RIP-1/c-FLIPL Induce Hepatic Cancer Cell Apoptosis Through Regulating Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL).

BACKGROUND Almost all hepatic cancer cells have resistance to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. c-FLIPL and RIP-1 are apoptotic negative regulatory factors. This study investigated the role of c-FLIPL and RIP-1 in hepatic cancer cell resistance to TRAIL-induced apoptosis. MATERIAL AND METHODS HepG2 cells were treated by TRAIL, RIP-1 siRNA, and/or BY11-7082. Cell viability was detected by MTT assay. Cell apoptosis was tested by flow cytometry. DISC component proteins, RIP-1, and p-p65 were measured by Western blot. Caspase-8 and caspase-3 were determined by spectrophotometry. RESULTS Single TRAIL treatment showed no significant impact on cell proliferation and apoptosis. HepG2 cells expressed high levels of RIP1 and c-FLIPL, while a high concentration of TRAIL upregulated RIP-1 and c-FLIPL expression but not DR4 and DR5. Single TRAIL treatment did not obviously activate caspase-8 and caspase-3. RIP-1 or c-FLIPL siRNA markedly induced cell apoptosis and enhanced caspase-8 and caspase-3 activities. Combined transfection obviously increased apoptotic cells. TRAIL markedly upregulated RIP-1 expression and enhanced p-p65 protein. Downregulating RIP-1 and/or BAY11-7082 significantly reduced NF-kB transcriptional activity, blocked cells in G0/G1 phase, weakened proliferation, elevated caspase-8 and caspase-3 activities, and promoted cell apoptosis. CONCLUSIONS TRAIL can enhance RIP1 and c-FLIPL expression in HepG2 cells. High expression of RIP1 and c-FLIPL is an important reason for TRAIL resistance. Downregulation of RIP1 and c-FLIPL can relieve caspase-8 suppression, activate caspase-3, and promote cell apoptosis. TRAIL mediates apoptosis resistance through upregulating RIP-1 expression, enhancing NF-kB transcriptional activity, and weakening caspase activity.

Carvedilol promotes mitochondrial biogenesis by regulating the PGC-1/TFAM pathway in human umbilical vein endothelial cells (HUVECs).

Carvedilol, a third-generation and nonselective ß-adrenoceptor antagonist, is a licensed drug for treating patients suffering from heart failure in clinics. It has been shown that Carvedilol protects cells against mitochondrial dysfunction. However, it's unknown whether Carvedilol affects mitochondrial biogenesis. In this study, we found that treatment with Carvedilol in HUVECs resulted in a significant increase of PGC-1α, NRF1, and TFAM. Notably, Carvedilol significantly increased mtDNA contents and the two mitochondrial proteins, cytochrome C and COX IV. In addition, MitoTracker Red staining results indicated that treatment with Carvedilol increased mitochondria mass. Mechanistically, we found that the effect of Carvedilol on the expression of PGC-1α is mediated by the PKA-CREB pathway. Importantly, our results revealed that stimulation of mitochondrial biogenesis by carvedilol resulted in functional gain of the mitochondria by showing increased oxygen consumption and mitochondrial respiratory rate. The increased expression of PGC-1α and mitochondrial biogenesis induced by Carvedilol might suggest a new mechanism of the therapeutic effects of Carvedilol in heart failure.

Interleukin 6 induces expression of NADPH oxidase 2 in human aortic endothelial cells via long noncoding RNA MALAT1.

Human abdominal aortic aneurysm (AAA) is characterized by the induction of intracellular and extracellular inflammatory cytokines and the production of reactive oxygen species (ROS) associated with localized inflammatory responses in the vascular wall. Recent studies have shown that greater circulating levels of the proinflammatory cytokine interleukin-6 (IL-6) are closely associated with AAA presence, suggesting that IL-6 plays an important role in the development of AAA. Previous in vivo studies have indicated that excess activities of NADPH oxidase (NOX), a major oxidase system for ROS production, promote AAA development. Furthermore, long noncoding RNAs (lncRNAs) are involved in the development of AAA. LncRNA MALAT1 has been found closely involved in endothelial cell functions and dysfunctions. In the present study, we explored the effects and the underlying mechanisms of IL-6 and MALAT1 on the expression/activity of NOXs in human aortic endothelial cells (HAOECs). Primary HAOECs with or without overexpression or knockdown of MALTA1 were cultured in the presence of IL-6. We found that IL-6 concentration- and time-dependently elevated the NOX activity as well as the MALAT1 level in HAOECs. Among different NOXs, only NOX2 was induced by IL-6. Overexpression and knockdown of MALAT1 respectively augmented and abolished IL6-induced expression of NOX2, NOX activity/cellular ROS production, and activation of the human NOX2 gene promoter, whereas MALAT1 alone in the absence of IL-6 treatment showed no significant effect. Knockdown of extracellular signal-regulated kinase (ERK) abolished IL6-induced expression of MALAT1. In conclusion, this study provides the first evidence that IL-6 induces expression/activity of NOX2 in HAOECs via inducing MALAT1 by an ERK-dependent mechanism. It adds new insights into the molecular mechanisms underlying AAA development.

