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

Abnormally low plasma cystine levels have been found in the late asymptomatic stage of HIV infection and several other diseases associated with progressive loss of skeletal muscle mass. The phenomenon is commonly associated with a low NK cell activity, skeletal muscle wasting or muscle fatigue and increased rates of urea production. In its extreme form, the negative nitrogen balance leads to overt cachexia and is associated with severe debilitation and psychological stress. The low NK cell activity is in most cases not life-threatening but may be disasterous in HIV infection, because it may compromise the initially stable balance between immune system and virus and trigger disease progression. This review summarizes briefly (i) the role of cysteine in the physiological regulation of body cell mass and the development of skeletal muscle wasting, and (ii) the role of glutathione in the immune system.
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PMID:Role of cysteine and glutathione in signal transduction, immunopathology and cachexia. 969 16

The aim of rehabilitation is to improve exercise capacity and, thereby, the autonomy of patients with cardiac failure. For many years, these patients were considered inapt to perform physical exercise and they are in the same situation at the dawn of the year 2000 as patients with myocardial infarction forty years ago. The symptoms of cardiac failure (dyspnoea of effort and muscular fatigue) are not only the consequence of pulmonary hypertension and decreased muscular perfusion. Prolonged interruption of exercise and long stays in bed or in a chair lead to anatomical and functional amyotrophy, which, in turns, incites to further inactivity. Deconditioned respiratory muscles cannot tolerate the increased load of hyperventilation. Neurohormonal changes cause vasoconstriction which reduces muscular perfusion. Physical training can significantly improve these abnormalities, though it does not seem to have a measurable effect on cardiac function; based on segmental work which enables performance of substantial efforts with a minimum of haemodynamic changes, it provides a 20 to 30% gain in capacity, mainly increasing the duration of submaximal exercise rather than maximum performance. Muscular fatigue is the symptom which is the most improved. Unfortunately the organisation, which is more difficult than in the post-infarction period, and the generalisation of the practice of long-term, well adapted physical training remains marginal although hundreds of thousands of patients could benefit; more than the inertia of the official instances concerning anything related to cardiac rehabilitation, it is the lack of interest shown by cardiologists and the absence of flexible structures within the health care organisation for elderly people which are responsible.
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PMID:[Rehabilitation by physical exercise in chronic heart failure]. 986 10

The purpose of this study was to determine whether spinal muscular atrophy affects masticatory muscle strength and mandibular range of motion. A sample of 15 subjects with spinal muscular atrophy was compared to a sample of age-matched and sex-matched controls. Maximum bite force, masticatory muscle electromyography activity, mandibular ranges of motion and masticatory muscle endurance were evaluated. Results showed that maximum bite forces were one-half as great for the sample with spinal muscular atrophy than for the controls, even though their EMG activity was not significantly different. Slopes of the relationship between electromyography activity and bite force were two to four times steeper for patients with spinal muscular atrophy than controls. Maximum opening and protrusion were reduced to approximately one-half control values. Fatigue times of patients with spinal muscular atrophy were reduced by 30% (17.9 seconds versus 11.1 seconds). We conclude that the masticatory muscles of patients with spinal muscular atrophy are weakened, that their muscles are less efficient, and that they fatigue more quickly than controls. In addition, mandibular movements of these patients take place over a more limited range than unaffected controls.
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PMID:Masticatory muscle function in patients with spinal muscular atrophy. 1035 53

Recently, a congenital myasthenic syndrome (CMS) with end-plate acetylcholine receptor (AChR) deficiency due to missense mutations in the genes for the AChR subunit was described. The first observed patient with this CMS was heteroallelic for the two epsilon-AChR subunit mutations epsilon1101insT and epsilon1293insG. This patient had only a moderate phenotype with mild muscle weakness and abnormal fatigue. We have now found homozygosity for the epsilon1293insG mutation in a severely affected CMS patient, who lost the ability to walk in midchildhood and shows profound weakness and muscle wasting. Our observation allows a genotype-phenotype correlation illustrating how differences in the AChR mutation haplotype can profoundly influence disease severity.
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PMID:Severe congenital myasthenic syndrome due to homozygosity of the 1293insG epsilon-acetylcholine receptor subunit mutation. 1097 46

