Gene/Protein Disease Symptom Drug Enzyme Compound
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Immunofluorescence and immunogold localization studies show that the two Ca(2+)-dependent proteinases (mu-calpain for the micromolar Ca(2+)-requiring proteinase and m-calpain for the millimolar Ca(2+)-requiring proteinase) and their protein inhibitor (calpastatin) are located exclusively intracellularly in normal rat soleus muscle. Quantitative immunogold studies indicate that binding of antibodies to both calpains and to calpastatin is approximately two times greater at the Z-disk of myofibrils than it is at the I-band or A-band regions. Mitochondria and nuclei in muscle cells contain both calpains and calpastatin at concentrations approximately one-tenth and one-fifth, respectively, of the concentration at the Z-disk, as estimated by antibody binding. Very little calpain or calpastatin was seen in the cytoplasmic intermyofibrillar spaces, and most of the calpain and calpastatin in muscle cells is associated with intracellular structures. Immunofluorescence results suggest that concentration of m-calpain but not mu-calpain or calpastatin is, in some instances, slightly higher near the intracellular surface of the plasma membrane than elsewhere in the muscle cell. Most m-calpain, however, is distributed throughout the interior of mature rat skeletal muscle cells. Denervation, or fasting and refeeding increases the concentration of the calpains and calpastatin in the muscle cell but does not change their distribution. Some mu- and m-calpain and calpastatin is found extracellularly in denervated soleus muscle or soleus muscle from fasting rats, but the extracellular calpains and calpastatin seem to originate from "leakage" of these proteins out of the cell because serum creatine kinase levels are much higher than normal in denervated or fasting rats.
Anat Rec 1992 Jan
PMID:Localization of the Ca(2+)-dependent proteinases and their inhibitor in normal, fasted, and denervated rat skeletal muscle. 153 66

Using monoclonal antibodies against the M and B subunit isoforms of creatine kinase (CK) we have investigated their distribution in developing human skeletal and cardiac muscle immunohistochemically. It is demonstrated that in skeletal muscle, a switch from CK-B to CK-M takes place around the week 8 of development, whereas in the developing heart, CK-M is the predominant isoform from the earliest stage examined onward (i.e., 4 1/2 weeks of development). In all hearts examined, local differences in concentration of the CK isoforms are observed. The CK-M expression in the developing outflow tract (OFT) and conduction system is described in detail. Between the weeks 5 and 7 of development, the distal portion of the OFT is characterized by low CK-M expression, whereas around the week 8-10 of development the myocardium around the developing semilunar valves in the OFT expresses a very high level of CK-M. At all stages examined, a relatively low CK-M level is observed in those regions in which the "slow" components of the conduction system do develop (e.g., the sinoatrial junction and atrioventricular junction), whereas a relatively high concentration of CK-M is observed in those areas that are destined to become the "fast" components, i.e., the subendocardial myocardium of the ventricles. The high expression of CK-M in the developing "fast components" of the conduction system contrasts with the relatively low expression of CK-M in the force-producing myocardium of the interventricular septum and free ventricular wall.
Anat Rec 1990 Oct
PMID:Spatial distribution of "tissue-specific" antigens in the developing human heart and skeletal muscle. I. An immunohistochemical analysis of creatine kinase isoenzyme expression patterns. 224 Jun 9

An outbreak of muscle stiffness and poor performance among 59 thoroughbreds at a Newmarket flat racing yard was investigated between the beginning of May and the end of June 1986. Over a third of the horses showed signs of muscular stiffness, and 38 had, at one or more of the sampling times, creatine kinase (CK) activities above 200 iu/litre and, or, aspartate aminotransferase (AST) activities above 300 iu/litre when they were sampled six to eight hours after exercise. The following season, at a similar time and stage of training, only four of 39 horses sampled had CK activities between 200 and 300 iu/litre, and three had AST activities between 500 and 600 iu/litre. Plasma samples from 18 animals sampled at the start of the investigation and 13 days later were tested for the presence of antibodies to equine herpesvirus (EHV). Ten of them showed a response highly suggestive of an EHV-1 infection. No significant abnormality was found in the fractional electrolyte values from seven randomly selected animals. Unusually high numbers of normally sized and stained fibres with centrally placed nuclei as well as groups of small muscle fibres were found in muscle biopsies taken from three animals which continued to have high enzyme activities and show recurrent signs of muscle stiffness.
Vet Rec 1990 Nov 10
PMID:An outbreak of the equine rhabdomyolysis syndrome in a racing yard. 227 Jun 35

An outbreak of muscle disease affected approximately 20 of 600 ewes in spring 1987 in south-east Scotland. The clinical signs were a flaccid paralysis of the hind limbs and in severe cases collapse. Serum creatine kinase and aspartate aminotransferase activities were increased. Clinically affected sheep had a mean reciprocal serum antibody titre in a sarcocystis immunofluorescence antibody test of 557 whereas 22 sheep from the same flock, sampled one year earlier, showed a mean reciprocal titre of only 51. Histologically a heavy infestation of sarcocysts, myodegeneration and a non-suppurative myositis centred on degenerating sarcocysts were observed in a wide range of skeletal muscles and myocardium from four affected sheep. Monensin sodium had been inadvertently included in the protein pellet used in the feed for one week before the onset of the disease.
Vet Rec 1989 Apr 22
PMID:A myopathy of sheep associated with sarcocystis infection and monensin administration. 250 29

