Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of different preparative procedures for electron microscopy on the size and shape of murine oncornaviruses has been studied. With conventional negative staining procedures using neutral sodium phosphotungstate, both murine mammary tumor virus and murine leukemia virus appeared in head-and-tail forms, with a peak head diameter of 122 and 130 nm, respectively. Negative staining with uranyl accetate gave round virions with peak diameters of 148 and 130 nm. Prefixed virus was round with peak diameters of 141 and 130 nm, respectively, in phosphotungstate, and 148 and 117 nm, respectively, in uranyl acetate. With thin sections, the peak diameters were 143 and 123 nm. The preservation of the spherical shape of the virus was obtained by glutaraldehyde fixation dehydration in alcholic solutions of uranyl acetate, and critical point drying. Under these conditions the viruses had peak diameters of 99 and 82 nm, respectively. The size of murine mammary tumor virus has always been found to be larger than murine leukemia virus in all preparations except for negative staining with neutral sodium phosphotungstate. Shadowing of the virion preparations revealed considerable flattening of the particles in all cases except for critical point drying. Negatively stained preparations did not cast any shadow, and thus thethickness of the particles could not be evaluated. Virus can be reversibly converted from spherical to head-and-tail forms by altering osmotic strength. Under most of the conditions used, murine mammary tumor virus gave a bimodal size distribution with significant numbers of particles that were smaller than the major virus size.
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PMID:The morphology of murine oncornaviruses following different methods of preparation for electron microscopy. 4 80

Scanning electron microscopy (SEM) is an invaluable tool for studying the surface morphology of isolated blood cells. We have used a simple preparative technique for SEM to study the erythrocytes from a case of Congenital Dyserythropoietic Anaemia type II and the leucocytes from healthy individuals or patients with leukaemia or lymphoma. This rapid and inexpensive technique for fixation and dehydration of blood cells was found to be equally reliable for obtaining micrographs of healthy or diseased leucocytes or erythrocytes.
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PMID:Scanning electron microscopy of blood cells. 31 84

The relatively high incidence of infectious disease in alcoholics is attributed to the immunosuppressive effects of alcohol. The potential role of alcohol as cofactor in HIV infection and in the development and expression of AIDS is suggested but unknown. In order to understand better the contribution of alcohol to immune dysfunction following HIV infection, we assessed the presence of specific markers on thymus and spleen cells in C57B1/6 mice infected with LP-BM5 murine leukemia virus and fed ethanol-containing diets. In the first experiments, mice were fed diets containing 0, 4.5, 5.5, and 6% (v/v) ethanol for 14 weeks. High ethanol exposure (6%) resulted in severe dehydration and death after 7 weeks. Although moderately low intakes of ethanol did not significantly modify percentages of T and B cells, they increased the absolute number of mature T, B, and CD4+ cells and decreased percentages of Thy 1.2+ cells. In the second experiment, mice were infected with LP-BM5 murine leukemia retrovirus and fed diets containing 5% ethanol in a regimen of 5 days of ethanol diet and 2 days of diet without alcohol for 12 weeks. Ethanol exposure in the retrovirally infected mice showed a marked decrease in Thy 1.2+ (P < 0.05). Moderate decreases in percentages of CD4+, CD8+, CD5+ cells and an increase in Ia+ cells were also observed in the retrovirus/infected ethanol-treated mice. Moderate ethanol consumption during retroviral infection induced mild/moderate changes on lymphoid cells. Ethanol consumption may accelerate the progression of murine AIDS through such changes in the lymphoid cells of the spleen.
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PMID:Modification of lymphoid subsets by chronic ethanol consumption in C57Bl/6 mice infected with LP-BM5 murine leukemia virus. 135 81

Of 6,099 children treated for malignancy, 16 (ages 3.5 to 18 years) developed acute appendicitis between 1962 and 1989. Fourteen had leukemia (ALL 10, AML 4). One each had rhabdomyosarcoma and Ewing's sarcoma. Active malignancy at diagnosis was noted in 10, 4 of whom had severe neutropenia (absolute neutrophil count less than 500/mm3). Of all the leukemics (2,794/6,099), abdominal pain during induction was a frequent complaint. The incidence of appendicitis, however, was low (0.5%). Nine of the 16 patients presented classically, facilitating prompt diagnosis and treatment. Six diagnoses were delayed. Three of these patients presented atypically with vague, nonlocalized pain, abdominal distention, lack of abdominal guarding, fever, dehydration, diarrhea, and unusual symptoms such as upper gastrointestinal bleeding. In each of these 6 patients the appendix was ruptured. Delays led to complications and deaths. Three patients required perioperative transfusions to treat excessive bleeding and two patients with ruptured appendicitis developed wound abscesses. Two patients died; in one, ruptured appendix was diagnosed only at autopsy. The other patient died of uncontrolled sepsis. Typhlitis occurring during induction chemotherapy may present similarly and is the main differential diagnosis. Typhlitis will usually improve with medical treatment alone. Nausea and vomiting (13/16), right lower quadrant pain (13/16), guarding (14/16), tachycardia (12/16), fever (10/16), and rebound tenderness (10/16) were the most frequent signs and symptoms of appendicitis. Persistent localized abdominal pain and guarding, lack of improvement with medical treatment, clinical deterioration, and the development of a mass were our indications for laparotomy. Despite major improvements in therapy, there is still a 37.5% error rate in our ability to accurately diagnose appendicitis in pediatric cancer patients.
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PMID:Acute appendicitis in children with leukemia and other malignancies: still a diagnostic dilemma. 152 62

