Design and Implementation of Chinese Common Braille Translation System Integrating Braille Word Segmentation and Concatenation Rules.

An important sign of the accessibility of Braille information is the realization of the mutual translation between Chinese and the Braille. Due to the irregularity and uncertainty of the Prevailing Mandarin Braille, coupled with the lack of a large-scale Braille corpus, the quality of Chinese-Braille translation seems to be poor. In July 2018, the National Language Commission released the "Chinese Common Braille Scheme" and advocated replacing the "Prevailing Mandarin Braille." Aimed at improving translation accuracy, this research, which is based on the self-built Chinese Common Braille corpus and combined with the HanLP (Han Language Processing) dictionary and the Chinese-Braille word corpus (a Braille word segmentation and concatenation dictionary for generating a unigram language model), uses the n-gram language model to design and implement a Chinese-Braille intertranslation system that integrates Chinese and Braille Word Segmentation and Concatenation Rules. More importantly, this research proposes an experimental plan for improving the Braille Word Segmentation and Concatenation Rules using a Chinese-Braille word corpus. Experiments show that in the field of educational literature, the accuracy rate of translation from Chinese to Chinese Common Braille has reached 95.01%, and the accuracy of Chinese Common Braille to Chinese translation has reached 90.15%.

Changes of choroidal structure in children with hyperopic amblyopia observed by EDI-OCT technique / 国际眼科杂志(Guoji Yanke Zazhi)

AIM: To compare the differences in choroidal structure between hyperopic amblyopia and normal children of the same age by the enhanced depth imaging optical coherence tomography(EDI-OCT)technique.METHODS: There were 35 cases in 50 eyes of children with hyperopic amblyopia visiting our hospital in January 2021 to December 2021 selected in the amblyopic group, and 30 cases in 51 eyes of healthy children who matched general data in the same period were selected in the control group. EDI-OCT examination was performed to measure the choroidal thickness(CT). After image processing, the total choroidal area(TCA), luminal area(LA), stromal area(SA)and choroidal vascularity index(CVI)were obtained.RESULTS: TCA(except inferior quadrant), SA(except inferior quadrant of the outer ring), LA and CT(except inferior and temporal quadrant )in the amblyopic group of each area were significantly larger than that in the control group(P<0.05), and there was no significant difference in CVI between the two groups except the temporal quadrant of the outer ring(P>0.05). There was no significant difference in CT for all degrees of hyperopic amblyopia, with the exception of the nasal quadrant(P>0.05).CONCLUSION: Hyperopic amblyopia is accompanied with abnormal choroidal structure. As the degree of hyperopia increases, TCA, LA and SA exhibit increasing trends. The changes in choroidal structure are presumed to be related to hyperopic amblyopia.

A novel mutation in the ALOX12B gene in hereditary ichthyosis: pedigree analysis for a female collodion baby / 中华皮肤科杂志

Objective:To investigate pathogenic genes and inheritance patterns in 3 consecutive collodion babies in a family.Methods:The proband was diagnosed as a collodion baby due to extensive dry and chapped skin all over the body at birth. Phenotypes of the proband's parents were normal, but their first and second children presented with dry and chapped skin at birth and died a few days after birth. DNA was extracted from peripheral blood samples of the patient and her parents for whole-exome capture sequencing, and candidate mutations were verified by Sanger sequencing.Results:Compound heterozygous mutations in the ALOX12B gene were identified in the infant, including a missense mutation c.1405 C>T (p.R469w) inherited from her father and a frameshift mutation c.68_69insC (p.L24fs) inherited from her mother.Conclusions:The infant was diagnosed with hereditary ichthyosis, which was inherited in an autosomal recessive manner. The missense mutation c.1405 C>T and frameshift mutation c.68_69insC in the ALOX12B gene may contribute to the clinical phenotype of this infant, and the frameshift mutation had not been reported in China or other countries.

