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David Jiang,Robert Weiss,Benjamin Lind,Omar Morcos,Cheong Jun Lee 대한혈관외과학회 2024 Vascular Specialist International Vol.40 No.2
Purpose: This study aims to examine predisposing anatomic factors and subsequent post-decompression functional outcomes among high-intensity athletes with thoracic outlet syndrome (TOS). Materials and Methods: A single-institution retrospective review was performed on a prospective database of patients with TOS from 2018 to 2023 who had undergone operative decompression for TOS. Demographics, TOS characteristics, predisposing anatomy, operative details, and postoperative outcomes were examined. The primary outcome was postoperative return to sport. Secondary outcomes included vascular patency. Results: A total of 13 patients who were engaged in high-demand athletic activity at the time of their diagnosis were included. Diagnoses included 8 (62%) patients with venous TOS, 4 (31%) patients with neurogenic TOS, and 1 (8%) patient with arterial TOS. Mixed vascular and neurogenic TOS was observed in 3 (23%) patients. The mean age of the cohort was 30 years. Abnormal scalene structure was observed in 12 (92%) patients, and abnormal bone structures were noted in 4 (27%) patients; 2 (15%) with cervical ribs and 3 (23%) patients with clavicular abnormalities. Prior ipsilateral upper extremity trauma was reported in 4 (27%) patients. Significant joint hypermobility was observed in 8 (62%) patients with a median Beighton score of 6. Supraclavicular cervical and/or first rib resection with scalenectomy was performed in all patients. One case of postoperative pneumothorax was treated non-operatively. Ten (77%) patients returned to sport. Duplex ultrasonography showed subclavian vein patency in all 8 patients with venous TOS and wide patency with no drop in perfusion indices in the patient with arterial TOS. Conclusion: Athletes with TOS who required operative intervention had a high incidence of musculoskeletal aberrations and joint hypermobility. Supraclavicular decompression was associated with a high success rate, with overall good functional outcomes and good likelihood of patients returning to preoperative high-intensity athletics.
Yang, Kun,Park, Chae G,Cheong, Cheolho,Bulgheresi, Silvia,Zhang, Shusheng,Zhang, Pei,He, Yingxia,Jiang, Lingyu,Huang, Hongping,Ding, Honghui,Wu, Yiping,Wang, Shaogang,Zhang, Lin,Li, Anyi,Xia, Lianxu,B Nature Publishing Group 2015 Immunology and Cell Biology Vol. No.
<P><I>Yersinia pestis</I> is a Gram‐negative bacterium that causes plague. After <I>Y. pestis</I> overcomes the skin barrier, it encounters antigen‐presenting cells (APCs), such as Langerhans and dendritic cells. They transport the bacteria from the skin to the lymph nodes. However, the molecular mechanisms involved in bacterial transmission are unclear. Langerhans cells (LCs) express Langerin (CD207), a calcium‐dependent (C‐type) lectin. Furthermore, <I>Y. pestis</I> possesses exposed core oligosaccharides. In this study, we show that <I>Y. pestis</I> invades LCs and Langerin‐expressing transfectants. However, when the bacterial core oligosaccharides are shielded or truncated, <I>Y. pestis</I> propensity to invade Langerhans and Langerin‐expressing cells decreases. Moreover, the interaction of <I>Y. pestis</I> with Langerin‐expressing transfectants is inhibited by purified Langerin, a DC‐SIGN (DC‐specific intercellular adhesion molecule 3 grabbing nonintegrin)‐like molecule, an anti‐CD207 antibody, purified core oligosaccharides and several oligosaccharides. Furthermore, covering core oligosaccharides reduces the mortality associated with murine infection by adversely affecting the transmission of <I>Y. pestis</I> to lymph nodes. These results demonstrate that direct interaction of core oligosaccharides with Langerin facilitates the invasion of LCs by <I>Y. pestis</I>. Therefore, Langerin‐mediated binding of <I>Y. pestis</I> to APCs may promote its dissemination and infection.</P>