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PurposeThe infiltration of immune cells and their roles of the infiltrating-immune cells in gastrointestinal stromal tumor (GIST) is still unclear. We aimed to discover the infiltration cell types and the relationship between the infiltrating-immune cells and the progression of GIST.Experimental designSingle-cell RNA sequencing were performed to discover types of the infiltrating-immune cells and to analyze CellChat between cells. Immunohistochemistry of 80 GIST samples were used to clarify the relation between macrophages and recurrence risk. In vitro, flow cytometry and Real-time PCR were performed to uncover a potential mechanism of tumor cell regulation of macrophages.ResultsTumor cells, macrophages, and T-cells were the predominant cell types. The MIF/CXCR4 axis was the most common ligand–receptor interaction between macrophages and tumor cells. As the risk increased, expression levels of CD68, CD206, MIF, and CXCR4 gradually increased. In vitro, we found that GIST882 was able to secrete MIF and GIST882 cell supernatant upregulated M2 polarization. Real-time PCR showed that expression levels of IL-10 mRNA and Arginase-1 mRNA were also the highest in the GIST882 cell supernatant group.ConclusionsThese findings identify that macrophages are the most abundant infiltrating cells in GIST. The MIF/CXCR4 axis is the most common ligand–receptor interaction between macrophages and tumor cells. GIST cells can regulate macrophage M2 polarization through the MIF/CXCR4 axis.

Abstract Metabolic heterogeneity of tumor microenvironment (TME) is a hallmark of cancer and a big barrier to cancer treatment. Cancer cells display diverse capacities to utilize alternative carbon sources, including nucleotides, under poor nutrient circumstances. However, whether and how purine, especially inosine, regulates mitochondrial metabolism to buffer nutrient starvation has not been well-defined yet. Here, we identify the induction of 5′-nucleotidase, cytosolic II (NT5C2) gene expression promotes inosine accumulation and maintains cancer cell survival in the nutrient-poor region. Inosine elevation further induces Rag GTPases abundance and mTORC1 signaling pathway by enhancing transcription factor SP1 level in the starved tumor. Besides, inosine supplementary stimulates the synthesis of nascent TCA cycle enzymes, including citrate synthesis (CS) and aconitase 1 (ACO1), to further enhance oxidative phosphorylation of breast cancer cells under glucose starvation, leading to the accumulation of iso-citric acid. Inhibition of the CS activity or knockdown of ACO1 blocks the rescue effect of inosine on cancer survival under starvation. Collectively, our finding highlights the vital signal role of inosine linking mitochondrial respiration and buffering starvation, beyond serving as direct energy carriers or building blocks for genetic code in TME, shedding light on future cancer treatment by targeting inosine metabolism.

The density of CD169+ macrophages has been reported to positively correlate with the number of CD8+ T cells, although this remains controversial. To better understand this topic, we conducted a meta-analysis. We searched the PubMed, Medline, and Web of Science databases for studies that were published before May 2022 and performed a meta-analysis of the incidence of low and high CD169 expression in groups based on CD8 expression using the random-effects model. A total of 10 studies were included in the meta-analysis. The incidence of high CD169 expression in lymph nodes was significantly lower than that of low CD169 expression in the low CD8 expression group (odds ratio (OR): 0.76, 95% confidence interval (CI): 0.6, 0.96); however, the incidence of high CD169 expression in lymph nodes was higher than that of low CD169 expression in the high CD8 expression group (OR: 1.50, 95% CI: 1.08, 2.07). We also found that the expression of CD169 in tumors was lower than that in nontumor tissues (standardized mean difference: −5.29, 95% CI: −7.47, −3.11). The overall survival and hazard ratio of patients with high and low CD169 expression was 0.45 (95% CI: 0.37, 0.55). This analysis showed that high CD169 expression was associated with a high CD8 expression, and low CD169 expression was associated with low CD8 expression. The risk of death was 55% lower for patients with high CD169 expression, and high CD169 expression may be associated with favorable survival outcomes in cancer patients. However, the number and heterogeneity of the studies should be taken into consideration when evaluating the analysis. High-quality randomized controlled trials on the association between CD169 and CD8 expression are needed to verify these effects.

