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( Ada W. Y. Tse ),( Larry H. Lai ),( C. C. Lee ),( Kelvin K. F. Tsoi ),( Vincent W. S. Wong ),( Yawen Chan ),( Joseph J. Y. Sung ),( Francis K. L. Chan ),( Justin C. Y. Wu ) 대한소화기기능성질환·운동학회 2010 Journal of Neurogastroenterology and Motility (JNM Vol.16 No.1
Introduction: Psychiatric comorbidity is common in patients with functional dyspepsia (FD) but a good screening tool for psychiatric disorders in gastrointestinal clinical practice is Lacking. Aims: 1) Evaluate the performance and optimal cut-off of 12-item General Health Questionnaire (GHQ-12) as a screening tool for psychiatric disorders in FD patients; 2) Compare health-related quality of Life (HRQoL) in FD patients with and without psychiatric comorbidities. Methods: Consecutive patients fulfilling Rome III criteria for FD without medical co-morbidities and gastroesophageal reflux disease were recruited in a gastroenterology clinic. The followings were conducted at 4 weeks after index oesophagogastroduodenoscopy: self-administrated questionnaires on socio-demographics, dyspeptic symptom severity (4-point Likert scale), GHQ-12, and 36-item short-form health survey (SF-36). Psychiatric disorders were diagnosed with Structured Clinical Interview for DSM-IV Axis I Disorders (SCID) by a trained psychiatrist, which served as reference standard. Results: 55 patients underwent psychiatrist-conducted interview and questionnaire assessment. 27 (49.1%) had current psychiatric disorders as determined by SCID (anxiety disorders: 38.2%, depressive disorders: 16.4%). Receiver operating characteristic curve analysis of GHQ-12 revealed an area under curve of 0.825 (95%CI: 0.698-0.914). Cut-off of GHQ-12 at 3 gave a sensitivity of 63.0% (95%CI = 42.4-80.6%) and specificity of 92.9% (95%CI = 76.5%-98.9%). Subjects with co-existing psychiatric disorders scored significantly Lower in multiple domains of SF-36 (mental component summary, general health, vitality and mental health). By multivariate Linear regression analysis, current psychiatric morbidities (Beta = -0.396, p = 0.002) and family history of psychiatric illness (Beta = -0.299, p = 0.015) were independent risk factors for poorer mental component summary in SF-36, while dyspepsia severity was the only independent risk factor for poorer physical component summary (Beta = -0.332, p = 0.027). Conclusions: Concomitant psychiatric disorders adversely affect HRQoL in FD patients. The use of GHQ-12 as a reliable screening tool for psychiatric disorders allows early intervention and may improve clinical outcomes of these patients.(J Neurogastroenterol Motil 2010;16:52-60)
Yu, Jun,Tao, Qian,Cheng, Yuen Y.,Lee, Kwan Y.,Ng, Simon S. M.,Cheung, Kin F.,Tian, Linwei,Rha, Sun Y.,Neumann, Ulf,Rö,cken, Christoph,Ebert, Matthias P. A.,Chan, Francis K. L.,Sung, Joseph J. Y. Wiley Subscription Services, Inc., A Wiley Company 2009 Cancer Vol.115 No.1
<P><B>Abstract</B></P><P><B>BACKGROUND:</B></P><P>Abnormal activation of the Wnt/β‐catenin signaling pathway is common and critical in the pathogenesis of digestive cancers. In this study, the authors investigated the promoter methylation of the dickkopf homolog 3 gene <I>Dkk‐3</I> in these cancers and its prognostic significance in gastric cancer.</P><P><B>METHODS:</B></P><P><I>Dkk‐3</I> methylation was assessed in 173 patients with gastric cancers (including 104 patients who were followed for up to 4090 days) and in 128 patients with colorectal cancer. Cell growth was evaluated by using a colony‐formation assay. For survival analyses, the authors used Kaplan‐Meier plots, the log‐rank test, and Cox proportional regression.