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Conservative Treatment of Thoracic Outlet Syndrome: A Narrative Review
SuYeon Kwon,Seoyon Yang 대한통증연구학회 2022 International Journal of Pain Vol.13 No.2
Thoracic outlet syndrome (TOS) refers to a group of disorders that result in the compression of the brachial plexus and subclavian axillary vessels in the area of the thoracic outlet. Patients with TOS can experience various symptoms, such as neuropathic pain, paresthesia, numbness, and weakness. There is no definite consensus on the appropriate treatment method for TOS, and the treatment usually varies depending on the type of TOS. For patients with venous or arterial TOS, thrombolysis or embolectomy is usually considered first; however, when they do not respond to these treatments, surgical treatments are indicated. Patients with neurogenic TOS are typically treated conservatively. Conservative treatment, including oral medications, injections, rehabilitation therapy, activity modification, and patient education, is used as the initial treatment. This narrative review provides a brief overview of the disease, possible treatments, and exercise protocols to help physicians treat TOS.
Kwon, Hyemi,Jeon, Min Ji,Kim, Won Gu,Park, Suyeon,Kim, Mijin,Song, Dong Eun,Sung, Tae-Yon,Yoon, Jong Ho,Hong, Suck Joon,Kim, Tae Yong,Shong, Young Kee,Kim, Won Bae Bioscientifica 2017 European journal of endocrinology Vol.176 No.4
<B>Objective</B><P>Papillary thyroid microcarcinoma (PTMC) accounts for most of the increase in thyroid cancer in recent decades. We compared clinical outcomes and surgical complications of lobectomy and total thyroidectomy (TT) in PTMC patients.</P><B>Design and methods</B><P>In this retrospective individual risk factor-matched cohort study, 2031 patients with PTMC were initially included. Patients who underwent lobectomy or TT were one-to-one matched according to individual risk factors, including age, sex, primary tumor size, extrathyroidal extension, multifocality and cervical lymph node (LN) metastasis.</P><B>Results</B><P>In total, 688 patients were assigned to each group. During the median 8.5 years of follow-up, 26 patients (3.8%) in the lobectomy group and 11 patients (1.6%) in the TT group had recurrences. The relative risk of recurrence was significantly less in the TT than that in the lobectomy group (hazard ratio (HR) 0.41; 95% confidence interval (CI) 0.21-0.81; <I>P</I> = 0.01). Most recurrences (84.6%) in the lobectomy group occurred in the contralateral lobe, and all patients were disease-free after completion of thyroidectomy. There were no significant differences in recurrence-free survival between the two groups after exclusion of contralateral lobe recurrences (HR, 2.75; 95% CI, 0.08-8.79; <I>P</I> = 0.08). There were significantly more patients with transient and permanent hypoparathyroidism in the TT than that in the lobectomy group (<I>P</I> < 0.001).</P><B>Conclusions</B><P>Lobectomy could be appropriate for most patients with PTMC when there is no evidence of extrathyroidal disease in the preoperative work-up. Preoperative and postoperative imaging studies are important for patients who undergo lobectomy for PTMC, because most recurrences are in the contralateral lobe.</P>
송우근,Suyeon Ahn,Ahreum Kwon,Youngsoo Oh,이상명 한국분자세포생물학회 2023 Molecules and cells Vol.46 No.6
Microtubule acetylation has been proposed as a marker of highly heterogeneous and aggressive triple-negative breast cancer (TNBC). The novel microtubule acetylation inhibitors GM-90257 and GM-90631 (GM compounds) cause TNBC cancer cell death but the underlying mechanisms are currently unknown. In this study, we demonstrated that GM compounds function as anti-TNBC agents through activation of the JNK/AP-1 pathway. RNA-seq and biochemical analyses of GM compound-treated cells revealed that c-Jun N-terminal kinase (JNK) and members of its downstream signaling pathway are potential targets for GM compounds. Mechanistically, JNK activation by GM compounds induced an increase in c-Jun phosphorylation and c-Fos protein levels, thereby activating the activator protein-1 (AP-1) transcription factor. Notably, direct suppression of JNK with a pharmacological inhibitor alleviated Bcl2 reduction and cell death caused by GM compounds. TNBC cell death and mitotic arrest were induced by GM compounds through AP-1 activation in vitro. These results were reproduced in vivo, validating the significance of microtubule acetylation/JNK/AP-1 axis activation in the anti-cancer activity of GM compounds. Moreover, GM compounds significantly attenuated tumor growth, metastasis, and cancer-related death in mice, demonstrating strong potential as therapeutic agents for TNBC.