Cell division cyclin 25C knockdown inhibits hepatocellular carcinoma development by inducing endoplasmic reticulum stress.

BACKGROUND: Cell division cyclin 25C (CDC25C) is a protein that plays a critical role in the cell cycle, specifically in the transition from the G2 phase to the M phase. Recent research has shown that CDC25C could be a potential therapeutic target for cancers, particularly for hepatocellular carcinoma (HCC). However, the specific regulatory mechanisms underlying the role of CDC25C in HCC tumorigenesis and development remain incompletely understood. AIM: To explore the impact of CDC25C on cell proliferation and apoptosis, as well as its regulatory mechanisms in HCC development. METHODS: Hepa1-6 and B16 cells were transduced with a lentiviral vector containing shRNA interference sequences (LV-CDC25C shRNA) to knock down CDC25C. Subsequently, a xenograft mouse model was established by subcutaneously injecting transduced Hepa1-6 cells into C57BL/6 mice to assess the effects of CDC25C knockdown on HCC development in vivo. Cell proliferation and migration were evaluated using a Cell Counting Kit-8 cell proliferation assays and wound healing assays, respectively. The expression of endoplasmic reticulum (ER) stress-related molecules (glucose-regulated protein 78, X-box binding protein-1, and C/EBP homologous protein) was measured in both cells and subcutaneous xenografts using quantitative real-time PCR (qRT-PCR) and western blotting. Additionally, apoptosis was investigated using flow cytometry, qRT-PCR, and western blotting. RESULTS: CDC25C was stably suppressed in Hepa1-6 and B16 cells through LV-CDC25C shRNA transduction. A xenograft model with CDC25C knockdown was successfully established and that downregulation of CDC25C expression significantly inhibited HCC growth in mice. CDC25C knockdown not only inhibited cell proliferation and migration but also significantly increased the ER stress response, ultimately promoting ER stress-induced apoptosis in HCC cells. CONCLUSION: The regulatory mechanism of CDC25C in HCC development may involve the activation of ER stress and the ER stress-induced apoptosis signaling pathway.

Upregulating KTN1 promotes Hepatocellular Carcinoma progression.

Background: Hepatocellular carcinoma (HCC) presents a common malignant tumor worldwide. Although kinectin 1 (KTN1) is the most frequently identified antigen in HCC tissues, the detailed roles of KTN1 in HCC remain unknown. This study seeks to clarify the expression status and clinical value of KTN1 in HCC and to explore the complicated biological functions of KTN1 and its underlying mechanisms. Methods: In-house reverse transcription quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression of KTN1 in HCC tissues. External gene microarrays and RNA-sequencing datasets were downloaded to confirm the expression patterns of KTN1. The prognostic ability of KTN1 in HCC was assessed by a Kaplan-Meier curve and a hazard ratio forest plot. The CRISPR/Cas9 gene-editing system was used to knock out KTN1 in Huh7 cells, which was verified by PCR-Sanger sequencing and western blotting. Assays of cell migration, invasion, viability, cell cycle, and apoptosis were conducted to explore the biological functions. RNA sequencing was performed to quantitatively analyze the functional deregulation in KTN1-knockout cells compared to Huh7-wild-type cells. Upregulated genes that co-expressed with KTN1 were identified from HCC tissues and were functionally annotated. Results: KTN1 expression was increased in HCC tissues (standardized mean difference [SMD] = 0.20 [0.04, 0.37]). High KTN1 expression was significantly correlated with poorer prognosis of HCC patients, and KTN1 may be an independent risk factor for HCC (pooled HRs = 1.31 [1.05, 1.64]). After KTN1-knockout, the viability, migration, and invasion ability of HCC cells were inhibited. The proportion of HCC cells in the G0-G1 phases increased after KTN1 knockout, which also elevated the apoptosis rates in HCC cells. Several cascades, including innate immune response, chemical carcinogenesis, and positive regulation of transcription by RNA polymerase II, were dramatically changed after KTN1 knockout. KTN1 primarily participated in the cell cycle, DNA replication, and microRNAs in cancer pathways in HCC tissues. Conclusion: Upregulation of KTN1 served as a promising prognosticator in HCC patients. KTN1 promotes the occurrence and deterioration of HCC by mediating cell survival, migration, invasion, cell cycle activation, and apoptotic inhibition. KTN1 may be a therapeutic target in HCC patients.

