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microRNAs (miRNAs) are low-molecular-weight non-coding RNAs that regulate various physiological and pathological functions through the regulation of gene expression at the post-transcriptional level. More and more evidence has shown that microRNA-27a (miRNA-27a) plays a role in the development and pathogenesis of liver diseases. By reviewing and updating related studies, this article introduces the research advances in the role of miRNA-27a in various liver diseases including fatty liver disease, hepatitis, hepatic fibrosis, and liver cancer and analyzes the role of miRNA-27a in liver regeneration and its potential as a biomarker, so as to provide a reference for future studies and more possibilities for new treatment ideas for chronic hepatic diseases.
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Nonalcoholic fatty liver disease (NAFLD) includes a series of diseases affected by various complex factors. Mitochondrial dysfunction often occurs in NAFLD and may lead to the progression of hepatitis and liver fibrosis. This article reviews the important role of mitochondrial oxidative stress, respiration, energy metabolism, quality control, and mitochondrial DNA in NAFLD and summarizes the current status of mitochondria-targeted therapy for NAFLD, hoping to provide a new direction for the research and clinical treatment of NAFLD.
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At present, more and more studies have been conducted on noninvasive diagnostic indicators for liver cirrhosis, but no consensus has been reached on the association of noninvasive diagnostic indicators with clinical outcome events and their predictive value. This article summarizes the value of noninvasive indicators, including serological markers, serum diagnostic models, and liver stiffness measurement (LSM), in predicting the clinical outcome events of liver cirrhosis. The noninvasive diagnostic method of serological markers (such as platelet count and FibroTest) combined with LSM can assess the stage of liver fibrosis and predict the outcome events and long-term prognosis of liver cirrhosis, and thus it has been included in Chinese and global guidelines and has been widely used in clinical practice. The use of new combinations (such as LSM combined with serological markers or diagnostic models) or a step-by-step calculation method shows the hope of modification to realize individualized dynamic clinical management of patients, reduce or avoid the occurrence of clinical outcome events of liver cirrhosis, and bring maximum benefit to patients with liver cirrhosis.
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Objective@#To understand the genotype distribution and molecular epidemiological characteristics of the group A rotavirus (RVA) in domestic sewage, and further explore the importance of environmental surveillance in investigating RVA regional circulation.@*Methods@#Sewage samples were collected monthly in the city of Yantai from January 2014 to December 2016. After concentration, total RNA was extracted, and RVA VP7 and VP4 coding regions were amplified via RT-PCR. PCR products were purified, cloned and Sanger sequenced. Genotyping and phylogenetic analysis was conducted based on the sequences.@*Results@#Thirty-six sewage samples were collected and 86.1% was positive with VP7 and VP4 sequences. A total of 205 VP7 and 239 VP4 nucleotide sequences were obtained, belonging to 4 G genotypes and 6 P genotypes. Among these, G9 (95.6%, 196/205), P[8] (58.6%, 140/239) and P[4] (28.0%, 67/239) were the most common genotypes. Phylogenetic analysis for G9, P[8] and P[4] sequences revealed co-circulation of multiple transmission chains in local population.@*Conclusions@#This study describes the genotype distribution and sequence characteristics of local RVA in Shandong province, and the result demonstrate that surveillance on environmental sewage is an effective way in investigating RVA molecular epidemiology.
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The data were drawn from injury hospitalization surveillance system in Shandong province. From 2012 to 2018, 164 cases of acute occupational poisoning were reported from five surveillance counties (cities, districts), accounting for 6.11% (164/2 683) of total accidental poisoning cases. The annual average reported incidence of acute occupational poisoning hospitalization was 1.15/100 000. The number of male cases was 3.3 times that of females (126 vs 38). The poisoning cases mainly occurred between January to May in a year and 5-7 AM within a day. Those cases were mainly caused by irritating gases (92 cases, 56.10%) and asphyxiating gases (53 cases, 32.32%), of which chlorine (71 cases) and carbon monoxide (50 cases) were the main reasons. The average hospitalization medical cost of acute occupational poisoning cases was 7 278.81 RMB per case.
