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| 1 | Helicobacter pylori associated chronic gastritis,clinical syndromes,precancerous lesions,and pathogenesis of gastric cancer development显示文摘Helicobacter pylori(H.pylori)infection is well known to be associated with the development of precancerous lesions such as chronic atrophic gastritis(AG),or gastric intestinal metaplasia(GIM),and cancer.Various molecular alterations are identified not only in gastric cancer(GC)but also in precancerous lesions.H.pylori treatment seems to improve AG and GIM,but still remains controversial.In contrast,many studies,including meta-analysis,show that H.pylori eradication reduces GC.Molecular markers detected by genetic and epigenetic alterations related to carcinogenesis reverse following H.pylori eradication.This indicates that these changes may be an important factor in the identification of high risk patients for cancer development.Patients who underwent endoscopic treatment of GC are at high risk for development of metachronous GC.A randomized controlled trial from Japan concluded that prophylactic eradication of H.pylori after endoscopic resection should be used to prevent the development of metachronous GC,but recent retrospective studies did not show the tendency.Patients with precancerous lesions(molecular alterations)that do not reverse after H.pylori treatment,represent the'point of no return'and may be at high risk for the development of GC.Therefore,earlier H.pylori eradication should be considered for preventing GC development prior to the appearance of precancerous lesions. | Jiro Watari Nancy Chen Peter S Amenta Hirokazu Fukui Tadayuki Oshima Toshihiko Tomita Hiroto Miwa Kheng-Jim Lim Kiron M Das | 2014 | World Journal of Gastroenterology2014，20，18： | 60 |
| 2 | Biomolecular basis of the role of diabetes mellitus in osteoporosis and bone fractures显示文摘Osteoporosis has become a serious health problem throughout the world which is associated with an increased risk of bone fractures and mortality among the people of middle to old ages.Diabetes is also a major health problem among the people of all age ranges and the sufferers due to this abnormality increasing day by day.The aim of this review is to summarize the possible mechanisms through which diabetes may induce osteoporosis.Diabetes mellitus generally exerts its effect on different parts of the body including bone cells specially the osteoblast and osteoclast,muscles,retina of the eyes,adipose tissue,endocrine system specially parathyroid hormone(PTH) and estrogen,cytokines,nervous system and digestive system.Diabetes negatively regulates osteoblast differentiation and function while positively regulates osteoclast differentiation and function through the regulation of different intermediate factors and thereby decreases bone formation while increases bone resorption.Some factors such as diabetic neuropathy,reactive oxygen species,Vitamin D,PTH have their effects on muscle cells.Diabetes decreases the muscle strength through regulating these factors in various ways and ultimately increases the risk of fall that may cause bone fractures. | Bipradas Roy | 2013 | World Journal of Diabetes2013，4，4： | 41 |
| 3 | Endoscopic Kyoto classification of Helicobacter pylori infection and gastric cancer risk diagnosis显示文摘Recent advances in endoscopic technology allow detailed observation of the gastric mucosa.Today,endoscopy is used in the diagnosis of gastritis to determine the presence/absence of Helicobacter pylori(H.pylori)infection and evaluate gastric cancer risk.In 2013,the Japan Gastroenterological Endoscopy Society advocated the Kyoto classification,a new grading system for endoscopic gastritis.The Kyoto classification organized endoscopic findings related to H.pylori infection.The Kyoto classification score is the sum of scores for five endoscopic findings(atrophy,intestinal metaplasia,enlarged folds,nodularity,and diffuse redness with or without regular arrangement of collecting venules)and ranges from 0 to 8.Atrophy,intestinal metaplasia,enlarged folds,and nodularity contribute to gastric cancer risk.Diffuse redness and regular arrangement of collecting venules are related to H.pylori infection status.In subjects without a history of H.pylori eradication,the infection rates in those with Kyoto scores of 0,1,and≥2 were 1.5%,45%,and 82%,respectively.A Kyoto classification score of 0 indicates no H.pylori infection.A Kyoto classification score of 2 or more indicates H.pylori infection.Kyoto classification scores of patients with and without gastric cancer were 4.8 and 3.8,respectively.A Kyoto classification score of 4 or more might indicate gastric cancer risk. | Osamu Toyoshima Toshihiro Nishizawa Kazuhiko Koike | 2020 | World Journal of Gastroenterology2020，26，5： | 44 |
