Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q0Z944 (hemoglobin)
 63,986 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

The efficacy of orally administered mycophenolic acid (MPA), an inhibitor of guanosine monophosphate (GMP) synthesis, for the treatment of psoriasis, was studied in a double-blind fashion. Of twenty-one patients completing the study period, ten of eleven patients treated with MPA had a greater than 25% decrease in severity score compared with only two of ten patients treated with placebo. The placebo group had a slight increase in severity score compared to almost 50% reduction in the average severity score of the MPA-treated group. After termination of the double-blind portion of the study, the placebo group was treated with MPA and showed a 60% decrease in severity score. Adverse effects encountered included anorexia, nausea, vomiting, and diarrhea. One patient had an uncomplicated episode of herpes zoster. Other than a mild decrease hemoglobin, no hematologic toxicity was noted.
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PMID:Efficacy of mycophenolic acid for the treatment of psoriasis. 39 32

Giant hypertrophic gastritis is a newly recognized disease of adult Baseji dogs similar to Menetrier's disease of man. It is characterized by weight loss, diarrhea, dry coat, pale membranes, anorexia, raised convoluted rugae in the body of the stomach, palpable fluid- and gas-filled intestines, colonic inflammation, and radiographically demonstrable dilated intestinal loops. Laboratory findings include leukocytosis, neutrophilia, low hemoglobin, hypoalbuminemia, hypobetaglobulinemia, hypergammaglobulinemia, decreased serum fatty acids, hypocholesterolemia, indicanuria, low fecal pH, and increased fecal fat and nitrogen. Four dogs studied had gastritis with hypertrophy and diffuse lymphocytosis and plasmacytosis of the small intestine.
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PMID:Giant hypertrophic gastritis of Basenji dogs. 85 Sep 91

Three groups of rabbits (A, B, and C; 6 rabbits/group) were fed a lead supplement of 25, 50, and 100 mg of Pb/kg of live weight/day for 87 days to compare the efficacies of 3 diagnostic tests--whole blood lead concentration, urinary delta-aminolevulinic acid (UALA), and fluorescent erythrocyte test (FET)--and to determine the clinicopathologic changes of experimentally induced lead poisoning in rabbits. All rabbits given lead had whole-blood lead concentrations greater then the maximum value (0.030 mg/dl) for control rabbits (group D), indicating that this measurement is a reliable indicator of lead ingestion. All group A rabbits (fed 25 mg of Pb/kg) and 66% negative UALA test results, with values less than the maximum value (0.12 mg/dl) for group D (control) rabbits. Only group C rabbits (fed 100 mg of Pb/kg) had consistently positive UALA FINDINGS. The test was therefore considered unreliable for detecting daily lead intakes less than 100 mg/kg of live weight of rabbits. All rabbits given lead had erythrocytes which fluoresced red when exposed to light rays with wavelenghts from 320 to 400 nm; fluorescence was not observed in erythrocytes of control rabbits. The FET appears to be a convenient and reliable diagnostic test for lead ingestion. In groups B and C, clinical signs of lead poisoning were mild, nonpersistent anemia characterized by the presence of poikilocytes, hupochromic erythrocytes, target cells, erythroblasts, erythrocytes with punctate basophilic stippling, reduced mean corpuscular hemoglobin concentrations, and relative lymphocytosis, neutropenia, and eosinopenia. One rabbit from the group fed the largest dose displayed partial anorexia.
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PMID:Chronic plumbism in rabbits: a comparison of three diagnostic tests. 115 38

Several studies have demonstrated the efficacy of cyclosporin A in modifying the initial course of Type 1 (insulin-dependent) diabetes mellitus in older children and adults but none have reported the effects in very young children. We treated 14 newly-diagnosed Type 1 diabetic patients aged 22 months to 95 months with cyclosporin A. Mean insulin dose at entry was 0.7 +/- 0.07 IU.kg-1.day-1. Initial cyclosporin A dose was 10 mg.kg-1.day-1. Insulin dose reached a nadir of 0.13 IU.kg-1.day-1 by 180 days. Mean glucagon-stimulated connecting peptide levels were maximal at 6 months (0.75 nmol/l) and were maintained while on cyclosporin A. Insulin was discontinued in four patients for 4, 12, 15 and 30 months respectively. In five other patients the insulin dose was less than 0.15 IU.kg-1.day-1 for at least 3 months. Glycated haemoglobin levels for all patients were within the normal range. Side effects included anorexia, stomach pains, poor weight gain, hypertrichosis, gum hyperplasia, mild anaemia and elevated creatinine. All patients have now discontinued cyclosporin A and all but one have been followed for 5 years after discontinuation. Reasons for discontinuing cyclosporin A included exposure to chicken pox (varicella), non-resolving otitis media, incomplete or no response and relapse. All side effects have resolved since the treatment was discontinued. Following discontinuation of cyclosporin A insulin requirements and glycated hemoglobin levels increased while glucagon-stimulated connecting peptide levels declined dramatically.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cyclosporin A treatment of young children with newly-diagnosed type 1 (insulin-dependent) diabetes mellitus. London Diabetes Study Group. 139 85

