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Página 1 a partir de 23 resultados
Do cytosine guanine dinucleotide (CpG) fragments induce vasoactive neuropeptide mediated fatigue-related autoimmune disorders?
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Autoimmune dysfunction of certain vasoactive neuropeptides (e.g., vasoactive intestinal peptide, pituitary adenylate cyclase activating polypeptide) may be implicated in a range of disorders associated with fatigue-like states (chronic fatigue syndrome, Gulf War syndrome) and even sudden infant
Recombinant human granulocyte-macrophage colony-stimulating factor and low-dose cytosine-arabinoside in the treatment of patients with myelodysplastic syndromes. A phase II study.
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As part of a multicenter trial 12 patients with myelodysplastic syndromes (MDS) were treated with 14-day-cycles of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF; 250 micrograms/m2 day s.c.). In addition, all patients received 20 mg/m2/day s.c. cytosine-arabinoside
Treatment of Philadelphia chromosome-positive chronic myelogenous leukemia with weekly polyethylene glycol formulation of interferon-alpha-2b and low-dose cytosine arabinoside.
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BACKGROUND
To evaluate the activity and toxicity of weekly Schering 54301, a polyethylene glycol formulation of interferon- alpha-2b (PEG-IFN-alpha-2b), with cytosine arabinoside (ara-C) in patients with chronic myelogenous leukemia (CML).
METHODS
Seventy-six patients with Philadelphia chromosome
Are vasoactive neuropeptide autoimmune fatigue-related disorders mediated via G protein-coupled receptors?
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Vasoactive neuropeptides such as pituitary adenylate cyclase activating polypeptide (PACAP), calcitonin gene related peptide (CGRP) and vasoactive intestinal peptide (VIP) have been implicated in a number of fatigue-related conditions. Associations of these vasoactive neuropeptides with heat shock
Epigenome-wide DNA methylation patterns associated with fatigue in primary Sjögren's syndrome.
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Chronic fatigue is a common, disabling and poorly understood phenomenon. Recent studies indicate that epigenetic mechanisms may be involved in the expression of fatigue, a prominent feature of primary SS (pSS). The aim of this study was to investigate whether DNA methylation profiles of whole blood
Chronic Fatigue Syndrome and DNA Hypomethylation of the Glucocorticoid Receptor Gene Promoter 1F Region: Associations With HPA Axis Hypofunction and Childhood Trauma.
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OBJECTIVE
Chronic fatigue syndrome (CFS) has been associated with hypothalamic-pituitary-adrenal axis hypofunction and enhanced glucocorticoid receptor (GR) sensitivity. In addition, childhood trauma is considered a major risk factor for the syndrome. This study examines DNA methylation of the GR
Cytokine gene polymorphisms and fatigue in breast cancer survivors: early findings.
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Converging evidence from basic and clinical studies suggests a role for proinflammatory cytokines in cancer-related fatigue, although the etiology of elevated inflammatory processes is unclear. We examined single nucleotide polymorphisms (SNPs) in the promoters of cytokine genes as genetic risk
Translational phase I trial of vorinostat (suberoylanilide hydroxamic acid) combined with cytarabine and etoposide in patients with relapsed, refractory, or high-risk acute myeloid leukemia.
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OBJECTIVE
To determine the maximum-tolerated dose (MTD) of the histone deacetylase inhibitor vorinostat combined with fixed doses of cytarabine (ara-C or cytosine arabinoside) and etoposide in patients with poor-risk or advanced acute leukemia, to obtain preliminary efficacy data, describe
Effect of the nucleotides CMP and UMP on exhaustion in exercise rats.
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The aetiology of muscle fatigue has yet not been clearly established. Administration of two nucleotides, cytosine monophosphate (CMP) and uridine monophosphate (UMP), has been prescribed for the treatment of neuromuscular affections in humans. Patients treated with CMP/UMP recover from altered
[Hypoplastic leukemia successfully treated with low-dose aclarubicin: a case report].
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Low-dose aclarubicin (LDACR) therapy is one of the differentiation induction therapy, such as low-dose cytosine arabinoside therapy, 1 alpha, 25 dihydroxy-vitamin D3 or retinoic acid therapy, for myelodysplastic syndrome and atypical leukemias. A 36-year-old female with hypoplastic acute myelogenous
Do vasoactive neuropeptide autoimmune disorders explain pyridostigmine's association with Gulf War syndrome?
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Gulf War syndrome (GWS) is a perplexing multi-symptom condition comprising a constellation of signs and symptoms consistently described in the literature. These include muscle fatigue and tiredness, malaise, myalgia, impaired cognition, ataxia, diarrhoea, bladder dysfunction, sweating disturbances,
[Mast cell leukemia evolved from RAEB-T (5q-syndrome) in a 12 year-old girl].
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A 12-year-old, female 5q- syndrome case of refractory anemia with excess of blasts in transformation (RAEB-T) evolving to mast cell leukemia is described. This case was admitted because of general fatigue, when her peripheral blood count revealed anemia and leukocytosis with basophil-like cells.
Success in bone marrow failure? Novel therapeutic directions based on the immune environment of myelodysplastic syndromes.
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Myelodysplastic syndromes (MDS) are clonal neoplasms of aging that are associated with BM failure, related cytopenias, fatigue, susceptibility to infections, bruising, bleeding, a shortened lifespan, and a propensity for leukemic transformation. Most frail, elderly patients are not candidates for
Hypoplastic acute leukemia.
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There have been few reports of acute leukemia presenting with a hypocellular bone marrow. All patients diagnosed as having acute leukemia were identified during a recent six-year interval who had blast cells plus promyelocytes of greater than 30% and marrow cellularity of needle biopsy less than or
A case of primary hepatic Burkitt's lymphoma.
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Burkitt's lymphoma is a rare disease that belongs to the aggressive non-Hodgkin's lymphoma. Herein, we report a case of primary hepatic Burkitt's lymphoma. A 19-year-old man visited the hospital for right upper quadrant pain. He felt fatigue for two months. Physical examination revealed hepatomegaly
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