| 4 | Histological changes of gastric mucosa after Helicobacter pylori eradication:a systematic review and meta-analysis显示文摘AIM:To systematically review pathological changes of gastric mucosa in gastric atrophy(GA)and intestinal metaplasia(IM)after Helicobacter pylori(H.pylori)eradication.METHODS:A systematic search was made of PubMed,Web of Science,EMBASE,ClinicalTrials.gov,OVID and the Cochran Library databases for articles published before March 2013 pertaining to H.pylori and gastric premalignant lesions.Relevant outcomes from articles included in the meta-analysis were combined using Review Manager 5.2 software.A Begg’s test was applied to test for publication bias using STATA 11software.χ2 and I2 analyses were used to assess heterogeneity.Analysis of data with no heterogeneity(P>0.1,I2<25%)was carried out with a fixed effects model,otherwise the causes of heterogeneity were first analyzed and then a random effects model was applied.RESULTS:The results of the meta-analysis showed that the pooled weighted mean difference(WMD)with 95%CI was 0.23(0.18-0.29)between eradication and non-eradication of H.pylori infection in antral IM with a significant overall effect(Z=8.19;P<0.00001)and no significant heterogeneity(χ2=27.54,I2=16%).The pooled WMD with 95%CI was-0.01(-0.04-0.02)for IM in the corpus with no overall effect(Z=0.66)or heterogeneity(χ2=14.87,I2=0%)(fixed effects model).In antral GA,the pooled WMD with 95%CI was 0.25(0.15-0.35)with a significant overall effect(Z=4.78;P<0.00001)and significant heterogeneity(χ2=86.12,I2=71%;P<0.00001).The pooled WMD with 95%CI for GA of the corpus was 0.14(0.04-0.24)with a significant overall effect(Z=2.67;P=0.008)and significant heterogeneity(χ2=44.79,I2=62%;P=0.0003)(random effects model).CONCLUSION:H.pylori eradication strongly correlates with improvement in IM in the antrum and GA in the corpus and antrum of the stomach. | Yan-Jun Kong Hong-Gang Yi Jun-Cheng Dai Mu-Xin Wei | 2014 | World Journal of Gastroenterology2014，20，19： | 24 |
| 5 | Type 2 diabetes mellitus and Alzheimer's disease显示文摘Epidemiological and biological evidences support a link between type 2 diabetes mellitus(DM2) and Alzheimer's disease(AD). Persons with diabetes have a higher incidence of cognitive decline and an increased risk of developing all types of dementia. Cognitive deficits in persons with diabetes mainly affect the areas of psychomotor efficiency, attention, learning and memory, mental flexibility and speed, and executive function. The strong epidemiological association has suggested the existence of a physiopathological link. The determinants of the accelerated cognitive decline in DM2, however, are less clear. Increased cortical and subcortical atrophy have been evidenced after controlling for diabetic vascular disease and inadequate cerebral circulation. Most recent studies have focused on the role of insulin and insulin resistance as possible links between diabetes and AD. Disturbances in brain insulin signaling mechanisms may contribute to the molecular, biochemical, and histopathological lesions in AD. Hyperglycemia itself is a risk factor for cognitive dysfunction and dementia. Hypoglycemia may also have deleterious effects on cognitive function. Recurrent symptomatic and asymptomatic hypoglycemic episodes have been suggested to cause sub-clinical brain damage, and permanent cognitive impairment. Futuretrials are required to clarify the mechanistic link, to address the question whether cognitive decline may be prevented by an adequate metabolic control, and to elucidate the role of drugs that may cause hypoglycemic episodes. | Mario Barbagallo Ligia J Dominguez | 2014 | World Journal of Diabetes2014，5，6： | 22 |
