Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0392674 (exhaustion)
 13,658 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 29-year-old woman presented to the emergency department with exhaustion, fatigue, and abdominal pain. She reported having received a diagnosis of bulimia nervosa 10 years before. On examination, she had a marked pallor and was severely malnourished. Laboratory analysis revealed a dramatically low hemoglobin level of 1.7 g/dL (ref: 11.5-15.8 g/dL). Serum iron was quantified as 1.4 micromol/L (ref: 7-26 micromol/L), ferritin as 5 ng/mL (ref: 10-120 ng/mL), and the level of serum transferrin as 212 mg/dL (ref: 200-360 mg/dL). A duodenal biopsy revealed villous atrophy in the mucosal layer indicative for celiac disease. This diagnosis was confirmed by serum levels of endomysial antibodies, tissue transglutaminase antibody, and antigliadin antibodies. The newly diagnosed gluten-sensitive enteropathy is likely to be in part responsible for the severe symptoms reported. The extent of hemoglobin decline in combination with an astonishing lack of critical symptoms seen in this patient is a rarity. We conclude that anorectic patients with severe anemia and malnutrition should be evaluated for the presence of additional somatic conditions.
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PMID:Very severe iron-deficiency anemia in a patient with celiac disease and bulimia nervosa: a case report. 1629 20

A solution containing chromate was treated using waste shot-blast fines recovered from surface finishing operations in a cast-iron foundry as a sorbent in batch and fixed-bed modes. Equilibrium experiments for initial chromate concentrations of 5 to 10 ppm produced a pH-adsorption edge that exhibits removal of chromium (Cr) over a broad pH range, with adsorption capacities that compare favorably to those reported for other adsorbents such as activated carbon and commercial iron oxides. Surface complexation modeling of adsorption equilibria suggests the formation of monodentate, inner-sphere complexes with chromate (CrO4(2-)) and bichromate (HCrO4(-)). Adsorption of Cr(VI) at iron oxy-hydroxide sites appears to be the primary mechanism of chromium removal at neutral pH. At lower pH values (for example, pH 4), reduction to Cr(III) is assumed to contribute to the increasing removal as a function of decrease in pH. There is also evidence to support the formation of Cr(III)-iron (Fe)(III) coprecipitate following Cr(VI) reduction by dissolved Fe(II). Using equilibrium constants for the two surface complexation reactions evaluated from a triple-layer model description of the oxide-water interface, chromate removal in a short fixed bed of fines was simulated using a dual mass-transfer kinetic model. Rate coefficients determined from model calibration of the short column were used to predict experimental breakthrough curves in columns with empty bed contact times (EBCTs) up to four times the short column. For an influent chromium concentration and pH of 5 ppm and 7.0, respectively, a solid-phase loading capacity of 9.5 +/- 0.3 mg/g was achieved at exhaustion. Predictive model runs indicate that, for this case, an EBCT of 2.0 to 2.5 minutes is optimum for achieving a target effluent concentration of less than or equal to 0.05 mg/L chromium as Cr(VI).
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PMID:Chromate removal by an iron sorbent: mechanism and modeling. 1655 70

Eighty-one patients with acutely progressive pulmonary tuberculosis (APPT) (a study group) and 63 patients with involutive pulmonary tuberculosis (a control group) were examined. The magnitude of a systemic inflammatory response was estimated by the values of acute phase reagents (APR) and the blood protein spectrum; the body's iron provision, the state of the hemostatic and fibrinolytic systems, the functional status of mononuclear leukocytes and neutrophils were determined by the basal level of oxygen-dependent and nitrite oxide metabolism and by the capacity of these systems to respond to specific stimulation. In APPT, along with increased APR levels reflecting the mobilization of various components of endogenous defense, the serum (plasma) was found to show the signs of metabolic decompensation as increased catabolic processes and hepatic protein-synthesizing dysfunction in the presence of intravascular inactivation of functionally significant proteins. Noteworthy is hypochromic anemia caused by the body's redistribution of iron (in the absence of its genuine deficiency) and by the reduced plasma concentration of transferring. The patients with APPT had a significant hypercoagulation syndrome with the signs of latent intravascular blood coagulation. Antimicrobial defensive processes involved mononuclear leukocytes and neutrophils wherein free radical oxidation and nitric oxide generation became intensive. In APPT, the permanent reirritation of these systems led to the exhaustion of functional reserves of cells and their response to specific stimulation diminished. In the neutrophils, rearrangement of their metabolism correlated with other manifestations of a systemic inflammatory response and in the mononuclear leukocytes, this correlated with the size of a bacterial population and with the presence of drug sensitivity/resistance of the causative agent.
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PMID:[Qualitative assessment of metabolic shifts accompanying the acutely progressive course of pulmonary tuberculosis]. 1700 60

