Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0030552 (
paresis
)
5,831
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Retinol (vitamin A), alpha-tocopherol (
vitamin E
), and Zn are micronutrients essential for health and performance. We determined the effects of parturition, lactation, and periparturient Ca status on plasma retinol, alpha-tocopherol, and Zn in 18 Jersey cows during the 2 wk before and after parturition. Six cows developed clinical milk fever. Prepartum plasma concentrations of retinol, alpha-tocopherol, and Zn decreased progressively in all animals. A nadir was reached at 1 d postpartum when concentrations declined to 38, 47, and 67%, respectively, of prepartal baseline concentrations. Plasma Zn returned to baseline concentrations within 3 d of calving, and plasma alpha-tocopherol returned toward baseline about 10 d after calving. Plasma retinol remained below baseline concentrations throughout the first 2 wk of lactation. The decline in plasma Zn observed at calving was more severe in cows with milk fever (parturient
paresis
) than in cows without milk fever. The decrease in plasma retinol and alpha-tocopherol observed at parturition was similar in cows with or without milk fever. These data document an acute decline in plasma retinol, alpha-tocopherol, and Zn in the immediate periparturient period and indicate that the decline in plasma Zn is more severe in cows with milk fever.
...
PMID:Decreased plasma retinol, alpha-tocopherol, and zinc concentration during the periparturient period: effect of milk fever. 227 48
Two horse farms, on which there was a high incidence of proven and suspected equine degenerative myeloencephalopathy (EDM), were studied. Symmetric ataxia and
paresis
, along with laryngeal adductor, cervicofacial, local cervical, and cutaneous trunci hyporeflexia, characterized the syndrome. Serum
vitamin E
concentration reflected a deficient state in affected and unaffected horses on both farms when compared with selected reference groups and with published values. A high incidence of the disease was evident in offspring of two particular sires on one farm. Vitamin E supplementation resulted in correction of the deficient state in most horses and was associated with a drastic reduction in the incidence of EDM on one farm from 40% to less than 10% the year following
vitamin E
supplementation. In addition, during the last year, the severity of signs in the few cases was dramatically reduced. This information substantiates the hypothesis that EDM is a
vitamin E
-responsive disorder of Equidae with a possible familial predisposition.
...
PMID:Equine degenerative myeloencephalopathy: a vitamin E deficiency that may be familial. 350 20
Modulation of acute monensin toxicosis in swine was evaluated in 2 studies. In study 1, 56 weanling male pigs were allotted to 14 groups of 4 each. Pigs in 7 groups were given tiamulin in the drinking water (to supply 7.7 mg/kg of body weight/day) for 3 days before and for 2 days after monensin administration. Monensin was given as a single oral dose (at 0, 7.5, 15, 25, 50, 75, or 100 mg/kg) to pigs in groups with or without tiamulin exposure. Prominent acute clinical signs of monensin toxicosis (hypermetria, hind limb ataxia,
paresis
, knuckling of hind limbs, and recumbency) developed by 2 to 6 hours after dosing in pigs given 15 or 25 mg of monensin/kg with tiamulin exposure, but not in pigs given the 15 or 25 mg of monensin/kg without tiamulin exposure. Also, the extent of monensin-induced skeletal muscle damage at 4 days after monensin dosing was enhanced in pigs given 7.5, 15, or 25 mg of monensin/kg and exposed to tiamulin. In study 2, 48 weanling male pigs were allotted to 8 groups of 6 each. Four groups of pigs were given 20 mg of monensin/kg orally, and 4 groups were given 100 mg of monensin/kg orally. For each monensin dose, a group was treated 24 hours before monensin administration with (i) selenium (Se)-
vitamin E
preparation, 0.25 mg of Se and 68 IU of d-alpha-tocopheryl acetate (
vitamin E
)/kg, IM; (ii)
vitamin E
only, 68 IU of d-alpha-tocopheryl acetate/kg; (iii) Se only, 0.25 mg of Se/kg; or (iv) vehicle.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Monensin toxicosis in swine: potentiation by tiamulin administration and ameliorative effect of treatment with selenium and/or vitamin E. 367 64
Paresis
of the limbs of two 4-month-old ostriches fed a diet predominantly of crushed maize was investigated. Raised levels of serum aspartate transaminase and creatine kinase were demonstrated in both birds. The less severely affected ostrich recovered after a single intramuscular injection of a
vitamin E
-selenium preparation but the other died despite therapy. An autopsy of the latter revealed focal pale areas in the thigh muscle. Microscopically affected muscle fibres showed degeneration, necrosis and regenerative changes. Fibrinoid degeneration and necrosis of some arterioles was observed as well as varying degrees of interstitial fibrosis. The above findings suggest a diagnosis of
vitamin E
-selenium deficiency.
