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

There is compelling evidence that micronutrients can profoundly affect immunity. We surveyed vitamin supplement use and circulating concentrations of 22 nutrients and glutathione in 64 HIV-1 seropositive men and women and 33 seronegative controls participating in a study of heterosexual HIV-1 transmission. We assayed antioxidants (vitamins A, C, and E; total carotenes), vitamins B6 and B12, folate, thiamin, niacin, biotin, riboflavin, pantothenic acid, free and total choline and carnitine, biopterin, inositol, copper, zinc, selenium, and magnesium. HIV-infected patients had lower mean circulating concentrations of magnesium (p < 0.0001), total carotenes (p = 0.009), total choline (p = 0.002), and glutathione (p = 0.045), and higher concentrations of niacin (p < 0.0001) than controls. Fifty-nine percent of HIV+ patients had low concentrations of magnesium, compared with 9% of controls (p < 0.0001). These abnormal concentrations were unrelated to stage of disease. Participants who took vitamin supplements had consistently fewer low concentrations of antioxidants, across HIV infection status and disease stage strata (p = 0.0006). Nevertheless, 29% of the HIV+ patients taking supplemental vitamins had subnormal levels of one or more antioxidants. The frequent occurrence of abnormal micronutrient nutriture, as found in these HIV+ subjects, may contribute to disease pathogenesis. The low magnesium concentrations may be particularly relevant to HIV-related symptoms of fatigue, lethargy, and impaired mentation.
 ...
PMID:Micronutrient profiles in HIV-1-infected heterosexual adults. 862 65

An amino acid formula produced in Japan is not supplemented with biotin since biotin is not permitted as a food additive. Biotin deficiency developed in an 11-month-old Japanese infant who had been diagnosed as a neonate with cow milk and soy bean allergy and fed with an amino acid formula and hypoallergenic rice processed by protease. Serum levels of zinc, essential fatty acids and biotinidase were within the normal range while that of biotin was below the normal range. Urinary 3-hydroxy-isovalerate and slightly elevated levels of plasma branched-chain amino acids disappeared 1 week after oral supplementation with 1 mg day-1 of biotin as did the symptoms of orificial skin lesions, lethargy, hypotonia and alopecia later. In summary, to prevent biotin deficiency, biotin should be added to the Japanese amino acid formula.
 ...
PMID:Biotin deficiency in an infant fed with amino acid formula and hypoallergenic rice. 881 58

Lethargy is characteristic of malnourished populations, but little is known about the biologic mechanism or consequences for cognitive performance. In the current experiment, 24-h activity patterns and performance of an attention task were studied in adolescent female monkeys (18-33 mo of age, n = 10/group) under conditions of moderate dietary zinc deprivation (2 micrograms Zn/g diet) and adequate dietary zinc (50 micrograms Zn/g). There were progressive decreases in daytime activity levels in the zinc-deprived group followed by slowing of growth around the time of the growth spurt. Attention performance was also impaired before the onset of growth retardation. Zinc-deprived monkeys failed to show the shift to later initiation of the rest phase of the diurnal cycle seen in controls in late adolescence. These data support previous findings that activity and attention can be affected during early stages of zinc deprivation before the onset of growth retardation.
 ...
PMID:Activity and attention in zinc-deprived adolescent monkeys. 894 16

Overliming and excessive application of superphosphate caused a zinc deficiency in the soil and so reduced the uptake of zinc by fodder plants. Bucks reared on such fodder had significantly (p < 0.01) less zinc in their hair compared with controls and suffered from 'conditioned zinc deficiency syndrome' with a significant (p < 0.01) loss of body weight, stunted growth, alopecia, lethargy, abnormal (kyphotic) gait, anorexia, digestive and respiratory problems. Oral supplementation with zinc sulphate very rapidly improved these conditions to near normality. Histological examination of samples of skin and testis from the zinc-deficient bucks revealed formation of excessive keratin, retention of nuclei in the stratum corneum and reduction in the width of the stratum granulosum in the skin, while samples of testis indicated degenerative changes, including atrophy of the seminiferous tubules, hyperplasia of the germinal epithelium and thickening of the walls of blood vessels.
 ...
PMID:Studies on 'zinc deficiency syndrome' in black bengal goats (Capra hircus) fed with fodder (Andropogon gayanus) grown on soil treated with an excess of calcium and phosphorus fertilizer. 944 77

