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ObjectiveThere is little evidence that adjuvant therapy after radical surgical resection of hepatocellular carcinoma (HCC) improves recurrence-free survival (RFS) or overall survival (OS). We conducted a multicentre, randomised, controlled, phase IV trial evaluating the benefit of an aqueous extract of Trametes robinophila Murr (Huaier granule) to address this unmet need.Design and resultsA total of 1044 patients were randomised in 2:1 ratio to receive either Huaier or no further treatment (controls) for a maximum of 96 weeks. The primary endpoint was RFS. Secondary endpoints included OS and tumour extrahepatic recurrence rate (ERR). The Huaier (n=686) and control groups (n=316) had a mean RFS of 75.5 weeks and 68.5 weeks, respectively (HR 0.67; 95% CI 0.55 to 0.81). The difference in the RFS rate between Huaier and control groups was 62.39% and 49.05% (95% CI 6.74 to 19.94; p=0.0001); this led to an OS rate in the Huaier and control groups of 95.19% and 91.46%, respectively (95% CI 0.26 to 7.21; p=0.0207). The tumour ERR between Huaier and control groups was 8.60% and 13.61% (95% CI −12.59 to −2.50; p=0.0018), respectively.ConclusionsThis is the first nationwide multicentre study, involving 39 centres and 1044 patients, to prove the effectiveness of Huaier granule as adjuvant therapy for HCC after curative liver resection. It demonstrated a significant prolongation of RFS and reduced extrahepatic recurrence in Huaier group.Trial registrationNCT01770431; Post-results.

Pancreatic cancer (PC) is one of the most aggressive malignancies, with a high mortality. Distant metastasis and recurrence are the main causes of PC-related deaths. MicroRNAs (miRNAs) have been reported in the serum or tumor tissue of cancer patients, including PC, which makes them potential biomarkers. The dysfunction of many miRNAs has been linked to PC occurrence and metastasis. In the current study, we found that miR-601 expression was significantly lower in PC samples, especially in metastatic compared to non-metastatic PC tissues. Gain-of-function and loss-of-function analysis showed that miR-601 suppressed PC cell proliferation and migration. One potential mechanism is that miR-601 inhibited the expression of Sirtuin 1 (SIRT1), which is a well-known regulator of PC development. We found that overexpression of SIRT1 could reverse the effect of miR-601 on PC cells. Our investigation therefore suggests that both miR-601 and SIRT1 are possible biomarkers for the early detection, and targets for the treatment of PC.

To identify biologically relevant genes associated with the pathogenesis of colorectal cancer (CRC), genome wide expression profiles of 17 pairs of CRC tumor and adjacent tissues, previously published in a DNA microarray study, were analyzed. Cytoscape, String tools and DAVID tools were used to investigate the biological pathways encoded by the genes identified as being either upregulated or downregulated in CRC, to determine protein‑protein interactions and to identify potential hub genes associated with CRC. As a result, a total of 3,264 genes were identified as being differentially expressed in CRC and adjacent tissues, including 1,594 downregulated and 1,670 upregulated genes. Furthermore, 306 genes were revealed to be clustered in a complex interaction network, and the top 20 hub genes in this network were determined by application of the Matthews Correlation Coefficient algorithm. In addition, the patterns of the expression levels of the 20 hub genes were investigated using reverse transcription‑quantitative polymerase chain reaction. Gene Ontology analysis revealed that four of the 20 hub genes encoded small subunit processome components (UTP3 small subunit processome component; UTP14 small subunit processome component; UTP 18 small subunit processome component; and UTP20 small subunit processome component) and a further four encoded WD repeat domains (WD repeat‑containing protein 3, WD repeat domain 12, WD repeat‑containing protein 43 and WD repeat‑containing protein 75). In conclusion, the present DNA microarray study identified genes involved in the pathogenesis of CRC. Furthermore, it was revealed that hub genes identified from among the total identified upregulated and downregulated genes in CRC encoding subunit processome components and WD repeat domains may represent novel target molecules for future treatments of CRC.

