Silencing circ_0000644 inhibits papillary thyroid cancer cell malignancy by combining with miR-671-5p to release the inhibition on ANXA2.

BACKGROUND: Papillary thyroid cancer (PTC) is life-threatening due to its malignant progression. Considerable evidence demonstrates that circular RNA (circRNA) regulates PTC development. This study aims to explore the mechanism of circ_0000644 modulating PTC malignant progression. METHODS: The RNA levels of circ_0000644, microRNA-671-5p (miR-671-5p) and annexin A2 (ANXA2) were detected by quantitative real-time polymerase chain reaction. Western blot was performed to check protein expression. Cell proliferation and cell apoptosis were investigated by 5-ethynyl-29-deoxyuridine and flow cytometry. Angiogenic capacity, migration and invasion were analyzed by tube formation assay and transwell assay. The interaction between miR-671-5p and circ_0000644 or ANXA2 was identified by dual-luciferase reporter assay. Xenograft mouse model assay was performed to analyze the effect of circ_0000644 on tumor formation in vivo. RESULTS: Circ_0000644 and ANXA2 expression was significantly upregulated, while miR-671-5p was downregulated in PTC tissues and cells when compared with control groups. Circ_0000644 knockdown inhibited PTC cell proliferation, tube formation, migration, and invasion, but induced apoptosis in vitro. Moreover, circ_0000644 knockdown led to delayed tumorigenesis in vivo. In addition, circ_0000644 acted as a miR-671-5p sponge and mediated PTC cell tumor properties through miR-671-5p. ANXA2 was identified as a target gene of miR-671-5p, and its overexpression relieved miR-671-5p-induced effects in PTC cells. Furthermore, circ_0000644 depletion inhibited ANXA2 production by combining with miR-671-5p. CONCLUSION: Circ_0000644 depletion repressed PTC cell tumor properties through the miR-671-5p/ANXA2 axis.

Real-Time Fluorescent Monitoring of Kinetically Controlled Supramolecular Self-Assembly of Atom-Precise Cu8 Nanocluster.

Kinetically stable and long-lived intermediates are crucial in monitoring the progress and understanding of supramolecular self-assembly of diverse aggregated structures with collective functions. Herein, the complex dynamics of an atomically precise CuI nanocluster [Cu8 (t BuC6 H4 S)8 (PPh3 )4 ] (Cu8a) is systematically investigated. Remarkably, by monitoring the aggregation-induced emission (AIE) and electron microscopy of the kinetically stable intermediates in real time, the directed self-assembly (DSA) process of Cu8a is deduced. The polymorphism and different emission properties of Cu NCs aggregates were successfully captured, allowing the structure-optical property relationship to be established. More importantly, the utilization of a mathematical "permutation and combination" ideology by introducing a heterogeneous luminescent agent of a carbon dot (CD) to Cu8a aggregates enriches the "visualization" fluorescence window, which offers great potential in real time application for optical sensing of materials.

The Impact of Cysteine-Rich Intestinal Protein 1 (CRIP1) on Thyroid Carcinoma.

BACKGROUND/AIMS: CRIP1 (cysteine-rich intestinal protein 1) has been found in several tumor types; however, its prognostic impact and role in cellular processes, particularly in thyroid carcinoma, are still unclear. METHODS: To elucidate the prognostic impact of CRIP1, we analyzed tissues from 58 primary invasive thyroid carcinomas using immunohistochemistry. Western blotting was performed to investigate CRIP1 protein expression in the thyrocyte cell line Nthy-ori 3-1 and four different thyroid carcinoma cell lines, K1, TPC-1, TT, and SW579. Endogenous expression of CRIP1 was suppressed using a siRNA (si-CRIP1). The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay was used to investigate cell viability. Flow cytometric analysis was used to detect cell cycle progression and cell apoptosis. The effects of silencing CRIP1 on cell migration and invasion were detected using the transwell assay. RESULTS: The immunohistochemistry results showed that CRIP1 was overexpressed in thyroid carcinoma. CRIP1 expression was associated with tumor size, TNM stage, and lymphatic metastasis, but not with age, gender, and tumor location. In addition, the expression of CRIP1 in K1, TPC-1, TT, and SW529 cells was higher than that in the Nthy-ori 3-1 cells. The highest expression was observed in the SW579 and TT cells. Furthermore, silencing CRIP1 inhibited the proliferation, migration, and invasion of thyroid carcinoma cell lines SW579 and TT. We also found that silencing CRIP1 induced G1 arrest and apoptosis of thyroid carcinoma cell lines SW579 and TT. CONCLUSION: In conclusion, CRIP1 acts as an oncogene in the cell proliferation, migration, and invasion processes of thyroid carcinoma. CRIP1 may serve well as an independent prognostic marker with significant predictive power for use in thyroid carcinoma therapy.