| 6 | Identifying high-risk individuals for gastric cancer surveillance from western and eastern perspectives: Lessons to learn and possibility to develop an integrated approach for daily practice显示文摘Current evidence shows that individuals with gastric dysplasia, severe and extensive gastric atrophy, extensive gastric intestinal metaplasia and the incomplete subtype of intestinal metaplasia are at high risk for gastric cancer(GC) development. There are several approaches to identifying these subjects,including noninvasive methods, esophagogastroduodenoscopy and histology.The main approach in Western countries is histology-based while that in Eastern countries with a high prevalence of GC is endoscopy-based. Regarding asymptomatic individuals, the key issues in selecting applicable approaches are the ability to reduce GC mortality and the cost-effectiveness of the approach. At present, population-based screening programs have only been applied in a few Asian countries with a high risk of GC. Pre-endoscopic risk assessment based on demographic and clinical features, such as ethnicity, age, gender, smoking and Helicobacter pylori status, is helpful for identifying subjects with high pre-test probability for a possibly cost-effective approach, especially in intermediate-and low-risk countries. Regarding symptomatic patients with indications for esophagogastroduodenoscopy, the importance of opportunistic screening should be emphasized. The combination of endoscopic and histological approaches should always be considered as endoscopy provides a real-time assessment of the patient’s risk level. In addition, imaging enhanced endoscopy(IEE) has been shown to facilitate targeted biopsies resulting in better correlation between endoscopic and histological findings. Currently, the use of IEE is recommended for endoscopic examinations, and the Operative Link for Gastric Intestinal Metaplasia or Operative Link on Gastritis Assessment grading systems are recommended for histological examinations whenever available. However,resource limitations are an important barrier in many regions worldwide. Thus,for an approach to be applicable in real-life practice, it should be not only evidence-based but also resource-sensitive. In this review, we discuss the current understanding and approaches to identifying high-risk individuals from western and eastern perspectives, as well as the possibility of an integrated, resourcesensitive approach. | Duc Trong Quach Toru Hiyama Takuji Gotoda | 2019 | World Journal of Gastroenterology2019，25，27： | 18 |
| 7 | NUTRITIONAL LIPID LIVER DISEASE OF GRASS CARP CTENOPHARYNGODON IDULLUS(C.et V.)显示文摘The inadequate nutrient content of pellet feeds widely used in recent years in China for grass carp forming led to lipid liver degeneration in the fish. The present studies show that the pathological features of lipid liver disease are anaemia and hepatic ceroidosis. Other clinical features are: the ratio of liver to body weight exceeds 3% and lipid content exceeds 5%. Extreme infiltration of hepaiocytes by lipid results in the following deteriorative effects: swelling of the liver cells, increase of lipid droplets in the cytoplasm and dislocation of the nucleus, loss of cytoplasm staining affinity, and increased activities of GOT and GPT in serum. Lipid liver degeneration of grass carp can be divided into three stages: 1) deposition of liver lipid; 2) lipid infiltration of hepatic parenchyma; 3) atrophy of liver nucleus. The causes of lipid liver degeneration are complicated, but the main cause is assumed to be an imbalance of nutrients in daily feed and the lack of some lipotropic substances. | 林鼎 毛永庆 蔡发盛 | 1990 | Chinese Journal of Oceanology and Limnology1990，8，4： | 16 |
| 8 | The mechanisms and treatments of muscular pathological changes in immobilization-induced joint contracture: A literature review显示文摘The clinical treatment of joint contracture due to immobilization remains difficult.The pathological changes of muscle tissue caused by immobilization-induced joint contracture include disuse skeletal muscle atrophy and skeletal muscle tissue fibrosis.The proteolytic pathways involved in disuse muscle atrophy include the ubiquitin-proteasome-dependent pathway,caspase system pathway,matrix metalloproteinase pathway,Ca2+-dependent pathway and autophagy-lysosomal pathway.The important biological processes involved in skeletal muscle fibrosis include intermuscular connective tissue thickening caused by transforming growth factor-β1 and an anaerobic environment within the skeletal muscle leading to the induction of hypoxia-inducible factor-1α.This article reviews the progress made in understanding the pathological processes involved in immobilization-induced muscle contracture and the currently available treatments.Understanding the mechanisms involved in immobilization-induced contracture of muscle tissue should facilitate the development of more effective treatment measures for the different mechanisms in the future. | Feng Wang Quan-Bing Zhang Yun Zhou Shuang Chen Peng-Peng Huang Yi Liu Yuan-Hong Xu | 2019 | Chinese Journal of Traumatology2019，22，2： | 15 |