The aim of this study was to investigate the long-term outcomes and perioperative outcomes of laparoscopic hepatectomy (LH) versus open hepatectomy (OH) for hepatocellular carcinoma (HCC) between well-matched patient groups.We retrospectively reviewed data from 1535 hepatocellular carcinoma patients who underwent liver resection between January 2002 and December 2016 at two Chinese centres. Propensity score matching of patients in a ratio of 1:1 was conducted and 157 patients were matched.The median blood loss (150 vs 380 ml, P 0.001) was significantly less with LH. The laparoscopic group had shorter hospital stay (6 vs 10 days, P 0.001) and less complication rate (6.4% vs 24.2%,P 0.001). There were no significant differences in overall survival and disease-free survival between LH and OH. There were no significant differences in perioperative and long-term outcomes.Laparoscopic hepatectomy is technically feasible and safe in selected patients. LH showed similar long-term outcomes, associated with less blood loss, shorter hospital stay, and fewer postoperative complications in selected patients with HCC compared with OH.

Downregulation of LRIG1 was found in many types of cancer. However, data concerning the possible mechanism of LRIG1 reduction in cancers were not reported yet. To analyze the regulation and function of LRIG1 in colorectal cancer (CRC), 6 cell lines, 46 paired tissues from primary CRC cases were employed in this study. In CRC cell lines, under-expression of LRIG1 was correlated with promoter region hypermethylation, and restoration of LRIG1 was induced by 5-Aza-2'-deoxyazacytidine treatment. Subsequently, we ectopically expressed LRIG1 in LRIG1 low-expressing HCT-116 cells and suppressed LRIG1 in LRIG1 high-expressing LoVo cells. We found that over-expression of LRIG1 inhibits cell proliferation and colony formation and tumor growth, while knockdown of LRIG1 promotes cell proliferation and colony formation. Decreased and increased EGFR/AKT signaling pathway may partially explain the lower and higher rates of proliferation in CRC cells transfected with LRIG1 cDNA or shRNA. In clinical samples, we compared the methylation, mRNA and protein expression of LRIG1 in samples of CRC tissues. A significant increase in LRIG1 methylation was identified in CRC specimens compared to adjacent normal tissues and that it was negatively correlated with its mRNA and protein expression. In conclusion, LRIG1 is frequently methylated in human CRC and consequent mRNA and protein downregulation may contribute to tumor growth by activating EGFR/AKT signaling.

MicroRNAs (miRNAs) are short, non-coding RNA molecules that act as regulators of gene expression. Circulating blood miRNAs have potential as cancer biomarkers. The main objective of the present study was to assess the effect of miRNA-23b (miR-23b) expression in plasma on the diagnosis and prognosis of colorectal cancer (CRC). Reverse transcription-quantitative polymerase chain reaction (PCR) was used to measure miR-23b expression levels, and methylation-specific PCR was used to test the promoter methylation status. Subsequently, the expression level of miR-23b in plasma samples was compared between CRC patients and healthy control individuals. The miR-23b expression levels were significantly lower in CRC cells and primary CRC tissues than in nonmalignant colorectal tissues (P

ObjectiveTo observe expression of SIRT3 in normal liver tissue, cirrhotic tissue and hepatocellular carcinoma (HCC) tissues, and to explore the significance of SIRT3 in primary HCC.MethodsSIRT3 expression was detected in 10 normal cases, 30 cases with, 30 HCC cases by immunohistochemical and Western-blotting method.ResultsImmunohistochemical assay showed that the SIRT3 positive expression rates were 100.0% (10/10), 96.7% (29/30) and 60.0% (18/30), respectively in normal group, paracancer group and HCC group. And the SIRT3 expression in HCC group was significantly lower than in normal group and paracancer group (P