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Background: Early diagnosis and staging of liver fibrosis are important for the prognosis and evaluating the survival of patients.Aims: To systematically assess the diagnostic value of transient elastography (TE) for staging of liver fibrosis in patients with chronic liver disease.Methods: PubMed,Embase,Cochrane Library,CNKI,Wanfang and VIP from Jan.2001 to Dec.2015 were retrieved to collect the articles with staging of liver fibrosis in patients with chronic liver disease by TE.Data extraction was conducted.Article quality was evaluated by quality assessment of diagnostic accuracy studies 2 (QUADAS2).Meta-analysis was conducted by Stata 12.0 software.Results: Twenty articles involving 5 748 patients were included.Meta-analysis showed that the combined sensitivity,specificity and AUC of TE for diagnosing significant fibrosis (≥F2) were 0.78 (95％ CI: 0.73-0.82),0.85 (95％ CI: 0.80-0.88) and 0.88 (95％ CI: 0.85-0.91),respectively.The combined sensitivity,specificity and AUC for advanced fibrosis (≥F3) were 0.89 (95％ CI: 0.86-0.91),0.88 (95％ CI: 0.85-0.91) and 0.94 (95％ CI: 0.92-0.96),respectively.The combined sensitivity,specificity and AUC for cirrhosis (F4) were 0.91 (95％ CI: 0.86-0.95),0.89 (95％ CI: 0.87-0.92) and 0.95 (95％ CI: 0.93-0.97),respectively.Conclusions: TE technique has a good diagnostic value in assessing significant fibrosis,advanced fibrosis and cirrhosis in patients with chronic liver disease,especially for advanced fibrosis and cirrhosis.
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Non-coding RNAs include microRNAs and long non-coding RNAs (lncRNAs) and are a group of RNAs in the product of genome transcription which do not encode proteins. In recent years, with the development of screening technology, more and more lncRNAs have been identified. Related studies show that these lncRNAs play an important role in the development and progression of liver diseases. This article reviews the research advances in the influence of lncRNAs on liver diseases and related mechanisms.
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Epithelial-mesenchymal transition (EMT) is a process by which epithelial cells lose their own features and become mesenchymal cells, and more and more studies have shown that EMT plays an important role in the invasion and metastasis of hepatocellular carcinoma (HCC). This article reviews the signaling pathways involved in the progression of HCC and molecules involved in the regulation of EMT, in order to provide a new direction for the treatment of HCC.
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Exosomes are extracellular vesicles with a diameter of 30-100 nm formed during the processes of "endocytosis-fusion-exocytosis".Exosomes can be released by various types of cells and may carry important biological molecules,such as lipids,proteins,and nucleic acids.They are also involved in signal transduction and exchange of substances between cells and can regulate the physiological and pathological processes in various systems.They also play an important role in liver diseases,including liver cancer,viral hepatitis,liver fibrosis,and alcoholic and non-alcoholic fatty liver disease.This article reviews the research advances in exosomes in liver diseases.
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Exosomes are extracellular vesicles with a diameter of 30-100 nm formed during the processes of "endocytosis-fusion-exocytosis".Exosomes can be released by various types of cells and may carry important biological molecules,such as lipids,proteins,and nucleic acids.They are also involved in signal transduction and exchange of substances between cells and can regulate the physiological and pathological processes in various systems.They also play an important role in liver diseases,including liver cancer,viral hepatitis,liver fibrosis,and alcoholic and non-alcoholic fatty liver disease.This article reviews the research advances in exosomes in liver diseases.
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Background: Studies showed that aberrant activation of JAK/STAT3 signaling pathway promoted the tumorigenesis and progression of hepatocellular carcinoma (HCC), and transforming growth factor-β1 (TGF-β1) has either tumor-suppressing or tumor-promoting effect in regulation of tumor progression.Aims: To investigate the effect of specific inhibition of JAK/STAT3 signaling pathway on HCC and whether TGF-β1 signaling pathway is involved in this process or not.Methods: Thirty Wistar rats were randomly divided into three groups: control group, HCC group, and HCC+AG490 group.In the latter two groups, diethylnitrosamine was administered in drinking water to induce HCC model, and in HCC+AG490 group, AG490, a specific inhibitor of JAK was injected intraperitoneally in the first week of model establishment.At the end of the 16th week, all rats were sacrificed.The maximum diameter of tumor nodules in the liver was recorded and the number of tumors with maximum diameter greater than 1 cm was counted.Expression and distribution of STAT3 and TGF-β1 in liver tissue were determined by real-time PCR, immunohistochemistry, and immunofluorescence.Results: Compared with the control group, expressions of STAT3 and TGF-β1 mRNA in liver tissue were significantly increased in HCC group (P<0.05).Phosphorylated STAT3 (p-STAT3) and TGF-β1 proteins were absent in liver tissue in control group, and both were up-regulated and co-expressed in HCC group.While in HCC+AG490 group, expressions of STAT3 and TGF-β1 mRNA were significantly lower than those in HCC group (P<0.05);the liver tissue was weakly positive for p-STAT3 and TGF-β1 proteins, and the number of tumor nodules greater than 1 cm and the maximum diameter were markedly reduced when compared with the HCC group [1.20±1.03 and (1.14±0.18) cm vs.4.30±1.06 and (1.78±0.27) cm, P all<0.05].Conclusions: Specific inhibition of JAK/STAT3 signaling pathway may restrain the tumorigenesis and progression of HCC partially by interfering TGF-β1 signaling pathway.
