Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical sarcocystosis was studied in 37 goats after inoculation with graded doses of sporocysts of Sarcocystis capracanis. Eight uninoculated goats served as controls. Clinical response varied with the dose. Goats inoculated with 10-40 million sporocysts died between 11 and 13 days after inoculation (DAI), from interstitial pneumonia, vasculitis, and necrosis of mesenteric lymph nodes. All goats inoculated with 100,000 or 1 million sporocysts died between 19 and 23 DAI; clinical signs were anorexia, fever (40-41 C), anemia, and weight loss. Four of 4 goats inoculated with 50,000 sporocysts and 1 of 4 inoculated with 10,000 sporocysts died 24, 28, 39, 68, and 61 DAI, respectively. Goats inoculated with 1,000 sporocysts and uninoculated goats remained clinically normal. After day 18 and before day 68, packed cell volume and hemoglobin content decreased to as low as 11% and 3.6 g/dl, respectively. Alanine aminotransferase and lactic dehydrogenase activities were inconsistently increased. Blood urea nitrogen and bilirubin values were increased, reaching as high as 63 mg/dl and 10 mg/dl, respectively. Histologically, thymic atrophy, vasculitis, hepatitis, cholangitis, myocarditis, generalized myositis, and encephalomyelitis were the main microscopic findings. The cause of the anemia in goats that died after day 19 was not determined.
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PMID:Sarcocystosis in goats: clinical signs and pathologic and hematologic findings. 678 65

The toxicity of cis-dichlorodiammineplatinum was evaluated in 41 patients who were treated for squamous cell carcinoma of the cervix or epithelial carcinoma of the ovary, with a dosage schedule of 60 mg/m2 every 3 weeks. Ototoxicity occurred in 33.3% of the patients serially tested, and anemia occurred in 48.8%. Leukopenia occurred in 29.9% and thrombocytopenia in 2.2% of courses administered. Nephrotoxicity was seen in 61% of patients as determined by evaluation of blood urea nitrogen and in 70.7% by serum creatinine elevation. Urine dipstick protein and 24 hour urinary protein determinations were evaluated. Suggestions are made in regard to the use of these determinations as a guide to modification of dose and duration of therapy.
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PMID:cis-Platinum in gynecologic cancer. III. Toxicity. 719 23

A total of 22 nonsplenectomized Hereford, Holstein-Friesian, and cross-bred 18-month-old cattle were used to assess the degree of protection conferred by previous infection with Babesia bovis or B bigemina against infection and disease from tick-borne challenge exposure with the heterologous species. Prior infection with B bigemina or B bovis did not significantly (P less than 0.05) reduce the susceptibility of cattle to tick-borne infection and disease caused by the heterologous species. Carrier infections were not activated during heterologous species challenge exposure, nor was the severity of the challenge-exposure infection aggravated. Immunologic cross reactivity in the indirect fluorescent antibody test was restricted to the period during and shortly after recovery. Homologous indirect fluorescent antibody titers persisted long after primary infections with B bovis, but gradually declined in B bigemina-immune cattle. Babesia bovis infections caused severe reactions characterized by high fever, pancytopenia, and death of 9 of 15 infected cattle. Total serum bilirubin and urea nitrogen values increased markedly within 24 hours preceding death and were often accompanied by clinical signs of CNS involvement (incoordination, opisthotonos, and paddling). Microscopic lesions were restricted largely to kidney, CNS, and liver parenchyma and were characterized by vascular congestion and aggregation of infected erythrocytes in small vessels. Babesia bigemina, in contrast, caused only mild fever and anemia despite prolonged parasitemia and marked thrombocytopenia. The absence of significant (P less than 0.05) heterologous species immunity indicated that protection of cattle from these 2 babesial parasites will require specific immunization against each species.
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PMID:Bovine babesiosis: pathogenicity and heterologous species immunity of tick-borne Babesia bovis and B bigemina infections. 721 29