The aim of this study was to investigate the trafficking patterns, radiation sensitivities, and functions of conventional dendritic cell (DC) subsets in the rat liver in an allotransplantation setting. We examined DCs in the liver, hepatic lymph, and graft tissues and recipient secondary lymphoid organs after liver transplantation from rats treated or untreated by sublethal irradiation. We identified two distinct immunogenic DC subsets. One was a previously reported population that underwent blood-borne migration to the recipient's secondary lymphoid organs, inducing systemic CD8(+) T-cell responses; these DCs are a radiosensitive class II major histocompatibility complex (MHCII)(+) CD103(+) CD172a(+) CD11b(-) CD86(+) subset. Another was a relatively radioresistant MHCII(+) CD103(+) CD172a(+) CD11b(+) CD86(+) subset that steadily appeared in the hepatic lymph. After transplantation, the second subset migrated to the parathymic lymph nodes (LNs), regional peritoneal cavity nodes, or persisted in the graft. Irradiation completely eliminated the migration and immunogenicity of the first subset, but only partly suppressed the migration of the second subset and the CD8(+) T-cell response in the parathymic LNs. The grafts were acutely rejected, and intragraft CD8(+) T-cell and FoxP3(+) regulatory T-cell responses were unchanged. The radioresistant second subset up-regulated CD25 and had high allostimulating activity in the mixed leukocyte reaction, suggesting that this subset induced CD8(+) T-cell responses in the parathymic LNs and in the graft by the direct allorecognition pathway, leading to the rejection.Conventional rat liver DCs contain at least two distinct immunogenic passenger subsets: a radiosensitive blood-borne migrant and a relatively radioresistant lymph-borne migrant. LNs draining the peritoneal cavity should be recognized as a major site of the intrahost T-cell response by the lymph-borne migrant. This study provides key insights into liver graft rejection and highlights the clinical implications of immunogenic DC subsets.

Chronic hepatitis B virus infection is the dominant global cause of hepatocellular carcinoma (HCC), especially hepatitis B virus-X (HBx) plays a major role in this process. HBx protein promotes cell cycle progression, inactivates negative growth regulators, and binds to and inhibits the expression of p53 tumor suppressor gene and other tumor suppressor genes and senescence-related factors. However, the relationship between HBx and autophagy during the HCC development is poorly known. Previous studies found that autophagy functions as a survival mechanism in liver cancer cells. We suggest that autophagy plays a possible role in the pathogenesis of HBx-induced HCC. The present study showed that HBx transfection brought about an increase in the formation of autophagosomes and autolysosomes. Microtubule-associated protein light chain 3, Beclin 1, and lysosome-associated membrane protein 2a were up-regulated after HBx transfection. HBx-induced increase in the autophagic level was increased by mTOR inhibitor rapamycin and was blocked by treatment with the PI3K-Akt inhibitor LY294002. The same results can also be found in HepG2.2.15 cells. These results suggest that HBx activates the autophagic lysosome pathway in HepG-2 cells through the PI3K-Akt-mTOR pathway.

Ischemia/reperfusion (I/R) injury can occur during small-for-size liver transplantation, resulting in delayed graft function and decreased long-term graft survival. The aim of the present study was to evaluate the effects of genetic overexpression of endothelial nitric oxide synthase (eNOS) in protecting hepatocytes against I/R injury in a rat model of small-for-size liver transplantation. L02 liver cells were transfected with the eNOS gene using an adenovirus (Ad-eNOS). eNOS expression was detected using quantitative polymerase chain reaction and western blot analysis. To evaluate the effect of eNOS overexpression, L02 cells were placed in a hypoxic environment for 12 h and immediately transferred to an oxygen-enriched atmosphere. For in vivo testing, rats pretreated with Ad-eNOS or control underwent small-for-size liver transplantation. At 6 h after reperfusion, the bile quantity, serum transaminase and nitric oxide (NO) levels, and histological outcomes were evaluated. Cell apoptosis was assessed by flow cytometry or TUNEL assay. In vitro, Ad-eNOS prevented apoptosis in L02 cells with an increase in the level of NO in culture supernatant. In vivo, Ad-eNOS pre-treatment significantly increased bile production, improved abnormal transaminase levels, diminished apoptosis among liver cells, and decreased hepatocellular damage at 6 h after I/R injury. The eNOS-mediated renal protective effects might be associated with the downregulation of tumor necrosis factor-α and a reduction in macrophage activation in the early stage of reperfusion in small-for-size liver allografts. eNOS-derived NO production significantly attenuates hepatic I/R injury. Thus, eNOS overexpression constitutes a promising therapeutic approach to prevent liver I/R injury following small-for-size liver transplantation.

