Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In rats the application of 10 mg/kg 6-amino-nicotinamide (6-AN) leads to an accumulation of 6-phosphogluconate, by inhibition of 6-phosphogluconate dehydrogenase in the pentose phosphate pathway, in the cells of the spinal cord. The accumulation reaches its maximum after 18-24 h. It seems that there exists a relationship between the accumulation of 6-phosphogluconate and the lesion of the neuroglia, which is found in electron microscopic studies. Symptoms of a spastic paresis only develop later when the spinal interneurones are destroyed as a consequence of the lesion of the neuroglia. The accumulation of 6-phosphogluconate almost exceeds the 400 fold of the norm. No considerable differences are found between the effects of a dose of 35 mg 6-AN/kg and one of 10 mg 6-AN/kg. Free gluconate is identified enzymically in the cells of the spinal cords of the rats treated with 6-AN. The compound is very probably formed by dephosphorylation and diffuses into the blood. 6-Phosphogluconate is an inhibitor of the phosphoglucose isomerase. Its accumulation shifts the equilibrium towards glucose 6-phosphate. The lactate concentration decreases as compared with the untreated controls. Muscular action potentials are recorded extracellularly with a concentric needle electrode from the musculus gastrocnemius of rats treated with 6-AN. First activations of the electromyograms are found 48 h after the application of 10 mg 6-AN/kg. The electrical activities increase during the time in which a progressive destruction of the interneurones occurs. The electromyogram displays a permanent state of excitation with high amplitudes and an increased frequency. The continuity and intensity of the increased activity recorded by the electromyograph is the most important pathological finding. p-Chlorophenyl-GABA and, still more so, chlorpromazine cause temporary reduction of the excitation processes and an electromyogram nearly at rest. Under the same conditions, haloperidol is only slightly effective. The symptoms developed by the chemical destruction of the interneurones of the spinal cord, with rigidity and spasticity of the hind limbs, are suitable for testing antispastic drugs.
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PMID:Spastic paresis after 6-aminonicotinamide: metabolic disorders in the spinal cord and electromyographically recorded changes in the hind limbs of rats. 13 91

The most obvious symptoms of rabies in farm animals and pets in South Africa and South-West Africa are discussed in the light of information obtained during routine examination of specimens for the 10-year-period 1967--1976. More than 55% of the cases encountered were cattle in which the most obvious symptoms were salivation (92%), bellowing (69%), aggressiveness (47%), paresis or paralysis (30%) and straining (12%). Unlike cattle, the most obvious symptom in goats was aggressiveness (83%). Salivation was observed in ony 29% of goats but, like bellowing in cattle, bleating was very obvious in 72% of cases. Sheep were usually quiet, but 67% were aggressive. Salivation was observed in 30%, while 27% showed an abnormal sexual desire. The second highest incidence of rabies was recorded in dogs (20%). Aggressiveness was the most obvious symptom (71%) followed by salivation (48%), paresis and paralysis (28%) and barking (11%). With the exception of salivation and paresis, which were rarely encountered, aggressiveness was the only symptom observed in cats. Several cats were encountered with rabies-like symptoms due to organic phosphate poisoning. The most obvious symptoms in horses and donkeys were aggressiveness (77%), paresis or paralysis 33%), the chewing of foreign matter (33%) and salivation 22%). It is obvious that other conditions can easily be confused with rabies. Therefore every possible cause for rabies-like behaviour must be considered and eliminated to avoid unnecessary destruction of animals.
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PMID:[Symptoms of rabies in pets and domestic animals in South Africa and South West Africa (author's transl)]. 55 Nov 89

Twenty-four lactating cows were fed a normal-calcium (.75% of dry matter) diet plus free-choice dicalcium phosphate supplement for 8 wk, a low-calcium (.25% of dry matter) diet for 9 wk, and a low-calcium (.25% of dry matter) diet plus free-choice supplement for 4 wk. The low-calcium diet did not appear to affect adversely feed intake, milk production, or plasma ions. Depression of plasma calcium by sequestration with a chelating agent was less following low intake of calcium than following adequate calcium intake. Presumably, lower calcium intake increased parathyroid hormone which resulted in a larger and more responsive calcium pool immediately mobilizable. Changes in plasma phosphorus and magnesium were similar among treatments. Low calcium intake for short times apparently will not affect intake or production and may increase resistance to calcium stress such as hypocalcemia and parturient paresis.
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PMID:Effects of a low calcium diet on feed intake, milk production, and response to blood calcium challenge in lactating Holstein cows. 81 74

