Objective:To understand the current status of gastroscopy in diagnosing gastric lesions in general population, and to recommend the optimal age for the first gastroscopy and intervals for repeated gastroscopy.Methods:The gastroscopy records of residents aged 18-80 years in Yinzhou District of Ningbo, Zhejiang Province, between April 2010 and December 2021 were analyzed retrospectively. The detections of gastric lesions across different years, age and genders were described. Goodness of fit tests were applied to compare the differences in detection rates of different lesions in first-time endoscopy in different age groups and different populations. Generalized additive models were used to fit the trend of age specific gastric lesion detection rate explore the optimal age for gastroscopy. The appropriate gastroscopy intervals were determined according to the progress of the gastric lesions detected in repeated gastroscopy.Results:A total of 237 751 participants with 344 398 gastroscopy records were included in analyses. A total of 5 597 cases of chronic atrophic gastritis (CAG), 9 796 cases of intestinal metaplasia (IM), 165 cases of low-grade intraepithelial neoplasia (LGIN), 52 cases of high-grade intraepithelial neoplasia (HGIN) and 435 cases of gastric cancer were detected by the first gastroscopy. The overall detection rate of gastric lesions increased significantly in age group 45-70 years, and remained stable after 70 years old, with LGIN and HGIN showing notable increases at 50 and 55 years old, respectively. Repeated gastroscopy detected CAG, IM, LGIN, and HGIN at a higher rate compared with the first gastroscopy. Normal/superficial gastritis progressed in 3-5 years, whereas CAG or more severe lesions progressed in 1-6 years.Conclusion:Gastroscopy is recommended for general population aged 45 years and above. Furthermore, gastroscopy can be performed every 3-5 years for individuals with normal endoscopy results and once a year for patients with CAG or more severe gastric lesions.

Objective:To explore the effect of alternating food restriction on blood glucose, body mass index (BMI) and blood lipids in overweight or obesity patients with type 2 diabetes mellitus.Methods:A prospective cohort study was used. Three hundred overweight or obesity type 2 diabetes mellitus patients with stable blood glucose control from December 2021 to February 2022 in Nanxiang Hospital, Jiading District of Shanghai City were selected. The patients were divided into alternating food restriction group (adopting alternating food restriction therapy, giving balanced meal plates, reducing 30% of calories intake every other day), low carbohydrate high protein group (adopting low carbohydrate and high protein therapy, giving low carbohydrate and high protein reduction meal plates, reducing 15% of calories intake every day) and balanced diet group (adopting balanced diet therapy, giving balanced meal plates) by random digits table method with 100 cases each. All three groups received intervention treatment for 6 months. The height and body mass before intervention and the end of intervention and 6 months after intervention were measured, and the BMI was calculated. The levels of glycosylated hemoglobin (HbA 1c), fasting blood glucose (FBG), 2 h postprandial blood glucose (2 h PBG), triacylglycerol (TG), total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) were measured. Results:At the end, 280 cases were completed the study. There were 90 cases in the alternating food restriction group, 90 cases in the low carbohydrate high protein group, and 100 cases in the balanced diet group. There were no statistical differences in HbA 1c, FBG, 2 h PBG, BMI, TG, TC and LDL-C before intervention among the three groups ( P>0.05). At the end of the intervention, the HbA 1c and FBG in alternating food restriction group and low carbohydrate high protein group were significantly lower than those in balanced diet group: (6.50 ± 0.39)% and (6.67 ± 0.30)% vs. (6.79 ± 0.32)%, (6.47 ± 0.61) and (6.80 ± 0.30) mmol/L vs. (6.94 ± 0.37) mmol/L, the indexes in alternating food restriction group were significantly lower than those in low carbohydrate high protein group, and there were statistical difference ( P<0.05); the 2 h PBG and BMI in alternating food restriction group and the low carbohydrate high protein group were significantly lower than those in balanced diet group: (8.83 ± 0.63) and (8.81 ± 0.70) mmol/L vs. (9.45 ± 0.85) mmol/L, (25.99 ± 2.13) and (26.53 ± 2.16) kg/m 2 vs. (27.24 ± 2.24) kg/m 2, and there were statistical differences ( P<0.05), there were no statistical differences in 2 h PBG and BMI between alternating food restriction group and the low carbohydrate high protein group ( P>0.05). Six months after intervention, the HbA 1c, 2 h PBG and BMI in alternating food restriction group were significantly lower than those in low carbohydrate high protein group and balanced diet group: (6.62 ± 0.29)% vs. (6.79 ± 0.19)% and (6.84 ± 0.23)%, (9.21 ± 0.53) mmol/L vs. (9.48 ± 0.66) and (9.55 ± 0.51) mmol/L, (25.60 ± 1.67) kg/m 2 vs. (27.26 ± 2.42) and (27.79 ± 2.49) kg/m 2, and there were statistical differences ( P<0.05), there were no statistical differences in HbA 1c, 2 h PBG and BMI between low carbohydrate high protein group and balanced diet group ( P>0.05). At the end of intervention and 6 months after intervention, there were statistical differences in TG, TC and LDL-C among the three groups ( P<0.05); among them, the TG in alternating food restriction group was significantly lower than that in low carbohydrate high protein group and the balanced diet group: (1.67 ± 0.70) mmol/L vs. (1.99 ± 0.89) and (2.49 ± 0.94) mmol/L, (1.70 ± 0.71) mmol/L vs. (2.04 ± 0.96) and (2.53 ± 1.08) mmol/L, and there were statistical differences ( P<0.05), there was no statistical difference in TG between the low carbohydrate high protein group and balanced diet group ( P>0.05). Conclusions:The alternating food restriction therapy in overweight or obesity patients with type 2 diabetes mellitus can not only reduce blood glucose, improve blood lipids, but also reduce BMI, and the overall effect is better than that of low carbohydrate high protein therapy.