| 9 | Prevalence of Helicobacter pylori infection and atrophic gastritis in patients with dyspeptic symptoms in Myanmar显示文摘AIM: To survey the detailed analyses for Helicobacter pylori(H. pylori) infection and gastric mucosal status in Myanmar.METHODS: A total of 252 volunteers with dyspeptic symptoms(155 female and 97 male; mean age of 43.6 ± 14.2 years) was participated in Yangon and Mandalay. The status of H. pylori infection was determined based on 5 different tests including rapid urease test, culture, histology, immunohistochemistry and serology. Histological scores were evaluated according to the update Sydney system and the Operative Link for Gastritis Assessment system. Pepsinogen(PG)Ⅰand PG Ⅱ were measured using enzyme-linked immunosorbent assays.RESULTS: The overall prevalence of H. pylori infectionwas 48.0%. There was no relationship between age and infection rate. Even in young group(less than 29 years old), the H. pylori infection rate was relatively high(41.9%). The prevalence of H. pylori infection was significantly higher in Yangon than that of Mandalay. H. pylori infection was significantly associated with the presence of gastric mucosal atrophy. All 7 subjects with peptic ulcer were infected with H. pylori. Although H. pylori-positive subjects showed stronger gastritis than H. pylori-negative subjects, most cases had mild gastritis.CONCLUSION: We revealed the prevalence of H. pylori infection in patients with dyspeptic symptoms in Myanmar. The H. pylori infection was a risk factor for peptic ulcer and stronger gastritis. | Thein Myint Seiji Shiota Ratha-korn Vilaichone New Ni Than Than Aye Miyuki Matsuda Trang Thi Huyen Tran Tomohisa Uchida Varocha Mahachai Yoshio Yamaoka | 2015 | World Journal of Gastroenterology2015，21，2： | 10 |
| 10 | Helicobacter pylori infection with atrophic gastritis: An independent risk factor for colorectal adenomas显示文摘BACKGROUND The significance of Helicobacter pylori(H.pylori)infection and atrophic gastritis(AG)in the prevalence of colorectal adenomas has been examined in a limited number of studies.However,these studies reported disputed conclusions.AIM To investigate whether H.pylori infection,AG,and H.pylori-related AG increase the risk of colorectal adenomas.METHODS This retrospective cross-sectional study included 6018 health-check individuals.The relevant data for physical examination,laboratory testing,13C-urea breath testing,gastroscopy,colonoscopy and histopathological examination of gastric and colorectal biopsies were recorded.Univariate and multivariate logistic regression analyses were performed to determine the association between H.pylori-related AG and colorectal adenomas.RESULTS Overall,1012 subjects(16.8%)were diagnosed with colorectal adenomas,of whom 143(2.4%)had advanced adenomas.Among the enrolled patients,the prevalence of H.pylori infection and AG was observed as 49.5%(2981/6018)and 10.0%(602/6018),respectively.Subjects with H.pylori infection had an elevated risk of colorectal adenomas(adjusted odds ratio[OR]of 1.220,95%confidence interval(CI):1.053-1.413,P=0.008)but no increased risk of advance adenomas(adjusted OR=1.303,95%CI:0.922-1.842,P=0.134).AG was significantly correlated to an increased risk of colorectal adenomas(unadjusted OR=1.668,95%CI:1.352-2.059,P<0.001;adjusted OR=1.237,95%CI:0.988-1.549,P=0.064).H.pylori infection accompanied by AG was significantly associated with an increased risk of adenomas(adjusted OR=1.491,95%CI:1.103-2.015,P=0.009)and advanced adenomas(adjusted OR=1.910,95%CI:1.022-3.572,P=0.043).CONCLUSION H.pylori-related AG was associated with a high risk of colorectal adenomas and advanced adenomas in Chinese individuals. | Qin-Fen Chen Xiao-Dong Zhou Dan-Hong Fang En-Guang Zhang Chun-Jing Lin Xiao-Zhen Feng Na Wang Jian-Sheng Wu Dan Wang Wei-Hong Lin | 2020 | World Journal of Gastroenterology2020，26，37： | 8 |
