Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Heart and other muscles of the rat contain two forms of ferritin separable in polyacrylamide gel electrophoresis. The cellular location of the fast- and slow-migrating ferritins was investigated using primary cultures of hindlimb skeletal muscle, and isolated myocardial cell populations. Muscle and non-muscle cells were isolated in good yield from hearts of adult rats pretreated with large doses of iron to increase their ferritin content. In virtually all cases, the isolated muscle cells contained traces only of the fast-migrating species and the non-muscle cells contained small amounts of the slow-migrating ferritin. During cell isolation, 90-100% of both ferritins was lost and could be recovered in the perfusates and solutions employed, while one third of the total tissue protein, and a larger percentage of creatine phosphokinase, was recovered in the isolated cells. Primary cultures of thigh muscle from adult rats which had differentiated into multi-nucleated myotubes, were incubated for 1-3 days with chelated iron. These cells contained substantial amounts of the electrophoretically fast migrating ferritin, with its characteristic larger Stokes' radius (determined by quantitative polyacrylamide gel electrophoresis). None of the slow-migrating ferritin species was detected, although hindlimb muscle from iron-treated rats contained both forms. It is concluded that the fast-migrating ferritin of muscle, which is much larger and more asymmetric than other ferritins, is confined to the muscle cell population, while the other form is predominantly or exclusively in the non-muscle cells. Both ferritins are lost preferentially over other proteins during procedures which injure muscle tissue.
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PMID:Cellular location of rat muscle ferritins and their preferential loss during cell isolation. 671 90

Within the past few years, the measurement of serum and tissue markers has had an increasing influence on clinical decisions about initial treatment and follow-up. Lung cancer illustrates the types and importance of these various markers. This review presents data concerning the most studied and interesting markers in non-small cell (NSCLC) and small cell lung cancer (SCLC). CEA, TPA, SCC-Ag, CYFRA 21-1, ferritin, CA19-9, CA50, CA242, H-K-N-ras mutations and p53 mutation seem to be the most prolific in NSCLC, while NSE, BN/GRP, CK-BB, NCAM, IL-2R, IGF-I, transferrin, ANP, mAb (cluster 5), Le-y and c-N-L-myc mutation are markers in SCLC patients. Some of these serum markers might be useful adjuncts for monitoring response to therapy, including early detection of tumour reactivation to allow curative therapy and rapid detection of treatment failure to allow change of the regimen. The study of these markers also may lead to a better understanding of the biological characteristics of lung cancer. The information derived from these biological studies represents the most promising avenue towards new treatment strategies, as well as attempts at secondary prevention.
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PMID:Clinical tumour markers in lung cancer. 753 17

A review of stage IV-S neuroblastoma is provided. The possible uses of prognostic features to guide treatment options in this group of infants with neuroblastoma are suggested. The biologic basis for the spontaneous regression of widespread tumor involvement in some infants with stage IV-S neuroblastoma is discussed. The reasons that some infants with IV-S disease progress to a fatal outcome, while most undergo maturation or involution and eventual long term cure are suggested. The influence of such factors as age at diagnosis, clinical staging, and tumor biology on eventual outcome are covered. Biological variables and markers discussed include: genetic (cytogenetics (1p deletions), nuclear genomic content), molecular biologic (N-myc oncogene amplification, mdr-1, ras, and trk, gene expression), immunological (major histocompatibility antigen density, cellular and humoral immunity), and biochemical (creatine kinase isoenzyme profile, neuron specific enolase, ferritin, chromatograffin, lactic acid dehydrogenase and catecholamine levels).
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PMID:Neuroblastoma stage IV-S. 763 37

Two enriched populations of Leydig cells (hLCI and hLCII) have been characterized in human testes; it is noteworthy, that in the presence of hCG the steroid ouput is higher in hLCII when compared to hLCI; conversely, the basal production of steroids is greater in hLCI than in hLCII. The addition of increasing amounts of seminiferous tubule-conditioned medium to the purified Leydig cells leads to a dose-related enhancement of the steroid production in both Leydig cell fractions under basal and hCG-stimulated conditions. It is therefore obvious that a paracrine factor (or factors) from seminiferous tubular origin influences positively and with a high efficiency the human Leydig cell function. The human Sertoli cell synthesizes lactate, estradiol-17beta and several proteins, namely transferrin, ferritin and inhibin. In the presence of germ cells the Sertoli cell production of estradiol-17beta is decreased whereas the transferrin and inhibin outputs are enhanced. In addition the lactate dehydrogenase, gamma-glutamyl transpepetidase, alkaline phosphatase and creatine phosphokinase activities have been quantitated in various human Sertoli cell preparations. It should be kept in mind that germ cells exert an important influence on the adult Sertoli cell secretory activity through either direct contact and/or via secreted factors; moreover germ cells potentialize the stimulating effect of FSH on the Sertoli cell function and indirectly the Leydig cell output of testosterone via the Sertoli cell secretion of paracrine factor(s).
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PMID:Paracrine control of human Leydig cell and Sertoli cell functions. 896 55

