Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Since July 1980, 90 patients have had 95 permanent pacemakers implanted via an iliac vein approach. An incision is made superior to the inguinal ligament and the iliac vein is cannulated with a single lead for the ventricle or two leads for the atrium and ventricle. The pulse generator is placed in the subcutaneous tissue of the abdomen lateral to the umbilicus via a second incision. Overall 28 pacemaker implants were for atrial pacing, 53 for ventricular pacing and 14 were dual chamber. Nine (21%) of the atrial leads displaced and required repositioning and 5 (7%) of the ventricular leads dislodged and required revision. Lead dislodgement, especially in the atrium, remains a major weakness of the approach, and decreases its utility. Eleven percent of the last 19 atrial leads have dislodged. Nevertheless, the method is simple to perform and is presented as an alternative to the usual pectoral implantation site.
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PMID:Iliac vein approach to permanent pacemaker implantation. 247 36

Lead poisoning resulting from exposure to lead in a domestic car battery workshop is reported in 10 children in 2 families. 2 girls, aged 2 10/12 and 1 8/12 years, respectively, from 1 of the families were hospitalized for investigation of nausea, vomiting, progressive muscular weakness and peripheral neuropathy. Serum lead levels were 52 and 49 mcg/dl, respectively. Subsequent screening of all members of this family, as well as those of the other family who lived in the same house, revealed abnormally elevated levels of serum lead in all the members of both families. The 2 girls were treated with chelating agents and improved clinically and their serum lead levels decreased to 29 and 34 mcg/dl, respectively. The domestic workshop was closed and the 2 families moved to another neighborhood. These cases illustrate the need to screen all family members and contacts of patients with lead poisoning, as well as the hazards of the uncontrolled use of lead in domestic workshops.
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PMID:[Lead poisoning in two families from a car battery workshop]. 270 78

An analysis of reported symptoms and their relationship with indicators of lead absorption--blood lead (Pb-B) and zinc protoporphyrin (ZPP)--and of arsenic absorption--urinary arsenic (As-U)--was undertaken among 680 active copper smelter workers. Lead and arsenic absorption in the copper smelter employees were characterized by the median values of 30.4 micrograms/dl for Pb-B, 41.5 micrograms/dl for ZPP, and 26 micrograms/L for As-U. Blood lead was 40 micrograms/dl or higher in 16.7% of cases, ZPP was 50 micrograms/dl or higher in 31.2%, and urinary arsenic was 50 micrograms/L or higher in 16.4% of currently active copper smelter workers. The number of reported symptoms (from a total of 14 symptoms) increased with ZPP levels; the relationship with Pb-B was less marked. Arsenic contributed relatively little. Mean Pb-B, ZPP, and As-U levels for subjects reporting each of the 14 symptoms were compared with those of subjects who did not report the symptoms. Mean Pb-B was found to differ significantly for one symptom, fatigue. Significant differences in mean ZPP levels were found for fatigue, sleep disturbances, weakness, paresthesia, and joint pain. Prevalence rates for these symptoms rose more markedly with increasing ZPP than with Pb-B levels. The results indicate a relationship between certain CNS and musculo-skeletal symptoms and increased lead absorption in this population. Adherence to exposure standards that preclude undue lead absorption and appropriate biological monitoring including ZPP levels, are necessary to prevent adverse, especially long-term, health effects.
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PMID:Effects of low-level lead and arsenic exposure on copper smelter workers. 387 20

The diagnosis and treatment of a case of lead poisoning in a honey buzzard (Pernis apivorus) are described. Presenting signs were diarrhoea and weakness. Lead poisoning was suspected after radiography and confirmed by measuring the lead concentration in a venous blood sample. Comparison values of venous lead concentrations in healthy racing pigeons (Columba livia) were established. A method for the removal of lead shor from the gizzard of birds with a bronchoscope and grasping forceps under fluoroscopic control is described.
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PMID:An unusual case of lead poisoning in a honey buzzard (Pernis apivorus). 401 56

