Effects of lameness, subclinical mastitis and loss of body condition on the reproductive performance of dairy cows.

A total of 318 cows were monitored in the pre-breeding postpartum period for the presence of three production stressors: lameness, subclinical mastitis and body condition score (BCS) loss. For each stressor, cows were given a classification of severely, moderately or non-affected based on mobility scores, somatic cell counts and BCS change. The number of days from calving to onset of the first luteal phase was greater in cows that had one severe production stressor (median 44 days) or two moderate production stressors (41 days) compared with cows that had no stressors (31 days) (P=0.02 and P=0.04, respectively). More than one severe stressor increased the interval further. There was no difference between cows with one moderate stressor (median 38 days) and those with none (P=0.13). The delay to the first luteal phase was significantly longer in cows with two moderate stressors if the onset of one stressor occurred at the time when resumption of ovarian activity was expected. The presence of these production stressors in early lactation had no effect on the interval from calving to establishment of the next pregnancy or the number of inseminations required despite the negative effect on the onset of the luteal phase.

Altered levels and distribution of amyloid precursor protein and its processing enzymes in Niemann-Pick type C1-deficient mouse brains.

Niemann-Pick type C (NPC) disease is an autosomal recessive neurodegenerative disorder characterized by intracellular accumulation of cholesterol and glycosphingolipids in many tissues including the brain. The disease is caused by mutations of either NPC1 or NPC2 gene and is accompanied by a severe loss of neurons in the cerebellum, but not in the hippocampus. NPC pathology exhibits some similarities with Alzheimer's disease, including increased levels of amyloid beta (Abeta)-related peptides in vulnerable brain regions, but very little is known about the expression of amyloid precursor protein (APP) or APP secretases in NPC disease. In this article, we evaluated age-related alterations in the level/distribution of APP and its processing enzymes, beta- and gamma-secretases, in the hippocampus and cerebellum of Npc1(-/-) mice, a well-established model of NPC pathology. Our results show that levels and expression of APP and beta-secretase are elevated in the cerebellum prior to changes in the hippocampus, whereas gamma-secretase components are enhanced in both brain regions at the same time in Npc1(-/-) mice. Interestingly, a subset of reactive astrocytes in Npc1(-/-) mouse brains expresses high levels of APP as well as beta- and gamma-secretase components. Additionally, the activity of beta-secretase is enhanced in both the hippocampus and cerebellum of Npc1(-/-) mice at all ages, while the level of C-terminal APP fragments is increased in the cerebellum of 10-week-old Npc1(-/-) mice. These results, taken together, suggest that increased level and processing of APP may be associated with the development of pathology and/or degenerative events observed in Npc1(-/-) mouse brains.