Chromosomal assignment of porcine EAD, EAO, LPR and P3 genes by linkage analysis

A two-point linkage analysis was performed between blood group (14), allotype (8), polymorphic protein (11), DNA type I (2), and microsatellite (2) loci in Wild Boar x Pietrain and Meishan x Pietrain three-generation families. The following new pairwise linkages were detected: LPR-EAN (Z_max= 60.68, Ø= 0.055), EAD-GH1 (Z_max= 17.43, Ø= 0.246), EAO—P3 (Z_max= 15.81, Ø= 0.239), and P3—S0003 (Z_max= 5.43, Ø= 0.312). This study and published mapping data enabled the localization of LPR (LPR allotype) to chromosome 9, EAD (erythrocyte antigen D) to chromosome 12, and EAO (erythrocyte antigen O) and P3 (P3 allotype) to the q arm of chromosome 6 with gene order SOOO3—P3—EAO, EAO being the most distal.     

Dietary omega-3 fatty acids attenuate cellular damage after a hippocampal ischemic insult in adult rats

The role of omega-3 polyunsaturated fatty acids (3PUFAs) on brain function is increasingly demonstrated. Here, the effect of dietary deprivation of essential 3PUFAs on some parameters related to neuroprotection was investigated. Rats were fed with two different diets: omega-3 diet and omega-3-deprived diet. To assess the influence of 3PUFAs on brain responses to ischemic insult, hippocampal slices were subjected to an oxygen and glucose deprivation (OGD) model of in vitro ischemia. The omega-3-deprived group showed higher cell damage and stronger decrease in the [³H]glutamate uptake after OGD. Moreover, omega-3 deprivation influenced antiapoptotic cell response after OGD, affecting GSK-3beta and ERK1/2, but not Akt, phosphorylation. Taken together, these results suggest that 3PUFAs are important for cell protection after ischemia and also seem to play an important role in the activation of antiapoptotic signaling pathways.     

Molecular analysis of carbohydrate N-acetylgalactosamine 4-O sulfotransferase 8 (CHST8) as a candidate gene for bovine spongiform encephalopathy susceptibility

Endogenous prion proteins (PrP) play the central role in the pathogenesis of transmissible spongiform encephalopathies. The carbohydrate N -acetylgalactosamine 4-O sulfotransferase 8 (CHST8) promotes the conversion of the cellular PrP^C into the pathogenic PrP^d. Six sequence variants within the CHST8 gene were identified by comparative sequencing and genotyped for a sample of 623 animals comprising bovine spongiform encephalopathy (BSE)-affected and healthy control cows representing German Fleckvieh (German Simmental), German Holstein (Holstein-Friesian) and Brown Swiss. Significant differences in the allele, genotype and haplotype frequencies between BSE-affected and healthy cows indicate an association of sequence variant g.37254017G>T with the development of the disease in Brown Swiss cattle.     

Genetic linkage studies between congenital adrenal hyperplasia and the HLA blood group system

Seventeen families with one or two children suffering from congenital adrenal hyperplasia (CAH) were not only typed for their HLA-A,B, and D antigens but also tested biochemically forCAH heterozygosity after ACTH stimulation. The lod score analysis showed a close genetic linkage betweenCAH andHLA, indicating that theC-21-hydroxylase deficiency gene(s) causing CAH in the homozygous deficient state are-located in close proximity to theHLA complex on chromosome 6 with an estimated recombination fraction of 0 to 5%. HLA typing in 21 unrelated CAH patients revealed a statistically significant association to the HLA-B5 antigen with a relative risk value of 5.8. There was a significant correlation (P=0.0025) between theHLA segregation data and theCAH heterozygosity test results in relatives of CAH patients although a few ‘false negative’ results in theCAH heterozygosity test were observed. Thus, the combination of HLA typing and this biochemical test at present provides the most precise approach for detecting CAH carriers in families of CAH patients.     

Effect of high-pressure-induced ice I-to-ice III phase transitions on inactivation of Listeria innocua in frozen suspension

The inactivation of Listeria innocua BGA 3532 at subzero temperatures and pressures up to 400 MPa in buffer solution was studied to examine the impact of high-pressure treatments on bacteria in frozen matrices. The state of aggregation of water was taken into account. The inactivation was progressing rapidly during pressure holding under liquid conditions, whereas in the ice phases, extended pressure holding times had comparatively little effect. The transient phase change of ice I to other ice polymorphs (ice II or ice III) during pressure cycles above 200 MPa resulted in an inactivation of about 3 log cycles, probably due to the mechanical stress associated with the phase transition. This effect was independent of the applied pressure holding time. Flow cytometric analyses supported the assumption of different mechanisms of inactivation of L. innocua in the liquid phase and ice I (large fraction of sublethally damaged cells due to pressure inactivation) in contrast to cells subjected to ice I-to-ice III phase transitions (complete inactivation due to cell rupture). Possible applications of high-pressure-induced phase transitions include cell disintegration for the recovery of intracellular components and inactivation of microorganisms in frozen food.     

Non‐Parametric Ecological Regression and Spatial Variation

Ecological studies aim to analyse the variation of disease risk in relation to exposure variables that are measured at an area unit level. In practice it is rarely possible to use the exposure variables themselves, either because the corresponding data are not available or because the causes of the disease are not fully understood. It is therefore quite common to use crude proxies of the real exposure to the disease in question. These proxies are rarely able to explain the disease variation and hence additional area level random effects are introduced to account for the residual variation. In this paper we investigate the possibility to model the effect of ecological covariates non‐parametrically, with and without additional random effects for the residual spatial variation. We illustrate the issues arising through analyses of simulated and real data on larynx cancer mortality in Germany, during the years of 1986 to 1990, where we use the corresponding lung cancer rates as a proxy for smoking consumption.