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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Toxicosis was induced in pregnant Holstein-Friesian heifers by giving polybrominated biphenyls a in gelatin capsules at the rate of 25 g/day. Initially, this dosage was approximately 67 mg/kg of body weight. Clinical signs were anorexia, excessive lacrimation and salivation, diarrhea, emaciation, dehydration, depression, and abortion. Fever was not evident during the experiment. Values for serum glutamic-oxalacetic transaminase, lactic dehydrogenase, blood urea nitrogen, and bilirubin were increased. Changes in packed cell volume, hemoglobin content, total erythrocyte and leukocyte counts, and differential leukocyte counts were minimal and reflected dehydration and secondary infection. The principal urine changes were decreased specific gravity and moderate proteinuria. Gross necropsy findings included dehydration; subcutaneous emphysema and hemorrhage; atrophy of the thymus; fetal death with concomitant necrosis of cotyledons; kidneys that were enlarged, pale tan to gray; thickened wall of the gallbladder; inspissated bile; edema of abomasal folds; mucoid enteritis; linear hemorrhage and edema of the rectal mucosa; and secondary pneumonia. Microscopic changes were most marked in the kidneys, gallbladder, and eyelid. In the kidney, the principal changes were extreme dilatation of collecting ducts and convoluted tubules, with epithelial degenerative changes of cloudy swelling, hydropic degeneration, and separation from the basement membrane. Common changes in the gallbladder were moderate to marked hyperplasia and cystic dilatation of the mucous glands in the lamina propria. The changes in the eyelids were characterized by hyperkeratosis, with accumulations of keratin in hair follicles of the epidermis and squamous metaplasia with keratin cysts in the tarsal glands. Clinical signs and lesions of toxicosis did not develop in heifers given the polybrominated biphenyls at the rate of 0.25 mg and 250 mg/day for 60 days. Initially these rates were approximately 0.00065 mg/kg and 0.65 mg/kg of body weight, respectively.
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PMID:Pathology of experimentally induced polybrominated biphenyl toxicosis in pregnant heifers. 18 92

Data are presented to show that ingestion of cadmium chloride by rats at low levels leads to alteration of zinc metabolism in the liver, even though the formation of metallothionein is not evident. A dose-response relationship between amount of cadmium ingested and degree of perturbation of zinc metabolism in liver was found. Oral cadmium was shown to cause emphysema and reduce pulmonary function in male rats; the effect was less severe or delayed in onset if dietary zinc concentration was high. Interference with copper and iron metabolism was shown to occur in rats given low levels of cadmium orally. Depression of copper and iron metabolism of the rat fetus was found to occur when dams received very low doses of cadmium during gestation, even though very little cadmium passed the placental barrier.
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PMID:Some effects of oral ingestion of cadmium on zinc, copper, and iron metabolism. 48 54

The effects of ip administration of methotrexate (MTX) on 3-month-old male Wistar rats were studied. We administered log doses from 125 to 2,000 mug/kg, five times per week for as long as 24 months. The massive doses were promptly lethal, and most rats receiving 500 mug or more/kg died within a few weeks. Severe hematopolietic depression and ulcerative gastrointestinal lesions were observed. Truly chronic intoxication was achieved with the lesser doses. Rats in this category developed serious liver damage, namely, varying degrees of fatty metamorphosis, necrosis, atrophy of hepatic cords, and fibrosis. Hematopoietic depletion occurred in the spleen and bone marrow. Hemosiderosis was prominent in the spleen and liver. Pulmonary lesions--chiefly emphysema, occasionally fibrosis--were found less consistently. These studies demonstrated the ability of MTX to induce lesions, most consistently hepatic, in the Wistar rat, and thus have provided an animal model to evaluate protective measures.
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PMID:Hepatotoxicity in Wistar rats following chronic methotrexate administration: a model of human reaction. 84 77

The effects of 1.0 per cent end-tidal halothane-oxygen anesthesia on spontaneous ventilation, ventilatory deadspace, functional residual capacity (FRC), and alveolar-arterial oxygen difference (A-aD-O-2) were measured in patients with chronic obstructive pulmonary disease and in normal patients of similar age. results obtained were compared with values obtained preoperatively from the same patients. The following were measured: 1) ventilation and ventilatory deadspace, breathing room air and breathing 100 per cent oxygen; 2) functional residual capacity (FRC) and alveolar-arterial oxygen tension difference (A-aD-O-2); 3) forced expiratory volume in 1 second (FEV1.0); 4) ventilatory response to exogenous carbon dioxide. Findings indicated that ventilation is depressed more during halothane anesthesia in patients with emphysema than in normal patients and that the extent of depression is best related to a preoperative measurement of FEV1.0 (P less than 0.001, r = 0.86). The depression in alveolar ventilation results primarily from a reduction in tidal volume. A-aD-O-2 and ventilatory deadspace-to-tidal volume ratio are increaded and FRC decreased with anesthesia in patients with COPD, but the changes are no greater than those found in normal patients.
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PMID:Anesthetic effects on ventilation in patients with chronic obstructive pulmonary disease. 111 64

Clinical and roentgenographic findings were compared in patients 40 years of age and over and in those under 40 who were treated for acute unilateral pneumothorax. Dyspnea and anxiety were pominent in the older individuals, although pneumothoraces were usually small. Because physical findings were often unreliable, roentgenograms were required. In the presence of pulmonary emphysema, loss of retractility prevented total collapse of the underlying lung. Increased intrapleural pressure caused over-expansion of the chest wall and the depression of the diaphragm without much mediastinal shifting. Partial collapse of emphysematous lobes demonstrated bullae that were not previously obvious. Respiratory failure developed in five patients over 40 years of age, but four of them recovered after relief of the pneumothorax. Mortality for the group was low and related to associated pulmonary diseases.
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PMID:Pneumothorax complicating pulmonary emphysema. 117 69

