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Query: UMLS:C0023418 (
leukemia
)
93,477
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Bovine paraplegic syndrome (BPS) is a debilitating cattle disease of unknown origin that is characterized by leukocytosis, lymphocytopenia and monocytopenia. The major clinical signs are difficulties in locomotion affecting hind limbs, hypoalgesia in the hind quarters, posterior paralysis and death within 72 to 96 hours after recumbency. To investigate the aetiological basis of BPS, we examined a possible association of the syndrome with infection by bovine immunodeficiency virus (BIV), a lentivirus implicated in immune system dysfunction and central nervous system lesions in cattle. Serum samples (n = 1,278) were collected from both healthy and BPS-prevalent cattle herds in Venezuela, and organ extracts were prepared from euthanized animals (n = 11) suspected of having BPS. Sera were analysed for reactivity to recombinant BIV and bovine
leukaemia
virus gag precursor proteins by immunoblot procedures. Serum reactivity to BIV ranged from 12 to 66% between groups of BPS prevalent herds. The percentage of samples reactive to BLV antigen was much lower (2 to 17%). Rabbits inoculated with extracts from BPS-afflicted animals exhibited an anamnestic immune response to BIV antigens as well as the presence of BIV gag antigens in their tissues. We present evidence for a possible association between BPS disease and a viral agent related to BIV. The role of BIV, in combination with
malnutrition
, in BPS is discussed.
...
PMID:Possible role of bovine immunodeficiency virus in bovine paraplegic syndrome: evidence from immunochemical, virological and seroprevalence studies. 857 5
Acquired deficiency
of antithrombin (AT), which in some patients could lead to thrombosis, has been a serious side effect of protocols which incorporate E. coli L-asparaginase (ASP) for the treatment of acute lymphoblastic
leukaemia
(ALL). In a longitudinal, prospective, non-randomized study children with ALL (n=27) were treated according to the protocol ALL-BFM-90. During the induction phase using prednisone, vincristine, daunorubicin and ASP, AT substitution was performed in 15/27 patients, when their plasma concentration decreased below 60% of normal with a concomitant increase of D-dimer formation. After the administration of the AT concentrate the patients, plasma concentration of AT increased and remained elevated after 18, 48, and 72 h. In addition, the plasma concentration of enhanced thrombin generation, D-dimer formation and plasminogen activator inhibitor 1 decreased towards normal levels. Although the observed laboratory findings may serve as evidence for a possible clinical benefit of AT substitution during ASP treatment, further randomized studies are requested to evaluate whether the use of prophylactic AT administration could reduce the incidence of thromboembolic events in childhood acute
leukaemia
.
...
PMID:Inhibition of hypercoagulation by antithrombin substitution in E. coli L-asparaginase-treated children. 859 91
Over 80% of children with cancer live in developing countries, where access to medical services is limited to varying degrees. In many of these countries, economic conditions and general health care have improved sufficiently to permit the development of more sophisticated medical services. The introduction of pediatric oncology programs becomes appropriate as deaths from
malnutrition
and infections decrease and cancer emerges as an important cause of childhood mortality. In the absence of such services, the worldwide war against pediatric cancer will ultimately be lost because of the rapidly growing pediatric populations in developing countries that now lack the facilities and expertise to treat childhood malignancies. We believe that the development of pediatric cancer centers in many of these countries is both appropriate and feasible. Partnerships in which established pediatric oncology centers work with the governments and private sectors of developing nations to implement key facilities are an efficient and cost-effective way to introduce such services. The challenges of these outreach efforts are significant -- as are the expected benefits.