Abstract Background Proximal gastrectomy with double-tract reconstruction (DTR) has been used for upper third gastric cancer as a function-preserving procedure. However, the safety and feasibility of laparoscopic proximal gastrectomy (LPG) with DTR remain uncertain. This study compared open proximal gastrectomy (OPG) with DTR and LPG with DTR for proximal gastric cancer. Methods Sixty-four patients who had undergone OPG with DTR and forty-six patients who had undergone LPG with DTR were enrolled in this case–control study. The clinical characteristics, surgical outcomes and postoperative nutrition index were analysed retrospectively. Results The operation time was significantly longer in the LGP group than in the OPG group (258.3 min vs 205.8 min; p = 0.00). However, the time to first flatus and postoperative hospital stay were shorter in the LPG group [4.0 days vs 3.5 days (p = 0.00) and 10.6 days vs 9.2 days (p = 0.001), respectively]. No significant difference was found between the two groups in the number of retrieved lymph nodes, complications or reflux oesophagitis. The nutrition status was assessed using the haemoglobin, albumin, prealbumin and weight levels from pre-operation to six months after surgery. No significant difference was found between the groups. Conclusion LPG with DTR can be safely performed for proximal gastric cancer patients by experienced surgeons.

Abstract Background Patients with lung adenocarcinoma (LUAD) have high mortality rate and poor prognosis. The LUAD cells display increased aerobic glycolysis, which generates energy required for their survival and proliferation. Deregulation of Wnt/β-catenin signaling pathway induces the metabolism switching and oncogenesis in tumor cells. RING finger protein 115 (RNF115) is an E3 ligase for ubiquitin-mediated degradation. Although the oncogenic functions of RNF115 have been revealed in breast tumor cells, the effect of RNF115 on lung cancer is still not clear. Methods RNF115 expression and its correlation with the features of LUAD patients were analyzed by using public database and our own cohort. The functions of RNF115 in proliferation and energy metabolism in LUAD cells were explored by downregulating or upregulating RNF115 expression. Results We demonstrated that RNF115 was overexpressed in LUAD tissues and its expression was positively correlated with the poor overall survival of LUAD patients. Moreover, RNF115 overexpression inhibited LUAD cell apoptosis and promoted cellular proliferation and metabolism in LUAD cells. On the contrary, RNF115 knockdown displayed reverse effects. Furthermore, the underlying mechanism of the biological function of RNF115 in LUAD was through regulating Wnt/β-catenin pathway via ubiquitination of adenomatous polyposis coli (APC). Conclusion The current study reveals a close association between RNF115 expression and prognostic conditions in LUAD patients and the oncogenic roles of RNF115 in LUAD at the first time. These findings may help establish the foundation for the development of therapeutics strategies and clinical management for lung cancer in future.

Abstract Background The recent emergence and dissemination of high-level mobile tigecycline resistance Tet(X) challenge the clinical effectiveness of tigecycline, one of the last-resort therapeutic options for complicated infections caused by multidrug-resistant Gram-negative and Gram-positive pathogens. Although tet(X) has been found in various bacterial species, less is known about phylogeographic distribution and phenotypic variance of different genetic variants. Methods Herein, we conducted a multiregional whole-genome sequencing study of tet(X)-positive Acinetobacter isolates from human, animal, and their surrounding environmental sources in China. The molecular and enzymatic features of tet(X) variants were characterized by clonal expression, microbial degradation, reverse transcription, and gene transfer experiments, while the tet(X) genetic diversity and molecular evolution were explored by comparative genomic and Bayesian evolutionary analyses. Results We identified 193 tet(X)-positive isolates from 3846 samples, with the prevalence ranging from 2.3 to 25.3% in nine provinces in China. The tet(X) was broadly distributed in 12 Acinetobacter species, including six novel species firstly described here. Besides tet(X3) (n = 188) and tet(X4) (n = 5), two tet(X5) variants, tet(X5.2) (n = 36) and tet(X5.3) (n = 4), were also found together with tet(X3) or tet(X4) but without additive effects on tetracyclines. These tet(X)-positive Acinetobacter spp. isolates exhibited 100% resistance rates to tigecycline and tetracycline, as well as high minimum inhibitory concentrations to eravacycline (2–8 μg/mL) and omadacycline (8–16 μg/mL). Genetic analysis revealed that different tet(X) variants shared an analogous ISCR2-mediated transposon structure. The molecular evolutionary analysis indicated that Tet(X) variants likely shared the same common ancestor with the chromosomal monooxygenases that are found in environmental Flavobacteriaceae bacteria, but sequence divergence suggested separation ~ 9900 years ago (7887 BC), presumably associated with the mobilization of tet(X)-like genes through horizontal transfer. Conclusions Four tet(X) variants were identified in this study, and they were widely distributed in multiple Acinetobacter spp. strains from various ecological niches across China. Our research also highlighted the crucial role of ISCR2 in mobilizing tet(X)-like genes between different Acinetobacter species and explored the evolutionary history of Tet(X)-like monooxygenases. Further studies are needed to evaluate the clinical impact of these mobile tigecycline resistance genes.