An infant with lamellar ichthyosis induced by CYP4F22 gene mutations / 中华皮肤科杂志

A 1-month-old male infant presented with skin flushing covering with collodion-like membrane all over the body at birth, and experienced gradual skin desquamation thereafter. At the age of 2 months, collodion-like membrane completely peeled off, and the patient presented with obvious scales and dry skin. Skin examination showed generalized dry skin, tense, glossy and transparent plastic wrapper-like membrane remaining on the front chest, large and disk-shaped white scales with an adherent center and free edges inlaid in the skin of the trunk and scalp. Genetic testing showed compound heterozygous mutations in the CYP4F22 gene of the patient, including the mutation c.1137G>A (p.W379X) inherited from his father and the mutation c.467G>A (p.R156H) inherited from his mother. The patient was diagnosed with lamellar ichthyosis.

Current status of secondary prevention medication usage and their relation with on-treatment platelet reactivity / 中国介入心脏病学杂志

Objective To observe the current status of secondary prevention medication usage and their relation with on-treatment platelet reactivity in patients with Acute Coronary Syndrome(ACS) treated with aspirin and clopidogrel. Methods A total of 176 patients hospitalized from 2014 to 2015 due to ACS in the Department of Cardiology, Peking University People's Hospital were enrolled and on-treatment platelet reactivity was tested by thromboelastography(TEG)and CYP2C19*2,*3 and*17 alleles were analysed. Details of secondary prevention medication and patients' clinical characteristics were recorded. The relation of secondary prevention medication and on-treatment platelet reactivity was analyzed by multi-logistic regression after adjusting for CYP2C19 alleles and clinical characteristics covariates.Results A 94.89% of patients was treated with statins while 80.68% with beta blocker. The platelet inhibition rate were (45.33±28.78)% and the high on-treatment platelet reactivity (HTPR) rate tested by TEG was 37.50%. In the multivariate logistic regression analysis, usage of β-blockers during hospitalization as well as phenotypes of CYP2C19*2,*3 and *17,clinical presentation with ST-segment elevation myocardial infarction and the length of stents were associated with HTPR defi ned by TEG. The percentage of HTPR rate was signifi cantly lower in patients treated with than those without β-blockers (72.73% vs. 85.45%,OR 0.18,95%CI 0.06-0.53,P=0.002)after adjusting genetic factors and other covariates.Conclusions There was a signifi cant correlation between beta blockers usage and high clopidogrel on-treatment platelet reactivity.

Efficacy of azithromycin versus doxycycline in the treatment of genital Chlamydia trachomatis infection: a meta-analysis / 中华皮肤科杂志

Objective To systematically evaluate the efficacy of azithromycin and doxycycline in the treatment of genital Chlamydia trachomatis infection.Methods Databases including Cochrane library,PubMed,EMBASE,CBMdisc,CNKI and Wanfang were searched from January 1,1980 to October 2017 for randomized controlled trials (RCTs) comparing the efficacy of azithromycin versus doxycycline in the treatment of genital Chlamydia trachomatis infection.In these RCTs,negative microbiological findings were defined as cure.Patients in the treatment group were treated with azithromycin,and those in the control group were treated with doxycycline.Two researchers independently extracted data and evaluated the quality of these RCTs.Statistical analysis was done by using Stata 12.0 software.Results A total of 24 research reports were enrolled,including 24 RCTs and 2 369 patients.There were 1 302 patients in the azithromycin group and 1 067 in the doxycycline group.Meta-analysis showed that there was a significant difference in the microbiological response rate between the treatment group and the control group.A fixedeffect model was used to combine the response rate,and showed that the response rate to doxycycline was superior to that to azithromycin,with a risk difference of 2.8％ (95％ CI,0.9％-4.6％).Conclusion The microbiological response rate to azithromycin is lower than that to doxycycline in the treatment of genital Chlamydia trachomatis infection,but more RCTs are required to confirm the clinical efficacy of doxycycline.

TET1 inhibits gastric cancer growth and metastasis by PTEN demethylation and re-expression.