Zinc chloride is a powerful corrosive agent. Reports of zinc chloride ingestion are uncommon, and there is little information about its toxicity and management. The authors report the clinical course of a 10-year-old girl who accidentally ingested an acid soldering flux solution (pH, 3.0; zinc chloride, 30% to < 60%). Systemic effects after the ingestion were unremarkable except for lethargy. Thus, chelation therapy was not considered. Severe gastric corrosion was caused by local caustic action. An antral stricture of the stomach approximately 3 weeks after the ingestion developed, and she underwent a modified Heineke-Mikulicz antropyloroplasty. Postoperatively, she made an uneventful recovery. On follow-up, although she was tolerating a normal diet, results of a barium meal showed her stomach to be totally aperistaltic. Results of a nuclear medicine study showed moderately delayed gastric emptying. Careful long-term follow-up is necessary, because there is potential risk for malignancy in the damaged stomach.
 ...
PMID:A case of zinc chloride ingestion. 957 76

An acute zinc chloride poisoning due to ingestion is a rare event. Symptoms include: corrosive pharyngeal lesions, vomiting and lethargy. Laboratory findings may include hyperglycaemia, hyperamylasaemia, exocrine pancreatic insufficiency and renal insufficiency. This case report describes an accidental zinc chloride poisoning in a child, with lethargy as the most pronounced clinical sign. Clinical evaluation and chelator therapy are discussed.
 ...
PMID:An acute zinc chloride poisoning in a child: was chelator therapy effective? 1040 22

An 11-yr-old captive-born female striped hyena (Hyaena hyaena) acutely developed lameness and swelling of the left front foot with anorexia, depression, and lethargy. Hematologic evaluation revealed regenerative anemia, azotemia, and other mild serum electrolyte and mineral abnormalities. Twenty radiographically visible coins and 10 coin fragments were removed by laparotomy and gastrotomy following unsuccessful medical therapy. The animal died during anesthetic recovery. Zinc serum levels were 41.0 ppm at first presentation and 36.0 ppm at the time of surgery, compared with concentrations of 1.78 ppm and 2.82 ppm for serum taken from this female and a male hyena 3 mo previously. Zinc toxicosis was diagnosed based on the similarity of clinical signs to those described in dogs, presence in the stomach of pennies minted after 1982 (when the zinc content of U.S. pennies was increased substantially), necropsy findings, and elevated serum and liver zinc values. The case highlights the risk posed by penny ingestion for subsequent zinc toxicosis in captive omnivores.
 ...
PMID:Zinc toxicosis in a captive striped hyena (Hyaena hyaena). 1123 34

We studied the prevalence of zinc deficiency in patients who were hospitalised in a geriatric ward and its association with risk factors for this deficiency and the possible symptoms. The serum zinc level was measured from 45 consecutive admissions to a geriatric ward and patient characteristics were collected. A peer group of healthy subjects originating from a population survey was used as a control group. The serum zinc measured in the admitted patients was significantly lower than the reference value for adults (65.8% had a lowered zinc level) and the serum zinc for healthy elderly. There was no association found with possible causes of zinc deficiency. In an univariate analysis lethargy was the only significant association to zinc deficiency. There was a reverse relationship between the sum of the number of present symptoms and the zinc proportion A lower zinc level is associated with symptoms of zinc deficiency. As more symptoms appear the probability of zinc deficiency is greater. The importance for the clinical practice based on present knowledge is discussed.
 ...
PMID:[Zinc deficiency in geriatric patients. A study on a geriatric department's wheeling and dealing]. 1201 44

