Search Results - (Author, Cooperation:S. W. Cho)

2018-08-31

Institute of Physics Publishing (IOP)

1748-0221

Physics

2015-01-30

Nature Publishing Group (NPG)

0028-0836

1476-4687

Biology

Chemistry and Pharmacology

Medicine

Natural Sciences in General

Physics

CRISPR-Cas Systems/*genetics ; Genetic Engineering/*methods ; Genome, Human/*genetics ; Humans ; Melanoma/*genetics ; Transcriptional Activation/*genetics

2018-02-28

Wiley-Blackwell

0007-0963

1365-2133

Medicine

2018-10-26

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Geosciences

Computer Science

Medicine

Natural Sciences in General

Physics

Medicine, Diseases, Online Only

1471-4159

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Evidence that stem cell factor (SCF) and c-Kit receptor tyrosine kinase expressed in the cerebellum during postnatal development, suggests a possible contribution of the SCF/Kit signaling pathway in the cerebellar development. In the present study, we prepared cerebellar cultures from C57Bl/6J mouse at postnatal day 6 to investigate the role of c-Kit receptor and SCF in regulation of cell growth and viability in the postnatal cerebellar cells. SCF increased the number of survival cells and density of calbindin and GFAP expression in the immunoblot analysis. Treatment with c-Kit antibody accelerated cellular loss in serum-free media and decreased the expression of calbindin and GFAP. The recovery effects of SCF on the cellular proliferation and the expression of functional proteins in the cultures containing c-Kit antibody suggest an involvement of SCF/Kit pathways in the control of postnatal development of cerebellar cells.

Electronic Resource

1365-2036

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background : It has been suggested that chronic, persistent, uncontrolled inflammations in the stomach could provide the basic step for the beginning of carcinogenesis. One of the potential clinical applications of rebamipide is the inhibition of the immunoinflammatory response in gastric mucosa imposed by Helicobacter pylori.Aim : To determine the implications of long-term rebamipide treatment in H. pylori infection, we studied the underlying moleculo-pathological changes in gastric lesions in mice infected with H. pylori (SS1 strain), following this treatment.Methods : C57BL/6 mice were sacrificed 24 and 50 weeks after H. pylori infection, respectively. Colonization rates of H. pylori, degree of gastric inflammation and other pathological changes including atrophic gastritis and metaplasia, serum levels of IL-1β, TNF-α, IFN-γ and IL-10, mRNA transcripts of various mouse cytokines and chemokines, and NF-κB binding activities, and finally the presence of gastric adenocarcinoma were compared between an H. pylori infected group (HP), and an H. pylori infected group administered with long-term rebamipide-containing pellet diets (HPR).Results : Serum levels of IL-1β, IFN-γ and TNF-α, the gastric mucosal expression of ICAM-1, HCAM and MMP, and transcriptional regulation of NF-κB-DNA binding were all significantly decreased in the HPR group compared with the HP group. An RNase protection assay showed, in the rebamipide administered group, significantly decreased mRNA levels of apoptosis-related genes such as caspase-8, FasL, Fas, TRAIL and various cytokines genes such as IFN-γ, RANTES, TNF-α, TNFR p75, IL-1β. In the experiment designed to provoke gastric cancer through MNU treatment with H. pylori infection, the incidence of gastric carcinoma was not different in either group. However, long-term administration of rebamipide showed the advantage of decreasing precancerous lesions like chronic atrophic gastritis and showed molecular evidence of attenuation of proliferation.Conclusion : The long-term administration of rebamipide should be considered in the treatment of H. pylori since it demonstrated molecular and biological advantages like a lessening of gastric inflammation and a possible chemopreventive effect.

Electronic Resource

1365-2036

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background : Gabapentin has been shown to reduce elements of central sensitization in human experimental hyperalgesia. It remains uninvestigated whether gabapentin has beneficial effects for irritable bowel syndrome associated with visceral hypersensitivity.Aims : To evaluate the effects of gabapentin on sensory and motor function of the rectum in patients with diarrhoea-predominant irritable bowel syndrome.Methods : Forty patients with diarrhoea-predominant irritable bowel syndrome completed this randomized, double-blind, placebo-controlled, parallel-grouped study. All patients received a barostat study and were subsequently randomized for 5-day treatment with gabapentin 300 mg/day and then 600 mg/day or placebo. On day 6, after subjects had their morning dose, the barostat experiment was repeated.Results : The threshold pressures for bloating, discomfort and pain significantly increased after gabapentin, but not after placebo. Significant increase in the pressure and corresponding wall tension inducing discomfort or pain were observed in the gabapentin group, but not in the placebo group. Rectal compliance significantly increased after gabapentin, but not after placebo. The postprandial increase of rectal tone was not affected by gabapentin.Conclusion : Our results show that gabapentin reduces rectal sensory thresholds through attenuating rectal sensitivity to distension and enhancing rectal compliance in diarrhoea-predominant irritable bowel syndrome patients. The clinical efficacy of this drug in irritable bowel syndrome patients warrants investigation.

