Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Six serologically negative sows were infected by intranasal instillation of porcine cytomegalovirus (PCMV) between 31 and 85 days of pregnacy. Four sows showed an afebrile anorexia and lethargy 14-25 days after infection and all 6 developed significant increases in indirect immunofluorescent (IIF) antibody titres within 35 days. Virus was recovered from nasal and/or cervical swabs from 2 sows during life and from lung macrophage cultures after death. At term the sows were killed and their fetuses harvested by caesarean section. The number of mummified and stillborn fetuses increased from 4/63 in 6 previous litters to 18/60 in the 6 present litters. Nine of 43 fetuses born alive were reared in isolators for up to 6 weeks but the majority were killed for examination on the day of birth. Virus was isolated from 16 piglets from 4 of the 6 litters examined; it was isolated most frequently from lungs and liver but also from spleen, kidney, brain and nasal mucosa. Unsuckled day-old pigs had insignificant IIF titres, irrespective of whether they were excreting virus or not. The 5 congenital excretors which were reared all died within 7 days but no death occurred among their 4 litter-mates. Post-natal infection of 2 of these piglets reared in contact with congenitally infected pigs was suggested by the recovery of virus from nasal swabs 17 and 27 days after birth and the subsequent rise in IIF titre to 1/256 by day 42.
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PMID:Experimental transplacental transmission of porcine cytomegalovirus. 19 22

Two newborn infants, male (A) and female (B), with lethal hyperammonaemia are described in the same family. In both, symptoms started on the second day of life. Lethargy and hypotonia were the most prominent initial findings and were followed by convulsions and coma. In both, blood ammonia levels rose to 570 mumol/u (795 microgram/100 ml) a few hours before death, which occurred on the third and fourth day of life respectively. Assay of liver urea cycle enzymes in baby B showed a complete absence of mitochondrial carbamyl phosphate synthetase activity.
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PMID:Neonatal hyperammonaemia with complete absence of liver carbamyl phosphate synthetase activity. 20 10

Extensive water, sodium, chloride, bicarbonate, and potassium losses occur in the diarrheal calf. The water loss is entirely from the extracellular space. In severe cases, hypovolemic shock occurs with the blood volume decreased by as much as one-half. Acidosis, which results from fecal bicarbonate loss, lactic acidosis, and renal dysfunction, results in tissue buffering, which in turn causes the efflux of cellular potassium ions. Although there is a total body potassium deficit, plasma potassium concentration is increased. This, in conjunction with an intracellular deficit, causes weakness, lethargy, and potassium cardiotoxicosis resulting in death. Hypoglycemia also contributes to the weakness and lethargy seem as calves become moribund. These losses from the body and shifts in fluids and electrolytes must be understood to develop the most effective rationale for supportive therapy.
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PMID:Pathophysiologic changes due to coronavirus-induced diarrhea in the calf. 21 8

The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.
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PMID:Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss. 21 10

A progressive neurological illness characterized by myoclonus, motor and sensory deficits, and lethargy occurred in a patient with Hodgkin's disease and was fatal within two months. A focal inclusion cell encephalitis was demonstrated by immunohistological means to be due to measles virus. Measles encephalitis must be considered a potential opportunistic agent in the immune-compromised host.
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PMID:Subacute measles encephalitis complicating Hodgkin's disease in an adult. 21 19

Inoculation of three- to four-week-old BALB/c mice with temperature-sensitive (ts) vesicular stomatitis virus mutant G41 produced a subacute neurological disease, initially characterized by development of lethargy, hunched posture, and ruffled fur within five to seven days after infection. More than 90% of infected mice developed these clinical signs. In approximately 60% of infected mice, the initial neurological signs proceeded to striking hind-limb paralysis and weight loss. These signs usually appeared by seven to nine days after infection and lasted for 21-28 days. Only 16% of the mice died as a result of infection; death usually occurred eight to 12 days after infection. Most of the infected mice recovered from the acute phase of disease and appeared normal by four weeks after infection. However, hind-limb paralysis persisted in 4% of the mice for as long as the mice were observed, i.e., 42 days. The mutant ts-G41 was recovered from the brains and spinal cords of infected mice for the first seven days after infection. Peak titers of virus were modest, 10(4)-10(5) pfu/ml in brain tissue and 10(3)-10(4) pfu/ml in spinal cord tissue. Virus isolated after in vivo infection was temperature-sensitive and thus not revertant wild-type virus. Although virus was recoverable by homogenization for only the first seven days of infection, use of cocultivation techniques permitted the detection of ts-G41 in brains and spinal cords of infected animals for as long as 21 days after infection. Virus recovered by cocultivation was also temperature-sensitive.
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PMID:Subacute infection with temperature-sensitive vesicular stomatitis virus mutant G41 in the central nervous system of mice. I. Clinical and virologic studies. 22 Mar 28