Nickel sulfate hexahydrate is used in nickel plating, as a mordant in dyeing and printing textiles, as a blackening agent for zinc and brass, and in the manufacture of organic nickel salts. Nickel sulfate hexahydrate was nominated by the National Cancer Institute to the NTP as part of a class study of nickel compounds for which there was little information on the toxic and carcinogenic effects of inhalation exposure. Male and female F344/N rats and B6C3F1 mice were exposed to nickel sulfate hexahydrate (greater than 98% pure) by inhalation for 16 days, 13 weeks, or 2 years. Genetic toxicology studies were conducted in L5178Y mouse lymphoma cells. 16-DAY STUDY IN RATS: Groups of five male and five female F344/N rats were exposed to 0, 3.5, 7, 15, 30, or 60 mg nickel sulfate hexahydrate/m(3) (equivalent to 0, 0.7, 1.4, 3.1, 6.1, or 12.2 mg nickel/m(3)). Rats were exposed on weekdays only, for a total of 12 exposure days during a 16-day period. Additional groups of four or five male and female F344/N rats were exposed to 0, 3.5, 15, or 30 mg nickel sulfate hexahydrate/m(3)for tissue burden studies. In the core study, two 60 mg/m(3) males, one 30 mg/m(3) female, and all 60 mg/m(3)females died before the end of the study. Final mean body weights of all exposed groups of males and females were significantly lower than those of the controls, as were mean body weight gains of male rats. Clinical findings included increased rates of respiration and reduced activity levels in rats in all exposure groups, except those exposed to 3.5 mg/m(3). Absolute lung weights of 60 mg/m(3) males and of all exposed groups of females were significantly greater than those of the controls, as were the relative lung weights of all exposed groups of males and females. Inflammation (including degeneration and necrosis of the bronchiolar epithelium) occurred in the lungs of all exposed groups of males and females. Atrophy of the olfactory epithelium occurred in the nasal passages of all exposed groups of males (except 60 mg/m(3)) and in 15, 30, and 60 mg/m(3) females. Lymphoid hyperplasia in the bronchial or mediastinal lymph nodes was observed in 30 mg/m(3) males and in 60 mg/m(3) males and females. The concentration of nickel in the lungs of all exposed groups of males and females was greater than in control animals. 16-DAY STUDY IN MICE: Groups of five male and five female B6C3F1 mice were exposed to 0, 3.5, 7, 15, 30, or 60 mg nickel sulfate hexahydrate/m(3). Mice were exposed on weekdays only, for a total of 12 exposure days during a 16-day period. Additional groups of five male and five female B6C3F1 mice were exposed to 0 or 3.5 mg nickel sulfate hexahydrate/m(3)for tissue burden studies. All core study mice exposed to 7 mg/m(3) or greater died before the end of the study; all control and 3.5 mg/m(3)mice survived to the end of the study. Final mean body weights and weight gains of 7, 15, 30, and 60 mg/m(3)males and females were significantly less than those of the controls, and clinical findings in these groups included emaciation, lethargy, and rapid respiration rates. Absolute and relative lung weights of male and female mice exposed to 7 mg/m(3) or greater were significantly greater than those of the controls. Only tissues from mice exposed to 0, 3.5, or 7 mg/m(3) were examined histopathologically. Inflammation occurred in the lungs of 3.5 and 7 mg/m(3) males and females; necrosis of the alveolar and bronchiolar epithelium was a component of the inflammation in 7 mg/m(3)males and females. In addition, atrophy of the olfactory epithelium of the nasal passages was observed in 3.5 mg/m(3) males and females. Nickel concentrations in the lungs of mice exposed to 3.5 mg/m(3) were greater than those in the controls. 