BACKGROUND Gastric ulcers(GUs)have a high risk of clinical morbidity and recurrence,and further exploration is needed for the prevention,diagnosis,and treatment of the disease.AIM To investigated the effects of a diet...BACKGROUND Gastric ulcers(GUs)have a high risk of clinical morbidity and recurrence,and further exploration is needed for the prevention,diagnosis,and treatment of the disease.AIM To investigated the effects of a diet plan on pepsinogen(PG)I,PG II,gastrin-17(G-17)levels and nutritional status in patients with GUs.METHODS A total of 100 patients with GUs treated between May 2022 and May 2023 were enrolled,with 47 patients in the control group receiving routine nursing and 53 patients in the experimental group receiving dietary nursing intervention based on a diet plan.The study compared the two groups in terms of nursing efficacy,adverse events(vomiting,acid reflux,and celialgia),time to symptom improvement(burning sensation,acid reflux,and celialgia),gastric function(PG I,PG II,and G-17 levels),and nutritional status[prealbumin(PA)and albumin(ALB)levels].RESULTS The experimental group showed a markedly higher total effective rate of nursing,a significantly lower incidence of adverse events,and a shorter time to symptom improvement than the control group.Additionally,the experimental group’s post-intervention PG I,PG II,and G-17 levels were significantly lower than preintervention or control group levels,whereas PA and ALB levels were significantly higher.CONCLUSION The diet plan significantly reduced PG I,PG II,and G-17 levels in patients with GUs and significantly improved their nutritional status.展开更多
Atrophic gastritis and intestinal metaplasia may progress to gastric malignancy.Non-invasive serum biomarkers have been extensively studied and proven to be useful as a screening tool to stratify risk and identify pat...Atrophic gastritis and intestinal metaplasia may progress to gastric malignancy.Non-invasive serum biomarkers have been extensively studied and proven to be useful as a screening tool to stratify risk and identify patients for endoscopy to detect early gastric cancer.These non-invasive biomarkers have been endorsed and recommended by many international consensus guidelines.In this letter,we reviewed the literature and evidence supporting the use of serum biomarkers as a dynamic test to monitor the status of atrophic gastritis.展开更多
AIM: To examine whether the fasting levels of serum gastrin-17 (G-17) are lower in Barrett's esophagus (BE)patients than in non-Barrett controls.METHODS: Nineteen patients with BE (presenting with a tubular segme...AIM: To examine whether the fasting levels of serum gastrin-17 (G-17) are lower in Barrett's esophagus (BE)patients than in non-Barrett controls.METHODS: Nineteen patients with BE (presenting with a tubular segment ≥2 cm long in lower esophagus and intestinal metaplasia of incomplete type ('specialized columnar epithelium') in endoscopic biopsies from the tubular segment below the squamocolumnar junction were collected prospectively from outpatients referred to diagnostic gastroscopy. The controls comprised 199 prospectively collected dyspeptic outpatients without BE or any endoscopically visible lesions in the upper GI tract.Fasting levels of serum G-17 (G-17fast) were assayed with an EIA test using a Mab highly specific to amidated G-17. None of the patients and controls received therapy with PPIs or other antisecretory agents.RESULTS: The mean and median levels of G-17fast in serum were significantly lower (P = 0.001) in BE patients than in controls. The positive likelihood ratios (LR+) of low G-17fast to predict BE in the whole study population at G-17fast levels ＜0.5, ＜1, or ＜1.5 pmol/L were 3.5, 3.0,and 2.8, respectively. Among patients and controls with healthy stomach mucosa, the LR+ were 5.6, 3.8, and 2.6,respectively. In the whole study population, serum G-17 was below 2 pmol/L in 15 of 19 BE patients (79%). The corresponding prevalence was 66 of 199 (33%) in controls (P＜0.001). The G-17fast was 5 pmol/L or more in only one of the 19 BE patients (5%). In controls, 76 of the 199 patients (38%) had such high serum G-17fast levels (P＜0.01).CONCLUSION: Serum levels of G-17fast tend to be lower in native patients with BE than in healthy controls.展开更多
