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)

Acute altitude illnesses include acute mountain sickness (AMS), a benign condition involving headache, nausea, vomiting, irritability, insomnia, dizziness, lethargy, and peripheral edema, and potentially lethal high-altitude cerebral edema and pulmonary edema (HAPE). Recent evidence is summarized that AMS is related to cerebral edema secondary at least in part to hypoxic cerebral vasodilation and elevated cerebral capillary hydrostatic pressure. This results in reduced brain compliance with compression of intracranial structures in the absence of altered global brain metabolism. It is postulated that these primary intracranial events elevate peripheral sympathetic activity that acts neurogenically in the lung possibly in concert with pulmonary capillary stress failure to cause HAPE and in the kidney to promote salt and water retention. The adrenergic responses are likely modulated by striking increases of aldosterone, vasopressin and atrial natriuretic peptide. The effects of exercise on altitude-induced illness and various therapeutic regimens (acetazolamide, CO2 breathing, dexamethasone, and alpha adrenergic inhibitors) are discussed in light of this hypothesis.
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PMID:A neurogenic basis for acute altitude illness. 816 37

We investigated the effects of a turf application of the insecticide diazinon AG500 on Canada geese (Branta canadensis) on a golf course in coastal Washington (USA). On both 19 and 26 March 1987, 1 ha of turf on a golf course located in Birch Bay, Washington was treated with diazinon AG500 at a target application rate of 2.2 kg active ingredient per hectare (AI/ha). Treated areas were then irrigated with 6 mm water. Grass and water samples were collected from three different sites one day before and 1, 3, 7 and 14 days after each application. Diazinon residues > or = 20 ppm were found in golf course grasses for one week after each application. Diazinon residues in study area ponds and creeks were > or = 17 ppb. Samples from two irrigation puddles one day post-application had 1.00 and 0.20 ppm of diazinon, respectively. Numbers of geese present declined following diazinon application; however, no goose mortality was observed. Geese spent 422 and 538 min feeding on the treated areas after the first and second diazinon applications, respectively. One goose feeding in treated areas demonstrated signs of poisoning (lethargy, ataxia) for several hours. Two other geese feeding in the treated areas may have been slightly intoxicated. During carcass searches, three American wigeon (Anas americana) carcasses were found. Based on brain cholinesterase (ChE) levels and gastrointestinal (GI) tract residues of diazinon present, we concluded that these wigeon died from diazinon poisoning. Numerous songbirds (Passeriformes) also fed on the treated turf but no apparent response to the insecticide was observed.
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PMID:Response of Canada geese to a turf application of diazinon AG500. 835 49

A healthy dog developed signs of lethargy and vomiting after ingesting water from a tide pool containing blue-green algae. Fulminant hepatic failure occurred, and the dog was euthanized 52 hours later. At necropsy, the liver was large, friable, and discolored a dark red. Histopathology showed hepatocyte dissociation, degeneration, and necrosis. The alga was identified as Microcystis aeruginosa, a known hepatotoxin. The intraperitoneal administration of lyophilized cell material from the bloom caused hepatic necrosis in mice.
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PMID:Clinical and pathologic findings of blue-green algae (Microcystis aeruginosa) intoxication in a dog. 837 55

Mannitol is an osmotic diuretic used in acute oliguric renal failure, acute cerebral edema, and acute glaucoma. It is metabolically inert and is excreted through the kidneys. So once renal function is impaired, mannitol accumulates and the movement of water into the intravascular space with resultant cellular dehydration. Two patients suffered reversible acute oliguric renal failure following mannitol infusion given as treatment for intracranial hypertension. Both patients experienced nausea and vomiting and became increasingly lethargic with edema of general body. Congestive heart failure occurred. Laboratory data showed severe dilutional hyponatremia with hyperosmolality. We successfully treated them with extracorporeal ultrafiltration method (ECUM) and hemodialysis (HD). Some discussions were presented about acute renal failure following mannitol infusion.
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PMID:[Acute renal failure following mannitol infusion]. 837 73