13-WEEK STUDY IN RATS: Groups of ten male and ten female F344/N rats were exposed to 0, 0.12, 0.25, 0.5, 1, or 2 mg nickel sulfate hexahydrate (equivalent to 0, 0.03, 0.06, 0.11, 0.22, or 0.44 mg nickel/m(3)), 5 days per week for 13 weeks. Additional groups of six male and six female F344/N rats were exposed to 0, 0.12, 0.5, or 2 mg nic mg nickel sulfate hexahydrate/m(3)for tissue burden studies. In the core study, one 2 mg/m(3)male rat died before the end of the study; all other males and all females survived until the end of the study. Final mean body weights and body weight gains of all exposed groups were similar to those of the controls. There were no significant clinical findings noted during the study. Exposure-related increases in neutrophil and lymphocyte numbers occurred and were most pronounced in female rats. With the exception of 0.12 mg/m(3)rats, absolute and relative lung weights of all exposed groups were generally significantly greater than those of the controls. Exposure-related increases in the incidence and severity of inflammatory lesions (alveolar macrophages, chronic inflammation, and interstitial infiltration) occurred in the lungs of all exposed groups of males and females. Lymphoid hyperplasia of the bronchial and/or mediastinal lymph nodes occurred in males exposed to 0.5 mg/m(3)or greater. Atrophy of the olfactory epithelium occurred in males and females exposed to 0.5, 1, and 2 mg/m(3)and in 0.25 mg/m(3)females. The concentration of nickel in the lungs of 0.5 and 2 mg/m(3) rats was greater than that in the lungs of control animals at 4, 9, and 13 weeks for males and at 13 weeks for females. 13-WEEK STUDY IN MICE: Groups of ten male and ten female B6C3F1 mice were exposed to 0, 0.12, 0.25, 0.5, 1, or 2 mg nickel sulfate hexahydrate, 5 days per week for 13 weeks. Additional groups of up to five or six male and female B6C3F1 mice were exposed to 0, 0.12, 0.5, or 2 mg nickel sulfate hexahydrate/m(3)for tissue burden studies. In the core study, four control males, three control females, and one 0.12 mg/m(3)male died before the end of the study; the deaths were not considered to be chemical related, and all other mice survived to the end of the study. The final mean body weights and body weight gains of all exposed groups were similar to those of the controls. There were no chemical-related clinical findings. Hematology changes similar to those reported in female rats occurred in female mice, but the mice were minimally affected. The absolute and relative lung weights of 1 mg/m(3)males and 2 mg/m(3)males and females were significantly greater than those of the controls. Increased numbers of alveolar macrophages occurred in all males and females exposed to 0.5 mg/m(3)or greater. Chronic active inflammation and fibrosis occurred in 1 and 2 mg/m(3)males and females. Lymphoid hyperplasia of the bronchial lymph node and atrophy of the olfactory epithelium in the nasal passages were observed in 2 mg/m(3)males and females. Nickel concentration in the lung of 2 mg/m(3)females was significantly greater than in control animals. 2-YEAR STUDY IN RATS: Groups of 63 to 65 male and 63 to 64 female rats were exposed to nickel sulfate hexahydrate by inhalation at concentrations of 0, 0.12, 0.25, or 0.5 mg/m(3) (equivalent to 0, 0.03, 0.06, or 0.11 mg nickel/m(3)). Animals were exposed for 6 hours plus T90 (8 minutes) 5 days per week for 104 weeks. Five male and five female rats from each group were evaluated at 7 months for histopathology; an additional seven males and seven females from each group were evaluated at 7 months for nickel tissue burden in the lung and kidney; and five males and five females from each group were evaluated at 15 months for alterations in hematology, nickel tissue burden in the lung and kidney, and histopathology. Survival, Body Weights, Clinical Findings, and Hematology The survival rates of all exposed groups of males and females were similar to those of the controls. Mean body weights of 0.5 mg/m(3)female rats were slightly lower (6&percnt; to 9&percnt;) than those of the controls throughout the second year of the study; final mean body weights of all exposed groups of males and 0.12 and 0.25 mg/m(3)females were similar to those of the controls. There were no clinical findings or hematology differences that were considered to be related to nickel sulfate hexahydrate administration. Pathology Findings No exposure-related neoplasms occurred in male or female rats exposed by inhalation to nickel sulfate hexahydrate for 2 years. Increased incidences of inflammatory lung lesions were generally observed in all exposed groups of male and female rats at the end of the study. The incidences of chronic active inflammation, macrophage hyperplasia, alveolar proteinosis, and fibrosis were markedly increased in male and female rats exposed to 0.25 or 0.5 mg/m(3). Increased incidences of lymphoid hyperplasia in the bronchial lymph nodes occurred in 0.5 mg/m(3)male and female rats at the end of the 2-year study. The incidences of atrophy of the olfactory epithelium in 0.5 mg/m(3)males and females were significantly greater than those in controls at the end of the study. Tissue Burden Analyses Lung nickel burdens in exposed male and female rats were greater than those in the controls at the 7- and 15-month interim evaluations, and lung nickel burdens values increased with increasing exposure concentration. 