The Correlation Relationship between P14ARF Gene DNA Methylation and Primary Liver Cancer.

BACKGROUND: Primary liver cancer is a common malignant tumor that causes serious damage to human health. DNA methylation is common in epigenetics. DNA methylation plays an important role in the process of primary liver cancer occurrence and development. The P14ARF gene is an important tumor suppressor gene. It was found that P14ARF methylation is associated with the degree of malignancy in multiple tumors. Therefore, this study aimed to investigate the relationship between P14ARF methylation level and primary liver cancer malignant degree. MATERIAL AND METHODS: Carcinoma tissues and adjacent tissues were collected from 87 primary liver cancer patients. Pyrosequencing was applied to obtain P14ARF methylation. Real-time PCR was used to detect P14ARF mRNA level. RESULTS: P14ARF methylation level in cancerous tissue was significantly higher than in the adjacent tissue (t=76.54, P<0.001). P14ARF methylation showed no significant difference in patients with different age, sex, smoking status, or drinking status. It did not present an obvious difference in tumors with different size. Its methylation level increased following the improvement of TNM stage (P<0.05). Compared with the adjacent tissue, P14ARF mRNA in carcinoma tissue decreased by 31% (t=28.91, P<0.001). P14ARF methylation showed a significant negative correlation with mRNA expression in cancerous tissue (r=-0.43, P<0.01). CONCLUSIONS: P14ARF mRNA level is regulated by DNA methylation in primary liver cancer. P14ARF gene DNA methylation may be associated with the occurrence of primary liver cancer occurrence and TNM staging.

[A new system for noninvasive esophageal varices pressure measurement based on airflow and laser technology].

OBJECTIVE: Combined the optical principle with automatic control technology and computer real-time image detection technology to develop a non-contact system for noninvasive esophageal varices pressure measurement. METHODS: The system included the adjustable air pump, laser device, image collection and analysis program. The feasibility and accuracy of the system were verified by in vitro experiments. RESULTS: The bionic vascular pressure measured by this system had good correlation and repeatability with the actual pressure. CONCLUSIONS: This system is accurate, feasible and has good application prospects.

EIF3B stabilizes PCNA by counteracting SYVN1-mediated ubiquitination to serve as a promotor in cholangiocarcinoma.

Cholangiocarcinoma, a prevalent hepatic malignancy, exhibits a progressively rising incidence. While Eukaryotic translation initiation factor 3 subunit B (EIF3B) has been implicated in the occurrence and development of various cancers, its specific roles in cholangiocarcinoma remain unexplored. Immunohistochemical (IHC) analysis was employed to detect EIF3B/PCNA expression in cholangiocarcinoma. Cells were manipulated using short hairpin RNA (shRNA)-mediated lentiviruses or overexpression plasmids. Statistical significance was assessed using the Student's t-test and one-way ANOVA, with P < 0.05 considered statistically significant. EIF3B exhibited robust expression in cholangiocarcinoma, demonstrating a significant correlation with the pathological grade of cholangiocarcinoma patients. Furthermore, modulation of EIF3B expression, either depletion or elevation, demonstrated the ability to inhibit or enhance cholangiocarcinoma cell survival and migration in vitro. Mechanistically, we identified Proliferating Cell Nuclear Antigen (PCNA) as a downstream gene of EIF3B, driving cholangiocarcinoma. EIF3B stabilized PCNA by inhibiting PCNA ubiquitination, a process mediated by E3 ligase SYVN1. Similar to EIF3B, PCNA levels were also abundant in cholangiocarcinoma, and knocking down PCNA impeded cholangiocarcinoma development. Intriguingly, silencing PCNA attenuated the promotion induced by EIF3B overexpression. Furthermore, the elevated P21 protein level in shEIF3B RBE cells was partially attenuated after UC2288 (P21 signaling pathway inhibitor) treatment. Our findings underscored the potential of EIF3B as a therapeutic target for cholangiocarcinoma. Unraveling its functions holds promise for the development of more specific and effective targeted therapy strategies.