| 11 | Characteristics and advantages of adeno-associated virus vector-mediated gene therapy for neurodegenerative diseases显示文摘Common neurodegenerative diseases of the central nervous system are characterized by progressive damage to the function of neurons, even leading to the permanent loss of function. Gene therapy via gene replacement or gene correction provides the potential for transformative therapies to delay or possibly stop further progression of the neurodegenerative disease in affected patients. Adeno-associated virus has been the vector of choice in recent clinical trials of therapies for neurodegenerative diseases due to its safety and efficiency in mediating gene transfer to the central nervous system. This review aims to discuss and summarize the progress and clinical applications of adeno-associated virus in neurodegenerative disease in central nervous system. Results from some clinical trials and successful cases of central neurodegenerative diseases deserve further study and exploration. | Yuan Qu Yi Liu Ahmed Fayyaz Noor Johnathan Tran Rui Li | 2019 | Neural Regeneration Research2019，14，6： | 6 |
| 12 | Can endoscopic atrophy predict histological atrophy? Historical study in United Kingdom and Japan显示文摘AIM: To assess the diagnostic concordance between endoscopic and histological atrophy in the United Kingdom and Japan.METHODS: Using published data,a total of 252 patients,126 in the United Kingdom and 126 in Japan,aged 20 to 80 years,were evaluated. The extent of endoscopic atrophy was classified into five subgroups according to a modified Kimura-Takemoto classification system and was compared with histological findings of atrophy at five biopsy sites according to the updated Sydney system.RESULTS: The strength of agreement of the extent of atrophy between histology and visual endoscopic inspection showed good reproducibili ty,wi th a weighted kappa value of 0.76(P < 0.001). Multivariate analysis showed that three factors were associated with decreased concordance: Japanese ethnicity [odds ratio(OR) 0.22,95% confidence interval(CI) 0.11-0.43],older age(OR = 0.32,95%CI: 0.16-0.66) and endoscopic atrophy(OR = 0.10,95%CI: 0.03-0.36). The strength of agreement between endoscopic and histological atrophy,assessed by cancer risk-oriented grading,was reproducible,with a kappa value of 0.81(95%CI: 0.75-0.87). Only nine patients(3.6%) were endoscopically underdiagnosed with antral predominant rather than extensive atrophy and were considered false negatives.CONCLUSION: Endoscopic grading can predict histological atrophy with few false negatives,indicating that precancerous conditions can be identified during screening endoscopy,particularly in patients in western countries. | Shin Kono Takuji Gotoda Shigeaki Yoshida Ichiro Oda Hitoshi Kondo Luigi Gatta Greg Naylor Michael Dixon Fuminori Moriyasu Anthony Axon | 2015 | World Journal of Gastroenterology2015，21，46： | 6 |
| 13 | Establishment of a mouse model of cancer cachexia with spleen deficiency syndrome and the effects of atractylenolide I显示文摘Cancer cachexia is a multifactorial metabolic syndrome that affects~50%–80%of cancer patients,and no effective therapy for cancer cachexia is presently available.In traditional Chinese medicine,a large portion of patients with cancer cachexia was diagnosed as spleen deficiency syndrome and treated with tonifying TCMs that produce clinic benefits.In this study we established a new animal model of spleen deficiency and cancer cachexia in mice and evaluated the therapeutic effects of atractylenolide I,an active component of tonifying TCM BaiZhu,in the mouse model.Cancer cachexia was induced in male BALB/c mice by inoculation of mouse C26 colon adenocarcinoma cells,whereas spleen deficiency syndrome was induced by treating the mice with spleen deficiency-inducing factors,including limited feeding,fatigue,and purging.The mouse model was characterized by both cachexia and spleen deficiency characteristics,including significant body weight loss,cancer growth,muscle atrophy,fat lipolysis,spleen,and thymus atrophy as compared with healthy control mice,cancer cachexia mice,and spleen deficiency mice.Oral administration of atractylenolide I(20 mg·kg?1per day,for 30 days)significantly ameliorated the reduction in body weight and atrophy of muscle,fat,spleen,and thymus in mice with spleen deficiency and cachexia.The established model of spleen deficiency and cancer cachexia might be useful in the future for screening possible anticachexia TCMs and clarifying their mechanisms. | Wan-li Zhang Na Li Qiang Shen Men Fan Xiao-dong Guo Xiong-wen Zhang Zhou Zhang Xuan Liu | 2020 | Acta Pharmacologica Sinica2020，41，2： | 6 |
