Portuguese highlight rapid clinical progress of pelvic MRI

When integrated with prior clinical evaluation and exclusion of organic disease,...

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Swiss give new advice on MRI technique for female pelvis

Consensus grows for switch from fluoroscopy to MRI in pelvic floor imaging

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WNT4 Acts Downstream of BMP2 to Mediate the Regulation of ATRA Signaling on RUNX1 Expression: Implications for Terminal Differentiation of Antler Chondrocytes

Abstract

Although ATRA is involved in regulating the proliferation and differentiation of chondrocytes, its underlying mechanism remains unknown. Here we showed that ATRA could stimulate the proliferation of antler chondrocytes and expression of COL X and MMP13 which were two well-known markers for hypertrophic chondrocytes. Silencing of CRABP2 prevented the induction of ATRA on chondrocyte terminal differentiation, while overexpression of CRABP2 exhibited the opposite effects. CYP26A1 and CYP26B1 weakened the sensitivity of antler chondrocytes to ATRA. Further analysis evidenced that ATRA might induce chondrocyte terminal differentiation and modulate the expression of BMP2, WNT4 and RUNX1 through RARα/RXRα. Knockdown of BMP2 enhanced the induction of ATRA on the expression of COL X and MMP13, whereas overexpression of BMP2 abrogated this effectiveness. WNT4 might mediate the effects of ATRA and BMP2 on chondrocyte terminal differentiation. Dysregulation of BMP2 impaired the regulation of ATRA on WNT4 expression. Administration of ATRA to antler chondrocytes transfected with RUNX1 siRNA failed to induce the differentiation. Conversely, rRUNX1 strengthened the stimulation of ATRA on the expression of COL X and MMP13. Simultaneously, RUNX1 was a downstream effector of BMP2 and WNT4 in chondrocyte terminal differentiation. Moreover, WNT4 might play an important role in the crosstalk between BMP2 and RUNX1. Attenuation of BMP2 or WNT4 enhanced the interaction between ATRA and RUNX1, while constitutive expression of BMP2 or WNT4 reversed the regulation of ATRA on RUNX1. Collectively, WNT4 may act downstream of BMP2 to mediate the effects of ATRA on the terminal differentiation of antler chondrocytes through targeting RUNX1. This article is protected by copyright. All rights reserved

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Nap Counteracts Hyperglycemia/Hypoxia Induced Retinal Pigment Epithelial Barrier Breakdown Through Modulation Of HIFs and VEGF Expression

Abstract

Diabetic macular edema (DME) is a common complication leading to a central vision loss in patients with diabetes. In this eye pathology, the hyperglycaemic/hypoxic microenvironment of pigmented epithelium is responsible for outer blood retinal barrier integrity changes.

More recently, we have shown that a small peptide derived from the activity-dependent neuroprotective protein (ADNP), known as NAP, counteracts damages occurring during progression of diabetic retinopathy by modulating HIFs/VEGF pathway. Here, we have investigated for the first time the role of this peptide on outer blood retinal barrier (BRB) integrity exposed to hyperglycaemic/hypoxic insult mimicking a model in vitro of DME. To characterize NAP role on disease's pathogenesis, we have analysed its effect on HIFs /VEGF system in human retinal pigmented epithelial cells, ARPE-19, grown in high glucose and low oxygen tension. The results have shown that NAP prevents outer BRB breakdown by reducing HIF1α /HIF2α, VEGF/VEGFRs and increasing HIF3 α expression, moreover it is able to reduce the percentage of apoptotic cells by modulating the expression of two death related genes, BAX and Bcl2. Further investigations are needed to determine the possible use of NAP in DME treatment. This article is protected by copyright. All rights reserved

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One Simple But Effective Action You Can Take for American Science - Today

The March for Science is over, but the fight for science is just getting started.

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Editorial Board Page

Publication date: May 2017
Source:Journal of Oral and Maxillofacial Surgery, Volume 75, Issue 5





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Vascularized Fascia Lata for Prevention of Postoperative Parotid Fistula Arising From Partial Parotidectomy During Neck Dissection

Publication date: May 2017
Source:Journal of Oral and Maxillofacial Surgery, Volume 75, Issue 5
Author(s): Lijuan Zeng, Canhua Jiang, Ning Li, Wen Liu, Fei Wang, Feng Guo
PurposePostoperative parotid fistula can occur after partial parotidectomy, which is a routine surgical procedure during neck dissection of oral cancers arising from or close to the oropharyngeal area. The aim of this study was to evaluate the reliability of vascularized fascia lata for the prevention of postoperative parotid fistula after neck dissection.Materials and MethodsA retrospective review was conducted of patients with oral cancer who underwent ablative resection involving the parotid tail and reconstruction using the anterolateral thigh (ALT) flap with a vascularized fascia lata paddle. The vascularized fascia lata paddle was used to seal off the parotid stump by tightly suturing the edges of the fascia lata and parotid wound together.ResultsTwenty-three patients (18 men and 5 women) with primary oral cancer arising from or close to the oropharyngeal area were enrolled. The mean area of parotid defect was 16.7 cm² and the mean area of fascia lata harvested was 21.8 cm². All flaps survived. Pressure dressing or anticholinergic drugs were not used in any case. During the follow-up period, there was no clinical evidence of the development of parotid fistula.ConclusionThe vascularized fascia lata paddle is a reliable option for the prevention of postoperative parotid fistula after neck dissection of oral cancer.



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Table of Contents

Publication date: May 2017
Source:Journal of Oral and Maxillofacial Surgery, Volume 75, Issue 5





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