Relationship between nonalcoholic fatty liver disease and chronic kidney disease could start in childhood

The relationship between nonalcoholic fatty liver disease (NAFLD) and chronic kidney disease (CKD) has gained considerable scientific interest in adults over the past few years. However, this association has recently emerged in children. Several published studies have suggested a role for NAFLD as a risk factor for CKD from the earliest age, with a potential influence of the major NAFLD risk polymorphisms, resulting in an increased risk of both cardiovascular and metabolic diseases. In view of the progressive course and increased cardiometabolic risk closely related to NAFLD and CKD, we focused on the link between these diseases in childhood.     

Aetiology of Legg-Calvé-Perthes disease:A systematic review

BACKGROUND Legg-Calvé-Perthes disease(LCPD) is a clinical condition affecting the femoral head of children during their growth. Its prevalence is set to be between 0.4/100000 to 29.0/100000 children less than 15 years of age with a peak of incidence in children aged from 4 years to 8 years. LCPD aetiology has been widely studied, but it is still poorly understood.AIM To analyse the available literature to document the up-to-date evidence on LCPD aetiology.METHODS A systematic review of the literature was performed regarding LCPD aetiology,using the following inclusion criteria: studies of any level of evidence, reporting clinical or preclinical results and dealing with the aetiology or pathogenesis of LCPD. Two reviewers searched the PubMed and Science Direct databases from their date of inception to the 20th of May 2018 in accordance with the Preferred Reporting Items for Systemic Reviews and Meta-Analyses guidelines. To achieve the maximum sensitivity of the search strategy, we combined the terms: ‘‘Perthes disease OR LCPD OR children avascular femoral head necrosis" with "pathology OR aetiology OR biomechanics OR genetics" as either key words or MeSH terms.RESULTS We include 64 articles in this review. The available evidence on LCPD aetiology is still debated. Several hypotheses have been researched, but none of them was found decisive. While emerging evidence showed the role of environmental risk factors and evidence from twin studies did not support a major role for genetic factors, a congenital or acquired predisposition cannot be excluded in disease pathogenesis. One of the most supported theories involved mechanical induced ischemia that evolved into avascular necrosis of the femoral head in sensible patients.CONCLUSION The literature available on the aetiology of LCPD presents major limitations in terms of great heterogeneity and a lack of high-profile studies. Although a lot of studies focused on the genetic, biomechanical and radiological background of the disease, there is a lack of consensus on one or multiple major actors of the etiopathogenesis. More studies are needed to understand the complex and multifactorial genesis of the avascular necrosis characterizing the disease.     

Serum osteocalcin and parathyroid hormone in healthy children assessed with two new automated assays

BACKGROUND: The recent introduction of new automated assays needs careful definition of reference values in healthy children. The aim of this study was to determine serum parathyroid hormone (PTH) and osteocalcin in a large group of healthy children according to age. METHODS: We selected 2,288 healthy children (1,079 girls, 1,209 boys), aged 2-16 years. Serum PTH and osteocalcin were assayed with a two-site immunochemiluminometric assay adapted on an automated analyzer, the Liaison. RESULTS: Significant differences were found between the mean serum values of PTH and osteocalcin in boys and girls in all age groups (p <0.001). Boys' and girls' PTH values ranged from 3.42-22.30 ng/l and 2.31-24.49 ng/l, respectively; serum osteocalcin ranged from 3.85-17.80 nmol/l in boys and 3.74-17.38 nmol/l in girls. CONCLUSIONS: The results of this study contribute to the establishment of reference values in healthy children for PTH and osteocalcin assays.     

Retracted: Inhibition of non‐neuronal α7‐nicotinic receptor reduces tumorigenicity in A549 NSCLC xenografts

Retraction: The following article from International Journal of Cancer, "Inhibition of non‐neuronal α7‐nicotinic receptor reduces tumorigenicity in A549 NSCLC xenografts", by Laura Paleari, Fausto Sessa, Alessia Catassi, Denis Servent, Gilles Mourier, Guido Doria‐Miglietta, Emanuela Ognio, Michele Cilli, Lorenzo Dominioni, Massimo Paolucci, Andrea Calcaterra, Alfredo Cesario, Stefano Margaritora, Pierluigi Granone and Patrizia Russo, published online in Wiley InterScience (http://www3.interscience.wiley.com) on 22 January 2009, Volume 125, Issue 1, pages 199‐211, has been retracted by agreement between the authors, the journal Editor in Chief, Peter Lichter, and Wiley Periodicals, Inc. The retraction has been agreed due to unverified data.     

Hyperbaric oxygen therapy prevents coagulation disorders in an experimental model of multiple organ failure syndrome

Objective To evaluate the effects of hyperbaric oxygen (HBO) therapy on the coagulation cascade using an experimental model of multiple organ failure syndrome (MOFS).Design MOFS was induced by zymosan (500 mg/kg i. p.) in rats. HBO therapy (2 ATA) was administered in a cylindrical steel chamber 4 and 11 h after zymosan administration. In a separate set of experiments animals were monitored for 72 h, and systemic toxicity was scored.Intervention Eighteen hours after zymosan administration, rats were killed and blood samples were used for analysis of hemocoagulative parameters, hemodynamics, and arterial blood gas.Main results Zymosan administration caused MOFS by affecting the coagulation cascade, as shown by a significant increase in plasma levels of fibrinogen, tissue plasminogen activator, inhibitor of tissue plasminogen activator of type 1, and plasma levels of fibrin degradation products vs. control rats. Zymosan-induced MOFS was also characterized by a significant increase in von Willebrand antigen plasma levels vs. controls. Moreover, zymosan administration induced a significant fall in mean arterial blood pressure and alteration in blood gas values. HBO therapy significantly reduced the derangements of coagulation cascade, the fall in mean blood pressure and alteration in blood gas induced by zymosan administration.Conclusions The hypercoagulability induced by zymosan could be responsible for organ failure and death. Our data demonstrate that HBO therapy significantly prevents the alteration in the coagulation cascade and arterial blood gas in an experimental model of MOFS.This article is discussed in the editorial available at:.     

Identification of a receptor necessary for Nogo-B stimulated chemotaxis and morphogenesis of endothelial cells

Nogo isoforms (Nogo-A and -B) have been implicated in regulating neural and cardiovascular functions, such as cell spreading and chemotaxis. Unlike the loop domain (Nogo-66) found in all Nogo isoforms that can interact with a neural-specific Nogo-66 receptor, the receptor for the amino terminus of Nogo-B that mediates vascular function is unknown. Here, we identify a previously uncharacterized Nogo-B receptor specific for the amino terminus of Nogo-B and show that Nogo-B receptor localizes with the ligand Nogo-B during VEGF and wound healing angiogenesis in vivo, mediates chemotaxis in a heterologous expression system and chemotaxis, and 3D tube formation in native endothelial cells. Thus, identification of this receptor may lead to the discovery of agonists or antagonists of this pathway to regulate vascular remodeling and angiogenesis.