[Retracted] Downregulation of ROS­FIG inhibits cell proliferation, colony­formation, cell cycle progression, migration and invasion, while inducing apoptosis in intrahepatic cholangiocarcinoma cells.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that the western blotting data shown in Fig. 9 were strikingly similar to data appearing in different form in other articles written by different authors at different research institutes that had either already been published elsewhere prior to the submission of this paper to International Journal of Molecular Medicine, or were under consideration for publication at around the same time. In view of the fact that certain of these data had already apparently been published previously, the Editor of International Journal of Molecular Medicine has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 34: 661­668, 2014; 10.3892/ijmm.2014.1823].

A Fluorescent Biosensor for Streptavidin Detection Based on Double-Hairpin DNA-Templated Copper Nanoparticles.

In this paper, we developed a sensitive, label-free and facile fluorescent strategy for detecting streptavidin (SA) based on double-hairpin DNA-templated copper nanoparticles (CuNPs) and terminal protection of small molecule-linked DNA. Herein, a special DNA hairpin probe was designed and synthesized, which contained two poly T single-stranded loops and a nick point in the middle of the stem. Inspired by the concept of the terminal protection interaction, the specific binding of SA to the biotinylated DNA probe can prevent the exonuclease degradation and keep the integrity of DNA probe, which can be used for synthesizing fluorescent CuNPs as a template. Conversely, the DNA probe would be digested by exonucleases and therefore, would fail to form CuNPs without SA. After systematic optimization, the detection range of SA concentration is from 0.5 to 150 nM with a low detection limit of 0.09 nM. Additionally, the proposed method was also successfully applied in the biological samples. Finally, the proposed method is sensitive, effective and simple, and can be potentially applied for predicting diseases and discovering new drugs.

[Comparison of endoscopic band ligation and propranolol for the primary prophylaxis of variceal bleeding in cirrhosis].

OBJECTIVE: To compare endoscopic variceal ligation (EVL) with propranolol for prophylaxis of first variceal bleeding. METHODS: We chose 168 patients with cirrhosis and esophageal varices in our hospital and allocated them to EVL and propranolol groups. Treatment effectiveness and safety in the 2 groups were observed. RESULTS: he parameters of two groups were similar before therapy. Follow-up period was 8-36 months. Variceal bleeding occurred in 24 (28.6%) of the EVL group and in 20 (23.9%) of the propranolol group (P>0.05). Overall mortality and death related to bleeding were similar (21.4% vs 17.9%; 7.1% vs 6.0%, P>0.05). Adverse events related to EVL were 43 (3 of them life-threatening) compared to 16 in the propranolol group (51.19% vs 19.05%, P<0.05). CONCLUSION: Propranolol may be the better choice in prophylaxis of variceal bleeding with similar effects and lower adverse events than with EVL.

GSG2 knockdown suppresses cholangiocarcinoma progression by regulating cell proliferation, apoptosis and migration.

Cholangiocarcinoma (CCA) is the second most common type of hepatocellular carcinoma characterized by high aggressiveness and extremely poor patient prognosis. The germ cell­specific gene 2 protein (GSG2) is a histone H3 threonine­3 kinase required for normal mitosis. Nevertheless, the role and mechanism of GSG2 in the progression and development of CCA remain elusive. In the present study, the association between GSG2 and CCA was elucidated. Firstly, we demonstrated that GSG2 was overexpressed in CCA specimens and HCCC­9810 and QBC939 cells by immunohistochemical (IHC) staining. It was further revealed that high expression of GSG2 in CCA had significant clinical significance in predicting disease deterioration. Subsequently, cell proliferation, apoptosis, cell cycle distribution and migration were measured by MTT, flow cytometry, and wound healing assays, respectively in vitro. The results demonstrated that downregulation of GSG2 decreased proliferation, promoted apoptosis, arrested the cell cycle and weakened migration in the G2 phase of CCA cells. Additionally, GSG2 knockdown inhibited CCA cell migration by suppressing epithelial­mesenchymal transition (EMT)­related proteins, such as N­cadherin and vimentin. Mechanistically, GSG2 exerted effects on CCA cells by modulating the PI3K/Akt, CCND1/CDK6 and MAPK9 signaling pathways. In vivo experiments further demonstrated that GSG2 knockdown suppressed tumor growth. In summary, GSG2 was involved in the progression of CCA, suggesting that GSG2 may be a potential therapeutic target for CCA patients.

