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

The influence of lead on iron absorption was investigated at various stages of development in rat pups exposed to lead first through mothers' milk and later in their solid diet. Hematocrit, hemoglobin, iron absorption, and tissue iron concentration were measured on d 14, 20, 23, 29, 35, 42, and 63 after birth. Both hematocrit and hemoglobin in the lead-exposed group were significantly below control levels at all periods earlier than d 42 and 63, respectively. Absorption of iron ([59Fe]-ferrous citrate in 10(-4)M FeSO4) from intestinal loops measured over 1/2 h remained at preweaning levels (10-12% of total activity added to the loop) for at least 1 wk after weaning in the lead-exposed rats, whereas in control animals iron absorption fell to adult levels (3-4%) at weaning. Spleen weight was significantly elevated in lead-exposed rats compared with control rats at all ages beyond d 14. However, spleen iron content (micrograms of Fe per gram of tissue) was not significantly elevated in the lead-exposed group before d 42. The results indicate that exposure to lead does not reduce iron absorption from the intestinal tract; thus alteration of intestinal iron absorption does not contribute to lead-induced anemia. Indeed, lead-exposed rats demonstrated increased iron uptake.
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PMID:Effect of exposure to lead on maturation of intestinal iron absorption of rats. 68 5

Hb M Akita disease is a cyanotic hemoglobinopathy found in Akita Prefecture, Japan. The abnormal hemoglobin was found to be the same as Hb M Hyde Park (beta92 His replaced by Tyr) by chemical analysis in 1967. In this disease signs of accelerated hemolysis (serum bilirubin, 2.4 mg/dl; splenomegaly, 2 finger breadths; Hb, 10.7 g/dl; reticulocyte index, 2.7) were noted, but the causes of its slight anemia were revealed to be fairly complex by ferrokinetic study, RBC life-span measurement, and 99mTc myeloscintigram. The anemia in this disease is caused not only by shortened erythrocyte survival (T 1/2 = 11.5 days by 51Cr-tagging method) and sequestration of red cells in the spleen (Spleen: liver ratio = 2.5 approximately 3.0 by 51Cr-surface counting), but also by slow supply of erythrocytes to the peripheral blood from the bone marrow, presumably, related to the existence of unstable Hb M Akita and its derivative (Hb Akita) in the erythroid cells. Both Carrell's isopropanol test and Heinz body formation test were positive. In spite of maximally increased total erythropoiesis (8 times as high as the normal level; M:E ratio = 0.22:1.0), supply of red cells from the bone marrow to the peripheral blood was significantly decreased. The distribution of hematopoietic sites throughout the body was reasonably uniform.
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PMID:Altered erythropoiesis and increased hemolysis in hemoglobin M Akita (M Hyde Park beta92 His replaced by Tyr) disease. 105 75

The proliferative activity of bone marrow from Rauscher Leukemia Virus infected mice was studied during the course of the disease. Spleen colony assay and thin-layer agar technique, both presumably reflecting the number of pluripotent hemopoietic stem cells, showed a 2.6 times increase in colony forming units (CFU-S resp. CFU-A) at 12 days after infection. The Bradley method of culturing colonies in agar, which is stated to reflect the number of myeloid precursor cells, resulted in a slower rise in colony forming units (CFU-C) with a maximum of 2.3 times increase at 19 days after infection. These results were compared to the differentiation patterns of the bone marrow at similar intervals after infection. The course of the CFU-C curve parallelled the rise in the number of the myeloblasts in the bone marrow. The pattern of CFU-A and CFU-S curves preceded the rise in number of CFU-C by 7 days. It was found, that RLV infection apart from causing an erythroblastosis in the spleen and a severe anemia is followed by a disappearance of neutrophil granulocytes from the bone marrow. The latter phenomenon is probably the primary cause of the increase of hemopoietic stem cells.
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PMID:The relation between the proliferative activity and the differentiation pattern of bone marrow cells from Rauscher leukemia virus infected BALB/c mice. 122 10

One-day-old chicks with no maternal antibodies to chicken anemia agent (CAA) were inoculated intramuscularly with CAA grown in MDCC-MSB1 cells. A control group of birds from the same source was inoculated intramuscularly with a lysate from uninfected MSB1 cells. Birds were killed at 8, 15, 22, 29, and 43 days postinoculation (PI), and the spleens were removed. Spleen cells were dispersed and stimulated with various concentrations of Concanavalin A (Con A), and lymphocyte transformation responses were determined. Supernatants from Con A-stimulated cultures were assayed for T-cell growth factor (TCGF) and interferon. Decreased lymphocyte transformation and TCGF production were demonstrated at 8 and 15 days PI. This was followed by a stimulation in activities before a return to control levels at 43 days PI. Interferon levels were elevated 8 days after infection. This was followed by a significant decrease in activity compared with controls at 15, 22, and 29 days PI, and a return to control levels by 43 days PI. The results suggest that CAA infection in young chickens can produce a dramatic decrease in immune competence, which, although transitory, is likely to seriously compromise the ability of birds to mount a successful immune response to invading pathogens.
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PMID:Effects of chicken anemia agent on lymphokine production and lymphocyte transformation in experimentally infected chickens. 172 73