Laminarin from Seaweed (Laminaria japonica) Inhibits Hepatocellular Carcinoma Through Upregulating Senescence Marker Protein-30.

Objective: This study aimed at investigating the specific roles of laminarin from seaweed (Laminaria japonica) in hepatocellular carcinoma (HCC) and its potential mechanisms related to senescence marker protein-30 (SMP-30). Materials and Methods: Human HCC cell lines, including Bel-7404 and HepG2, were incubated with different concentrations of laminarin (0, 5, 15, 25, 35, and 45 mg/mL). The cell viability and apoptosis rates were detected by WST-8 cell proliferation assay and flow cytometry, respectively. Hepa 1-6 tumor-bearing mice were injected with different concentrations of laminarin (400, 800, and 1200 mg/kg·d), and tumor volume and weight were measured. The expression of SMP-30 was detected in laminarin-treated Bel-7404 and HepG2 HCC cells and LO2 normal liver cells by quantitative real-time PCR and Western blotting. Results: The treatment with laminarin (48 h) significantly decreased the viability and increased the apoptosis rates of Bel-7404 and HepG2 cells in a dose-dependent manner. The injection of laminarin also significantly decreased the tumor volumes (beginning on the 10th day) and tumor weights (30 d post-injection) of mice in a dose-dependent manner. In addition, the treatment with laminarin (35 mg/mL for 48 h) significantly upregulated SMP-30 in Bel-7404 and HepG2 cells but not in LO2 cells. Conclusion: Laminarin inhibited the proliferation of Bel-7404 and HepG2 cells and inhibited the growth of tumors in Hepa 1-6 tumor-bearing mice by upregulating SMP-30.

Characterization of Heterozygous HTRA1 Mutations in Taiwanese Patients With Cerebral Small Vessel Disease.

BACKGROUND AND PURPOSE: Homozygous and compound heterozygous mutations in the high temperature requirement serine peptidase A1 gene (HTRA1) cause cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy. However, heterozygous HTRA1 mutations were recently identified to be associated with autosomal dominant cerebral small vessel disease (SVD). The present study aims at investigating the clinical features, frequency, and spectrum of HTRA1 mutations in a Taiwanese cohort with SVD. METHODS: Mutational analyses of HTRA1 were performed by Sanger sequencing in 222 subjects, selected from a cohort of 337 unrelated patients with SVD after excluding those harboring a NOTCH3 mutation. The influence of these mutations on HTRA1 protease activities was characterized. RESULTS: Seven novel heterozygous mutations in HTRA1 were identified, including p.Gly120Asp, p.Ile179Asn, p.Ala182Profs*33, p.Ile256Thr, p.Gly276Ala, p.Gln289Ter, and p.Asn324Thr, and each was identified in 1 single index patient. All mutations significantly compromise the HTRA1 protease activities. For the 7 index cases and another 2 affected siblings carrying a heterozygous HTRA1 mutation, the common clinical presentations include lacunar infarction, intracerebral hemorrhage, cognitive decline, and spondylosis at the fifth to sixth decade of life. Among the 9 patients, 4 have psychiatric symptoms as delusion, depression, and compulsive behavior, 3 have leukoencephalopathy in anterior temporal poles, and 2 patients have alopecia. CONCLUSIONS: Heterozygous HTRA1 mutations account for 2.08% (7 of 337) of SVD in Taiwan. The clinical and neuroradiological features of HTRA1-related SVD and sporadic SVD are similar. These findings broaden the mutational spectrum of HTRA1 and highlight the pathogenic role of heterozygous HTRA1 mutations in SVD.

Homocysteine induces vascular inflammatory response via SMAD7 hypermethylation in human umbilical vein smooth muscle cells.