Patients suffering from malignant disease will probably develop some metabolic abnormality of electrolytes. Hypernatremia is defined as an elevation of serum natrium over 150 mEq/l and caused by decrease of water intake, low level of ADH secretion and impaired response of kidney to ADH. Hyponatremia below 135 mEq/l of serum natrium is caused by SI-DAH, sick cell syndrome and increased loss of natrium from the kidney. On the other hand, hyperkalemia is defined as an elevation of serum kalium over 5.0 mEq/l and caused by acute tumor cell lysis syndrome, adrenal and renal insufficiency. Hypokalemia is caused by kalium loss from kidney and hypersecretion of mineral corticoid. Hypercalcemia is found in the high frequency among patients with malignant disease. Hypercalcemia is defined as an elevation of serum calcium over 11.0 mg/dl, although the most important aspect is the level of ionized calcium. The excess calcium causes defective urinary concentration with polydipsia, nausea and vomiting leading to volume depletion. At serum calcium levels about 13.8 mg/dl, there may be rapid deterioration or renal function, dehydration, coma and cardiac arrhythmias. Hypercalcemia is rarely the first manifestation of cancer. There are three principle pathogenic causes of malignant hypercalcemia, 1) hypercalcemia is a feature of several hematological cancers, including Burkitt's lymphoma, T cell leukemia, but most commonly with myeloma. The hypercalcemia in these myeloma patients is due to the secretion of an osteoclast activator, a lymphokine by the myeloma cells. 2) all patients with bony metastases have biochemical evidence of increased bone resorption. However, not all patients with bony metastases develop hypercalcemia. Probably the hypercalcemia is due partially to increased renal tubular reabsorption of calcium, mediated by a humoral factor, with activity similar to that of parathormone. 3) hypercalcemia in the patients without bony metastases is due to increased bone resorption caused by the ectopic secretion by the tumor. Mildly symptomatic patients will benefit from modest salt loading. They are dehydrated and replacement of the extracellular fluid is the first line of treatment. This may require 4-10 l normal saline/24 h. In addition, frusemide will increase calcium excretion. Calcitonin may be given subcutaneously or intravenously to refuse the mobilisation of calcium from bone. Glucocorticoids are unhelpful, but will prolong the effect of calcitonin. A diphosphonate is also useful.
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PMID:[Palliative therapy in cancer. 4. Palliation of the symptoms from a malignant tumor. (2)]. 169 56

Cancrum oris is predominantly seen in children in underdeveloped countries where widespread malnutrition, dehydration and epidemic infections are present. In the western world, it is sometimes found in immunosuppressed adults with predisposing conditions such as leukaemia and infection associated with malnutrition. Early diagnosis and an intensive therapeutic approach are the key to a favourable prognosis of noma-like necro-ulcerative lesions. The prognosis is significantly improved if the predisposing condition can be removed. Two cases are presented and the treatment is discussed.
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PMID:Cancrum oris-like lesions. 162 72