2-YEAR STUDY IN MICE: Groups of 80 male and 80 female mice were exposed to nickel sulfate hexahydrate by inhalation at concentrations of 0, 0.25, 0.5, or 1 mg/m(3) (equivalent to 0, 0.06, 0.11, or 0.22 mg nickel/m(3)). Animals were exposed for 6 hours plus T90 (8 minutes) 5 days per week for 104 weeks. Five male and five female mice from each group were evaluated at 7 months for histopathology; five males and five females from each group were evaluated at 7 months for nickel tissue burden in the lung and kidney; five males and five females from each group were evaluated at 15 months for alterations in hematology and histopathology; and five males and five females from each group were evaluated at 15 months for nickel tissue burden in the lung and kidney. Survival, Body Weights, Clinical Findings, and Hematology The survival rates of all exposed groups of males and females were similar to those of the controls. The mean body weights of 1 mg/m(3)males and of all exposed groups of females were lower than those of the controls during the second year of the study. There were no clinical findings or hematology differences considered to be related to chemical exposure. Pathology Findings Inflammatory lesions of the lung generally occurred in all exposed groups of male and female mice at the end of the 2-year study. These lesions included macrophage hyperplasia, chronic active inflammation, bronchialization (alveolar epithelial hyperplasia), alveolar proteinosis, and infiltrating cells in the interstitium. Incidences of macrophage hyperplasia and/or lymphoid hyperplasia occurred in the bronchial lymph nodes of most of the 1 mg/m(3)males and females and in some 0.5 mg/m(3)females at the end of the 2-year study. Atrophy of the olfactory epithelium was observed in 0.5 and 1 mg/m(3)males and in all exposed groups of females at the end of the 2-year study. Tissue Burden Analyses At the 7- and 15-month interim evaluations, lung nickel burden parameters measured in control and exposed groups were below the limit of detection. Absolute lung weights of 0.5 and 1 mg/m(3)lung burden study females were significantly greater than those of the controls at 15 months. GENETIC TOXICOLOGY: Nickel sulfate hexahydrate (500 to 800 g/mL) was tested for induction of trifluorothymidine resistance in L5178Y mouse lymphoma cells. A positive response was observed in the absence of S9. The test was not performed with S9. CONCLUSIONS: Under the conditions of these 2-year inhalation studies, there was no evidence of carcinogenic activity of nickel sulfate hexahydrate in male or female F344/N rats exposed to 0.12, 0.25, or 0.5 mg/m(3) (0.03, 0.06, or 0.11 mg nickel/m(3)). There was no evidence of carcinogenic activity of nickel sulfate hexahydrate in male or female B6C3F1 mice exposed to 0.25, 0.5, or 1 mg/ m3 (0.06, 0.11, or 0.22 mg nickel/m(3)). Exposure of rats to nickel sulfate hexahydrate by inhalation for 2 years resulted in increased incidences of chronic active inflammation, macrophage hyperplasia, alveolar proteinosis, and fibrosis of the lung; lymphoid hyperplasia of the bronchial lymph node; and atrophy of the olfactory epithelium. Exposure of mice to nickel sulfate hexahydrate by inhalation for 2 years resulted in increased incidences of chronic active inflammation, bronchialization (alveolar epithelial hyperplasia), macrophage hyperplasia, interstitial infiltration, and alveolar proteinosis of the lung; lymphoid and macrophage hyperplasia of the bronchial lymph node; and atrophy of the olfactory epithelium. Synonyms: Blue salt; hexahydrate, nickel (2+) salt; nickel monosulfate hexahydrate; nickel (2+) sulfate hexahydrate; nickel (II) sulfate hexahydrate; nickel sulphate hexahydrate; nickelous sulfate hexahydrate; nickelous sulphate hexahydrate; single nickel salt, sulfuric acid
 ...
PMID:NTP Toxicology and Carcinogenesis Studies of Nickel Sulfate Hexahydrate (CAS No. 10101-97-0) in F344 Rats and B6C3F1 Mice (Inhalation Studies). 1258 12