Homocysteine (Hcy) can induce atherosclerosis through the inflammatory response and DNA methylation disorder. Our recent study has reported a novel epigenetic modified gene related to atherosclerosis -SMAD7. To further understand the pathogenesis of atherosclerosis, the current study was designed to investigate an inflammatory role of Hcy in human umbilical vein smooth muscle cells (HUVSMCs) through interfering with SMAD7 methylation. Using MALDI-TOF MS, we found that Hcy increased DNA methylation levels of SMAD7 promoter in a dose and time-dependent manner in HUVSMCs. Meanwhile, both SMAD7 mRNA and protein levels were decreased along with the increase of Hcy concentrations and treating time. Decreased SMAD7 levels led to up regulation of pro-inflammatory cytokines (TNF-α and IL-1ß) expression in HUVSMCs. Furthermore, we found that activation of NF-κB pathway was the mechanism by which reduced Smad7 levels enhanced vascular inflammation. Thus, Hcy is able to activate NF-κB-mediated vascular inflammatory response via inducing hypermethylation of SMAD7 promoter in HUVSMCs. The in vitro findings supplement our recent clinical study that SMAD7 methylation as a novel marker in atherosclerosis and further elucidate the role of Hcy in atherogenesis.

Clinical and Molecular Characterization of PMP22 point mutations in Taiwanese patients with Inherited Neuropathy.

Point mutations in the peripheral myelin protein 22 (PMP22) gene have been identified to cause demyelinating Charcot-Marie-Tooth disease (CMT) and hereditary neuropathy with liability to pressure palsy (HNPP). To investigate the mutation spectrum of PMP22 in Han-Chinese population residing in Taiwan, 53 patients with molecularly unassigned demyelinating CMT and 52 patients with HNPP-like neuropathy of unknown genetic causes were screened for PMP22 mutations by Sanger sequencing. Three point mutations were identified in four patients with demyelinating CMT, including c.256 C > T (p.Q86X) in two, and c.310delA (p.I104FfsX7) and c.319 + 1G > A in one each. One PMP22 missense mutation, c.124 T > C (p.C42R), was identified in a patient with HNPP-like neuropathy. The clinical presentations of these mutations vary from mild HNPP-like syndrome to severe infantile-onset demyelinating CMT. In vitro analyses revealed that both PMP22 p.Q86X and p.I104FfsX7 mutations result in truncated PMP22 proteins that are almost totally retained within cytosol, whereas the p.C42R mutation partially impairs cell membrane localization of PMP22 protein. In conclusion, PMP22 point mutations account for 7.5% and 1.9% of demyelinating CMT and HNPP patients with unknown genetic causes, respectively. This study delineates the clinical and molecular features of PMP22 point mutations in Taiwan, and emphasizes their roles in demyelinating CMT or HNPP-like neuropathy.

Molecular identification of Uncaria (Gouteng) through DNA barcoding.

BACKGROUND: While DNA barcoding is an important technology for the authentication of the botanical origins of Chinese medicines, the suitable markers for DNA barcoding of the genus Uncaria have not been reported yet. This study aims to determine suitable markers for DNA barcoding of the genus Uncaria (Gouteng). METHODS: Genomic DNA was extracted from the freshly dried leaves of Uncaria plants by a Bioteke's Plant Genomic DNA Extraction Kit. Five candidate DNA barcode sites (ITS2, rbcL, psbA-trnH, ITS, and matK) were amplified by PCR with established primers. The purified PCR products were bidirectionally sequenced with appropriate amplification primers in an ABI-PRISM3730 instrument. The candidate DNA barcodes of 257 accessions of Uncaria in GenBank were aligned by ClustalW. Sequence assembly and consensus sequence generation were performed with CodonCode Aligner 3.7.1. The identification efficiency of the candidate DNA barcodes was evaluated with BLAST and nearest distance methods. The interspecific divergence and intraspecific variation were assessed by the Kimura 2-Parameter model. Genetic distances were computed with Molecular Evolutionary Genetics Analysis 6.0. RESULTS: The accessions of the five candidate DNA barcodes from 11 of 12 species of Uncaria in China and four species from other countries were included in the analysis, while 54 of total accessions were submitted to GenBank. In a comparison of the interspecific genetic distances of the five candidate barcodes, psbA-trnH exhibited the highest interspecific divergence based on interspecific distance, theta prime, and minimum interspecific distance, followed by ITS2. The distribution of the interspecific distance of ITS2 and psbA-trnH was higher than the corresponding intraspecific distance. Additionally, psbA-trnH showed 95.9 % identification efficiency by both the BLAST and nearest distance methods regardless of species or genus level. ITS2 exhibited 92.2 % identification efficiency by the nearest distance method, but 87 % by the BLAST method. CONCLUSION: While psbA-trnH and ITS2 (used alone) were applicable barcodes for species authentication of Uncaria, psbA-trnH was a more suitable barcode for authentication of Uncaria macrophylla.