Reproductive toxicity of 2-ethylhexanoic acid (2-EHA) was studied in Wistar rats. The animals (24 animals per sex per group) were given 2-EHA as a sodium salt in drinking water at daily doses of 100, 300, or 600 mg/kg. Control animals received plain water. Male rats were exposed to 2-EHA for 10 weeks and females for 2 weeks prior to mating, both sexes during the mating period and females during the entire gestation and lactation period. 2-EHA caused a slight but dose-dependent decrease in fertility; time to mating increased at 300 and 600 mg/kg and even total infertility ensued. 2-EHA slightly decreased sperm quality in males. The spermatozoa were significantly less motile at 100 and 600 mg/kg and abnormal sperm occurred more frequently at the two highest dose levels. The average litter size was reduced by 16% in the dose group receiving 600 mg/kg. The birth weights of the pups were unaffected but the body weight gain was transiently slower during lactation at 600 mg/kg. Several pups appeared abnormal (kinky tail, lethargic, slightly paralyzed legs) and the physical development assessed by several landmarks (opening of eyes, eruption of teeth, hair growth) and reflexes (grip reflex, cliff avoidance) was delayed at 300 and 600 mg/kg. In another experiment, a single dose of 600 mg/kg 2-EHA was given to pregnant females by gavage on Gestational Day 4, 5, 6, or 7 and the number of implantations were counted on Gestational Day 10. Administration on Day 6 decreased the number of implantations and caused resorptions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of 2-ethylhexanoic acid on reproduction and postnatal development in Wistar rats. 840 83

A 15-year-old mare mule was presented with a 2-month history of weight loss, lethargy, and anorexia. Clinicopathologic abnormalities were consistent with liver disease. Repeated urinalysis revealed hyposthenuria, but water intake and a water deprivation test were normal, suggesting adequate renal function. Ultrasonography revealed pulmonary, hepatic, and renal masses. Cytologic and histologic examination of pulmonary aspirates and hepatic biopsies, respectively, revealed polygonal neoplastic cells with many mitotic figures, the cells having the characteristics of adenocarcinoma. Necropsy confirmed a primary renal adenocarcinoma with metastasis to liver, lung, lymph nodes and the opposite kidney.
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PMID:Metastatic renal adenocarcinoma in a mule. 841 57

A total of 28 male spinal cord injury (SCI) patients were enrolled in an open label study to evaluate the efficacy and safety of terazosin to improve voiding. All patients were started on 1 mg daily dose at bedtime. The dosage was gradually increased to 1-2 mg twice daily, depending upon patient tolerance and a minimum acceptable systolic blood pressure of 90 mm Hg. Urodynamic evaluation was done in 24 patients prior to and one week after a maximum tolerated dose was established for at least 48 hours. The maximum dose varied from 1 to 5 mg daily. Subjective improvement in voiding was noticed in 50 percent of patients. Objective assessment with urodynamics showed a mean drop in maximum voiding pressure of 35 cm H2O (range 9-65 cm H2O) in only 42 percent of patients. Subjective improvement in voiding occurred in 14 of 17 patients with absent detrusor sphincter dyssynergia. The drug was discontinued in three patients with side effects of syncope in one patient, lethargy in another and body rash in the third. Because the tolerance dose of terazosin is variable and the therapeutic response is unpredictable, urodynamic monitoring is recommended to accomplish a useful outcome.
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PMID:Efficacy and safety of terazosin to improve voiding in spinal cord injury patients. 859 Oct 69

A nonsurgical rabbit model of enteric Shigella infection was developed for studying the pathogenesis and immunology of shigellosis and for evaluating Shigella vaccine candidates. In this model, rabbits are made susceptible to Shigella infection by a pre-inoculation conditioning procedure consisting of a 36-h nonfeeding period, with 250 mg of tetracycline administered in 250 ml of drinking water, 75 mg of cimetidine given intravenously, and two 15-ml doses of 5% sodium bicarbonate given orally immediately before orogastric administration of the bacterial inoculum. Lastly 2 ml of tincture of opium is administered intraperitoneally. With a virulent strain, Shigella flexneri 2a, the clinical and pathologic characteristics of shigellosis in this rabbit model were studied. Twenty hours after oral inoculation of 10(10) bacteria, all six experimental rabbits developed diarrhea and were lethargic or moribund, whereas the four control rabbits inoculated with sterile broth remained healthy. Histologic examination revealed severe, diffuse, necrotizing ileitis with hemorrhage in experimental rabbits, whereas no lesions were found in the controls. Although the major site of necrosis in this rabbit model was the ileum, as opposed to the colon in humans and nonhuman primates, the histologic morphology of the lesion was the same in the various hosts. Because it is relatively inexpensive and convenient, this model should facilitate study of the pathophysiology and immunology of shigellosis, thereby speeding development of oral vaccines, which can be tested in this animal model.
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PMID:Pathologic study of a rabbit model for shigellosis. 869 22

