biochemically. In addition a heterozygous nonsense mutation (p.C18X; c.54C>A) was identified in a fourth case. Conclusions: This study demonstrates that recessive PDX1 mutations are a rare but important cause of isolated permanent neonatal diabetes in patients without pancreatic hypoplasia/agenesis. Inclusion of the PDX1 gene in mutation screening for permanent neonatal diabetes is recommended as a genetic diagnosis reveals the mode of inheritance, allows accurate estimation of recurrence risks and confirms the requirement for insulin treatment. © 2013 The Authors. Diabetic Medicine © 2013 Diabetes UK.Diabetes UKEuropean Union FP

Type 2 Diabetes Risk Alleles Are Associated With Reduced Size at Birth

OBJECTIVE: Low birth weight is associated with an increased risk of type 2 diabetes. The mechanisms underlying this association are unknown and may represent intrauterine programming or two phenotypes of one genotype. The fetal insulin hypothesis proposes that common genetic variants that reduce insulin secretion or action may predispose to type 2 diabetes and also reduce birth weight, since insulin is a key fetal growth factor. We tested whether common genetic variants that predispose to type 2 diabetes also reduce birth weight. RESEARCH DESIGN AND METHODS: We genotyped single-nucleotide polymorphisms (SNPs) at five recently identified type 2 diabetes loci (CDKAL1, CDKN2A/B, HHEX-IDE, IGF2BP2, and SLC30A8) in 7,986 mothers and 19,200 offspring from four studies of white Europeans. We tested the association between maternal or fetal genotype at each locus and birth weight of the offspring. RESULTS: We found that type 2 diabetes risk alleles at the CDKAL1 and HHEX-IDE loci were associated with reduced birth weight when inherited by the fetus (21 g [95% CI 11-31], P = 2 x 10(-5), and 14 g [4-23], P = 0.004, lower birth weight per risk allele, respectively). The 4% of offspring carrying four risk alleles at these two loci were 80 g (95% CI 39-120) lighter at birth than the 8% carrying none (P(trend) = 5 x 10(-7)). There were no associations between birth weight and fetal genotypes at the three other loci or maternal genotypes at any locus. CONCLUSIONS: Our results are in keeping with the fetal insulin hypothesis and provide robust evidence that common disease-associated variants can alter size at birth directly through the fetal genotype

Exocrine pancreatic dysfunction is common in hepatocyte nuclear factor 1β–associated renal disease and can be symptomatic

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