Cultural perspectives of interventions for managing diabetes and asthma in children and adolescents from ethnic minority groups.

Both diabetes and asthma are increasingly being recognized as health problems for ethnic groups. Because of cultural differences, ethnicity is reported to be a risk factor for poorer quality in health care, disease management and disease control. Ethnic groups are at risk for poorer quality of life and increased disease complications when compared with non-ethnic counterparts living in the same country. There is little known about how culture is addressed in interventions developed for ethnic groups. The aim of this paper is to systematically review the cultural perspectives of interventions for managing diabetes and asthma in children, adolescents and/or their families from ethnic minority groups. A total of 92 records were identified that were potentially relevant to this review following which, 61 papers were excluded. The full texts of remaining papers (n= 31) were then read independently by both authors, and agreement was reached to exclude a further 27 papers that did not meet inclusion criteria. A total of four papers were eligible for inclusion in this review. Findings indicate that despite growing concerns about health disparities between ethnic and non-ethnic groups in relation to both asthma and diabetes in childhood, there has been little effort to develop cultural specific interventions for ethnic groups. By systematically reviewing asthma and diabetes interventions we have highlighted that few interventions have been developed from a cultural perspective. There are a limited number of interventions published that add knowledge on the specific elements of intervention that is needed to effectively and sensitively educate other cultures. More work is required into identifying which strategies or components of cultural interventions are most effective in achieving positive health outcomes for children, adolescents and/or their families from ethnic groups.

Saccharomyces cerevisiae HOC1, a suppressor of pkc1, encodes a putative glycosyltransferase.

The Saccharomyces cerevisiae gene PKC1 encodes a protein kinase C isozyme that regulates cell wall synthesis. Here we describe the characterization of HOC1, a gene identified by its ability to suppress the cell lysis phenotype of pkc1-371 cells. The HOC1 gene (Homologous to OCH1) is predicted to encode a type II integral membrane protein that strongly resembles Och 1p, an alpha-1,6-mannosyltransferase. Immunofluorescence studies localized Hoc1p to the Golgi apparatus. While overexpression of HOC1 rescued the pkc1-371 temperature-sensitive cell lysis phenotype, disruption of HOC1 lowered the restrictive temperature of the pkc1-371 allele. Disruption of HOC1 also resulted in hypersensitivity to Calcofluor White and hygromycin B, phenotypes characteristic of defects in cell wall integrity and protein glycosylation, respectively. The function of HOC1 appears to be distinct from that of OCH1. Taken together, these results suggest that HOC1 encodes a Golgi-localized putative mannosyltransferase required for the proper construction of the cell wall.

Sequence analysis of two genomic regions containing the KIT and the FMS receptor tyrosine kinase genes.

The KIT and FMS tyrosine kinase receptors, which are implicated in the control of cell growth and differentiation, stem through duplications from a common ancestor. We have conducted a detailed structural analysis of the two loci containing the KIT and FMS genes. The sequence of the approximately 90-kb KIT locus reveals the position and size of the 21 introns and of the 5' regulatory region of the KIT gene. The introns and the 3'-untranslated parts of KIT and FMS have been analyzed in parallel. Comparison of the two sequences shows that, while introns of both genes have extensively diverged in size and sequence, this divergence is, at least in part, due to intron expansion through internal duplications, as suggested by the discrete extant analogies. Repetitive elements as well as exon predictions obtained using the GRAIL and GENEFINDER programs are described in detail. These programs led us to identify a novel gene, designated SMF, immediately downstream of FMS, in the opposite orientation. This finding emphasizes the gene-rich characteristic of this genomic region.

Analysis of a 62 kb DNA sequence of chromosome X reveals 36 open reading frames and a gene cluster with a counterpart on chromosome XI.

We have sequenced a 61.989 bp stretch located between genes RAD7 and FIP1 of Saccharomyces cerevisiae chromosome X. This stretch contains 36 open reading frames (ORFs) of at least 100 codons. Fourteen of these correspond to sequences previously published as HIT1, CDC8, YAP17, CBF1, NAT1, RPA12, CCT5, TOR1, RFC2, PEM2, CDC11, MIR1, STE18 and GRR1. The proteins deduced from four ORFs (YJR059w, YJR065c, YJR075w, YJR078w) have significant similarity to proteins of known function from yeast or other organisms, including S. cerevisiae serine/threonine-specific protein kinase. Schizosaccharomyces pombe Act2 protein, S. cerevisiae mannosyltransferase OCH1 protein and mouse indoleamine 2,3-dioxygenase, respectively. Four of the remaining 18 ORFs have similarity to proteins with unknown function, six are weakly similar to other known sequences, while another eight exhibit no similarity to any known sequence. In addition, three tRNA genes have been recognized. Three genes clustered within 22 kb (YJR059w, YJR061w and TOR1) have counterparts arranged within 15 kb on the left arm of chromosome XI.

Revised nucleotide sequence of the COR region of yeast Saccharomyces cerevisiae chromosome X.

The COR region, a gene cluster located on chromosome X of Saccharomyces cerevisiae and including genes CYC1, UTR1, UTR3, OSM1, tRNA(Gly) and RAD7, was sequenced within the framework of the European Union genome systematic sequencing project. It was compared with previously published sequences to be found in GenBank under the acronym YSCCORA. While some of the discrepancies observed can be readily ascribed to polymorphism, others most probably result from sequencing errors. A revised version of the sequence of the COR cluster is given.