Objective: To investigate the correlation of serum pepsinogen Ⅰ/Ⅱ ratio and gastrin-17 content with malignant proliferation of cancer cells in patients with gastric cancer. Methods:Superficial gastritis group (n=247...Objective: To investigate the correlation of serum pepsinogen Ⅰ/Ⅱ ratio and gastrin-17 content with malignant proliferation of cancer cells in patients with gastric cancer. Methods:Superficial gastritis group (n=247), gastric ulcer group (n=159) and gastric cancer group (n=97) who were pathologically diagnosed by gastroscopy in Chongqing wanzhou district people's hospital of 5 between August 2016 and August 2017 were selected, and the differences in serum pepsinogen Ⅰ/Ⅱ ratio and gastrin-17 content as well as proliferation and apoptosis gene expression in lesion tissue were compared among the three groups. Pearson test was used to evaluate the correlation of pepsinogen Ⅰ/Ⅱ ratio and gastrin-17 content with malignant proliferation activity of cancer cells in patients with gastric cancer. Results: Serum pepsinogenⅠ/Ⅱ ratio and gastrin-17 content in gastric cancer group were lower than those in gastric ulcer group and superficial gastritis group. Proliferation genes EIF5A2, MACF1 and PIK3CD mRNA expression levels in gastric cancer group were higher than those in gastric ulcer group and superficial gastritis group whereas SIRT1 mRNA expression level was lower than that in gastric ulcer group and superficial gastritis group;apoptosis gene Livin mRNA expression level was higher than that in gastric ulcer group and superficial gastritis group whereas Bad and Noxa mRNA expression levels were lower than those in gastric ulcer group and superficial gastritis group;serum pepsinogen Ⅰ/Ⅱ ratio and gastrin-17 content in gastric cancer group were negatively correlated with EIF5A2, MACF1, PIK3CD and Livin mRNA expression levels, and positively correlated with SIRT1, Bad and Noxa mRNA expression levels. Conclusion: The serum pepsinogen Ⅰ/Ⅱ ratio and gastrin-17 content abnormally reduce in patients with gastric cancer, and the specific levels are directly correlated with gastric cancer cell proliferation and apoptosis activity.展开更多
BACKGROUND Hepatocellular carcinoma(HCC)is an inflammation-associated tumor with a dismal prognosis.Immunotherapy has become an important treatment strategy for HCC,as immunity is closely related to inflammation in th...BACKGROUND Hepatocellular carcinoma(HCC)is an inflammation-associated tumor with a dismal prognosis.Immunotherapy has become an important treatment strategy for HCC,as immunity is closely related to inflammation in the tumor microenvir-onment.Inflammation regulates the expression of programmed death ligand-1(PD-L1)in the immunosuppressive tumor microenvironment and affects im-munotherapy efficacy.Interleukin-17A(IL-17A)is involved in the remodeling of the tumor microenvironment and plays a protumor or antitumor role in different tumors.We hypothesized that IL-17A participates in tumor progression by affe-cting the level of immune checkpoint molecules in HCC.The upregulation of PD-L1 expression in HCC cells by IL-17A was assessed by reverse transcription PCR,western blotting,and flow cytometry.Mechanistic studies were conducted with gene knockout models and pathway inhibitors.The function of IL-17A in immune evasion was explored through coculture of T cells and HCC cells.The effects of IL-17A on the malignant biological behaviors of HCC cells were evaluated in vitro,and the antitumor effects of an IL-17A inhibitor and its synergistic effects with a PD-L1 inhibitor were studied in vivo.RESULTS IL-17A upregulated PD-L1 expression in HCC cells in a dose-dependent manner,whereas IL-17A receptor knockout or treatment with a small mothers against decapentaplegic 2 inhibitor diminished the PD-L1 expression induced by IL-17A.IL-17A enhanced the survival of HCC cells in the coculture system.IL-17A increased the viability,G2/M ratio,and migration of HCC cells and decreased the apoptotic index.Cyclin D1,VEGF,MMP9,and Bcl-1 expression increased after IL-17A treatment,whereas BAX expression decreased.The combination of IL-17A and PD-L1 inhibitors showed synergistic antitumor efficacy and increased cluster of differentiation 8+T lymphocyte infiltration in an HCC mouse model.CONCLUSION IL-17A upregulates PD-L1 expression via the IL-17A receptor/phosphorylation-small mothers against decapenta-plegic 2 signaling pathway in HCC cells.Blocking IL-17A enhances the therapeutic efficacy of PD-L1 antibodies in HCC in vivo.展开更多
基金the Ethic Committee of Lujiang County Hospital of Traditional Chinese Medicine.
