Gene/Protein Disease Symptom Drug Enzyme Compound
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Following sudden exposure to extreme cold, a group of 15-week-old pigs exhibited strange nervous signs which included arching the back, a high stepping gait, violent tremors of the whole body and screaming. The animals lowered themselves and once sitting, the tremors and screaming stopped. But if forced to rise, these signs recurred. When the pigs returned to a warmer environment, they rapidly recovered. An acute clinical myopathy caused by a marginal vitamin E deficiency was suspected. Other stress-induced factors, such as circulatory collapse caused by movement from a warm to a cold environment, were also thought to have contributed towards the myopathy.
Vet Rec 1979 Sep 22
PMID:Suspected acute myopathy of pigs. 51 11

In an outbreak of a degenerative myopathy six animals from a group of 20 intensively reared yearling bulls were affected. With one exception there was no history of stress or unaccustomed exercise. The diet was found to be deficient in vitamin E and selenium and it is thought that the rapid growth rate of the bulls concurrent with a continuing myodegeneration was sufficient to precipitate clinical disease.
Vet Rec 1977 Feb 05
PMID:Degenerative myopathy in housed yearling bulls. 84 29

An outbreak of acute myopathy occurred in a group of 23 Hereford cross and Aberdeen Angus cross 18-month-old heifers, running outside with a bull in February. One morning two were found recumbent, five were ataxic and one had fallen into a river and drowned. Subsequently two of the ataxic ones became recumbent. Serum creatine phosphokinase values were found to be directly proportional to the severity of the clinical manifestations. Myoglobinuria was not observed. Serum calcium, magnesium and inorganic phosphate levels were all within the normal ranges. Treatment of affected animals with selenium and/or alpha-tocopherol had no clear effect; from biochemical estimations carried out, the selenium and alpha-tocopherol status of both affected and unaffected animals was considered adequate. Five recovered, two spontaneously without treatment, but the two most severely affected did not improve with therapy and had to be slaughtered 13 and 25 days respectively after the onset of symptoms.
Vet Rec 1977 Apr 09
PMID:Acute myopathy in outwintered cattle. 86 42

Two 10-month-old heifers from a group of 20 young stock showed symptoms closely resembling paralytic myoglobinuria. One animal died five days after the onset of the symptoms and the other recovered slowly with selenium and vitamin E therapy. Histological examination of muscle tissue from the dead animal showed a myopathy resembling that due to vitamin E deficiency.
Vet Rec 1975 Sep 06
PMID:Myopathy in young cattle associated with possible myoglobinuria. 116 61

Unacceptably high mortalities in rainbow trout fry (Oncorhynchus mykiss) six to 10 weeks after they started to feed were recorded in two spring water trout hatcheries in Northern Ireland in May 1989. Muscle degeneration and necrosis were consistent with histopathological findings in both outbreaks, and this myopathy was similar to that previously described in salmonids and other species associated with vitamin E and selenium deficiency. A feed trial was designed to investigate the hypothesis that the vitamin E requirement of rainbow trout fry on these farms was higher than the current minimum recommendations. Three groups of fry were fed diets containing 147, 239 and 532 iu/kg alpha-tocopherol. The mortality in the groups was inversely related to the dietary alpha-tocopherol concentration, and there was severe myopathy in fry fed the diet containing 147 iu/kg alpha-tocopherol, mild myopathy in fry fed 239 iu/kg alpha-tocopherol but no myopathy in fry fed 532 iu/kg alpha-tocopherol.
Vet Rec 1992 Mar 14
PMID:Vitamin E-responsive myopathy in rainbow trout fry (Oncorhynchus mykiss). 156 35

To investigate annulate lamellae (AL) with nuclear changes, ultrastructural time course studies were done of the reversible end-plate myopathy in the soleus muscles of rats exposed chronically to a high dose of the anticholinesterase drug neostigmine. At the earliest stage (2 hours) in which severe subjunctional damage involving a nuclear lesion (nuclear pyknosis) was prominent, AL profiles were undetectable. At the intermediate stage (7, 21 days), in which the subjunctional organelles tended to cluster and nuclear pyknosis often accompanied degenerative features, most AL laid near the surface of the abnormal nuclei, where there were signs of elimination or formation of pores, as well as a progression of changes leading to the loss of pores. At the late stage (56 days), in which muscle repair was nearly completed and euchromatic nuclei usually were found, there was a concomitant enhanced formation of false nuclear inclusions and of the AL profiles in these sites. Pores are packed on nuclear envelopes, which detach themselves from the nucleus and take the same profile as AL. This phenomenon can be envisioned not only in the euchromatic but also in the abnormal (pyknotic or degenerated) nuclei. Following nuclear reconstitution, the nuclear envelope folding is accelerated to induce the usual pattern of AL organization, i.e., budding from the invaginated nuclear envelope.
Anat Rec 1989 Sep
PMID:Annulate lamellae-soleplate nuclei associations in skeletal muscle fibers of rats during chronic high-dose exposure to neostigmine. 254 12

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

An abnormality of chromosome 16 in an eight year-old male was associated with a multiple congenital anomalies syndrome characterized by myopathy, cataracts, blepharophimosis, microcephaly, failure to grow, profound mental retardation, moderate sensorineural hearing loss, grand mal seizures, bilateral inguinal hernia, and thoracolumbar kyphoscoliosis. Magnetic resonance imaging of the head demonstrated absence of the corpus callosum and extensive loss of brain parenchyma in the occipital regions. Chromosome analysis from peripheral blood of the patient showed a recombinant chromosome 16 [46, XY, rec (16), dup (p13.1----p13.3) del (q22----q24)]. The mother had a pericentric inversion of chromosome 16 [46, XX, inv(16) (p13.1;q22)]. Independent recombinant DNA studies have shown that the breakpoints of these chromosomal rearrangements flank the alpha-globin gene cluster locus.
 ...
PMID:Multiple congenital anomalies syndrome with myopathy in chromosome 16 abnormality. 381 61

Selenium deficient barley grown in Northern Ireland was treated with sodium hydroxide to deplete it of vitamin E. Housed cattle fed a complete diet based on this treated barley developed nutritional degenerative myopathy, showing that spontaneous myopathy in yearling cattle can be the result of vitamin E and selenium deficiency alone. The diet used is as effective and cheaper than others presently in use for inducing degenerative myopathy.
Vet Rec 1986 Feb 15
PMID:Use of sodium hydroxide treated selenium deficient barley to induce vitamin E and selenium deficiency in yearling cattle. 396 28


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