Neurologic evaluation of the equine head and neurogenic dysphagia

Neurologic evaluation should be performed in horses with diseases of the head. Although neurologic examination should focus on assessing behavior, mental status, and cranial nerve evaluation, evaluation of neurologic function of other body regions should be performed. Neurologic evaluation of the head can be performed expediently by practitioners to provide useful diagnostic and prognostic information. The numerous causes of dysphagia can be classified as obstructive, painful, or neurogenic. Common causes of neurogenic dysphagia are summarized, and methods for initial diagnosis and management are described. Maintaining adequate nutrition and preventing aspiration pneumonia are principal concerns in managing horses with neurogenic dysphagia.     

Increase of aminotransferases

Elevated aminotransferases activities are frequent in medical practice. In acute elevations, the mains causes are generally easily found (viral, drug-induced, toxic, ischemic). In moderate or prolonged elevations, the most frequent causes are steatosis (alcoholic, diabetes, obesity) and chronic hepatitis (viral B, D, C, drug-induced and auto-immune diseases.     

Effect of increased afterload on cardiac lipoprotein lipase and VLDL receptor expression

Fatty acids are a major source of fuel for energy production by myocytes. Lipoprotein lipase (LPL) and very low density lipoprotein (VLDL) receptor are abundantly expressed by the heart and skeletal muscles. LPL and possibly VLDL receptor represent the primary route of access to fatty acids contained in circulating triglyceride-rich lipoproteins. Physical exercise and thyroid hormone, which promote energy consumption, upregulate LPL expression in skeletal muscles. This study tested the hypothesis that increased cardiac workload might modulate myocardial LPL and/or VLDL receptor expressions. Accordingly, cardiac tissue LPL activity, LPL and VLDL receptor proteins and mRNA abundance were studied in Sprague-Dawley rats 4 weeks after induction of severe thoracic aorta constriction or sham operation. Elevation of afterload with thoracic aortic constriction led to a significant cardiomegaly and a marked upregulation of cardiac LPL activity, LPL mRNA and LPL protein abundance, but did not modify VLDL receptor mRNA or protein abundance. Thus, increased cardiac workload in this model results in upregulation of myocardial LPL expression which can enhance fatty acid availability to accommodate the heart's increased energy requirement.     

Activation of p38 mitogen-activated protein kinase by lipopolysaccharide in human neutrophils requires nitric oxide-dependent cGMP accumulation

This study examined the signal transduction pathway(s) leading to phosphorylation of p38 in human neutrophils stimulated with lipopolysaccharide and formyl peptides. Blockade of the nitric oxide (NO) pathway in neutrophils with the NO synthase inhibitor N-nitro-L-arginine methyl ester or by treatment with the NO scavenger 2-phenyl-tetramethylimidazoline-1-oxyl-3-oxide attenuated phosphorylation of the mitogen-activated protein kinase p38 in response to lipopolysaccharide but not fMet-Leu-Phe. Using the NO releasing agents S-nitroso-N-acetylpenicillamine and sodium nitroprusside it was determined that nitric oxide is sufficient to cause an increase in phosphorylation of p38. Increasing cellular cGMP with phosphodiesterase inhibitors, by stimulation of soluble guanylyl cyclase with YC-1 or with exogenous dibutyryl cGMP resulted in mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 3,6 (MEK3,6) activation and phosphorylation of p38. This phenomenon was specific for MEK3,6, because these agents had no effect on the phosphorylation state of MEK1,2. A role for protein kinase G but not protein kinase A downstream of lipopolysaccharide but not formylmethionylleucylphenylalanine was shown using the specific inhibitors KT5823 and H89, respectively. These data indicate that activation of p38 by fMet-Leu-Phe and lipopolysaccharide involve different mechanisms, and that activation of protein kinase G by NO-dependent stimulation of guanylyl cyclase is necessary and sufficient for phosphorylation of p38 downstream of lipopolysaccharide.     

Sublethal concentrations of mercury in river otters: monitoring environmental contamination

Hair, muscle, and liver mercury concentrations were determined in river otter (Lutra canadensis) carcasses collected from the lower coastal plain and piedmont of Georgia. Mean muscle and hair mercury concentrations were greater (P < 0.001) in otters from the lower coastal plain (4.42 and 24.25 mg/kg wet wt, respectively) compared to otters from the piedmont (1.48 and 15.24 mg/kg, respectively). Liver tissue from lower coastal plain otters averaged 7.53 mg/kg mercury. Mean fetus brain and muscle mercury concentrations were 1.03 and 1.58 mg/kg wet wt, respectively, and fetal muscle mercury concentrations were correlated (r = 0.92) with maternal muscle mercury concentrations. Comparison of mercury concentrations found in Georgia otters to those associated with adverse effects in otter and mink (Mustela vison), indicate sublethal contamination with concentrations in some individuals approaching that observed in experimentally dosed individuals that developed clinical signs of mercurialism. Mercury concentrations in fish from the lower coastal plain approached or exceeded concentrations demonstrated to be toxic to experimentally dosed otters.