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

Juzen-taiho-to (TJ-48) is prepared by extracting a mixture of ten kinds of medicinal plants. This prescription has long been used traditionally against anemia, anorexia, extreme exhaustion and fatigue. TJ-48 may now provide new advantages with little toxicity in combination with chemotherapy or radiation therapy, and promising results have actually been obtained in terms of preventing leukemia in cancer patients who have taken antitumor agents. The combination of TJ-48 and mitomycin C (MMC) produced significantly longer survival in p-388 tumor-bearing mice than MMC alone, and TJ-48 decreased the diverse effects of MMC such as leukopenia, thrombopenia and weight loss. However, mechanisms of the pharmacological action are still unclear. One of the possible mechanisms of the action of TJ-48 may be some effects on immune responses. Therefore we studied the effects of TJ-48 on immune response in mice and characterization of immunologically active substances. TJ-48 augmented antibody production and activated macrophage by oral administration of TJ-48, but reduced the MMC-induced immunosuppression in mice. TJ-48 showed a mitogenic activity in splenocytes but not in thymocytes, and an anti-complementary activity was also observed. Anti-complementary activity and mitogenic activity were both observed in high-molecular polysaccharide fraction but not in low-molecular weight fraction. Of several polysaccharide fractions in TJ-48, only pectic polysaccharide fraction (F-5-2) showed potent mitogenic activity. F-5-2 was also shown to have the highest anti-complementary activity. However, the polygalacturonan region is essential for the expression of the mitogenic activity, but that the contribution of poly-galacturonan region to the anti-complementary activity is less. F-5-2 activates complement via alternative complement pathway and induces the proliferation of B cells but does not differentiate those cells from antibody producing cells.
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PMID:[Chemical characterization and biological activity of the immunologically active substances in Juzen-taiho-to (Japanese kampo prescription)]. 278 80

To determine the effects of a variety of doses of cocaine on endurance capacity, rats were injected intraperitoneally with either 0.1, 0.5, 2.5, 12.5, or 20 mg/kg body wt 20 min before running to exhaustion at 26 m/min up a 10% grade. Animals given saline ran 116 +/- 9 (SE) min. At doses of 12.5 and 20 mg/kg, cocaine reduced endurance time significantly (34 and 74%, respectively). At rest the drug had no effect on liver or fast-twitch muscle glycogen but significantly reduced (20-40%) soleus glycogen at the two highest doses. However, at exhaustion, the quantity of glycogen depleted in the fast-twitch red and white vastus muscles was similar in all groups despite the reduced run times of the animals receiving a higher dose implying a greater rate of glycogenolysis due to cocaine. Blood lactate in the 20 mg/kg group (9.9 +/- 1.2 mM) at exhaustion was nearly twice that of the saline controls at exhaustion (5.1 +/- 0.6). Before exercise plasma norepinephrine (at doses of 2.5, 12.5 and 20 mg/kg) was higher than saline controls and remained higher (20 mg/kg groups) at exhaustion. We conclude that high doses of cocaine cause rapid muscle glycogen depletion and early fatigue. The mechanism by which cocaine causes these effects is not clear.
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PMID:Effect of various doses of cocaine on endurance capacity in rats. 291 43

The purpose of this study was to test the hypothesis that efferent sympathetic neural discharge is coupled with the development of muscle fatigue during voluntary exercise in humans. In 12 healthy subjects (aged 20-34 yr) we measured heart rate (HR), arterial blood pressure (AP), and noncontracting, skeletal muscle sympathetic nerve activity (MSNA) in the leg (peroneal nerve) before (control) and during each of three trials of submaximal (30% of maximum) isometric handgrip exercise performed to exhaustion. In six of the subjects of eletromyographic (EMG) activity of the exercising forearm was also measured. HR and AP increased significantly (P less than 0.05) in the 1st min of exercise in all trials. In contrast, neither MSNA nor EMG activity increased significantly above control during the 1st min of exercise, but both parameters subsequently increased in a progressive and parallel manner (P less than 0.05). The overall correlation coefficient between MSNA and EMG activity (144 observations) was 0.85 (P less than 0.001). With successive trials the magnitudes of the increases in HR, AP, MSNA, and EMG activity were greater at any absolute point in time during exercise. These results indicate that sympathetic activation to noncontracting skeletal muscle is directly related to the development of muscle fatigue (as assessed by the change in EMG) during prolonged isometric exercise in humans. Furthermore, our findings demonstrate that previous fatiguing contractions alter the time course of the sympathetic neural adjustments to exercise.
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PMID:Sympathetic activation is associated with increases in EMG during fatiguing exercise. 291 61