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<p><b>OBJECTIVE</b>To investigate the epidemiological status of cholestasis in first-hospitalized patients with chronic liver disease in Shanghai, and to provide a scientific basis for developing prevention and treatment measures.</p><p><b>METHODS</b>From April 2005 to September 2014, 5,146 first-hospitalized patients in Shanghai with a diagnosis of chronic liver disease were enrolled in this study. Clinical data of the 4,660 patients who fit the study criteria for participation were collected for retrospective analysis.Diagnosis of cholestasis was made according to serum alkaline phosphatase (ALP) levels higher than 1.5 times the upper limit normal (ULN) and gamma-glutamyltransferase (GGT) levels higher than 3 times the ULN. The incidence rate of cholestasis was assessed for relation to age, sex, etiology, and type of liver disease, and statistically compared to the general clinical data and specific biochemical indicators with potential sex-related differences. T-test and chi-square test were performed for the statistical analyses.</p><p><b>RESULTS</b>Of the 4,660 study participants, 10.26% had cholestasis; the prevalence of cholestasis increased with increasing age in male patients. The distribution of the cholestasis incidence according to the type of chronic liver disease was: 75.00%, primary sclerosing cholangitis; 42.86%, primary biliary cirrhosis; 35.97%, hepatic tumor; 30.77%, autoimmune hepatitis; 28.31%, drug-induced liver disease; 16.46%, alcoholic hepatitis; 13.98%, cryptogenic cirrhosis; 12.99%, schistosomal cirrhosis; 7.53%, alcoholic cirrhosis; 7.32%, mixed cirrhosis; 5.94%, viral liver cirrhosis; 2.70%, nonalcoholic fatty liver disease. There was no significant difference in the prevalence of cholestasis between the two sexes. In the patients with cholestasis, the levels of GGT and total bilirubin were significantly different between the two sexes.</p><p><b>CONCLUSION</b>The incidence rate of cholestasis in first-hospitalized patients with chronic liver disease was 10.26%, and the rate increased with increased age. Patients with primary sclerosing cholangitis or primary biliary cirrhosis had higher incidence rates of cholestasis. Incidence rates of cholestasis of the various chronic liver diseases were not related to sex.</p>
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Humans , Male , Bilirubin , China , Cholestasis , Chronic Disease , Incidence , Liver Diseases , Prevalence , Retrospective Studies , gamma-GlutamyltransferaseABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of TGF-beta1 and STAT3 signaling in liver fibrosis using a rat model system and to determine the therapeutic mechanism of AG490 in relation to this signaling pathway.</p><p><b>METHODS</b>Rats were randomly divided into a control group and DENA-induced liver fibrosis model group, and then subdivided into AG490 treatment groups. During fibrosis development, liver tissue samples were collected at different time points (0, 4 and 8 weeks) and evaluated according to the Scheuer scoring system. Expression of STAT3, TGFbeta1, alpha-SMA, E-cadherin, MMP2 and TIMP1 was measured by PCR (mRNA) and immunohistochemistry and western blotting (protein).</p><p><b>RESULTS</b>Increasing degrees of inflammation and fibrosis were observed in liver tissues of DENA-treated rats throughout model establishment. The mRNA expression of TGFbeta1 and STAT3 was significantly increased in DENA-induced rats with advanced fibrosis (AF) compared to those with early fibrosis (EF) (P = 0.034 and P = 0.012 respectively). The protein expression of TGF-beta1, phospho-Smad2, alpha-SMA, E-cadherin, STAT3 and phospho-STAT3 was significantly increased in DENA-induced rats with AF compared to the unmodeled control group (P = 0.048, P = 0.003, P = 0.002, P = 0.028, P = 0.009 and P = 0.039). The protein expression of E-cadherin was lower in the DENA-induced rats with AF than in those with EF (P = 0.026). STAT3 and TGF-beta1 co-expression was detected in AF tissues. DENA-induced AG490-treated rats with AF showed substantially lower protein expression of STAT3, TGF-beta1, MMP2 and TIMP1 compared to DENA-induced untreated rats with AF (P = 0.006, P = 0.018, P = 0.010 and P = 0.005); in addition, the degrees of fibrosis and inflammation were also greatly reduced in the DENA-induced AG490-treated rats with AF compared to DENA-induced untreated rats with AF (P = 0.042 and P = 0.021). Conclusions STAT3 signal transduction may regulate the TGF-beta1 pathway and affect liver fibrosis, especially in the advanced phase. AG490 can inhibit TGFbeta1-STAT3 signaling, resulting in reversal of liver fibrosis.</p>
