Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a study of 16 patients with aplastic anaemia, an attempt has been made to relate ferrokinetic data to haematological measurements and clinical course. There was a positive relationship of cellularity on trephine biopsy with plasma iron clearance and erythrocyte iron turnover, but not with red cell utilisation. Bone marrow aspirate provided less reliable information on erythropoietic function than did trephine biopsy. There was good correlation between all the ferrokinetic parameters and reticulocyte count, but not between reticulocyte count and marrow cellularity, even by trephine. Patients whose ferrokinetic studies indicate a less severe erythroid depression (i.e., plasma clearance T 1/2 less than 200 min and red cell utilisation greater than 35%) are more likely to survive without transplantation than those with more abnormal ferrokinetic results, but such studies alone are of only limited value in clinical management of the individual patient.
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PMID:Ferrokinetic studies and prognosis in aplastic anaemia. 678 93

Twenty-five children with acute lymphoblastic leukemia (ALL) were tested for natural killer (NK) and K-cell activity in vitro using the nonsensitized myeloid/erythroid cell line K562 and the K562 sensitized with rabbit antithymocyte globulin, respectively. The patients consisted of two groups: 1) 13 patients in continuous first remission undergoing maintenance chemotherapy and 2) 12 patients in remission for at least five years in whom chemotherapy had been discontinued at least six months before this study. The first group consistently demonstrated a marked depression in their NK activity and antibody-dependent cell-mediated cytotoxicity (K-cell activity), as compared with normal controls. In contrast, normal levels of cytotoxicity were found in the second group of patients off of all chemotherapy. One patient studied while on chemotherapy and on two occasions following discontinuation of maintenance medications demonstrated that while NK and K-cell activity was depressed during therapy, normal activity returned within days when immunosuppressive therapy was stopped. Thus, present modes of chemotherapy clearly had a profound effect on the in vitro NK and K-cell activity; however, no long-term effect on these functions was noted in our studies.
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PMID:Immunologic evaluation of long-term effects of childhood ALL chemotherapy: analysis of in vitro NK- and K-cell activities of peripheral blood lymphocytes. 680 72

Three preadipocyte cell lines that have been independently derived from bone marrow stroma (Lanotte et al, 1982) have been tested for their capacity to produce granulocyte, macrophage, and erythroid colony-stimulating factors (CSFs). All elaborated colony-stimulating material that was active upon adult mouse marrow granulocyte/macrophage colony-forming cells (M-CFC) but not foetal liver GM-CFC. The major activity was characterised as a monocyte-macrophage colony-stimulating factor (M-CSF), and the pattern of colony stimulation was similar to that seen after addition of highly purified L-cell CSF. Furthermore, the stimulating activity was specifically neutralised by rabbit anti-L cell CSF antibodies. No evidence was found for stimulation of multipotential or erythroid colony-forming cells, only few granulocytic colonies were detected, and the stimulating activity had no mouse strain restriction. All cell lines produced large quantities of M-CSF; however, the production was found to be modulated during the adipogenesis process. A peak in M-CSF production corresponded to the period of growth arrest after confluence of the stromal cells was reached and when adipocyte maturation was at an early stage. A marked depression in M-CSF secretion was associated with the final steps of adipocyte maturation.
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PMID:Production of monocyte/macrophage colony-stimulating factor by preadipocyte cell lines derived from murine marrow stroma. 698 Aug 87