Abstract Background Matrix metalloproteinase 7 (MMP7), as the smallest member of the matrix metalloproteinase family, has been verified to be implicated in cancer progression, especially metastasis. However, its expression pattern and function in tongue cancer is not clear. Methods The expression of MMP7 in human tongue squamous cell carcinoma (TSCC) specimens compared with their respective paired nontumour tissues by real-time PCR and immunohistochemical staining. The effect of MMP7 on the proliferation, apoptosis, migration, invasion of tongue cancer cells was tested in appropriate ways after MMP7 siRNA knockdown or overexpression. The effect of MMP7 on lymph node metastasis in vivo was analyzed using a high-metastasis orthotopic nude mouse tongue transplanted tumour model. Results We found markedly elevated expression of MMP7 in human TSCC specimens compared with their respective paired nontumour tissues, and this high expression was correlated with the patients’ lymph node metastasis. Furthermore, the results of molecular functional assays confirmed that MMP7 promotes cell proliferation, migration and invasion of TSCC cells. Knockdown of MMP7 inhibited lymph nodes metastasis in vivo. Conclusions MMP7 plays an oncogenic role in carcinogenesis and metastasis of tongue cancer, and may serve as a potential therapeutic target for tongue cancer.

The newly emerged tigecycline-inactivating enzymes Tet(X3) and Tet(X4), which are associated with high-level tigecycline resistance, demonstrated significantly higher activities in comparison to that of the prototypical Tet(X) enzyme, threatening the clinical efficacy of tigecycline as a last-resort antibiotic to treat multidrug-resistant (MDR) Gram-negative bacterial infections. However, the molecular mechanisms leading to high-level tigecycline resistance remain elusive.

ABSTRACTPlasmid-mediated antimicrobial resistance has emerged as one of the principal global issues, posing significant threats to public health. Herein, we reported a mobile tigecycline resistance mechanism Tet(X4) on both plasmid and chromosome in Escherichia coli strains from migratory birds in China. Besides tigecycline, these tet(X4)-positive strains also exhibited elevated MICs to the FDA newly approved tetracycline antibiotics, eravacycline (4 µg/ml) and omadacycline (8 µg/ml). Worrisomely, the tet(X4)-carrying plasmids and chromosome also shared high homology with the plasmids from human. Taken together, Tet(X4) represents another emerging antimicrobial threat and collective efforts from different sectors are needed to control its further spread.

Purposes. Mesenteric venous thrombosis (MVT) is a serious condition. The current study aimed to identify risk factors of intestinal necrosis (IN) in patients with MVT to predict the onset of patients. Methods. Data pertaining to patients diagnosed with MVT between 2014 and May 2018 were reviewed. Patients’ characteristics and risk factors of IN were assessed. Results. Seventy-eight patients were included in our study, of whom all cases were diagnosed as superior mesenteric venous thrombosis. There were fifty-eight cases (74%) with intestinal necrosis and twenty cases (26%) without intestinal necrosis. Multivariate analysis of factors associated with IN was organ failure (odds ratio (OR): 4.1; 95% confidence interval (95%CI): 1.26–8.59; P=0.028), elevated serum lactate (OR:3.6; 95% CI: 1.51–5.47; P=0.024), bowel loop dilation on computerized tomography (CT) scan (OR: 2.8; 95% CI: 1.32–7.23; P=0.031), and the time between onset of symptoms and operation (OR: 4.8; 95% CI: 1.36–9.89; P=0.012). Area under the receiver operating characteristics curve for the diagnosis of IN with MVT was 0.901 (95%CI: 0.809–0.993; P=0.000) depending on the different number of predictive factors. Conclusion. Predictive risk factors for IN with MVT were organ failure, elevated serum lactate level, bowel loop dilation on CT, and the time between onset of symptoms and operation. However, this result is from a retrospective study and further long-term, large-sample prospective studies are required to confirm this finding.