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Animals , Rats , Disease Models, Animal , Liver Cirrhosis , Metabolism , Rats, Sprague-Dawley , STAT3 Transcription Factor , Metabolism , Signal Transduction , Transforming Growth Factor beta1 , Metabolism , Tyrphostins , PharmacologyABSTRACT
<p><b>OBJECTIVE</b>To investigate whether gene expression profiles can be used to determine risk genes and predict HBV-related cirrhosis progression to liver carcinoma using Significance Analysis of Microarray (SAM) and Prediction Analysis of Microarray (PAM) methods.</p><p><b>METHODS</b>The Affymetrix GeneChip was used to establish the gene expression profiles of liver tissues from 15 patients with chronic hepatitis B and cirrhosis or hepatocellular carcinoma (HCC). Differentially expressed genes (fold-change more than 2; P value less than 0.01) were selected by GeneSpring GX software. Risk genes related to cirrhosis and liver carcinoma were generated by SAM and PAM methods. Real-time PCR was used to verify the expression of risk genes in the liver tissues.</p><p><b>RESULTS</b>Samples were clustered into the cirrhosis subgroup (n =15) or the HCC subgroup (n =15). A total of 497 differentially expressed genes were identified, SAM identified 162 significant genes, including 18 up-regulated genes and 144 down-regulated genes (fold-change:-1.46 to 1.28). PAM identified 22 genes with a "poor risk signature" (defined with a threshold of 5.5), which were associated with classifying cirrhosis and liver carcinoma; of these risk genes, 4 were down-regulated and 18 were up-regulated in the HCC group compared to the cirrhosis group (fold-change: 2.038 to 7.897, P value less than 0.01). The correction of classification was more than 80% . FOXP1, SPINK1 and KCNJ16 were verified by real-time PCR as differently expressed in the two subgroups (P value =0.011, 0.002 and 0.004, respectively).</p><p><b>CONCLUSION</b>The altered gene profiles of carcinogenesis in HBV-related cirrhosis involves hundreds of genes. The combination of three "poor risk genes" may represent potential targets for diagnosis and prediction of liver carcinoma progression.</p>
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Adult , Female , Humans , Male , Middle Aged , Carcinoma, Hepatocellular , Genetics , Pathology , Gene Expression Profiling , Hepatitis B, Chronic , Genetics , Pathology , Liver Cirrhosis , Genetics , Pathology , Virology , Liver Neoplasms , Genetics , Pathology , Microarray Analysis , Oligonucleotide Array Sequence Analysis , TranscriptomeABSTRACT
Purpose:To prove that electroacupuncture pudendal nerve stimulation(EPNS)can exactly excites the pudendal nerve.by simultaneous measurements of pelvic floor muscle (PFM) movements(perineal ultrasound),vaginal pressure and pelvic floor surface myoelectricity.Methods:Long needles(acupuncture needles)were deeply inserted into four sacral points and electrifled to stimulate the Pudendal nerves.When EPNS Was performed.perineal ultrasound B-mode images of PFM movements(contractions),M-mode PFM movement curves;vaginal pressure and pelvic floor surface electromyogram were recorded simultaneously by use of an urodynamic instrument with video suite(Medtronic Duet Encompass).Simultaneous records were also obmined under three conditions in the process of the nerve stimulation:1) pausing electric stimulation;2)reducing the intensity of electric stimulation(to about 2/7 of the original);3)drawing back the two lower needles to make the tips 1-2 cm away from the original position.Results:Thirty-five female patients with stress incontinence(aged 54.9±9.81 received EPNS and the simultaneous measurements.When EPNS was performed correctly,the patient felt rhythmic and cephalad PFM contractions with the urethra as the center.Simultaneous records showed the following:1) cranio-caudal PFM movements on the B.mode image;2)the M-mode curves indicating the PFM contractions (amplitude:about 1 mm,n=31,14 cases≥1 mm and 17 cases＜1 mm);3)A sawtooth curve of changes in vaginal pressure[amplitude:2.61±1.69(0.7-5.6)cmH2O,n=34];4)pelvic floor myoelectric waves[amplitude:23.9±25.3(5-96)μV,n=34].The amplitude of a PFM movement curve conformed basically to that of a vaginal pressure curve.If the electric current was stopped or its intensity was reduced to about 2/7 of the original or during the process of the nerve stimulation the two lower needles were gradually drawn back until the tips were 1-2 cm away from the original positions,then B-mode PFM movements,M-mode curves and sawtooth changes in vaginal pressure disappeared.Conclusion:Electroacupuncture pudendal nerve stimulation can exactly excites the pudendal nerve and effectively contract the pelvic floor muscles.
