Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0015672 (fatigue)
 51,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High-dose chemotherapy with autologous stem cell support (HDC-ASCS) can produce high complete remission rates in patients with metastatic breast cancer (MBC). However, the majority of those so treated will relapse within 3 years. The ability of such patients to tolerate further myelosuppressive chemotherapy may be limited and the best therapy is undefined. In this retrospective study we assessed the role of capecitabine as initial therapy after relapse. Ten patients (median age = 47 years; oestrogen receptor-positive, n = 4; visceral disease, n = 6; prior anthracycline, n = 8, prior taxanes, n = 10), whose disease progressed at a median of 246 days (range 69-480) after HDC-ASCS and who were treated with capecitabine (2500 mg/m2 per day for 2 weeks of a 3-week cycle) as initial therapy for relapse, were assessed retrospectively for response and toxicity. They received a median of eight cycles (range 4-24) of capecitabine. The toxicities encountered while receiving capecitabine were: hand-foot syndrome (grade 1, n = 3; grade 2, n = 4; grade 3, n = 1); diarrhoea (grade 1, n = 1; grade 2, n = 3); nausea (n = 2) and fatigue (n = 5). Haematological toxicity was seen in only one patient. No patient required hospitalization for toxicity. Three achieved a complete remission, four a partial remission and three disease stabilization. After a median follow-up of 183 days from commencing capecitabine (range 97-540), all patients were alive and five were in remission. Five progressed after remissions that lasted between 63 and 252 days. Oral capecitabine is an active and well-tolerated agent when used alone as first-line therapy in patients who have relapsed after HDC-ASCS for MBC.
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PMID:Use of capecitabine as first-line therapy in patients with metastatic breast cancer relapsing after high-dose chemotherapy and autologous stem cell support. 1182 80

When a mouse is put into a cylinder too narrow for it to turn (its front end being blocked with a thin plastic strip), the mouse gnaws away the plastic to escape. Hence, the weight reduction in the plastic can be used as an index of 'gnawing activity (GA).' GA was high at first, but decreased with time. Training augmented GA, but not the activity of the histamine-forming enzyme (histidine decarboxylase [HDC]: a proposed marker of muscle fatigue) in the masseter muscle. In trained mice, GA was higher at night than in the daytime, and was decreased by starvation. In mice prevented from reaching the strip, the elevation of serum cortisol was greater than that seen in mice able to gnaw at it. As such gnawing is a form of voluntary behavior, these results suggest that our experimental system may be useful for (i) the quantitative study of voluntary muscle activity associated with physical or mental fatigue or motivation, and (ii) the study of an animal's response to stress when it has, or alternatively does not have, an apparent way of escape.
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PMID:Gnawing behavior of a mouse in a narrow cylinder: a simple system for the study of muscle activity, fatigue, and stress. 1221 15

Pharmacologic effects of propolis were investigated in this article. The results suggested that propolis has pharmacologic functions in many aspects. It is a new-type medicine derived from animal in pharmacology and food both. To small mouse, propolis showed the functions of anti-fatigue and endurance to lack of oxygen. To high-blood-lipid-model mouse, it prevented increase of blood-mucus and blood lipid(TC, TG, LDL-C) (P < 0.05-0.01), but there were insignificant changes to red-blood-cell proportion (HCT) and high-density lipoprotein chelesteral (HDC-C). To small immunosuppessive-model mouse, propolis could strengthen macrophagocyte phagocytosis in the abdominal-cavity (P < 0.05), and increase the thymus-index (P < 0.05), but there were insignificant changes to the spleen-index. The LD50 > 7500 mg/kg to small mouse.
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PMID:[Study on the pharmacologic effect of propolis]. 1257 90

Histamine has been referred to as an anorexic factor that decreases appetite and fat accumulation and affects feeding behavior. Tuberomammillary histaminergic neurons have been implicated in central mediation of peripheral metabolic signals such as leptin, and centrally released histamine inhibits ob gene expression. Here we have characterized the metabolic phenotype of mice that completely lack the ability to produce histamine because of targeted disruption of the key enzyme in histamine biosynthesis (histidine decarboxylase, HDC). Histochemical analyses confirmed the lack of HDC mRNA, histamine immunoreactivity, and histaminergic innervation throughout the brain of gene knockout mouse. Aged histamine-deficient (HDC-/-) mice are characterized by visceral adiposity, increased amount of brown adipose tissue, impaired glucose tolerance, hyperinsulinemia, and hyperleptinemia. Histamine-deficient animals are not hyperphagic but gain more weight and are calorically more efficient than wild-type controls. These metabolic changes presumably are due to the impaired regulatory loop between leptin and hypothalamic histamine that results in orexigenic dominance through decreased energy expenditure, attenuated ability to induce uncoupling protein-1 mRNA in the brown adipose tissue and defect in mobilizing energy stores. Our results further support the role of histamine in regulation of energy homeostasis.
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PMID:Hyperleptinemia, visceral adiposity, and decreased glucose tolerance in mice with a targeted disruption of the histidine decarboxylase gene. 1296 41