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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Injection of plasma from experimentally induced anemic toad with intact testis increases erythropoiesis in starved toads evidenced by the increase of red blood cell, hemoglobin and hematocrit, whereas the plasma of castrated and phenylhydrazine-HCl treated anemic toad failed to do so. It can be suggested that the erythropoiesis stimulating factor (ESF) is produced from the testis of toad and the production of this factor (ESF) was found to increase during anemia in an attempt to correct the anemic condition.
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PMID:Studies on the erythropoietic effect of plasma from anemic toads both with and without testis. 46 79

34 subjects including 5 probands with pernicious anemia, 3 probands with severe atriphic body gastritis and 26 of their first-degree relatives were studied gastroscopically, bioptically, functionally and immunologically. In general, members of the same family revealed a trend to behave similarly with respect to the parameters studied. Signs of A-gastritis (severe atrophy of gastric body glands with a normal or almost normal antrum, achlorhydria, hypergastrinemia and parietal cell antibodies), with intrinsic factor antibodies in the gastric juice and diminished intrinsic factor secretion without anemia were found both in families of probands with atrophic gastritis and pernicious anemia. This suggests a close etiopathogenetic relation of this type of mucosal lesion to overt pernicious anemia. Determination of HCl output and serum gastrin level enabled us to distinguish two differently behaving subgroups in the series, one of them with characteristics of overt adult pernicious anemia. Very low intrinsic factor secretion was found almost exclusively in connection with the presence of intrinsic factor antibodies in the gastric juice and always with severe atrophy of gastric body glands.
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PMID:Gastric lesion and pernicious anemia: a family study. 63 45

We describe a spot test for detecting deficiency of uroporphyrinogen I synthase (EC 4.3.1.8), which is characteristic of intermittent acute porphyria. The specimens used for enzyme assay are 6.5-mm filter paper discs saturated with dried blood (less than 15 mul) that was collected by direct application from a fingerstick or from venipuncture, with or without anticoagulant. The enzyme in such specimens is stable for at least nine days at -20 or c degrees C or for two days at room temperature. The discs are incubated with porphobilinogen (0.11 mmol/liter) in tris(hydroxymethyl)aminomethane HCl buffer, pH 8.2, in the dark at 37 degrees C for 3.5 h. Trichloroacetic acid is added and, after centrifugation, the supernate is examined visually with a long-wavelength ultraviolet lamp. Samples from normal and porphyric subjects are readily differentiated, both by color and intensity of the resulting porphyrin fluorescence. Anemia is a potential source of falsely positive tests, but one may accurately determine the concentration of hemoglobin in the whole blood on the filter paper discs. Moreover, the fluorescence of normal but anemic samples clearly differs qualitatively from that of porphyric specimens. Another source of falsely positive tests, variation in enzyme activity creating an overlap zone of normal and porphyric results, has not been a confounding problem. The method thus seems to offer promise for screening populations for this disorder.
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PMID:A spot test for uroporphyrinogen I synthase, the enzyme that is deficient in intermittent acute porphyria. 100 Jul 96

Fractional contents of hemoglobins of the peripheral blood, spleen and the bone marrow was studied in intact and anemic rats by using electrophoresis in polyacrylamide gel. Anemia was caused by injection of phenylhydrazine (HCl) into the animals. The principal regularities in the formation of the heterogeneous system of hemoglobin, depending on its source and the animal condition, was established. Possible mechanisms responsible for the rebuilding of the fractional contents of the protein investigated and its biological sense are discussed.
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PMID:[Heterogeneous hemoglobin system in anemic rats]. 101 10

Incorporation of 3H-thymidine into cells of bone marrow, spleen and intestinal mucosa was studied in rats with anemia, caused by administration of phenyl hydrazine-HCl. Optimal duration for administration of the labelled precursor was determined and the doses of 3H-thymidine required to produce 3H-DNA with the definite specific radioactivity were established. The isolation of the labelled preparations of DNA from rat spleen after incorporation of 2-2.5 muCi of 3H-thymidine is described; their physico-chemical properties were studied. The specific radioactivity of 3H-DNA was equal to 5-10(6)--10-10(6) disintegrations per 1 min per 1 mg.
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PMID:[Preparation of labelled DNA from animal tissues]. 121 71

1. Cohorts of [3H]thymidine-labelled erythrocytes were examined over a 42-day period in goldfish (Carassius auratus L.) recovering from phenylhydrazine HCl-induced anemia under normoxic conditions at 20 +/- 1 degree C and maintained with minimal disturbance on a high nutritional plane. 2. As judged by changes in primary and derived hematological variables, maturation required 16-20 days. 3. Similar estimates were obtained using cytomorphic variables obtained by image analysing methods. 4. These suggest that juvenile red cells in this species can be identified on the basis of the following characteristics: major axis less than 9.2 microM; one-sided surface area not greater than approximately 50 microns2; axis ratio greater than 0.774; form factor greater than 0.938. 5. Corresponding values for mature cells are: major axis greater than 11.2 microns; area greater than 68.5 microns2; axis ratio less than 0.716; form factor less than 0.912. 6. These criteria, with values for dividing and karyorrhectic cell numbers, offer a basis for more detailed and dynamic characterization of the erythron during response to environmental variation than has previously been possible.
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PMID:Maturation of the goldfish (Carassius auratus) erythrocyte. 135 5

