• Title/Summary/Keyword: Liver retraction

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V-shaped Liver Retraction during a Laparoscopic Gastrectomy for Gastric Cancer

  • Oh, Dong-Kyo;Hur, Hoon;Kim, Jun-Young;Han, Sang-Uk;Cho, Yong-Kwan
    • Journal of Gastric Cancer
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    • v.10 no.3
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    • pp.133-136
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    • 2010
  • Purpose: The aim of this study was to evaluate the effectiveness of our retraction method for achieving a good operative field for the adequate lymph node dissection during laparoscopic gastrectomy in view of short term surgical outcome. Materials and Methods: This study prospectively enrolled 19 patients who underwent laparoscopic gastrectomy for early gastric cancer. The procedure was simply performed by putting the laparoscopic sigle suture in the phrenoesophageal ligament, and then the string was pulling and tying over the sternum. Surgical outcomes of these patients were evaluated. Results: Under V-shaped liver retraction, the mean operating time and mean number of retrieved lymph nodes was 166.3 minute and 31.37, respectively. And the results were satisfactory compared to open or conventional laparoscopic gastric surgery. Conclusions: V-shaped liver retraction requires no extra port or assistant's hands, and prevents additional injury to any intra-abdominal organ. And this method can easily, efficiently and safely enable to achieve a good operative field for the lymph node dissection near the lesser curvature of the stomach.

Induction of Oxidative Stress and Cytoskeleton Damage by Cadmium in WB-F344 Rat Liver Epithelial Cells (랫드간장상피세포에서 카드뮴에 의한 산화적 스트레스 및 Cytoskeleton 손상 유발에 관한 연구)

  • 정상희;조명행;조준형
    • Toxicological Research
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    • v.14 no.4
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    • pp.577-585
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    • 1998
  • Cadmium is an important industrial and environmental pollutant and has adverse effects on cell growth and metabolism, although the mechanisms of its cellular toxicity are still unclear. This study was performed to elucidate the cytotoxic mechanism of cadmium in the viewpoint of oxidative stress and cytoskeleton alterations in WB-F344 rat liver epithelial cells. 200 $\mu\textrm{M}$ $CdCl_2$ caused a severe disassembling of microtubule and micro filament and an apparent cell retraction under an observation with fluorescence micoscope. (equation omitted)-tubulin and F-actin protein were highly thiolated at 20 min and then disappeared from 1 hour after the treatment of 200 $\mu$M CdCl$_2$in the immunoblot analysis. Intracellular GSH was decreased from 1hr to 24 hrs by 66.6 or 200 $\mu\textrm{M}$ of $CdCl_2$. Intracellular protein thiol was also decreased by 22.2, 66.6 and 200 $\mu\textrm{M}$ of $CdCl_2$ at 1 hour after its treatment. The product of lipid peroxidation (malondialdehyde) was increased from 4 hrs by 66.6 and 200$\mu\textrm{M}$ of $CdCl_2$. These data indicate that cadmium induces oxidative stress involving disassembling of microtubule and micro filament, thiolation of (equation omitted)-tubulin and actin protein, depletion of GSH and protein thiol, and increase of lipid peroxidation.

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[Retraction] A Review on the Role of Irisin in Insulin Resistance and Type 2 Diabetes Mellitus

  • Gizaw, Mamo;Anandakumar, Pandi;Debela, Tolessa
    • Journal of Pharmacopuncture
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    • v.20 no.4
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    • pp.235-242
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    • 2017
  • Irisin is a novel hormone like polypeptide that is cleaved and secreted by an unknown protease from fibronectin type III domain-containing protein 5 (FNDC5), a membrane-spanning protein and which is highly expressed in skeletal muscle, heart, adipose tissue, and liver. Since its discovery in 2012, it has been the subject of many researches due to its potent physiological role. It is believed that understanding irisin's function may be the key to comprehend many diseases and their development. Irisin is a myokine that leads to increased energy expenditure by stimulating the 'browning' of white adipose tissue. In the first description of this hormone, increased levels of circulating irisin, which is cleaved from its precursor fibronectin type III domain-containing protein 5, were associated with improved glucose homeostasis by reducing insulin resistance. Irisin is a powerful messenger, sending the signal to determine the function of specific cells, like skeletal muscle, liver, pancreas, heart, fat and the brain. The action of irisin on different targeted tissues or organs in human being has revealed its physiological functions for promoting health or executing the regulation of variety of metabolic diseases. Numerous studies focus on the association of irisin with metabolic diseases which has gained great interest as a potential new target to combat type 2 diabetes mellitus and insulin resistance. Irisin is found to improve insulin resistance and type 2 diabetes by increasing sensitization of the insulin receptor in skeletal muscle and heart by improving hepatic glucose and lipid metabolism, promoting pancreatic ${\beta}$ cell functions, and transforming white adipose tissue to brown adipose tissue. This review is a thoughtful attempt to summarize the current knowledge of irisin and its effective role in mediating metabolic dysfunctions in insulin resistance and type 2 diabetes mellitus.

Potential drug targets in the GPCR-$G{\alpha}_{12}/G{\alpha}_{13}$ signaling pathways

  • Kim, Sang-Geon
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 2008.04a
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    • pp.89-99
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    • 2008
  • GPCRs are large families of cell surface receptors that transmit signals through conformational changes upon ligand activation and an interaction with the heterotrimeric G-proteins. GPCRs regulate the cell-signaling pathways and participate in the regulation of physiological processes through the G-proteins defined by their ${\alpha}$ subunits. A family of 20 G protein-coupled receptors (GPCRs) that provide a large class of tractable drug targets for new anti-inflammatory drugs and, in certain instances, for the treatment of the inflammatory indications such as atherosclerosis, rhinitis, asthma, pulmonary disease and arthritis. In view of the important findings showing that $G{\alpha}_{12}/G{\alpha}_{13}$ regulate the various cellular processes such as actin-stress fiber formation, neurite retraction, platelet aggregation, gene induction, and apoptosis, we became interested in whether, after coupling to the activated GPCRs, the G-proteins and their downstream molecules might be involved in the pathologic processes of chronic inflammatory diseases (e.g., liver fibrosis). In this symposium, the possible link of the G-proteins with the pathophysiology will be discussed with the aim of finding potential new drug targets.

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