Impact of cytoreductive surgery on survival in gastric cancer patients with peritoneal metastasis / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To investigate the survival benefit of cytoreductive surgery in gastric cancer patients with peritoneal metastasis.</p><p><b>METHODS</b>Clinicopathological data of 151 advanced gastric adenocarcinoma patients with extensive peritoneal metastasis who were identified by surgical exploration between May 2008 and April 2015 in Xijing Hospital of Digestive Diseases were analyzed retrospectively. Of all the patients, 32 cases were treated by cytoreductive surgery with local radical tumor resection and regional lymph node cleaning, combined with fluorouracil-based adjuvant chemotherapy after surgery (cytoreductive surgery combined with chemotherapy group); 39 caseswere only treated by cytoreductive surgery group(cytoreductive surgery group);23 caseswere treated bysurgical exploration combined with fluorouracil-based adjuvant chemotherapy after surgery(surgical exploration combined with chemotherapy group) and 57 cases were only treated bysurgical exploration (surgical exploration group). The overall survival of four groups were analyzed and compared.</p><p><b>RESULTS</b>Among the 151 patients, 148 (98.0%) patients were followed up. The median follow up time was 7.2 months (range 1.4-61.2). The median survival of cytoreductive surgery combined with chemotherapy group, cytoreductive surgery group, surgical exploration combined with chemotherapy group and surgical exploration group was 11.9(95% CI: 8.8-15.1) months, 7.1(95% CI: 3.2-11.1) months, 8.2(95% CI:4.6-11.8) and 5.4(95% CI:4.4-6.4) months, respectively(P < 0.01).</p><p><b>CONCLUSIONS</b>Cytoreductive surgery can prolong the survival of gastric adenocarcinoma patients with extensive peritoneal metastasis. Cytoreductive surgery combined with chemotherapy may provide more benefit for patients, and can be used as a choice of treatment in these patients.</p>

Survival rate of proximal and total gastrectomy in treatment of esophagogastric junction adenocarcinoma (Siewert II( Types) / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To compare the survival rate of proximal gastrectomy and total gastrectomy in the treatment of esophagogastric junction (EGJ) adenocarcinoma (Siewert II( types), and to provide reference for clinical choice.</p><p><b>METHODS</b>A total of 533 patients with Siewet II( type EGJ adenocarcinoma were screened. All the patients underwent radical operations and were pathologically diagnosed as Siewet II( type EGJ adenocarcinoma in Xijing Hospital of Digestive Diseases from May 2008 to March 2014. These patients all had complete followed-up data. Finally, 234 patients were enrolled into the retrospective study, and divided into proximal gastrectomy group(117 patients) and total gastrectomy group (117 patients) based on the matching of age, sex, tumor size, TNM staging, and differentiation. The survival rate was compared between the two groups.</p><p><b>RESULTS</b>In proximal gastrectomy and total gastrectomy group, the overall 3-year survival rate was 65.6% and 62.6% respectively, and the overall 5-year survival rate was 53.8% and 44.5% respectively. No significant difference was found between the two groups (P=0.768). In subgroup analyses of 3-year survival rate between proximal gastrectomy group and total gastrectomy group, the results were as follows: 72.8% and 80.4% respectively (P=0.423) for tumor diameter ≤4 cm, 57.9% and 46.5% (P=0.239) for tumor diameter >4 cm, 83.3% and 83.3% (P=0.998) for high differentiated EGJ adenocarcinoma, 68.2% and 53.3% (P=0.270) for moderate differentiated EGJ adenocarcinoma, 56.1% and 69.6% (P=0.280) for poorly differentiated EGJ adenocarcinoma, 64.8% and 56.0% (P=0.451) for mucinous EGJ adenocarcinoma, 80.0% and 76.9% (P=0.912) for T1-2 stage EGJ adenocarcinoma, 64.3% and 60.4% (P=0.610) for T3 stage, 50.0% and 62.5% (P=0.953) for T4a stage, 92.3% and 100% (P=0.380) for stage I( EGJ adenocarcinoma, 79.6% and 66.3%(P=0.172) for stage II(, 42.6% and 49.5% (P=0.626) for stage I I(. All above differences between the two groups were not significant(all P>0.05).</p><p><b>CONCLUSION</b>Proximal gastrectomy and total gastrectomy are comparable in terms of 3-year and 5-year survival rates.</p>