The development of organophosphorus-induced delayed neurotoxicity (OPIDN) was studied in the European ferret (Mustela putorius furo). A single oral or dermal dose of 250, 500, or 1000 mg tri-o-tolyl phosphate (TOTP)/kg body weight was administered to adult male ferrets. Corn oil served as the vehicle in the oral test and 95% ethanol was the vehicle in the dermal test. At 48 h posttreatment, half the animals in each group were killed by cervical dislocation for assessment of whole-brain neuropathy target esterase (NTE) activity. The remaining 5 animals per group were observed and examined neurologically on a daily basis for a subsequent 54 d. All ferrets dosed dermally with 1000 mg TOTP/kg body weight developed clinical signs characteristic of OPIDN ranging from ataxia to partial paresis. Ferrets administered 250 and 500 mg TOTP/kg body weight via the dermal route displayed variable degrees of hind limb weakness and ataxia. Of the animals dosed orally, only those in the 1000 mg TOTP/kg body weight group showed clinical signs indicative of OPIDN. These signs did not progress beyond mild ataxia. Small amounts of axonal degeneration were noted in the dorsolateral part of the lateral funiculus and in the fasciculus gracilis of spinal cords in ferrets receiving dermal doses of 1000 mg TOTP/kg body weight. Whole-brain neuropathy target esterase activity was also maximally inhibited (46%) in animals receiving 1000 mg TOTP/kg dermally. These results suggest that the ferret is a species that is susceptible to OPIDN.
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PMID:Delayed neurotoxic effects of tri-o-tolyl phosphate in the European ferret. 291 34

To investigate the cat as a test animal for organophosphorous compound-induced delayed neurotoxicity, tri-o-cresyl phosphate (TOCP) was applied directly on the unprotected back of the neck of young adult cats. Single dermal doses, ranging from 250 to 2000 mg/kg TOCP, or subchronic daily administration of 1 to 100 mg/kg produced delayed neurotoxic effects in the cat. Severity of delayed neurotoxicity depended on the dose and duration. Clinical signs were characterized by hindlimb weakness, ataxia, and paresis. Electromyographic abnormalities resulting from acute denervation were observed in most cats that developed a neurologic deficit. No changes were seen in the motor nerve conduction, thus suggesting that the deficits were in the terminal branch rather than being diffuse lesions in the peripheral nerves. These results correlated well with histopathologic results showing lesions in the most distal portion of the longest tracts in both central and peripheral nervous systems. In the spinal cord, histopathologic studies showed that the ascending tracts of the upper cervical levels and descending tracts of the lumbosacral regions were affected most frequently. Although this study shows that the cat, like the chicken, is susceptible to TOCP-induced delayed neurotoxicity, it demonstrates two differences between the cat and the chicken: greater sensitivity of the cat to the acute effect of TOCP, and greater extent of recovery or improvement of the cat from delayed neurotoxicity. This recovery was demonstrated by: improvement of clinical signs, gain in body weight, disappearance of electromyographic abnormalities, and regeneration of peripheral nerves. Dermal administration of a single 100-mg/kg dose or subchronic 0.5-mg/kg doses of TOCP did not produce delayed neurotoxicity.
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PMID:Electromyographic, neuropathologic, and functional correlates in the cat as the result of tri-o-cresyl phosphate delayed neurotoxicity. 395 42

The neurotoxic effects of tri-o-cresyl phosphate (TOCP) were studied in the cat to define the elements of neurologic testing and to correlate dysfunction with the results of histopathologic studies. Neurologic examination of treated cats categorized clinical signs of TOCP-induced delayed neurotoxicity in the cat into four stages: leg weakness, mild ataxia, severe ataxia, and paresis. These deficits correlated well with histopathological lesions found in the central and peripheral systems. The improvement seen, is attributed to regeneration and/or collateral sprouting of remaining axons of peripheral nerves that would not be expected in tracts of the central nervous system.
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PMID:Neurologic manifestations of tri-O-cresyl phosphate delayed neurotoxicity in cats. 664 17

The following parameters were tested in clinically intact dairy cows and those afflicted with parturitional paresis, over a period from four weeks before to 16 weeks after parturition: calcium, inorganic phosphate (PA), magnesium, alkaline phosphatase (AP), glucose, total protein, mineral mass/fat-free dry matter (A/FFT), mineral mass/volume of fresh skeletal bioptate (A/V). Literature data regarding the behaviour patterns of Ca, PA, Mg, AP, and glucose were confirmed. The dynamics of physiological mineral catabolism and mineral anabolism were expressed by the A/V changes more clearly than they had been reflected in A/FFT. The criterion A/V should be included as a function of age in the spectrum of parameters of metabolic monitoring.
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PMID:[Follow-up studies on the behavior of mineral metabolic parameters with particular reference to the degree of skeletal minearlization in the milch cow in the period 4 weeks ante- to 16 weeks postpartum]. 719 72