Leukemia
1996 Mar
PMID:St Jude Children's Research Hospital's International Outreach Program. 864 77
Deficiency
in p53-mediated cell death is common in human cancer, contributing to both tumorigenesis and chemoresistance. In an attempt to restore p53, we evaluated in vitro infectivity and cytotoxicity of a wild type (w.t.) p53-expressing adenovirus (Ad-p53) toward a panel of human cancer cell lines (n = 19). At a multiplicity of infection of 30, both Ad-p53 and adenovirus expressing beta-galactosidase (Ad-LacZ) infected greater than 99% of cells derived from brain, lung, breast, ovarian, colon, and prostate cancer, but failed to infect
leukemia
or lymphoma cells. Ad-p53, but not Ad-LacZ, infection of cancer cells was followed by nuclear accumulation of the CDK inhibitor p21WAFI/CIPI, cell cycle arrest and loss of viability. Ad-p53 induced apoptotic death in cancer cells that express mutant p53, including multi-drug resistant cells, but fewer deaths were observed in some w.t. p53 expressing cells. Ad-p53-infected SKBr3 breast cancer cells were more sensitive to cytotoxicity of the DNA damaging drugs mitomycin C or Adriamycin, but not the M-phase specific drug vincristine. Our results suggest that Ad-p53 is capable of infecting and killing cancer cells of diverse tissue origins (including multi-drug resistant cancer cells), that p21WAFI/CIPI may be a useful marker of p53 infectivity and that there may be synergy between Ad-p53 and either mitomycin C or Adriamycin induced cell death in tumors with p53 mutations.
...
PMID:In vitro evaluation of a p53-expressing adenovirus as an anti-cancer drug. 870 13
An acute transient swelling of the parotid glands is recorded after general anaesthesia in orthopaedic surgery. The first differential diagnosis is bacterial parotitis; other causes of gland enlargement are viral infections, lymphoma,
leukemia
, sarcoidosis, Sjogren's syndrome,
malnutrition
cirrhosis, vomiting, and poor oral hygiene. Excluding the above mentioned conditions, the most probably factors involved in our case are drugs used for anaesthesia, congestion of the venous drainage of the gland because of parasympathetic stimula during tracheal intubation and head positioning during surgery.
...
PMID:[Transitory swelling of a parotid gland following general anesthesia. Description of a case]. 891 36
LP-BM5 Murine
leukemia
virus (MuLV) infection of C57BL/6 mice develop a disease that has many features in common with human acquired immunodeficiency syndrome (AIDS), in particular abnormal lymphoproliferation and severe immunodeficiency. Thus, this MAIDS model may be useful for evaluation of potent antirival agents in vivo.
Deficiency
in antioxidant micronutrients such as selenium, zinc, and glutathione have been observed in AIDs and AIDS-related complex (ARC) patients. In the present study, the MAIDS model was used to evaluate immunological and oxidative effect of Se as sodium selenite. Results indicated that Se treatment 0.1 mg/kg/d (p.o.) inhibited splenomegaly and sera IgG elevation effectively. In addition to abnormal immunity, oxidative imbalance possibly existed in MAIDS model, as lipid peroxide increased significantly in spleen and whole blood glutathione peroxidase (GSH-Px) activity decreased markedly. Se supplementation had good protective effect.
...
PMID:Effect of selenium supplementation on mice infected with LP-BM5 MuLV, a murine AIDS model. 952 61
Deficiency
in DNA repair capability is considered to be responsible for oncogenesis. Hereditary and sporadic cancers in various tissues have been reported to have mutations at the DNA repair genes. In this study we analysed two excision repair genes (ERCC1 and XPCC) and two mismatch repair genes (hMSH2 and hMTH1) in the leukaemic blasts of newly diagnosed paediatric patients by use of reverse transcriptase (RT)-polymerase chain reaction (PCR). Analysis of the leukaemic blasts from 15 patients demonstrated no alterations at the XPCC, hMSH2 or hMTH1 genes. Blasts from one patient with acute mixed lineage
leukaemia
revealed an abnormally migrated product of the ERCC1 gene by RT-PCR. His leukaemic blasts showed a reduced expression of ERCC1 protein by Western blotting. Since bone marrow cells at remission showed only normally migrated product, the ERCC1 gene mutation was considered to be specific for the leukaemic blasts. This is the first report describing a mutation at the ERCC1 gene in acute childhood
leukaemia
.
...