This in vitro study aimed to accelerate the remineralization of a completely demineralized dentine collagen block in order to regenerate the dentinal microstructure of calcified collagen fibrils by a novel electric field-aided biomimetic mineralization system in the absence of non-collagenous proteins. Completely demineralized human dentine slices were prepared using ethylene diamine tetraacetic acid (EDTA) and treated with guanidine hydrochloride to extract the bound non-collagenous proteins. The completely demineralized dentine collagen blocks were then remineralized in a calcium chloride agarose hydrogel and a sodium hydrogen phosphate and fluoride agarose hydrogel. This process was accelerated by subjecting the hydrogels to electrophoresis at 20 mA for 4 and 12 h. X-ray diffraction (XRD), scanning electron microscopy (SEM), energy dispersive X-ray spectroscopy (EDX), and transmission electron microscopy (TEM) were used to evaluate the resultant calcification of the dentin collagen matrix. SEM indicated that mineral particles were precipitated on the intertubular dentin collagen matrix; these densely packed crystals mimicked the structure of the original mineralized dentin. However, the dentinal tubules were not occluded by the mineral crystals. XRD and EDX both confirmed that the deposited crystals were fluorinated hydroxyapatite. TEM revealed the existence of intrafibrillar and interfibrillar mineralization of the collagen fibrils. A novel electric field-aided biomimetic mineralization system was successfully developed to remineralize a completely demineralized dentine collagen matrix in the absence of non-collagenous proteins. This study developed an accelerated biomimetic mineralization system which can be a potential protocol for the biomineralization of dentinal defects.

Multiple primary malignant neoplasms are two or more malignancies in an individual without any relationship between the tumors. Multiple primary malignancies are relatively rare but have increased in recent decades. Two cancers are commonly observed among those with multiple primary malignancies, but two malignancies of stomach and liver are relatively rare to be reported. Mechanisms of the tumors were unclear; we described a patient who had stomach carcinoma presenting with a synchronous liver cancer and investigated his family history; we suggest that family history may be a key risk factor and early detection for additional primary malignancies should be needed for patients who had specific cancer history in their pedigree. Early diagnosis may be the key risk factor affecting prognosis.

Objective: To investigate the effect of programmed death-ligand 1 (PD-L1) gene polymorphism on pathological characteristics and clinical prognosis quality in patients with esophageal cancer. Methods: 86 patients with esophageal cancer treated in our hospital from January 2014 to January 2017 were selected as the observation group, and 100 healthy patients were selected as the control group during the same period. The single nucleotide polymorphisms of rs2890658, rs17718883, rs2297136 and rs4143185 at different sites were determined. And the impact of PD-L1 gene polymorphism on pathological features and prognosis of esophageal cancer were analyzed. Results: The observation group finally completed 84 cases, and the control group included 99 cases. There were differences between the observation group and the control group in the PD-L1 different genetic locus rs17718883, rs2890658, rs2297136 (P<0.05). The PD-L1 locus rs17718883 was related to the pathological type and degree of differentiation of esophageal cancer, the difference was statistically significant (P<0.05), rs2890658 was related to the degree of differentiation of esophageal cancer, the difference was statistically significant (P<0.05). Log-rank test showed that the genotype of rs17718883 in patients with esophageal cancer was related to prognostic survival, and the difference was statistically significant (P<0.05). Cox proportional hazards model analysis showed that age, degree of differentiation, lymph node metastasis, and rs17718883 genotype were independent factors in the prognosis of patients with esophageal cancer, and the difference was statistically significant (P<0.05). Conclusion: The polymorphisms of rs17718883 and rs2890658 loci of PD-L1 gene have an impact on the clinicopathological characteristics of patients with esophageal cancer, and the polymorphisms of rs17718883 locus of PD-L1 gene have an impact on the clinical prognosis quality. [ABSTRACT FROM AUTHOR]

Itis the challenging and desirable aim of biomineralization studiesto regenerate tooth tissue microstructures and to accelerate the speedof available biomimetic remineralization protocols for potential usein clinical dentistry. In this study, we developed a novel electrophoresis-aidedcalcium and phosphate agarose hydrogel system that can be used toquickly regenerate tooth tissue microstructure. After remineralization for 12 h, a demineralized dentin collagen matrix was remineralizedwith intrafibrillar and interfibrillar hydroxyapatites that mimickedthe structure of the original calcified dentin collagen matrix. Theprecipitated hydroxyapatites were densely packed, occluded the exposeddentinal tubules, and regularly and homogeneously distributed alongthe collagen fibrils in a "string-of-beads" structurewithin the dentin collagen matrix. Needle-like hydroxyapatite crystalswere densely packed, with their c-axis parallel toone another, to form the enamel-like tissue that precipitated ontothe remineralized dentin surface. This study provides a potentialprotocol for inducing the self-healing of dentin defects. [ABSTRACT FROM AUTHOR]