Analysis of risk factors and prognosis of esophagojejunal anastomotic leakage in gastric cancer patients after curative total gastrectomy / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To identify the risk factors of esophagojejunal anastomotic leakage (EJAL) and its impact on prognosis of gastric cancer patients after curative total gastrectomy.</p><p><b>METHODS</b>Clinical and follow-up data of 1254 gastric cancer patients who underwent radical total gastrectomy at the Department of Digestive Surgery, Xijing Hospital, from January 2012 to May 2015 were retrospectively collected. Risk factors of EJAL and prognostic factors of patients were analyzed respectively. In order to reduce the influences of other prognostic factors on survival, patients with and without EJAL were selected using Gmatch methods based on the results of prognostic factor analysis. Survival of those with or without EJAL was examined before and after match respectively.</p><p><b>RESULTS</b>EJAL occurred in 31 of 1 254 patients(2.5%). The leakage was diagnosed at a median of 6 (range, 4-12) days after surgery. Multivariate analysis demonstrated that preoperative low serum albumin(<35 g/L)(P=0.018), pulmonary insufficiency(P=0.006), long duration of operation(≥240 min)(P=0.001) were independent risk factors of EJAL. All the patients were followed up for 3-40(median 18) months. Multivariate analysis showed that age(≥65, P=0.000), intraoperative blood transfusion (P=0.016), EJAL (P=0.000), tumor location (distal, P=0.020; total, P=0.001), depth of invasion (T4, P=0.005) and lymph node metastasis (N2, P=0.002, N3, P=0.000) were prognostic predictors. Twenty-six patients with EJAL were successfully matched to 104 patients without EJAL in a ratio of 1/4 ratio. Patients with EJAL had a significantly worse overall 3-year survival rate than those without (44.3% vs. 66.7%, P=0.002).</p><p><b>CONCLUSIONS</b>EJAL after curative total gastrectomy leads to worse survival. Patients with preoperative low serum albumin, pulmonary insufficiency and long duration of operation should be taken care of during perioperative period to prevent the occurrence of EJAL.</p>

Comparison of long-term survival and postoperative complications between Billroth I( and II( reconstruction in patients with distal gastric cancer / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To compare the long-term survival and postoperative complications of distal gastric cancer patients between Billroth I((BI() and Billroth II((BII() reconstruction.</p><p><b>METHODS</b>Clinicopathological data of 992 patients with distal gastric cancer who underwent D2 curative gastrectomy in our department from May 2008 to April 2015 were recorded, including 207 patients of BI( reconstruction and 785 of BII( reconstruction, were retrospectively analyzed. Patients presenting a previous history of cancer, gastric resection or cytotoxic chemotherapy, and those presenting liver or intraperitoneal tumor dissemination or unresectable infiltration into contiguous organs were excluded. Patients in BI( and BII( group were selected using gmatch methods based on age (±10 years), gender, tumor size (±1 cm), differentiated degree and depth of invasion in order to reduce the selection bias of clinicopathological characteristics. The final number of patients matched was 191 respectively.</p><p><b>RESULTS</b>Compared with BII( group, the BI( group had a significantly shorter operation time (181.7 min vs. 220.7 min, P=0.000) and a shorter postoperative hospitalization stay (7.6 days vs. 8.1 days, P=0.046). The postoperative complications including anastomotic leakage, wound dehiscence, wound infection, intraperitoneal hemorrhage, intestinal obstruction, duodenal stump fistula, pulmonary infection and fever had no significant difference(P>0.05). Three-year survival between two groups was comparable (82.9% vs. 78.7%, P=0.379).</p><p><b>CONCLUSIONS</b>Compared with BII(, BI( reconstruction is more suitable for patients with distal gastric cancer.</p>