...
PMID:Suspected vitamin E-selenium deficiency in two ostriches. 663 92
A progressive neurologic syndrome developed in six children with longstanding cholestatic liver disease. The neurologic abnormalities included areflexia, gait disturbance, decreased proprioceptive and vibratory sensation, and
paresis
of gaze. Serum
vitamin E
concentrations were uniformly low. Neuropathological studies carried out in two of the three fatal cases revealed degeneration of the posterior column, selective loss of large-caliber, myelinated axons in peripheral nerve, and spheroids in the gracile and cuneate nuclei. These lesions are similar to those found in animals with experimentally induced vitamin E deficiency. We therefore speculate that the neurologic syndrome in these children may be the result of chronic
vitamin E
malabsorption.
...
PMID:A progressive neurologic syndrome in children with chronic liver disease. 745 84
Nutritional and management strategies for dairy cattle are designed to prepare the cow for lactation and to minimize the incidence of metabolic diseases around calving. However, strategies initiated during the dry period should also consider the potential effects on the calf prior to and after calving. Fetal requirements for energy and protein are significant, particularly during the last trimester of gestation. Energy requirements increase to 1.3 to 1.5 times maintenance in late pregnancy; therefore, the formulation of rations for dry cows must contain sufficient energy to support fetal growth plus maintenance. Protein requirements during pregnancy increase, particularly during the last 2 mo. Colostrum is a source of immune components and nutrients to the neonate and contains more protein, immunoglobulins (Ig), nonprotein nitrogen, fat, ash, vitamins, and minerals than does milk. Because some vitamins do not cross the placental barrier, colostrum is the primary source of these nutrients for the calf after birth. Colostrum from cows that are not supplemented with
vitamin E
during the dry period may provide inadequate
vitamin E
to calves after birth. The Ig concentration in colostrum is not markedly affected by prepartum protein nutrition; diets containing high crude protein (CP) generally increase the nonprotein fraction of colostrum, but low CP diets do not affect the CP or Ig concentration of colostrum. However, data from beef calves suggest that absorption of IgG may be impaired when low protein diets are fed during the dry period. Diets for dry cows may be balanced to reduce the cation to anion ratio, which may reduce the incidence of parturient
paresis
. Recent research also suggests that these diets might increase the incidence of calves born in respiratory acidosis, which may impair the acquisition of passive immunity.
...
PMID:Nutrient and immunity transfer from cow to calf pre- and postcalving. 981 84
Turkey knockdown was diagnosed in three of five flocks of hen turkeys on a single farm within a 12-mo period. The age of birds in the flocks affected ranged from 6 wk 2 days to 7 wk 4 days. The attack rate ranged from 0.02% to 0.30% with a case fatality rate in affected birds ranging from 0 to 74%. The diagnosis was made on the basis of clinical signs and histopathologic lesions associated with knockdown. The feed in all flocks contained bacitracin methylene disalicylate and monensin (Coban). Affected birds were recumbent, demonstrated
paresis
, and were unable to vocalize. Postmortem examination revealed few significant lesions although pallor of the adductor muscles and petechiation in adductor and gastrocnemius muscles were noted. Birds that had been recumbent for extended periods were severely dehydrated. Consistent microscopic lesions included degeneration, necrosis, and regeneration of adductor, gastrocnemius, and abdominal muscles. No lesion in cardiac tissue was noted. Results of our investigation indicated that changes in water consumption,
vitamin E
status, and brooder to finisher movement correlated with the occurrence of knockdown. Turkey knockdown was defined in 1993 as any condition identified in a turkey flock that has affected the neuromuscular system to a degree that a turkey is unable to walk or stand. This definition was later modified to...neuromuscular or skeletal systems to a degree that a turkey is unable to walk or stand properly. Knockdown may be associated with numerous feed, management, or disease factors alone or in combination. Dosage of monensin, feed restriction/gorging, water restriction, heat stress, copper, mycotoxins, sodium chloride in feed, and sulfa drugs have all been suggested as contributing factors; however, laboratory studies to duplicate this have not been successful. This report presents observations from a single farm at which three of five hen flocks in a single year experienced knockdown. When a flock was reported as affected, a detailed investigation was initiated within 3 hr. The fifth flock was followed on a twice weekly basis from 0 to 8 wk of age to determine if initiating events were evident, but knockdown did not occur.