Ten-Eleven Translocation 1 (TET1) is a member of ten eleven translocation enzymes, which convert 5-methylcytosine (5-mC) to 5-hydroxymethylcytosine (5-hmC). TET1 can promote CpG islands demethylation in specific genes and often absent in various cancers. Herein, we found that TET1 expression and 5-hmC content were low in gastric tumors compared to its adjacent non-tumor tissues. Cell proliferation, migration and invasion were enhanced upon TET1 knockdown in gastric cancer cells in vitro. This phenomenon was confirmed by an animal xeongraft model. We also found that TET1 directly binds to the promoter region of PTEN and activates its transcription through demethylation of CpG islands. TET1 knockdown activated AKT and FAK pathways, which were suppressed by PTEN. The activation of AKT and FAK facilitated tumor migration, invasion and accelerated cell growth. In conclusion, we found a novel mechanism that TET1 suppresses tumor cell growth, migration and invasion through demethylation of CpG island in PTEN promoter by increasing 5-hmC content. The re-expressed PTEN subsequently down regulates AKT and FAK activity.

Epigenetic silencing of microRNA-149 in cancer-associated fibroblasts mediates prostaglandin E2/interleukin-6 signaling in the tumor microenvironment.

Tumor initiation and growth depend on its microenvironment in which cancer-associated fibroblasts (CAFs) in tumor stroma play an important role. Prostaglandin E2 (PGE2) and interleukin (IL)-6 signal pathways are involved in the crosstalk between tumor and stromal cells. However, how PGE2-mediated signaling modulates this crosstalk remains unclear. Here, we show that microRNA (miR)-149 links PGE2 and IL-6 signaling in mediating the crosstalk between tumor cells and CAFs in gastric cancer (GC). miR-149 inhibited fibroblast activation by targeting IL-6 and miR-149 expression was substantially suppressed in the CAFs of GC. miR-149 negatively regulated CAFs and their effect on GC development both in vitro and in vivo. CAFs enhanced epithelial-to-mesenchymal transition (EMT) and the stem-like properties of GC cells in a miR-149-IL-6-dependent manner. In addition to IL-6, PGE2 receptor 2 (PTGER2/EP2) was revealed as another potential target of miR-149 in fibroblasts. Furthermore, H. pylori infection, a leading cause of human GC, was able to induce cyclooxygenase-2 (COX-2)/PGE2 signaling and to enhance PGE2 production, resulting in the hypermethylation of miR-149 in CAFs and increased IL-6 secretion. Our findings indicate that miR-149 mediates the crosstalk between tumor cells and CAFs in GC and highlight the potential of interfering miRNAs in stromal cells to improve cancer therapy.

Androgen receptor promotes gastric cancer cell migration and invasion via AKT-phosphorylation dependent upregulation of matrix metalloproteinase 9.

Androgen receptor (AR) plays an important role in many kinds of cancers. However, the molecular mechanisms of AR in gastric cancer (GC) are poorly characterized. Here, we investigated the role of AR in GC cell migration, invasion and metastatic potential. Our data showed that AR expression was positively correlated with lymph node metastasis and late TNM stages. These findings were accompanied by activation of AKT and upregulation of matrix metalloproteinase 9 (MMP9). AR overexpression induced increases in GC cell migration, invasion and proliferation in vitro and in vivo. These effects were attenuated by inhibition of AKT, AR and MMP9. AR overexpression upregulated MMP9 protein levels, whereas this effect was counteracted by AR siRNA. Inhibition of AKT by siRNA or an inhibitor (MK-2206 2HC) decreased AR protein expression in both stably transfected and parental SGC-7901 cells. Luciferase reporter and chromatin immunoprecipitation assays demonstrated that AR bound to the AR-binding sites of the MMP9 promoter. In summary, AR overexpression induced by AKT phosphorylation upregulated MMP9 by binding to its promoter region to promote gastric carcinogenesis. The AKT/AR/MMP9 pathway plays an important role in GC metastasis and may be a novel therapeutic target for GC treatment.

RhoGDI2 confers resistance to 5-fluorouracil in human gastric cancer cells.