| 14 | NKX6.3 protects against gastric mucosal atrophy by downregulatingβ-amyloid production显示文摘BACKGROUND Atrophic gastritis is characterized by loss of appropriate glands and reduction in gastric secretory function due to chronic inflammatory processes in gastric mucosa. Moreover, atrophic gastritis is considered as a precancerous condition of gastric cancer. However, little is known about the molecular mechanism underlying gastric mucosal atrophy and its contribution to gastric carcinogenesis.Thus, we hypothesized that transcription factor NKX6.3 might be involved in maintaining gastric epithelial homeostasis by regulating amyloid β(Aβ)production.AIM To determine whether NKX6.3 might protect against gastric mucosal atrophy by regulating Aβ production.METHODS We identified NKX6.3 depletion induced cell death by cell count and Western blot assay. Production and mechanism of Aβ oligomer were analyzed by enzymelinked immunosorbent assay, Western blot, immunoprecipitation, real-timequantitative polymerase chain reaction and immunofluorescence analysis. We further validated the correlation between expression of NKX6.3, Helicobacter pylori CagA, Aβ oligomer, apolipoprotein E(ApoE), and β-secretase 1(Bace1) in 55 gastric mucosae.RESULTS NKX6.3 depletion increased both adherent and floating cell populations in HFE-145 cells. Expression levels of cleaved caspase-3,-9, and poly ADP ribose polymerase were elevated in floating HFE-145^(shNKX6.3) cells. NKX6.3 depletion produced Aβ peptide oligomers, and increased expression of ApoE, amyloid precursor protein, Aβ, Bace1, low-density lipoprotein receptor, nicastrin, high mobility group box1, and receptor for advanced glycosylation end product proteins. In immunoprecipitation assay, γ-secretase complex was stably formed only in HFE-145^(shNKX6.3) cells. In gastric mucosae with atrophy, expression of Aβpeptide oligomer, ApoE, and Bace1 was detected and inversely correlated with NKX6.3 expression. Treatment with recombinant Aβ 1-42 produced Aβoligomeric forms and decreased cell viability in HFE-145^(shNKX6.3) cells. Additionally,NKX6.3 depletion increased expression of inflammatory cytokines and cyclooxygenase-2.CONCLUSION NKX6.3 inhibits gastric mucosal atrophy by regulating Aβ accumulation and inflammatory reaction in gastric epithelial cells. | Jung Hwan Yoon Yeon Soo Lee Olga Kim Hassan Ashktorab Duane T Smoot Suk Woo Nam Won Sang Park | 2019 | World Journal of Gastroenterology2019，25，3： | 6 |
| 15 | Protective effects of oral glutathione on fasting-induced intestinal atrophy through oxidative stress显示文摘AIM To determine whether oral glutathione(GSH)administration can alleviate the effects of fasting-induced intestinal atrophy in the small intestinal mucosa. METHODS Rats were divided into eight groups.One group was fed ad libitum,another was fed ad libitum and received oral GSH,and six groups were administrated saline(SA)or GSH orally during fasting.Mucosal height,apoptosis,and cell proliferation in the jejunum were histologically evaluated.i NOS protein expression(by immunohistochemistry),nitrite levels(by high performance liquid chromatography,as a measure of NO production),8-hydroxydeoxyguanosine formation(by ELISA,indicating ROS levels),glutathione/oxidized glutathione(GSH/GSSG)ratio(by enzymatic colorimetric detection),andγ-glutamyl transpeptidase(Ggt1)mR NA levels in the jejunum(by semi-quantitative RT-PCR)were also estimated. RESULTS O r a l G S H a d m i n i s t r a t i o n w a s d e m o n s t r a t e d t o drastically reduce fasting-induced intestinal atrophy in the jejunum.In particular,jejunal mucosal height was enhanced in GSH-treated animals compared to SA-treated animals[527.2±6.9 for 50 mg/kg GSH,567.6±5.4 for 500 mg/kg GSH vs 483.1±4.9(μm),P<0.01at 72 h].This effect was consistent with decreasing changes in GSH-treated animals compared to SA-treated animals for iN OS protein staining[0.337±0.016for 50 mg/kg GSH,0.317±0.017 for 500 mg/kg GSH vs 0.430±0.023(area of staining part/area of tissue),P<0.01 at 72 h]and NO[2.99±0.29 for 50 mg/kg GSH,2.88±0.19 for 500 mg/kg GSH vs 5.34±0.35(nmol/g tissue),P<0.01 at 72 h]and ROS[3.92±0.46for 50 mg/kg GSH,4.58±0.29 for 500 mg/kg GSH vs6.42±0.52(8-OHdG pg/μg DNA),P<0.01,P<0.05at 72 h,respectively]levels as apoptosis mediators in the jejunum.Furthermore,oral GSH administration attenuated cell proliferation decreases in the fasting jejunum[182.5±1.9 for 500 mg/kg GSH vs 155.8±3.4(5-Brd U positive cells/10 crypts),P<0.01 at 72h].Notably,both GSH concentration and Ggt1 m RNA expression in the jejunum were also attenuated in rats following oral administration of GSH during fasting as compared with fasting alone[0.45±0.12 vs 0.97±0.06(nmol/mg tissue),P<0.01;1.01±0.11 vs 2.79±0.39(Ggt1 m RNA/Gapdh m RNA),P<0.01 for 500 mg/kg GSH at 48 h,respectively]. CONCLUSION Oral GSH administration during fasting enhances jejunal regenerative potential to minimize intestinal mucosal atrophy by diminishing fasting-mediated ROS generation and enterocyte apoptosis and enhancing cell proliferation. | Hiroyuki Uchida Yukari Nakajima Kazuo Ohtake Junta Ito Masahiko Morita Ayako Kamimura Jun Kobayashi | 2017 | World Journal of Gastroenterology2017，23，36： | 5 |
