60%) and normal IVD (26.09%) groups (P = 0.001). Similarly,
DR5 mRNA levels differed between groups (P = 0.025). However, there were no differences in DcR2 protein or mRNA levels.
Conclusion. The current results indicate that disc cells, after herniation, undergo apoptotic cell death via the DR5/TRAIL pathway.”
“Problem alcohol use is common among problem drug users (PDU) and associated with adverse health outcomes. Primary care has an important role in the overall stepped approach to alcohol treatment, especially screening and brief intervention (SBI).
To discuss three themes that emerged from an exploration of the literature on SBI for problem alcohol use in drug users attending primary care.
Material for this discussion paper was gathered from three biomedical I-BET-762 in vivo databases (PubMed, PsycINFO and Cochrane library), conference proceedings and online resources of CX-4945 supplier professional organisations or national health agencies.
Themes discussed in this paper are: (a) the potential of primary care for delivery
of alcohol SBIs to PDUs, (b) screening methods and (c) application of brief interventions to PDUs.
Although SBI improves health outcomes associated with problem alcohol use in the general population, further research is needed among high-risk patient groups, especially PDUs.”
“Background: Pseudoxanthoma elasticum (PXE) is an autosomal recessive metabolic disorder with ectopic mineralization in the skin, eyes and cardiovascular system. PXE is caused by mutations in ABCC6.
Objective: To examine 54 unrelated South African PXE patients for ABCC6 PXE causing mutations.
Methods: Patients were screened for Mutations in ABCC6 using two strategies. The first involved a comprehensive screening of all the ABCC6 exons and flanking learn more regions by dHPLC or sequencing whereas the second involved screening patients only for the common PXE mutations. The ABCC6 gene was screened in ten white and ten black healthy unrelated South Africans in order to examine the level
of common non-PXE associated variation.
Results: The Afrikaner founder mutation, R1339C, was present in 0.41 of white ABCC6 PXE alleles, confirming the founder effect and its presence in both Afrikaans- (34/63 PXE alleles) and English-speakers (4/28). Eleven mutations were detected in the white patients (of European origin), including two nonsense mutations, 6 missense mutations, two frameshift mutations and a large deletion mutation. The five “”Coloured”" patients (of mixed Khoisan, Malay, European and African origin) included three compound heterozygotes with R1339C as one of the mutations. The three black patients (sub-Saharan African origin) were all apparent homozygotes for the R1314W mutation. Blacks showed a trend towards a higher degree of neurtral variation (18 variants) when compared to whites (12 variants).