[Treating superficial hemangioma in children according to local blood flow].

OBJECTIVE: To treat superficial hemangioma in children according to the local blood flow. METHODS: A total of 98 children with superficial hemangiomas admitted to our hospital from January 2005 to June 2009, and their clinical data were analyzed. RESULTS: According to the local blood flow velocity, 98 children were treated with injections or injection plus surgical treatment, respectively. Ninety-four children (95.9%) were cured. CONCLUSION: Injection therapy is effective for children with superficial hemangioma, but we should arrange individualized treatment according to the local blood flow in children.

[Treatment for chronic venous ulceration of the leg by subfascial endoscopic perforator vein surgery].

OBJECTIVE: To observe the effect of subfascial endoscopic perforator vein surgery (SEPS) in the treatment of chronic venous ulceration of the legs. METHODS: Chronic venous ulceration for 91 patients with 102 limbs was treated by SEPS from January 2005 to July 2008. The effect of SEPS on chronic venous ulceration of the leg, the symptoms during and after the operation, and the durations of hospital treatment were analyzed. RESULTS: The symptoms of the 102 legs conducted by SEPS operation, except the pigmentation, were obviously improved (P<0.01). Its cicatrisation rate, the recrudesce rate, and the cut infection rate were 93.1%, 1.96%, and 1.0%, respectively. The time of the operation was short and the hemorrhage was small during the surgery. The durations of hospitalization and the cicatrisation time of ulceration were (6.5+/-3.4) d and (12.2+/-13.7) d, respectively. CONCLUSION: SEPS is simple and effective in treating chronic venous ulceration of the leg, and particularly effective for patients classified into C5 and C6 in clinical-etiological-anatomical-pathophysiology (CEAP).

Depletion of the lncRNA RP11-567G11.1 inhibits pancreatic cancer progression.

BACKGROUND: Pancreatic cancer is one of the most lethal malignancies, as demonstrated by its 5-year survival rate of less than 10%. The poor response of pancreatic cancer to conventional therapeutics, especially against cancer stem cells (CSCs), is the primary obstacle to improving patient survival. Emerging evidence indicates that the long non-coding RNA (lncRNA) RP11-567G11.1 is up-regulated in pancreatic cancer tissues and that its expression is associated with poor prognosis. This study aimed to elucidate the mechanism by which RP11-567G11.1 influences survival in pancreatic cancer. METHODS: We evaluated the expression of RP11-567G11.1 in pancreatic cancer tissues via in situ hybridization. We also constructed RP11-567G11.1 knockdown cell models and used CCK8 and flow cytometry to detect the function of this lncRNA. Western blotting and qPCR were used to detect the expression levels of factors related to RP11-567G11.1. RESULTS: The results illustrated that RP11-567G11.1 was significantly up-regulated in poorly differentiated pancreatic cancer tissues as compared to its expression in non-tumor tissues. Additionally, depletion of RP11-567G11.1 in pancreatic cancer cells inhibited proliferation and cell cycle progression, induced apoptosis, suppressed the stem cell-like phenotype, and increased sensitivity to gemcitabine. Also depletion of RP11-567G11.1 in pancreatic cancer cells inhibited factors downstream of the NOTCH signaling pathway. CONCLUSION: RP11-567G11.1 plays a crucial role in pancreatic cancer. Importantly, depletion of RP11-567G11.1 boosts the sensitivity of pancreatic cancer cells to gemcitabine, suggesting that this lncRNA is a promising target for pancreatic cancer treatment.

[Comparison of treatment response in primary hepatocellular carcinomas with contrast-enhanced ultrasonography and contrast-enhanced helical CT].

