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)

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

In June-July 1983, staff from the Centre for Community Medicine at the All India Institute of Medical Sciences, in New Delhi, India, interviewed 145 mothers of children younger than 5 years old living in Garhkhera and Atali in Haryana State, India, to determine the usage rate of oral rehydration salt (ORS) and to use the results to design an educational campaign to prevent diarrhea and diarrhea-related deaths. Atali residents received their water through pipes while those in Gahrkhera received their water from handpumps. Diarrheal incidence stood at 2.88 episodes/child/year. Just 24.1% defined diarrhea accurately (i.e., WHO's definition = 3 loose stools/day). 40% defined diarrhea to be more than 6 stools/day. Only 29.7% knew about sugar salt solution or commercial ORS and only 9.7% of them could correctly prepare it. 38% of mothers gave a child with diarrhea a liquid, mainly weak tea or curd. 81.4% continued to feed a child during a diarrheal episode, but the investigators could not determine whether the amount was lower than normal because of a decrease in appetite. Breast-feeding mothers continued to breast feed during diarrhea. 64% did not know the danger signs (e.g. duration of at least 3 days, at least 6 stools/day, blood in stools, and lethargy), indicating a need to seek medical care. The most frequently reported danger signs were duration of at least 3 days (17%) and at least 6 stools/day (14%). These findings showed limited knowledge about diarrhea and diarrhea management. The additional campaign should focus on the danger signs.
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PMID:Knowledge and practices regarding diarrhea in rural mothers of Haryana. 142 47

The cause of the yearly death of an estimated 1,000 to 2,000 migrating dabbling ducks (Anas spp.) and 10 to 50 swans (Cygnus buccinator and C. columbianus) has remained a mystery for the last ten years in Eagle River Flats (ERF), a 1,000 ha estuarine salt marsh near Anchorage, Alaska, used for artillery training by the U.S. Army. We have gathered evidence that the cause of this mortality is the highly toxic, incendiary munition white phosphorus (P4). The symptoms of poisoning we observed in wild ducks included lethargy, repeated drinking, and head shaking and rolling. Death was preceded by convulsions. Farm-reared mallards dosed with white phosphorus showed nearly identical behavioral symptoms to those of wild ducks that became sick in ERF. White phosphorus does not occur in nature but was found in both the sediments where dabbling ducks and swans feed and in the gizzards of all carcasses collected in ERF. We hypothesize that feeding waterfowl are ingesting small particles of the highly toxic, incendiary munition P4 stored in the bottom anoxic sediments of shallow salt marsh ponds.
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PMID:White phosphorus poisoning of waterfowl in an Alaskan salt marsh. 147 72

Two male infants with hyperpigmentation, vomiting, lethargy and weight loss were reported. Hypoglycemia, hyponatremia, hypochloremia, hyperkalemia and metabolic acidosis were suggestive diagnosis of salt losing adrenocortical insufficiency. The absence of ambiguous genitalia, low 24 hour urinary 17 KS and pregnanetriol excretion precluded congenital adrenal hyperplasia. Low basal levels of plasma aldosterone and cortisol and low 24 hour urinary 17 OHCS excretion with disability to increase their corticosteroid secretions after ACTH stimulation as well as furosemide and theophylline infusions were supportive for the diagnosis of congenital adrenal hypoplasia. The definitive diagnosis was confirmed by ultrasonogram and computerized tomography. Family histories suggested X-linked recessive inheritance in these reported cases. Evidence of progressive postnatal adrenocortical degeneration was documented by progressive deterioration of adrenocortical functions beginning from mineralocorticoid to total corticosteroid deficiencies. The increased brain serotonin synthesis as the associated pathology of X-linked congenital adrenal hypoplasia was proposed on the basis of elevated basal plasma GH and PRL levels in the reported cases, taken together with an incidence of congenital LH deficiency and persistent ACTH hypersecretion in corticosteroid treated patients reported elsewhere.
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PMID:X-linked congenital adrenal hypoplasia: proposal pathogenesis. 273 38

About 150 waterfowl died and another 250 became weak and lethargic from suspected salt poisoning after using White Lake, a highly saline lake in Mountrail County, North Dakota. Frigid temperatures made fresh water unavailable, forcing the birds to ingest the saline waters with resultant toxic effects. Sick birds recovered when removed from the salt water and released into fresh water marshes. Brain sodium levels were higher in dead geese submitted for necropsy than in controls.
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PMID:Salt toxicosis in waterfowl in North Dakota. 362 5

Although used as a condiment and essential supplement since pre-Biblical times, chlorine as a part of the molecule salt has received little research effort by large animal nutritionists. Its low cost and the continued popularity of salt as a condiment and sodium supplement has precluded the appearance of chloride deficiencies. There is great variation in the chloride and sodium content of feedstuffs fed to lactating cows so that some formulations require no supplemental chloride or sodium. Chloride is highly available from feedstuffs, and when dietary chloride is low, the cow can reduce sharply her losses of chloride in urine, feces, skin secretions, and to some degree in milk. Clinical symptoms of chloride deficiency in the lactating cow include pica, lethargy, anorexia, lowered milk yield, constipation, and cardiovascular depression. Metabolic changes are expressed as a severe primary hypochloremia, secondary hypokalemia, and metabolic alkalosis. Requirement for chloride by the lactating cow is about .20%; a working allowance of .25% seems reasonable for cows in positive energy balance. With gradual resolution of the requirements for chloride and more data on chloride in feedstuffs, use of supplemental salt for either sodium or chloride can be reduced greatly.
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PMID:Mineral utilization by the lactating cow--chlorine. 370 Jul 98