This investigation examined the acute response of serum lipoprotein(a) (Lp(a)) concentration immediately after, and during several days following, level and downhill motorized treadmill running. Eight males ran for 1 h on a level motorized treadmill at an intensity producing 90% maximum heart rate (MHR). On a separate occasion, three males and three females performed downhill (negative 13.4% incline) treadmill running at an intensity producing 75-80% MHR. For both protocols, serial blood samples were taken pre- and post-exercise and at the same time of day 1, 3, 5, and 7 days following exercise. Levels of Lp(a), creatine kinase (CK), C-reactive protein (CRP), and ferritin were measured. Repeated measures statistical analysis (Friedman ANOVA) showed no significant change in the median level of Lp(a) (level run, 5.0 mg.dl-1; downhill run, 7.45 mg.dl-1) across time following either protocol. After level running, ferritin levels 5 and 7 d post-exercise were significantly (P < 0.05) lower compared with immediately and 1 d post-exercise measures (Friedman ANOVA). Following level running, the Wilcoxon signed rank test showed significant (P < 0.05) elevations in CK levels immediately, 1 and 5 d post-exercise compared with pre-exercise values. Following downhill running. CK level was significantly elevated up to 3 d post-exercise (Wilcoxon signed rank). Calculated plasma volume did not change significantly following either protocol. These data suggest that Lp(a) does not change acutely in response to level or downhill treadmill running up to 60 min duration.
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PMID:Acute effects of treadmill running on lipoprotein(a) levels in males and females. 910 24

The aim of the present prospective longitudinal study was to investigate the hormonal response in overtrained athletes at rest and during exercise consisting of a short-term exhaustive endurance test on a cycle ergometer at an intensity 10% above the individual anaerobic threshold. Over a period of 19+/-1 months, 17 male endurance athletes (cyclists and triathletes; age 23.4+/-1.6 yr; VO2max. 61.2+/-1.8 mL x min(-1) x kg(-1); means+/-SEM) were examined five times on two separate days under standardized conditions. Short-term overtraining states (OT, N=15) were primarily induced by an increase of frequency of high-intensive bouts of exercise or competitions without increase of the total amount of training. OT was compared with normal training states intraindividually (NS, N=62). During OT, the time to exhaustion of the exercise test was significantly decreased by 27% on average. At rest and during exercise, the concentrations in plasma and the nocturnal excretion in urine of free epinephrine and norepinephrine were not significantly changed during OT. At physical rest, the concentrations of (free) testosterone, cortisol, luteinizing hormone, follicle-stimulating hormone, adrenocorticotropic hormone, growth hormone, and insulin during OT were comparable with those during NS. A significantly (P < 0.025) lower maximal exercise-induced increase of the adrenocorticotropic hormone and growth hormone, as well as a trend for a decrease of cortisol (P=0.060) and insulin (P=0.036), was measured. The response of free catecholamines as well as the ergometric performance of an all-out 30-s test was unchanged. Serum urea, uric acid, ferritin, and activity of creatine kinase showed no differences between conditions. In conclusion, the results confirm the hypothesis of a hypothalamo-pituitary dysregulation during OT expressed by an impaired response of pituitary hormones to exhaustive short-endurance exercise.
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PMID:Impaired pituitary hormonal response to exhaustive exercise in overtrained endurance athletes. 952 87

Free radical species have been implicated as important agents involved in myocardial ischemic and reperfusion injuries. Superoxide is capable of mobilizing iron from ferritin and the released iron can cause hydroxyl formation from H2O2. The aim of this study was to evaluate the time-dependent increase in lipid peroxidation assessed by plasma thiobarbituric acid reactive substances (TBARS) and the relationship between lipid-peroxidation and the iron status. Peripheral venous blood samples were obtained from 17 men with acute myocardial infarction (AMI) before thrombolytic treatment (T0) and 1, 2, 3, 4, 8, 12, 16, 20, 24 and 48 hours after commencing fibrinolytic treatment. The concentration of TBARS, the parameters of iron metabolism, serum myoglobin, creatine kinase, and creatine kinase-MB were measured. Early reperfusion was judged by regression of sinus tachycardia (ST) elevation and reduction of chest pain. Recanalization of coronary artery was evaluated by a late coronary angiography 24-96 hours after thrombolysis. After thrombolytic therapy, the TBARS level was raised from 2.98 +/- 0.80 (T0) to 4.57 +/- 1.24 (peak), and decreased to 2.96 +/- 0.40 nmol/mL plasma at T48 (T0 vs peak: P < 0.001, peak vs T48: P < 0.001, T0 vs T48: NS). The mean time of the peak was observed at 9.7 +/- 7.5 hours. The iron increased significantly from 0.67 +/- 0.34 (T0) to 1.15 +/- 0.52 mg/L (peak), and returned to the pre-reperfusion to levels: 0.53 +/- 0.28 UI/L at T48 (TO vs peak: P < 0.001, peak vs T48: P < 0.001, T0 vs T48: NS). The mean time of the peak was observed at 9.4 +/- 7.3 hours. In return, no correlation was found between the increase of plasma creatine-kinase activity, myoglobin and iron or between the biochemical markers and time of fibrinolytic therapy. The results confirmed the importance of the temporal relationship between lipid peroxidation and iron status after thrombolytic therapy. Our results are in agreement with the concept that antioxidant agents used in association with thrombolytic therapy might be useful.
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PMID:Plasma iron status and lipid peroxidation following thrombolytic therapy for acute myocardial infarction. 956 80