Resistance to 5-fluorouracil (5-FU) in patients with gastric cancer is a serious therapeutic problem and major efforts are underway to understand the underlying mechanisms. We have previously identified RhoGDI2 as a contributor to 5-FU resistance in colon cancer cells using 2D electrophoresis and mass spectrometry and the current study aimed to further investigate this role. The expression of RhoGDI2 in seven gastric cancer cell lines was positively correlated with resistance to 5-FU. Lower 5-FU sensitivity of isolated tumor cells from patients with gastric cancer was also associated with higher RhoGDI2 expression. Ectopic expression of RhoGDI2 in gastric cancer cells increased the resistance to 5-FU and reverted low dose 5-FU-induced G2/M phase arrest without affecting the population of sub-G1 cells. Overall, these findings suggest that RhoGDI2 is associated with 5-FU resistance and is a potential therapeutic target for enhancing chemotherapy efficacy in gastric cancer.

microrna expression signature of gastric cancer cells relative to normal gastric mucosa.

micrornas (miRNAs) play an important role in a wide range of physiological and developmental processes by negatively regulating the expression of target genes at the post-transcriptional level. In this study, we investigated the differential miRNA expression signature between gastric cancer cells and normal gastric mucosa to determine changes in miRNA expression during gastric cancer development. We analyzed the global miRNA expression profiles of 9 gastric cancer cell lines and 6 normal gastric mucosa lines using miRNA microarrays. In addition, we performed quantitative real-time PCR (Q-PCR) to validate the results. Correlations between the miRNA expression profile and tumor clinicopathological parameters were analyzed. We found that 17 miRNAs were upregulated in gastric cancer cell lines and 146 miRNAs were downregulated compared to normal gastric mucosa. Using microarray data and Q-PCR validation, 15 miRNAs were finally selected. These candidate miRNAs were associated with gastric cancer clinicopathology to various degrees. High expression levels of hsa-miR-93 were found to predict poor survival (median, 16 vs. 40 months; log-rank test p<0.05). These findings suggest that miRNAs play vital roles in human gastric cancer. The findings may also provide clues toward understanding the molecular functions of miRNAs in various biological processes.

[Screening and identification of genes associated with multi-drug resistance in colonic cancer].

OBJECTIVE: To identify novel multi-drug resistance-related genes, and to explore the mechanisms of multi-drug resistance. METHODS: Multi-drug resistant cell line Lovo/5-FU was established by incubation with increasing dose of 5-FU. The sensitivity to 5-FU and cis-diaminodichloroplatinum (CDDP) was measured by MTT assay. Two dimensional electrophoresis plus mass spectrum(2-DE/MS) was used to identify the differentially expressed protein between Lovo and Lovo/5-FU. The identified protein was then verified by Western blot analysis. RESULTS: The IC50 concentrations of Lovo/5-FU to 5-FU and CDDP were increased by 31 and 3 times, compared with Lovo (both P<0.01). 2DE-MS showed that CAP-G and RhoGDI2 were up-regulated, whereas 6-PGL, DCI, Prdx-6 and Maspin were down-regulated in Lovo/5-FU. Western blot analysis confirmed that the expression levels of RhoGDI2 and CAP-G in Lovo/5-FU were increased by 6.14 and 2.98 fold respectively (both P<0.01), whereas Maspin was decreased to 5.2% of Lovo(P<0.01). CONCLUSIONS: Multi-gene and multi-pathway are involved in the development of multi-drug resistance of colorectal cancer cells. CAP-G, RhoGDI2 and Maspin are potential multi-drug resistant genes.

[Interaction of SerpinB5 and MAFbx in gastric cancer cell and its action site].