Infectious anaemia in Atlantic salmon (Salmo salar) was studied by recording gross and light microscopic changes, and the development of lesions was studied in relation to haematocrit values. Gross lesions were characterised by ascites formation, congestion and enlargement of liver and spleen, congestion of the foregut and petechiae in the peritoneum. Histologically, lesions were demonstrated in the liver, being characterised by congestion in early stages (that is, haematocrit values around 25), dilatation of the sinusoids, and in later stages (haematocrit values 25 to 15) formation of blood-filled spaces bearing morphological resemblance to peliosis hepatis. At low haematocrit values (around 10), these changes comprised large areas of the liver parenchyma, that is, blood-filled areas coalesced, presenting islets of degenerate and necrotic hepatocytes. At this stage, haemorrhagic necroses were found. Spleen and kidney lesions were characterised by congestion. In the foregut, congestion and bleeding in lamina propria were observed. Liver lesions became more disseminated and severe with decreasing haematocrit values. Hypoxia due to anaemia alone cannot fully explain the development of the liver lesions.
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PMID:A morphological study of the gross and light microscopic lesions of infectious anaemia in Atlantic salmon (Salmo salar). 178 86

Spleen abscesses are infrequent, and are encountered in 0.4 to 0.7%-of the autopsy series. They are diagnosed late and their prognosis is poor. The authors report about 5 cases of spleen abscesses observed at Dakar's University Surgical Clinic over a period of 30 years. The patients were young adults, including one case of sickle-cell anemia. In spite of numerous clinical signs in all cases, the abscess was diagnosed late. In three patients, ultrasound allowed establishing the diagnosis and initiating percutaneous treatment, with no success in two cases. The procedure had consisted in total splenectomy in all cases. One patient died 2 months after surgery, after the evacuation of a hematoma in the splenic compartment. The other 4 patients, seen 7, 4, 3 months and 15 years after total splenectomy, no longer presented with any symptom. The authors emphasize the rarity of spleen abscesses; the fact that the diagnosis is often established late, in spite of the progress made in non-invasive medical imaging, including CT and ultrasound; the physiopathology, etiology and treatment of the disease, the latter still being surgical.
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PMID:[Splenic abscess. Apropos of 5 cases]. 188 Jan 83

Levels of mature lymphocytes, granulocytes, macrophages, platelets, their progenitor cells, and cytokines were monitored in the blood, marrow, and spleen during fatal or nonfatal murine malarial infections. In all four malaria models, before anemia developed, there was a lymphopenia, a rapid lymphocyte depletion in the marrow with a compensating rise in spleen lymphocytes, thrombocytopenia with increased megakaryocytic progenitor cell numbers, and monocyte increases in the bone marrow and later the spleen. The development of anemia was associated with a monocytosis and neutropenia, an increase in granulomonocytic progenitor cells in the spleen, and a reduction of spleen lymphocytes. Spleen granulocytes, monocytes, and their progenitor cells increased two- to threefold more in nonfatal than in fatal malaria and the spleen lymphocyte pool became severely depleted in fatal malaria. The data suggest that a defective effector cell response was of importance for the fatal outcome of the disease. Other than an early rise in serum macrophage colony stimulating factor levels in fatal infections, changes in levels of the regulators of these effector cells did not correlate well with the outcome of the infection.
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PMID:Changes in hemopoietic and regulator levels in mice during fatal or nonfatal malarial infections. II. Nonerythroid populations. 214 42