A de-illumination scheme for face recognition based on fast decomposition and detail feature fusion.

Almost all the face recognition algorithms are unsatisfied due to illumination variation. Feature with high frequency represents the face intrinsic structure according to the common assumption that illumination varies slowly and the face intrinsic feature varies rapidly. In this paper, we will propose an adaptive scheme based on FBEEMD and detail feature fusion. FBEEMD is a fast version of BEEMD without time-consuming surface interpolation and iteration computation. It can decompose an image into sub-images with high frequency matching detail feature and sub-images with low frequency corresponding to contour feature. However, it is difficult to determine by quantitative analysis that which sub-images with high frequency can be used for reconstructing an illumination-invariant face. Thus, two measurements are proposed to calculate weights for quantifying the detail feature. With this fusion technique, one can reconstruct a more illumination-neutral facial image to improve face recognition rate. Verification experiments using classical recognition algorithms are tested with Yale B, PIE and FERET databases. The encouraging results show that the proposed scheme is very effective when dealing with face images under variable lighting condition.

Stream-data-clustering based adaptive alarm threshold setting approaches for industrial processes with multiple operating conditions.

The setting of alarm thresholds is a critical concern of alarm management systems in industrial processes. Conventional alarm thresholds less consider changes of operating conditions in production processes, which degrades the effectiveness of alarm management systems. In response to this problem, this paper proposes an adaptive alarm threshold setting approach based on stream data clustering (SDC). Firstly, we develop a stream data clustering algorithm termed as a-DenStream algorithm which realizes industrial flow data clustering through online micro-clustering and offline integration. Subsequently, we develop the C-BOUND algorithm to extract the edges of the clustering results. In response to alarms associated with multiple operating conditions, segmentations are conducted to set alarm threshold groups and build a multi-condition alarm threshold model. Consequently, an adaptive alarm threshold setting method based on model matching is created. The effectiveness of the proposed method is demonstrated by experiments on a coal gasification chemical process. The proposed method provides a potential application for industrial processes with multiple operating conditions alarm managements.

Preventive effect of Ibrolipim on suppressing lipid accumulation and increasing lipoprotein lipase in the kidneys of diet-induced diabetic minipigs.

BACKGROUND: The role of renal lipoprotein lipase (LPL) per se in kidney diseases is still controversial and obscure. The purpose of this study was to observe the preventive effects of Ibrolipim, a LPL activator, on lipid accumulation and LPL expression in the kidneys of minipigs fed a high-sucrose and high-fat diet (HSFD). METHODS: Male Chinese Bama minipigs were fed a control diet or HSFD with or without 0.1 g/kg/day Ibrolipim for 5 months. Body weight, plasma glucose, insulin, lipids, LPL activity, and urinary microalbumin were measured. Renal tissue was obtained for detecting LPL activity and contents of triglyceride and cholesterol, observing the renal lipid accumulation by Oil Red O staining, and examining the mRNA and protein expression of LPL by real time PCR, Western Blot and immunohistochemistry. RESULTS: Feeding HSFD to minipigs caused weight gain, hyperglycemia, hyperinsulinemia, hyperlipidemia and microalbuminuria. HSFD increased plasma LPL activity while it decreased the mRNA and protein expression and activity of LPL in the kidney. The increases in renal triglyceride and cholesterol contents were associated with the decrease in renal LPL activity of HSFD-fed minipigs. In contrast, supplementing Ibrolipim into HSFD lowered body weight, plasma glucose, insulin, triglyceride and urinary albumin concentrations while it increased plasma total cholesterol and HDL-C. Ibrolipim suppressed the renal accumulation of triglyceride and cholesterol, and stimulated the diet-induced down-regulation of LPL expression and activity in the kidney. CONCLUSIONS: Ibrolipim exerts renoprotective and hypolipidemic effects via the increase in renal LPL activity and expression, and thus the increased expression and activity of renal LPL play a vital role in suppressing renal lipid accumulation and ameliorating proteinuria in diet-induced diabetic minipigs.

