Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
11,506 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

Toxicosis was induced in pregnant Holstein heifers by feeding FireMaster BP-6 (polybrominated biphenyls) in daily oral doses of 25 g/head/day for 33--60 days. The individual heifers were dosed until each became moribund (days 33, 36, 39, 40, 41, or 66), at which time they were necropsied. Gross findings included dehydration, subcutaneous emphysema and hemorrhage, atrophy of the thymus, fetal death with concomitant necrosis of cotyledons, thickened wall of the gallbladder, inspissated bile, edema of abomasal folds, mucoid enteritis, linear hemorrhage and edema of the rectal mucosa, and secondary pneumonia. The livers were enlarged approximately 40%. Kidneys were approximately double the normal size and were pale tan to grey in color. The perirenal lymph nodes were enlarged and edematous. Microscopic changes were the most marked in the kidneys, gallbladder and eyelid. Extreme dilatation of collecting ducts and convoluted tubules with epithelial degenerative changes of cloudy swelling, hydropic degeneration and separation from the basement membrane were principal changes in the kidney. Hyperkeratosis with accumulations of keratin in hair follicles of the epidermis and squamous metaplasia with keratin cysts in the tarsal glands were characteristic findings in sections of eyelids. Moderate to marked hyperplasia and cystic dilatation of the mucous glands in the lamina propria were common changes in the gallbladder. Foci of fatty degeneration and glycogen depletion were observed in liver sections. Necropsy of heifers immediately after 60 days exposure to 0.25 and 250 mg/head/day of PBB showed no gross or histopathological signs indicating toxicosis. Following parturition, at approximately 220 days after the PBB doses, heifers from the 0.25 and 250 mg/head/day groups and their calves were necropsied and displayed no signs of toxicosis.
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PMID:Effects of PBB on cattle. II. Gross pathology and histopathology. 20 62

The clinical presentation and surgical treatment of thoracic anomalies--developmental malformations of the respiratory tract, congenital chylothorax or mediastinal masses--in 15 infants are reported. The age range at operation was 2 weeks to 8 months. The diagnoses were lobar emphysema (3 cases), bronchogenic cyst (3), cystic adenomatoid malformation (1), enteric duplication (2), hyperplastic thymus (2), neuroblastoma (1), chylothorax (1), cystic lymphangiectasia (1) and tracheal stenosis (1). The most common symptom was respiratory embarrassment, with acute development in half of the cases. The diagnosis could be established or suspected from chest radiography in 14 of the 15 infants. All were submitted to thoracotomy. None died postoperatively, but three had major complications. At postoperative follow-up 13 of 14 patients were free from respiratory symptoms.
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PMID:Surgical management of thoracic anomalies in infants. Respiratory-tract malformations, congenital chylothorax and mediastinal masses. 338 51

Groups of F344/N rats and B6C3F1 mice were exposed to aerosols of nickel subsulfide (Ni3S2) 6 hr/day for 12 days not including weekends. Actual exposure concentrations were within 3% of target (target = 10.0, 5.0, 2.5, 1.2, 0.6, and 0.0 mg Ni3S2/m3). Nickel lung burdens of exposed rats and mice increased linearly with exposure concentration. Two male rats and all mice exposed to 10.0 mg Ni3S2/m3 died before the end of the exposures. Exposure to Ni3S2 had no effect on the natural killer cell activity of mouse spleen cells. Lesions in rats and mice related to inhalation of Ni3S2 were found in the nasal epithelium, lung, and bronchial lymph nodes. The most extensive lesions were found in the lung and included necrotizing pneumonia. Emphysema developed in rats exposed to 5.0 or 10.0 mg Ni3S2/m3, while fibrosis developed in mice exposed to 5.0 mg Ni3S2/m3. Degeneration of the respiratory epithelium and atrophy of the olfactory epithelium of the nose occurred in rats exposed to as low as 0.6 mg Ni3S2/m3 and mice exposed to 1.2 mg/m3. Results indicate that inhalation exposure of rats and mice to Ni3S2 aerosol concentrations near the current threshold limit value (TLV) for nickel compounds (1 mg/m3 for Ni metal and roasting fume and dust and 0.1 mg/m3 as Ni for soluble compounds) can produce lesions in the respiratory tract. Atrophy of lymphoid tissues (spleen, thymus, and bronchial lymph nodes) was found in animals of the highest exposure concentration. Degeneration of the testicular germinal epithelium was also observed in mice and rats that survived 5.0 or 10.0 mg/m3 exposure concentrations.
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PMID:Comparative inhalation toxicity of nickel subsulfide to F344/N rats and B6C3F1 mice exposed for 12 days. 365 67

Ectopic thymic tissue can present a diagnostic dilemma when it is located in the posterior mediastinum. The diagnosis can be made by awareness of it and by use of computed tomography (CT) and magnetic resonance imaging (MRI). Rarely, ectopic thymus are reported to cause airway obstruction. In infants ectopic thymic tissue should also be considered in the differential diagnosis of secondary pneumonias and emphysema especially located in the upper lung zones.
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PMID:Ectopic thymic tissue: a cause of emphysema in infants. 1033 93