The clinical chemical changes induced by Anaplasma marginale infection were determined in 16 adult, intact cows infected with either of 2 virulent isolates and in 8 others treated with a live sheep-attenuated A marginale vaccine and were compared with the clinical chemical analyses in 7 noninfected controls. Blood samples from the cows were analyzed for various serum components and during clinical disease. Cows infected with the 2 virulent isolates had maximum erythrocyte parasitemias (0.5% to 66%) between 1 and 11 days of patency (DP); 7 of the 16 infected animals died within 5 to 12 DP. Cows given the sheep-attenuated anaplasma vaccine had maximum parasitemias (0.1% to 4.2%) between 1 and 16 DP and none died. Infection with the virulent isolates produced severe anemia (mean RBC count = about 2 million/mm3) and caused increases in serum total bilirubin (TBILI), direct bilirubin (DBILI), serum urea nitrogen (SUN), alkaline phosphatase (ALP), and serum aspartate aminotransferase (AST) that were significantly higher than comparable changes in control values. These increases were highest after peak parasitemias in surviving animals. Vaccination with the attenuated isolate produced a mild anemia (mean RBC count = about 5 million/mm3) and a significant increase only in ALP. Marked increase in TBILI, DBILI, SUN, ALP, and AST were detected 0 to 1 day before death in 3 cows. However, such increases were not observed 2 to 4 days before death in the other cows that died.
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PMID:Clinical chemistry of anaplasmosis: blood chemical changes in infected mature cows. 725 83

Pigs receiving a limited ration of 1 kg commercial feed per day were infected daily with 50,000 Oesophagostomum dentatum larvae. The animals exhibited serious diarrhoea and anorexia. Although there was neither anaemia nor hypoproteinaemia, there was a significant decrease in plasma sodium and an increase in blood urea nitrogen at the end of the experiment. Large numbers of third and fourth stage larvae were found in the ileal, caecal and colonic mucosae. Only fourth stage larvae, never adults, were observed in the lumen. A continual expulsion of large quantities of third and fourth stage larvae were demonstrated in the faeces beginning with the appearance of diarrhoea. Neither Vibrio coli, Salmonella spp nor Balantidium coli contributed to the course of the enteritis.
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PMID:Experimental infection of pigs with Oesophagostomum dentatum: pathogenesis and parasitology of repeated mass infection. 731 9

Investigation of pharmacokinetics of certain drugs in experimental models of glomerulonephritis would facilitate development of dose schedules for dogs with this disease. Polymerized polyvinyl alcohol (PVA)-induced glomerulonephritis was investigated in healthy, 15-week-old purebred Beagle dogs. Three dogs were injected daily with 20 ml of 5% (w/v) PVA (125,000 molecular weight, 88% hydrolyzed) in phosphate-buffered saline solution. One control was given only phosphate-buffered saline solution. Determinations were made of complete blood count, PCV, serum urea nitrogen, specific gravity, urine pH, and protein. Tissue specimens were taken for light microscopic and electron microscopic examinations. Injections were stopped after 3 weeks due to severe CNS depression and anemia in the principals. Proteinuria appeared shortly before dogs were euthanatized, but there were no other signs of renal disease. The dominant lesions were foam cell formation in glomeruli and diffuse vacuolation of splenic red pulp cells. Lesions were also visible in electron microscopic sections of glomeruli. Abnormalities were not observed in the control dog. Due to the severity of the nonrenal lesions, PVA (the type used here) is not useful for creating a model of renal disease in dogs.
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PMID:Polyvinyl alcohol toxicosis as a model of glomerulonephritis in Beagle dogs. 740 71

Oral administration of lead-containing paint to rhesus monkeys induced anemia, more profound in older primates. Erythrocytes were microcytic and hypochromic, but tended to become macrocytic terminally. Stippled erythrocytes were increased in all poisoned monkeys, especially in those with high blood lead levels and anemia. Proteinuria, glycosuria, casts and sloughed tubular cells containing acid-fast inclusion bodies were found on urinalysis. Terminal elevations of blood urea nitrogen were associated with profound anemia and renal tubular damage. Repeated blood lead values over 200 microgram/dl were associated with a moribund termination while monkeys which had levels under 100 microgram/dl remained apparently healthy. Behavioral studies in a small number of subclinically poisoned juveniles and neonates failed to reveal deficiencies of visual acuity or cognitive ability, nor was there evidence of alterations in levels of activity.
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PMID:Experimental lead paint poisoning in nonhuman primates. II. Clinical pathologic findings and behavioral effects. 744 15