To investigate the role of autophagy in the injury of HepG-2 cells induced by hepatitis B virus x protein (HBx).After HBx transfection, the cells were used to detect the formation of autophagosomes and observed by transmission electron microscopy, monodansylcadaverine (MDC) staining autophagic vacuole (AV), immunofluorescent ce staining microtubule-associated protein light chain 3 ( MAP1-LC3 ) protein, and Western blotting examining the ratio of LC3-II/LC3-I (gray level: 0.760 ± 0.078 vs 0.520 ± 0.086, P0.05), beclin 1 (gray level: 0.875 ± 0.093 vs 0.220 ± 0.087, P0.05)and lysosome associated membrane protein 2a ( lamp2a ) protein (gray level: 0.320 ± 0.061 vs 0.120 ± 0.064, P0.05) levels.(1) HBx transfected upregulated the expression of LC3-II, LC3-I, beclin 1 and lamp2a protein. (2) HBx transfected brought about an increase in the formation of autophagosomes and autolysosomes.HBx activates the autophagic lysosome pathway in HepG-2 cells through the LC3/beclin1 pathway.

The present study aimed to investigate the effects of small interfering (si)RNA interference of connexin 37 (Cx37) on subcutaneous gastric tumours in mice. Constructed lentiviruses carrying siRNA against Cx37 significantly knocked down Cx37 mRNA and protein expression in vitro. A total of 60 mice with gastric cancer were randomly divided into the Cx37 siRNA group, the mock‑siRNA group and the control group. Cx37 siRNA, mock‑siRNA and saline were separately injected (with the lentiviruses transfected into the gastric cancer cells). Following six weeks, the Cx37 mRNA expression, Cx37 protein expression and tumor apoptosis were detected using semiquantitative reverse transcription‑polymerase chain reaction, western blot analysis and terminal deoxynucleotidyl transferase‑mediated dUTP nick end labelling, respectively. Six weeks following lentiviral transfection, the Cx37 mRNA levels in the Cx37 siRNA group, mock‑siRNA group and saline group decreased to 42, 63 and 67%, respectively (P

The 4-1BB signal pathway plays a key role in organ transplantation tolerance. In this study, we have investigated the effect of gene silencing of 4-1BB by RNA interference (RNAi) on the acute rejection in rats with liver transplantation. The recombination vector of lentivirus that contains shRNA targeting the 4-1BB gene (LV-sh4-1BB) was constructed. The liver transplantation was performed using the two-cuff technique. Brown-Norway (BN) recipient rats were infected by the recombinant LVs. The results showed that gene silencing of 4-1BB by RNAi downregulated the 4-1BB gene expression of the splenic lymphocytesin vitro, and the splenic lymphocytes isolated from the rats with liver transplantation. LV-sh4-1BB decreased the plasma levels of liver injury markers including AST, ALT, and BIL and also decreased the level of plasma IL-2 and IFN-γin recipient rats with liver transplantation. Lentivirus-mediated delivery of shRNA targeting 4-1BB gene prolonged the survival time of recipient and alleviated the injury of liver morphology in recipient rats with liver transplantation. In conclusion, our results demonstrate that gene silencing of 4-1BB by RNA interference inhibits the acute rejection in rats with liver transplantation.

