A seven day running training period increases basal urinary hepcidin levels as compared to cycling

BACKGROUND: This investigation compared the effects of an extended period of weight-bearing (running) vs. non-weight-bearing (cycling) exercise on hepcidin production and its implications for iron status. METHODS: Ten active males performed two separate exercise training blocks with either running (RTB) or cycling (CTB) as the exercise mode. Each block consisted of five training sessions (Day 1, 2, 4, 5, 6) performed over a seven day period that were matched for exercise intensity. Basal venous blood samples were obtained on Day 1 (D1), and on Recovery Days 3 (R3) and 7 (R7) to assess iron status, while basal and 3 h post-exercise urinary hepcidin levels were measured on D1, D2, D6, as well as R3 and R7 (basal levels only) for each condition. RESULTS: Basal urinary hepcidin levels were significantly elevated (p </= 0.05) at D2, R3 and R7 as compared to D1 in RTB. Furthermore, 3 h post-exercise urinary hepcidin levels on D1 were also significantly higher in RTB compared to CTB (p </= 0.05). In CTB, urinary hepcidin levels were not statistically different on D1 as compared to R7. Iron parameters were not significantly different at D1 compared to R3 and R7 during both conditions. CONCLUSIONS: These results suggest that basal hepcidin levels may increase over the course of an extended training program, especially if a weight-bearing exercise modality is undertaken. However, despite any variations in hepcidin production, serum iron parameters in both RTB and CTB were unaffected, possibly due to the short duration of each training block. In comparing running to cycling, non-weight-bearing activity may require more training sessions, or sessions of extended duration, before any significant changes in basal hepcidin levels appear. Chronic elevations in hepcidin levels may help to explain the high incidence of iron deficiency in athletes

Toxic iron species in lower-risk myelodysplastic syndrome patients : course of disease and effects on outcome

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Hepcidin-25 in Chronic Hemodialysis Patients Is Related to Residual Kidney Function and Not to Treatment with Erythropoiesis Stimulating Agents

Hepcidin-25, the bioactive form of hepcidin, is a key regulator of iron homeostasis as it induces internalization and degradation of ferroportin, a cellular iron exporter on enterocytes, macrophages and hepatocytes. Hepcidin levels are increased in chronic hemodialysis (HD) patients, but as of yet, limited information on factors associated with hepcidin-25 in these patients is available. In the current cross-sectional study, potential patient-, laboratory- and treatment-related determinants of serum hepcidin-20 and -25, were assessed in a large cohort of stable, prevalent HD patients. Baseline data from 405 patients (62% male; age 63.7±13.9 [mean SD]) enrolled in the CONvective TRAnsport STudy (CONTRAST; NCT00205556) were studied. Predialysis hepcidin concentrations were measured centrally with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Patient-, laboratory- and treatment related characteristics were entered in a backward multivariable linear regression model. Hepcidin-25 levels were independently and positively associated with ferritin (p<0.001), hsCRP (p<0.001) and the presence of diabetes (p = 0.02) and inversely with the estimated glomerular filtration rate (p = 0.01), absolute reticulocyte count (p = 0.02) and soluble transferrin receptor (p<0.001). Men had lower hepcidin-25 levels as compared to women (p = 0.03). Hepcidin-25 was not associated with the maintenance dose of erythropoiesis stimulating agents (ESA) or iron therapy. In conclusion, in the currently studied cohort of chronic HD patients, hepcidin-25 was a marker for iron stores and erythropoiesis and was associated with inflammation. Furthermore, hepcidin-25 levels were influenced by residual kidney function. Hepcidin-25 did not reflect ESA or iron dose in chronic stable HD patients on maintenance therapy. These results suggest that hepcidin is involved in the pathophysiological pathway of renal anemia and iron availability in these patients, but challenges its function as a clinical parameter for ESA resistance

NTBI levels in C282Y homozygotes after therapeutic phlebotomy

Abstract C282Y homozygotes exposed to sustained elevated transferrin saturation (TS) may develop worsening clinical symptoms. This might be related to the appearance of non‐transferrin bound iron (NTBI) when TS≥50% and labile plasma iron (LPI) when TS levels reach 75–80%. In this study, NTBI levels were examined in 219 randomly selected untreated and treated C282Y homozygotes. Overall, 161 of 219 had TS ≥ 50%, 124 of whom had detectable NTBI (≥0.47 µM, 1.81 µM [0.92–2.46 µM]) with a median serum ferritin 320 µg/L (226–442 µg/L). Ninety of 219 homozygotes had TS ≥ 75%, and all had detectable NTBI (2.21 µM [1.53–2.59 µM] with a median ferritin 338 µg/L [230–447 µg/L]). Of 125 homozygotes who last had phlebotomy ≥12 months ago (42 months [25–74 months], 92 had TS levels ≥ 50%, and 70 of these had NTBI ≥ 0.47 µM (2.06 µM [1.23–2.61µM]). Twenty‐six of these 70 had a normal ferritin. Fifty‐five of 125 had TS ≥ 75%, and NTBI was detected in all of these (2.32 µM [1.57–2.77 µM]) with a median ferritin 344 µg/L (255–418 µg/L). Eighteen of these 55 had a normal ferritin. In summary, NTBI is frequently found in C282Y homozygotes with TS ≥ 50%. Furthermore, C282Y homozygotes in the maintenance phase often have TS ≥ 50% together with a normal ferritin. Therefore, monitoring the TS level during the maintenance phase is recommended as an accessible clinical marker of the presence of NTBI

Serum hepcidin following autologous hematopoietic cell transplantation : an illustration of the interplay of iron status, erythropoiesis and inflammation

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A sorption compressor with a single sorber bed for use with Linde-Hampson cold stage

A sorption compressor cell basically consists of a container that is filled with an adsorbent. When such a cell is thermally cycled, a pressure difference is created by the subsequent adsorption and desorption of the gas. As a consequence, a single sorption compressor cell inherently provides an intermittent flow. A Joule–Thomson expansion stage requires a more or less continuous flow. The standard way to obtain a continuous flow out of a sorption compressor is to use three or more compressor cells that are operated out of phase. This paper presents an alternative compressor concept that uses only one compressor cell, two buffer volumes and two check valves. Such a compressor is easier to construct and to operate and has a higher reliability at the expense of a slight variation in the cooler’s cold-end temperature. The principle was demonstrated using a sorption compressor cell that is filled with Maxsorb [The Kansai Coke & Chemicals Co. Ltd., 1-1 Oh-Hama, Amagasaki, Japan 660] activated carbon, is equipped with a gas-gap heat switch, and uses xenon as the working fluid. A flow of 0.52 mg/s was achieved with a low pressure of 1.39 bar and a high pressure of 17.0 bar, giving a theoretical cooling power of 42 mW at 172 K. A sensitivity analysis on several control parameters has been performed experimentally