Publications by authors named "Jeong Soo Ahn"

Purpose: This study aimed to investigate the neuroprotective effects of vitamin E for preventing chemotherapy-induced peripheral neuropathy (CIPN).

Methods: A comprehensive search from 1973 through July 2011 identified randomized controlled trials (RCTs) that reported the preventive effects of vitamin E on CIPN. The relative risk (RR) of CIPN with vitamin E supplementation, compared with placebo, was assessed with the Bayesian random effect model and expressed as RR with a 95 % credible-interval (CrI).

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Aim: To evaluate the association between acid suppressive drug use and the development of gastric cancer.

Methods: A systematic search of relevant studies that were published through June 2012 was conducted using the MEDLINE (PubMed), EMBASE, and Cochrane Library databases. The search included observational studies on the use of histamine 2-receptor antagonists (H₂RAs) or proton pump inhibitors and the associated risk of gastric cancer, which was measured using the adjusted odds ratio (OR) or the relative risk and 95%CI.

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Background: Previous case-control studies have reported inconsistent findings regarding the association between proton pump inhibitor (PPI) use and colorectal cancer (CRC) risk. We investigated these associations using meta-analysis.

Methods: We searched MEDLINE (PubMed), EMBASE, and the Cochrane Library in April 2011.

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Objective: To perform meta-analyses using observational studies to assess the association between the use of selective serotonin reuptake inhibitors (SSRIs) and the risk of colorectal cancer.

Methods: A systematic search of relevant studies published through February 2012 was carried out using the Medline (PubMed), Embase, and Cochrane Library databases. We reviewed the observational studies that were associated with our subject and carried out a meta-analysis.

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Purpose: Previous studies have reported inconsistent findings regarding the association between the use of acid-suppressive drugs such as proton pump inhibitors (PPIs) and histamine 2 receptor antagonists (H(2)RAs) and fracture risk. We investigated this association using meta-analysis.

Methods: We searched MEDLINE (PubMed), EMBASE, and the Cochrane Library from inception through December 2010 using common key words.

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One of the characteristics of the senescent cell is apoptotic resistance. Gelsolin, a Ca(2+)-dependent actin regulatory protein, is believed to regulate the intracellular movements which are necessary for cell growth, proliferation, and differentiation. Recently, gelsolin was suggested to play a role in apoptotic resistance, which led us to examine its involvement in the apoptotic resistance of senescent cells.

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Gelsolin, a Ca(2+)-dependent actin regulatory protein, was recently suggested to participate in apoptosis regulation. In this study, we found that the level of gelsolin is elevated in senescent human diploid fibroblasts (HDFs) and also in the tissues of old rats, i.e.

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Hyporesponsiveness to growth factors is one of the fundamental characteristics of senescent cells. We previously reported that the up-regulation of caveolin attenuates the growth factor response and the subsequent downstream signal cascades in senescent human diploid fibroblasts. Therefore, in the present experiment, we investigated the modulation of caveolin status in senescent cells to determine the effect of caveolin on mitogenic signaling efficiency and cell cycling.

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Lysophosphatidic acid (LPA) is a lipid mitogen that acts through G-protein-coupled receptors. LPA responsiveness has been reported to be dependent on the senescent state of the cells. To solve the mechanism underlying, we observed LPA-dependent cAMP status and found its age-dependent contrasting profile such as high level of cAMP in the senescent cells vs its low level in the young cells.

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Human diploid fibroblasts (HDF) do not divide indefinitely and eventually lead to an arrest of cell division by a process termed cellular or replicative senescence. Irreversible growth arrest of senescent cells is strongly related to the attenuated response to growth factors. Recently, we reported that up-regulation of caveolin in the senescent cells is responsible for the attenuated response to growth factors.

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