Hepatocellular carcinoma (HCC) has the features of high incidence rate, low survival rate, poor treatment outcome, and complex pathogenesis. In recent years, many studies have shown that long non-coding RNA (lncRNA) MALAT1 is upregulated in HCC and can promote the proliferation, invasion, and metastasis of HCC cells, and it can also guide the diagnosis, prognostic evaluation, and treatment of HCC in clinical practice. This article reviews the current status of research on lncRNA MALAT1 in HCC and discusses its expression pattern, mechanism of action, and clinical significance in predicting and monitoring the progression of HCC, so as to gain a deep understanding of the role of lncRNA MALAT1 in the progression of HCC. It is pointed out that lncRNA MALAT1 is expected to become a potential biomarker for the diagnosis and prognostic evaluation of HCC and may be used as a therapeutic target in clinical practice.

Objective:To investigate the expression level of C-type lectin domain family 4 member G ( CLEC4 G) in liver disease tissues and its correlation with the clinicopathological characteristics of hepatocellular carcinoma (HCC) patients. Methods:The cancer tissue and the corresponding adjacent tissues (at least 2 cm from the edge of the cancer tissue), cut in surgeries from January to December in 2019, of 40 HCC patients in Zhuzhou Central Hospital, as well as 10 normal liver tissue samples (seen as far away as possible from the edge of the cancer tissue with naked eyes) and 10 liver cirrhosis samples were analyzed retrospectively. The tumor genome atlas (TCGA) database was used to screen the HCC transcriptome data sets, and bioinformatics methods were used to make expression heat maps and box maps which can help analyze the difference of CLEC4 G in cancer and adjacent tissues. The mRNA expression level of CLEC4 G was detected by conducting real-time fluorescence quantitative PCR (qRT-PCR), and the protein expression level of CLEC4G was detected by immunohistochemistry (IHC). The measurement data were expressed as mean±standard deviation ( Mean± SD). Group t test was used for inter-group comparison. The counting information was expressed as a percentage (%). The χ2 test was adopted to analyze the correlation between CLEC4 G expression level and the clinicopathological features of patients. Results:The expression level of CLEC4 G in cancer tissues was significantly decreased in heat map compared with that in adjacent tissues. In the box figure, the relative expression of CLEC4 G mRNA in the cancer tissues was (82.5±18.9) and (3 354.4±296.2) in paracancer tissues, with statistically significant difference ( P<0.001). Respectively, qRT-PCR and IHC showed that mRNA of CLEC4 G were abundant in normal liver tissues (3 301.3±286.4), while they were very little in liver cancer tissues (63.6±32.9), significantly decreasing in liver cirrhosis (1 742.6±208.7) and paracancer tissues (1 553.2±249.9), with statistically significant difference ( P<0.001). Moreover, low CLEC4 G expression level was associated with tumor vascular metastasis in HCC patients. Conclusions:CLEC4 G is highly expressed in normal liver tissue, but with the progression of malignant liver disease, it is significantly decreased with little expression in HCC tissue. It can be expected to be a good marker for the pathological diagnosis of HCC.