PMID:Analysis of mutations at the DNA repair genes in acute childhood leukaemia. 982 20
The results of the treatment of acute lymphoblastic leukemia (ALL) in children depend not only on the biologic diversity of the
leukemia
cell, the multi-drug treatment schedule and the individual variability of drug metabolism, but also on the socioeconomic and cultural background of the leukemic child. Social and cultural disparity is very marked in underdeveloped countries and has been increasing in industrialized nations. The prognostic influences of these factors are poorly documented and sometimes mistakenly attributed to differences in ethnic origin. We have investigated in Brazil the relative impact of
malnutrition
and socioeconomic status on the outcome of ALL, adjusting for the known influence of biologic factors. Children with ALL (n = 167) treated with a Berlin-Frankfurt-Munster-based protocol were studied prospectively. At a median follow-up of 1623 days, the estimated probability of disease-free survival was 43 +/- 4%. The main cause for interruption of remission was bone-marrow relapse. Socioeconomic indicators of poverty (poor housing conditions, low per capita income and energy consumption) were significantly associated with a greater risk of relapse in univariate analysis. They were consolidated in a single index, socioeconomic status (SES), defined by the product of monthly per capita income times mean familial daily energy consumption. Other unfavorable findings included age, z score for the height for age at diagnosis (HAZ) below-1.28 and the z score for weight for age below-1.28. After adjustment in Cox's multivariate model, only HAZ and poor SES remained as predictive factors for relapse. Poor prognosis for leukemic children of low SES is just another indicator of social inequality.
...
PMID:Low socioeconomic status is a strong independent predictor of relapse in childhood acute lymphoblastic leukemia. 987 80
Leptin, the product of the ob gene, is a pleiotropic molecule that regulates food intake as well as metabolic and endocrine functions. Leptin also plays a regulatory role in immunity, inflammation, and hematopoiesis. Alterations in immune and inflammatory responses are present in leptin- or leptin-receptor-deficient animals, as well as during starvation and
malnutrition
, two conditions characterized by low levels of circulating leptin. Both leptin and its receptor share structural and functional similarities with the interleukin-6 family of cytokines. Leptin exerts proliferative and antiapoptotic activities in a variety of cell types, including T lymphocytes,
leukemia
cells, and hematopoietic progenitors. Leptin also affects cytokine production, the activation of monocytes/macrophages, wound healing, angiogenesis, and hematopoiesis. Moreover, leptin production is acutely increased during infection and inflammation. This review focuses on the role of leptin in the modulation of the innate immune response, inflammation, and hematopoiesis.
...
PMID:Leptin in the regulation of immunity, inflammation, and hematopoiesis. 1103 63
The thiamin transporter encoded by SLC19A2 and the reduced folate carrier (RFC1) share 40% homology at the protein level, but the thiamin transporter does not mediate transport of folates. By using murine
leukemia
cell lines that express no, normal, or high levels of RFC1, we demonstrate that RFC1 does not mediate thiamin influx. However, high level RFC1 expression substantially reduced accumulation of the active thiamin coenzyme, thiamin pyrophosphate (TPP). This decreased level of TPP, synthesized intracellularly from imported thiamin, resulted from RFC1-mediated efflux of TPP. This conclusion was supported by the following observations. (i) Efflux of intracellular TPP was increased in cells with high expression of RFC1. (ii) Methotrexate inhibits TPP influx. (iii) TPP competitively inhibits methotrexate influx. (iv) Loading cells, which overexpress RFC1 to high levels of methotrexate to inhibit competitively RFC1-mediated TPP efflux, augment TPP accumulation. (v) There was an inverse correlation between thiamin accumulation and RFC1 activity in cells grown at a physiological concentration of thiamin. The modulation of thiamin accumulation by RFC1 in murine
leukemia
cells suggests that this carrier may play a role in thiamin homeostasis and could serve as a modifying factor in thiamin
nutritional deficiency
as well as when the high affinity thiamin transporter is mutated.
...
PMID:Impact of the reduced folate carrier on the accumulation of active thiamin metabolites in murine leukemia cells. 1103 62
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