The diagnosis of cancer has traditionally been associated with malnutrition and wasting. Oncology patients are at risk for nutrition-related problems because of the cancer itself, as well as the treatment prescribed. Clinical manifestations of cachexia include anorexia, weight loss, muscle wasting, and fatigue, resulting in poor performance status. Control of symptoms, such as anorexia, nausea and vomiting, and mucositis is imperative in the management of cancer cachexia. Current pharmacologic therapies, as well as complementary and alternative methods, are presented. The nurse plays a key role in ensuring that the nutritional needs of oncology patients are met.
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PMID:Management of cancer cachexia. 1128 21

Patients treated with nucleoside analogue reverse transcriptase inhibitors (NRTIs) develop a varying degree of myopathy or neuropathy after long-term therapy. Zidovudine (AZT) causes myopathy; zalcitabine (ddC), didanosine (ddl) and lamuvidine (3TC) cause neuropathy; stavudine (d4T) and fialuridine (FIAU) cause neuropathy or myopathy and lactic acidosis. The tissue distribution of phosphorylases responsible for phosphorylation of NRTIs relates to their selective tissue toxicity. The myopathy is characterized by muscle wasting, myalgia, fatigue, weakness and elevation of CK. The neuropathy is painful, sensory and axonal. In vitro, NRTIs inhibit the gamma-DNA polymerase, responsible for replication of mtDNA, and cause mtDNA dysfunction. In vivo, patients treated with AZT, the best studied NRTI, develop a mitochondrial myopathy with mtDNA depletion, deficiency of COX (complex IV), intracellular fat accumulation, high lactate production and marked phosphocreatine depletion, as determined with in vivo MRS spectroscopy, due to impaired oxidative phosphorylation. Animals or cultured cells treated with NRTIs develop neuropathy, myopathy, or cell destruction with similar changes in the mitochondria. There is evidence that the NRTI-related neuropathy is also due to mitochondrial toxicity. The NRTIs (AZT, ddC, ddl, d4T, 3TC) contain azido groups that compete with natural thymidine triphosphate as substrates of DNA pol-gamma and terminate mtDNA synthesis. In contrast, FIAU that contains 3'-OH groups serves as an alternate substrate for thymidine triphosphate with DNA pol-gamma and is incorporated into the DNA causing permanent mtDNA dysfunction. The NRTI-induced mitochondrial dysfunction has an influence on the clinical application of these agents, especially at high doses and when combined. They have produced in humans a new category of acquired mitochondrial toxins that cause clinical manifestations resembling the genetic mitochondrial disorders.
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PMID:Peripheral neuropathy and antiretroviral drugs. 1129 2

There are two different clinical scenarios in which a decision on hormonal therapy either initially after diagnosis of deferred until the occurrence of signs and symptoms for presently asymptomatic prostate cancer is needed: A more recently described cohort of men with prostate cancer who underwent definitive therapy for putatively curable disease experiencing a rising PSA (biochemical relapse / progression), and a more classical group of men with prostate cancer who were unwilling or unfit to undergo local therapy with curative intent. Long-term hormonal treatment will expose patients to the risk of substantial adverse side effects such as muscle wasting, chronic fatigue, osteoporosis and others, in addition to an overall increase in treatment costs. On the other hand, a potential prolongation of survival and a delay in the development of clinical symptoms may serve as arguments for early treatment. A number of studies have been conducted in which early hormonal treatment delays the time to progression and reduces the cancer-related complication rate such as urinary obstruction and bone fractures. However, results on overall survival remain inconclusive and quality-of-life issues will become more and more important in light of the extended life span of patients with asymptomatic prostate cancer in recent years. Ongoing clinical trials such as EORTC 30991 are needed to provide further information on this important issue.
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PMID:Early versus deferred hormonal treatment for asymptomatic prostate cancer. 1145 13