...
PMID:Turkey knockdown in successive flocks. 1100 29
Vitamin A toxicosis and vitamin E deficiency was diagnosed in a commercial rabbit-breeding colony and was associated with reproductive abnormalities, abortions, and poor survivability of kits in the breeding colony.
Paresis
and muscular dystrophy were noted in juvenile rabbits. Another group of New Zealand White rabbits from the same commercial colony was used to assess the effect of
vitamin E
-based therapy on clinical signs, reproduction, and vitamin A and E serum and liver levels. Blood samples were taken before and after dietary changes and
vitamin E
therapy. Serum
vitamin E
remained low after feeding a diet containing the recommended levels of
vitamin E
. Administration of
vitamin E
for 2 weeks lowered the serum vitamin A levels and increased the
vitamin E
serum and liver levels. In conclusion,
vitamin E
therapy appears to be an effective treatment for hypervitaminosis A.
...
PMID:Vitamin A toxicity and vitamin E deficiency in a rabbit colony. 1526 66
Senile dementia was the third most common admission diagnosis for New York psychiatric hospitals at the start of the twentieth century and the distinction between vascular and senile dementia was understood by psychiatrists even then. The term Alzheimer's disease (AD) was originally introduced to distinguish a pre-senile dementia from the common general
paresis
, but Alzheimer raised the possibility that pre-senile AD might not be distinguishable in clinical or histological terms from senile dementia. By the late 1970s it had become clear that the most common disorder producing dementia in elderly people was clinically and pathologically identical to pre-senile AD. AD is malignant, reducing remaining life expectancy by almost half and raising the risk of death over five years threefold (cancer raises it fourfold). Synapse loss associated with beta amyloid oligomers is a strong determinant of cognitive decline in patients with AD. Tau-containing neurofibrillary tangles usefully track disease severity. Unmodifiable risk factors include mutations in three genes which affect the production or metabolism of beta amyloid, the risk factor gene for Apolipoprotein [see symol in text]4 and female gender. The overriding risk factor is age, the prevalence of AD doubling with every five years of age until 90. Low education, head injury and low folate levels are examples of potentially modifiable risk factors. Since a delay of onset of five years would halve the number of patients with the disease, clinical trials for such putative protective factors as estrogens, folic acid,
vitamin E
, statins, and NSAIDs have begun. Cognitive and leisure activity may be protective against the development of AD but any protective function can only be confirmed by clinical trials.
...
PMID:Luigi Amaducci memorial award winner's paper 2003. A neurologist's view of Alzheimer's disease and dementia. 1555 52
Four adult ostriches developed sudden onset
paresis
and were unable to stand up when disturbed. After treatment with selenium and
vitamin E
, one of the birds could stand and move normally. The others died and post mortem examination revealed pale patches in the thigh muscles. Histopathological examination showed degeneration of skeletal muscles as seen in nutritional myopathy. Serum selenium and
vitamin E
levels were low whereas aspartate aminotransferase and creatine kinase levels were very high. All remaining birds on the farm were given multimineral and
vitamin E
supplement and no more cases were seen.
...
PMID:Selenium-vitamin E responsive myopathy in farmed ostriches (Struthio camelus) in Botswana. 1848 8
1
2
Next >>