Dose levels for these studies were selected mainly on the basis of subchronic studies, although consideration was also given to workplace exposure levels and proposed mechanism of tumor formation with structurally similar compounds. For the chronic study, groups of 60 male and 60 female Sprague-Dawley CD (Registered Trademark of Charles River Breeding Laboratories, Portage, MI) rats were given 0, 0.25, 1.5, or 9.0 mg/kg/day paranitroaniline (PNA) by gavage in corn oil for a period of 2 years. Parameters monitored included clinical observations, ophthalmoscopic exams, body weights, food consumption, hematology, clinical chemistry, and urinalysis at regular intervals throughout the study. All gross lesions and over 40 tissues were examined histologically for all control and high-dosage-level animals. Gross lesions, spleens, and livers of low- and mid-dosage groups were also examined histologically. For the reproduction study, groups of 15 male and 30 female rats, designated as F0 generation, were given PNA at the same levels as the chronic study for 14 weeks prior to mating and during mating, gestation, and lactation. Selected groups of 15 male and 30 female rats of the F1 generation received the same dose of PNA for 18 weeks prior to mating and during mating, gestation, and lactation. F2 pups were observed through weaning at which time they were euthanized. Observations made during the study included body weights, food consumption, mating and fertility indices, pup and litter survival indices, and histopathology of selected tissues. In the chronic study, except for a slight decrease in survival of high-dose male rats late in the study, survival in all treated groups was comparable to controls. Blood methemoglobin levels were elevated in the mid- and high-dosage groups, while slight anemia was observed in the high-dosage group also. Spleen weights were significantly increased in the high-dosage groups. An accumulation of brown pigment was observed in the cytoplasm of the sinusoidal macrophages or littoral cells of the liver and in the reticuloendothelial cells of the spleen. No treatment-related increase in tumor incidence was observed. In the reproduction study, no consistent pattern of effect from treatment between the F0 and F1 generation was seen in mating, pregnancy, or fertility indices. Thus, administration of PNA at levels which produced significant methemoglobinemia and low-level anemia in the rat and histological changes in the spleen produced no tumors or reproducible effects on reproductive performance.
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PMID:Chronic toxicity, oncogenic potential, and reproductive toxicity of p-nitroaniline in rats. 225 23

This work characterizes the erythropoietic interplay of the spleen, blood, and bone marrow in a lethal murine malaria, strain 17XL P. yoelii. This malaria runs a fulminant 7 day course in BALB/c/ByJ mice, marked by high levels of parasitized reticulocytes with death likely due to anemia. We have quantitated the levels of burst forming units-erythroid (BFU-E), the early, niche-seeking, largely erythropoietin-unresponsive erythropoietic precursors, and of colony forming units-erythroid (CFU-E), the more differentiated sessile erythropoietin-responsive precursors, in bone marrow, blood, and spleen, through the course of this malaria. A decline in marrow BFU-E began on day 2, but recovered, relatively, after day 3. Marrow cellularity declined, being but 75% normal on day 6. Spleen weight increased about 5-fold within 6 days with enlargement of erythroid, lymphoid, macrophage, and stromal compartments. Splenic BFU-E increased in the first 24 hr and 5-fold by day 6. Splenic CFU-E increased in the first 24 hr and into day 4. They then declined and showed a secondary, large-scale, sustained rise interrupted by death. Because the spleen was enlarging, a greater than 60-fold increase in the absolute number of splenic CFU-E occurred at the time of death. Marrow CFU-E followed the same pattern as splenic CFU-E, but the terminal increase represented but a 4-fold absolute increase because of declining marrow cellularity. High levels of erythropoietin occurred only late in the course of disease, likely in response to profound anemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of splenic control of murine malaria: tissue culture studies of the erythropoietic interplay of spleen, bone marrow, and blood in lethal (strain 17XL) Plasmodium yoelii malaria in BALB/c mice. 277 62

Spleen cells taken from mice infected as adults with two different variants of the spleen focus-forming virus (SFFV), SFFVP and SFFVA, as well as spleen cells taken from mice infected as newborns with Friend murine leukemia virus (F-MuLV) were assayed in a proliferation assay in the presence or absence of the erythroid hormone erythropoietin (Epo). Infection of NIH Swiss mice with SFFV resulted in excessive proliferation of erythroid cells that could still differentiate, and spleen cells taken from these mice were able to incorporate high levels of tritiated thymidine ([3H]dThd) in the absence of Epo, even in the presence of antibodies to Epo. In contrast, the level of proliferation of spleen cells from SFFVA-infected mice, but not those from SFFVP-infected mice, could be greatly enhanced by the addition of Epo to the cultures. Infection of newborn mice with F-MuLV resulted in the generation of Friend mink cell focus-inducing virus, which caused excessive proliferation of erythroid cells that appeared to be blocked in differentiation, resulting in severe anemia. Spleen cells from these mice were unable to proliferate in the absence of Epo. However, when increasing doses of Epo were added to the cultures, the cells proliferated at levels equivalent to the levels seen with SFFV. These results indicate that a proliferation assay based on the incorporation of [3H]dThd into spleen cells in response to Epo can be used as a quantitative means of assessing and comparing the effects of erythroleukemia-inducing retroviruses on the proliferation of their target cells.
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PMID:Employment of a [3H]thymidine-incorporation assay to distinguish the effects of different Friend erythroleukemia-inducing retroviruses on erythroid cell proliferation. 345 16


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