Obesity increases gastroesophageal reflux disease through several factors. As a result, Barrett's esophagus, esophageal adenocarcinoma, and gastroesophageal junctional gastric cancer are increasing. Existing studies usually defined obesity by body mass index and analyzed the correlation. Recently, more studies have shown that central obesity is a more important variable in upper gastrointestinal diseases related to gastroesophageal reflux. Studies have reported that weight loss is effective in reducing gastroesophageal reflux symptoms. Obesity also affects functional gastrointestinal diseases. A significant correlation was shown in upper abdominal pain, reflux, vomiting, and diarrhea rather than lower abdominal diseases.

No abstract available.
Basal Ganglia Diseases/diagnostic imaging/drug therapy/*etiology ; Calcinosis/diagnostic imaging/drug therapy/*etiology ; Calcium/therapeutic use ; Dietary Supplements ; Female ; Humans ; Hypoparathyroidism/*complications/diagnosis/drug therapy ; Middle Aged ; Tomography, X-Ray Computed ; Treatment Outcome ; Vitamin D/therapeutic use

Endoscopic treatment for obesity, especially intragastric balloon insertion, is on the rise in Korea. From 2016 to 2019, we performed intragastric balloon placement for the treatment of obesity in 12 patients at a single tertiary center. One balloon was removed on the next day due to nausea and severe abdominal pain, and the remaining 11 patients were followed up for 6 months. Body weight reduction of 8.9±5.4 kg was achieved, and the body mass index was reduced by 3.3±2.0 kg/m2. Significant effects regarding total body weight loss and excess weight loss were noted. The effect of weight reduction was greatest within 1 month after the procedure. Low density lipoprotein cholesterol significantly decreased by 18.0±18.2 mg/dL, but there were no significant changes in blood pressure, fasting blood glucose, total cholesterol, triglyceride, and high density lipoprotein cholesterol. Common adverse events were nausea and epigastric pain, but no serious adverse events occurred. Further studies regarding the long-term effects of endoscopic treatment for obesity and the improvement of metabolic syndrome are needed.

Endoscopic treatment for obesity, especially intragastric balloon insertion, is on the rise in Korea. From 2016 to 2019, we performed intragastric balloon placement for the treatment of obesity in 12 patients at a single tertiary center. One balloon was removed on the next day due to nausea and severe abdominal pain, and the remaining 11 patients were followed up for 6 months. Body weight reduction of 8.9±5.4 kg was achieved, and the body mass index was reduced by 3.3±2.0 kg/m2. Significant effects regarding total body weight loss and excess weight loss were noted. The effect of weight reduction was greatest within 1 month after the procedure. Low density lipoprotein cholesterol significantly decreased by 18.0±18.2 mg/dL, but there were no significant changes in blood pressure, fasting blood glucose, total cholesterol, triglyceride, and high density lipoprotein cholesterol. Common adverse events were nausea and epigastric pain, but no serious adverse events occurred. Further studies regarding the long-term effects of endoscopic treatment for obesity and the improvement of metabolic syndrome are needed.

BACKGROUND: The S100A2 gene, also known as S100L or CaN19, encodes a protein comprised of 99-amino acids, is a member of the calcium-binding proteins of EF-hand family. According to a recent study, this gene was over-expressed in several early and malignant carcinomas compared to normal tissues. To elucidate the role of S100A2 protein in the process during carcinogenesis, production of monoclonal antibody specific to the protein is essential. METHODS: First, cDNA sequence coding for ORF region of human S100A2 gene was amplified and cloned into an expression vector to produce GST fusion protein. Recombinant S100A2 protein and subsequently, monoclonal antibody to the protein were produced. The specificity of anti-S100A2 monoclonal antibody was confirmed by immunoblot analysis of cross reactivity to other recombinant proteins of S100A family (GST-S100A1, GST-S100A4 and GST-S100A6). To confirm the relation of S100A2 to cervical carcinogenesis, S100A2 protein in early cervical carcinoma tissue was immunostained using the monoclonal antibody. RESULTS: GST-S100A2 recombinant protein was purified by affinity chromatography and then fusion protein was cleaved and S100A2 protein was isolated. The monoclonal antibody (KK0723; Korean patent pending #2001-30294) to the protein was produced and the antibody did not react with other members of EF-hand family proteins such as S100A1, S100A4 and S100A6. CONCLUSION: These data suggest that anti-S100A2 monoclonal antibody produced in this study can be very useful for the early detection of cervical carcinoma and elucidation of mechanism during the early cervical carcinogenesis
Animals ; Calcium-Binding Proteins ; Carcinogenesis ; Chromatography, Affinity ; Clinical Coding ; Clone Cells ; DNA, Complementary ; Ecthyma, Contagious ; Humans* ; Recombinant Proteins ; Sensitivity and Specificity

