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Sang Min Park,Soo Youn Lee,Mi-Hyang Jung,Jong-Chan Youn,Darae Kim,Jae Yeong Cho,Dong-Hyuk Cho,Junho Hyun,Hyun-Jai Cho,Seong-Mi Park,Jin-Oh Choi,Wook-Jin Chung,Seok-Min Kang,Byung-Su Yoo 대한심장학회 2023 Korean Circulation Journal Vol.53 No.7
Most patients with heart failure (HF) have multiple comorbidities, which impact their quality of life, aggravate HF, and increase mortality. Cardiovascular comorbidities include systemic and pulmonary hypertension, ischemic and valvular heart diseases, and atrial fibrillation. Non-cardiovascular comorbidities include diabetes mellitus (DM), chronic kidney and pulmonary diseases, iron deficiency and anemia, and sleep apnea. In patients with HF with hypertension and left ventricular hypertrophy, renin-angiotensin system inhibitors combined with calcium channel blockers and/or diuretics is an effective treatment regimen. Measurement of pulmonary vascular resistance via right heart catheterization is recommended for patients with HF considered suitable for implantation of mechanical circulatory support devices or as heart transplantation candidates. Coronary angiography remains the gold standard for the diagnosis and reperfusion in patients with HF and angina pectoris refractory to antianginal medications. In patients with HF and atrial fibrillation, long-term anticoagulants are recommended according to the CHA2DS2-VASc scores. Valvular heart diseases should be treated medically and/or surgically. In patients with HF and DM, metformin is relatively safer; thiazolidinediones cause fluid retention and should be avoided in patients with HF and dyspnea. In renal insufficiency, both volume status and cardiac performance are important for therapy guidance. In patients with HF and pulmonary disease, beta-blockers are underused, which may be related to increased mortality. In patients with HF and anemia, iron supplementation can help improve symptoms. In obstructive sleep apnea, continuous positive airway pressure therapy helps avoid severe nocturnal hypoxia. Appropriate management of comorbidities is important for improving clinical outcomes in patients with HF.
( Sung Soo Park ),( Seung Hoon Kim ),( Mihee Kim ),( Jong Wook Kim ),( Yoo Mi Ko ),( Sung Kyoung Kim ),( So Hyang Kim ),( Chi Hong Kim ) 대한결핵 및 호흡기학회 2015 Tuberculosis and Respiratory Diseases Vol.78 No.4
Although influenza A (H1N1) virus leads to self-limiting illness, co-infection with bacteria may result in cases of severe respiratory failure due to inflammation and necrosis of intra-airway, as pseudomembranous tracheobronchitis. Pseudomembranous tracheobronchitis is usually developed in immunocompromised patients, but it can also occur in immunocompetent patients on a very rare basis. We report a case of pseudomembranous tracheobronchitis complicated by co-infection of inflenaza A and Staphylococcus aureus, causing acute respiratory failure in immunocompetent patients.
TNF-Like Ligand 1A is a promising biomarker of disease activity in rheumatoid arthritis
( Yoo Jin Hong ),( Yun Jong Lee ),( Kichul Shin ),( Byoong Yong Choi ),( Sung Hae Chang ),( Hae Won Kim ),( In Ah Choi ),( Eun Young Lee ),( Eun Bong Lee ),( Yeong Wook Song ) 대한내과학회 2011 대한내과학회 추계학술대회 Vol.2011 No.-
Yoo, Taesik,Ham, Sun Ah,Lee, Won Jin,Hwang, Seon In,Park, Jin-A,Hwang, Jung Seok,Hur, Jinwoo,Shin, Ho-Chul,Han, Sung Gu,Lee, Chi-Ho,Han, Dong Wook,Paek, Kyung Shin,Seo, Han Geuk American Diabetes Association 2018 Diabetes Vol.67 No.3
<P>Peroxisome proliferator-activated receptor (PPAR) delta plays a pivotal role in metabolic homeostasis through its effect on insulin signaling. Although diverse genomic actions of PPAR delta are postulated, the specific molecular mechanisms whereby PPARd controls insulin signaling have not been fully elucidated. We demonstrate here that short-term activation of PPAR delta results in the formation of a stable complex with nuclear T-cell protein tyrosine phosphatase 45 (TCPTP45) isoform. This interaction of PPAR delta with TCPTP45 blocked translocation of TCPTP45 into the cytoplasm, thereby preventing its interaction with the insulin receptor, which inhibits insulin signaling. Interaction of PPAR delta with TCPTP45 blunted interleukin 6-induced insulin resistance, leading to retention of TCPTP45 in the nucleus, thereby facilitating deactivation of the signal transducer and activator of transcription 3 (STAT3)-suppressor of cytokine signaling 3 (SOCS3) signal. Finally, GW501516-activated PPAR delta improved insulin signaling and glucose intolerance in mice fed a high-fat diet through its interaction with TCPTP45. This novel interaction of PPAR delta constitutes the most upstream component identified of the mechanism downregulating insulin signaling.</P>
TNF-like ligand 1A is a promising biomarker of disease activity in rheumatoid arthritis
( Yoo Jin Hong ),( Yun Jong Lee ),( Ki Chul Shin ),( Byoong Yong Choi ),( Sung Hae Chang ),( Hae Won Kim ),( In Ah Choi ),( Eun Young Lee ),( Eun Bong Lee ),( Yeong Wook Song ) 대한내과학회 2011 대한내과학회 추계학술대회 Vol.2011 No.1
Background: Rheumatoid arthritis (RA) is an autoimmune disease characterized by chronic inflammation of multiple joints. TN -like ligand 1A (TL1A), a ligand belonging to the TNF superfamily, is expressed by endothelial cells, lymphocytes, monocytes and plasma cells. These are also the key cell lineages participating in the pathogenesis of RA. Moreover, TL1A is up-regulated by proinflammatory cytokines TNF- and IL-1. We thereby examined the serum and synovial fluid levels of TL1A in patients with RA. In addition, we investigated the relationship between serum TL1A concentration and clinical parameters in RA patients. Methods: Serum samples were obtained from 232 patients with RA and 29 with osteoarthritis (OA). Thirty-eight and 27 synovial fluid (SF) samples were collected from respective group of patients. Additional 45 serum samples before and after (14 weeks) anti-TNF- treatment were collected from RA patients. TL1A concentrations were measured by ELISA. Clinical parameters were acquired at the time of sampling. Results: Serum concentrations of TL1A in RA patients were significantly higher than those in OA patients (mean±SD, 1327.4±3858.8 pg/ml vs. 150.3±269.6 pg/ml, p<0.0001). The SF levels of TL1A were elevated in patients with RA compared with those in OA (965.7±1617.2 vs. 271.4±238.9, p=0.013). Levels of TL1A were significantly increased in SF than serum in matched samples (RA; p=0.006, OA; p<0.0001). Serum levels of TL1A decreased substantially with anti-TNF- treatment (p=0.002). Serum levels of TL1A correlated well with DAS28-ESR (r=0.170, p=0.021), DAS28-CRP (r=0.166, p=0.037), SDAI (r=0.201, p=0.016), CDAI (r=0.195, p=0.011) and rheumatoid factor positivity (r=0.876, p=0.044). Conclusion: Serum and SF levels of TL1A were significantly increased in RA patients compared with OA patients, and correlated well with clinical parameters representing disease activity.Our results support that TL1A could be a potential biomarker in assessing disease activity and treatment response in RA patients.