Objective: To investigate the association between the connexin 37 C1019T polymorphism and Helicobacter pylori infection in patients with gastric cancer. Methods: 388 patients with gastric cancer (GC), 204 with chronic superficial gastritis (CSG) were studied. H. pylori was detected by gastric mucosal biopsies biopsy dyeing method. Connexin 37 gene polymorphism 1019 site genotypes were determined by gene sequencing technology. Genotypes and alleles frequencies were compared. Results: (1) Connexin37 gene 1019 site distribution frequency (CC type, TC type, TT type) in the CSG group was 18.1%, 45.1% and 36.8%; in the stomach cancer group it was 35.1%, 45.9% and 19.%, conforming to the Hardy-Weinberg euilibrium. (2) In comparison with CSG group, the frequency of Connexin37 C allele was higher in the gastric cancer group (58.0% vs 40.7%, OR = 2.01, 95%CI = 1.58-2.57, P < 0.01). The prevalence of gastric cancer risk was significantly increased in the carriers of C allele (CC+TC) than in TT homozygote (OR = 2.47, 5%CI = 1.68- 3.610. (3) Gastric cancer patients complicated with Hp infection 211 cases, gastric cancer group of the male patients with HP positive patients with 187 cases, 40 cases of female patients with negative patients, 24 cases were HP positive, negative in 137 cases, control group male patients, 28 cases were Hp positive, negative in 95 patients, female patients with Hp positive 6 cases, 75 cases were negative. On hierarchical analysis, the male group OR value was 15.9 (95%CI to 9.22-27.3), and the female OR was 2.19 (95%CI 0.88-5.59), indicating a greater contribution in males (P

In order to investigate whether the presence of distant metastases is associated with serum lipid abnormalities.The fasting serum lipid profile and various clinicopathological data of 324 breast cancer patients with and without synchronous distant metastases were collected and analyzed. The serum lipid profile, including total cholesterol (TC), triglycerides (TG), low-density (LDL-C) and high-density lipoprotein cholesterol (HDL-C) was determined. The nutritional status, the serum albumin was measured and body mass index (BMI) was calculated. Univariate analysis and multiple logistic regression analysis were carried out to investigate the association of serum lipid profile with distant metastases.Univariate analysis showed that the distant metastasis rate was significantly higher in the breast cancer patients with an higher level of serum TC, TG, LDL-C, and LDL-C/HDL-C ratio (P0.05). Multiple logistic regression analysis showed that higher serum levels of TC, LDL-C and LDL-C/HDL-C ratio were independent risk factors for distant metastasis in breast cancer (OR = 2.324, 2.648 and 4.862, respectively).Hyperlipidemia is significantly associated with the distant metastasis in breast cancer patients. Monitoring of serum lipid profile may be helpful to predict the occurrence of distant metastasis in breast cancer patients.

Although changes in serum lipid profile have been reported in CRC, the specific association between serum lipid profile and lymph node stages remains uncertain.Fasting serum lipid profile, including TC, TG, HDL-C and LDL-C was retrospectively evaluated in 968 patients undergoing curative resection for primary CRC. To determine the nutritional status, the serum albumin levels were measured and BMI was calculated. Statistical analyses were performed to investigate the association of serum lipid profile with lymph node stages.Serum lipid levels correlated well with rate of lymph node metastasis and high LDL-C and low HDL-C levels tended to present more advanced lymph node stages. The observed elevation of the LDL-C/HDL-C ratio for patients with N2 stage was statistically significant when compared with patients with N1 stage. When separated by gender, multivariate logistic regression analysis showed that both LDL-C levels and LDL-C/HDL-C ratio had independent association with advanced N2 stage in males, but not in females. In addition, LDL-C/HDL-C ratio might be a more effective biomarker for identifying N2 stage than LDL-C levels alone (OR value: 2.85 vs. 1.63).Elevated serum LDL-C levels and an increased LDC-C/HDL-C ratio might favour development of lymph node metastasis and LDCC/HDL-C ratio might be a more effective biomarker for identifying advanced N2 stage than LDL-C levels alone, especially for male patients with CRC.