Pulse transit time for quantifying inspiratory effort in patients with obstructive sleep apnea.

OBJECTIVES: To investigate the feasibility of pulse transit time (PTT) as a quantitative measure of inspiratory effort in patients with obstructive sleep apnea (OSA). METHODS: Nineteen moderate to severe OSA patients were included to undergo overnight polysomnography simultaneously with esophageal pressure (P(es)) and PTT. The quantitative relationships between the size of P(es) variations (ΔP(es)) and PTT variations (ΔPTT) on a breath-by-breath basis in obstructive apneas were assessed. RESULTS: A total of 19,833 breaths from 6,087 obstructive apneas were analyzed. There were good correlations with r = 0.779 ± 0.095 (mean ± SD) between ΔP(es) and ΔPTT based on overnight sleep. The correlation coefficients for supine and lateral position were of the approximated magnitude (r = 0.783 ± 0.060 and 0.757 ± 0.106, respectively), whereas they were lower in rapid eye movement (REM) sleep (r = 0.564 ± 0.140) compared with non-rapid eye movement (NREM) sleep (r = 0.787 ± 0.071). In NREM sleep, the regression lines of ΔPTT against ΔP(es) were plotted with intercepts (5.1 ± 2.1 ms) and slopes (0.35 ± 0.08 ms·cm H(2)O(-1)). CONCLUSIONS: PTT showed good ability in detecting changes of inspiratory effort in overnight sleep and was proved to be a clinically useful method in quantifying increases in inspiratory effort in NREM sleep. Hence, PTT has prospects to become an alternative to P(es) in respiratory sleep studies.

A novel detection of correlated alarms with delays based on improved block matching similarities.

Statistical analysis method has emerged as a general approach to detect relation alarms in the process industries. However, the delay between related alarms is the main cause leading to wrong analysis results from traditional approaches to detect correlated alarms. This paper proposed a novel detection of correlated alarms based on block matching similarities with delay (BMS-d). First, blocking alarm data sequence method is to transform alarm data into time node sequences, which is able to reduce the calculation burden of the correlation analysis. Second, a novel maximal block correlation coefficient method is presented to estimate the correlation delay between alarms. Third, a novel method is proposed to detect correlated alarms based on the block matching similarities and related alarm delay information. A numerical case and TE process are employed to demonstrate the effectiveness and efficiency of the proposed method.

[An epidemiological survey on saturnism among children due to lead pollution released from township enterprise].

OBJECTIVE: To understand the current situations of saturnism and blood lead levels of children resided in village and circumjacent areas, and to know its relations with sex, age and other factors on children' s health as to providing some evidences for prevention and control. METHODS: An epidemiological survey was conducted for finding out the pollution sources and for a better understanding of the surrounding environment. All 221 children under 14 years old, from the lead pollution villages and surrounding establishments were enrolled, and their blood lead levels were detected by graphite atomizer absorption spectrophotometer method. Symptoms of the saturnism were investigated through a standardized questionnaire. SPSS13.0 software was administrated for data analysis. RESULTS: High blood lead level identification rate was 66.06% (146/221), and saturnism rate 32.13% (71/221). The children's blood lead levels among group 1, group 2, group 3 in this village and jade factory were (161.20 +/- 32.94), (176.60 +/- 43.62), (258.00 +/-106.08) and (238.01 +/- 55.20) microg/L respectively and the significant differences were observed through Kruskal-Wallis test (chi2 = 51.84, df= 3, P<0. 01). The blood lead levels of children from group 3 in this village and the jade factory were higher than those of other two groups. No correlation was found between children's age and blood lead level (r = 0.10, P = 0.13). There was a significant difference in blood lead levels between boys and girls (t' = 3.83, P<0.01). With the children's blood lead levels rising, the occurrence rate of main saturnism symptoms was significantly increased. This survey suggested that the pollution source was a coarse lead smelter. CONCLUSION: The blood lead level should ke overwhelmingly increased among children who live nearby the higher level of lead blood, that living nearby the lead smeltery,might result in stautnism and negative effect on children's healthy.

