Circulating Sclerostin responses to acute weight and non weight bearing sport activity in pre adolescent males

Mechanical loading, i.e. physical activity and/or exercise, promotes bone formation during growth. Sclerostin, a glycoprotein, mediates osteocytes' response to mechanical loading by inhibiting the Wnt/lf-catenin pathway thereby inhibiting bone formation.Published versio

Age-Dependent Changes in the Size of Adenotonsillar Tissue in Childhood: Implications for Sleep-Disordered Breathing

Objective To analyze age-associated changes in linear and cross-sectional area (CSA) measurements of adenoid, tonsils, and pharyngeal lumen. Study design Measurements were completed in head magnetic resonance imaging examinations performed for diagnostic purposes. Linear and nonlinear regression models were applied to describe the effect of age on the size of soft tissues and upper airway. Results Magnetic resonance imaging data were analyzed in 149 children without snoring (aged 0-15.9 years) and in 33 children with snoring (aged 1.6-15 years). In the children without snoring, adenoid size increased during the first 7-8 years of life and then decreased gradually [% (adenoid oblique width/ mental spine-clivus length) = 11.38 + 1.52 (age) - 0.11 (age)(2), R-2 = 0.22, P < .01; adenoid CSA = 90.75 + 41.93 (age) - 2.47 (age)(2); R-2 = 0.50; P < .01]. Nasopharyngeal airway CSA increased slowly up to age 8 years and rapidly thereafter. Similar patterns were noted for the tonsils and oropharyngeal airway. In contrast, in children with snoring, adenoid and tonsils were large irrespective of age, and nasopharyngeal airway size increased slowly with age. Conclusions In children without snoring, growing adenotonsillar tissue narrows the upper airway lumen to variable degrees only during the first 8 years of life. In contrast, in children with snoring, appreciable pharyngeal lymphoid tissue enlargement is present during the preschool years and persists beyond the eighth birthday. (J Pediatr 2013;162:269-74)

Mast cells co-expressing CD68 and inorganic polyphosphate are linked with colorectal cancer

<div><p>Inflammation is a hallmark of colorectal cancer (CRC). Neutrophils are well-known mediators in tumor biology but their role in solid tumors, including CRC, was redefined by neutrophil extracellular traps (NETs). Given that it was recently demonstrated that platelet-derived polyP primes neutrophils to release NETs, we examined surgical specimens from CRC to investigate the presence of polyP, as a possible NET inducer. Biopsies with adenomas, hyperplastic polyps, inflammatory bowel disease and healthy colon tissues were used as controls. In all cases, the presence of polyP was apparent, with the main source of polyP being the mast cells. In all CRC and all adenomas with high-grade dysplasia, a substantial number of mast cells, more than 50%, co-expressed intracellularly polyP with CD68 surface antigen (CD68+), but this was not the case in the other examined disorders. PolyP-expressing mast cells were detected in close proximity with tumor cells and neutrophils, suggesting polyP expression by CD68+ mast cells among the stimuli which prime neutrophils to release NETs, in CRC. Moreover, the detection of CD68+ polyP-expressing mast cells could represent a potential prognostic marker in colorectal adenomas and/or carcinomas.</p></div

PolyP-expressing cells are positive for mast cell tryptase and CD68 in human colon cancer.

<p>Confocal microscopy for <b>(A)</b> polyP / tryptase and <b>(C)</b> polyP / CD68 staining in sections of colonic adenocarcinoma specimens. <b>(B and D)</b> Data from six independent experiments presented as mean ± SD. Blue: PI, Green: (A and C) JC-D8 polyP-specific fluorescent probe, Red: (A) mast cell tryptase or (C) CD68. (A and C) One representative out of ten independent experiments is shown. Original magnification x600. Scale bar– 5μm. *P < 0.05, **P < 0.001, NS–not significant, HG–high grade.</p

Presence of polyP in human colon cancer.

<p>Confocal microscopy for polyP staining in sections of colonic adenocarcinoma specimens from (A) the main mass and (B) the surgical margin. Blue: PI, Green: JC-D8 polyP-specific fluorescent probe. One representative out of ten independent experiments is shown. Original magnification x600, Scale bar– 5μm.</p

CD68+ mast cells are important sources of polyP in CRC and adenomas with high-grade dysplasia, and are localized next to neutrophils in CRC.

<p>Confocal microscopy for <b>(A)</b> Tryptase / CD68, <b>(B)</b> polyP / NE and <b>(C and D)</b> polyP / CD68 staining in sections of <b>(A and B)</b> colonic adenocarcinoma specimens and adenomas with <b>(C)</b> high- or <b>(D)</b> low-grade dysplasia. Blue: PI, Green: (A) mast cell tryptase or (B and D) JC-D8 polyP-specific fluorescent probe, Red: (A, C and D) CD68 or (B) NE. One representative out of (A and B) ten or (C and D) six independent experiments is shown. Original magnification x600. Scale bar– 5μm. HG–high grade, LG–low grade.</p