Blocking the 4-1BB/4-1BB ligand (4-1BBL) signal may modulate the secretion of Th1/Th2 cytokines and prolong the survival of the grafts, which play a key role in organ transplantation tolerance. The aim of this study was to investigate the role of blockade of the 4-1BB/4-1BBL co-stimulatory pathway with 4-1BBL monoclonal antibody (mAB) in acute rejection of rat orthotopic liver transplantation.The orthotopic liver transplantation model was set up, while male Lewis rats were used as liver donors and Brown-Norway rats as recipients. The recipient rats were intravenously injected with anti 4-1BBL mAB or isotype control antibody. Groups were monitored for graft survival after transplantation. Plasma chemistry, including aspartate transaminase (AST), alanine aminotransferase (ALT), and bilirubin (BIL), was assayed. The concentrations of interleukin (IL)-2, IL-10 and interferon (IFN)-gamma in plasma were also measured by enzyme-linked immunosorbent assay. Allograft histology images were collected under light microscope and electron microscope.Isotype antibody treated recipients exhibited elevated plasma levels of liver injury markers including AST, ALT and BIL, progressive portal and venous inflammation and cellular infiltration of the liver allografts, and a mean graft survival time (MST) of 10.9 days. Administration of anti 4-1BBL mAB resulted in a decrease in plasma levels of liver injury markers and the concentrations of IL-2, IL-10 and IFN-gamma. The histological grade of rejection on day 7 decreased and MST (17.3 days) increased substantially.These results demonstrate that attenuation of acute rejection follows the blockade of the 4-1BB/4-1BBL co-stimulatory pathway with 4-1BBL monoclonal antibody and strongly suggest it is a promising strategy to prevent progression of graft rejection by suppressing T cell-mediated immunity.

The antitumor role of Ras association domain family 1A (RASSF1A) gene and its potential molecular mechanisms are not well understood. The objective of this study was to observe the antitumor ability of RASSF1A in hepatocellular carcinoma, and study the mechanisms of cell apoptosis induced by RASSF1A.After stably transfecting a RASSF1A (wild-type or mutant) expression vector into the BEL-7402 hepatocellular carcinoma cell line, RT-PCR and Western blotting was used to detect the RASSF1A expression levels in recombinant cells. The effects of wild-type RASSF1A on cell growth were observed in vitro by analyzing cell proliferation rate, cell colony formation, and in vivo by analyzing tumorigenesis in nude mice. In addition, the effect of RASSF1A gene expression on the chemosensitivity of human hepatocellular carcinoma cells to antitumor drugs was examined by inhibition of cell proliferation and the percentage of apoptotic cells.Wild-type RASSF1A, not the mutant, suppressed cell growth in vitro and in vivo. Re-expression of wild-type RASSF1A could enhance the inhibition of cell proliferation and the percentage of apoptotic cells following cell treatment with mitomycin, but had no significant effect when combined with adriamycin, etoposide, 5-fluorouracil and cisplatin treatment.Wild-type RASSF1A inhibits cell growth and enhances cell chemosensitivity to mitomycin in hepatocellular carcinoma, suggesting that RASSF1A may serve as a new target for gene therapy in hepatocellular carcinoma patients.

To investigate the role of duodenum in regulation of ghrelin and body mass index (BMI) and the correlation between ghrelin and BMI after subtotal gastrectomy.Forty-two patients with T(0-1)N(0-1)M(0) gastric cancer were divided into two groups after gastrectomy according to digestive reconstruction pattern, Billroth I group (n=23) and Billroth II group (n=19) respectively. Plasma ghrelin levels were determined by radioimmunoassay (RIA) before and at day 1, 7, 30 and 360 after gastrectomy,and BMIs were also measured.Two groups had identical postoperative trends in ghrelin alterations during the early stage, both dropping to nadir at day 1 (36.7% vs 35.7%), then markedly increasing at day 7 (51.0% vs 51.1%). At day 30, ghrelin level of Billroth I group was slightly higher than that of Billroth II group. At day 360, ghrelin level of Billroth I group recovered to 93.6%, approaching though lower than preoperative level and no significant difference was displayed, while ghrelin level of Billroth II group recovered only to 81.6% of preoperational level and significant difference existed (P=0.033). Compared with preoperative levels, ghrelin of two groups decreased by 6.9% and 18.4% while BMI by 3.3% and 6.4% respectively, liner regression correlations were revealed in both groups between decrease magnitudes(R(1)(2)=0.297,P=0.00;R(2)(2)=0.559,P0.001).Anatomico-physiological duodenum compensatively promotes ghrelin recovery, accordingly enhances BMI after gastrectomy. Regarding patients with insufficient ghrelin secretion, ghrelin is positively correlated with BMI.