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Objective To investigate stem cell factor(SCF)expression in activated pancreatic stellate cell(PSC)and the effect of SCF on adhesion between PSC and mast cell(MC).Methods PSC of SD rat was separated and activated by pancreatic tissue culture;the expression of SCF mRNA and protein was detected bv RT-PCR and immunachemistry.SCF was blocked with different dose of anti-SCF antibody,the rate of adhesion between PSC and MC was determined by thiomn blue stain and β-hexasaminidase assay.PSC was stimulated by 10 μg/ml mitomycin-C and was co-cultured with MC,then the growth of MC was observed at 2,3,5 day,respectively.Results Activated PSC expressed SCF mRNA and protein,the number of adhered MC in the control,1mg/ml and 10 mg/ml antibody groups was 48±10,28±8,and 23±9,respectively;the difference between antibody and control group was statistically significant(P＜0.05).One day after PSC and MC was co-cultured without serum.there were MC adhesion;3 days later the rate of adhesion increased;5 days later the adhesion appeared bulk-like and lots of colonies were present,while PSC basically disappeared.Conclusions Activated PSC may synthesize,express SCF and induced adhesion and growth of MC.
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Objective To investigate the influence of Lipoprotein lipase (LPL)/Hepatic lipase (HL) on hyperlipidemie acute necrotizing pancreatitis (HLANP) in rats. Methods The rats were fed with hyperlipidemic feed for 4 weeks, then the rats were injected with 5% sodium taurocholate into pancreatic duct to induce HLANP model. Seventy-two rats were randomly assigned to HLANP and control groups, and then each group was subdivided into 6 subgroups (n = 6) at 0, 3, 6, 12, 24 and 48 h. Serum amylase, cholesterol, triglyeride (TG), free fatty acid (FFA) levels and serum LPL, HI. activities were determined. Under the light-microscopy and electron microscopy, the histopathologic and uhrastructure changes of pancreas were observed; the HL mRNA expressions were detected by RT-PCR; HL protein expressions HL were assessed by immunohistoehemical staining. Results The serum amylase levels reached peak values at 12 h after ANP induction in the two groups, the mean values were 7 176U/L and 6 366U/L, which were significantly higher than those of baseline values (P <0.05) ; serum levels of cholesterol in HLANP group at 0 ～ 12 h were higher than those of control group, however, only at 0 h the difference (1.19±0.49 vs 0. 32±0.14 mmol/L) was significant (P < 0.05) ; serum levels of FFA in HLANP group were not significantly different when compared with those of control group; serum levels of LPL and HL at 3 h were (17.5±7) U/L and (18.6±3.9) U/L, which were significantly higher than those of control group (8.9±3.4 U/L and 9.5±2. 1 U/L, P < 0.05). The pancreatic tissues necrosis levels were significantly increased in HLANP groups (3, 6, 24 and 48 h) than those of control group at corresponding time points (P < 0.05). lipid droplet deposition, rough endoplasmic reticulum distension, zymogen granule reduction, and chondriosome swelling in acinar cells of pancreatic tissues in HLANP group were found. The HI, mRNA expressions at 3 h and 6 h in HLANP group were 1.1±0.09 and 0.89±0.08, which were significantly higher than those in control group (0. 11 ± 0.01 and 0.15±0. 03, P <0.05). HL proteins were positively expressed in pancreatic tissues of two groups before ANP was induced, and HL proteins were strongly positively expressed after ANP induction. Conclusions Lipase (LPL/HL) expression increased in HLANP rats, and the content of serum protein increased, which resulted in lipids decomposition and increased the severity of ANP. LPL/HL may be one of the key lipids metabolic enzymes aggravating HLANP.