The Shengenaqi oral liquid has a function of improving the inspiration and can be used in the treatment of chronic bronchitis, pulmonary emphysema and pulmonary heart disease etc. In the research, animal models for TCM dyspnea of deficiency were made by inhaling papain and injection hydrocotison into the abdominal eavity and afterwards, treated with Shengenaqi oral liquid. The effects showed: The medicine can improve the susfainability of swimming mice, increase the ability of cold tolerance and prevent the thymus from atrophy. The SOD activity in the lung tissue of mice can be improved and MDA be decreased.
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PMID:[Pharmacological studies on shengenaqi oral liquid on animal model for TCM dyspnea of deficiency]. 1257 69

The CT appearance of a pathologically proven spontaneous multiloculated multiseptated pneumomediastinum in a newborn baby has not been reported in the English literature. Our baby was delivered vaginally at term and developed mild respiratory distress after birth. The antenatal history was unremarkable apart from borderline oligohydramnios. The multiple septa seen within the pneumomediastinum on CT on day 3 may simulate an underlying 'bubbly' lung lesion like congenital cystadenomatoid malformation or congenital lobar emphysema, but actually represent anatomically known fascia surrounding the thymus. Furthermore, in neonates, air in the mediastinum often loculates locally and tends not to dissect widely as in adults.
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PMID:Spontaneous multiloculated multiseptated pneumomediastinum in a newborn baby: the spinnaker sail is rigged-CT features with pathologic correlation. 1285 66

Pulmonary emphysema is a major component of the morbidity and mortality of chronic obstructive pulmonary disease (COPD). Currently there are no predictive biomarkers for COPD. Initial steps toward identifying potentially predictive biomarkers involve utilizing well-characterized mainstream smoke (MS) exposure conditions (dose-response) to identify changes in biomarkers of effect (inflammation, tissue injury, oxidative stress) in emphysema-susceptible and -resistant mouse strains. C57Bl/6 mice have been reported to develop emphysema when exposed chronically to cigarette smoke, while similarly exposed ICR mice do not. Male C57Bl/6 and ICR mice were exposed 2 h/day for 7 consecutive days to MS from a standard reference cigarette (2R4F) at 75, 250, and 600 microg total particulate matter (TPM)/L or filtered air. To confirm exposure, blood samples were collected toward the end of the last exposure and analyzed for carboxyhemoglobin, nicotine, and cotinine. Bronchoalveolar lavage (BAL) fluid samples were collected 2 or 12 h postexposure and analyzed for biomarkers of effect. MS dose differed slightly between strains. More necrosis was observed in nasal epithelium of exposed C57Bl/6 mice. Exposure concentration-dependent increases in apoptosis, chemokines, and neutrophil counts were greater in ICR mice. Similar increases in thymus and activated-regulated chemokine were only observed in C57Bl/6 mice. BAL fluid cells of C57Bl/6 mice appear to undergo necrosis, while the BAL fluid cells of ICR mice appear to undergo apoptosis following MS exposure. Utilizing two strains of mice we identified MS-responsive biomarkers of effect that may be predictive of COPD pathology. Chronic MS exposures are needed to link these biomarkers with emphysema.
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PMID:Characterization of mainstream cigarette smoke-induced biomarker responses in ICR and C57Bl/6 mice. 1537 Oct 58

The usefulness of radiologic examination in the diagnosis of aspiration pneumonia in infants. The aim of the study was to estimate whether the connection between the localisation and radiological findings on the plain X-ray chest examination exists in the group of 121 infants and young children, age 1 to 24 month (77 boys and 44 girls), treated for pneumonia and gastroesophageal reflux disease (GERD), established by 24-hour esophageal pH-monitoring. In all children the diagnosis of pneumonia were made on admission to hospital by physical and X-ray chest examinations. GERD, in accordance with consensus ESPAGAN, was diagnosed in the group of 65 children. Children with abnormal results of pH-monitoring had significantly more changes in the lower parts of the right lung and in the intermediate and the lower parts of the left lung. There were no difference in radiological appearance between the changes suspected to the aspiration etiology and other pneumonic changes in the group of 56 children with normal pH-investigation. Additionally, there was no significant difference in the frequency of atelectasis, emphysema and/or enlargement of the thymus between both groups.
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PMID:[Effect of gastroesophageal reflux in children on x-ray imaging of the lungs]. 1599 46

Fibroblast growth factor 23 null mice (Fgf-23-/-) have a short lifespan and show numerous biochemical and morphological features consistent with premature aging-like phenotypes, including kyphosis, severe muscle wasting, hypogonadism, osteopenia, emphysema, uncoordinated movement, T cell dysregulation, and atrophy of the intestinal villi, skin, thymus, and spleen. Furthermore, increased vitamin D activities in homozygous mutants are associated with severe atherosclerosis and widespread soft tissue calcifications; ablation of vitamin D activity from Fgf-23-/- mice, by genetically deleting the 1alpha(OH)ase gene, eliminates atherosclerosis and ectopic calcifications and significantly rescues premature aging-like features of Fgf-23-/- mice, resulting in prolonged survival of Fgf-23-/-/1alpha(OH)ase-/- double mutants. Our results indicate a novel role of Fgf-23 in developing premature aging-like features through regulating vitamin D homeostasis. Finally, our data support a new model of interactions among Fgf-23, vitamin D, and klotho, a gene described as being associated with premature aging process.
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PMID:Premature aging-like phenotype in fibroblast growth factor 23 null mice is a vitamin D-mediated process. 1643 65


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