The incidence, cost and factors associated with foot lameness in dairy cattle in south-western Victoria

A survey of 73 dairy farms in south-western Victoria was conducted to assess the cost and mean herd incidence of foot lameness for the period from calving to the end of November, 1985, and to identify the herd, management and environmental factors associated with foot lameness. The mean herd size was 125 cows (range 82 to 220). Lameness occurred in 64 (88%) herds, and the mean herd incidence was 7.0% (range 0.0 to 30.9%). The main clinical signs associated with lameness were the presence of overworn and/or bruised soles, or stones lodged in the interdigital cleft. Factors associated with lameness were: property and herd size, age of cow, bail feeding, voluntary entry into the bails, and features of the farm track including its length, the presence of steep slopes, the type of surface material, presence and treatment of broken sections and maintenance including rolling history. The association of these factors with specific clinical signs was examined. The mean cost was estimated to be $42.90 per lame cow due to loss of production, treatment, the culling or death of lame cows, and extra man hours spent managing lame cows. It was concluded that the site, construction, maintenance and use of the farm track were of major importance to the incidence of lameness in herds in this area and recommendations for reducing lameness are made.     

Chronic cervical compressive myelopathy in horses: patterns of astrocytosis in the spinal cord

The distribution and morphology of fibrous astrocytes in the cervical spinal cord of normal horses and horses with chronic compressive myelopathy were demonstrated using immunohistochemical staining for glial fibrillary acidic protein. In the spinal cord from normal horses, astrocytes with stellate cell bodies and short processes were irregularly distributed in grey matter. In the white matter, their cell bodies were small and angular in areas adjacent to grey matter and larger and more stellate-shaped in the subpial area. Astrocyte processes were fine, and evenly distributed in a predominantly radial pattern in transverse sections of cord. Gliosis was marked in the spinal cords of horses with cervical compressive myelopathy. In the grey matter at the level of compression astrocytes were often enlarged and rounded, with short, blunt processes, but the gliosis was generally mild. In the white matter, gliosis was obvious in areas of nerve fibre swelling and degeneration at the level of compression and in areas of ascending and descending Wallerian degeneration. The fine radial pattern of astrocyte fibres was replaced by a dense, irregular arrangement. Gliosis persisted in the cords of chronically affected horses after active nerve fibre degeneration had subsided. The areas of gliosis coincided with the areas of Marchi staining for degenerating myelin and with areas of myelin loss in osmium tetroxide post-fixed tissue. Histological observations were consistent with astrocytes replacing areas of extracellular space that remained after nerve fibre degeneration. it is concluded that astrocytic gliosis is a prominent and persistent alteration of the spinal cord of horses with chronic cervical compressive myelopathy.     

Quantitation of hepatic glycogenolysis and gluconeogenesis in fasting humans with 13C NMR

The rate of net hepatic glycogenolysis was assessed in humans by serially measuring hepatic glycogen concentration at 3- to 12-hour intervals during a 68-hour fast with 13C nuclear magnetic resonance spectroscopy. The net rate of gluconeogenesis was calculated by subtracting the rate of net hepatic glycogenolysis from the rate of glucose production in the whole body measured with tritiated glucose. Gluconeogenesis accounted for 64 +/- 5% (mean +/- standard error of the mean) of total glucose production during the first 22 hours of fasting. In the subsequent 14-hour and 18-hour periods of the fast, gluconeogenesis accounted for 82 +/- 5% and 96 +/- 1% of total glucose production, respectively. These data show that gluconeogenesis accounts for a substantial fraction of total glucose production even during the first 22 hours of a fast in humans.     

Hematotoxicity in workers exposed to low levels of benzene

Benzene is known to have toxic effects on the blood and bone marrow, but its impact at levels below the U.S. occupational standard of 1 part per million (ppm) remains uncertain. In a study of 250 workers exposed to benzene, white blood cell and platelet counts were significantly lower than in 140 controls, even for exposure below 1 ppm in air. Progenitor cell colony formation significantly declined with increasing benzene exposure and was more sensitive to the effects of benzene than was the number of mature blood cells. Two genetic variants in key metabolizing enzymes, myeloperoxidase and NAD(P)H:quinone oxidoreductase, influenced susceptibility to benzene hematotoxicity. Thus, hematotoxicity from exposure to benzene occurred at air levels of 1 ppm or less and may be particularly evident among genetically susceptible subpopulations.     

Fusion of cells by flipped SNAREs

The SNARE (soluble N-ethylmaleimide-sensitive factor attachment protein receptor) hypothesis suggests that pairs of proteins known as vesicle (v-) SNAREs and target membrane (t-) SNAREs interact specifically to control and mediate intracellular membrane fusion events. Here, cells expressing the interacting domains of v- and t-SNAREs on the cell surface were found to fuse spontaneously, demonstrating that SNAREs are sufficient to fuse biological membranes.     

Caenorhabditis elegans p53: role in apoptosis, meiosis, and stress resistance

We have identified a homolog of the mammalian p53 tumor suppressor protein in the nematode Caenorhabditis elegans that is expressed ubiquitously in embryos. The gene encoding this protein, cep-1, promotes DNA damage-induced apoptosis and is required for normal meiotic chromosome segregation in the germ line. Moreover, although somatic apoptosis is unaffected, cep-1 mutants show hypersensitivity to hypoxia-induced lethality and decreased longevity in response to starvation-induced stress. Overexpression of CEP-1 promotes widespread caspase-independent cell death, demonstrating the critical importance of regulating p53 function at appropriate levels. These findings show that C. elegans p53 mediates multiple stress responses in the soma, and mediates apoptosis and meiotic chromosome segregation in the germ line.