This review examines the effects of parenteral nutrition(PN) or enteral nutrition(EN) on pancreatic exocrine secretion and severe acute pancreatitis(SAP). There is no evidence that PN support in SAP affects the underlying disease process,but it may prevent the malnutrition and complications.In recent years,EN is considered to be used in that it preserves gut barrier function.PN,in contrast,may result in mucosal atrophy,bacterial translocation and increased rates of catheter related sepsis.The effects of EN on pancreatic exocrine secretion and natural course of SAP are discussed.The safety and feasibility of EN in SAP have been established. EN may even be superior to PN.Some patients,however,cannot tolerate enteral feeding and PN still has a role.

The tight junction of intestinal epithelium plays an important role in maintaining the function of intestinal barrier and regulating the cell differentiation. The intestinal epithelial cells interact with neighboring cells and the extracellular matrix and then affect the epithelial barrier as well as the proliferation, polarization, and apoptosis of cells. As an important cell junction, the tight junction of intestinal epithelium participates in a series of signal transduction pathways including the classic cyclic adenosine monophosphate-protein kinase A-cyclic adenosine monophosphate response element-binding, inositol trisphosphate, Ras-mitogen-activated protein kinase, phosphatidylinositol 3-kinase, and in some special pathways including zonula occludents protein 1-associated Y-box factor,cyclin related protein, phosphorylation, and methylation. Furthermore, regulations of gene and protein expression of the tight junction are also complex, while disorders of such regulations may lead to clinical diseases, such as disruption of the intestinal barrier, refractory infection, and even cancers. This article reviews the research advances in gene expressions, related signal transduction, and self-regulation in the tight junction of intestinal epithelium.

Many peptide transporters have been identified in mammals, among which PepT1 has been widely studied. PepT1, a member of proton-coupled oligopeptide transporter (POT) superfamily, is a peptide transporter of low affinity and high capacity and is mainly expressed in the brush border membrane of intestinal epithelial cells. PepT1 plays an important role in the absorption of di/tri-peptide (the degradation products of protein in intestinal tract). Meanwhile, it mediates the transport of peptide-like drugs and the bacterial products. Therefore,the changes of the functional expression of PepT1 in the gastrointestinal tract may dramatically affect the internal and external environmental stability and drug absorption. This paper reviews the structural features and function,distribution, transport mechanisms, and regulatory factors of PepT1.

The relationship of the nutritional and colorectal tumor was reviewed.The epidemiology of oral nutrition and colorectal tumor was investigated.The nutritional support in patients with colorectal tumor was discassed.The use of some amino acids and fatty acids might not only improve the hosts nutritional condition,but also serve as methods to treat tumor.

Objective To investigate the clinical values of serum histidine decarboxylase(HDC),intestinal fatty acid binding protein(I-FABP),and diamine oxidase(DAO)for diagnosing intestinal mucosal injury (IMI)in patients with intestinal obstruction.Methods The expression levels of serum HDC,I-FABP,and DAO in 28 patients with strangulated intestinal obstruction,19 patients with simple intestinal obstruction,17 patients with acute simple appendicitis,and 20 healthy control were determined by enzyme-linked immunosorbent assay (ELISA)before clinical treatment,and then the areaa under receiver operating characteristic curves(AUC)of these diagnostic indicators were compared.In addition,the incidences of systemic inflammatory response syndrome (SIRS)and infectious complications were closely observed.The difference of the expressions of HDC,I-FABP,and DAO and their relationship with SIRS and infectious complications were compared among these patients and controls.Results The expression levels of serum HDC, I-FABP, and DAO were the highest in patients with strangulated intestinal obstruction (all P < 0.001), and the expression levels of these three indicators were significantly higher in patients with simple intestinal obstruction than in those with acute simple appendicitis or healthy controls (all P<0.05).The AUC of HDC (0.913) was significantly larger than that of I-FABP (0.877, P =0.000) and DAO (0.873, P = 0.000).When the cut-off value of HDC ≥31.00 ng/ml, the sensitivity, specificity, false negative rate, and false positive rate of HDC were 74.5% , 94.6% , 25.5% , and 5.4% , respectively,which were all better than those of I-FABP and DAO.There were significant differences of the incidence of SIRS ( P = 0.046) and abdominal infection (P = 0.027) among patients with strangulated intestinal obstruction, patients with simple intestinal obstruction, and patients with acute simple appendicitis, while lung infection showed no such significant difference (P = 0.728).The expression level of serum HDC was significantly higher in patients with strangulated intestinal obstruction who were also suffered from SIRS ( P = 0.000) or abdominal infection ( P =0.002) than that of uninfected patients.Meanwhile, the expression levels of serum I-FABP and DAO were significantly higher in the SIRS patients with strangulated intestinal obstruction than that of uninfected patients ( P = 0.027, P=0.017, respectively).The expression levels of HDC, I-FABP, and DAO were significantly correlated with the incideces of SIRS and abdominal infection ( all P < 0.05 ) , among which the level of HDC and the incidence of SIRS had the highest correlation (R = 0.608, P = 0.001).Conclusion HDC can be an effective indicator for diagnosing IMI in patients with intestinal obstruction.

Protein phosphatase 2A(PP2A)is a major Ser/Thr phosphatase involved in sevelral cellular signal transduction pathways.The reversible phosphorylation of proteins is accomplished by opposing activities of kinases and phosphatases.PP2A controls the specific dephosphorylation of thousands of phosphoprotein substrates and thus regulates physiological and biochemical processes of organism.The changes of the physiological activities of PP2A closely relate to apoptosis and regeneration of injured intestinal epithelial cell,and PP2A may be a regulatory factor in balancing the apoptosis and regeneration of intestinal epithehal cell.

Colorectal cancer (CRC) is a malignant digestive tract tumor resulted from genetic and environmental factors and can be accompanied by a series of gene mutations.The etiology of CRC,particularly the role of gut microbiota imbalance,has became a hot research topic along with the increase of its prevalance.In this article,we elucidate the potential roles and mechanisms of streptococcus gallolyticus,fusobacterium,Escherichia coli,Bacteroides fragilis,and helicobacter wlori in the development of CRC,with an attempt to further understand the functions of microbiota,search for possible specific carcinogenic strains,and improve the management of CRC.

Human guts harbor abundant microbes that regulate many aspects of host physiology.However,bacterial imbalance or dysbiosis in the gut due to the dietary or environmental changes may cause colorectal cancer (CRC).Therefore,it is theoretically and clinically important to explore the correlation between possible carcinogenic bacteria and CRC and thus reduce CRC incidence by regulating intestinal microecological balance through the application of microecological preparations.

Intestinal ischemia is a severe and life-threatening acute abdomen. Although its incidence is low,early diagnosis remains relatively difficult. The efficiencies of conventional laboratory biochemical tests are low. In recent years, many new markers for the early diagnosis of intestinal ischemia have been developed. In this article,we summarize their diagnostic efficiencies and relevant factors.

Acquired growth hormone resistance(AGHR) in critical illness may be defined as the combination of a raised serum growth hormone concentration,low serum insulin-like growth factor-1 concentration and a reduced anabolic response to exogenous GH.GH given to reverse catabolism in critical illness increased mortality.Therefore,it has the theoretical significance and clinical value for better understanding of the mechanism of AGHR.The mechanism of AGHR and its prevention and cure are reviewed.