</P><P><B>RESULTS:</B></P><P><I>Dkk‐3</I> was silenced or down‐regulated in 12 of 17 gastric cancer cell lines (70.6%) and in 3 of 9 colon cancer cell lines (33.3%). The loss of gene expression was associated with promoter methylation, which could be restored by demethylating agents. Ectopic expression of <I>Dkk‐3</I> suppressed colony formation. Moreover, methylation of <I>Dkk‐3</I> was detected in 117 of 173 primary gastric tumors (67.6%) and in 67 of 128 colorectal tumors (52.3%). The clinical significance and the prognostic value of <I>Dkk‐3</I> methylation also were examined in 104 gastric cancers and in 84 colorectal cancers. Multivariate analysis indicated that <I>Dkk‐3</I> methylation was associated significantly and independently with poor disease survival (relative risk, 2.534; 95% confidence interval, 1.54–4.17; <I>P</I> = .002) in gastric cancer, but not in colorectal cancer. Kaplan‐Meier survival curves revealed that patients who had <I>Dkk‐3</I> methylated gastric cancers had a significantly shorter survival (median, 0.76 years) compared with patients who did not have <I>Dkk‐3</I> methylation (median, 2.68 years; <I>P</I> < .0001; log‐rank test).</P><P><B>CONCLUSIONS:</B></P><P>Epigenetic silencing of the <I>Dkk‐3</I> gene by promoter methylation was a common event in gastric cancer and was associated with a poor outcome in such patients. Cancer 2009. © 2008 American Cancer Society.</P>
Modern Interpretation of Giant Cell Tumor of Bone: Predominantly Osteoclastogenic Stromal Tumor
Yuhree Kim,,Saqib Nizami,Hana Goto,Francis Y. Lee 대한정형외과학회 2012 Clinics in Orthopedic Surgery Vol.4 No.2
Owing to striking features of numerous multinucleated cells and bone destruction, giant cell tumor (GCT) of bone, often calledas osteoclastoma, has drawn major attractions from orthopaedic surgeons, pathologists, and radiologists. The name GCT or osteoclastomagives a false impression of a tumor comprising of proliferating osteoclasts or osteoclast precursors. The underlyingmechanisms for excessive osteoclastogenesis are intriguing and GCT has served as an exciting disease model representing a paradigmof osteoclastogenesis for bone biologists. The modern interpretation of GCT is predominantly osteoclastogenic stromal celltumors of mesenchymal origin. A diverse array of infl ammatory cytokines and chemokines disrupts osteoblastic differentiation andpromotes the formation of excessive multi-nucleated osteoclastic cells. Pro-osteoclastogenic cytokines such as receptor activatorof nuclear factor kappa-B ligand (RANKL), interleukin (IL)-6, and tumor necrosis factor (TNF) as well as monocyte-recruiting chemokinessuch as stromal cell-derived factor-1 (SDF-1) and monocyte chemoattractant protein (MCP)-1 participate in unfavorable osteoclastogenesisand bone destruction. This model represents a self-suffi cient osteoclastogenic paracrine loop in a localized area. Consistent with this paradigm, a recombinant RANK-Fc protein and bisphosphonates are currently being tried for GCT treatment inaddition to surgical excision and conventional topical adjuvant therapies.
권혁권,Mahesh Chandra Patra,신현준,Xiangai Gui,asma,Suresh Panneerselvam,김동진,송석종,홍리원,김경수,김양균,Francis Y. Lee,함대현,이상호,최상둔 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
Toll-like receptors (TLRs) recognize pathogen/damage-associated molecular patterns and initiate inflammatory signaling cascades. Occasionally, overexpression of TLRs leads to the onset of numerous inflammatory diseases, necessitating the development of selective inhibitors to allow a protective yet balanced immune response. Here, we demonstrate that a novel peptide (TIP1) derived from Toll/interleukin-1 receptor (TIR) domain-containing adapter protein inhibited multiple TLR signaling pathways (MyD88-dependent and MyD88-independent) in murine and human cell lines. TIP1 also inhibited NLRP3-mediated IL-1β secretion, as we validated at both the protein and mRNA levels. Biophysical experiments confirmed that TIP1 specifically binds to the BB loop of the TLR4-TIR domain. Animal studies revealed that TIP1 inhibited the secretion of lipopolysaccharide (LPS)-induced proinflammatory cytokines in collagen-induced arthritis (CIA) and kaolin/carrageenan-induced arthritis (K/C) rodent models. TIP1 also rescued animals from sepsis and from LPS-induced kidney/liver damage. Importantly, TIP1 ameliorated the symptoms of rheumatoid arthritis in CIA and K/C rodent models, suggesting that TIP1 has therapeutic potential for the treatment of TLR-mediated autoimmune/inflammatory diseases.