We investigated the effect of a novel analgesic compound, flupirtine on the respiratory center in 8 healthy controls and patients with lung emphysema (n = 6), bronchial asthma (n = 7) and lung fibrosis (n = 5). All patients received a in a double blind, randomized fashion on three separate study days 100 mg and 200 mg flupirtine and placebo, respectively. Respiratory drive was estimated from measurements of CO2-rebreathing curves and mouth occlusion pressure at rest and during CO2-rebreathing performed before, 1.5 and 3 hours after medication. We were unable to detect any significant depression of respiratory drive neither in the controls nor in the patients and therefore suggest that flupirtine is a safe analgetic compound even in patients with severe obstructive and restrictive lung function impairment.
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PMID:[The effect of flupirtine on respiratory drive in healthy probands and patients with various lung diseases]. 147 68

Many studies of age-related cognitive decline have failed to distinguish between usual and successful aging. Although some degree of cognitive impairment is associated with aging, when one looks at average performance, there is great variability among individuals, with many showing little or no deleterious effects of aging on intellectual abilities. Many of the risk factors for dementia and for conditions associated with cognitive impairments can be treated or controlled. Among the preventable causes of cognitive decline are the following: AIDS, Alcohol and drug abuse, Cerebrovascular disease, Exposure to organic solvents or lead, Head trauma, Overmedication, Syphilis. Other conditions that may cause cognitive decline can be controlled or treated: Atherosclerosis, Depression, Diabetes, Emphysema, High blood pressure, Obesity, Sleep disorders, Thyroid dysfunction. In addition, it may be possible to enhance the cognitive performance of even healthy elderly people through changes in diet and lifestyle. Recent data raise the possibility that improved prenatal and perinatal care and greater access to educational opportunities may result in a decreased incidence of dementia in future generations of older adults. Although they are rapidly becoming more numerous, the efficacy of cognitive training programs in preventing or slowing cognitive decline has not yet been demonstrated. Nevertheless, such programs may ameliorate cognitive impairment by reducing the psychiatric disabilities associated with anxiety and depression. The general principle underlying these strategies for limiting cognitive impairment with age is to maximize brain reserve and minimize brain damage.
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PMID:Preventing cognitive decline. 157 76

A path analysis model examined interrelationships among variables significantly associated with chronic dyspnea in chronic bronchitis and emphysema (CBE) and the relative influence of these variables on each other and on functional status and quality of life. Results from the 45 adults (mean age, 61) with moderate CBE disease severity showed that dyspnea severity has a sizable effect on functional status and quality of life. Disease severity was more strongly related to functional status than to quality of life. Depression and mastery had the strongest total effects on quality of life. Dyspnea severity had strong but separate effects on functional status and quality of life. From these preliminary results, it is suggested that a direct focus on psychologic interventions to ameliorate depression and improve mastery is likely to improve quality of life with some resultant positive effect on functional status.
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PMID:Disease and symptom severity, functional status, and quality of life in chronic bronchitis and emphysema (CBE). 221 71

This study explores the association between familial alcoholism and the presence of certain conditions in nonalcoholic family members. Depression, obesity, functional bowel syndrome, asthma/emphysema, trauma, and genitourinary problems are conditions suggested by prior studies to be more common in families of alcoholics than in those without an alcoholic family member. Cross-sectional data were collected from a convenience sample of adults in the waiting room of a midwestern, university based family practice clinic. The respondents were classified in two groups: those with little likelihood of familial alcoholism and those with probable familial alcoholism. The groups were matched for race and age, creating two demographically similar groups which were then analyzed as cohorts. The prevalence rates of the conditions of interest in the respondents were calculated in the two groups and compared using the chi-square test for statistical significance. Significant differences in prevalence rates of depression and obesity were found. Trends were found for differing rates of functional bowel syndrome and asthma/emphysema. No differences were found for trauma and genitourinary problems. If differences in disease prevalence truly exist between family members of alcoholic and nonalcoholic individuals, this awareness could enhance the diagnosis and treatment of the conditions of interest in the nonalcoholic relative as well as the alcoholic individual. Family members could be a powerful screening tool for alcoholism.
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PMID:Self-reported illnesses in family members of alcoholics. 232 89

We previously described a technique for en bloc double-lung transplantation that was initially applied to select patients with cystic fibrosis and emphysema. This procedure is quite complex and associated with several limitations, including a substantial incidence of airway ischemia, postoperative myocardial depression, and cardiac denervation. To address these problems we have developed a simpler procedure for replacing both lungs. The operation is done through a transverse thoracosternotomy and involves sequential replacement of the two lungs. Positive features include separate bronchial anastomoses to reduce ischemic airway complications, elimination of the need for total cardiopulmonary bypass and a period of ischemic cardiac arrest, improved exposure to reduce intraoperative and postoperative hemorrhage, and maintenance of cardiac innervation. Additionally, the technique can be more easily mastered and widely applied. Details of the procedure and its initial clinical application in 3 patients having emphysema, cystic fibrosis, and bronchiolitis obliterans following previous double-lung transplantation, respectively, are described. All 3 patients recovered without complication. Postoperative function was excellent in spite of lung ischemic times ranging up to 91/2 hours.
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PMID:Improved technique for bilateral lung transplantation: rationale and initial clinical experience. 233 34


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