Hypernatremia resulting in neurologic symptoms ranging from lethargy to coma, and with underlying lesions of cerebral hemorrhage and thrombosis, has been reported in human beings. Herein we report two cases of cerebral infarction with venous thrombosis in cynomolgus monkeys. Both animals were severely hypernatremic because of water deprivation, with serum sodium levels of 185 and 193 meq/liter, respectively. At necropsy, there were bilateral multiple hemorrhagic and malacic areas visible on the surface of the cerebrum and extending into the parenchyma, primarily involving the occipital lobes. These lesions were interpreted microscopically as infarcts because, in addition to hemorrhage and necrosis, multiple thrombi were present in small and medium-sized veins of gray matter and meninges. The pathogenesis of hypernatremia-induced cerebral lesions is believed to involve cellular dehydration that caused shrinkage of the brain. Because the vasculature of the brain is tightly adherent to the skull, this shrinkage results in tearing of blood vessels, with consequent hemorrhage and thrombosis.
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PMID:Cerebral infarction in two cynomolgus macaques (Macaca fascicularis) with hypernatremia. 881 42

2-Ethylhexanol (2EH) is a weak nongenotoxic hepatic peroxisome proliferator in the rat. It is a high-volume chemical intermediate in the preparation of the plasticizers bis-(2-ethylhexyl) adipate (DEHA), bis-(2-ethylhexyl) phthalate (DEHP), and tris-(2-ethylhexyl) phosphate (TEHP), which are weak hepatocellular tumorigens in female mice. In consequence, the oncogenic potential of 2EH was evaluated in male (M) and female (F) rats and mice (50 animals/sex/group). Oral gavage doses of 2EH in 0.005% aqueous Cremophor EL (polyoxyl-35 castor oil) were given five times a week to rats: 0 (water), 0 (vehicle), 50, 150, and 500 mg/kg for 24 months, and to mice: 0 (water), 0 (vehicle), 50, 200, and 750 mg/kg for 18 months. Statistical comparisons of data were made between vehicle controls and treatment groups. There were no differences of biological significance between data from vehicle and water control groups. In rats, there were no dose-related changes at 50 mg/kg. There was reduced body weight gain at 150 mg/kg (M, 16; F, 12%) and 500 mg/kg (M, 33; F, 31%) and an increased incidence of lethargy and unkemptness. There were dose-related increases in relative liver, stomach, brain, kidney, and testis weights at sacrifice. Female rat mortality was markedly increased at 500 mg/kg. There was marked aspiration-induced bronchopneumonia in rats at 500 mg/kg; hematologic, gross, and microscopic changes, including tumors, were otherwise comparable among all rat groups. In mice at 50 and 200 mg/kg there were no dose-related changes and essentially no time-dependent or time-independent adverse trends in liver tumor incidence at the 5% significance level. At 750 mg/kg mouse body weight gain was reduced (M, 26; F, 24%), and mortality increased (M and F, 30%) versus vehicle controls. At 750 mg/kg there was a slight increase in nonneoplastic focal hyperplasia in the forestomach of mice (M 5/50, F 4/50) versus vehicle controls (M 1/50, F 1/50). There were increases in mouse relative liver (F, 21%) and stomach (M, 13%; F, 19%) weights at 750 mg/kg. There was a 12% incidence of hepatic basophilic foci and an 18% incidence of hepatocellular carcinomas in male mice at 750 mg/kg, not statistically significant compared with either control by Fisher's exact test. There was a 12% incidence of hepatic basophilic foci and a 10% incidence of hepatocellular carcinomas in female mice at 750 mg/kg, statistically significant (p < 0.05) compared with vehicle but not with water controls by Fisher's exact test. There were no metastases. Time-dependent and -independent statistical analyses showed an adverse trend in the incidence of hepatocellular carcinomas in male and female mice, correlated with toxicity (expressed as mortality) at 750 mg/kg. The time-adjusted incidence of hepatocellular carcinomas in male mice (18.8%) was within the historical normal range at the testing facility (0-22%), but that in females (13.1%) lay outside the normal range (0-2%). Under the conditions of these studies 2EH was not oncogenic in rats, but there were weak adverse trends in hepatocellular carcinoma incidence in mice at high dose levels which may have been associated with toxicity. The major effects of chronic dosing were mortality in female rats at 500 mg/kg and in male and female mice at 750 mg/kg, accompanied by reductions in body weight gain in rats at 150 and 500 mg/kg and in mice at 750 mg/kg. Direct comparison of any tumorogenic effects of 2EH given alone to female mice with those due to 2EH formed in vivo from DEHA, DEHP, or TEHP is limited by the high mortality caused by 2ER in female mice at equivalent doses of 2EH. While 2EH may be a contributing factor in the hepatocellular carcinogenesis in female mice associated with the chronic administration of DEHA and DEHP, it is unlikely to be the entire proximate carcinogen.
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PMID:Oncogenicity testing of 2-ethylhexanol in Fischer 344 rats and B6C3F1 mice. 899 51


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