Acute renal failure was diagnosed by clinical, necropsy and histological criteria in 39 flocks (20 low ground, 13 hill and six marginal upland) in areas served by six veterinary investigation centres. Forty-eight lambs of 12 different breeds or crosses were investigated. The mean age of affected lambs was 38 days (range seven to 84 days); 21 lambs (44 per cent) were aged seven to 28 days, while only eight (17 per cent) were older than two months. Mortality in clinically affected lambs was almost 100 per cent, with no response to various treatments. Histological examination showed that 40 lambs (83 per cent) had nephrosis, while the rest had toxic tubular necrosis, interstitial nephritis or tubular damage associated with oxalate crystal deposits. Only about half of the lambs had any evidence of enteric infections or enteropathy. Acutely ill lambs had azotaemia, haemoconcentration and proteinuria; some lambs had glycosuria or haematuria. Samples of plasma from 22 lambs with nephrosis were compared with similar samples from 82 incontact but asymptomatic lambs. The clinically affected group had significantly elevated plasma urea, creatinine, total protein, globulin, phosphorus and chloride concentrations and significantly reduced plasma calcium concentrations compared with healthy lambs. Affected lambs had a significant reduction also in the calcium:phosphorus ratio. No significant differences between groups was found in plasma concentrations of albumin, glucose, lactate, glycerol, creatine kinase, alkaline phosphatase, sodium, potassium or magnesium.
Vet Rec 1989 Jan 07
PMID:Acute nephropathy in young lambs. 291 11

The clinical pathology and histopathology of two groups of Atlantic salmon with severe degenerative myopathy (pancreas disease) is described and compared with a third healthy group. One affected group was anorexic and had low plasma protein and albumin levels while the other was feeding and had normal levels. Both diseased groups had plasma and tissue vitamin E and selenium levels lower than the healthy group. Similarly, creatine kinase values were raised in affected groups. If representative of the syndrome as a whole, the results suggest that the myopathy of pancreas disease has a basis in a vitamin E-selenium deficiency, but whether primary or induced is not clear. The results also demonstrate that the myopathy and pancreatic atrophy do not inevitably lead to anorexia or any other clinically obvious sign of disease, despite both cardiac and oesophageal involvement.
Vet Rec 1986 Sep 20
PMID:Clinical pathology of myodegeneration (pancreas disease) in Atlantic salmon (Salmo salar). 377 31

A myopathy of horses at grass in east and south east Scotland was recognised in the autumn and winter of 1984 and the spring of 1985. The clinical signs resembled those of paralytic myoglobinuria. Grossly increased creatine kinase activities and the passage of dark brown urine were consistent features. However, the horses were not in training, most of them died and the muscles affected were those of posture and respiration rather than movement. The condition may be unrelated to nutritional myopathy because all the cases had adequate levels of alpha-tocopherol although their selenium status varied from normal to deficient. The clinical and pathological findings in 12 cases are presented and the differential diagnosis and possible aetiologies discussed.
Vet Rec 1986 Nov 01
PMID:Acute myopathy in horses at grass in east and south east Scotland. 379 93

A herd of lactating British Friesian cows was divided into two equal groups. After 14 days during which all the cows had free access to water one group (restricted) was allowed only 50 per cent of the voluntary water intake of the other group (control). After four days when the experiment was terminated, the milk yield of the restricted group had fallen to 74 per cent of that of the control group and their mean body-weight was reduced by 14 per cent. In the restricted group there were significant increases in the concentrations of urea, sodium, total protein and copper in serum, in the osmolality of serum, in the plasma activities of the enzymes creatine kinase and glutamate-oxaloacetate transaminase and in the packed cell volume of blood. The restricted cows behaved very aggressively around their water trough and spent more time in its vicinity. They spent less time lying down than the cows of the control group and some of them were not seen to drink and were withdrawn from the experiment before the end of four days. In a second experiment half the herd was allowed approximately 90 per cent of the water intake of the control group for 14 days. Decreases in milk yield and body-weight and changes in blood composition were much smaller and difficult to detect. However, changes in behaviour were still easily recognised although not as marked as in the first experiment.
Vet Rec 1980 Jun 28
PMID:Effect of reduced water intake by lactating dairy cows on behaviour, milk yield and blood composition. 719 26

Blood samples were taken before and after a cross country race over the marathon distance of 42 km. There was a rise in blood glucose and plasma free fatty acids and glycerol associated with a rise in plasma cortisol and glucagon but the fall in insulin was not significant (P > 0.05). Plasma potassium and albumin concentrations increased, calcium decreased and there was no change in sodium or bicarbonate concentrations. There was an increase in plasma urea, creatinine, uric acid, bilirubin and isocitrate dehydrogenase but no change in alkaline phosphatase. There was a rise in plasma creatine kinase. These results of a competitive race are compared with those of the 80 km non-competitive Golden Horseshoe Ride.
Vet Rec 1980 Dec 06
PMID:A biochemical study of the Arab Horse Society's marathon race. 746 99

During the summer of 1992 renal failure was diagnosed in 232 grazing cattle in 85 herds on the west coast of Norway. The salient clinical signs were depression, anorexia and melaena or fresh blood in the faeces; diarrhoea was also commonly observed. The serum concentrations of creatinine, urea, magnesium and phosphorus, and the activities of glutamate dehydrogenase, aspartate aminotransferase and creatine kinase were above normal and the serum calcium concentration was below normal. Post mortem examinations consistently revealed renal tubular necrosis. In some cases there was liver necrosis and also erosions at the base of the tongue, in the oesophagus and in the jejunum and colon. The toxicity was probably caused by the plant Narthecium ossifragum (bog asphodel).
Vet Rec 1995 Sep 09
PMID:Nephrotoxicity of Narthecium ossifragum in cattle in Norway. 750 63


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