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RISS 인기검색어
- 검색키워드
- 저자 : Ming-Tsung Lai (검색결과 3 건)
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Po-Ju Lai,Sheng-Fen Wang,Tsung-Ting Tsai,Yun-Da Li,Ping-Yeh Chiu,Ming-Kai Hsieh,Fu-Cheng Kao 대한척추신경외과학회 2021 Neurospine Vol.18 No.4
Objective: Surgical treatment of severe infectious spondylodiskitis remains challenging. Although minimally invasive percutaneous endoscopic drainage and debridement (PEDD) may yield good results in complicated cases, outcomes of patients with extensive structural damage and mechanical instability may be unsatisfactory. To address severe infectious spondylodiskitis, we have developed a surgical technique called percutaneous endoscopic interbody debridement and fusion (PEIDF), which comprises endoscopic debridement, bone-graft interbody fusion, and percutaneous posterior instrumentation. Methods: Outcomes of PEIDF in 12 patients and PEDD in 15 patients with infectious spondylodiskitis from April 2014 to July 2018 were reviewed retrospectively. Outcome were compared between 2 kinds of surgical procedures. Results: Patients in PEIDF group had significantly lower rate of revision surgery (8.3% vs. 58.3%), better kyphosis angle (-5.73°±8.74 vs. 1.07°±2.70 in postoperative; 7.09°±7.23 vs. 0.79°±4.08 in kyphosis correction at 1 year), and higher fusion rate (83.3% vs. 46.7%) than those who received PEDD. Conclusion: PEIDF is an effective approach for treating infectious spondylodiskitis, especially in patients with spinal instability and multiple medical comorbidities.
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( Man Chin Hua ),( Hsun Chin Chao ),( Tsung Chieh Yao ),( Ming Wei Lai ),( Jing Long Huang ),( The Patch Study Group ) 대한소화기학회 2013 Gut and Liver Vol.7 No.4
Background/Aims: The aim of this study was to investigate whether genetic variations at positions -1082, -819, and 592 in the interleukin (IL)-10 promoter affect IL-10 production in children with irritable bowel syndrome (IBS). Methods: Ninety-four children with IBS and 102 children as healthy controls (HCs) were enrolled. Genomic DNA was extracted, and IL-10 -1082, -819, and -592 polymorphisms were detected by direct sequencing from all participants. Peripheral blood mononuclear cells (PBMCs) from 46 IBS children and 38 HCs were isolated and cultured with and without 5 ng/mL Escherichia coli lipopolysaccharide (LPS). IL-10 levels in the culture supernatants were measured by enzyme-linked immunosorbent assay. Results: There were no significant differences in the distribution of IL-10 -1082, -819, and -592 polymorphisms or in the allele and haplotype frequencies between IBS children and HCs. PBMCs from children with IBS had significantly lower IL-10 levels after LPS stimulation than PBMCs from HCs (p=0.011); however, LPS-induced IL-10 levels in PBMCs with different genotypes of -819 and 592 polymorphisms were not significantly different between IBS patients and HCs. Conclusions: Although significantly lower LPS-induced IL-10 production by PBMCs was noted, it is unlikely that IL-10 production was fully genetically determined in our IBS children. ClinicalTrials.gov identifier: NCT01131442. (Gut Liver 2013; 7:430-436)
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Antioxidative and Hepatoprotective Effects of Magnolol on Acetaminophen-induced Liver Damage in Rats
Yung-Hsiang Chen,Feng-Yen Lin,Po-Len Liu,Yi-Tsau Huang,Jen-Hwey Chiu,Yi-Chun Chang,Kee-Ming Man,Chuang-Ye Hong,Yen-Yi Ho,Ming-Tsung Lai 대한약학회 2009 Archives of Pharmacal Research Vol.32 No.2
Acute liver failure (ALF), an often fatal condition characterized by massive hepatocyte necrosis, is frequently caused by drug poisoning, particularly with acetaminophen (N-acetyl-p-aminophenol/APAP). Hepatocyte necrosis is consecutive to glutathione (GSH) depletion and mitochondrial damage caused by reactive oxygen species (ROS) overproduction. Magnolol, one major phenolic constituent of Magnolia officinalis, have been known to exhibit potent antioxidative activity. In this study, the anti-hepatotoxic activity of magnolol on APAP-induced toxicity in the Sprague-Dawley rat liver was examined. After evaluating the changes of several biochemical parameters in serum, the levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) were elevated by APAP (500 mg/kg) intraperitoneal administration (8 and 24 h) and reduced by treatment with magnolol (0.5 h after APAP administration; 0.01, 0.1, and 1 μg/kg). Histological changes around the hepatic central vein, lipid peroxidation (thiobarbituric acid-reactive substance/TBARS), and GSH depletion in liver tissue induced by APAP were also recovered by magnolol treatment. The data show that oxidative stress followed by lipid peroxidation may play a very important role in the pathogenesis of APAP-induced hepatic injury; treatment with lipid-soluble antioxidant, magnolol, exerts anti-hepatotoxic activity. Our study points out the potential interest of magnolol in the treatment of toxic ALF.
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