The one-humped camel is a typical desert animal. It has the capability of withstanding the harsh climatic changes and the scarcity of food and water, in addition to the high-ambient temperature. The prevalence of diabetes mellitus in two different groups of the one-humped camel, group (A) control (n = 102) camels and group (B) high-calorie diet-fed camels (n = 103), in Al-Ain region (UAE) was studied using biochemical and radioimmunoassay techniques. In this article, 7% of the control camels have diabetes mellitus (blood glucose level: > or =140 mg/dL) compared to 21% of the high-calorie-fed camels. Plasma insulin level was significantly (P < 0.05) lower in group B compared to group A. The low insulin level in camels consuming high-caloric diet could be a sign of exhaustion of pancreatic beta cells. The hematological parameters were nearly similar in both groups and no significant differences were seen. Liver and kidney enzymes were normal in both groups. Iron and copper were significantly (P < 0.005) higher in the high-calorie-fed camels compared with the control. Our study indicates that high-caloric feed consumption in camels is associated with the development of disorders in glucose metabolism leading to diabetes mellitus.
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PMID:Effect of high-calorie diet on the prevalence of diabetes mellitus in the one-humped camel (Camelus dromedarius). 1715 18

Uraemic patients are exposed either to iron deficiency due to impaired digestive n associated with various blood losses (particularly in dialysis patients) or iron verload related to blood transfusions in the pre-erythropoetin era or excessive intravenous iron supplementation. The central role of hepcidin in the regulation of oral iron absorption d its effects in uraemia have been recently evidenced. The increased haemoglobin synthesis induced by erythropoiesis stimulating agents (ESA) enhances iron requirements. In case of exhaustion of tissue reserves and/or insufficient exogenous supply, iron deficiency develops which is the major limiting factor for ESA efficacy. Careful biological follow-up is mandatory to detect early iron deficiency or overload, the latter being considered as possibly increasing the uraemic patients' susceptibility to bacterial or viral infections. Intravenous administration of Vitamin C, by enhancing the release of iron from the reticuloendothelial system towards transferrin increases the circulating iron available for erythropoiesis and contributes to the optimisation of ESA efficacy.
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PMID:[Iron metabolism pre and post the erythropoietin era]. 1737 76

This investigation examined the effect of intramuscular iron injections on aerobic-exercise performance in iron-deficient women. Sixteen athletes performed a 10-min steady-state submaximal economy test, a VO2max test, and a timed test to exhaustion at VO2max workload. Subjects were randomly assigned to an iron-supplemented group (IG) receiving intramuscular iron injections or to a placebo group (PG). Twenty days after the first injection, exercise and blood testing were repeated. A final blood test occurred on Day 28. Post supplementation, no differences were found between the groups' submaximal or maximal VO2, heart rate, or blood lactate (P > 0.05). Time to exhaustion was increased in the IG (P < 0.05) but was not greater than that of the PG (P > 0.05). The IG's serum ferritin (SF) was significantly increased on Days 20 and 28 (mean +/- standard error: 19 +/- 3 to 65 +/- 11 to 57 +/- 12 microg/L; P < 0.01), with a percentage change from baseline significantly greater than in the PG (P < 0.01). It was concluded that intramuscular iron injections can effectively increase SF without enhancing submaximal or maximal aerobic-exercise performance in iron-depleted female athletes.
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PMID:Effect of iron injections on aerobic-exercise performance of iron-depleted female athletes. 1769 84

Following World War II, Americans feared their iron ore supplies were depleted. The steel industry attempted to increase supplies by exploring foreign countries for new, high-grade hematite ores and experimenting with technology that upgraded low-grade domestic taconite ores into acceptable, but apparently uneconomical, pellets. Government did little at first, but the Korean War renewed fears of domestic resource exhaustion. Congress quickly enacted loan guarantees, rapid tax write-offs, and other tax policies that helped commercialize taconite pellets for national defense. These policies lingered long after the Korean War ended. Other policies bolstering taconite were enacted on the state level well after taconite had replaced hematite as industry's ore of choice. Understanding how government policies helped to develop pelletized lean iron ore may help in thinking about current policy suggestions aimed at easing our energy crisis or other mineral shortages. For taconite, too much government help came too late.
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PMID:Iron ore: from depletion to abundance. 1778 4