The infectivity and pathogenicity of newly discovered baculovirus, CuniNPV (family Baculoviridae, genus Nucleopolyhedrovirus) originally isolated from the mosquito Culex nigripalpus Theobald, was evaluated in laboratory bioassys against thirteen species and four genera of mosquitoes native to the northeastern U.S. Purified virus at a dosage rate of 1.6 x 10(7) occlusion bodies/ml with 10 mM Mg2+ added was used in exposures with second through fourth instars at temperatures ranging from 17 to 27 degrees C. High infection rates and accompanying mortality were achieved in Cx. pipiens L. (83.0-14.4%), Cx. pipiens f. molestus (80.4% infection), and Cx. salinarius Coquillett (48.0-43.1%). Cx. restuans Theobald was also susceptible but infection rates were lower (21.3-12.5%). The gross pathology associated with infection was identical to that reported in Cx. nigripalpus. Infected larvae were lethargic and were often suspended at the water surface. Development of CuniNPV was observed in the nuclei of the midgut epitheial cells in the gastric caeca and posterior region of the stomach of host larvae. One hundred percent mortality was observed in all larvae that exhibited gross symptoms of infection within 4-d p.i. Cx. territans Walker (subgenus Neoculex Dyar) was the only Culex mosquito that was not susceptible. No infections were obtained with any species of Aedes [Ae. vexans (Meigen)], Culiseta [Culiseta morsitans (Theobald)] or Ochlerotatus [Ochlerotatus canadensis (Theobald), Oc. cantator (Coquillett), Oc. communis (De Geer), Oc. excrucians (Walker), Oc. japonicus (Theobald), Ochlerotatus stimulans (Walker), and Ochlerotatus triseriatus (Coquillett)]. The host range of CuniNPV appears to be restricted to Culex mosquitoes within the subgenus Culex. An inhibitory effect on transmission of CuniNPV was observed when a liver powder/Brewer's yeast mixture was used as a source of food reinforcing the critical role of Mg2+ and sensitivity of the infection process to the presence other divalent cations (Cu2+, Fe2+, and Zn2+) in the larval medium that interfered with the infection process. The high infectivity and pathogenicity of CuniNPV for the principal vectors of West Nile virus in North America make CuniNPV an attractive candidate for future development as a biopesticide.
 ...
PMID:Infectivity and pathogenicity of a novel baculovirus, CuniNPV from Culex nigripalpus (Diptera: Culicidae) for thirteen species and four genera of mosquitoes. 1468 Jan 19


<< Previous 1 2 3 4 5 6 Next >>