Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
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Clinical differences were determined between granulomatous meningoencephalomyelitis, distemper, and suppurative meningoencephalitis in the dog. Dogs with granulomatous meningoencephalomyelitis had "head" signs on examination, which progressed to profound caudal fossa abnormalities, changes in mental status, and tetraparesis. Dogs with distemper had a gradual onset of posterior paresis; tetraparesis and occasional vestibular signs developed later in the course of disease. Dogs with suppurative meningoencephalitis had lethargy and anorexia at the time of examination, which progressed to nuchal rigidity, mental depression, tetraparesis, and profound alterations in consciousness. Analysis of cerebral spinal fluid was useful in distinguishing suppurative meningoencephalitis from the other 2 diseases. Twenty-seven cases of inflammatory disease of the CNS in dogs were reviewed. Comparisons of history, results of physical and neurologic examinations, ancillary data, and response to treatment were made. It appeared that certain clinical and neurologic features contributed to the diagnosis of these diseases.
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PMID:Differential diagnosis of granulomatous meningoencephalomyelitis, distemper, and suppurative meningoencephalitis in the dog. 394 14

Grass hay produced in the Coeur d'Alene River Basin of northern Idaho was fed to a group of 4 ponies. The hay contained Pb in concentration of 423 +/- 82 mg/kg and Cd in concentration of 10.8 +/- 1.4 mg/kg, resulting in daily exposures of the ponies to approximately 7.4 mg of Pb/kg and 0.19 mg of Cd/kg/day. The results in this group of ponies were compared with those from a group fed noncontaminated grass hay and given a daily dose of 10 mg of Pb/kg of body weight, in the form of lead acetate. Clinical toxicologic signs, hematologic changes, and blood and tissue Pb concentrations were similar in the 2 groups. However, the severity of the disease process appeared to be greater in the ponies fed the Pb- and Cd-contaminated hay. This was shown clearly by the shorter interval between onset of clinical changes and death in the ponies fed contaminated hay. The possibility of multiple heavy metal effects is discussed. Clinical toxicologic signs observed include incoordination, labial paresis, pharyngeal paresis, CNS depression, anorexia, and body weight loss. Anemia or marginal anemia was common and was often accompanied by the appearance of nucleated RBC and Howell-Jolly bodies in peripheral blood. Neither the hematologic response nor the blood Pb concentrations were reflective of the severity of poisoning, although blood Pb concentrations were greater than 0.35 micrograms/ml once clinical signs of toxicity were observed. Liver, kidney, spleen, brain, and bone Pb concentrations and liver, kidney, and brain Cd concentrations were increased in both the ponies fed contaminated hay and the ponies given lead acetate.
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PMID:Experimental lead toxicosis in ponies: comparison of the effects of smelter effluent-contaminated hay and lead acetate. 716 58

In guinea-pigs, the oral and subcutaneous LD50 values were very similar (cf. 0,173 mg/kg over 48 h with 0,116 mg/kg over 24 and 48 h). When dosed subcutaneously, a cumulative effect was observed. Intravenous administration of cotyledoside to anaesthetized guinea-pigs resulted in: dyspnoea, increased heart rates and blood pressures, and electrocardiagraphic changes typical of cardiac glycoside poisoning. A positive cardiac inotropic effect was succeeded by a positive chronotropic one. In sheep, acute and subacute intoxication resulted in ruminal, respiratory and cardiac changes. The signs included ruminal stasis, cyanosis, cardiac arrhythmia, ectopic foci and AV dissociation, followed by hypotension and progressive respiratory and cardiac failure. The skeletal muscles were affected in only 1 sheep vide infra. In chronically intoxicated sheep typical clinical signs of "krimpsiekte" developed, e.g. weakness, reluctance to stand, unsteadiness on feet, tremor and paresis of hindquarter muscles, paresis of the neck, arching of the back and standing with the feet close together. Respiratory function was affected in all 3 cases; ruminal stasis, with concomitant loss of appetite occurring in one, and a transient change in heart function in another. The syndrome induced by acute cotyledoside poisoning is similar to that of other cardiac glycosides, but the paretic signs of chronic intoxication resemble "krimpsiekte", a disease associated only with intoxication with the plants of the family Crassulaceae.
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PMID:Studies on South African cardiac glycosides. II. Observations on the clinical and haemodynamic effects of cotyledoside. 718 41