Lead subacetate (0.5g) and 1000 units of vitamin D were given three times a week to four newly-weaned rhesus monkeys. In addition, two animals received only the vitamin D. The poisoned animals had an increase in the urinary excretion of delta-aminolevulinic acid, an elevated content of lead in the blood, and a fall in hemoglobin concentration. Between 6 and 18 weeks the animals suddenly developed ataxia, nystagmus, generalized weakness, and convulsions. At this time the animals were killed by perfusion of fixative and the brain prepared for light and electron microscopic studies. Definite morphological evidence of disease was confined to the central nervous system, except for one animal which showed the characteristic renal inclusions of lead poisoning. All animals showed PAS-positive globules associated with blood vessels and an exudative edema involving the white matter of the cerebral hemispheres and cerebellum. Ultra-structurally, this appeared as a granular precipitate within an expanded extracellular space. Alterations of nerve fibers were not seen in the white matter but axonal swelling was observed in the cerebral cortex. The perikaryon and neuropil appeared normal. The control animals showed no significant cerebral changes.
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PMID:Experimental acute lead encephalopathy in the juvenile rhesus monkey. 420 57

Strychnine toxicosis is characterized by inducible tetanic seizures and metaldehyde poisoning by fine fasciculations progressing to generalized tremors and seizures. Intoxication with 1080 causes seizures, random running movements, vomiting, defecation, urination, acidosis and hyperglycemia. Intoxication with rodenticides causing coagulopathy is characterized by hemorrhage into body cavities but not necessarily external hemorrhage. Anticholinesterase insecticides cause salivation, urination and defecation, while chlorinated hydrocarbon insecticides cause CNS disturbances. Ethylene glycol intoxication results in ataxia, depression, coma, vomiting and tachypnea, followed by acute renal failure. Urea poisoning causes bloat and CNS signs in cattle. Monensin intoxication in horses lasts several days and causes stiffness, colic, uneasiness and recumbency. Salt poisoning results in depression, seizures and hypernatremia. Lead poisoning is associated with central and peripheral nervous system signs, as well as increased numbers of nucleated RBC and basophilic stippling of RBC. Arsenic poisoning results in GI pain, diarrhea, weakness and death. Copper toxicosis in sheep is manifested by hemolytic anemia, hemoglobinemia and hemoglobinuria. Plants that may intoxicate domestic animals include sorghum, greasewood, halogeton, water hemlock, Japanese yew, larkspur, lupine, milk-weed, philodendron, oleander, castor bean and precatory bean.
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PMID:Practical toxicologic diagnosis. 649 3

Ten clinically normal male beagle dogs were used in the study. Two dogs served as control, 4 received 2 mg lead/kg daily and 4 received 5 mg lead/kg/daily. Lead was administered for 13 weeks, after which one-half of each experimental group was treated with calcium ethylene diaminetetraacetate (CaEDTA) for 5 days. All animals were then monitored for another 4 weeks. Blood lead levels, haematology, blood glutathione concentration, and the number of bone marrow cells with stainable iron granules were measured weekly during the 18-week experimental period. Clinical signs of poisoning were observed only in one dog in the high dose group after 6 weeks. The signed included emaciation, anorexia, muscular weakness, evidence of abdominal pain and depression. These signs were reversed with cessation of lead dosing and CaEDTA treatment. Blood lead levels and the number of marrow cells with non-haeme iron increased in both lead-dosed groups; nucleated red blood cells increased only in high lead dosed group. There was a trend for an increased packed cell volume in all groups; however, the high lead dosed group did not increase as fast. No significant changes were observed in blood glutathione concentration and in other haematologic parameters. There were no differences in the parameters studied between the dogs treated with CaEDTA and those not so treated. Blood lead levels and the number of nucleated red blood cells decreased after cessation of lead administration and the number of marrow cells with iron also tended to decrease after lead removal.
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PMID:Effect of chronic lead on the haematology, blood glutathione and bone marrow non-haeme iron of dogs. 676 21