Microcirculatory detection of Toll-like receptor 4 in rat pancreas and intestine.

This paper was aimed to detect Toll-like receptor 4 (TLR4) microcirculatory expression and localization in rat pancreas and intestine. Acute pancreatitis (AP) was induced by twice injections of cerulein (20 mug in total) and acute necrotizing pancreatitis (ANP) was induced by intraductal injection of 5% taurocholate (1 ml/kg.bw). Reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry (IHC) were used to detect and localize TLR4 in the pancreas and intestine. Results showed that RT-PCR of RNA isolated from pancreatic and intestinal tissue yielded the predicted amplicon for TLR4; IHC analysis localized TLR4 expression to the endothelium of pancreatic arteriole, venule, acinar capillary network and sinusoidal capillary of endocrine islet; TLR4 expression in intestine was principally in the microvascular endothelium and leucocytes within the mucosa lamina propria. TLR4 staining in intestine was more intense in taurocholate-induced pancreatitis (TIP) than that in cerulein-induced pancreatitis (CIP). In conclusion, TLR4 could be detected in the pancreatic and intestinal microcirculation, suggesting TLR4 involved in the microcirculatory impairment in AP; the more intense intestinal TLR4 expression in TIP suggests a potential risk for secondary infection.

[Distribution of micrometastatic nodules of low rectal cancer in mesorectum: a pathological study using whole-mount sections].

OBJECTIVE: To investigate the regional spread of micrometastatic nodules in the mesorectum from low rectal cancer, and provide further pathological evidence to optimize radical resection procedure for rectal cancer. METHODS: A total of 62 patients with low rectal cancer underwent low anterior resection and total mesorectal excision (TME) was included in this study. Surgical specimens were sliced transversely and serial embedded blocks were made at 2.5 mm interval, and paraffin sections were stained with hematoxylin and eosin. The mesorectum on whole-mount sections was divided into three regions: outer region of mesorectum (ORM), middle region of mesorectum (MRM) and inner region of mesorectum (IRM). Microscopic spread were examined microscopically on the sections for the distribution in different mesorectal regions, frequency, types, involvement of lymphatic system and correlation with the primary tumor. RESULTS: Microscopic spread of the tumor in mesorectum and ORM was observed in 38.7% (24/62) and 25.8% (16/62) of the patients, respectively. Circumferential resection margin (CRM) involved by microscopic tumor foci occurred in 6.5% (4/62) of the patients, and distal mesorectum (DMR) involvement was recorded in 6.5% (4/62) with a spread extent within 3 cm of distal border of the main lesions. Most (20/24) of the patients with microscopic spread in mesorectum were in TNM stage III. CONCLUSION: Results of the present study support that complete excision of mesorectum without destruction of the ORM is essential for surgical management of low rectal cancer, and an optimal DMR clearance resection margin should not be less than 4 cm.

MiR-1180 promoted the proliferation of hepatocellular carcinoma cells by repressing TNIP2 expression.

MicroRNAs (miRNAs) are short, non-coding RNAs with post-transcriptional regulatory function, playing crucial roles in cancer development and progression of hepatocellular carcinoma (HCC). Previous studies have indicated that miR-1180 was implicated in diverse biological processes. However, the underlying mechanism of miR-1180 in HCC has not been intensively investigated. In this study, we aimed to investigate the role of miR-1180 and its target genes in HCC. We found that miR-1180 expression was significantly increased in HCC cells and clinical tissues compared with their corresponding controls. Overexpression of miR-1180 promoted cell proliferation in HCC cell line HepG2. TNFAIP3 interacting protein 2 (TNIP2), a potential target gene of miR-1180, and were validated by a luciferase assay. Further studies revealed that miR-1180 regulated cell proliferation of HCC by directly suppressing TNIP2 expression and the knockdown of TNIP2 expression reversed the effect of miR-1180-in on HCC cell proliferation. In summary, our data indicated that miR-1180 might act as a tumor promoter by targeting TNIP2 during development of HCC.

