• Title/Summary/Keyword: Fatty infiltration

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Systemic TM4SF5 overexpression in ApcMin/+ mice promotes hepatic portal hypertension associated with fibrosis

  • Joohyeong, Lee;Eunmi, Kim;Min-Kyung, Kang;Jihye, Ryu;Ji Eon, Kim;Eun-Ae, Shin;Yangie, Pinanga;Kyung-hee, Pyo;Haesong, Lee;Eun Hae, Lee;Heejin, Cho;Jayeon, Cheon;Wonsik, Kim;Eek-Hoon, Jho;Semi, Kim;Jung Weon, Lee
    • BMB Reports
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    • v.55 no.12
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    • pp.609-614
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    • 2022
  • Mutation of the gene for adenomatous polyposis coli (APC), as seen in ApcMin/+ mice, leads to intestinal adenomas and carcinomas via stabilization of β-catenin. Transmembrane 4 L six family member 5 (TM4SF5) is involved in the development of non-alcoholic fatty liver disease, fibrosis, and cancer. However, the functional linkage between TM4SF5 and APC or β-catenin has not been investigated for pathological outcomes. After interbreeding ApcMin/+ with TM4SF5-overexpressing transgenic (TgTM4SF5) mice, we explored pathological outcomes in the intestines and livers of the offspring. The intestines of 26-week-old dual-transgenic mice (ApcMin/+:TgTM4SF5) had intramucosal adenocarcinomas beyond the single-crypt adenomas in ApcMin/+ mice. Additional TM4SF5 overexpression increased the stabilization of β-catenin via reduced glycogen synthase kinase 3β (GSK3β) phosphorylation on Ser9. Additionally, the livers of the dualtransgenic mice showed distinct sinusoidal dilatation and features of hepatic portal hypertension associated with fibrosis, more than did the relatively normal livers in ApcMin/+ mice. Interestingly, TM4SF5 overexpression in the liver was positively linked to increased GSK3β phosphorylation (opposite to that seen in the colon), β-catenin level, and extracellular matrix (ECM) protein expression, indicating fibrotic phenotypes. Consistent with these results, 78-week-old TgTM4SF5 mice similarly had sinusoidal dilatation, immune cell infiltration, and fibrosis. Altogether, systemic overexpression of TM4SF5 aggravates pathological abnormalities in both the colon and the liver.

Multidetector CT Findings of Acquired Spondylolysis and Spondylolisthesis after Posterior Lumbar Laminectomy (요추 후방 감압술에서 발생한 후천적 척추분리증과 척추전방전위증의 다중검출 전산화단층촬영 소견)

  • Hyein Yun;Ji Young Hwang;Jeong Hyun Yoo
    • Journal of the Korean Society of Radiology
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    • v.81 no.3
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    • pp.644-653
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    • 2020
  • Purpose We aimed to analyze postoperative multidetector CT (MDCT) of acquired spondylolysis and spondylolisthesis after posterior lumbar laminectomy. Materials and Methods We enrolled 74 patients, from 2003 to 2017, who underwent posterior lumbar laminectomy with both pre and postoperative MDCT. The patients were categorized into the following two groups: group 1 without fusion and group 2 with fusion. We analyzed laminectomy width, level and location of spondylolysis or spondylolisthesis, facet changes, and fatty infiltration of paraspinal muscles on postoperative MDCT. Results Incidence of spondylolysis or spondylolisthesis was 4 of 20 patients in group 1 and 2 of 54 patients in group 2. The laminectomy width (%) was defined as the percentage of the width of laminectomy to total lamina length. Mean laminectomy width (%) in patients with spondylolysis or spondylolisthesis was 54.0 in group 1 and 53.2 in group 2, in contrast to that in patients without spondylolysis or spondylolisthesis, which was 35.0 in group 1. The spondylolysis was observed at the level of the laminectomy and below pars interarticularis in group 1 and below the fusion mass at isthmic region in group 2. Conclusion MDCT facilitates the diagnosis of postsurgical acquired spondylolysis and spondylolisthesis and demonstrates typical location of spondylolysis. Greater laminectomy width has been associated with occurrence of acquired spondylolysis and spondylolisthesis.

Hepatoprotective Effects of Semisulcospira libertine Hydrolysate on Alcohol-induced Fatty Liver in Mice (알코올성 지방간 유발 마우스에서 다슬기 유래 가수분해물의 간 보호 효과)

  • Song, Eun Jin;Cho, Kyoung Hwan;Choo, Ho Jin;Yang, Eun Young;Jung, Yoon Kyoung;Seo, Min Gyun;Kim, Jong Cheol;Kang, Eun Ju;Ryu, Gi Hyung;Park, Beom Yong;Hah, Young-Sool
    • Food Engineering Progress
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    • v.21 no.4
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    • pp.318-325
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    • 2017
  • Alcoholic steatosis is a fundamental metabolic disorder and may precede the onset of more severe forms of alcoholic liver disease. In this study, we isolated enzymatichydrolysate from Semisulcospira libertine by alcalase hydrolysis and investigated the protective effect of Semisulcospira libertine hydrolysate on liver injury induced by alcohol in the mouse model of chronic and binge ethanol feeding (NIAAA). In an in vitro study, the hydrolysate protects HepG2 cells from ethanol toxicity. Liver damage was assessed by histopathological examination, as well as by quantitating activities of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase (ALP). After the administration of S. libertina hydrolysate, fat accumulation and infiltration of inflammatory cells in liver tissues were significantly decreased in the NIAAA mouse model. The elevated levels of serum AST, ALT, and ALP activities, along with the lipid contents of a damaged liver, were recovered in experimental mice administrated with S. libertina hydrolysate, suggesting its role in blood enzyme activation and lipid content restoration within damaged liver tissues. Moreover, treatment with S. libertine hydrolysate reduced the expression rate of cyclooxygenase (COX-2), interleukin $(IL)-1{\beta}$, and IL-6, which accelerate inflammation and induces tissue damage. All data showed that S. libertine hydrolysate has a preventive role against alcohol-induced liver damages by improving the activities of blood enzymes and modulating the expression of inflammation factor, suggesting S. libertine hydrolysate could be a commercially potential material for the restoration of hepatotoxicity.