| 16 | Eradication rate and histological changes after Helicobacter pylori eradication treatment in gastric cancer patients following subtotal gastrectomy显示文摘AIM: To investigate the eradication rate and histological changes after Helicobacter pylori(H. pylori) eradication treatment following subtotal gastrectomy for gastric cancer.METHODS: A total of 610 patients with H. pylori infection who had undergone surgery for either early or advanced gastric adenocarcinoma between May 2004 and December 2010 were retrospectively studied. A total of 584 patients with proven H. pylori infection after surgery for gastric cancer were enrolled in this study. Patients received a seven day standard triple regimen as first-line therapy and a 10 d bismuthcontaining quadruple regimen as second-line therapy in cases of eradication failure. The patients underwent an esophagogastroduodenoscopy(EGD) between six and 12 mo after surgery, followed by annual EGDs. A further EGD was conducted 12 mo after confirming the result of the eradication and the histological changes. A gastric biopsy specimen for histological examination and Campylobacter-like organism testing was obtained from the lesser and greater curvature of the corpus of the remnant stomach. Histological changes in the gastric mucosa were assessed using the updated Sydney system before eradication therapy and at follow-up after 12 mo.RESULTS: Eradication rates with the first-line and second-line therapies were 78.4%(458/584) and 90%(36/40), respectively, by intention-to-treat analysis and 85.3%(458/530) and 92.3%(36/39), respectively, by per-protocol analysis. The univariate and multivariate analyses revealed that Billroth Ⅱ surgery was an independent factor predictive of eradication success in the eradication success group(OR = 1.53, 95%CI: 1.41-1.65, P = 0.021). The atrophy and intestinal metaplasia(IM) scores 12 mo after eradication were significantly lower in the eradication success group than in the eradication failure group(0.25 ± 0.04 vs 0.47 ± 0.12, P = 0.023; 0.27 ± 0.04 vs 0.51 ± 0.12, P = 0.015, respectively). The atrophy and IM scores 12 mo after successful eradication were significantly lower in the Billroth Ⅱ group than in the Billroth I group(0.13 ± 0.09 vs 0.31 ± 0.12, P = 0.029; 0.32 ± 0.24 vs 0.37 ± 0.13, P = 0.034, respectively).CONCLUSION: Patients with H. pylori following subtotal gastrectomy had a similar eradication rate to patients with an intact stomach. H. pylori eradication is recommended after subtotal gastrectomy. | Jae Jin Hwang Dong Ho Lee Kyu Keun Kang Ae-Ra Lee Hyuk Yoon Cheol Min Shin Young Soo Park Nayoung Kim | 2015 | World Journal of Gastroenterology2015，21，13： | 5 |
| 17 | Base editing-mediated splicing correction therapy for spinal muscular atrophy显示文摘Dear Editor,Spinal muscular atrophy(SMA)is a devastating autosomal recessive motor neuron disease.1,2 Infants with more severe forms of type I SMA die before the age of 2 if no intervention is provided.1,2 Spinraza and zolgensma have been approved by the FDA as SMA therapeutics for pediatric patients.1,2 However,as an antisense oligonucleotide(ASO)based therapy,spinraza requires four loading doses,followed by three annual maintenance doses.The patients would be subjected to repeated intrathecal injections in the procedure.Zolgensma is a single-dose gene-replacement therapy for SMA,but unfortunately is unreliable in maintaining a high,stable level of gene expression.These issues have limited the therapeutic effects of the two approved drugs for SMA. | Xiang Lin Haizhu Chen Ying-Qian Lu Shunyan Hong Xinde Hu Yanxia Gao Lu-Lu Lai Jin-Jing Li Zishuai Wang Wenqin Ying Lixiang Ma Ning Wang Erwei Zuo Hui Yang Wan-Jin Chen | 2020 | Cell Research2020，30，6： | 5 |