文摘BACKGROUND Gastric ulcers(GUs)have a high risk of clinical morbidity and recurrence,and further exploration is needed for the prevention,diagnosis,and treatment of the disease.AIM To investigated the effects of a diet plan on pepsinogen(PG)I,PG II,gastrin-17(G-17)levels and nutritional status in patients with GUs.METHODS A total of 100 patients with GUs treated between May 2022 and May 2023 were enrolled,with 47 patients in the control group receiving routine nursing and 53 patients in the experimental group receiving dietary nursing intervention based on a diet plan.The study compared the two groups in terms of nursing efficacy,adverse events(vomiting,acid reflux,and celialgia),time to symptom improvement(burning sensation,acid reflux,and celialgia),gastric function(PG I,PG II,and G-17 levels),and nutritional status[prealbumin(PA)and albumin(ALB)levels].RESULTS The experimental group showed a markedly higher total effective rate of nursing,a significantly lower incidence of adverse events,and a shorter time to symptom improvement than the control group.Additionally,the experimental group’s post-intervention PG I,PG II,and G-17 levels were significantly lower than preintervention or control group levels,whereas PA and ALB levels were significantly higher.CONCLUSION The diet plan significantly reduced PG I,PG II,and G-17 levels in patients with GUs and significantly improved their nutritional status.
文摘Atrophic gastritis and intestinal metaplasia may progress to gastric malignancy.Non-invasive serum biomarkers have been extensively studied and proven to be useful as a screening tool to stratify risk and identify patients for endoscopy to detect early gastric cancer.These non-invasive biomarkers have been endorsed and recommended by many international consensus guidelines.In this letter,we reviewed the literature and evidence supporting the use of serum biomarkers as a dynamic test to monitor the status of atrophic gastritis.
文摘AIM: To examine whether the fasting levels of serum gastrin-17 (G-17) are lower in Barrett's esophagus (BE)patients than in non-Barrett controls.METHODS: Nineteen patients with BE (presenting with a tubular segment ≥2 cm long in lower esophagus and intestinal metaplasia of incomplete type ('specialized columnar epithelium') in endoscopic biopsies from the tubular segment below the squamocolumnar junction were collected prospectively from outpatients referred to diagnostic gastroscopy. The controls comprised 199 prospectively collected dyspeptic outpatients without BE or any endoscopically visible lesions in the upper GI tract.Fasting levels of serum G-17 (G-17fast) were assayed with an EIA test using a Mab highly specific to amidated G-17. None of the patients and controls received therapy with PPIs or other antisecretory agents.RESULTS: The mean and median levels of G-17fast in serum were significantly lower (P = 0.001) in BE patients than in controls. The positive likelihood ratios (LR+) of low G-17fast to predict BE in the whole study population at G-17fast levels ＜0.5, ＜1, or ＜1.5 pmol/L were 3.5, 3.0,and 2.8, respectively. Among patients and controls with healthy stomach mucosa, the LR+ were 5.6, 3.8, and 2.6,respectively. In the whole study population, serum G-17 was below 2 pmol/L in 15 of 19 BE patients (79%). The corresponding prevalence was 66 of 199 (33%) in controls (P＜0.001). The G-17fast was 5 pmol/L or more in only one of the 19 BE patients (5%). In controls, 76 of the 199 patients (38%) had such high serum G-17fast levels (P＜0.01).CONCLUSION: Serum levels of G-17fast tend to be lower in native patients with BE than in healthy controls.
