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        Assessment of Esophageal Motor Disorders Using High-resolution Manometry in Esophageal Dysphagia With Normal Endoscopy

        Dan Wang,Xiu Wang,Yao Yu,Xiaowen Xu,Jing Wang,Yuting Jia,Hong Xu 대한소화기 기능성질환∙운동학회 2019 Journal of Neurogastroenterology and Motility (JNM Vol.25 No.1

        Background/Aims The distribution and esophageal motor characteristics of Chinese patients with esophageal dysphagia who exhibit no structural abnormalities on esophagogastroduodenoscopy remain unclear. Our aim is to assess the esophageal motor patterns using high-resolution manometry (HRM) and classify them according to the Chicago classification version 3.0 (CC v3.0). Furthermore, we compared the CC v3.0 and the previous version 2.0 (CC v2.0) for diagnosis of motor disorders. Methods Two hundred thirty-six (mean age 48.4 ± 12.2 years, 61.9% female) patients with esophageal dysphagia were included for analysis of motor function using HRM. All participants were administered a questionnaire to determine Eckardt scores before HRM. Results According to the CC v3.0, 57 (24.2%) patients showed evidence of esophagogastric junction outflow obstruction and were classified as Group 1. Eighteen (7.6%) patients with major disorders of peristalsis were classified as Group 2. Minor disorders of peristalsis (Group 3) were much more frequent (129 [54.7%] patients). Thirty-two (13.6%) patients had normal esophageal manometry were classified as Group 4. All patients with abnormal pH or pH impedance monitoring (n = 44) had minor motor disorders (ineffective esophageal motility [IEM] = 34, fragmented peristalsis = 10). Based on motor category, the Eckardt score was 4.7 ± 0.1 in Group 1, 4.5 ± 0.3 in Group 2, 3.5 ± 0.1 in Group 3, and 3.9 ± 0.1 in Group 4. Conclusions IEM was the most common esophageal motor disorder in patients with esophageal dysphagia who showed no structural abnormality on endoscopy. While a high Eckardt score suggests outflow obstruction or a major motor disorder, a low score suggests IEM.

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        Differential Hrd1 Expression and B-Cell Accumulation in Eosinophilic and Non-eosinophilic Chronic Rhinosinusitis With Nasal Polyps

        Kun Chen,Miaomiao Han,Mengyao Tang,Yadong Xie,Yuting Lai,Xianting Hu,Jia Zhang,Jun Yang,Huabin Li 대한천식알레르기학회 2018 Allergy, Asthma & Immunology Research Vol.10 No.6

        Purpose: Hrd1 has recently emerged as a critical regulator of B-cells in autoimmune diseases. However, its role in the pathogenesis of chronic rhinosinusitis with nasal polyps (CRSwNP) remains largely unexplored. This study aimed to examine Hrd1 expression and B-cell accumulation and their possible roles in CRSwNP. Methods: Quantitative real-time polymerase chain reaction, immunohistochemistry, enzyme-linked immunosorbent assay and Western blotting were used to assess gene and protein expression in nasal tissue extracts. Cells isolated from nasal tissues and peripheral blood mononuclear cells were characterized by flow cytometry. Local antibody production was measured in tissue extracts with a Bio-Plex assay. Additionally, changes in Hrd1 expression in response to specific inflammatory stimuli were measured in cultured dispersed polyp cells. Results: Nasal polyps (NPs) from patients with eosinophilic CRSwNP (ECRS) had increased levels of Hrd1, B-cells and plasma cells compared with NPs from patients with non-eosinophilic CRSwNP (non-ECRS) or other control subjects (P < 0.05). The average Hrd1 levels in B-cells in NPs from ECRS patients were significantly higher than those from non-ECRS patients and control subjects (P < 0.05). NPs also contained significantly increased levels of several antibody isotypes compared with normal controls (P < 0.05). Interestingly, Hrd1 expression in cultured polyp cells from ECRS patients, but not non-ECRS patients, was significantly increased by interleukin-1β, lipopolysaccharide and Poly(I:C) stimulation, and inhibited by dexamethasone treatment (P < 0.05). Conclusions: Differential Hrd1 expression and B-cell accumulation between the ECRS and non-ECRS subsets suggests that they can exhibit distinct pathogenic mechanisms and play important roles in NP.

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