The aim of this study was to compare resting energy expenditure (REE) obtained by indirect calorimetry (IC) and Hams-Benedict (H-B) equations, and to examine whether hypocaloric nutrition support could improve protein nutritional status in mechanically ventilated patients with chronic obstructive pulmonary disease (COPD). Thirty-three COPD patients (20 males, 13 females) were recruited and REE was measured by IC. Measured RE (REEm) was compared to predictive REE by H-B equations (REEH-B) and its corrected values. Correlation between REEm and APACHE II score was also analyzed. Patients were randomly divided into hypocaloric energy group (50%-90% of REEm, En-low) and general energy group (90%-130% of REEm, En-gen) for nutrition support. The differences of albumin, prealbumin, transferrin, hemoglobin, and lymphocyte count before and after 7 days nutrition support were observed. Results show that REEH-B and REEH-B x 1.2 were significantly lower than REEm (p<0.01). REEm positively correlated with APACHE II score (p<0.05 or p<0.01). After nutrition support, hemoglobin decreased significantly in En-gen group (p<0.05); lymphocyte count in both groups, and transferrin and prealbumin in the En-low group increased significantly (p<0.05 or p<0.01). Our data suggest that 1) these patients' REE were increased; 2) since 1C is the best method to determine REE, in the absence of IC, H-B equations (with standard body weight) can be used to calculate REE, but the value should be adjusted by correction coefficients derived from APACHE II; 3) low energy nutrition support during mechanical ventilation in COPD patients might have better effects on improving protein nutritional status than high energy support. [ABSTRACT FROM AUTHOR]

Purpose: To evaluate the effectiveness of resecting liver metastases of gastrointestinal stromal tumors (GISTs), when performed in conjunction with imatinib treatment. Methods: Forty-one patients with pathologically diagnosed GIST and liver metastases were randomly assigned to an operation group (neoadjuvant therapy + resection + adjuvant therapy with imatinib) or a nonoperation group (imatinib alone). Patients were monitored for up to 36 months, and survival was analyzed. Results: We monitored 39 patients throughout the 36-month follow-up period, recording 1- and 3-year survival rates of 100% and 89.5% in the operation group and 85% and 60% in the nonoperation group, respectively. There was a significant difference in overall survival between the operation and nonoperation groups ( P = 0.03). Furthermore, resection improved the survival of patients who responded poorly to 6 months of preoperative imatinib treatment, compared with that of their counterparts in the nonoperation group ( P = 0.04). Conclusion: These findings suggest that surgical intervention in combination with imatinib treatment is more effective than imatinib alone against GIST liver metastases, with minimal complications and side effects. [ABSTRACT FROM AUTHOR]

Studies investigating the association between genetic polymorphism of glutathione S-transferase T1 ( GSTT1) and gastric cancer risk have reported conflicting results. Therefore, we conducted this meta-analysis to provide more precise evidence. We searched the databases Medline, PubMed, Embase, and China National Knowledge Infrastructure up to July 30, 2009. Thirty-six studies with 4,357 gastric cancer cases and 9,796 controls were selected. Odds ratio (OR) and 95% confidence intervals (CI) were calculated based on fixed- and random-effects models. The combined results based on all studies showed there was a significant link between GSTT1 null genotype and gastric cancer risk (OR = 1.14, 95%CI = 1.01–1.28). In subgroup analysis stratified on the basis of ethnic group, we also observed positive association between GSTT1 polymorphism and gastric cancer risk among Caucasians (non-Europeans + non-Americans), but not among East Asians. When stratifying by control source, the overall ORs for population- and hospital-based studies were 1.09 (95%CI = 0.94–1.28) and 1.17 (95%CI = 1.03–1.34), respectively. Subjects with both GSTM1 and GSTT1 negative genotypes had increased gastric cancer risk compared with those who had nonnull genotypes of both GST genes. Subgroup analyses for Helicobacter pylori infection and smoking habit did not reveal any significant association between GSTT1 polymorphism and gastric cancer development. This meta-analysis suggests that GSTT1 gene polymorphism may be not associated with increased gastric cancer risk among Europeans, Americans, and East Asians. More large-scale studies based on the same racial group are needed. [ABSTRACT FROM AUTHOR]