OBJECTIVE: To investigate the value of contrast-enhanced ultra sonography for non-surgical treatment response in hepatocellular carcinomas. METHODS: Non-surgical therapies were performed on 56 patients (64 liver neoplasms) who were diagnosed by ultrasonography-guided biopsy before the therapy. Contrast-enhanced ultrasonography(CEUS) and contrast-enhanced helical CT were performed to assess the treatment response. RESULTS: Forty-six of the 64 lesions were not enhanced with CEUS.Partial enhancement was demonstrated in the other 18 lesions. Forty-eight of the 64 lesions were not enhanced with contrast-enhanced helical CT. Partial enhancement were demonstrated in the other 16 lesions.The sensitivity, specificity, and accuracy were 94.4%, 97.8%, and 96.9% for CEUS and 83.3%, 97.8%, and 93.8% for contrast-enhanced helical CT (P>0.05). CONCLUSION: CEUS is a good method in assessing the non-surgical treatment response in hepatocellular carcinomas and is more sensitive and useful than contrast-enhanced helical CT in assessing the treatment response of transcatheter hepatic arterial chemoembolization.

MicroRNA-212 targets FOXA1 and suppresses the proliferation and invasion of intrahepatic cholangiocarcinoma cells.

[This retracts the article DOI: 10.3892/etm.2016.3824.].

Serum angiotensin-converting enzyme 2 is an independent risk factor for in-hospital mortality following open surgical repair of ruptured abdominal aortic aneurysm.

Open surgical repair (OSR) is a conventional surgical method used in the repair a ruptured abdominal aortic aneurysm (AAA); however, OSR results in high perioperative mortality rates. The level of serum angiotensin-converting enzyme 2 (ACE2) has been reported to be an independent risk factor for postoperative in-hospital mortality following major cardiopulmonary surgery. In the present study, the association of serum ACE2 levels with postoperative in-hospital mortality was investigated in patients undergoing OSR for ruptured AAA. The study enrolled 84 consecutive patients underwent OSR for ruptured AAA and were subsequently treated in the intensive care unit. Patients who succumbed postoperatively during hospitalization were defined as non-survivors. Serum ACE2 levels were measured in all patients prior to and following the surgery using ELISA kits. The results indicated that non-survivors showed significantly lower mean preoperative and postoperative serum ACE2 levels when compared with those in survivors. Multivariate logistic regression analysis also showed that, subsequent to adjusting for potential confounders, the serum ACE2 level on preoperative day 1 showed a significant negative association with the postoperative in-hospital mortality. This was confirmed by multivariate hazard ratio analysis, which showed that, subsequent to adjusting for the various potential confounders, the risk of postoperative in-hospital mortality remained significantly higher in the two lowest serum ACE2 level quartiles compared with that in the highest quartile on preoperative day 1. In conclusion, the present study provided the first evidence supporting that the serum ACE2 level is an independent risk factor for the in-hospital mortality following OSR for ruptured AAA. Furthermore, low serum ACE2 levels on preoperative day 1 were found to be associated with increased postoperative in-hospital mortality. Therefore, the serum ACE2 level on preoperative day 1 may be a potential biomarker or prognostic factor for in-hospital mortality following OSR for ruptured AAA.

MicroRNA-212 targets FOXA1 and suppresses the proliferation and invasion of intrahepatic cholangiocarcinoma cells.

MicroRNAs (miRNAs), which are a class of small RNAs, have been shown to negatively regulate the expression of their target genes by directly binding to the 3'-untranslated region (3'-UTR) of mRNA. miRNA dysregulation has been associated with the pathogenesis of numerous types of human cancer. However, the role of miRNAs in intrahepatic cholangiocarcinoma (ICC) has yet to be fully elucidated. The present study aimed to investigate the role of miR-212 in the growth and metastasis of ICC in vitro, as well as the underlying mechanism. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting were used to examine mRNA and protein expression. An MTT assay and transwell assay were conducted to determine cell proliferation and invasion rates. The results of the RT-qPCR demonstrated that miR-212 was downregulated in the majority of investigated ICC tissues, as compared with their matched adjacent non-tumor tissues. In addition, miR-212 expression was shown to be markedly downregulated in three ICC cell lines, as compared with human intrahepatic biliary epithelial cells. Furthermore, restoration of miR-212 expression significantly suppressed the proliferation and invasion of ICC QBC939 cells. Forkhead box protein A1 (FOXA1) was predicted to be a putative target of miR-212 by bioinformatics analysis with TargetScan. Therefore, a luciferase reporter assay was conducted to confirm that miR-212 was able to directly bind to the 3'-UTR of FOXA1 mRNA. In addition, using western blot analysis, the protein expression of FOXA1 was shown to be negatively regulated by miR-212 in ICC QBC939 cells. In conclusion, it was demonstrated that FOXA1 was frequently upregulated in various ICC tissues and cell lines. The results of the present study suggested that miR-212 inhibits the proliferation and invasion of ICC cells by directly targeting FOXA1, and thus may be considered a potential candidate for the treatment of ICC.

