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951.
This study describes the effects of floor system, digital dermatitis (DD) and interdigital dermatitis and heel-horn erosion (IDHE) on locomotion performance in 225 dairy cows of 12 commercial dairy herds. Nine herds were kept in cubicle houses with concrete passageways (either solid, slatted, or grooved concrete) and three herds were kept in straw yards. Animals were at most five times examined at monthly intervals for lesion severity of DD and IDHE and for locomotion score. Locomotion score was rated on a scale ranging from 1 to 5 (from normal to severe) and disturbed locomotion (lameness) was defined as a score > or =3. A logistic regression model was used to analyze the 943 observations using lameness (yes/no) as outcome variable. The proportion of observations scored as lame (locomotion score > or =3) increased from 18% 1 month after trimming to 29% at 4 months after trimming. Severe lesions of DD and IDHE were associated with a significantly higher proportion of lame cows. The proportion of animals with disturbed locomotion increased from 16% to 40% as the severity of DD increased and from 17% to 30% with increasing severity of IDHE lesions. Locomotion performance highly differed between the cubicle house and straw yard group. Only 1% of all gaits in straw yard cows were scored as lame, while in cubicle housed cows these percentages varied from 24% to 46% with grooved floors showing the highest average locomotion score. Due to the extreme low incidence of lameness in straw yards, the statistical analysis had to be restricted to observations on concrete floors (n=744). The logistic regression model with lameness (yes/no) as dependent variable and random effects of cow and herd resulted in Odds Ratios for severe DD and IDHE of, respectively, 3.2 and 3.2, both significantly larger than unity. Cows housed at grooved concrete floors showed the highest OR of 6.5 compared to solid concrete floors. Recovery of lameness was poor as disturbance in gait lasted several months.  相似文献   
952.
Hyperchylomicronaemia was identified in a four-week-old Siamese kitten with lethargy, in-appetence, hindlimb ataxia and profound anaemia. The kitten was euthanased and at necropsy a thrombus was found occluding the caudal aorta. Two littermates later presented with lethargy, inappetence and hypertriglyceri-daemia which resolved after being weaned on to a low fat diet. A similar condition was subsequently diagnosed in a kitten born to the same sire but a different queen. The expression of hyperchylomicronaemia in two related litters was suggestive of an inherited, familial defect in the function of lipoprotein lipase (LPL). The activity of this enzyme was reduced in all three parents, the two recovered cases and two related, but apparently unaffected kittens, compared with a control group of unrelated cats belonging to the breeder. This reduction in activity was not attributable to defective activation of LPL by its serum cofactor apolipoprotein C-II or the presence in plasma of a factor that inhibited LPL. The gene that codes for LPL was examined by restriction fragment length polymorphism analysis using a human LPL cDNA probe. The results showed that the cat has a similar, but not identical, LPL gene to man. However, there were no differences in the restriction fragment patterns obtained from affected, unaffected and control animals.  相似文献   
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