The Glutathione S-transferases (GSTs) play multiple roles in the pathogenesis and treatment of cancer. Studies investigating the association between Glutathione S-transferase M1 (GSTM1) null genotype and gastric cancer risk report conflicting results. The purpose of this study was to quantitatively summarize the evidence for such a relationship. This meta-analysis included 35 studies, which included 4,505 gastric cancer cases and 9,062 controls. The combined results based on all studies showed that the GSTM1 null genotype was associated with an increased risk of gastric cancer (OR = 1.15, 95% confidence interval [CI] = 1.02, 1.29). When stratifying for race, results were similar among Asians (OR = 1.24, 95% CI = 1.07, 1.44) except Caucasians (OR = 1.04, 95% CI = 0.88, 1.24). When stratifying by the location, stage, Lauren’s classification, histological differentiation, lymph node metastasis, smoking, and Helicobacter pylori infection of gastric cancer, we observed that patients with diffuse classification had a significantly higher frequency null genotype (OR = 4.80, 95% CI = 1.65,13.94) than those with intestinal classification among Caucasians. This meta-analysis suggests that the GSTM1 null genotype may be associated with gastric cancer among Asians. [ABSTRACT FROM AUTHOR]

Studies investigating the association between interleukin10 (IL10) -592 promoter polymorphism and gastric cancer risk report conflicting results. The objective of this study was to quantitatively summarize the evidence for such a relationship. Two investigators independently searched the MEDLINE and Embase databases. This meta-analysis included ten case–control studies, which included 1,715 gastric cancer cases and 2,783 controls. The combined results based on all studies showed that there was no significant difference in genotype distribution (AA odds ratio [OR] = 0.88, 95% confidence interval [CI] = 0.66, 1.18; AC OR = 1.09, 95% CI = 0.95, 1.24; CC OR = 1.03, 95% CI = 0.89, 1.18) between gastric cancer and noncancer patients. When stratifying for race, the results were similar, except that patients with gastric cancer had a significantly lower frequency of AA (OR = 0.67, 95% CI = 0.52, 0.87) and a higher frequency of AC (OR = 1.34, 95% CI = 1.07, 1.68) than noncancer patients among Asians. When stratifying by the location of gastric cancer, we found that patients with cardia gastric cancer had a significantly lower frequency of AA (OR = 0.41, 95% CI = 0.20, 0.84) than those with noncardia gastric cancer among Caucasians. When stratifying by Lauren’s classification of gastric cancer, we found that patients with diffuse gastric cancer had a significantly higher frequency of AA (OR = 1.91, 95% CI = 1.07, 3.41) than those with intestinal gastric cancer among Caucasians. This meta-analysis suggests that the IL10 -592 promoter polymorphism may be associated with gastric cancer among Asians, and that differences in genotype distribution may be associated with the location and Lauren’s classification of gastric cancer. [ABSTRACT FROM AUTHOR]

Studies investigating the association between aspirin use and gastric cancer risk have reported conflicting results. The objective of this study was to quantitatively summarize the evidence for such a relationship. Two investigators independently searched the Medline, PubMed, Embase, and Academic Search Premier (EBSCO) databases. Fourteen studies with a total number of 5,640 gastric cancer cases were identified. Most of the study populations were Caucasian. The combined results based on all studies showed there was no statistically significant difference between aspirin use and gastric cancer risk (odds ratio (OR) = 0.80, 95% confidence intervals (CI) = 0.54–1.19). When stratifying by study designs and gender, results were similar except for cohort and randomized controlled trial (RCT) studies (OR = 0.72, 95% CI = 0.62–0.84). When stratifying by location and Helicobacter pylori ( H. pylori) infection, we observed there were lower risks in noncardia gastric cancer (OR = 0.62, 95% CI = 0.55–0.69) and H. pylori-infected individuals (OR = 0.62, 95% CI = 0.42–0.90) for aspirin users. Among Caucasians, there were lower risks for noncardia gastric cancer (OR = 0.73, 95% CI = 0.62–0.87) and H. pylori-infected individuals (OR = 0.62, 95% CI = 0.42–0.90) also. This meta-analysis indicated that regular use of aspirin may be associated with reduced risk of noncardia gastric cancer, especially among Caucasians; for H. pylori-infected subjects the result was similar. [ABSTRACT FROM AUTHOR]