Knockdown of Sall4 inhibits intrahepatic cholangiocarcinoma cell migration and invasion in ICC-9810 cells.

In spite of improvements in surgical technology, the resectability and curability of intrahepatic cholangiocarcinoma (ICC) are still low. Our previous study showed that the strong Sal-like protein 4 (Sall4)-positive cases had shorter overall survival compared to Sall4-negative cases, indicating an oncogenic role of Sall4 in ICC. In this study, we aimed to explore the precise mechanism of Sall4 on ICC cell invasion and metastasis. We evaluated the expression of Sall4, PTEN, and Bmi-1 in 28 cases of adjacent tissues and 175 cases of ICC tissues by using immunohistochemical staining. We found that the expression of Sall4 and Bmi-1 was significantly increased in ICC tissues compared with the adjacent tissues, while PTEN expression was reduced in ICC tissues compared with the adjacent tissues, and there was a reverse relationship between Sall4 and PTEN in ICC, whereas there was a positive correlation in Sall4 and Bmi-1 expression in ICC. In addition, overall survival analysis showed that ICC patients with low PTEN exhibited a worse prognosis than ICC patients with high PTEN, and lower Bmi-1 expression showed a better prognosis than ICC patients with high Bmi-1. By a battery of experiments in vitro, we demonstrated that Sall4 promotes ICC cell proliferation, and progression of ICC might be through PTEN/PI3K/Akt and Bmi-1/Wnt/ß-catenin signaling and enhancing epithelial-mesenchymal transition process. Thus, Sall4 may be a potential target for the treatment of ICC metastasis.

MicroRNA-101 inhibits the migration and invasion of intrahepatic cholangiocarcinoma cells via direct suppression of vascular endothelial growth factor-C.

MicroRNAs (miRs) have important roles in the pathogenesis of human malignancy. It has previously been suggested that deregulation of miR­101 is associated with the progression of intrahepatic cholangiocarcinoma (ICC); however, the exact role of miR­101 in the regulation of ICC metastasis remains largely unknown. The present study demonstrated that the expression levels of miR­101 were significantly decreased in ICC tissue, as compared with matched adjacent normal tissue. Furthermore, miR­101 was downregulated in the ICC­9810 human ICC cell line, as compared with in the normal human intrahepatic biliary epithelial cell (HIBEC) line. Vascular endothelial growth factor (VEGF)­C was identified as a target gene of miR­101 in ICC­9810 cells. The expression of VEGF­C was negatively regulated by miR­101 at the post­transcriptional level in ICC­9810 cells. Further investigation demonstrated that overexpression of miR­101 markedly suppressed the migration and invasion of ICC­9810 cells, and these effects were similar to those observed following VEGF­C knockdown. Conversely, restoration of VEGF­C reversed the inhibitory effects of miR­101 overexpression on ICC­9810 cell migration and invasion, thus suggesting that miR­101 may suppress ICC­9810 cell migration and invasion, at least partly via inhibition of VEGF­C. It was also demonstrated that the mRNA and protein expression levels of VEGF­C were frequently upregulated in ICC tissue and cells, and its expression level was inversely correlated with that of miR­101 in ICC tissue. In conclusion, the present study identified important roles for miR­101 and VEGF­C in ICC, suggesting that miR­101/VEGF­C signaling may be a promising diagnostic and/or therapeutic target for ICC.

A study on new method of noninvasive esophageal venous pressure measurement based on the airflow and laser detection technology.

Using optics combined with automatic control and computer real-time image detection technology, a novel noninvasive method of noncontact pressure manometry was developed based on the airflow and laser detection technology in this study. The new esophageal venous pressure measurement system was tested in-vitro experiments. A stable and adjustable pulse stream was produced from a self-developed pump and a laser emitting apparatus could generate optical signals which can be captured by image acquisition and analysis system program. A synchronization system simultaneous measured the changes of air pressure and the deformation of the vein wall to capture the vascular deformation while simultaneously record the current pressure value. The results of this study indicated that the pressure values tested by the new method have good correlation with the actual pressure value in animal experiments. The new method of noninvasive pressure measurement based on the airflow and laser detection technology is accurate, feasible, repeatable and has a good application prospects.