To study the color distribution of the anterior teeth in elder people.612 anterior teeth from 137 people aging from 60 to 81 years and 200 anterior teeth from 100 young people aging from 20 to 40 years were collected. A digital colorimeter was used to measure the value of L*,a*,b* of the teeth, and the chromatism (deltaE) was calculated according to the formula deltaE=(deltaL*(2)+deltaa*(2)+deltab*(2))1/2. All data were analyzed with SAS 6.12 software package for Student's t test.Totally, there were 612 vital anterior teeth from elder people, including 201 central incisors,199 lateral incisors and 212 canines, were collected. No difference was found between the teeth on the right side and the left side in terms of L*,a*,b*value(P0.05). The mean value of L*,a*,b* of the central incisors was 71.2+/-6.22,0.97+/-1.12,15.9+/-5.04, respectively and that of the lateral incisors and the canines were 69.6+/-5.52,0.6+/-1.18,13.9+/-4.15 and 68.4+/-5.99,0.15+/-1.02,19.6+/-4.87, respectively.The mean value of L*,a*,b* of the central incisors and the canines from the youngster was 75.82,-0.11,12.68 and 72.07,1.22,17.92, respectively.There were significant differences between the central incisors and the lateral incisors as well as the canines (P0.05) in terms of L* value. Meanwhile difference was also found among the incisors and the canines in terms of a* and b* value(P0.05). The deltaE between the central incisors and the lateral incisors was 2.945NBS, and the value between the canines and the central incisors as well as the lateral incisors was 4.629NBS and 5.832NBS, respectively, indicating that the color difference could be perceived visually. Compared to the youngster, the teeth of the elder people demonstrated a lower L* and a* value, but a higher b* value (P0.05).Among elder people, the central incisors look much brighter than the lateral incisors and canines, while the canines have more redness and yellowness than the incisors, and the color of the lateral incisors exhibits lighter than the central incisors and the canines. Compared to the teeth from younger people, the teeth from elder people look much darker and yellower but less red. Supported by Shanghai Leading Academic Discipline Project (Grant No.T0202).

Background and Aim: The tumor-suppressing role of Ras-association domain family 1A (RASSF1A) has been described in several systems. In this study, we tested its tumor-suppressing ability and the potential molecular mechanisms in hepatocellular carcinoma (HCC) from Qidong County. Methods: Reverse transcription polymerase chain reaction and Northern blotting were employed to detect the expression of RASSF1A in HCC. After establishing stable RASSF1A (wild type or mutant) expressing ‘qi dong gan ai yan jiu suo’ ([Qidong Institute of Liver Cancer] QGY)-7703 cell lines, we tested the effects of RASSF1A expression on cell growth by cell proliferation rate, cell colony formation, and cell cycle progression. We also tested the effects of RASSF1A expression on tumorigenesis in nude mice and on cellular sensitivity to mitomycin treatment. Results: The RASSF1A transcript was not found in 75% (three of four) of HCC cell lines and 67% (32/48) of HCC primary biopsies. The stepwise regression analyses indicated that the loss of RASSF1A expression was more frequent in patients who were hepatitis B virus surface antigen positive (HBsAg+) compared to those who were HBsAg(−), both in tumor and corresponding non-cancerous tissues. The wild-type (wt)-RASSF1A expression in the QGY-7703 cell line resulted in fewer and smaller clones, decreased xenograft tumor volume and weight, and G1/S arrest in vitro and in vivo. The wt-RASSF1A expression also decreased the cyclin D1 protein expression, which appeared to be at the level of post-transcriptional control. In addition, the wt-RASSF1A expression increased cell growth inhibition and the percentage of cells with sub-G1 DNA content when the cells were treated with mitomycin. Conclusion: RASSF1A is a tumor suppressor in HCC. The loss of RASSF1A expression may be related to HBsAg+ in hepatocarcinogenesis. Its inactivation may play an important role in the development of HCC.