We describe the mapping and identification of the gene for hereditary myopathy with lactic acidosis (HML). HML is characterized by low physical performance, resulting in physical exertion that causes early exhaustion, dyspnoea and palpitations. Using an autosomal recessive mode of inheritance, we mapped the trait to chromosome 12q23.3-24.11, with a maximum lod score of 5.26. The 1.6-Mb disease-critical region contained one obvious candidate gene-ISCU-specifying a protein involved in iron-sulphur cluster assembly. IscU is produced in two isoforms; one cytosolic and one mitochondrial, coded for by different splice variants of the ISCU gene. Mutational analysis of all exon and intron sequences as well as 1000 bp of the promoter of the ISCU gene revealed one intron mutation that was specific for the disease haplotype. The mutation is located in a region with homology to the interferon-stimulated response element (ISRE), but we could not see any effect of the mutation on expression levels in vitro or in vivo. We did, however, observe a drastic difference in the splicing pattern between patients and controls. In controls the mRNA was, as expected, mainly in the mitochondrial form, while in the patients a larger mRNA transcript was predominant. Sequencing of the product revealed that the mutation activates cryptic splice sites in intron 5 resulting in aberrant mRNA containing 100 bp of the intron. To conclude, our data strongly suggest that an intron mutation in the ISCU gene, leading to incorrectly spliced mRNA, is the cause of myopathy with lactic acidosis in this family.
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PMID:Myopathy with lactic acidosis is linked to chromosome 12q23.3-24.11 and caused by an intron mutation in the ISCU gene resulting in a splicing defect. 1829 49

Diabetes is a disorder characterized by beta-cell loss or exhaustion and insulin deficiency. At present, knowledge is lacking on the underlying causes and for the therapeutic recovery of the beta-cell mass. A better understanding of diabetes pathogenesis could be obtained through exact monitoring of the fate of beta-cells under disease and therapy conditions. This could pave the way for a new era of intervention by islet replacement and regeneration regimens. Monitoring the beta-cell mass requires a reliable method for noninvasive in vivo imaging. Such a method is not available at present due to the lack of a beta-cell-specific contrast agent. The only existing method to monitor islet cells in vivo consists of labeling islet transplants with iron nanoparticles prior to transplantation and visualization of the transplanted islets by magnetic resonance imaging (MRI). Therefore, accurate assessment of the native beta-cell mass is still limited to autopsy studies. Endeavors to find a biological structure specific for beta-cells led to the discovery of potential candidates that have been tested for noninvasive imaging. Among them are the ligand to the vesicular monoamine transporter type 2 (VMAT-2), which is called dihydrotetrabenazine (DTBZ), antibodies to zinc transporter (ZnT-8) and the monoclonal antibody IC2. While DTBZ and antibodies to ZnT-8 showed binding activities to more than beta-cells, the anti-IC2 monoclonal antibody showed binding properties exclusively to insulin-producing beta-cells. This effect was demonstrated in many previous investigations, and has been further substantiated more recently. Thus, at present, IC2 seems to be the only useful marker for noninvasive functional imaging of native beta-cells. Experiments with a radioisotope-chelated IC2 structure on pancreas ex vivo showed that the tracer specifically bound to the beta-cell surface and could be detected by nuclear imaging. In the near future, these promising findings may offer a new way to monitor the beta-cell mass in vivo under disease and therapy conditions so that we can learn more about diabetes pathogenesis and options for disease prevention.
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PMID:Imaging the Beta-cell mass: why and how. 1854 65

The cybernetic modeling framework developed by Ramkrishna and co-workers has been applied to a case of bacterial metabolite production, namely the production of siderophores (iron-chelating agents) associated with iron-limiting fermentation conditions. Experimental growth data showed that, even though final biomass levels were controlled by exhaustion of the carbon source, iron-limiting conditions also affected the biomass yield. A structured model which includes the process of an iron-limiting energy resource production was able to quantitatively account for this apparent dual-substrate limitation over a wide range of batch and continuous operating conditions. The experiments data also showed quite large difference in iron uptake over the wide range of operating condition and iron levels investigated. The inclusion in the model of the processes of low and high (siderophore-mediated) affinity iron transport, and siderophore production led to simulation results that were in good quantitative agreement with the siderophore, medium and cell iron levels, in both batch and steady-state continuous culture operating conditions.
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PMID:Cybernetic modeling of iron-limited growth and siderophore production. 1860 82


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