We studied biliary excretion of sodium and chloride in 17 infants with external bile drainage through a "biliostomy" and describe four additional children who became ill from sodium depletion following external biliary drainage procedures for biliary tract anomalies. In the 17 infants, the mean +/- SD bile sodium concentration was 122 +/- 15 mEq/L. The mean +/- SD serum sodium concentration was low (132 +/- 7 mEq/L) (normal, 138 to 145 mEq/L). The mean +/- SD bile volume was 388 +/- 317 mL/day at one year following surgery (range, 40 to 1,000 mL/day). In the four children, clinical manifestations of sodium depletion (lethargy, anorexia, dehydration, and malnutrition) necessitated hospital admission. At that time, the serum sodium concentration ranged from 109 to 129 mEq/L, and the simultaneous urinary sodium concentration ranged from 0 to 5 mEq/L. Although dietary sodium was normal, biliary losses exceeded dietary intake, resulting in salt and water depletion despite renal conservation. Children with biliary drainage procedures are at risk for sodium depletion and should be monitored closely and supplemented accordingly until biliostomy closure is performed.
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PMID:Sodium homeostasis in infants with biliary drainage procedures. 370 30

Presented is the case of a normal two-month-old girl who developed seizures secondary to water intoxication. The infant had been fed 20 to 30 oz of water daily for three days, while her usual formula was withheld because of vomiting and diarrhea. On the day of admission, the infant exhibited signs of water intoxication in the form of lethargy, vomiting, and seizures. Hyponatremia, hypothermia, and hyperglycemia were noted on admission, and are common features of the syndrome. The patient responded well to fluid restriction and salt replacement. Previous reports have attributed water intoxication to feeding mismanagement, vigorous hydration, dilute formulas, and swimming lessons.
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PMID:Water intoxication with seizures. 396 5

Congenital adrenocortical unresponsiveness to ACTH is characterized by hyperpigmentation, muscular weakness, and episodes of hypoglycemia, with lethargy or coma and convulsion, and without signs or symptoms of salt wasting. Endocrinological evaluation reveals low levels of serum and urinary glucocorticoids, elevated levels of plasma ACTH and unresponsiveness to exogenous ACTH. On the other hand, aldosterone secretion or excretion is normal and is elevated during a low sodium diet. We reported on two patients with this syndrome. Case A, a 4 year-old-girl, showed skin hyperpigmentation, hypoglycemia, convulsion and coma. She was tall wlth a marked advance of bone age. Case B, a 4 year-old-boy, showed skin hyperpigmentation, fatigability and muscular weakness. Both of them revealed low urinary excretion of THE, THF, cortolone, and beta-cortolone and low levels of plasma cortisol. The levels of urinary glucocorticoids and plasma cortisol did not respond to ACTH administration. During a low sodium diet, urinary aldosterone excretion was elevated, urinary sodium excretion ws decreased, and the patients were able to conserve sodium normally. We also summerized other reported cases and discussed the etiology of this syndrome.
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PMID:[2 cases of congenital adrenocortical unresponsiveness to ACTH (author's transl)]. 625 Sep 21

The premenstrual syndrome (PMS) is a complex of symptoms that usually occurs seven to ten days before menses in large numbers of women. These symptoms typically cease during the 24 hours after the onset of menses. PMS affects many areas of the body, with each afflicted woman having her personal set of symptoms. Frequently encountered signs and symptoms include breast tenderness and swelling, weight gain, headache, abdominal cramping and bloating, food cravings, thirst, nausea, joint pain, acne, dizziness, hyperalgesia and one or more psychologic symptoms: irritability, lethargy and fatigue, depression, anxiety, hostility and aggression. Theories relating PMS to hormonal imbalance, vitamin deficiency or psychosomatic aberration have failed to explain this condition fully. Treatments using hormones, vitamins, oral contraceptives or diuretics have failed to relieve all the symptoms of PMS. The prostaglandin (PG) theory proposes that these nearly ubiquitous substances, produced in pathophysiologic amounts in brain, breast, gastrointestinal tract, kidney and reproductive tract, can trigger many of the PMS symptoms. If that is true, then a PG inhibitor could counteract excessive PG production and successfully control those PMS symptoms related to prostaglandin excess or imbalance. Therapy based upon this theory can proceed to the use of PG inhibitors in conservative steps. First, permanent deletion of xanthine-containing beverages (coffee, tea, cola and chocolate) from the diet can reduce nervousness, irritability and breast tenderness. Luteal phase salt restriction, with a mild diuretic used if necessary the last week before menses, adds to this effect. For the 20-25% of women who need more help, either a PG inhibitor or natural progesterone (to oppose the action of PGs), given when PMS begins, brings relief. In women with depressive PMS complaints, small daily doses of an antidepressant may prove helpful.
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PMID:The use of prostaglandin inhibitors for the premenstrual syndrome. 635 May 80


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