by Sfakianakis G. Alexandros
Anapafseos 5,Agios Nikolaos Lasithi Crete 72100 Greece,00302841026182,00306948891480

Παρασκευή, 1 Σεπτεμβρίου 2017

Grafting materials for alveolar cleft reconstruction: a systematic review and best-evidence synthesis

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Publication date: Available online 31 August 2017
Source:International Journal of Oral and Maxillofacial Surgery
Author(s): C. Wu, W. Pan, C. Feng, Z. Su, Z. Duan, Q. Zheng, C. Hua, C. Li
The purpose of this study was to compare the efficacy of alveolar bone reconstruction for alveolar cleft patients performed with the traditional iliac graft or alternative/supplementary bone grafting materials. Electronic databases, relevant journals, and reference lists of the included studies were searched to the end of June 2016. A best-evidence synthesis was performed to draw conclusions. A total of 38 studies were included, which provided 25 pieces of evidence: seven of moderate evidence and 18 of insufficient evidence. The seven pieces of moderate evidence indicated that (1) bone morphogenetic protein 2 bound to absorbable collagen sponge shares similar cleft repair efficacy to the iliac graft; (2) covering the iliac graft with an acellular dermis matrix membrane may increase bone retention for unilateral cleft patients; (3) mixing iliac graft with platelet-rich plasma may increase bone retention for skeletally mature patients, but (4) does not achieve the same result for younger patients; and compared with the iliac graft, (5) the mandible graft is more effective, whereas (6) the cranium graft and (7) rib graft are less effective for alveolar cleft reconstruction. The efficacy of the remaining grafting materials was supported by insufficient evidence. More well-designed controlled studies are needed to ascertain the long-term clinical results of alveolar cleft reconstruction.



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Venous Diverticula Causing Pulsatile Tinnitus Treated With Coil Embolization and Stent Placement With Resolution of Symptoms: Report of Two Cases and Review of the Literature.

Objective: To report two cases of pulsatile tinnitus caused by complex venous diverticula with successful treatment via coil embolization and stent placement followed by complete resolution of symptoms. We also review the literature pertaining to venous diverticula causing pulsatile tinnitus treated using endovascular techniques. Patients: Two women patients, aged 27 and 29 years, presented to our institution with 3-month histories of pulsatile tinnitus. In each case, non-invasive imaging and conventional digital subtraction angiography (DSA) confirmed the presence of a complex right transverse-sigmoid sinus junction diverticulum. Intervention: Both patients underwent stent-assisted coil embolization of the venous diverticula. Main Outcome and Results: Clinical and DSA follow-up at 6 and 12 months confirmed resolution of symptoms with obliteration of the venous diverticulum. We also performed a PubMed database search for the period January 1995 through June 2016 using the terms pulsatile tinnitus, venous aneurysm/diverticulum, stent-assisted coil embolization, and endovascular treatment and identified reports of 14 additional patients treated using endovascular techniques. Conclusions: Venous sinus diverticula causing pulsatile tinnitus can be successfully treated with stent-assisted coil embolization with complete resolution of clinical symptoms. This is in concordance with 13 case reports in the literature involving 14 patients with venous sinus diverticula treated using endovascular techniques. Copyright (C) 2017 by Otology & Neurotology, Inc. Image copyright (C) 2010 Wolters Kluwer Health/Anatomical Chart Company

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Venous Diverticula Causing Pulsatile Tinnitus Treated With Coil Embolization and Stent Placement With Resolution of Symptoms: Report of Two Cases and Review of the Literature.

Objective: To report two cases of pulsatile tinnitus caused by complex venous diverticula with successful treatment via coil embolization and stent placement followed by complete resolution of symptoms. We also review the literature pertaining to venous diverticula causing pulsatile tinnitus treated using endovascular techniques. Patients: Two women patients, aged 27 and 29 years, presented to our institution with 3-month histories of pulsatile tinnitus. In each case, non-invasive imaging and conventional digital subtraction angiography (DSA) confirmed the presence of a complex right transverse-sigmoid sinus junction diverticulum. Intervention: Both patients underwent stent-assisted coil embolization of the venous diverticula. Main Outcome and Results: Clinical and DSA follow-up at 6 and 12 months confirmed resolution of symptoms with obliteration of the venous diverticulum. We also performed a PubMed database search for the period January 1995 through June 2016 using the terms pulsatile tinnitus, venous aneurysm/diverticulum, stent-assisted coil embolization, and endovascular treatment and identified reports of 14 additional patients treated using endovascular techniques. Conclusions: Venous sinus diverticula causing pulsatile tinnitus can be successfully treated with stent-assisted coil embolization with complete resolution of clinical symptoms. This is in concordance with 13 case reports in the literature involving 14 patients with venous sinus diverticula treated using endovascular techniques. Copyright (C) 2017 by Otology & Neurotology, Inc. Image copyright (C) 2010 Wolters Kluwer Health/Anatomical Chart Company

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Abnormalities of T cell receptor repertoire in CD4+ regulatory and conventional T cells in patients with RAG mutations: implications for autoimmunity