This study assessed the safety and efficacy of structured triglyceride (ST) for parenteral nutrition. A meta-analysis of all the relevant randomized controlled trials (RCTs) was performed. Clinical trials were identified from the following electronic databases: MEDLINE, EMBASE, the Cochrane Controlled Trials Register, Chinese Bio-medicine Database. The search was undertaken in March 2005. Language was restricted to Chinese and English. Literature references were checked at the same time. Only RCTs were extracted and evaluated by two reviewers independently of each other. The statistical analysis was performed by RevMan4.2 software which was provided by the Cochrane Collaboration. A P value of <0.05 was considered statistically significant. Ten RCTs involving 236 patients were included. Eight of them compared ST with the long-chain triglyceride (LCT), and the combined results showed that the ST had significant effect on resting energy expenditure (weighted mean difference [WMD] = 1.54, 95%CI [1.26, 1.82], P<0.00001), plasma glycerol (WMD = 0.14, 95%CI [0.06, 0.22], P=0.0007), free fatty acids (WMD = 0.24, 95%CI [0.10, 0.37], P=0.0006), and β-hydroxybutyric acid (WMD = 0.14, 95%CI [0.06, 0.22], P=0.0007), but no differences was found regarding nitrogen balance (standardized mean difference [SMD] = 0.64, 95%CI [-0.30, 1.59], P= 0.18), respiratory quotient (WMD = -0.02, 95%CI [-0.04, 0.01], P=0.18), and plasma triglycerides (WMD = -0.10, 95%CI [-0.30, 0.10], P=0.32). Only two RCTs compared ST with the physical mixture of medium- and long-chain triglyceride (MCT/LCT), data from trials were not combined due to clinical differences between trials, and conclusions can not be drew from the present data. ST appeared to be safe and well tolerated. Further trials are required, especially compared with the MCT/LCT, with sufficient size and rigorous design. [ABSTRACT FROM AUTHOR]

This study assessed the safety and efficacy of growth hormone (GH) and glutamine (GLN) combined with a modified (high-carbohydrate-low-fat, HCLF) diet in patients with short bowel syndrome. A meta-analysis of alt the relevant clinical trials was performed. Clinical trials were identified from the following electronic databases: MEDLINE, EMBASE, the Cochrane Controlled Trials Register, Chinese Bio-medicine Database. The search was undertaken in May 2004. Language was restricted to Chinese and English. Literature references were checked at the same time. Clinical trials were extracted and evaluated by two reviewers independently of each other. The statistical analysis was performed by RevMan4.2 software which was provided by the Cochrane Collaboration. A P value of <0.05 was considered statistically significant. Thirteen trials involving 258 patients were included. The combined results showed that GH, GLN and HCLF diet had positive treatment effect on body weight (weighted mean difference [WMD] = 2.44, 95%Cl [1.62, 3.27], P<0.0000I), stool output (WMD = -376.49, 95%Cl [-600.35, -152.63], P=0.001), lean body mass (WMD = 2.16, 95%Cl [0.91, 3.41], P=0.0007), absorption of carbohydrates (WMD = 6.21, 95%Cl [5.27, 7.15], P<0.00001), absorption of nitrogen (WMD = 10.83, 95%CI [5.22, 16.44], P=0.0002), absorption of D-xylose (WMD = 0.37, 95%Cl [0.29, 0.44], P<0.00001), and off TPN (total parenteral nutrition) (odds ratios [OR] = 64.63, 95%Cl [15.51, 269.22], P<0.00001). But there were no improvements in fat mass (WMD = -1.50, 95%Cl [-3.48, 0.48], P=0. 14), absorption of energy (WMD = 7.48, 95%Cl [-7.22, 22.17], P=0.32), and absorption of fat (WMD = 7.16, 95%Cl [-2.95, 17.28], P=0.17). Most patients had side effects that are known to occur during treatment with high doses (0.14 mg/kg/day) of GH. No serious adverse effects occurred during active treatment with low doses (&les;0.1 mg/kg/day) of GH. Treatment with a combination of low-dose GH, GLN and HCLF diet is effective without any major adverse effects in patients with short bowel syndrome. Further trials are required, especially in children, with sufficient size and rigorous design. [ABSTRACT FROM AUTHOR]