Electronic Resource

1365-2036

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background : Long-term evaluation of gastric pathology after H. pylori infection is very important in order to reveal its clinical implications, since debate still exists on the gastric carcinogenesis provoked by H. pylori infection in animal models.Aim : Either to evaluate the long-term outcome of H. pylori infection or to determine how H. pylori could provoke gastric cancer in the mice model.Methods : Four-week-old specific pathogen free C57BL/6 mice (n = 115) were infected with SS1, the mouse-adapted H. pylori strain. After 4, 8, 16, 24, 36, 50 and 80 weeks of bacterial infection, the H. pylori-infected mice were sacrificed.Results : After 80 weeks of infection, almost all the H. pylori-infected mice developed hyperplastic gastritis, but did not show any evidence of gastric adenoma, dysplasia or carcinoma. PCNA positive cells were most abundant after 50 weeks and tended to decrease thereafter up to 80 weeks, whereas apoptosis began to be noted 8 weeks after H. pylori infection, showing 7–8 apoptotic cells/high power field, and tending to increase as time passed. Normally observed neutral mucin decreased during the experiment, showing the most marked decrease 50 weeks after H. pylori infection. In contrast, acidic mucin was noted from 50 weeks after infection.Conclusion : The SS1-infected mouse seems to be a suitable animal model for H. pylori-related research, and H. pylori itself does not induce gastric cancer in normal wild-type mouse model following long-term exposure, which could be explained by the balance that exists between cell proliferation and apoptosis.

Electronic Resource

0301-0104

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Chemistry and Pharmacology

Physics

Electronic Resource

1573-2568

HELICOBACTER PYLORI ; REBAMIPIDE ; OXIDATIVE STRESS ; CYTOKINE ; ERADICATION

Springer Online Journal Archives 1860-2000

Medicine

Abstract The aim of the present study was to determinethe efficacy of a new combination regimen including anantioxidant, a proton pump inhibitor, and antibioticsagainst Helicobacter pylori and to document the changes of oxidative stress and cytokinesinvolved in H. pylori-associated gastric inflammation.From 57 patients with endoscopically diagnosed gastricand/or duodenal ulcers associated with H. pylori infection five gastric antral biopsy specimenswere taken for the diagnosis of H. pylori and for theexperimental measures. The patients were then treatedeither with lansoprazole 30 mg + amoxicillin 1.5 g (LAgroup; 21 patients) or lansoprazole 30 mg amoxicillin1.5 g + rebamipide 300 mg (LAM group; 36 patients) fortwo weeks. Four weeks after the initiation of treatment,the patients were endoscoped again and biopsy specimens were obtained. Mucosalmalondialdehyde (MDA) levels; myeloperoxidase (MPO)activities; superoxide dismutase; catalase; glutathioneperoxidase; cytokines IL-1, IL-6, TNF-α; andchemokines IL-8, GRO-α, RANTES (regulated onactivation normal T expressed and secreted) weremeasured. Using paraffin-embedded tissue sections, insitu terminal deoxyribonucleotide transferase (TdT)mediated dUTP nick end labeling (TUNEL) for apoptosisand immunohistochemical staining for inducible nitricoxide synthase (iNOS) were performed. Two weeks oftreatment with the LA regimen resulted in 57.4%eradication rates of H. pylori, whereas two weeks oftreatment with the LAM regimen resulted in 75.0%eradication rates. Eradication rates between these twogroups were statistically significantly different (P〈 0.05). Mucosal MDA levels and MPO activities weresignificantly lower in the LAM group than the LA group.Mucosal levels of cytokines IL-1, IL-6, and TNF-αand of chemokines IL-8, GRO-α, and RANTES were all significantly decreased after the treatmentof H. pylori, especially so in the LAM group. Theapoptotic index and iNOS score were significantlyreduced after the eradication of H. pylori. The addition of an antioxidative drug to the eradicationregimen against H. pylori has advantages either inaugmenting the eradication rates of H. pylori or indecreasing the oxidative stress and cytokines levelsgenerated by H. pylori infection.

Electronic Resource