| 18 | Diagnosis of Spinal Muscular Atrophy:A Simple Method for Quantifying the Relative Amount of Survival Motor Neuron Gene 1/2 Using Sanger DNA Sequencing显示文摘Background: Spinal muscular atrophy (SMA) is caused by homozygous deletion or compound heterozygous mutation of survival motor neuron gene 1 (SMN1), which is the key to diagnose SMA. The study was to establish and evaluate a new diagnostic method for SMA. Methods: A total of 1494 children suspected with SMA were enrolled in this study. Traditional strategy, including multiplexed ligation-dependent probe amplification (MLPA) and TA cloning, was used in 1364 suspected SMA children from 2003 to 2014, and the 130 suspected SMA children were tested by a new strategy from 2015 to 2016, who were also verified by MLPA combined with TA cloning. The SMN1 and SMN2 were simultaneously amplified by polymerase chain reaction using the same primers. Mutation Surveyor software was used to detect and quantify the SMN1 variants by calculating allelic proportions in Sanger sequencing. Finally, turnaround time and cost of these two strategies were compared. Results: Among 1364 suspected SMA children, 576 children had SMN1 homozygous deletion and 27 children had SMN1 compound heterozygous mutation. Among the 130 cases, 59 had SMN1 homozygous deletion and 8 had heterozygous deletion: the SMN1-specific peak proportion on exon 7 was 34.6 ± 1.0% and 25.5 ± 0.5%, representing SMN1:SMN2 to be 1:2 and 1:3, respectively. Moreover, five variations, including p.Ser8Lysfs *23 (in two cases), p.Leu228*, p.Pro218Hisfs *26, p.Ser143Phefs*5, and p.Tyr276His, were detected in 6/8 cases with heterozygous deletion, the mutant allele proportion was 31.9%, 23.9%, 37.6%, 32.8%, 24.5%, and 23.6%, which was similar to that of the SMN1-specific site on exon 7, suggesting that those subtle mutations were located in SMN1. All these results were consistent with MLPA and TA cloning. The turnaround times of two strategies were 7.5 h and 266.5 h, respectively. Cost of a new strategy was only 28.5% of the traditional strategy. Conclusion: Sanger sequencing combined with Mutation Surveyor analysis has potential application in SMA diagnosis. | Yan-Yan Cao Wen-Hui Zhang Yu-Jin Qu Jin-Li Bai Yu-Wei Jin Hong Wang Fang Song | 2018 | Chinese Medical Journal2018，，24： | 5 |
| 19 | Denervated muscle extract promotes recovery of muscle atrophy through activation of satellite cells. An experimental study显示文摘Purpose: The objective of the present study was to determine whether a denervated muscle extract(DmEx) could stimulate satellite cell response in denervated muscle.Methods: Wistar rats were divided into 4 groups: normal rats, normal rats treated with DmEx, denervated rats, and denervated rats treated with DmEx. The soleus muscles were examined using immunohistochemical techniques for proliferating cell nuclear antigen, desmin, and myogenic differentiation antigen(MyoD), and electron microscopy was used for analysis of the satellite cells.Results: The results indicate that while denervation causes activation of satellite cells, DmEx also induces myogenic differentiation of cells localized in the interstitial space and the formation of new muscle fibers. Although DmEx had a similar effect in nature on innervated and denervated muscles, this response was of greater magnitude in denervated vs. intact muscles.Conclusion: Our study shows that treatment of denervated rats with DmEx potentiates the myogenic response in atrophic denervated muscles. | Eduardo Aguera Salvador Castilla Evelio Luque Ignacio Jimena Ignacio Ruz-Caracuel Fernando Leiva-Cepas Jos Pea | 2019 | Journal of Sport and Health Science2019，8，1： | 4 |
| 20 | The Impacts of Simulated Microgravity on Rat Brain Depended on Durations and Regions显示文摘Objective To explore the dynamic impacts of simulated microgravity(SM) on different vital brain regions of rats. Methods Microgravity was simulated for 7 and 21 days, respectively, using the tail-suspension rat model. Histomorphology, oxidative stress, inflammatory cytokines and the expression of some key proteins were determined in hippocampus, cerebral cortex and striatum. Results 21-day SM decreased brain derived neurotrophic factor and induced neuron atrophy in the cerebral cortex. Strong oxidative stress was triggered at day 7 and the oxidative status returned to physiological level at day 21. Inflammatory cytokines were gradually suppressed and in striatum, the suppression was regulated partially through c-Jun/c-Fos. Conclusion The results revealed that the significant impacts of SM on rat brain tissue depended on durations and regions, which might help to understand the health risk and to prevent brain damage for astronauts in space travel. | CHEN Bo ZHANG Yu Shi LI George CHO Jun-Lae DENG Yu Lin LI Yu Juan | 2019 | Biomedical and Environmental Sciences2019，32，7： | 4 |
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