The erythroid status and levels of splenic plaque-forming cells (PFC) to sheep red blood cells (SRBC) were monitored in mice subsequent to acute phenylhydrazine (PHZ)-induced hemolytic anemia. From ferrokinetic measurements, we noted a shift in erythropoiesis from bone marrow to spleen. The levels of splenic PFC were significantly depressed following PHZ-induced erythroid differentiation. Although this immune depression may reflect competition at the stem cell levels, whereby pluripotent stem cells (CFU-s) are preferentially differentiated into the erythroid line at the expense of lymphopoietic pathways, other possibilities cannot be excluded. In this regard, we have shown that loading of the mononuclear phagocyte system (MPS) by PHZ-damaged erythrocytes effected profound depressions in splenic PFC numbers. Lastly, in addition to the well-documented increases in CFU-s migration from marrow to spleen during enhanced erythropoiesis, we noted increased migration of B lymphocytes (as assessed by PFC) in marrow-shielded lethally-irradiated mice given PHZ. We also provide data which show that PHZ-damaged RBC evoke increased migration of CFU-s in normal mice, indicating a possible involvement of the MPS in stem cell migration.
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PMID:Splenic plaque-forming cells (PFC) and stem cells (CFU-s) during acute phenylhydrazine-induced enhanced erythropoiesis. 700 67

Myelomonocytic myeloproliferative disease in a horse was diagnosed on the basis of hematologic, enzymatic, and histopathologic findings. It was characterized clinically by depression, weight loss splenomegaly, lymphadenopathy, coagulopathy, and bacteremia. Hematologic findings included severe refractory anemia, thrombocytopenia, monocytosis, and pleomorphic leukocytes, with a left shift of the myeloid series. The serum lysozyme concentration was 14.5 microgram/ml (normal, less than 5 microgram/ml). The bone marrow contained many immature cells of the myeloid series and had a myeloid-to-erythroid ratio of 30.5 to 1. The horse died after brief hospitalization. Necropsy revealed generalized lymphadenopathy and hemorrhages throughout the body. Histopathologically, primitive cells were seen in several tissues. Cells that proliferated in the bone marrow were primarily myeloblastic, with some additional erythropoietic cells. Myeloblastic cells with evidence of normal erythropoiesis were seen in numerous lymph nodes and in the spleen, whereas primarily normal erythropoietic cells proliferated in the adrenal glands. Myeloid blast-type cells predominated in the lungs, myocardium, liver, and kidneys.
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PMID:Myelomonocytic myeloproliferative diseases in a horse. 705 85

The time-response curve for hematocrit following s.c. injection of 400 microgram of indomethacin (IM) in a single dose into adult female mice showed a maximal depression at 3 days after IM with return to normal values by 11-12 days. The effect was dose-related showing a plateau with doses of IM above 400 microgram. The total circulating red cell volume was 68% of control and the plasma volume 117% of control 3 days after IM injection, recovering thereafter. At the same time, erythroid tissue iron uptake (microgram/h) was 67% higher in IM-treated than in non-injected mice. In mice with suppressed erythropoiesis due to daily i.p. injections of 0.06 microgram/g of actinomycin D, injection of IM induced a marked and rapid loss of cells from the circulation. Macroscopic and microscopic examinations of IM-treated mice at autopsy showed no indication of internal bleeding or other abnormalities. Serum non-conjugated bilirubin concentration was 2.2 times higher in IM-injected mice than in controls 3 days after drug administration. These results indicate that IM injection into mice in the experimental conditions reported here appears to induce a transient hemolytic state which is responsible for the depression of the red cell mass and the subsequent increase in the erythropoietic rate to compensate it. Both the decreased red cell volume and the increased plasma volume are responsible for the depression of the hematocrit value.
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PMID:Effect of indomethacin on red cell volume, iron kinetics and red cell survival in mice. 711 22