It is sometimes necessary for the practitioner to transfuse the ruminant with whole blood or plasma. These techniques are often difficult to perform in practice and are time-consuming, expensive, and stressful to the animal. Acute loss of 20-25% of the blood volume will result in marked clinical signs of anemia, including tachycardia and maniacal behavior. The PCV is only a useful tool with which to monitor acute blood loss after intravascular equilibration with other fluid compartments has occurred. An acutely developing PCV of 15% or less may require transfusion. Chronic anemia with PCV of 7-12% can be tolerated without transfusion if the animal is not stressed and no further decline in erythrocyte mass occurs. Seventy-five per cent of transfused bovine erythrocytes are destroyed within 48 hours of transfusion. A transfusion rate of 10-20 ml/kg, recipient weight, is necessary to result in any appreciable increase in PCV. A nonpregnant donor can contribute 10-15 ml of blood/kg body weight at 2-4 week intervals. Sodium citrate is an effective anticoagulant, but acid citrate dextrose should be used if blood is to be stored for more than a few hours. Blood should not be stored more than 2 weeks prior to administration. Heparin is an unsuitable anticoagulant because the quantity of heparin required for clot-free blood collection will lead to coagulation defects in the recipient. Blood crossmatching is only rarely performed in the ruminant. In field situations, it is advisable to inject 200 ml of donor blood into the adult recipient and wait 10 minutes. If no reaction occurs, the rest of the blood can probably be safely administered as long as volume overload problems do not develop. Adverse reactions are most commonly seen in very young animals or pregnant cattle. Signs of blood or plasma transfusion reaction include hiccoughing, tachycardia, tachypnea, sweating, muscle tremors, pruritus, salivation, cough, dyspnea, fever, lacrimation, hematuria, hemoglobinuria, collapse, apnea, and opisthotonos. Intravenous epinephrine HCl 1:1000 can be administered (0.2 to 0.5 ml) intravenously or (4 to 5 ml) intramuscularly if clinical signs are severe. Pretreatment with antipyretics and slowing the administration rate may decrease the febrile response. Blood or plasma administered too rapidly will also result in signs of cardiovascular overload, acute heart failure, and pulmonary hypertension and edema. Furosemide and slower administration of blood or plasma should alleviate this problem.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Use of blood and blood products. 217 38

An economical vitamin B6-deficient ration, which was palatable to broiler chickens, was prepared and fed to 1-day-old broiler chicks. The experimental ration was a glucose-soybean meal diet. Vitamin B6 was removed by washing the soybean meal with water. Microbiological analysis revealed that the washed ration contained .45 mg vitamin B6 activity/kg. Experimental rations were formulated to contain .5, 1.0, and 3.0 mg added pyridoxine HCl/kg of ration. These supplemental levels produced total pyridoxine concentrations, as assayed, of .95, 1.48, and 3.18 mg pyridoxine HCl activity/kg of diet. Chicks were grown to 7 weeks of age and characteristic B6 deficiency traits, including increased mortality, decreased body weight gain, and increased incidence of abnormal leg conformation, were quantitated or observed. An extensive hematological evaluation at 4 weeks of age indicated that this marginal B6 deficiency resulted in increased erythrocyte numbers, decreased mean corpuscular hemoglobin levels, and increased erythrocyte fragility. No changes in hematocrits, total hemoglobin level, intracellular hemoglobin concentration, or reticulocyte number were found. These results indicate that anemia did not occur in broilers experiencing a moderate vitamin B6 deficiency. The hematological condition is described as microcytic, normochromic polycythemia.
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PMID:Hematology of chicks experiencing marginal vitamin B6 deficiency. 673 14

We report a 78-year-old man with progressive gait disturbance, dementia, and dysphagia. He was apparently well until 75 years of age in 1989 when he had an insidious onset of gait disturbance. In October of 1991, he was treated with levodopa and amantadine HCl in another hospital, but he developed visual hallucination right after these medications, and the drugs were discontinued. He also developed difficulty in swallowing with frequent aspiration pneumonia. He was admitted to our hospital on January 13, 1992. On admission, the patient was chronically ill Japanese man; his blood pressure was 118/70 mmHg, body temperature 35.4 degrees C, and heart rate 72 and regular. No anemia or jaundice was noted; lungs were clear and no heart murmur was audible. The abdomen was flat but rigid to palpation without tenderness; no organomegaly was noted. On neurologic examination, he was alert but disoriented to all spheres; he was apparently demented and the score of the mini-mental test was 11. He did not appear to have aphasia or apraxia. Cranial nerves appeared intact, but he had a mask-like face and a slight limitation in the upward gaze; his voice was small. He was unable to stand or walk; he showed marked akinesia and moderate rigidity in his neck and the trunk. Deep reflexes were generally elicited normally or slightly weakly. Plantar response was extensor on the left and flexor on the right. No grasp reflex was present. Sensory examination showed questionable loss of touch in the glove- and -stocking distribution.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A 78-year-old man with progressive gait disturbance, dysphagia, and dementia]. 819 46

The report concerns a 30-year-old factory worker, employed in a small galvanizing plant for over ten years in the burnishing, copper- and nickel-plating of small metal articles for the shoe industry. Acute arsine poisoning was attributed to the use of a dilute solution of CuSO4 (3%), HCl (32%), and As2O3 (2%) for burnishing metal (Fe-Zn) shoelace eyelet holes, in the absence of local exhaust ventilation and with no respiratory protection. Arsine caused severe intravascular hemolysis with a rapid drop in hematocrit and hemoglobin levels. Other body organs were involved as a result of the hypoxic effect of anemia and hemolysis, or as a direct toxic effect of the arsine itself. Our experience confirms that exchange transfusion is capable of rapidly arresting the adverse effects of arsine. The importance of preventive measures and worker information to avoid acute arsine poisoning is emphasized.
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PMID:Acute arsine intoxication as a consequence of metal burnishing operations. 921 49


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