We compared two different populations living in central Tibet with the purpose of establishing standard values for different anthropometric parameters in a rural population. Later on, these values were used as references for a similar study on a KBD population. One group (KBD) (n=1,246) came from the endemic areas, and the other group, serving as the control population (n=815), came from non-endemic areas. Both groups included children and adults and were of the Mongoloid type; they were farmers or semi-nomads. Height, weight, segment length, joint perimeter, joint diameter, joint movement were recorded. Also more subjective information such as general feeling of tiredness, rapid fatigue at work, work limitation, joint pain, muscle weakness, muscular atrophy, dwarfism, flatfoot, and waddling gate was also collected. Those variables were compared between the two groups.
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PMID:Anthropometry and clinical features of Kashin-Beck disease in central Tibet. 1148 26

Fatigue is the most frequently reported symptom by cancer patients. Many of these patients perceive fatigue as the most distressing symptom associated with their illness because it imposes limitations on their physical activity level. Skeletal muscle wasting, which occurs as part of cancer cachexia, is one of the mechanisms that contribute to fatigue. Cancer-induced skeletal muscle wasting may occur despite normal food intake and is not prevented by nutritional supplementation. Evidence suggests that endurance exercise ameliorates cancer-related fatigue. There is no compelling evidence to support that exercise-induced reduction in fatigue is related to preservation of muscle mass. Resistance exercise attenuates muscle wasting associated with a variety of catabolic conditions. However, its effects on cancer-induced muscle wasting have not been adequately studied. This article describes the physiological mechanisms implicated in the induction of cancer-related muscle wasting, summarizes findings from endurance and resistance exercise studies in relation to fatigue and muscle wasting during cancer and selected clinical conditions, and proposes directions for future research.
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PMID:Cancer-induced fatigue and skeletal muscle wasting: the role of exercise. 1154 40

In planning the optimum treatment for patients with neuromuscular diseases (NMD), it is essential to know as much as possible about their functional state. Assessment of the strength of certain muscles is the most direct measure of motor deficiency. In the development of normative data needed for patients with NMD, the use of torque measurements is required. Forty-nine patients (31 men and 18 women),f rom 18 to 54 years (mean age 33 +/- 8.9 years), were included in the study. Five groups of patients, each having one of five different NMDs, were formed. We tested unilaterally the biceps brachii muscle that normally generates the highest torque. For this purpose an eletronic brace enabling isometric measurements of torque during elbow flexion was designed. The patients produced three maximum voluntary elbow flexions that lasted about 3 s and separated by a pause of about 3 s. Force development was rapid with continuous build-up and isometric. About 15 s later the patients produced the last maximum voluntary elbow flexion, keeping it as stable aspossible for a period of 30 s. Patients with mitochondrial myopathy (MM), having the shortest mean half fatigue time (4.3 s), elicited the highest mean torque in both short maximum voluntary elbow flexions (1.34 Nm) as well as in the 30 s-long maximum voluntary elbow flexions. In contrast, patients with facioscapulohumeral muscular dystrophy (MD-FSH), having the longest mean half-fatigue time (15.4 s), elicited the lowest mean torque in both the short maximum voluntary (0.29 Nm) as well as in 30 s-long maximum voluntary elbow flexions. Patients with Becker muscular dystrophy (MD-B), having a mean half-fatigue time (11.1 s) slightly shorter than the patients with MD-FSH, elicited a higher mean torque in both the short (0.82 Nm) and the 30 s-long elbow flexions. Finally, patients with limb-girdle muscular dystrophy (MD-RM) and spinal muscular atrophy type 3 (SMA3), having a similar mean half-fatigue time (6.9 s for patients with MD-RM and 7.4 s for patients with SMA3), also elicited similar torque in both short (0.45 Nm for patients with MD-RM and 0.65 Nm for patient with SMA3) and 30 s-long elbow flexions. The results of the study show that the methodology developed to quantitative measure the torque of elbow flexions in patients with NMD enables the characteristics and natural course of NMD to be more objectively documented. Accordingly, the optimum treatmentforpatients with NMD could be restored.
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PMID:Evaluation of the strength of elbow flexors in patients with neuromuscular diseases. 1178 Jul 64


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