Relationship between serum calcium or phosphate levels and mortality stratified by parathyroid hormone level: an analysis from the MBD-5D study

Introduction: There is limited evidence about the association between calcium and phosphate levels and mortality stratified by intact parathyroid hormone (iPTH) level. Methods: We investigated whether differences in iPTH level affect the relationship between calcium and phosphate levels and all-cause mortality in hemodialysis patients with secondary hyperparathyroidism (SHPT). Calcium and phosphate levels were categorized as low (< 8.5 mg/dL,  < 4.0 mg/dL), medium (≥ 8.5–< 9.5 mg/dL,  ≥ 4.0–< 7.0 mg/dL), and high (≥ 9.5 mg/dL,  ≥ 7.0 mg/dL), respectively. iPTH levels were grouped into < 300 or ≥ 300 pg/mL. Adjusted incidence rate ratios (aIRRs) were analyzed by weighted Poisson regression. Results: For calcium, patients with higher iPTH (≥ 300 pg/mL) had significantly higher all-cause mortality rates in the high than in the medium category (aIRR 1.99, 95% confidence interval [CI] 1.16–3.42), and tended to have a higher mortality rate in the low category (aIRR 2.04, 95% CI 0.94–4.42). Patients with lower iPTH (< 300 pg/mL) had higher mortality rates in the high than in the medium category (aIRR 1.65, 95% CI 1.39–1.96). For phosphate, the mortality rate was significantly higher in the high than in the medium category in patients with higher and lower iPTH (aIRR 3.23, 95% CI 1.63–6.39 for iPTH ≥ 300 pg/mL; aIRR 1.58, 95% CI 1.06–2.36 for iPTH < 300 pg/mL). Conclusion: High calcium and phosphate levels were associated with increased risk of mortality irrespective of iPTH level

A mechanism of the large-scale damping in the CMB anisotropy

We present a mechanism through which a certain class of short-distance cutoff affects the CMB anisotropies at large angular scales. Our analysis is performed in two steps. The first is given in an intuitive way, using the property of the inflationary universe that quantum fluctuations of an inflaton field become classical after crossing the Hubble horizon. We give a condition for a cutoff to yield a damping on large scales, and show that the holographic cutoff introduced in the preceding paper (hep-th/0307029) does satisfy the condition. The second analysis is carried out by setting an initial condition such that each mode of inflaton starts as the vacuum fluctuation of the Hamiltonian when being released from the constraint of cutoff. The first intuitive discussion is then shown to be correct qualitatively.Comment: 31 pages, 14 figures, final version, to appear in Nuclear Physics

Structure of 136Sn and the Z = 50 magicity

The first 2+ excited state in the neutron-rich tin isotope 136Sn has been identified at 682(13) keV by measuring γ -rays in coincidence with the one proton removal channel from 137Sb. This value is higher than those known for heavier even-even N = 86 isotones, indicating the Z = 50 shell closure. It compares well to the first 2+ excited state of the lighter tin isotope 134Sn, which may suggest that the seniority scheme also holds for 136Sn. Our result confirms the trend of lower 2+ excitation energies of even-even tin isotopes beyond N = 82 compared to the known values in between the two doubly magic nuclei 100Sn and 132Sn. © The Author(s) 2014.published_or_final_versio

Autosomal dominant pseudohypoaldosteronism type 1 with a novel splice site mutation in MR gene

<p>Abstract</p> <p>Background</p> <p>Autosomal dominant pseudohypoaldosteronism type 1 (PHA1) is a rare inherited condition that is characterized by renal resistance to aldosterone as well as salt wasting, hyperkalemia, and metabolic acidosis. Renal PHA1 is caused by mutations of the human mineralcorticoid receptor gene (<it>MR</it>), but it is a matter of debate whether <it>MR </it>mutations cause mineralcorticoid resistance via haploinsufficiency or dominant negative mechanism. It was previously reported that in a case with nonsense mutation the mutant mRNA was absent in lymphocytes because of nonsense mediated mRNA decay (NMD) and therefore postulated that haploinsufficiency alone can give rise to the PHA1 phenotype in patients with truncated mutations.</p> <p>Methods and Results</p> <p>We conducted genomic DNA analysis and mRNA analysis for familial PHA1 patients extracted from lymphocytes and urinary sediments and could detect one novel splice site mutation which leads to exon skipping and frame shift result in premature termination at the transcript level. The mRNA analysis showed evidence of wild type and exon-skipped RT-PCR products.</p> <p>Conclusion</p> <p>mRNA analysis have been rarely conducted for PHA1 because kidney tissues are unavailable for this disease. However, we conducted RT-PCR analysis using mRNA extracted from urinary sediments. We could demonstrate that NMD does not fully function in kidney cells and that haploinsufficiency due to NMD with premature termination is not sufficient to give rise to the PHA1 phenotype at least in this mutation of our patient. Additional studies including mRNA analysis will be needed to identify the exact mechanism of the phenotype of PHA.</p