The change of sleeping and lying posture of Japanese black cows after moving into new environment

Objective Environmental change is one of the stressful events in livestock production. Change in environment disturbs cow behavior and cows require several days to regain a stable behavioral pattern. Sleeping posture (SP) and lying posture (LP) have been used as indicators for animal that are relaxed and well-acclimated to their environment. The aim of this study was to examine the time required by Japanese black cows for stabilization of SP and LP after moving into new environment. Methods Seven pregnant Japanese black cows were used. Cows were moved into new tie-stall shed and their sleeping and lying posture measured 17 times during 35 experimental days. Both SP and LP were detected by accelerometer fixed on middle occipital and hip-cross, respectively. Daily total time, frequency, and average bout of both SP and LP were calculated. Results Daily SP time was the shortest on day 1 and increased to the highest on day 3. It then decreased until day 9, after that stabilized about 65 min/d till the end of experiment. Daily LP time changed in same manner as daily SP time. The average SP bout was the longest on day 1, and then decreased to stable level on day 7. On the other hand, the average LP bout was the shortest on day 1, and it increased to stable level on day 7. Conclusion These results showed that pregnant Japanese black cows needed 1 week to stabilize their SP. However, there were different change patterns between the average SP and LP bout, even though the change pattern of daily SP and LP time were similar

Targeted Deletion of Both Thymidine Phosphorylase and Uridine Phosphorylase and Consequent Disorders in Mice

Thymidine phosphorylase (TP) regulates intracellular and plasma thymidine levels. TP deficiency is hypothesized to (i) increase levels of thymidine in plasma, (ii) lead to mitochondrial DNA alterations, and (iii) cause mitochondrial neurogastrointestinal encephalomyopathy (MNGIE). In order to elucidate the physiological roles of TP, we generated mice deficient in the TP gene. Although TP activity in the liver was inhibited in these mice, it was fully maintained in the small intestine. Murine uridine phosphorylase (UP), unlike human UP, cleaves thymidine, as well as uridine. We therefore generated TP-UP double-knockout (TP(−/−) UP(−/−)) mice. TP activities were inhibited in TP(−/−) UP(−/−) mice, and the level of thymidine in the plasma of TP(−/−) UP(−/−) mice was higher than for TP(−/−) mice. Unexpectedly, we could not observe alterations of mitochondrial DNA or pathological changes in the muscles of the TP(−/−) UP(−/−) mice, even when these mice were fed thymidine for 7 months. However, we did find hyperintense lesions on magnetic resonance T(2) maps in the brain and axonal edema by electron microscopic study of the brain in TP(−/−) UP(−/−) mice. These findings suggested that the inhibition of TP activity caused the elevation of pyrimidine levels in plasma and consequent axonal swelling in the brains of mice. Since lesions in the brain do not appear to be due to mitochondrial alterations and pathological changes in the muscle were not found, this model will provide further insights into the causes of MNGIE