Early inhalant allergen sensitization at component level: an analysis in atopic Dutch children.

Background: Allergic rhinitis is a common respiratory disease in children and sensitization to inhalant allergens plays a significant role in its development. However, limited knowledge exists regarding sensitization profiles of inhalant allergen components in atopic children, particularly in the very young individuals. Understanding these profiles could provide insights into the early development of allergic rhinitis.

Tolerance Induction in Cow's Milk Allergic Children by Heated Cow's Milk Protein: The iAGE Follow-Up Study.

Accelerating the induction of tolerance to cow's milk (CM) reduces the burden of cow's milk allergy (CMA). In this randomised controlled intervention study, we aimed to investigate the tolerance induction of a novel heated cow milk protein, the iAGE product, in 18 children with CMA (diagnosed by a paedriatric allergist). Children who tolerated the iAGE product were included.

ALEX versus ISAC multiplex array in analyzing food allergy in atopic children.

ALEX multiplex array is a relatively new multiplex allergy test which analyses more than 120 allergen extracts and 170 molecular components. ISAC is the most used and studied multiplex array to date, offering 112 molecular components. In ten atopic children with multiple food allergies good agreement was observed between ALEX and ISAC sIgE results for nearly all shared food components.

Introduction of Heated Cow's Milk Protein in Challenge-Proven Cow's Milk Allergic Children: The iAGE Study.

The introduction of baked milk products in cow's milk (CM) allergic children has previously been shown to accelerate induction tolerance in a selected group of children. However, there is no standardized baked milk product on the market. Recently, a new standardized, heated and glycated cow's milk protein (HP) product was developed.

Improving Successful Introduction after a Negative Food Challenge Test: How to Achieve the Best Result?

Oral food challenges (OFC) confirm or exclude the presence of a food allergy. The outcome can be positive (allergic symptoms), inconclusive, or negative (no symptoms). In the case of a negative OFC, parents and children are advised to introduce the challenged food allergen into their diet.

Food Allergy and Asthma: Is There a Link?

Purpose Of Review: To describe and understand the links and interactions between food allergy and asthma.

Recent Findings: Food allergy and asthma are characterized by an increasing prevalence. Moreover, food allergy and asthma often coexist.

Small percentage of anaphylactic reactions treated with epinephrine during food challenges in Dutch children.

Background: Severe allergic reactions, including anaphylaxis, occur during oral food challenges (OFCs) and the first-line treatment of anaphylaxis is epinephrine.

Objective: To evaluate the percentage of anaphylactic reactions treated with epinephrine during OFCs and to identify associated factors for the administration of epinephrine.

Methods: Children who underwent an OFC with peanut, hazelnut, cow's milk, hen's egg, or cashew nut from 2005 through 2015 in the Netherlands were evaluated.

Ovarian insufficiency and pubertal development after hematopoietic stem cell transplantation in childhood.

Background: Ovarian insufficiency (OI) and infertility are common and devastating late effects of cancer treatment and hematopoietic stem cell transplantation (HSCT). In children, gonadal insufficiency may subsequently lead to abnormal pubertal development. The aim of this study was to assess the cumulative incidence of OI and the need for hormonal induction of pubertal development after HSCT in childhood.

Fetal mesenchymal stromal cells differentiating towards chondrocytes acquire a gene expression profile resembling human growth plate cartilage.

We used human fetal bone marrow-derived mesenchymal stromal cells (hfMSCs) differentiating towards chondrocytes as an alternative model for the human growth plate (GP). Our aims were to study gene expression patterns associated with chondrogenic differentiation to assess whether chondrocytes derived from hfMSCs are a suitable model for studying the development and maturation of the GP. hfMSCs efficiently formed hyaline cartilage in a pellet culture in the presence of TGFβ3 and BMP6.

Mechanisms of growth plate maturation and epiphyseal fusion.

Longitudinal growth occurs within the long bones at the growth plate. During childhood, the growth plate matures, its total width decreases and eventually it disappears at the end of puberty with complete replacement by bone along with cessation of longitudinal growth. The exact mechanism of epiphyseal fusion is still not completely understood and experimental studies are complicated by the fact that there is a species difference between humans and rabbits that do fuse their growth plates and rodents that do not.

Genome-wide screening in human growth plates during puberty in one patient suggests a role for RUNX2 in epiphyseal maturation.

In late puberty, estrogen decelerates bone growth by stimulating growth plate maturation. In this study, we analyzed the mechanism of estrogen action using two pubertal growth plate specimens of one girl at Tanner stage B2 and Tanner stage B3. Histological analysis showed that progression of puberty coincided with characteristic morphological changes: a decrease in total growth plate height (P=0.

Expression of vascular endothelial growth factor in the growth plate is stimulated by estradiol and increases during pubertal development.

Longitudinal bone growth is regulated in the growth plate. At the end of puberty, growth velocity diminishes and eventually ceases with the fusion of the growth plate through mechanisms that are not yet completely understood. Vascular endothelial growth factor (VEGF) has an important role in angiogenesis, but also in chondrocyte differentiation, chondrocyte survival, and the final stages of endochondral ossification.

Epiphyseal fusion in the human growth plate does not involve classical apoptosis.

By the end of puberty, growth ceases and epiphyseal fusion occurs through mechanisms not yet completely understood. Human growth plate tissues were collected in various pubertal stages including a unique late pubertal growth plate, which was about to fuse. Apoptosis was studied by TUNEL staining, immunolocalization of pro- and antiapoptotic proteins, and electron microscopy (EM).

Catch-up growth after hypothyroidism is caused by delayed growth plate senescence.

Catch-up growth is defined as a linear growth rate greater than expected for age after a period of growth inhibition. We hypothesized that catch-up growth occurs because growth-inhibiting conditions conserve the limited proliferative capacity of growth plate chondrocytes, thus slowing the normal process of growth plate senescence. When the growth-inhibiting condition resolves, the growth plates are less senescent and therefore grow more rapidly than normal for age.

BNP is a transcriptional target of the short stature homeobox gene SHOX.

Short stature due to SHOX deficiency represents a common congenital form of growth failure and is involved in the aetiology of 'idiopathic' short stature and the growth deficits and skeletal anomalies in Leri-Weill, Langer and Turner syndromes. Although much is known on the clinical and molecular aspects of SHOX haploinsufficiency, the integration of SHOX in the signalling pathways regulating bone growth is currently not defined. Here we identify NPPB encoding the natriuretic peptide, BNP, a well-known cardiac and natriuretic peptide hormone, as a transcriptional target of SHOX.

The role of p27Kip1 in the regulation of growth plate chondrocyte proliferation in mice.

p27/Kip1, a cyclin-dependent kinase inhibitor, negatively regulates proliferation of multiple cell types. The goal of this study was to assess the role of p27 in the spatial, temporal, and conditional regulation of growth plate chondrocyte proliferation. p27 mRNA expression was detected by real-time RT-PCR in all zones of the mouse growth plate at levels approximately 2-fold lower than in the surrounding bone.

Depletion of resting zone chondrocytes during growth plate senescence.

With age, the growth plate undergoes senescent changes that cause linear bone growth to slow and finally cease. Based on previous indirect evidence, we hypothesized that this senescent decline occurs because growth plate stem-like cells, located in the resting zone, have a finite proliferative capacity that is gradually depleted. Consistent with this hypothesis, we found that the proliferation rate in rabbit resting zone chondrocytes (assessed by continuous 5-bromo-2'-deoxy-uridine labeling) decreases with age, as does the number of resting zone chondrocytes per area of growth plate.