Nutritional or secondary hyperparathyroidism in a litter of German shepherd dogs is reported. The bitch lost interest in the litter 2 weeks post partum, the owner proceeded to feed the pups on a mainly meat diet (low in calcium) together with whole wheat bread (high in phosphate) until they were presented at Onderstepoort at the age of 6 weeks. Clinically the pups showed poor growth, posterior paresis and pain on palpation of the long bones. Radiological examination revealed decreased bone density and thickness of bone cortices. A diagnosis of nutritional or secondary hyperparathyroidism was made. The diet was corrected and in addition the pups were treated with a balanced supplement of calcium and phosphate with very good clinical response. The pathophysiology of nutritional or secondary hyperparathyroidism as well as ricketts and hypertrophic osteodystrophy as differential diagnoses are discussed.
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PMID:[Nutritional or secondary hyperparathyroidism in a German shepherd litter]. 725 68

Varying doses of 1 alpha-hydroxycholecalciferol (1 alpha-HCC) (50, 150, 250 and 350 micrograms) in propylene glycol were injected intramuscularly into 30 dry adult Israeli Friesian cows. Fourteen of these animals received a second dose; four were given 250 or 350 micrograms 48 hours after the first dose and 10 were given 350 micrograms 72 hours after the first dose. Plasma calcium rose after 24 hours at all dose levels except 50 micrograms. A dose-dependent peak in plasma calcium was reached after three to four days, followed by a return to baseline five days (150 micrograms) and eight days (250 and 350 micrograms) post injection respectively. Repeating the injection 48 or 72 hours later increased the time span by three and four days respectively. The effect of plasma inorganic phosphate was double that on plasma calcium. Plasma magnesium declined slightly three days post injection. High calcium feeding in conjunction with one or two injections of 350 micrograms 1 alpha-HCC did not modify the response of plasma calcium. An injection of 350 micrograms of 1 alpha-HCC was given once to 40 parturient paresis-prone cows of the same breed and twice at 72-hour intervals to 37 such cows. Six of the animals received 5 mg of flumethasone together with the second injection and 13 received it 48 hours later. This was to induce parturition, which occurred within 24 to 48 hours. None of the cows injected earlier than 24 hours prepartum developed parturient paresis in comparison with 22 out of 60 control animals which did. The results suggest that 1 alpha-HCC is useful in the prevention of bovine parturient paresis.
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PMID:Observations of the use of 1 alpha hydroxycholecalciferol in the prevention of bovine parturient paresis. 743 21

A "hen model" or organophosphorus induced delayed neuropathy (OPIDN) has been developed using white leghorn exposed acutely to one of five dosages of tri-ortho-cresyl phosphate (TOCP), between 300 to 700 mg/Kg. Neuropathy target esterase was studied in brain and peripheral nerve 24 and 48 hrs following exposure. Behavioral symptoms abnormality was assessed from days 1 through 20 after exposure using a 7 point rating scale and neuropathological examination was conducted on sample collected from animals on days 0, 7, 14 and 21. Neuropathological abnormalities were indicated by damage scores between 0 (no damage) and 4 (gliosis of brain tissue, myelin loss, appearance of axonal foci etc and more than 55% degeneration of peripheral nerve fibres). TOCP (600 and 700 mg/Kg, orally) was able to inhibit NTE more than 75% in brain and peripheral nerves. TOCP at the same dosage was also capable of resulting maximal levels of neuropathological score at 4. After exposure to doses weight loss was observed abruptly in a greater extent at the beginning leading to a change in weight gain till the end of the experiment. Behavioral signs were also dose dependent. Symptoms (gain abnormality, ataxia, paresis) were noted on the early stage of experiment. Inhibition of NTE was 65% could not be reached in hens given TOCP without causing lethality and no significant ataxia or lesions developed in those birds. Behavioral signs were also observed to be late onset. These data indicate that more than 75% inhibition of peripheral nerve NTE after 24 hr exposure was predictive of severe behavioral abnormalities and pathology in the hen whereas less peripheral NTE inhibition was indicative of less severe behavioral abnormalities and a lower score for neuropathological damage.
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PMID:Biochemical, neuropathological and behavioral studies in hens induced by acute exposure of tri-ortho-cresyl phosphate. 755 52


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