Oak poisoning occurred in crossbred cattle due to eating immature tender oak (Quercus incana) leaves. Mortality was 70%. The animals exhibited anorexia, severe constipation and brisket edema. The feces were hard, pelleted and coated with blood and mucous. Significant reductions in blood hemoglobin and mean corpuscular hemoglobin, and significant elevations in serum bilirubin were observed. Serum urea nitrogen and creatinine were greatly increased. There was bilirubinuria, proteinuria, hypoproteinemia and hypocalcemia, and greatly increased activities of serum aspartate aminotransferase, lactate dehydrogenase and alkaline phosphatase. The levels of tannins and condensed tannins were 97.7 mg tannic acid equivalent and 5.8 mg catechin equivalent/g of dry leaves. There was extensive nephro- and hepatotoxicity in the affected cattle due to hydrolysable tannins and simple phenols in the oak leaves.
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PMID:Oak (Quercus incana) leaf poisoning in cattle. 150 80

A 63-year-old white woman was admitted to the hospital for bilateral total knee arthroplasty. She was given prophylactic subcutaneous heparin therapy postoperatively. Three days later, she had a brief hypotensive episode and an unexplained drop in hemoglobin level. Seven days postoperatively, she became confused and disoriented while complaining of pain in her right side and, later, under her left breast. She also had nausea, vomiting, anorexia, and a vague feeling of "illness." Her condition deteriorated progressively, with blood pressure falling to 65/40 mm Hg and a temperature of 39.7 degrees C. Blood, urine, and cerebrospinal-fluid culture samples showed no evidence of infection. A diagnosis of acute adrenal insufficiency was made. Following corticosteroid therapy, the patient's condition improved markedly. Of interest in our patient was that she had had no antecedent hypotension, sepsis, fever, or surgical complications. Acute adrenal hemorrhage is often overlooked because the symptoms are attributed to other conditions, especially to sepsis. Acute adrenal hemorrhage should be suspected in any stressed patient in whom an abrupt deterioration associated with back or abdominal pain, hypotension, and unexplained fever are noted. Suspicion should be raised regarding those patients who are receiving anticoagulant therapy (including subcutaneous heparin prophylaxis) at the time of deterioration. With increased awareness, more cases of acute bilateral adrenal hemorrhage and subsequent adrenal insufficiency can be recognized ante mortem and treated.
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PMID:Prophylactic subcutaneous heparin therapy as a cause of bilateral adrenal hemorrhage. 155 45

Idarubicin, a new analogue of daunorubicin, was administered i.v. at a dose of 15 mg/m2 to 31 previously treated patients with unfavorable non-Hodgkin's lymphoma. Clinical characteristics included median age, 69 years; performance status, 1; and prior chemotherapeutic regimens, 1. Twenty of the patients were relapsing after prior therapy and 11 were refractory; 29 had received prior anthracycline or anthracenedione. Responses were observed in 43% of patient (3 complete remission and 10 partial remission) with a median duration of 10+ months (2-29+ months). Idarubicin was well tolerated with nonhematological toxicities (nausea/vomiting, mucositis, and anorexia) seen in less than 50% of patients. Median hematological values during the first cycle for this dosage included WBC, 1,300/mm3; platelets, 129,000/mm3; and hemoglobin, 10.9 mg/dl. With dose escalation, hematological toxicity was dose limiting. Symptomatic cardiac toxicity was observed in one patient who had received maximum dose doxorubicin and radiotherapy. Median values for the cardiac ejection fraction during the full course of therapy for the entire group of patients were 0.62 (initial) and 0.60 (final). Idarubicin in i.v. form is an active drug in previously treated patients with unfavorable non-Hodgkin's lymphoma.
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PMID:Phase II study of intravenous idarubicin in unfavorable non-Hodgkin's lymphoma. 161 62

Erythrocytosis and microcytosis have been described in strains of genetically hypertensive rats and in essentially hypertensive humans. Published discussion of these phenomena has centered around their relationship to observed alterations in ionic transport and the pathogenesis of hypertension. In presenting data for another strain of spontaneously hypertensive rats in which these findings are exhibited, we note that erythroid cell size decreases concurrently with the increase in cell numbers so that the hematocrit and the mean corpuscular hemoglobin concentration remain constant. Data from the literature support the hypothesis that erythroid cell size is inversely proportional to cell count in a large number of species. Erythrocytosis, as it develops in the neonatal rat, is a consequence of the marked immaturity of this species at birth. Erythrocytosis in the spontaneously hypertensive rat is not due to a difference in the affinity of its hemoglobin for oxygen or to significant tissue anorexia. Microcytosis in the spontaneously hypertensive rat is the consequence of a continuation of the linear volume decrease with age of its erythroid cells seen in the normotensive animals and may be accounted for by the production of smaller cells with concomitant regulation of individual cell volume.
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PMID:Inverse changes in erythroid cell volume and number regulate the hematocrit in newborn genetically hypertensive rats. 194 11

A multi-institutional collaborative phase II study of (2"R)-4-O-tetrahydropyranyladriamycin (THP) was performed by intravenous administration to patients with advanced or recurrent gastric cancer. The administration schedules were (1) 40-60 mg/body every 3 or 4 weeks and (2) 20-40 mg/body once a week. Of 58 registered patients, 49 cases were eligible and 37 cases were evaluable for response. The therapeutic results were 1 CR, 4 PR, 14 NC and 18 PD. The response rate of the evaluable cases was 13.5%. The side effects were mainly bone marrow suppression and digestive symptoms. In particular, the frequency of leukopenia was a high 75.5%, while there was a decrease in hemoglobin in 38.8% and anorexia in 30.6%. The frequency and severity of alopecia, which is a known problem with anthracyclines, were slight, and no abnormal electrocardiograms were observed.
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PMID:[Phase II study of (2" R)-4'-O-tetrahydropyranyladriamycin (THP) in patients with advanced or recurrent gastric cancer. Clinical study group of THP for gastric cancer in Japan]. 206 2


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