Metformin potentiates the anticancer activities of gemcitabine and cisplatin against cholangiocarcinoma cells in vitro and in vivo.

Metformin, an oral biguanide drug used to treat type 2 diabetes, has displayed anticancer activities in several types of cancer cells. The combination of gemcitabine and cisplatin is the standard chemotherapy regimen for cholangiocarcinoma, but its benefit is limited. The present study aimed to investigate whether metformin could enhance the activities of gemcitabine and cisplatin against cholangiocarcinoma, and the underlying mechanisms. Metformin inhibited the proliferation of human cholangiocarcinoma RBE and HCCC-9810 cells and induced cell cycle arrest at the G0/G1 phase by increasing the activation of AMP-activated protein kinase (AMPK) pathways. Metformin upregulated the expression of p21Waf1 and p27kip1, and downregulated the expression of cyclin D1, a key protein required for cell cycle progression. The combination of gemcitabine and cisplatin inhibited the proliferation and induced the apoptosis of human cholangiocarcinoma cells by inducing the phosphorylation of AMPK, downregulating cyclin D1, and activating caspase-3. Administration of metformin enhanced the efficacy of gemcitabine and cisplatin to suppress the growth of cholangiocarcinoma tumors established in experimental models by inhibiting cell proliferation and inducing cell apoptosis through their effects on AMPK, cyclin D1 and caspase-3. Given that metformin has been used to treat type 2 diabetes patients for over half a century due to its superior safety profile, the results presented here indicate that metformin may be a potent agent for enhancing the efficacy of gemcitabine and cisplatin in the treatment of cholangiocarcinoma.

Significant Association Between Adiponutrin and Hepatocellular Carcinoma Risk.

ADPN I148M polymorphism has been consistently reported to play a role in liver-associated diseases, such as alcoholic liver disease, chronic hepatitis C, and liver fat and fibrosis in nonalcoholic fatty liver disease. This significant association was also indicated in a series of hepatocellular carcinoma (HCC) studies, where the significance may be affected due to the small sample sizes. The aim of this study was to reexamine the ADPN-HCC association by use of meta-analysis. Biweekly computer-based literature searches plus manual screening were undertaken in an effort to identify all studies that met the predefined inclusion criteria. The Mantel-Haenszel method was selected to estimate risk effects (odds ratio [OR] and 95% confidence interval [CI]). To examine reliability of the pooled risk effects, we additionally performed sensitivity analysis and publication bias tests. Ten studies (1335 HCC patients and 2927 HCC-free controls) were identified for the meta-analysis. We found significantly increased risk of HCC attributable to presence of ADPN I148M polymorphism, with the highest risk associated with the M/M genotype under the recessive model of inheritance (OR = 2.23, 95% CI = 1.87-2.67, between-study heterogeneity: P = 0.468). The significant increase persisted in Caucasian and African when data were stratified by ethnicity. Subgroup analysis according to source of controls revealed similar risk effects. Our meta-analysis indicates that I148M polymorphism in the ADPN gene may independently contribute to the progression of HCC irrespective of the etiologies.

Common Variants of the Prostaglandin-Endoperoxide Synthase 2 Gene and Hepatocellular Carcinoma Susceptibility.

Hepatocellular carcinoma (HCC) is a heterogeneous disease with substantial genetic constitution. Previous work has evaluated the effect of prostaglandin-endoperoxide synthase 2 (PTGS2) variants (-765G/C, -1195A/G, and +8473T/C) on the development of HCC, but the conclusions are inconsistent. We conducted a meta-analysis in this work. Data from 7 case-control studies were combined to assess the association between PTGS2 variants and HCC. The risk of HCC (OR and 95% CI) was estimated using either the fixed- or the random-effects model according to the Q test. No significant association was identified for -765G/C and +8473T/C. However, we identified a significantly decreased risk in relation to the GG genotype of -1195A/G (OR = 0.70, 95% CI = 0.50-0.98 for GG versus AA). We also observed a similar decrease (OR = 0.47, 95% CI = 0.23-0.95 for GG versus AA) in Caucasian samples. Variant -1195A/G in the promoter PTGS2 may protect against the malignant progression of HCC. This significant association suggests that -1195A/G could be used as a biomarker of HCC.