Preexistent feline leukemia virus (FeLV) infection greatly potentiated the severity of the transient primary and chronic secondary stages of feline immunodeficiency virus (FIV) infection. Of 10 FeLV-FIV carrier cats, 5 died of experimentally induced FIV infection, compared with 2 deaths in 10 cats infected only with FeLV and 1 death in 7 cats infected only with FIV. FIV-infected cats with preexistent FeLV infections developed severe depression, anorexia, fever, diarrhea, dehydration, weight loss, and leukopenia 4 to 6 weeks after infection and were moribund within 2 weeks of the onset of signs, whereas cats infected only with FIV developed much milder self-limiting gross and hematologic abnormalities. Pathologic findings in dually infected cats that died were similar to those observed previously in cats dying from uncomplicated primary FIV infection but were much more widespread and severe. Coinfection of asymptomatic FeLV carrier cats with FIV did not increase the levels of FeLV p27 antigen present in their blood over that seen in cats infected with FeLV alone. The amount of proviral FIV DNA was much higher, however, in dually infected cats than in cats infected only with FIV; there was a greater expression of FIV DNA in lymphoid tissues, where the genome was normally detected, and in nonlymphoid tissues, where FIV DNA was not usually found. Dually infedted cats that recovered from the primary stage of FIV infection remained more leukopenic than cats infected with FIV or FeLV alone, and their CD4+/CD8+ T-lymphocyte ratios were inverted. One of these cats developed what was considered to be an opportunistic infection. It was concluded, therefore, that a preexistent FeLV infection in some way enhanced the expression and spread of FIV in the body and increased the severity of both the resulting transient primary and chronic secondary stages of FIV infection. This study also demonstrated the usefulness of the FIV model in studying the role of incidental infectious diseases as cofactors for immunodeficiency-causing lentiviruses.
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PMID:Feline leukemia virus infection as a potentiating cofactor for the primary and secondary stages of experimentally induced feline immunodeficiency virus infection. 215 26

Reformatski condensation of benzyl 2-bromopropionate with 4-carbomethoxybenzaldehyde, followed by dehydration afforded benzyl 2-methyl-p-carbomethoxycinnamate (4a). Hydrogenation over a Pd catalyst gave the hydrocinnamic acid 5a. Conversion to the chloromethyl (6a) and azidomethyl ketone (7a) was followed by hydrogenation to the aminomethyl ketone (8a). Direct N-alkylation by 2,4-diamino-5-nitro-6-chloropyrimidine followed by reductive ring closure in Zn-HOAc and subsequent saponification of the benzoate ester yielded 4-amino-4-deoxy-9-methyl-10-deazapteroic acid (11a). Coupling with diethyl L-glutamate and saponification afforded 9-methyl-10-deazaminopterin (13a). The 9-ethyl analogue (13b) was similarly prepared from benzyl 2-bromobutyrate. The 9-methyl analogue (13a) was 21 times more potent than MTX as an inhibitor of cell growth in L1210 cells. The reason for this enhanced cytotoxicity in L1210 is unclear, since enzyme inhibition and transport parameters were similar to those of MTX. In human Manca leukemia cells growth inhibition was not dramatic and paralleled MTX.
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PMID:Synthesis and antifolate properties of 9-alkyl-10-deazaminopterins. 229 20

Mice ingesting 30 to 50% D2O (heavy water, deuterium oxide) developed a dose-dependent depression of formed peripheral blood elements in 4 to 9 days. The principal mechanism of anemia and thrombocytopenia is impaired hematopoiesis. Despite pancytopenia in the peripheral blood, bone marrow cellularity and morphology remained normal. Upon replacement of D2O with tap water, platelet and neutrophil concentrations returned to normal within 48 to 72 hr. In contrast, blood lymphocyte concentrations remained low for several weeks. B-lymphocytes may be more affected by deuteration than other lymphocyte subsets. In vivo reticuloendothelial cell function, as assessed by 51Cr-labeled sheep erythrocyte clearance, was unaffected by D2O. Although a dose-dependent decrease in fluid intake occurred during deuteration, hematocytopenia was not a consequence of dehydration. In view of the known kinetics of D2O in biological systems, the rapid response of myeloid elements to deuteration must be due primarily to the solvent (nonmetabolic) isotope effect. Prolonged deuteration has proven toxic when included in regimens for treatment of neoplasia, including leukemia, in animal models. The present study shows that modulation of hematopoiesis by D2O is possible without invoking the toxicities associated with prolonged deuteration.
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PMID:Effects of deuteration on hematopoiesis in the mouse. 283 49

Persistent neutropenia (0-0.6 X 10(9) neutrophils/l) was documented during a 10-month period in a 4-year-old spayed female domestic shorthair cat that was presented for anorexia and depression. Salient abnormalities detected on physical examination were fever (40.3 degrees C), dehydration, and gingivitis. The cat was neutropenic (0.5 X 10(9) neutrophils/l) and enzyme-linked immunosorbent assay (ELISA) test for feline leukemia virus was negative. A bone marrow aspirate showed decreased numbers of mature granulocytic cells. In vitro bone marrow cultures for colony-forming units-granulocyte/macrophage (CFU-GM) were performed comparing bone marrow from the patient with that of a normal cat. The patient had fewer CFU-GM than the control. The number of CFU-GM increased when bone marrow mononuclear cells were cultured in the presence of 10(-5) and 10(-6) mol/l of hydrocortisone, but the cat did not respond to oral prednisolone therapy. The pathogenesis of the neutropenia in this cat remains obscure, but resembles the chronic idiopathic neutropenia syndrome of man.
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PMID:Chronic idiopathic neutropenia in a cat. 322 55


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