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あぁかがさざただなはばぱまやゃらわゎんいぃきぎしじちぢにひびぴみりうぅくぐすずつづっぬふぶぷむゆゅるえぇけげせぜてでねへべぺめれおぉこごそぞとどのほぼぽもよょろを

アァカサザタダナハバパマヤャラワヮンイィキギシジチヂニヒビピミリウゥクグスズツヅッヌフブプムユュルエェケゲセゼテデヘベペメレオォコゴソゾトドノホボポモヨョロヲ ―

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á à Á À é è É È ç Ç ê

Ä Ö Ü ä ö ü ß

ְ ֳ ֲ ֱ ָ ַ ֵ ֶ ִ ֹ ּ ֻ ׂ ׁ ּ פ ם ן ו ט א ר ק ף ך ל ח י ע כ ג ד ש ץ ת צ מ נ ה ב

‘ ’ “ ” 〔〕〈〉「」『』【】＂（）［］｛｝

± × ÷ ≠ ≤ ≥ ∞ ∴ ♂ ♀ ∠ ⊥ ⌒ ∂ ∇ ≡ ≒ ≪ ≫ √ ∽ ∝ ∵ ∫ ∬ ∈ ∋ ⊆ ⊇ ⊂ ⊃ ∪ ∩ ∧ ∨ ￢ ⇒ ⇔ ∀ ∃ ∮ ∑ ∏ ＋－＜＝＞

、。 · ‥ … ¨ 〃 ― ∥ ＼ ∼ ´ ～ ˇ ˘ ˝ ˚ ˙ ¸ ˛ ¡ ¿ ː ！＇，．／：；？＾＿｀｜

½ ⅓ ⅔ ¼ ¾ ⅛ ⅜ ⅝ ⅞ ¹ ² ³ ⁴ ⁿ ₁ ₂ ₃ ₄

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′ ″ ℃ Å ￠￡￥ ¤ ℉ ‰ ＄％Ｆ￦㎕㎖㎗ ℓ ㎘㏄㎣㎤㎥㎦㎙㎚㎛㎜㎝㎞㎟㎠㎡㎢㏊㎍㎎㎏㏏㎈㎉㏈㎧㎨㎰㎱㎲㎳㎴㎵㎶㎷㎸㎹㎀㎁㎂㎃㎄㎺㎻㎽㎾㎿㎐㎑㎒㎓㎔ Ω ㏀㏁㎊㎋㎌㏖㏅㎭㎮㎯㏛㎩㎪㎫㎬㏝㏐㏓㏃㏉㏜㏆

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ⅰ ⅱ ⅲ ⅳ ⅴ ⅵ ⅶ ⅷ ⅸ ⅹ Ⅰ Ⅱ Ⅲ Ⅳ Ⅴ Ⅵ Ⅶ Ⅷ Ⅸ Ⅹ

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1
Identification of Medium-Length Antineurofilament Autoantibodies in Patients with Anti-N-Methyl-D-Aspartate Receptor Encephalitis

Shisi Wang,Cancan Xu,Xiaobo Sun,Yifan Zhou,Yaqing Shu,Shangzhou Xia,Zhengqi Lu,Wei Qiu,Xiaofen Zhong,Lisheng Peng 대한신경과학회 2020 Journal of Clinical Neurology Vol.16 No.3
- 원문보기
Background and Purpose Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is a severe central nervous system disorder mediated by NMDAR antibodies that damages neurons. We investigated the correlation between cytoskeletal autoantibodies and the clinical severity in patients with anti-NMDAR encephalitis. Methods Non-NMDAR autoantibodies were identified by screening matched cerebrospinal fluid (CSF) and the serum samples of 45 consecutive patients with anti-NMDAR encephalitis and 60 healthy individuals against N-methyl-D-aspartate receptor 1-transfected and nontransfected human embryonic kidney 293T cells. Immunocytochemistry was performed to assess antibody binding in rat brain sections and primary cortical neurons. Cell-based assays and Western blotting were applied to identify autoantibodies targeting medium neurofilaments (NFMs). We compared clinical characteristics between patients with NMDAR encephalitis who were positive and negative for anti-NFM-autoantibodies. Results Anti-NFM autoantibodies were detected in both the serum and CSF in one patient (2%) and in the serum only in six patients (13%). No antibodies were detected in the serum of healthy controls (7/45 vs. 0/60, p=0.0016). Four of the seven patients with anti-NFM autoantibodies in serum were children (57%), and three (43%) had abnormalities in brain magnetic resonance imaging. These patients responded well to immunotherapy, and either no significant or only mild disability was observed at the last follow-up. Anti-NMDAR encephalitis did not differ with the presence of anti-NFM autoantibodies. Conclusions Anti-NFM autoantibodies may be present in patients with anti-NMDAR encephalitis, indicating underlying neuronal damage. A large cohort study is warranted to investigate the clinical differences between patients with NMDAR encephalitis according to their anti- NFM antibody status.
2
Activating SIRT3 in peritoneal mesothelial cells alleviates postsurgical peritoneal adhesion formation by decreasing oxidative stress and inhibiting the NLRP3 inflammasome

Shen Tianli,Wu Yunhua,Wang Xingjie,Wang Zijun,Li Enmeng,Zhou Cancan,Yue Chenyang,Jiang Zhengdong,Wei Guangbing,Lian Jie,Xu Qinhong,Li Xuqi 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
- 원문보기
Peritoneal adhesions (PAs) are a serious complication of abdominal surgery and negatively affect the quality of life of millions of people worldwide. However, a clear molecular mechanism and a standard therapeutic strategy for PAs have not been established. Here, we developed a standardized method to mimic the pathological changes in PAs and found that sirtuin 3 (SIRT3) expression was severely decreased in adhesion tissues, which was consistent with our bioinformatics analysis and patient adhesion tissue analysis. Thus, we hypothesized that activating SIRT3 could alleviate postsurgical PAs. Sirt3-deficient (Sirt3−/−) mice exhibited many more PAs after standardized abdominal surgery. Furthermore, compared with wild-type (Sirt3+/+) mice, Sirt3-deficient (Sirt3−/−) mice showed more prominent reactive oxygen species (ROS) accumulation, increased levels of inflammatory factors, and exacerbated mitochondrial damage and fragmentation. In addition, we observed NLRP3 inflammasome activation in the adhesion tissues of Sirt3−/− but, not Sirt3+/+ mice. Furthermore, mesothelial cells sorted from Sirt3−/− mice exhibited impaired mitochondrial bioenergetics and redox homeostasis. Honokiol (HKL), a natural compound found in several species of the genus Magnolia, could activate SIRT3 in vitro. Then, we demonstrated that treatment with HKL could reduce oxidative stress and the levels of inflammatory factors and suppress NLRP3 activation in vivo, reducing the occurrence of postsurgical PAs. In vitro treatment with HKL also restored mitochondrial bioenergetics and promoted mesothelial cell viability under oxidative stress conditions. Taken together, our findings show that the rescue of SIRT3 by HKL may be a new therapeutic strategy to alleviate and block postsurgical PA formation.