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Publication date: Available online 31 August 2017
Source:Journal of Allergy and Clinical Immunology
Author(s): Jared H. Rowe, Brian D. Stadinski, Lauren A. Henderson, Lisa Ott de Bruin, Ottavia Delmonte, Yu Nee Lee, M. Teresa de la Morena, Rakesh K. Goyal, Anthony Hayward, Huang Chiung-Hui, Maria Kanariou, Alejandra King, Taco W. Kuijpers, Jian Yi Soh, Benedicte Neven, Jolan E. Walter, Eric S. Huseby, Luigi D. Notarangelo




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Abnormalities of T cell receptor repertoire in CD4+ regulatory and conventional T cells in patients with RAG mutations: implications for autoimmunity

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Publication date: Available online 31 August 2017
Source:Journal of Allergy and Clinical Immunology
Author(s): Jared H. Rowe, Brian D. Stadinski, Lauren A. Henderson, Lisa Ott de Bruin, Ottavia Delmonte, Yu Nee Lee, M. Teresa de la Morena, Rakesh K. Goyal, Anthony Hayward, Huang Chiung-Hui, Maria Kanariou, Alejandra King, Taco W. Kuijpers, Jian Yi Soh, Benedicte Neven, Jolan E. Walter, Eric S. Huseby, Luigi D. Notarangelo




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Πέμπτη, 31 Αυγούστου 2017

Quaking RNA-Binding Proteins Control Early Myofibril Formation by Modulating Tropomyosin

Publication date: Available online 31 August 2017
Source:Developmental Cell
Author(s): Aline Bonnet, Guillaume Lambert, Sylvain Ernest, François Xavier Dutrieux, Fanny Coulpier, Sophie Lemoine, Riadh Lobbardi, Frédéric Marc Rosa
Skeletal muscle contraction is mediated by myofibrils, complex multi-molecular scaffolds structured into repeated units, the sarcomeres. Myofibril structure and function have been extensively studied, but the molecular processes regulating its formation within the differentiating muscle cell remain largely unknown. Here we show in zebrafish that genetic interference with the Quaking RNA-binding proteins disrupts the initial steps of myofibril assembly without affecting early muscle differentiation. Using RNA sequencing, we demonstrate that Quaking is required for accumulation of the muscle-specific tropomyosin-3 transcript, tpm3.12. Further functional analyses reveal that Tpm3.12 mediates Quaking control of myofibril formation. Moreover, we identified a Quaking-binding site in the 3′ UTR of tpm3.12 transcript, which is required in vivo for tpm3.12 accumulation and myofibril formation. Our work uncovers a Quaking/Tpm3 pathway controlling de novo myofibril assembly. This unexpected developmental role for Tpm3 could be at the origin of muscle defects observed in human congenital myopathies associated with tpm3 mutation.

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Teaser

Bonnet et al. explore how de novo myofibril formation is regulated within the differentiating muscle cell. In zebrafish, they identify Quaking RNA-binding proteins and tropomyosin-3 as essential regulators. Quaking controls early steps of myofibril assembly by promoting tropomyosin-3 transcript accumulation, through physical interaction with its 3′ UTR.


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Arp2/3 Complex Is Required for Macrophage Integrin Functions but Is Dispensable for FcR Phagocytosis and In Vivo Motility

Publication date: Available online 31 August 2017
Source:Developmental Cell
Author(s): Jeremy D. Rotty, Hailey E. Brighton, Stephanie L. Craig, Sreeja B. Asokan, Ning Cheng, Jenny P. Ting, James E. Bear
The Arp2/3 complex nucleates branched actin, forming networks involved in lamellipodial protrusion, phagocytosis, and cell adhesion. We derived primary bone marrow macrophages lacking Arp2/3 complex (Arpc2−/−) and directly tested its role in macrophage functions. Despite protrusion and actin assembly defects, Arpc2−/− macrophages competently phagocytose via FcR and chemotax toward CSF and CX3CL1. However, CR3 phagocytosis and fibronectin haptotaxis, both integrin-dependent processes, are disrupted. Integrin-responsive actin assembly and αM/β2 integrin localization are compromised in Arpc2−/− cells. Using an in vivo system to observe endogenous monocytes migrating toward full-thickness ear wounds we found that Arpc2−/− monocytes maintain cell speeds and directionality similar to control. Our work reveals that the Arp2/3 complex is not a general requirement for phagocytosis or chemotaxis but is a critical driver of integrin-dependent processes. We demonstrate further that cells lacking Arp2/3 complex function in vivo remain capable of executing important physiological responses that require rapid directional motility.

Graphical abstract

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Teaser

Using a combination of cell culture-based and in vivo mouse experiments, Rotty et al. demonstrate that the actin-nucleating Arp2/3 complex is not absolutely required for macrophage FcR phagocytosis, chemotaxis, or in vivo monocyte directional motility. Rather, the complex has a critical role in regulating integrin-dependent macrophage processes.


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