MicroRNA-223 (miR-223) is located on chromosome X, and is highly conserved in the process of evolution. In recent years, many studies have shown that miR-223 is abnormally expressed in a variety of digestive system tumors, such as esophageal cancer, gastric cancer, liver cancer, pancreatic cancer and colorectal cancer. MiR-223 can participate in the proliferation, apoptosis and invasion of tumor cells through a variety of signal pathways, which is expected to become a marker for the diagnosis and prognosis of digestive system tumors.

Severe acute pancreatitis is a common clinical acute abdominal disease, characterized by acute onset, rapid progression, high risk, poor prognosis and so on. Due to the high mortality of this disease, it has been the focus and difficulty of clinical research. The traditional treatment of severe acute pancreatitis mainly include fasting and parenteral nutrition. However, recently, international and national consensus suggest that early enteral nutrition is fit for severe acute pancreatitis, although the timing of early enteral nutrition has been controversial. The article summarizes the optimal timing of early enteral nutrition for severe acute pancreatitis.

Objective To observe the changes of serum complements and proinflammatory cytokines in rats with sepsis, and to explore the possible mechanism.Methods 120 healthy male Wistar rats were randomly divided into three groups: normal control group (n = 15), sham operation group (n = 15) and sepsis group [cecum ligation and puncture (CLP) operation,n = 90]. The sepsis rats were sacrificed on 24, 48 and 72 hours after modeling. The level of serum complements (C5, C5a) and cytokines tumor necrosis factor-α (TNF-α), interleukin (IL-1, IL-6), high mobility group box 1 (HMGB1), macrophage migration inhibitory factor (MIF) were detected by enzyme linked immunosorbent assay (ELISA).Results Compared with normal control group and sham operation group, the levels of serum complements C5, C5a and IL-1β were significantly increased at 24 hours after CLP in sepsis group [C5 (ng/L): 1.60±0.19 vs. 1.04±0.20, 1.09±0.09; C5a (ng/L): 0.20±0.02 vs. 0.18±0.01, 0.18±0.02; IL-1β (ng/L): 700.20±111.41 vs. 475.87±108.96, 592.29±121.57; allP < 0.05]; then the levels of C5, C5a and IL-1β declined, the level of serum C5 were also higher than normal control group at 48 hours and 72 hours after CLP (ng/L: 1.17±0.24, 1.27±0.24 vs. 1.04±0.20, bothP < 0.05). In sepsis group the level of serum TNF-α (ng/L: 51.33±1.96, 51.06±1.64) was lower than that in normal control group (59.53±3.06) and sham operation group (57.91±2.72) at 48 hours and 72 hours (allP < 0.05). There was a time dependent rise of serum HMGB1 in sepsis group, which level was much higher than that in normal control group and sham operation group at 72 hours after CLP (ng/L: 472.21±20.94 vs. 406.00±43.16, 404.41±35.39, bothP < 0.05). There were no significant differences of MIF, and IL-6 level between groups at each time points.Conclusions Complement system led to uncontrolled inflammatory response and immune dysfunction through the release of proinflammatory cytokines and inflammatory mediators, which maybe one of the important mechanism of the pathology of sepsis.