The effect of chronic oral led acetate administration on canine bone marrow was studied. Two dogs (group 1) were used as controls, 4 dogs (group 2) were given 2 mg of lead/kg of body weight daily, and 4 dogs (group 3) were given 5 mg of lead/kg daily. After a 7-day stabilizaion period, lead dosing was conducted for 91 days (13 weeks), after which half of each group was treated with calcium ethylenediaminetetraacetic acid. All dogs were then observed for another 28 days (4 weeks). Blood lead values and bone marrow cellular changes were monitored once a week during the 126 days (18 weeks) of study. Lead-dosed dogs had lower weight gains than the controls. Clinical signs of toxicosis were observed after 6 weeks in one dog in group 3. Anorexia, body weight loss, CNS depression, muscular weakness, and trembling were seen. Blood lead concentrations increased in all group 2 and 3 dogs. Lead caused increases in bone marrow segmented neutrophils and myeloid series cells, and increased myeloid:erythroid ratios. Blood lead concentrations and myeloid:erythroid ratios decreased after cessation of lead administration.
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PMID:Effect of chronic lead exposure on the canine bone marrow. 677 50

Lead causes peripheral neuropathy, which may lead to radial palsy or other peripheral palsy. In milder cases weakness has been reported especially in the wrist extensors. Several reports have confirmed that even in neurologically symptom-free lead workers motor and sensory conduction velocities slow down and also electromyographic abnormalities like denervation activity and loss or changes in the motor unit potentials appear. When individual exposure to lead has been monitored for long term, an exposure-effect relationship and also an exposure-response relationship have been shown concerning lead exposure and slowing of nerve conduction velocities and also concerning frequency of abnormally slow conduction velocities.
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PMID:Lead poisoning: neurophysiological aspects. 696 50

Previous studies have suggested cardiac taurine is released into the plasma in response to hypoxemia (low blood oxygen levels) during the pathogenesis of pulmonary hypertension syndrome (PHS, ascites). In the present study, broilers reared under cool temperature conditions (16 C) were provided tap water (control group), tap water supplemented with taurine, or tap water supplemented with the taurine transport antagonist beta-alanine. When compared with control values, taurine supplementation consistently elevated free taurine concentrations in the plasma but not in cardiac tissues, whereas beta-alanine supplementation consistently reduced free taurine concentrations in cardiac tissues but not in the plasma. Neither the incidence of PHS nor specific predictors of PHS susceptibility (electrocardiogram Lead II S-wave amplitude, % saturation of hemoglobin with oxygen, heart rate, right to total ventricular weight ratio) were affected by taurine or beta-alanine supplementation. Cardiopulmonary hemodynamic evaluations were conducted to compare control and beta-alanine supplemented broilers breathing room air or air containing 12% oxygen (low oxygen challenge). While breathing room air, the betaalanine-supplemented broilers had higher baseline values for cardiac output (186.2 vs. 146.9 mL/min/kg BW) and pulmonary arterial pressure (27.4 vs. 22.4 mm Hg), similar values for mean systemic arterial pressure (100 vs. 104 mm Hg) and pulmonary vascular resistance (0.062 vs. 0.064 resistance units), and lower values for total peripheral resistance (0.228 vs. 0.296 resistance units) when compared with control broilers breathing room air. During low oxygen challenges, the beta-alanine-supplemented broilers exhibited larger reductions in cardiac output, mean systemic arterial pressure, and pulmonary arterial pressure and greater increases in pulmonary vascular resistance than control broilers. These observations indicate that beta-alanine-supplemented broilers breathing room air had a higher systemic demand for oxygen as evidenced by their lower total peripheral resistance (systemic vasodilation) and had a capacity sufficient to pump a higher cardiac output and, thereby, maintain a similar mean systemic arterial pressure when compared with control broilers. However, cardiac function rapidly deteriorated in beta-alanine-supplemented broilers during low oxygen challenges, leading to substantially greater reductions in cardiac output, stroke volume, and mean systemic arterial pressure when compared with control broilers. Concurrent changes in pulmonary arterial pressure within the beta-alanine group reflect interactions between cardiac output and pulmonary vascular resistance. Overall, depleting cardiac taurine did not appear to initiate PHS, but systemic hypoxemia developing during the mid- to late-pathogenesis of PHS may expose and incipient cardiac weakness attributable to depleted taurine reserves.
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PMID:Taurine, cardiopulmonary hemodynamics, and pulmonary hypertension syndrome in broilers. 1173 78


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