OBJECTIVE: To explore the interaction between SerpinB5 and MAFbx in gastric cancer cell and to identify the interaction sites. METHODS: The interaction between SerpinB5 and MAFbx was screened and validated by yeast two-hybrid screening and co-immunoprecipitation. The expression of MAFbx was analyzed after SerpinB5 expression being modified by RNA interference and pGBKT7-SerpinB5 transfection. The impact of SerpinB5 on the expression of MAFbx was studied in gastric cancer cell line SUN-16. A model of MAFbx was constructed by homology modeling. The related residues for interaction were analyzed by Autodock4.0. RESULTS: The interaction between SerpinB5 and MAFbx was validated. The expression of MAFbx changed along with SerpinB5 expression. Amino acids including PRO261, ASN361, and LYS362 were key residue in the interaction of SerpinB5 and MAFbx. CONCLUSION: SerpinB5 interacts with MAFbx in gastric cancer cell. Amino acids including PRO261, ASN361, and LYS362 are potential binding sites.

microRNA-21 promotes tumor proliferation and invasion in gastric cancer by targeting PTEN.

Gastric cancer is one of the most common carcinomas in China. microRNAs, a type of non-coding RNA, are important specific regulators and are involved in numerous bioprocesses of an organism. microRNA-21 (miR-21) has been identified as the most suitable choice for further investigation because it is overexpressed in nearly all solid tumors; furthermore, it has been demonstrated that miR-21 is involved in the genesis and progression of human cancer. It has been reported that PTEN, an important tumour suppressor, is regulated by multiple miRNAs. Thus, in this study we focused on the expression and significance of miR-21 in gastric cancer tissues, and the role of miR-21 in the biological behaviour and the expression of PTEN in gastric cancer cells. Real-time PCR was used to detect miR-21 expression in gastric cancer tissues, the adjacent normal tissues, and the gastric cell lines. The gastric cancer cell line BGC-823 was transfected with pre-miR-21/miR-21 inhibitor to overexpress/downregulate miR-21. The influence of miR-21 on the biological behaviour of gastric cancer cells was evaluated using the CCK-8 kit, FCMs, the scratch healing assay and the transwell test. Western blotting and the Luciferase Reporter Assay were used to evaluate the change of PTEN expression after lowered expression of miR-21 in gastric cancer cell lines. Real-time PCR analysis indicated that miR-21 exhibited higher expression in gastric cancer tissues compared to the adjacent non-tumor tissues. miR-21 expression was significantly associated with the degree of differentiation of the tumour tissues (P=0.004), as well as local invasion and lymph node metastasis (P<0.01). After transfection, pre-miR21 BGC-823 cells grew faster than the negative and control groups (P<0.01). The reduction in miR-21 expression demonstrated a remarkable effect on the biological behaviour of gastric cancer cells (P<0.05); the pre-miR-21-transfected cells healed more quickly compared to the control cells in the scratch healing assay, whereas the transwell test indicated that cell migration in vitro was notably inhibited with the downregulation of miR-21 (P<0.05). The western blot results and Luciferase Reporter Assay demonstrated that PTEN expression was remarkably increased after miR-21 inhibition (P<0.05). microRNA-21 expression was upregulated in gastric carcinoma tissues and was significantly associated with the degree of differentiation of tumour tissues, local invasion and lymph node metastasis. Overexpression of miR-21 promoted BGC-823 cell growth, invasion and cell migration in vitro, whereas downregulation of miR-21 exhibited a stronger inhibitory effect on the biological behaviour of gastric cancer cells; additionally, miR-21 inhibition may upregulate the PTEN expression level, which indicates that PTEN may be a target gene for gastric cancer initiation and development.

Interaction of SerpinB5 and MAFbx in gastric cancer cell and its action site / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To explore the interaction between SerpinB5 and MAFbx in gastric cancer cell and to identify the interaction sites.</p><p><b>METHODS</b>The interaction between SerpinB5 and MAFbx was screened and validated by yeast two-hybrid screening and co-immunoprecipitation. The expression of MAFbx was analyzed after SerpinB5 expression being modified by RNA interference and pGBKT7-SerpinB5 transfection. The impact of SerpinB5 on the expression of MAFbx was studied in gastric cancer cell line SUN-16. A model of MAFbx was constructed by homology modeling. The related residues for interaction were analyzed by Autodock4.0.</p><p><b>RESULTS</b>The interaction between SerpinB5 and MAFbx was validated. The expression of MAFbx changed along with SerpinB5 expression. Amino acids including PRO261, ASN361, and LYS362 were key residue in the interaction of SerpinB5 and MAFbx.</p><p><b>CONCLUSION</b>SerpinB5 interacts with MAFbx in gastric cancer cell. Amino acids including PRO261, ASN361, and LYS362 are potential binding sites.</p>

