A multimedia educational module for the restoration of single-tooth implants

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Hepcidin levels in acute kidney injury following cardiopulmonary bypass grafting.

Contains fulltext : 80563.pdf (publisher's version ) (Closed access

Hepcidin levels in patients with renal disease.

Contains fulltext : 80564.pdf (publisher's version ) (Closed access

Reproducibility of and correspondence among different hepcidin forms in blood and urine and their relationships to iron status in healthy, male Guatemalan volunteers observed over 9 weeks

Contains fulltext : 97314.pdf (publisher's version ) (Open Access)BACKGROUND/AIMS: Prohepcidin and the active form hepcidin-25 are two variants of the peptide hormone hepcidin for iron homoeostasis. Their regulatory role and usefulness as biomarkers of the iron status are uncertain. Our aim is to describe the intra-individual variance of serum and urinary hepcidin-25 and prohepcidin concentrations, the mutual associations of the 4 hepcidin formats, and their correspondence with iron status variables in male Guatemalan volunteers. METHODS: Eight healthy adult males provided serial samples of serum and urine without previous iron dosing over 6 intervals during a 9-week protocol period. Prohepcidin was assayed by a commercial enzyme immunoassay, and hepcidin-25 species in serum and urine were analysed by time-of-flight mass spectrometry after prior enrichment procedures. RESULTS: Serum hepcidin-25 levels correlated significantly with urinary hepcidin-25 concentrations, whereas serum and urinary prohepcidin were not associated with one another or with the homologous or converse formats for hepcidin-25. Serum ferritin and transferrin saturation were significantly correlated with serum hepcidin-25 concentrations, but not with urine hepcidin-25 or with either format of prohepcidin. CONCLUSION: Hepcidin-25 shows correspondence across biological fluids, and the background 'status' of hepcidin activation may be related to the host's iron stores, whereas prohepcidin concentrations showed no promise in this regard

Novel urine hepcidin assay by mass spectrometry.

Contains fulltext : 48998.pdf (publisher's version ) (Closed access)The hepatic peptide hormone hepcidin is the central regulator of iron metabolism and mediator of anemia of inflammation. To date, only one specific immuno-dot assay to measure hepcidin in urine had been documented. Here we report an alternative approach for quantification of hepcidin in urine by surface-enhanced laser desorption/ionization time-of-flight mass spectrometry (SELDI-TOF-MS). Peptide peaks were detected corresponding to the 3 forms of hepcidin normally found in urine. The identity of the peptide peak equivalent to hepcidin-25 was confirmed using synthetic human hepcidin-25. Validation of our MS data on samples with various hepcidin levels showed a strong correlation with previous immuno-dot assay results (Spearman R = 0.9275, P < .001). Most importantly, this hepcidin assay clearly discriminates between relevant clinical iron disorders. In conclusion, this novel MS urine hepcidin assay is easy to perform and available to a wide audience. This enables the implementation of hepcidin measurements in large clinical studies

Serum hepcidin levels are elevated in the metabolic syndrome.

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Acute dietary carbohydrate manipulation and the subsequent inflammatory and hepcidin responses to exercise

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Standardized serum hepcidin values in Dutch children: Set point relative to body iron changes during childhood

Contains fulltext : 218317.pdf (Publisher’s version ) (Open Access)BACKGROUND: Use of serum hepcidin measurements in pediatrics would benefit from standardized age- and sex-specific reference ranges in children, in order to enable the establishment of clinical decision limits that are universally applicable. PROCEDURE: We measured serum hepcidin-25 levels in 266 healthy Dutch children aged 0.3-17 years, using an isotope dilution mass spectrometry assay, standardized with our commutable secondary reference material (RM), assigned by a candidate primary RM. RESULTS: We constructed age- and sex-specific values for serum hepcidin and its ratio with ferritin and transferrin saturation (TSAT). Serum hepcidin levels and hepcidin/ferritin and TSAT/hepcidin ratios were similar for both sexes. Serum hepcidin and hepcidin/ferritin ratio substantially declined after the age of 12 years and TSAT/hepcidin ratio gradually increased with increasing age. Serum hepcidin values for Dutch children 12 years (n = 96) were 1.9 nmol/L (median); 0.1-13.1 nmol/L (p2.5-p97.5) and 0.9 nmol/L; 0.0-9.1 nmol/L, respectively. Serum ferritin was the most significant correlate of serum hepcidin in our study population, explaining 15.1% and 7.9% of variance in males and females, respectively. Multivariable linear regression analysis including age, blood sampling time, iron parameters, ALT, CRP, and body mass index as independent variables showed a statistically significant negative association between age as a dichotomous variable (12 years) and log-transformed serum hepcidin levels in both sexes. CONCLUSIONS: We demonstrate that serum hepcidin relative to indicators of body iron is age dependent in children, suggesting that the set point of serum hepcidin relative to stored and circulating iron changes during childhood

Sustained Exposure to High Carbohydrate Availability Does Not Influence Iron-Regulatory Responses in Elite Endurance Athletes

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Timing of post-exercise carbohydrate ingestion: influence on IL-6 and hepcidin responses

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