The effect of fatigue (running to exhaustion) on the Vmax activity of the key glycolytic enzymes measured at saturating substrate concentrations in muscles, liver and brain of sedentary and trained (running on a treadmill one h/day at 20 m/min, five days/week for six months) female Zucker fatty rats and their lean littermates was investigated. In the sedentary rats, fatigue increased the activity of phosphofructokinase (PFK) in the red vastus muscle by 82% in lean, and 120% in obese rats. In the trained rats, fatigue increased PFK activity by 28% in the white vastus muscle of lean rats. In the lean animals, hexokinase (HK) activity was decreased by 26% in the red vastus of sedentary rats, and by 29% in the white vastus of trained rats upon fatiguing. Pyruvate kinase (PK) activity was also decreased by 29% in the white vastus of fatigued lean animals. Training by itself had no effect on the activity of glycolytic enzymes, except PK activity which was increased by 27% in the cortex of the lean animals. It is concluded that in the Zucker rat, these glycolytic enzymes may play a differential role in regulating glycolysis during exercise and fatigue; the extent of their involvement differs depending upon the type of tissue studied and exercise. In view of the reported short half-life (7-17 h) of PFK and its covalent modification, it is suggested that the total content and/or phosphorylation status of the enzyme may be affected in animals subjected to long-term fatigue.
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PMID:Effect of exercise on glycolytic enzymes of Zucker fatty rats. 297 74

The purpose of this study was to examine the Ca2+-Mg2+ myofibrillar ATPase and protein composition of cardiac and skeletal muscle following strenuous activity to voluntary exhaustion. Sprague-Dawley rats (200 g) were assigned to a control and exercised group, with the run group completing 25 m.min-1 and 8% grade for 1 hour. Following activity, the myocardial Ca2+-Mg2+ myofibrillar ATPase activity -pCa relationship had undergone a rightward shift in the curve. Electrophoretic analysis revealed a change in the pattern of cardiac myofibrillar protein bands, particularly in the 38-42 Kdalton region. Enzymatic analysis of myofibrillar proteins from plantaris muscle, revealed no change in Ca2+ regulation following exercise. Electronmicrographic and electrophoretic analysis revealed extensively disrupted sarcomeric structure and a change in the ratio of several plantaris myofibrillar proteins. No difference was observed for myosin: Actin: tropomyosin ratios; however a dramatic reduction in 58 and 95 Kdalton proteins were evident. The results indicate that prolonged running is associated with similar responses in cardiac and skeletal muscle myofibrillar protein compositions. The abnormalities in myofibrillar ultrastructure may implicate force transmission failure as a factor in exercised-induced muscle damage and/or fatigue.
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PMID:Influence of exercise on cardiac and skeletal muscle myofibrillar proteins. 297 50

Ten patients with adrenal cortical carcinoma were treated from 1966 to 1986. There were 7 males and 3 females. The typical clinical manifestations, marked increase of 17-ketosteroid, 17-hydroxycorticoids and DHA, and negative dexamethasone suppression test were essential for the diagnosis. Of the ten patients, eight had secretive function and their 17-ketosteroid and 17-hydroxycorticoids varied from 36.8-93 mg% and 32.5-150 mg%, respectively. DHA was measured in 5 cases with the result of 6.95-44mg%. Those without secretive functions or obvious endocrine disturbances were usually misdiagnosed as kidney tumor, splenomagaly, liver tumor or pancreatic mass. Wood had summarized that nonsecretive ACC patients commonly had fever, pain, exhaustion syndrome (emaciation, fatigue, perspiration, anorexia), mass and distant metastasis. Adrenal scan, IVU, abdominal aortic arteriography, retroperitoneal pneumography and CT were helpful in localization. The differential diagnosis between ACC and adenoma by pathology was difficult. It is generally agreed that if the mass is larger than 100 grams, capsulated, having blood or lymphatic vessel invasion, hemorrhage, necrosis and calcification or even distant metastasis, malignant tumor should be considered. Surgical removal of the tumor is the only effective treatment. For advanced or recurrent lesions, selective adrenal artery thrombosis could be used. One of the ten patients was thus treated by this facilitated subsequent surgery. Postoperative chemotherapy, such as O.P-DDD, might be used in some cases.
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PMID:[Adrenal cortical carcinoma (ACC)--report of 10 cases]. 297 73