Study on prognosis relationship between ABO blood groups of patients with gastric cancer / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To investigate the relationship of ABO blood group with the clinicopathological characteristics in patients with gastric cancer and to assess whether the ABO blood group was associated with prognosis.</p><p><b>METHOD</b>Clinicopathological and follow-up data of 2838 patients with gastric cancer who underwent radical gastrectomy in our department from June 2008 to October 2013 were analyzed retrospectively. The distribution of ABO blood group under different clinicopathological characteristics and the overall 5-year survival of ABO blood group were compared.</p><p><b>RESULTS</b>There were no significant differences in clinicopathological characteristics among patients with different ABO blood groups (all P>0.05). The 5-year overall survival(OS) rates were 57.3% for patients with blood type A, 54.7% for type B, 57.4% for type O, and 53.5% for type AB. Though there was no significance difference of survival among ABO blood groups(P=0.722), while the subgroup analysis indicated that stage III( patients of blood group Non-AB had a poorer OS compared to those of blood group AB(25.2% vs. 44.7%, P=0.014); smoking patients of blood group Non-AB had a poorer OS compared to those of blood group AB(53.4% vs. 74.9%, P=0.044).</p><p><b>CONCLUSION</b>Neither clinicopathological characteristics nor overall survival are associated with the ABO blood group, however, stage III( and smoking patients of blood group Non-AB have a poorer OS compared to those of blood group AB.</p>

Conditionally ablated Pten in prostate basal cells promotes basal-to-luminal differentiation and causes invasive prostate cancer in mice.

Prostate glands comprise two major epithelial cell types: luminal and basal. Luminal cells have long been considered the cellular origin of prostate cancer (CaP). However, recent evidence from a prostate regeneration assay suggests that prostate basal cells can also give rise to CaP. Here, we characterize Pten-deficient prostate lesions arising from keratin 5-expressing basal cells in a temporally controlled system in mice. Pten-deficient prostate lesions arising from basal cells exhibited luminal phenotypes with higher invasiveness, and the cell fate of Pten-deficient basal cells was traced to neoplastic luminal cells. After temporally ablating Pten in keratin 8-expressing luminal cells, luminal-derived Pten-deficient prostate tumors exhibited slower disease progression, compared with basal-derived tumors, within 13 weeks after Pten ablation. Cellular proliferation was significantly increased in basal-derived versus luminal-derived Pten-deficient prostate lesions. Increased tumor invasion into the smooth muscle layer and aberrantly regulated aggressive signatures (Smad4 and Spp1) were identified exclusively in basal-derived Pten-deficient lesions. Interestingly, p63-expressing cells, which represent basal stem and progenitor cells of basal-derived Pten-deficient prostate lesions, were significantly increased, relative to cells of the luminal-derived prostate lesion. Furthermore, castration did not suppress cellular proliferation of either basal-derived or luminal-derived Pten-deficient prostate tumors. Taken together, our data suggest that, although prostate malignancy can originate from both basal and luminal populations, these two populations differ in aggressive potential.

Significance of stem cell transcription factor Nanog expression in hepatocellular carcinoma / 中华全科医师杂志

From August 2007 to April 2011,hepatocellular carcinoma (HCC) (n =40),paraHCC tissues (n =10),seminoma (n =10) and cavernous hemangioma (n =10) were selected.And the method of immunohistochemical streptavidin-perosidase was applied to detect the protein expression of Nanog.The expression ratios of Nanog were 17/40 (42％),1/10,0/10 and 5/5 in HCC,para-HCC tissues,seminoma and cavernous hemangioma respectively.Its expression showed no significant correlation with the patient gender,age,serum alpha fetoprotein (AFP),hepatitis B surface antigen (HBsAg),differentiation,Child grade and TNM stage ( P ＞ 0.05 ).It may be used as a surface marker of liver cancer stem cell.