文摘Objective: To investigate the correlation of serum pepsinogen Ⅰ/Ⅱ ratio and gastrin-17 content with malignant proliferation of cancer cells in patients with gastric cancer. Methods:Superficial gastritis group (n=247), gastric ulcer group (n=159) and gastric cancer group (n=97) who were pathologically diagnosed by gastroscopy in Chongqing wanzhou district people's hospital of 5 between August 2016 and August 2017 were selected, and the differences in serum pepsinogen Ⅰ/Ⅱ ratio and gastrin-17 content as well as proliferation and apoptosis gene expression in lesion tissue were compared among the three groups. Pearson test was used to evaluate the correlation of pepsinogen Ⅰ/Ⅱ ratio and gastrin-17 content with malignant proliferation activity of cancer cells in patients with gastric cancer. Results: Serum pepsinogenⅠ/Ⅱ ratio and gastrin-17 content in gastric cancer group were lower than those in gastric ulcer group and superficial gastritis group. Proliferation genes EIF5A2, MACF1 and PIK3CD mRNA expression levels in gastric cancer group were higher than those in gastric ulcer group and superficial gastritis group whereas SIRT1 mRNA expression level was lower than that in gastric ulcer group and superficial gastritis group;apoptosis gene Livin mRNA expression level was higher than that in gastric ulcer group and superficial gastritis group whereas Bad and Noxa mRNA expression levels were lower than those in gastric ulcer group and superficial gastritis group;serum pepsinogen Ⅰ/Ⅱ ratio and gastrin-17 content in gastric cancer group were negatively correlated with EIF5A2, MACF1, PIK3CD and Livin mRNA expression levels, and positively correlated with SIRT1, Bad and Noxa mRNA expression levels. Conclusion: The serum pepsinogen Ⅰ/Ⅱ ratio and gastrin-17 content abnormally reduce in patients with gastric cancer, and the specific levels are directly correlated with gastric cancer cell proliferation and apoptosis activity.
基金Supported by the Natural Science Foundation of Gansu Province,No.21JR7RA373 and No.24JRRA295.
文摘BACKGROUND Hepatocellular carcinoma(HCC)is an inflammation-associated tumor with a dismal prognosis.Immunotherapy has become an important treatment strategy for HCC,as immunity is closely related to inflammation in the tumor microenvir-onment.Inflammation regulates the expression of programmed death ligand-1(PD-L1)in the immunosuppressive tumor microenvironment and affects im-munotherapy efficacy.Interleukin-17A(IL-17A)is involved in the remodeling of the tumor microenvironment and plays a protumor or antitumor role in different tumors.We hypothesized that IL-17A participates in tumor progression by affe-cting the level of immune checkpoint molecules in HCC.The upregulation of PD-L1 expression in HCC cells by IL-17A was assessed by reverse transcription PCR,western blotting,and flow cytometry.Mechanistic studies were conducted with gene knockout models and pathway inhibitors.The function of IL-17A in immune evasion was explored through coculture of T cells and HCC cells.The effects of IL-17A on the malignant biological behaviors of HCC cells were evaluated in vitro,and the antitumor effects of an IL-17A inhibitor and its synergistic effects with a PD-L1 inhibitor were studied in vivo.RESULTS IL-17A upregulated PD-L1 expression in HCC cells in a dose-dependent manner,whereas IL-17A receptor knockout or treatment with a small mothers against decapentaplegic 2 inhibitor diminished the PD-L1 expression induced by IL-17A.IL-17A enhanced the survival of HCC cells in the coculture system.IL-17A increased the viability,G2/M ratio,and migration of HCC cells and decreased the apoptotic index.Cyclin D1,VEGF,MMP9,and Bcl-1 expression increased after IL-17A treatment,whereas BAX expression decreased.The combination of IL-17A and PD-L1 inhibitors showed synergistic antitumor efficacy and increased cluster of differentiation 8+T lymphocyte infiltration in an HCC mouse model.CONCLUSION IL-17A upregulates PD-L1 expression via the IL-17A receptor/phosphorylation-small mothers against decapenta-plegic 2 signaling pathway in HCC cells.Blocking IL-17A enhances the therapeutic efficacy of PD-L1 antibodies in HCC in vivo.