Aberrant Expression of CCAT1 Regulated by c-Myc Predicts the Prognosis of Hepatocellular Carcinoma.

BACKGROUND: CCAT1 has been reported to be linked with pathogenesis of malignancies including colon cancer and gastric cancer. However, the regulatory effect of CCAT1 in hepatocellular carcinoma (HCC) remains unclear. The purpose of this research was to identify any role of CCAT1 in the progression of HCC. MATERIALS AND METHODS: Real time-PCR was performed to test the relative expression of CCAT1 in HCC tissues. A computation screen of CCAT1 promoter was conducted to search for transcription-factor-binding sites. The association of c-Myc with CCAT1 promoter in vivo was tested by Pearson correlation analysis and chromatin immunoprecipitation assay. Additionally, Kaplan-Meier analysis and Cox proportional hazards analyses were performed. RESULTS: c-Myc directly binds to the E-box element in the promoter region of CCAT, and when ectopically expressed increases promoter activity and expression of CCAT1. Moreover, Kaplan-Meier analysis demonstrated that the patients with low expression of CCAT1 demonstrated better overall and relapse-free survival compared with the high expression group. Cox proportional hazards analyses showed that CCAT1 expression was an independent prognostic factor for HCC patients. CONCLUSIONS: The findings demonstrated CCAT1, acting as a potential biomarker in predicting the prognosis of HCC, is regulated by c-Myc.

Association of PTEN gene polymorphisms with liver cancer risk.

OBJECTIVE: To find out if there are any relationship between three single nucleotide polymorphisms (SNPs) of phosphatase and tensin homolog (PTEN) gene (rs1234213, rs1234220, and rs2299939) and the susceptibility of liver cancer. METHODS: Genotypes of the three SNPs in the PTEN gene were achieved utilizing polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Comparison of genotypes and alleles distribution differences between the case and the control subjects was accomplished with χ(2) test. The analysis of linkage disequilibrium (LD) and haplotypes of the three SNPs was performed using SHEsis software. We adopted odds ratios (ORs) with 95% confidence intervals (95% CIs) to show the relative risk of liver cancer. RESULTS: TC genotype and C allele of rs1234220 polymorphism showed much more frequently in cases than in controls, reflecting that the TC genotype and the C allele may be linked to the increased risk of liver cancer (OR=2.225, 95% CI=1.178-4.204; OR=1.941, 95% CI=1.124-3.351). Rs2299939 polymorphism showed an opposite result that the GT genotype probably reduce the risk of liver cancer (OR=0.483, 95% CI=0.259-0.900). Statistical significance was not found in the distribution differences of the genotypes of rs1234213 between two groups. LD and haplotype analysis results of the three SNPs showed that the T-C-G haplotype frequency was much higher in cases than in healthy objects, which proved that the T-C-G haplotype might be a susceptibility haplotype for liver cancer (OR=3.750, 95% CI=1.396-10.077). CONCLUSIONS: PTEN gene polymorphisms might relate to liver cancer risk.

PIK3CA polymorphisms associated with susceptibility to hepatocellular carcinoma.

PURPOSE: Our study was carried out to explore the relationship of PIK3CA rs17849071 and rs17849079 polymorphisms with the susceptibility to hepatocellular carcinoma (HCC) in Chinese Han population. METHODS: 150 HCC patients and 152 healthy individuals were recruited in the case and control groups respectively. The genotypes of PIK3CA rs17849071 and rs17849079 polymorphisms were detected with polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The linkage disequilibrium and haplotypes were analyzed with Haploview software. Differences in frequencies of genotypes, alleles, and haplotypes between the case and control groups were checked with χ(2) test. The controls were matched with the cases in age and gender. The relative risk of HCC was represented by odds ratio (OR) and 95% confidence interval (95% CI). RESULTS: Significant difference in frequencies of GG genotype and G allele in PIK3CA rs17849071 polymorphism existed between the two groups (P=0.040; P=0.028), indicating that rs17849071 was closely related to the increased risk of HCC (OR=2.919, 95% CI=1.007-8.460; OR=1.642, 95% CI=1.051-2.564). Furthermore, TT genotype also significantly increased the susceptibility to HCC (OR=3.438, 95% CI=1.050-11.250) and so was T allele (OR=1.521, 95% CI=1.052-2.199). The haplotype analysisshowed that G-T haplotypes were higher in cases than that of controls (P=0.030), which suggested that G-T might be a susceptible haplotype to HCC. CONCLUSIONS: The PIK3CA rs17849071 and rs17849079 polymorphisms may increase the risk of HCC either independently or synergistically.