Screening and identification of genes associated with multi-drug resistance in colonic cancer / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To identify novel multi-drug resistance-related genes, and to explore the mechanisms of multi-drug resistance.</p><p><b>METHODS</b>Multi-drug resistant cell line Lovo/5-FU was established by incubation with increasing dose of 5-FU. The sensitivity to 5-FU and cis-diaminodichloroplatinum (CDDP) was measured by MTT assay. Two dimensional electrophoresis plus mass spectrum(2-DE/MS) was used to identify the differentially expressed protein between Lovo and Lovo/5-FU. The identified protein was then verified by Western blot analysis.</p><p><b>RESULTS</b>The IC50 concentrations of Lovo/5-FU to 5-FU and CDDP were increased by 31 and 3 times, compared with Lovo (both P<0.01). 2DE-MS showed that CAP-G and RhoGDI2 were up-regulated, whereas 6-PGL, DCI, Prdx-6 and Maspin were down-regulated in Lovo/5-FU. Western blot analysis confirmed that the expression levels of RhoGDI2 and CAP-G in Lovo/5-FU were increased by 6.14 and 2.98 fold respectively (both P<0.01), whereas Maspin was decreased to 5.2% of Lovo(P<0.01).</p><p><b>CONCLUSIONS</b>Multi-gene and multi-pathway are involved in the development of multi-drug resistance of colorectal cancer cells. CAP-G, RhoGDI2 and Maspin are potential multi-drug resistant genes.</p>

SerpinB5 interacts with KHDRBS3 and FBXO32 in gastric cancer cells.

Mammary serine protease inhibitor B5 (SerpinB5) is a potential oncogene in gastric cancer (GC); however, the molecular mechanism by which SerpinB5 promotes oncogenesis remains elusive. In this study, SerpinB5-associated proteins were selected based on yeast two-hybrid screening and microarray analysis after RNA interference and were validated using co-immunoprecipitation (Co-IP) and RNA Co-IP. The expression profiles of the interacting proteins were analyzed by Western blotting and immunohistochemistry. The effects of SerpinB5 on KHDRBS3 and FBXO32 expression in GC cells were analyzed using real-time PCR and Western blotting after the expression of SerpinB5 was modified. By yeast two-hybrid screening and microarray analysis, FBXO32 and KHDRBS3 were found to be SerpinB5-interacting proteins. The interactions were confirmed by Co-IP. An RNA co-immunoprecipitation assay found that KHDRBS3 interacted with FBXO32 mRNA. The expression of SerpinB5 was much stronger in the nucleus of GC cells. FBXO32 was expressed at higher levels in the cytoplasm of GC cells. KHDRBS3 was primarily detected in the nucleus of normal mucosal cells. SerpinB5 expression was modified in GC cells, KHDRBS3 mRNA levels remained stable, however, FBXO32 mRNA levels changed 24 h after changes in KHDRBS3 protein levels were detected. In conclusion, SerpinB5 interacts with KHDRBS3 and FBXO32, and KHDRBS3 can interact with FBXO32 mRNA.

Cell cycle dependent genes from the gastric cancer cell MKN45 can affect tumorigenesis.

