Gene/Protein Disease Symptom Drug Enzyme Compound
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 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a retrospective study of 632 patients with pituitary disease we diagnosed pituitary insufficiency without hypersecretion of any pituitary hormone in 122 patients. Patients were substituted with sex hormones (76%), hydrocortisone (74%) and/or L-thyroxine (77%). 76% had additional growth hormone deficiency, as shown by an increase of growth hormone of less than 5 ng/ml after i.v. administration of L-arginine. In 17% of all patients the diagnosis of osteoporosis was proven or suspected radiologically. 57% had low bone mass of lumbar spine (dualphotonabsorptiometry) and 73% had low bone mass of the proximal forearm (singlephotonabsorptiometry). BMD values of pituitary insufficient patients were in the same range as those of patients with established osteoporosis. More than half of all patients (53%) complained of tiredness, exhaustion and muscle weakness. 40% suffered from adipositas. 77% had hyperlipidemia (68% hypertriglyceridemia and 42% hypercholesterinemia), 18% had hypertension. 14% of the patients had arteriosclerotic events in their history (myocardial infarction or stroke). These figures are higher than incidences shown in the German PROCAM-study. These data show an increased prevalence of osteoporosis and vascular diseases. This is in contrast to the general opinion, that patients with pituitary insufficiency are adequately treated by substitution with adrenal, thyroid and sex hormones. Whether other factors such as the additional growth hormone deficiency are responsible for these diseases has to be examined in prospective studies.
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PMID:[Increased prevalence of osteoporosis and arteriosclerosis in conventionally substituted anterior pituitary insufficiency: need for additional growth hormone substitution?]. 176 81

Understanding the reaction of bone to physical exercise is important for the development of strategies to increase and maintain bone mass. In this study the aim was to investigate the relationship among exercise intensity, physical capacity, and the biochemical responses, estimated by measuring biochemical markers of bone metabolism in serum. As a complement to the circulating concentrations we also accounted for the plasma volume shifts during and after exercise. The study included 10 men and 10 women, mean age 29 years, with a wide range of physical capacity, who performed a standardized running exercise test on a motor-driven treadmill with loads corresponding to 47 and 76% of VO2 max (maximal oxygen uptake) followed by a maximal effort until exhaustion. Total work time was about 35 minutes. Venous blood samples were drawn at rest, after each load, and after 30 minutes and 24 hours of recovery. The reductions in plasma volume during exercise were 4.3% (P < 0.05) and 15.1% (P < 0.001) whereas after 24 hours in recovery there was an expansion of 7.5% (P < 0.001). There were marked, intensity-related, increases of PICP and tALP concentrations (P < 0.001) during exercise. Since these were of the order of plasma volume reduction they did not correspond to a change in the calculated circulating amount (content). However, as the concentrations returned to basal during recovery, the total circulating amounts were increased at this point (P < 0.05). Osteocalcin was also increased during recovery (P < 0.01), although concentrations were unchanged during the entire study. The amount (P < 0.001) and concentration (P < 0. 05) of ICTP were also increased during follow-up. Serum PTH concentrations rose (P < 0.05) in proportion to the intensity of exercise and remained elevated during recovery. The subjects' VO2 max demonstrated positive relationships to the biochemical responses to exercise in bone and BMD of the legs, and a negative relationship to basal PTH levels. Bone turnover and PTH secretion was stimulated by exercise, and low basal levels of PTH and high BMD were induced by a high level of physical fitness. These observations correlate well with the favorable effects of exercise and training on bone mass.
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PMID:Bone metabolism during exercise and recovery: the influence of plasma volume and physical fitness. 926 9

Muscular dystrophies are heritable, heterogeneous neuromuscular disorders and include Duchenne and Becker muscular dystrophies (DMD and BMD, respectively). DMD patients exhibit progressive muscle weakness and atrophy followed by exhaustion of muscular regenerative capacity, fibrosis, and eventually disruption of the muscle tissue architecture. In-frame mutations in the dystrophin gene lead to expression of a partially functional protein, resulting in the milder BMD. No effective therapies are available at present. Cell-based therapies have been attempted in an effort to promote muscle regeneration, with the hope that the host cells would repopulate the muscle and improve muscle function and pathology. Injection of adult myoblasts has led to the development of new muscle fibers, but several limitations have been identified, such as poor cell survival and limited migratory ability. As an alternative to myoblasts, stem cells were considered preferable for therapeutic applications because of their capacity for self-renewal and differentiation potential. In recent years, encouraging results have been obtained with adult stem cells to treat human diseases such as leukemia, Parkinson's disease, stroke, and muscular dystrophies. Embryonic stem cells (ESCs) can be derived from mammalian embryos in the blastocyst stage, and because they can differentiate into a wide range of specialized cells, they hold potential for use in treating almost all human diseases. Several ongoing studies focus on this possibility, evaluating differentiation of specific cell lines from human ESCs (hESCs) as well as the potential tumorigenicity of hESCs. The most important limitation with using hESCs is that it requires destruction of human blastocysts or embryos. Conversely, adult stem cells have been identified in various tissues, where they serve to maintain, generate, and replace terminally differentiated cells within their specific tissue as the need arises for cell turnover or from tissue injury. Moreover, these cells can participate in regeneration of more than just their specific tissue type. Here we describe multiple types of muscle- and fetal-derived myogenic stem cells, their characterization, and their possible use in treating muscular dystrophies such as DMD and BMD. We also emphasize that the most promising possibility for the management and therapy of DMD and BMD is a combination of different approaches, such as gene and stem cell therapy.
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PMID:Stem cell therapies to treat muscular dystrophy: progress to date. 2062 90