Objective To explore the effect and mechanism of CD4+CD25+Tregs(Tregs)on the protective efficacy of glutha?tione?S?transferase(GST)against Schistosoma japonicum in mice. Methods Female BALB/c mice were divided randomly into five groups:a normal control group,an infected control group,an anti?CD25mAb group,a GST immunization group and a com?bination group with GST immunization and anti?CD25 mAb. The GST group and combination group were injected percutaneously with GST 50μg each mouse,the other two groups were injected with equal volume PBS. The immunization was performed for 3 times for two?week interval,and 2 weeks after the last immunization,each mouse was challenged with 40 S. japonicum cercaria. Two weeks post?infection,the combination group and anti?CD25 mAb group were injected intraperitoneally with 300μg anti?CD25 mAb each mouse. The mice were succumbed 2 weeks,3 weeks,4 weeks and 5 weeks post?infection respectively. The per?centages of CD4+CD25+Tregs in splenocytes of mice were measured with flow cytometer. The levels of IFN?γ,IL?2,IL?4,IL?5 and TGF?βin cell cultural supernatants were determined by sandwich?ELISA after stimulation with Con A. The liver sections were stained with hematoxylin and eosin. Results The worm burden in the combination group(15.80 ± 2.74)was significantly lower than those of the infected control group(27.78 ± 3.15),anti?CD25 mAb group(21.50 ± 4.21),and GST group(20.84 ± 6.46). Compared to those of the infected control group,the percentages of CD4+CD25+Tregs were significantly higher in the GST group,while the percentages of CD4+CD25+Tregs were significantly lower post?anti?CD25 mAb?administration. Regardless of GST administration,the levels of IFN?γ,IL?2,IL?4 and IL?5 after anti?CD25 mAb were significantly higher than those of the in?fected control groups. There were no significant differences of egg granuloma and the level of TGF?βbetween each group. Con?clusion CD4+CD25+Tregs could be partially blocked by anti?CD25 mAb while Th1 and Th2 type immunization response could be enhanced,which plays a role in improving the protective efficacy of GST against of S. japonicum.

AIM:MicroRNAs ( miRNAs) were recognized to play significant roles in cardiac hypertrophy .But, it remains unknown whether cyclin/Rb pathway is modulated by miRNAs during cardiac hypertrophy .This study investigates the potential roles of microRNA-1 (miR-1) and microRNA-16 (miR-16) in modulating cyclin/Rb pathway during cardiomyocyte hypertrophy .METHODS:An animal model of hypertrophy was established in a rat with abdominal aortic constriction (AAC).In addition, a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocyte .RESULTS:miR-1 and-16 expression were markedly de-creased in hypertrophic myocardium and hypertrophic cardiomyocytes in rats .Overexpression of miR-1 and -16 suppressed rat cardiac hypertrophy and hypertrophic phenotype of cultured cardiomyocytes .Expression of cyclins D1, D2 and E1, CDK6 and phosphorylated pRb was increased in hypertrophic myocardium and hypertrophic cardiomyocytes , but could be reversed by enforced expression of miR-1 and -16.CDK6 was validated to be modulated post-transcriptionally by miR-1, and cyclins D1, D2 and E1 were further validated to be modulated post-transcriptionally by miR-16.CONCLUSION: Attenuations of miR-1 and -16 provoke cardiomyocyte hypertrophy via derepressing the cyclins D1, D2, E1 and CDK6, and activating cyclin/Rb pathway.

AIM:To investigate the effect of miR-214 on cardiomyocyte hypertrophy and the expression of the potential target genes . METHODS:A cell model of hypertrophy was established based on angiotensin-Ⅱ( Ang-Ⅱ)-induced neonatal mouse ventricular car-diomyocytes (NMVCs).Dual luciferase reporter assay was performed to verify the interaction between miR-214 and the 3’ UTR of MEF2C.The expression of MEF2C and hypertrophy-related genes at mRNA and protein levels was determined by RT-qPCR and Wes-tern blotting, respectively.RESULTS:The expression of ANP, ACTA1,β-MHC and miR-214 was markedly increased in Ang-Ⅱ-in-duced hypertrophic cardiomyocytes .Dual luciferase reporter assay revealed that miR-214 interacted with the 3’ UTR of MEF2C, and miR-214 was verified to inhibit MEF2C expression at the transcriptional level .The protein expression of MEF2C was markedly in-creased in the hypertrophic cardiomyocytes .Moreover, miR-214 mimic, in parallel to MEF2C siRNA, inhibited the expression of hy-pertrophy-related genes in Ang-Ⅱ-induced NMVCs.CONCLUSION:MEF2C is a target gene of miR-214, which mediates the effect of miR-214 on attenuating cardiomyocyte hypertrophy .