The effects of chitosan-coated dialdehyde cellulose (Chitosan DAC), a newly developed oral adsorbent of urea and ammonia, were examined in rats with progressive chronic renal failure (CRF) induced by adriamycin. CRF rats induced by repeated injections of adriamycin were fed a diet containing chitosan DAC (5% content) or Kremezin (5% content), an oral charcoal adsorbent (AST-120) under strict paired-feeding for four months. CRF rats that received both a normal diet and Kremezin showed progressive azotemia, hyperphosphatemia, hyperlipidemia, proteinuria, and anemia, and began to die from 9 weeks after feeding started. In contrast, chitosan DAC-treatment showed marked prolongation of the survival period and decreases in blood urea nitrogen, serum creatinine, and serum phosphate. In addition, chitosan DAC-treatment ameliorated anemia in CRF rats, although hyperlipidemia and proteinuria were not improved. Furthermore, fecal weight, fecal water content, fecal nitrogen and fecal sodium were markedly increased, and the apparent protein ratio was decreased in CRF rats fed a diet containing chitosan DAC for 9 weeks. In contrast, none of these effects were observed in CRF rats receiving Kremezin. These observations suggest the further possibility of using oral adsorbent therapy for CRF patients.
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PMID:[Pharmacological properties of chitosan-coated dialdehyde cellulose (chitosan DAC), a newly developed oral adsorbent (II). Effect of chitosan DAC on rats with chronic renal failure induced by adriamycin]. 755 38

The rats were fed with adenine to establish the chronic renal insufficiency anemia model, and the relationship between renal functional impairment and reticulocytes, hemoglobin and erythropoietin (EPO) synthesis was observed to explore the mechanism of Bushen Shengxue drugs in improving the hemopoietic function. The results showed that the Bushen Shengxue drugs could significantly lower the serum creatinine and blood urea nitrogen of renal insufficiency rats, and through the promotion of EPO gene expression, the animals' anemic status was improved.
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PMID:[Effect of bushen shengxue recipe on EPO gene expression of chronic renal insufficiency anemia in rats]. 764 45

Anemia is an invariable consequence of end-stage renal failure (ESRF) and recombinant erythropoietin has dramatically improved the quality of life of patients with ESRF. As an alternative approach, we developed a myoblast gene transfer system for the systemic delivery of human erythropoietin (EPO). We recently reported that transplantation of 4 x 10(7) cells of a C2 myoblast cell clone that stably secretes high level of functional human EPO, increased hematocrit from 44.6 +/- 3.0 to 71.2 +/- 7.9(%) in 2 wk, and the increase was sustained for at least 12 wk in nude mice. A renal failure model was created by a two-step nephrectomy in nude mice, and myoblasts were transplanted 3 wk after the second nephrectomy, when mean blood urea nitrogen level had increased from 26.3 +/- 6.1 to 85.4 +/- 24.0 (mg/dl) and the hematocrit had decreased from 45.2 +/- 2.7 to 33.9 +/- 3.7(%). After transplantation, the hematocrit markedly increased to 68.6 +/- 4.2(%) 2 wk, and to 68.5 +/- 4.0(%) 7 wk after the transplantation. Serum human EPO concentration determined by ELISA indicated a persistent steady EPO production from the transplanted muscle cells 8 wk after the transplantation. The fate of transplanted myoblasts in uremic mice was monitored by transplanting the EPO-secreting clone which had also been transduced with BAG retrovirus bearing the beta-galactosidase gene. 8 wk later, X-gal positive myofibers were detected in the entire transplanted area. The results demonstrate that myoblasts can be transplanted in uremic mice, and that myoblast gene transfer can achieve sufficient and sustained delivery of functionally active EPO to correct anemia associated with renal failure in mice.
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PMID:Myoblast transfer of human erythropoietin gene in a mouse model of renal failure. 770 87


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