The effects of nutrition-induced abnormal food metabolism in the Southern Plains woodrat (Neotoma micropus): comparisons of variations of the Western diet.

We investigated the effects of several modifications of the Western diet on a medium-sized rodent, Neotoma micropus, that lives in the area of the wildland-urban interface. We conducted a laboratory study of the response of N. micropus to high fat-high fructose (HFHF), high fat-high sucrose (HFHS), high fat-low sugar (HFLSu) and control (low fat-low sugar) diets. We found a significant increase in hepatic lipid deposition and a significant decrease in podocytes in those animals that consumed the HFHF and HFLSu diets compared to those on the HFHS and control diets. We found no significant differences in Bowman's space or hepatic collagen formation. We predict that N. micropus in the wild, with access to anthropogenic resources, will show similar effects as a result of the consumption of anthropogenic resources.

Resistance to malignant catarrhal fever in American bison (Bison bison) is associated with MHC class IIa polymorphisms.

The Rhadinovirus ovine herpesvirus-2 (OvHV-2) is the most common causative agent of malignant catarrhal fever (MCF) in clinically susceptible ruminants including cattle and bison. American bison (Bison bison) are highly susceptible to clinical MCF. Nevertheless, approximately 20% of bison on ranches or in feedlots become infected with the virus without developing clinical disease. Defining the genetic basis for differences in susceptibility between bison could facilitate development of improved control strategies for MCF. One genetic region that influences susceptibility to infectious diseases is the major histocompatibility complex (MHC). In this study, a Bison bison (Bibi) DRB3 oligonucleotide microarray was used to type 189 bison from 10 herds where MCF outbreaks had occurred. Binary logistic regression was used to classify DRB3 alleles as resistant (R), susceptible (S) or neutral (N). Animals were reclassified using six DRB3 genotype categories: N/N, N/R, N/S, R/S, R/R and S/S. Analysis of homogeneity across herds showed that there was a herd effect. Consequently, a penalized logistic regression model was run with herd and genotype categories as the explanatory variables. The R/R genotype was associated with resistance to MCF (P = 0.0327), while the S/S genotype was associated with clinical MCF (P = 0.0069). This is the first evidence that MHC class IIa polymorphism is associated with resistance or susceptibility to OvHV-2-induced MCF.

Major histocompatibility antigen expression on the bovine placenta: its relationship to abnormal pregnancies and retained placenta.

In viviparous animals, regulation of expression of major histocompatibility complex (MHC) class I antigens by the trophoblast cells, which constitute the outermost layer of the placenta, seems to be critical for maternal immunological acceptance of an allogeneic fetus. Cattle are unusual in this regard, since the bovine trophoblast cells, in specific regions of the uterine/placental interface, normally express MHC class I antigens during the third trimester of gestation. This expression appears to be biologically relevant as MHC class I compatibility between a cow and her fetus has been associated with an increased incidence of placental retention. We have found significant differences in lymphocyte populations, cytokine production, and trophoblast cell apoptosis in the placentomes of MHC-compatible and -incompatible pregnancies at parturition. This suggests that maternal immunological recognition of fetal MHC class I proteins triggers an immune/inflammatory response that contributes to placental separation at parturition in cattle. Early in pregnancy, a complete shutdown of MHC class I expression by trophoblast cells appears to be critical for normal placental development and fetal survival. In bovine somatic cell nuclear transfer (SCNT) pregnancies, there is an extremely high rate of fetal loss between days 30 and 90 of pregnancy. We have shown that in bovine SCNT pregnancies, between days 34 and 63 of gestation, there is both abnormal expression of MHC class I antigens by trophoblast cells and an abnormal accumulation of lymphocytes within the uterine stroma. Consequently, it is likely that activation of the maternal mucosal immune system, within the uterus at the same time when placentomes are being established, interferes with the process of placentome development and leads to immune-mediated abortion. Our data suggest that bovine MHC-compatible pregnancies provide a unique model for studying regulation of the uterine immune system, as well as immune-mediated placental rejection.

Validation of a 20-minute steady-state jog as an estimate of peak oxygen uptake in adolescents.

Distance run tests are often used to estimate peak oxygen uptake (peak VO2) in children. This study examined the concurrent validity of a 20-min steady-state jog (20MSSJ). The sample consisted of 43 boys and 32 girls who performed a 20MSSJ and completed a maximal treadmill test 1 week later. Peak VO2 was measured by indirect calorimetry. Subject characteristics were as follows: boys, mean age = 15.1 +/- 1.0 years, mean peak VO2 = 46.4 +/- 7.7 ml.kg-1 x min-1, mean 20MSSJ = 2.3 +/- 0.5 miles; girls, mean age = 15.3 +/- 1.1 years, mean peak VO2 = 40.4 +/- 5.1 ml.kg-1 x min-1, mean 20MSSJ = 2.1 +/- 0.5 miles. The correlation between 20MSSJ and peak VO2 was .68 across boys and girls. The regression slopes of the boys and girls were common, but the intercepts differed, F (1, 72) = 10.9, p < .05. The influence of weight and skinfold fat was examined. Separate models were developed, and the R for each was increased to .79 (SEE = 4.45 ml.kg-1 x min-1) for the model using weight and .80 (SEE = 4.36 ml.kg-1 x min-1) for the model using sum of skinfolds. The regression equations are as follows: peak VO2 = 35.10 + 6.19 (Run) + 2.96 (Gender) -0.26 (Skinfold fat) peak VO2 = 33.94 + 7.64 (Run) + 5.84 (Gender) -0.18 (Weight) (Run = 20MSSJ performance in miles; Gender; females = 0, males = 1; Skinfold fat = sum of two-site skinfolds in mm; Weight = body weight in kg).(ABSTRACT TRUNCATED AT 250 WORDS)