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Objective To investigate the mechanism of hypedipidemia on pancreas of rats by comparative proteomic analysis.Methods Ten male SD rats were randomly divided into two groups,the experimental group Was fed with high lipid forage and the control group Was fed with normal food.Pancreatic samples from the two groups were harvested six weeks later.Differential protein analysis Was performed using differential in-gel electrophoresis(DIGE),and characterizing the protein biomarkers using tandem mass spectrometry.Western blot Was used to confirm the expression of significantly changed proteins.Results Compared to the normal pancreas tissue,a total of 3 protein spot-features were found to be significantly increased and 11 significantly decreased in pancreatic samples with hyperlipidemia.Significantly increased proteins in hyperlipidemia pancreatic samples were arginaseⅡ,ribonuclease inhibitor and glyeine amidinotransferase,which increased by 2.19,1.82 and 1.12 fold,respectively.Significantly decreased proteins in hyperlipidemia group were tyrosyl-tRNA synthetase,alpha-amylase,triacylglycerol lipase,DJ-1protein,Cu,Zn superoxide dismutase,which dicreased by 2.48,2.37,1.85,1.73 and 1.65 folds,respectively.Western blot analysis revealed increased arginase Ⅱ levels and decreased alpha-amylase in pancreatic samples with hyperlipidemia.Conclusions Pancreas wag possibly injured by hyperlipidemia via increase of arginase Ⅱ.Decreased amylase and lipase may be the protection mechanism of pancreas.
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Objective To investigate the expression and polymorphism of lipoprotein lipase (LPL) gene and their association with acute hyperlipidemic pancreatitis(HLP). Methods A total of 120 patients Were assigned to HLP group (n=20), acute pancreatitis (AP) group (n=50) and control group (n= 50). Serum levels of triglyceride (TG), cholesterol (Ch), free fatty acid (FFA), lipoprotein and apolipoprotein and serum LPL/HL activities were determined. The mRNA expressions of LPL/HL and LPL gene intron 8 polymorphisms were detected by RT-PCR and PCR-RFLP, respectively. Results The serum levels of TG, Ch, FFA and ApoE were significantly higher in HLP group than those in AP group and control group (P<0.05). The serum level of HDL was lower in HLP group than that in AP group and control group(P<0.05). The serum LPL/HL activities were significantly higher in HLP group than that in AP and control groups. The expression of LPL mRNA was up-regulated and intron 8 Hind Ⅲ H2 allele frequency was significantly inereased in the HLP group compared to control group(0.90/0.72, P<0.05). H1 allele frequency was significantly decreased in the HLP and AP groups compared to control group(0.10/0.28 and 0.14/0.28, respectively). Conclusions The high allele frequency of LPL gene intron 8 Hind H2 result in the increase of activities and expression of LPL mRNA, which exacerbate the development of HLP through changing TG metabolism such as FFA accumulation.
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Objective To investigate the potential influencing factors which possibly effected the gut barrier function.The effort was made to establish a clinical evaluation system of gut barrier dysfunc- tion.Methods Fifty-three critically ill patients with an APACHEⅡscore of 8 or more and 27 patient which APACHEⅡscore was 6 or less were recruited.Plasma was reserved for measurement of endo- toxin,tumor necrosis factor-?,diamine oxidase,D-lactic acid and high sensitive C reactive protein,uri- nary excretion of lactulose and mannitol and the urinary content of intestinal fatty acid binding protein (IFABP) were determined as well.Analyses was achieved by univariate,multivariate analysis and receiver operating characteristic curve.Results In the logistic regression models,gut barrier was affect- ed by many factors.The ratio of lactulose and mannitol in urine,the urinary content of IFABP of 24 hours and endotoxin level of plasma were identified as the most intimate factors which could associate with gut barrier function.The optimal operating point of plasma endotoxin,ratio of urinary lactulose and mannitol and content of urinary IFABP of 24 hours were 0.145,17 ng and 0,055 EU/ml respectively based on the results of receiver operating characteristic curve,the sensitivity and specificity were 84.5% vs 88%,78% vs 88% and 78% vs 78%.The doubtable value interval of urinary ratio of lactulose and mannitol was limited as 0.178 to 0.082.Conclusion Gut barrier dysfunction should be suspected when critically ill patients presented eertains gastrointestinal symptoms and had the proofs of increasing intesti- nal permeability,hypoperfusion of gut and higher level of plasma endotoxin.