BACKGROUND/AIMS: To investigate the cell cycle dependent genes involved in gastric tumorigenesis, possibly determining the relationship between the cell cycle and tumorigenesis. METHODOLOGY: MKN45 cells were collected every hour from Oh to 12h after release from G2/M and G1/S blocks. Nine samples (a-i), chosen at key times of the cell cycle, were prepared for RNA isolation and cDNA microarray analysis. RESULTS: In 2001 viable clones, 959 genes showed periodic variations during the cell cycle. Among 2001 genes that were clustered, a series of up-regulated genes were assigned to different cell cycle phases. Many periodically dependent genes in the cell cycle were ubiquitously expressed and participated in various cell physiological functions, such as transcription, translation, ubiquitination and signal transduction. These cell cycle dependent genes could affect cancer cell proliferation, apoptosis, activation of oncogenes and inactivation of tumor suppressor genes. CONCLUSIONS: We provided a comprehensive understanding of the gene expression profile involved in gastric cancer cell cycles and laid a foundation for further research on mechanisms of gastric tumorigenesis.

Serum DJ-1 as a diagnostic marker and prognostic factor for pancreatic cancer.

OBJECTIVE: DJ-1 is an oncoprotein secreted by cancer cells. Therefore, it might be a diagnostic or prognostic biomarker for pancreatic cancer (PC). METHODS: The study involved 47 patients with PC, 43 with chronic pancreatitis, and 40 healthy subjects. We assayed the serum level of DJ-1 and the conventional tumor marker carbohydrate antigen 19-9 (CA 19-9) to define the diagnostic and prognostic value of DJ-1 for PC. RESULTS: Serum DJ-1 level was elevated in patients with PC compared with those with chronic pancreatitis and healthy individuals. The area under the curve (AUC) of serum DJ-1 was higher than CA 19-9 (DJ-1 vs. CA19-9, 0.8735 ± 0.0356 vs. 0.6647 ± 0.0572 ng/mL), and an 87.5% sensitivity was reached with a combination of serum DJ-1 and CA19-9. No association of serum DJ-1 level with tumor node metastasis (TNM) classification or tumor resectability was found. However, after resection, the median serum DJ-1 level was decreased from 2.00 to 0.78 ng/mL. In addition, higher serum DJ-1 was correlated with shorter overall survival as analyzed by both Kaplan-Meier test (P = 0.018) and COX regression analysis (P = 0.013). The median overall survival time of PC patients with serum DJ-1 level greater than or equal to 2.06 ng/mL was 7.00 ± 1.11 months, whereas that of patients with lower DJ-1 levels was 13.0 ± 2.5 months. CONCLUSIONS: These findings indicate the potential clinical significance for serum DJ-1 level to be used for the diagnosis and prognosis prediction of patients with PC.

Silencing invariant chains of dendritic cells enhances anti-tumor immunity using small-interfering RNA.

BACKGROUND: Genetic modification of dendritic cells (DCs) has been used as an effective approach to enhance anti-tumor immunity. RNA interference (RNAi), which can cause the degradation of any RNA in a sequence-specific manner, is a post-transcriptional gene silencing mechanism. In this study, small-interfering RNA (siRNA) specific for the Ii gene was transfected into DCs, and the anti-tumor immunity of Ii-silenced DCs was assessed. METHODS: The silencing effect of siRNA was evaluated by Western blotting and real-time PCR analyses. In vitro cytotoxic activity of T cells was evaluated using a Cytotox 96(®) non-radioactive cytotoxicity assay kit. The time to tumor onset and the tumor volumes were used as reliable indices to assess the anti-tumor immunity in vivo. To further examine the mechanisms underlying the anti-tumor immunity, flow cytometry analysis was used. RESULTS: The Ii expression of DCs was significantly reduced after Ii siRNA transfection. Significant in vitro anti-tumor ability was exhibited when DCs were co-transfected with Ii siRNA plus endogenous tumor antigen (P < 0.05). Furthermore, tumor growth was greatly inhibited when mice were immunized with DCs transfected with Ii siRNA plus tumor antigen prior to or subsequent to tumor implantation. Flow cytometry analysis in vitro and in vivo indicated that both CD4(+) and CD8(+) T cells were significantly activated in the Ii siRNA group (P < 0.05). CONCLUSION: Silencing of the Ii gene of DCs may offer a potential approach to enhance DC-based anti-tumor immunity.