Two polymorphisms of USF1 gene (-202G>A and -844C>T) may be associated with hepatocellular carcinoma susceptibility based on a case-control study in Chinese Han population.

Hepatocellular carcinoma (HCC) is a prototype of liver cancer, which is closely related to manifested metabolism of lip and glucose. Upstream transcription factor 1 (USF1) is an important transcription factor in human genome, and it regulates the expression of multiple genes associated with lipid and glucose metabolism. This study aims at investigating the correlation between seven common USF1 polymorphisms (i.e., -1994 G>A, -202 G>A, 7998 A>G, -844 C>T, 9042 C>G, 9441 T>C, and -2083 G>A) and the risk of HCC. Elucidation of the interaction might be of vital importance to the diagnosis and prognosis of HCC. One hundred and fifty-five HCC patients and 160 healthy controls from a Chinese Han population were involved in this study. Tag single-nucleotide polymorphisms (SNPs) were identified with reference to CBI-dbSNP and HapMap databases. DNA was extracted from blood samples, and matrix-assisted laser desorption-ionization time-of-flight mass spectrometry (MALDI-TOF-MS) was conducted to determine the polymorphisms of USF1. Odds ratio (OR) and 95% confidence interval were applied to evaluate the difference of genotype distribution. Seven SNPs were selected to be representatives. No significant difference was observed concerning -1994 G>A, 7998 A>G, 9042 C>G, 9441 T>C, and -2083 G>A polymorphisms (all P > 0.05). A significantly elevated genotype frequency regarding -202 G>A polymorphism was observed in HCC patients [AA vs. GG: OR 2.13 (1.13-4.01), P = 0.019; AA vs. GG+GA: OR 2.22 (1.32-3.75), P = 0.003; A allele vs. G allele: OR 1.46 (1.07-2.01), P = 0.018]. Subjects carrying mutant -844 C>T genotypes also had a higher risk of HCC [CT vs. CC: OR 1.88 (1.17-3.04), P = 0.009; CT+TT vs. CC: OR 1.83 (1.17-2.86), P = 0.008; T allele vs. C allele: OR 1.49 (1.06-2.09), P = 0.020]. Further studies are recommended to validate our findings in different ethnicity and to clarify the functional relationship between USF1 polymorphisms and the susceptibility of HCC.

[Analysis of risk factors for anastomotic infectious complications following bowel resection for Crohn disease].

OBJECTIVE: To investigate the risk factors for anastomotic infectious complications after bowel resection in patients with Crohn disease. METHODS: Clinical data of 124 patients with Crohn disease undergoing bowel resection between January 1990 and October 2012 were analyzed retrospectively. The risk factors were identified by χ(2) test and Logistic regression. RESULTS: Fourteen patients (12.3%, 14/114) developed anastomotic infectious complications in the postoperative period, including anastomotic leak (n=7), intra-abdominal abscess (n=6), and enterocutaneous fistula (n=1). Crohn disease activity index (CDAI)>150 (OR=2.185, 95%CI:1.098-6.256, P=0.040), steroid usage (OR=2.674, 95%CI:1.118-8.786, P=0.027), and the presence of preoperative abscess/fistula (OR=3.447, 95%CI:1.254-10.462, P=0.014) were identified as independent risk factors of anastomotic infectious complications. In the absence of these 3 risk factors, the rate of anastomotic infectious complication was 5.7% (3/53), which increased to 11.4% (4/35) when one risk factor was present, 21.1% (4/19) when two risk factors were present, and 42.9% (3/7) when all the 3 risk factors were present. CONCLUSIONS: CDAI>150, steroid usage and preoperative abscess/fistula are associated with higher rates of anastomotic infectious complications following bowel resection for Crohn disease. A prudent management should be carried out if risk factors can not be eliminated preoperatively.