Three proteins have been identified in the eye lens of the octopus, Octopus dofleini. A 22 kDa protein comprising 3-5% of the soluble protein of the lens is 35-43% identical to a family of phosphatidylethanolamine-binding proteins of vertebrates. Other members of this family include the immunodominant antigen of the filarial parasite, Onchocerca volvulus, putative odorant-binding proteins of Drosophila and a protein with unknown function of Caenorhabditis elegans. We have called this protein O-crystallin on the basis of its abundance in the transparent lens. O-Crystallin mRNA was detected only in the lens. Two tryptic peptides of another octopus lens protein, less abundant than O-crystallin, showed 80% identity to arginine kinase of invertebrates, a relative of creatine kinase of vertebrates. Finally, ferritin cDNA was isolated as an abundant cDNA from the octopus lens library. Northern blots showed that ferritin mRNA is not lens-specific.
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PMID:O-Crystallin, arginine kinase and ferritin from the octopus lens. 1035 Jun 26

Resistance to thyroid hormone (RTH), a syndrome characterized by variable tissue hyposensitivity to thyroid hormone (TH), is linked to mutations in the thyroid hormone receptor (TR) beta gene. We report a new family with a heretofore unreported mutation, P247L. The proposita, a 31-year-old female, presented with goiter and palpitations. RTH was suspected because of elevated serum free thyroxine (FT4) level with a normal thyrotropin (TSH). Sequencing the TRbeta gene revealed a mutation causing replacement of a proline at position 247 with leucine. Seven family members were heterozygous for the mutation, two of whom also had evidence of autoimmune thyroid disease. The mutant TRbeta had a Ka for triiodothyronine (T3) 30% that of the wild-type TRbeta, approximately a threefold reduction in T3-induced transactivation and a low level dominant negative activity when tested with a positively regulated reporter gene. In vivo sensitivity to TH was evaluated in three affected subjects by measurement of the responses to graded doses of levotriiodothyronine (LT3). Peak TSH responses to TRH were reduced and were not completely suppressed at even the highest dose of LT3, (0.9, 0.2, and 0.2, compared to < 0.01 microU/mL in unaffected controls), confirming pituitary resistance to TH in all three subjects. In contrast, peripheral tissues responded variably to LT3: serum cholesterol decreased in all by 15%-25%, serum creatine kinase decreased by 15% in two subjects and increased 35% in another, but serum ferritin and sex hormone-binding globulin increased in only one of the three affected individuals that were tested. Basal metabolic rate and sleeping pulse did not change in three and two individuals, respectively. Hyporesponsiveness to exogenous TH established the clinical diagnosis of RTH in one member of the family with a mutant TRbeta but normal tests of thyroid function at baseline. Three affected subjects had an axis I diagnosis of major depression but had Wechsler Intelligence Scale for Children, III (WISC-III) full-scale IQs (FSIQs) in the normal range. This novel TRbeta mutation is associated with a realtively mild RTH. Results of responses to LT3 underscore the variable phenotype of RTH.
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PMID:A novel point mutation in cluster 3 of the thyroid hormone receptor beta gene (P247L) causing mild resistance to thyroid hormone. 1064 58

Birds have evolved alternate physiologic strategies to contend with dehydration, starvation, malnutrition, and reproduction. Basic anatomic and functional differences between birds and mammals impact clinical chemistry values and their evaluation. Interpretation of the results of standard biochemical analyses, including BUN, alanine aminotransferase, aspartate aminotransferase, creatine kinase, gamma glutamyltransferase, bilirubin, ammonia, alkaline phosphatase, cholesterol, bile acids, glucose, albumin, globulins, calcium, phosphorus, prealbumin (transthyretin), fibrinogen, iron, and ferritin, is reviewed and discussed in relation to these physiological differences. The use and interpretation of alternative analytes appropriate for avian species, such as uric acid, biliverdin, glutamate dehydrogenase, and galactose clearance, also are reviewed. Normal avian urine and appropriate use of urinalysis, an integral part of laboratory diagnosis in mammalian species that frequently is omitted from avian diagnostic protocols, is discussed.
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PMID:Clinical chemistry of companion avian species: a review. 1218 2


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