Twenty-three 2- to 5-month-old Beagle dogs were fed a purified thiamine-deficient ration (2 to 3 micrograms of thiamine/100 g of ration) at a rate of 40 to 70 g/kg of body weight/day depending on age. Eleven dogs were used as principles, 6 as pair-fed controls, and 6 as ad libitum-fed controls. Controls were treated once a week with an IM dose of 300 micrograms of thiamine hydrochloride/kg of body weight. Three stages of clinical disease occurred in the principals: (i) an initial short (18.0 +/- 7.9 days) stage of induction, during which the dogs usually grew suboptimally, but were otherwise healthy, (ii) an intermediate stage of preliminary clinical signs of deficiency, characterized by a variable period (58.5 +/- 37.0 days) of progressive inappetance, failure to grow, loss of body weight, and coprophagia, and (iii) a terminal stage, which, in most dogs, was abrupt in onset and short (7.6 +/- 6.0 days) and consisted of either a neurologic syndrome or sudden unexpected death syndrome. Eight of the principals developed the neurologic syndrome characterized by anorexia, emesis, CNS depression, paraparesis, sensory ataxia, torticollis, circling, exophthalmos, tonic-clonic convulsions, profound muscular weakness, recumbency, and then died. Common reflex abnormalities included exaggerated patella reflex, proprioceptive and supporting reflex deficits, induced torticollis and ventroflexion of head, and absent eye menace (blink) reflex. Three other principals developed the sudden unexpected death syndrome. Common signs of deficiency were inappetance and paresis. Two were found dead and 1, with severe ECG abnormalities (including elevation of ST segment and tall or deeply inverted T waves), was killed.
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PMID:Experimentally induced thiamine deficiency in beagle dogs: clinical observations. 719 32

Lasalocid was given to horses in a series of sequentially increasing single oral doses ranging between 5 and 30 mg/kg of body weight, with an appropriate washout period between treatments. One of the 5 horses died after a dosage of 15 mg/kg, 1 of 3 horses died after 21 mg/kg, 1 of 3 horses died after 22 mg/kg, and 1 of 2 horses died after 26 mg/kg. The LD50 of lasalocid for horses was estimated to be 21.5 mg/kg. Monensin was given to horses in a similar manner at dosages of 1, 2, and 3 mg/kg of body weight. One of the 2 horses died after a dosage of 2 mg/kg and 1 horse died after a dosage of 3 mg/kg. The clinical signs of toxicosis observed in horses given either drug were progressive and included depression, ataxia, paresis, and paralysis with partial anorexia. Intermittent profuse sweating was observed before death in horses given monensin.
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PMID:Toxic effects of lasalocid in horses. 727 Oct 10

The acute and subchronic toxicity of monenzine (preparation Elancoban -- 100 of Elanco Co., USA) to male lambs for fattening aged 3-4 months and weighing 16-28.5 kg was studied. It was established that the single per oral dose of 5 mg/kg weight of the natrium monoenzine salt causes a temporary lack of appetitie but no changes in the behavior and the general state of the animals. The use of a 10 and 30 mg/kg weight dose of the preparation led to death of the lambs on the 72nd-120th hour. The toxicity was clinically manifested by anurexia, arumination, ataxia, paresis, and paralysis of the limbs, tachicardia, taxipnea, hypothermia and showed down and weakened rumen movements. Erosive rumitis and abomasis, catharrhalhemorrhagis duodenitis, hemorrhages on the epicardis, hyperremia and parenchymal organ oedema, 3-4 times increased gall-bladder with numerous nodes having a sunken center on its walls were observed pathologo-anatomically, while microscopically blood vessel disturbances (hyperremia, hemorrhages and oedema) of the lungs, heart, spleen, endocrinal glands (thyroid, adrenal and hypophysis), the brain, and the leptomeninges, liver distrophy, distrophic nephrosis and necrotic holecystitis were obvious. Following a long term (30 days) application to the fodder in 10 and 50 g/t doses, monenzine-natrium does not have a negative effect on the behaviour, general condition, clinical and biochemical blood composition and the structural build up of the inner organs, but in the first 5-10 days of the treatment it causes loss of appetite. Additional specific investigations are needed to elucidate the effect of the preparation on body gain.
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PMID:[Acute and subchronic monensin toxicity for lambs]. 741 27