Focal electrodes were used to record the spontaneous miniature potentials generated on delimited patches of innervated membrane in the Torpedo electric organ. The main population of miniature potentials followed a bell-shaped amplitude distribution. In addition, we observed a second class of spontaneous events that were smaller and whose amplitude distribution was skewed. These subminiatures formed an homogenous population together with the regular miniatures with respect to their time course versus amplitude relationship. They were thus probably generated at the same sites. The proportion of potentials that were subminiature was less than 10% in resting, freshly excised tissue, but it increased markedly: (i) when the tissue was kept for 24-28 h in vitro after excision; (ii) in the period following a brief heat challenger or (iii) stimulation to exhaustion; and (iv) in the presence of dinitrophenol or dinitrofluorobenzene. In all these conditions, we measured the acetylcholine, adenosine 5'-triphosphate and creatine phosphate content of the tissue and found a correlation between the relative number of subminiature potentials and the lack of energy rich molecules. It is concluded that subminiature potentials are present in the electric organ as in neuromuscular junctions. They are probably produced at the same sites as the regular miniature potentials and their relative occurrence seems to increase greatly when the nerve terminals are in a state of energy deficiency.
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PMID:Spontaneous quantal and subquantal transmitter release at the Torpedo nerve-electroplaque junction. 303 36

Clinical and biochemical findings in skeletal muscle in 11 patients with chronic fatigue myalgia syndromes of unknown aetiology are reported. All patients had severe asthenia for from one to 10 years with greatly limited exercise capacity and protracted exhaustion after minor exercise. Diffuse myalgia was prominent and was exacerbated for hours to days after exercise. Assay of skeletal muscle carnitine, phosphorylase, all glycolytic enzymes and the mitochondrial marker enzymes monoamine oxidase, isocitrate dehydrogenase and cytochrome oxidase were normal. These findings lend no support to the presence of a major defect in muscle intermediary energy pathways in this syndrome.
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PMID:Chronic fatigue and myalgia syndrome: mitochondrial and glycolytic studies in skeletal muscle. 303 60

Myalgic Encephalomyelitis or post-viral fatigue syndrome is a common disorder, which has been known previously under a variety of different names, i.e., Iceland disease or Royal Free disease. It may occur in epidemics or sporadically. The cause is unknown, with patients complaining of exhaustion, fatigue, muscle aches and pains, and invariable psychiatric symptoms such as emotional lability, poor memory/concentration, and depression. Present-day research points to the cause as a metabolic disorder secondary to persistent viral infection.
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PMID:Postviral fatigue syndrome. 306 94

To examine fatigue mechanisms in an unselected series of patients with excess fatigue ("effort syndromes") their muscle function was compared with that of normal subjects. Voluntary performance was assessed with a cycle ergometer to exhaustion and by maximal isometric contractions of the quadriceps femoris. The mean maximal heart rate in patients during ergometry was 89% of the predicted rate, and quadriceps strength was either normal or was inappropriate for the available muscle, which suggested submaximal effort. Contractile performance was examined in the absence of volition with stimulated contractions of the adductor pollicis. During stimulated fatiguing activity patients were neither weaker nor more fatigable than controls; thus the excess fatigue experienced by the patients was not due to a defect of the contractile apparatus. The increased perception of effort must therefore be due to impairment of central rather than peripheral mechanisms. The optimal approach to treatment of effort syndromes combines physical and psychological techniques.
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PMID:Normal muscle strength and fatigability in patients with effort syndromes. 314 92


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