Clinical usefulness of the (chloride-90)/phosphate ratio for distinguishing primary hyperparathyroidism from hypercalcemia due to other causes

In order to obtain a good separation line between patients with primary hyperparathyroidism (1 degree HPT) and those with non-parathyroidal hypercalcemia (NPHC), serum chloride (Cl) and phosphate (P) concentrations were analyzed. Ninety-nine per cent of the patients with 1 degree HPT had a Cl/P ratio greater than or equal to 33, but 29% of patients with NPHC were also included in this range. When the (Cl-90)/P ratio was used to separate into two groups, 98% of the patients with 1 degree HPT had a ratio greater than or equal to 5.0, and 94% of the patients with NPHC had a ratio less than 5.0. From these results, while high sensitivity was achieved both with the Cl/P and (Cl-90)/P ratios, the (Cl-90)/P ratio provided higher specificity. Therefore we conclude that the (Cl-90)/P ratio was excellent in distinguishing 1 degree HPT from other types of hypercalcemia.     

Characterization of Astrocytes in the Minocycline-Administered Mouse Photothrombotic Ischemic Stroke Model

Neurochemical Research - Astrocytes, together with microglia, play important roles in the non-infectious inflammation and scar formation at the brain infarct during ischemic stroke. After ischemia...     

Stage-specific roles of fibulin-5 during oxidative stress-induced renal carcinogenesis in rats

By using a rat model of renal cell carcinoma (RCC) induced by ferric nitrilotriacetate (Fe-NTA), this study performed genome-wide analysis to identify target genes during carcinogenesis. It screened for genes with decreased expression in RCCs, with simultaneous loss of heterozygosity, eventually to focus on the fibulin-5 (fbln5) gene. Oxidative damage via Fe-NTA markedly increased Fbln5 in the proximal tubules. RCCs presented lower levels of Fbln5. However, a fraction of RCCs presenting pulmonary metastasis revealed significantly higher levels of Fbln5 than those without metastasis, accompanied by immunopositivity of RCC cells and myofibroblast proliferation. Experiments revealed that RCC cell lines showed lower expression of fbln5 than its non-transformed counterpart NRK52E, but that fbln5 transfection to RCC cell lines changed neither proliferation nor migration/invasion. The data suggest that Fbln5 plays a role not only in the tissue repair and remodelling after renal tubular oxidative damage but also in RCC metastasis, presumably as a cytokine.     

Urinary stone analysis in a patient with hyperuricemia to determine the mechanism of stone formation

In order to determine the mechanism of urinary stone formation in patients with hyperuricemia, we analyzed the crystal components and matrix proteins in a urinary stone from such a patient. Micro-area X-ray spectrometry and infrared (IR) spectroscopy suggested that the outside of the stone was composed of calcium oxalate monohydrate (COM) and the inside of uric acid (UA). Proteomic analysis identified 37 and 14 proteins from the inside and outside of the stone, respectively, as matrix proteins. The proteins that were identified in an ethylenediaminetetraacetic acid (EDTA) fraction were able to bind calcium ions. Thus, calcium-binding proteins may play a significant role in the formation of urinary stones in patients with hyperuricemia.     

LINE1 family member is negative regulator of HLA-G expression

Class Ia molecules of human leucocyte antigen (HLA-A, -B and -C) are widely expressed and play a central role in the immune system by presenting peptides derived from the lumen of the endoplasmic reticulum. In contrast, class Ib molecules such as HLA-G serve novel functions. The distribution of HLA-G is mostly limited to foetal trophoblastic tissues and some tumour tissues. The mechanism required for the tissue-specific regulation of the HLA-G gene has not been well understood. Here, we investigated the genomic regulation of HLA-G by manipulating one copy of a genomic DNA fragment on a human artificial chromosome. We identified a potential negative regulator of gene expression in a sequence upstream of HLA-G that overlapped with the long interspersed element (LINE1); silencing of HLA-G involved a DNA secondary structure generated in LINE1. The presence of a LINE1 gene silencer may explain the limited expression of HLA-G compared with other class I genes.