In contrast to its lethargy at physiological pH, horse heart cytochrome c can be oxidized at room temperature by the axial inner sphere oxidant bromomalononitrile (BMN) at higher acidities. The following stoichiometry obtains: 2Fe11 c + BrCH(CN2) + H+ leads to 2FeIII c + CH2(CN)2 + Br-, and the rate law is given by: rate = k2(FeIIc)(BMN). At an ionic strength of 1.0 (KCl), second-order rate constants vary from 300 l. per mol per sec (pH 2-3) to 0(pH 9). Below pH 6 there is a noticeable increase in rate with ionic strength while there is no specific salt effect for the process. At pH 7.4 there is no influence of added salt (0.01-1.0 M) upon the slow rate of reaction. The vast changes in rate occur over a pH region (3-6) in which only very minor changes in the visible spectrum of the cytochrome are manifest. The results are interpreted in terms of a conformational isomerism of cytochrome c in which the effective redox geometry alters from a predominantly "short C" form (in which an axial position is available for substitution) at lower pH's to a predominantly "C" form (axial positions encumbered) in the physiological region. At 5 degrees, pH 7.4, both hemes of beef heart cytochrome oxidase are oxidized by the addition of BMN (k2 = 29 plus or minus 3 l. per mol per sec). However, the reaction is inhibited by potassium cyanide and the protein containing iron(II) cyt alpha along with the cyano adduct of iron(II) or iron(III) cyt alpha3 is inert. The results demonstrate cytochrome alpha3 as the site of reaction and that alpha reduces alpha3 in the process. Cytochrome oxidase does catalyze the oxidation of cytochrome c with BMN as substrate. Taken together the results provide additional support for a recent theory and they demonstrate BMN to be an efficient probe for the effective redox geometry of a hemoprotein in solution.
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PMID:Conformational isomerism and effective redox geometry in the oxidation of heme proteins by alkyl halides, cytochrome c, and cytochrome oxidase. 23 44

To determine the hepatic and intestinal toxicity of sodium cyanate, this compound was administered to rats by orogastric tube (PO) or intraperitoneal injection (IP). At low dosage (50 mg. per kilogram per day PO for 8 weeks), the animals showed no clinical effects other than mild lethargy. They had normal intestinal absorption studies, but demonstrated decreased liver G6PD activity and a slight increase in hepatic glycogen. At higher dose levels (200 mg. per kilogram per day PO for 10 days, 400 mg. per kilogram per day PO for 3 days, and 100 mg. per kilogram per day IP for 10 days), the animals became very lethargic and developed hind-limb paralysis; many animals died during the period of dosing. The severity and rate of onset of symptoms increased proportionally with the dose level. Liver sections from rats receiving these higher doses showed striking increases in glycogen deposition. Activities of hepatic enzymes involved in glycogen synthesis and degradation were measured in rats receiving 200 mg. per kilogram per day PO or 100 mg. per kilogram per day IP. Significant decreases were noted in the activities of glucose-6-phosphatase and G6PD in PO-dosed rats. The activities of phosphorylase, UDPG-pyrophosphorylase, glycogen synthetase, phosphoglucomutase, and debrancher did not differ from control rats. In IP-dosed rats, significant decreases were observed in the activities of glucose-6-phosphatase, G6PD, phosphorylase, and UDPG-pyrophosphorylase, but not in the other glycogen-related enzymes. Our data suggest that sodium cyanate affects several enzymes of hepatic glycogen metabolism but that the enzymes vary in their susceptibility (glucose-6-phosphatase and G6PD greater than phosphorylase and UDPG pyrophosphorylase.
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PMID:In vivo hepatic and intestinal toxicity of sodium cyanate in rats: cyanate-induced alterations in hepatic glycogen metabolism. 23 70

Eighty-four patients have undergone surgical exploration following a clinical diagnosis of hyperpathyroidism over a 20-year period. Urinary tract calculi were the major indication for exploration, and 90% of these patients had recurrent calculi. Osteitis fibrosa was a rare presentation of hyperparathyroidism. Lethargy, sometimes profound, was an important symptom, in some instances the dominant feature. Persistent hypercalcaemia remains the chief diagnostic investigation, with helpful confirmation from estimation of the parathyroid hormone level. Little attempt was made in this series to utilize preoperative localization techniques, reliance being placed on meticulous bloodless surgery to find normal and abnormal parathyroid tissue. Eighty-five explorations were carried out in the 84 patients. Seventy-four of the explorations were successful, converting the patient to a normocalcaemic state. Of these, 63 had a single adenoma (86%).
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PMID:Twenty years' experience with parathyroid exploration. 28 Dec 16

Seven patients with cancer complicated by nonmetastatic sagittal sinus thrombosis were encountered in a 7-year period. Five had hematologic malignancies and two had solid tumors. There were two different presentations. In the first, neurologic signs and symptoms (e.g., headaches, seizures, hemiparesis, lethargy) occurred suddenly in five patients shortly after initiation of cancer therapy. Four of these five patients recovered with minimal residua; the fifth died as a direct result of the sinus thrombosis. The second presentation occurred in the two patients with terminal cancer who declined gradually without focal signs; both patients died. Only arteriography can reliably establish the diagnosis of sagittal sinus occlusion. In patients with cancer, sagittal sinus occlusion probably results from a "hypercoagulable state" associated with the systemic neoplasm.
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PMID:Nonmetastatic superior sagittal sinus thrombosis complicating systemic cancer. 28 38


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