Significance of aminopeptidase N/CD13 expression in hepatocellular carcinoma / 国际外科学杂志

Objective To study aminopeptidase N/CD13 expression in hepatocellular carcinoma and its relationship with clinical data and proguosis in patients with hepatocellular carcinoma.Methods The immunohistochemical SP method was used to detect the CD13 monoclonal antibody in 40 cases of hepatocellular carcinoma,10 cases of corresponding para-carcinoma and 10 cases of cavernous hemangioma.Results Forty cases ( 100％ ) hepatocellular carcinoma tissues were seen varying degrees of CD13 expression,3 (30％) corresponding para-carcinoma tissues were weakly positive,and 10 cases of cavernous hemangioma with no expression.The expression rate of CD13 was not significantly correlated with the patient gender,age,serum AFP value,HbsAg,differentiation,CHILD grade and TNM stage (P＞0.05).But the expression of CD13 was closely related with the patient serum AFP value,HbsAg,differentiation ( P ＜ 0.05 ).By the survival function graph we could find the expression rate was negativly correlated with survival in patients,but the expression was not significantly correlated with tumor relapse.Conclusion CD13 can be used as the surface marker of liver cancer stem cells,and it is expected to become an effective indicator of prognosis in patients with hepatocellular carcinoma.

Aquaculture and food crisis: opportunities and constraints.

Fish farming, now well known as aquaculture, has been well recognized since the ancient era. The first written document on fish culture was published in China in 475 BC, and the first koi pond was constructed at the Japanese Imperial Palace grounds during 71-130 AD. In recent years, aquaculture has progressively played an important role in the provision of: animal protein and gourmet cuisines, job opportunities, and foreign currency for developing countries. Asian countries produce around 91 percent of the world's total aquaculture production. Among the top ten aquaculture-producing countries, nine are from Asia. The current global population consist of more than 6.5 billion individuals; over one billion of which face hunger problem. In the highly populated Asia-Pacific region with moderately high-productivity, 642 million people are still facing hunger. Being a proficient and potential source of animal protein, aquaculture will play an increasing and important role in solving the world food problem in the future. This paper discusses both the opportunities and constraints in the aquaculture industry, specifically in the Asia-Pacific region, and its possible role in solving the current global food crisis. Strategies including promotion and adoption of traceability and HACCP systems for food safety, and marketing management for aquaculture products are also suggested. It is hoped that traditional administration of aquaculture management for survival, profit, as well as food safety will successfully match sustainability management to meet the urgent global need for food.

The rsmA-like gene rsmA(Xcc) of Xanthomonas campestris pv. campestris is involved in the control of various cellular processes, including pathogenesis.

RsmA is an RNA-binding protein functioning as a global post-transcriptional regulator of various cellular processes in bacteria and has been demonstrated to be an important virulence regulator in many animal bacterial pathogens. However, its function in other phytopathogenic bacteria is unclear, except for the Erwinia carotovora RsmA, which acts as a negative virulence regulator. In this work, we investigated the function of the rsmA-like gene, named rsmA(Xcc), of the phytopathogen Xanthomonas campestris pv. campestris. Deletion of rsmA(Xcc) resulted in complete loss of virulence on the host plant Chinese radish, hypersensitive response on the nonhost plant pepper ECW-10R, and motility on the surface of an agar plate. The rsmA(Xcc) mutant displayed a significant reduction in the production of extracellular amylase, endoglucanase, and polysaccharide, but a significant increase in intracellular glycogen accumulation and an enhanced bacterial aggregation and cell adhesion. Microarray hybridization and semiquantitative reverse-transcription polymerase chain reaction analysis showed that deletion of rsmA(Xcc) led to significantly reduced expression of genes encoding the type III secretion system (T3SS), T3SS-effectors, and the bacterial aggregate dispersing enzyme endo-beta-1,4-mannanase. These results suggest that rsmA(Xcc) is involved in the control of various cellular processes, including pathogenesis of X. campestris pv. campestris.