Medical records of 10 dogs in which fungal infection was diagnosed between 1982 and 1990 were reviewed. In each dog, infection was determined to be caused by a single species of fungus, either Aspergillus terreus, Penicillium sp, Paecilomyces sp, Chrysosporium sp, or Pseudallescheria boydii. Nine dogs were German Shepherd Dogs; 1 was a German Shepherd Dog cross, and 9 were females. The most common clinical signs were signs of neck or back pain (9 dogs), weight loss (7 dogs), anorexia (6 dogs), pyrexia (6 dogs), paresis (3 dogs), and paralysis (3 dogs). All 10 dogs had evidence of multiple sites of diskospondylitis. Urine sediment was examined in 6 dogs, and all 6 had fungal hyphae. Urine samples from these dogs produced a medium to heavy pure growth of fungi when placed on Sabaraud's medium. Predisposing causes were not identified in any of the dogs. Four dogs were euthanatized immediately after diagnosis because of paralysis or paresis. The other 6 dogs were treated, and 4 of the 6 received itraconazole. One dog was euthanatized for an unrelated problem after 21 months of treatment; 1 dog was still alive after 4 years of continuous treatment with itraconazole. The other 4 dogs were euthanatized because of eventual paralysis or paresis. Our results suggest that German Shepherd Dogs are predisposed to infection with opportunistic fungi, possibly because of a specific inability to mount an effective response. This predisposition needs to be further studied.
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PMID:Disseminated opportunistic fungal disease in dogs: 10 cases (1982-1990). 760 96

In a prospective study, the prevalence of 15 physical symptoms and symptom groups was evaluated in 1635 cancer patients referred to a pain clinic. In addition to pain, patients suffered an average of 3.3 symptoms: insomnia (59%), anorexia (48%), constipation (33%), sweating (28%), nausea (27%), dyspnea (24%), dysphagia (20%), neuropsychiatric symptoms (20%), vomiting (20%), urinary symptoms (14%), dyspepsia (11%), paresis (10%), diarrhea (6%), pruritus (6%), and dermatological symptoms (3%). While symptom prevalence was influenced by tumor site, pain intensity, and opioid treatment, only a minor relationship was seen between symptoms and gender, age, or tumor stage. The data emphasize that it is not sufficient to simply address pain during the treatment of patients with cancer pain; a more global approach to symptom management is necessary.
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PMID:Prevalence and pattern of symptoms in patients with cancer pain: a prospective evaluation of 1635 cancer patients referred to a pain clinic. 796 90

There are (at least) two types of receptor for cholecystokinin (CCK)/gastrin peptides. Highly potent specific antagonists are available for both types. The CCKA-receptor mediates classical CCK-like effects on the gut. Antagonists given to man inhibit pancreatic enzyme secretion and generally shorten gastrointestinal transit times. Potential clinical indications include anorexia, gastro-paresis, pseudo-paresis, pseudo-obstruction, severe constipation and chronic pancreatitis. However gallbladder contraction is markedly inhibited and this led to gallstone formation in baboons. This will obviously have to be avoided if CCKA antagonists are to be used in man. CCKB-receptors mediate the effects of gastrin on the gut and the effects of CCK in the brain. They inhibit gastrin-stimulated acid secretion. If used in acid-peptic disease they might inhibit the trophic effects of gastrin on enterochromaffin cells. CCKB-antagonists can also inhibit the growth of some gastrin-dependent tumours, including certain human colonic cancer cell lines which produce gastrin. CCKB-antagonists have a potent anxiolytic-like effect in animals, and this effect might become their main clinical application.
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PMID:CCK/gastrin antagonists--clinical perspectives. 826 65

Plasma cell myelomas in horses have been reported infrequently. Data from 10 cases, 9 from the literature and 1 new case, are used to characterize the disease in the horse. Hot-blooded horses (7/10), specifically Quarter Horses (4/10), were most often affected. Median age at diagnosis was 11 years (range, 3 mo-22 yr) and both male (5) and female horses (5) were represented equally. Clinical findings included weight loss (6/8), anorexia (4/8), fever (4/8), limb edema (4/8), pneumonia (3/8), rear leg paresis/ataxia (3/8), epistaxis (3/8), palpable lymphadenopathy (2/8), and bone pain (2/8). Anemia (8/8) was present routinely, and in three horses, RBCs were macrocytic. Leukopenia (2/8), thrombocytopenia (2/8), and circulating plasma cells (3/8) were variable findings. Except for abnormal protein concentrations and hyponatremia (3), abnormal results from serum biochemical analysis including hypocholesterolemia (1), hypercalcemia (1), and azotemia (1) were reported infrequently. Hyperproteinemia (8/9), hypoalbuminemia (7/9), and hyperglobulinemia (8/9) were characteristic but not invariable findings. Monoclonal proteins (7/7) were detected in the alpha 2, beta, or gamma region by serum electrophoresis. The paraprotein's heavy chain, determined in four horses, was a subclass of IgG. Three horses had decreased concentrations of normal immunoglobulins. Variable proteinuria (trace to 4+) was detected by routine urinalysis in four of six horses. Bence Jones proteinuria was detected in one of five horses (heat precipitation) and monoclonal proteins were detected in two of three electrophoresed urine samples. Three of the horses had lytic bone lesions detected radiographically. Bone marrow aspirates were diagnostic in two of five horses.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma cell myeloma in the horse. A case report and literature review. 833 11


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