To study the influence of the try-in pastes on the color of all-ceramic veneers made by Ips-empress II system.50 discolored teeth were collected and restored with all-ceramic veneers. Five try-in pastes including A1, A3, transleucent(Trt), white opaque(WOT) and B0.5 opaque(B0.5),which were different in shade, were respectively used to try in before cementing. The color was measured by the ShadeEye, a digital colorimeter, and expressed in terms of 3 coordinate values (L*,a*,b*) of the CIEL*a*b* system. Then the color differences(deltaEa*b*) of all-ceramic veneers[deltaEa*b*=(deltaL*(2)+deltaa*(2)+deltab*(2))(1/2)] as well as the value of L*deltaC(ab)[C(ab)=(a*(2)+b*(2))(1/2)] and H(ab)[H(ab)=arctan(b*/a*)]were calculated. Meanwhile,the thickness of the measurement point was measured and recorded. One-way ANOVA was used to analyze deltaEa*b* as well as L*,C(ab) and Hab.The average thickness of the ceramic was 1.088mm, and the colour of the veneers after try in with WOT paste and B0.5 paste performed a higher L* value than the other pastes (P0.05).And the veneers also showed a higher C(ab) value after try in with WOT,B0.5 and A3 paste than the A1 and Trt paste (P0.05). No significant differences were found in Hab value after these 50 veneers tried in with these five kinds of pastes.It's more advisable to choose the WOT or the B0.5 luting agent to cement the veneer when the abutment tooth is severely discolored, while the Trt or the A1 shade and A3 shade luting resin may be more appropriate if the abutment tooth doesn't discolor or a little compared with the adjacent tooth.

Several reports have showed that three histologic variables (venous invasion, regional lymph node status, and depth of primary tumor penetration) were associated with the prognosis of colorectal adenocarcinoma patients. Based on these variables, a new classification system has been recommended. This study was designed to evaluate prognostic significance and risk factors of neoplasm in low and middle rectal cancer.Four hundreds and eighty-four consecutive patients with low and middle rectal cancer were treated by the abdominoperineal resection (APR) (356 patients) and the low anterior resection(LAR) (128 patients) between 1990 and 1996. To determine the independent prognostic variables, the variables were evaluated both univariately and multivariately from the perspectives of oncologic outcome.The 5-year survival rate for all patients was 71.1% (344/484), 63.5% (226/356) for APR and 92.2% (118/128) for LAR/SSR, respectively (P0.01). The resulting multivariate analysis using Cox regression showed that the three tumor variables were significantly associated with the 5-year survival (P0.01), the independent prognostic variables included venous invasion, tumor size, and TNM stages.The three tumor variables identified in multivariate analysis as bearing the strongest independent effect on the 5-year survival in low and middle rectal cancer were (in order to decrease prognostic impact) venous invasion, tumor size, and TNM stages. These three tumor variables may be used as important bases for a new classification system.

AIM: To investigate the role of the duodenum in the regulation of plasma ghrelin levels and body mass index (BMI), and the correlation between them after subtotal gastrectomy. METHODS: Forty-two patients with T0-1N0-1M0 gastric cancer were divided into two groups after gastrectomy according to digestive reconstruction pattern, Billroth I group (n = 23) and Billroth II group (n = 19). Ghrelin levels were determined with radioimmunoassay (RIA) before and on d 1, 7, 30 and 360 after gastrectomy, and BMI was also measured. RESULTS: The two groups had identical postoperative trends in ghrelin alterations during the early stage, both decreasing sharply to a nadir on d 1 (36.7% vs 35.7%), then markedly increasing on d 7 (51.0% vs 51.1%). On d 30, ghrelin levels in the Billroth I group were slightly higher than those in the Billroth II group. However, those of the Billroth I group recovered to 93.6% on d 360, which approached, although lower than, the preoperative levels, and no statistically significant difference was observed. Those of the Billroth II group recovered to only 81.6% and manifested significant discrepancy with preoperative levels (P = 0.033). Compared with preoperative levels, ghrelin levels of the two groups decreased by 6.9% and 18.4% and BMI fell by 3.3% and 6.4%, respectively. The linear regression correlations were revealed in both groups between decrease of ghrelin level and BMI (R12 = 0.297, P = 0.007; R22 = 0.559, P < 0.001). CONCLUSION: Anatomically and physiologically, the duodenum compensatively promotes ghrelin recovery and accordingly enhances BMI after gastrectomy. Regarding patients with insufficient ghrelin secretion, ghrelin is positively associated with BMI.