Search

Objective: To review the literature regarding associations between developmental motor delay (DMD) and pediatric obesity. We hope to identify potential interventions that can improve motor coordination at an early age, thereby minimizing the deterring factors of physical activity down the road., Design: An integrative review was undertaken using search combinations to best identify potential publications. Manuscripts were reviewed, summarized, and discussed in detail. An experienced clinician in pediatric obesity reviewed the final searches for substantive content., Criteria: Inclusion criteria include English language studies or publications, children ≤18 years old, publication/study relates to DMD and pediatric obesity. Excluded publications regarded topics of pediatric obesity that have been extensively studied such as maternal and family histories of obesity, isolated nutritional or physical interventions to improve obesity without discussion of DMD., Results: 21 publications were included for review. Papers fell into three main categories regarding the association between pediatric obesity and DMD: 1) Motor function - negative association with motor function and obesity 2) Motor Development - lower levels of motor function are associated with decreased levels of exercise, and 3) Role of Intervention - specific physical activity intervention showed improvements in motor function., Conclusions: Motor function deficits appear to be associated with obesity. However, it is not well understood if children with obesity have delayed motor skills as a consequence of their weight or if the DMD is a risk factor for the development of obesity; existing studies do not provide an answer., (Copyright © 2020 Asia Oceania Association for the Study of Obesity. Published by Elsevier Ltd. All rights reserved.)

Background: Tympanostomy tube (TT) insertion is a common procedure in children with otitis media with effusion. Post-TT otorrhea (PTTO) is a frequent post-operative complication. Biofilms are involved in chronic PTTO cases., Objective: To describe and qualitatively analyze the geometry and sites prone to biofilms on removed TTs, relatively to their position in the ear, past medical/surgical history and PTTO presence., Methods: Biofilms presence and topographic distribution on TTs were ex vivo evaluated by using scanning electron microscope, confocal microscope and stereo-microscope., Results: Forty-eight TTs from 30 children were analyzed. Indications for removal were: 71% due to retained TTs (average time from insertion: 24.4 ± 15.1 months), 23% due to chronic PTTO, and 6% due to TT obstruction/dysfunction. Different types of bacterial biofilms were detected on all TTs, regardless the time from their insertion nor their types. Biofilms were observed more on the perpendicular junction and on the internal lumen, and more biofilm colonies were detected on the medial part, facing the middle ear mucosa. TTs removed from children with PTTO exhibited more biofilm colonies when compared to their peers. Of the 16 children who underwent adenoidectomy concomitantly with TT insertion, 10 (62%) children were sent for TT removal due to retained TTs, and 6 (38%) children due to chronic PTTO (p = 0.03)., Conclusion: Descriptive analysis of biofilm topographic distribution demonstrated adhesions on specific TT areas: perpendicular junctions and the internal lumen. Such "prone zones" may be the future target areas for changes in TT geometry or can be specifically coated with anti-biofilm materials., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Burning mouth syndrome (BMS) is characterized by a spontaneous and chronic sensation of burning in the oral mucosa, with no apparent signs. The underlying pathophysiological and neuropathic mechanisms remain unclear. Here, we attempt to elucidate some of these mechanisms using proteomic profiling and bioinformatic analyses of whole-saliva (WS) from BMS patients compared to WS from healthy individuals. Qualitative and quantitative proteomic profiling was performed using two dimensional gel electrophoresis (2-DE) and quantitative mass spectrometry (q-MS). In order to improve protein visibility, 21 high abundance proteins were depleted before proteomic profiling. Quantitative proteomic analysis revealed 100 BMS specific proteins and an additional 158 proteins up-regulated by more than threefold in those with BMS. Bioinformatic analyses of the altered protein expression profile of BMS group indicated high correlations to three cellular mechanisms including the neurotrophin signaling pathway. Based on this finding, we suggest that neurotrophin signaling pathway is involved in the pathophysiology of BMS by amplifying P75NTR activity, which in turn increases neural apoptosis thereby reducing sub-papillary nerve fiber density in the oral mucosa.

Salivary glands (SGs) are irreversibly damaged by irradiation (IR) treatment in head and neck cancer patients. Here, we used an animal irradiation model to investigate and define the molecular mechanisms affecting SGs following IR, focusing on saliva proteome and global transcription profile of submandibular salivary gland (SSG) tissue.We show that saliva secretion was gradually reduced to 50% of its initial level 12 weeks post-IR. Saliva protein composition was further examined by proteomic analysis following mass spectrometry (MS) analysis that revealed proteins with reduced expression originating from SSGs and proteins with increased expression derived from the serum, both indicating salivary tissue damage. To examine alterations in mRNA expression levels microarray analysis was performed. We found significant alterations in 95 genes, including cell-cycle arrest genes, SG functional genes and a DNA repair gene.Tissue damage was seen by confocal immunofluorescence of α-amylase and c-Kit that showed an increase and decrease, respectively, in protein expression. This was coherent with real-time PCR results.This data indicates that IR damages the SSG cells' ability to produce and secrete saliva and proteins, and maintain the physiological barrier between serum and saliva. The damage does not heal due to cell-cycle arrest, which prevents tissue regeneration. Taken together, our results reveal a new insight into IR pathobiology.