The capability of chronic beta 2-adrenoceptor activation to effectively stimulate erythrocyte production in vivo was investigated in mice which had been treated with the hematopoiesis inhibiting agent busulfan. A relatively low dose (5 mg/kg i.p.) of busulfan produced moderate depression of erythropoiesis 10 days after a single injection, as determined by 59Fe-incorporation into erythrocytes. Administration of albuterol (1 mg/kg s.c. twice daily), a selective beta 2-adrenergic agonist, significantly enhanced erythropoiesis for 5--10 days after the injection of busulfan. In a long-term study with albuterol at the same dose a significant increase in hematocrit values as well as in the circulating erythrocyte mass was found in busulfan (5 mg/kg i.p. weekly) treated mice when compared to saline-busulfan treated control mice. Simultaneous injections of the beta-adrenergic blocking agent propanolol (4 mg/kg i.p.) diminished the effect of albuterol on erythropoiesis. Albuterol at a lower dose (0.1 mg/kg) had no significant effect on erythrocyte mass. In view of recent findings, which have shown that the proliferation of the pluripotent hemopoietic stem cell pool is blocked by busulfan, it is concluded that the main site of beta 2-adrenergic action on erythropoiesis is on the erythroid committed stem cell pool. In addition, enhanced release of erythropoietin from the kidney following the application of albuterol may contribute to beta 2-adrenergic stimulation of erythropoiesis.
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PMID:beta 2-Adrenergic stimulation of erythropoiesis in busulfan treated mice. 720 79

In 3 experiments, 45 castrated male weanling pigs (4 to 6 weeks old) were used to determine the hematologic alterations induced by adriamycin (ADR) given IV at 0.64, 1.6, or 3.2 mg/kg of body weight/week. The effect of selenium-vitamin E (Se-E) supplements on ADR toxicosis was evaluated. Mortality, decreased survival time, growth depression, leukopenia, and anemia were dose related in ADR-treated pigs. At 0.64 mg of ADR/kg/week for 16 weeks, important clinical or hematologic alterations did not develop. At 1.6 mg of ADR/kg/week for 13 weeks, mortality was 100%, mean survival time ws 65.7 days (min-max, 49 to 92 days), and moderate growth depression and marked leukopenia and anemia were present from weeks 7 to 13. At 3.2 mg of ADR/kg/week for 4 weeks, mortality was 100% and mean survival time was 22.0 days (min-max, 18 to 26 days); marked growth depression, leukopenia, and mild anemia developed (week 4). Cytologic study of smears of bone marrow from pigs that died of ADR toxicosis (3.2 mg/kg/week) revealed marked hypoplasia and evidence of decreased production and increased destruction of erythroid and myeloid cells. Beneficial effect of Se-E supplementation against ADR toxicosis was seen only in the pigs given 1.6 mg/kg/week, where prolonged survival and delayed onset of leukopenia and anemia was observed.
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PMID:Effect of selenium-vitamin E on hematologic alterations of adriamycin toxicosis in young pigs. 727 Oct 34

Plethoric mice treated with pharmacological doses of estradiol have decreased concentration of erythropoietin-responsive cells (ERC) in the marrow. We used the methylcellulose-culture system for growth of erythroid stem cells (CFU-E and BFU-E) to define more accurately these estrogen-induced changes. As an animal model we utilized plethoric mice given repeated injections of estradiol cypionate and found that at 14 days after the onset of treatment there was no significant change in the concentration of femoral CFU-E whereas there was a significant decrease of the BFU-E content. Both CFU-E and BFU-E increased progressively in the spleen over a 42-day period. Addition of estradiol directly to the cell-culture system showed no effect on CFU-E growth but induced a significant depression of BFU-E growth. This depression seemed to require the presence of adherent cells. It is our hypothesis that estrogens suppress only the early stages of erythroid proliferation and/or differentiation by a mechanism involving possibly the stromal (adherent) cells of the marrow microenvironment.
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PMID:The effect of estrogens on erythroid stem cells in polycythemic mice. 732 99

After a base-line period (14 days), five cats were orally given 50 mg of chloramphenicol every 12 hours for 21 days. Clinical signs of toxicosis were CNS depression, reduced intake of food and water, and weight loss. Changes in peripheral blood included lower platelet counts after treatment for 1 week and fewer neutrophils after treatment for 3 weeks; one cat developed lymphocytopenia after 1 week and neutropenia after 2 weeks. Changes in bone marrow at the end of treatment comprised vacuolation of early myeloid cells and lymphocytes, and reduced myeloid maturation ratio, and some cats also had reduced marrow cellularity, or increased myeloid:erythroid ratio, or both of these.
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PMID:Further observations on chloramphenicol toxicosis in cats. 736 2


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