Stem cell factor (SCF) is an early-acting cytokine inducing proliferative synergy with other cytokines in hematopoietic cells. We earlier showed that p21 was synergistically induced in SCF synergy and the p44/42 MAPK pathway was essential for the transcriptional control of p21. SCF synergy accompanies protein synthesis. p70S6K implicated in translational control in many other systems has not been shown in SCF synergy induced system. GM-CSF dependent human cell line MO7e was stimulated with GM-CSF with SCF, and investigated activation of p70S6K by using phospho-specific antibody. A possible contribution of p70S6K to SCF synergy was examined by measuring p21 induction as a model system. p70S6K was slightly activated by GM-CSF alone and markedly activated by SCF alone. Combined stimulation with these two cytokines synergistically activated p70S6K resulting in persistent activation. Addition of the pathway- specific inhibitors for PI3K or FRAP/TOR, two upstream pathways of p70S6K resulted in abolishment of p70S6K phosphorylation and also significant reduction of p21 protein level. These data suggest that synergistically activated p70S6K by GM-CSF plus SCF involves, at least in part, protein translational control including regulation of p21 protein.
1-Phosphatidylinositol 3-Kinase/metabolism ; Drug Synergism ; Enzyme Activation ; Granulocyte-Macrophage Colony-Stimulating Factor/*pharmacology ; Hematopoietic Stem Cells/*enzymology ; Human ; Phosphorylation/drug effects ; Protein-Serine-Threonine Kinases/metabolism ; Ribosomal Protein S6 Kinases, 70kD/antagonists & inhibitors/*metabolism ; Stem Cell Factor/*pharmacology ; Tacrolimus Binding Protein 1A/metabolism

Background/Aims: Point mutations in the 23S ribosomal RNA gene have been associated with Helicobacter pylori clarithromycin resistance. This study aimed to detect the prevalence of these point mutations and to investigate the role of different point mutations in the success of eradication therapy. Methods: We retrospectively investigated a total of 464 consecutive patients who underwent an endoscopic examination and dual-priming oligonucleotide-based multiplex polymerase chain reaction for H. pylori between June 2014 and October 2019. For 289 patients with negative point mutations, standard triple therapy was used in 287 patients, and the bismuth-quadruple regimen was used in two patients. For 175 patients with positive point mutations (A2142G, A2143G, and both mutations), standard triple and bismuth-quadruple therapies were used in 37 patients and 138 patients, respectively. Results: The eradication rates of standard triple and bismuth-quadruple therapies showed no significant difference in mutation-negative patients or those with the A2142G point mutation.However, the eradication rate with bismuth-quadruple therapy was significantly higher than that with standard triple therapy in the group with the A2143G mutation or with the double mutation.The eradication rates for standard triple and bismuth-quadruple therapies, respectively, were 25.8% and 92.1% in the per-protocol group (p<0.001) and 24.2% and 85.2% in the intention-totreat analysis (p<0.001). Conclusions The A2143G point mutation is the most prevalent cause of clarithromycin resistance. Bismuth-quadruple therapy is superior to standard triple therapy in patients with the A2143G or double point mutation.

Background/Aims: Point mutations in the 23S ribosomal RNA gene have been associated with Helicobacter pylori clarithromycin resistance. This study aimed to detect the prevalence of these point mutations and to investigate the role of different point mutations in the success of eradication therapy. Methods: We retrospectively investigated a total of 464 consecutive patients who underwent an endoscopic examination and dual-priming oligonucleotide-based multiplex polymerase chain reaction for H. pylori between June 2014 and October 2019. For 289 patients with negative point mutations, standard triple therapy was used in 287 patients, and the bismuth-quadruple regimen was used in two patients. For 175 patients with positive point mutations (A2142G, A2143G, and both mutations), standard triple and bismuth-quadruple therapies were used in 37 patients and 138 patients, respectively. Results: The eradication rates of standard triple and bismuth-quadruple therapies showed no significant difference in mutation-negative patients or those with the A2142G point mutation.However, the eradication rate with bismuth-quadruple therapy was significantly higher than that with standard triple therapy in the group with the A2143G mutation or with the double mutation.The eradication rates for standard triple and bismuth-quadruple therapies, respectively, were 25.8% and 92.1% in the per-protocol group (p<0.001) and 24.2% and 85.2% in the intention-totreat analysis (p<0.001). Conclusions The A2143G point mutation is the most prevalent cause of clarithromycin resistance. Bismuth-quadruple therapy is superior to standard triple therapy in patients with the A2143G or double point mutation.