Flow regimes identification of air water counter current flow in vertical annulus using differential pressure signals and machine learning.

This study investigates the gas-liquid two-phase counter-current flow through a vertical annulus, a phenomenon prevalent across numerous industrial fields. The presence of an inner pipe and varying degrees of eccentricity between the inner and outer pipes often blur the clear demarcation of flow regime boundaries. To address this, we designed a vertical annulus with adjustable eccentricity (outer and inner diameters of 125 mm and 75 mm, respectively). We conducted gas-liquid counter-current flow experiments under specific conditions: gas superficial velocity ranging from 0.06 to 5.04 m/s, liquid superficial velocity from 0.01 to 0.25 m/s, and five levels of eccentricity (e = 0, 0.25, 0.5, 0.75, 1). We collected differential pressure data at two distinct height distances (DP1: 50 mm and DP2: 1000 mm). We used vectors, composed of both the probability density functions (PDFs) of the differential pressure signals and the power spectral density (PSD) reduced via Principal Component Analysis, as features. Using the CFDP clustering algorithm-based on local density-we clustered the flow regimes of the experimental data, thereby achieving an objective and consistent identification of the flow regime of gas-liquid two-phase counter-current flow in a vertical annulus. Our analysis reveals that for DP1, the main differences in the PSD of various flow regimes occur within the 0.5-1 Hz range. Among the three flow regimes involved, the slug flow exhibits the highest power intensity, followed by the bubbly flow, with the churn flow having the least. In terms of differential pressure distribution, the bubbly and churn flows have a concentrated distribution, while the slug flow is more dispersed. For DP2, the PSD differences primarily exist within the 0.5-2 Hz range. The churn flow has the highest power intensity, followed by the slug flow, with the bubbly flow being the weakest. Here, the bubbly flow's differential pressure distribution is concentrated, while the slug and churn flows are more dispersed. Based on the results of the flow regime classification, we generated a flow regime map and analyzed the influence of annulus eccentricity on the flow regime. We found that in most cases, pipe eccentricity does not significantly affect the flow regime. However, in the transition region-such as the bubbly to slug flow transition zone-flows with medium eccentricity values (e = 0.5, 0.75) are more likely to transition to slug flow. We compared the visual recognition results of flow regimes with the clustering results. 4.04% of the total samples showed different results from visual recognition and clustering, primarily located in the flow regime transition area. Since visually distinguishing flow regimes in these areas is typically challenging, our methodology offers an objective classification approach for gas-liquid two-phase counter-current flow in a vertical annulus.

Clinical efficacy and mechanism study of mid-frequency anti-snoring device in treating moderate obstructive sleep apnea-hypopnea syndrome.

BACKGROUND: Obstructive sleep apnea-hypopnea syndrome (OSAHS) is primarily caused by airway obstruction due to narrowing and blockage in the nasal and nasopharyngeal, oropharyngeal, soft palate, and tongue base areas. The mid-frequency anti-snoring device is a new technology based on sublingual nerve stimulation. Its principle is to improve the degree of oropharyngeal airway stenosis in OSAHS patients under mid-frequency wave stimulation. Nevertheless, there is a lack of clinical application and imaging evidence. AIM: To investigate the clinical efficacy and mechanisms of a mid-frequency anti-snoring device in treating moderate OSAHS. METHODS: We selected 50 patients diagnosed with moderate OSAHS in our hospital between July 2022 and August 2023. They underwent a 4-wk treatment regimen involving the mid-frequency anti-snoring device during nighttime sleep. Following the treatment, we monitored and assessed the sleep apnea quality of life index and Epworth Sleepiness Scale scores. Additionally, we performed computed tomography scans of the oropharynx in the awake state, during snoring, and while using the mid-frequency anti-snoring device. Cross-sectional area measurements in different states were taken at the narrowest airway point in the soft palate posterior and retrolingual areas. RESULTS: Compared to pretreatment measurements, patients exhibited a significant reduction in the apnea-hypopnea index, the percentage of time with oxygen saturation below 90%, snoring frequency, and the duration of the most prolonged apnea event. The lowest oxygen saturation showed a notable increase, and both sleep apnea quality of life index and Epworth Sleepiness Scale scores improved. Oropharyngeal computed tomography scans revealed that in OSAHS patients cross-sectional areas of the oropharyngeal airway in the soft palate posterior area and retrolingual area decreased during snoring compared to the awake state. Conversely, during mid-frequency anti-snoring device treatment, these areas increased compared to snoring. CONCLUSION: The mid-frequency anti-snoring device demonstrates the potential to enhance various sleep parameters in patients with moderate OSAHS, thereby improving their quality of life and reducing daytime sleepiness. These therapeutic effects are attributed to the device's ability to ameliorate the narrowing of the oropharynx in OSAHS patients.

Berberine improved the microbiota in lung tissue of colon cancer and reversed the bronchial epithelial cell changes caused by cancer cells.

Objective: The lung is a common organ for colon cancer metastasis, and the objective of this experiment was to explore the protective effect of berberine on lung tissue or alveolar epithelial cells induced by colon cancer. Methods: Thirty-six BALB/c nude mice were used to establish a xenograft model of colon cancer with the HT29 cell line and were treated with berberine and probiotics. Human bronchial epithelial BEAS-2B cells were induced by conditioned medium (CM) from the colon cancer cell lines HT29 and RKO and were treated with berberine. Lung tissues were collected to detect the changes in the microbiota using 16S rDNA sequencing and the expression of inflammatory cytokines. The expression of E-cadherin and N-cadherin in BEAS-2B cells was detected by cellular immunofluorescence. The changes in cell proliferation were detected by the CCK-8 assay. Western blotting was used to detect E-cadherin, N-cadherin, collagen I, fibronectin, PDGF-ß, and RAD51 expression in BEAS-2B cells. Results: The richness and evenness of the microbiota in the lung tissues of mice with colon cancer were significantly lower than those of the control group. Berberine significantly increased the abundances of Bacteroidetes, Bacteroidia, Bacteroidales, Lactobacillaceae, Lactobacillus and Acinetobacter in the lung tissue of mice with colon cancer, with reduced abundances of Actinobacteria, Bacillales, Staphylococcaceae and Staphylococcus. Berberine or probiotics significantly increased the alpha diversity of the lung microbiota. Compared with probiotics, berberine significantly enhanced the abundance of microbiota involved in the metabolism of lysosomes, flavone and flavonol biosynthesis, glycosaminoglycan degradation, and glycosphingolipid biosynthesis-ganglio. Berberine increased IL-6 and IL-10 and decreased IL-17 and IFN-γ expression in lung tissue (P > 0.05), but berberine-probiotics significantly decreased IL-17 and IFN-γ and increased IL-10 expression (P < 0.05). Colon cancer cells could not induce BEAS-2B proliferation but decreased the expression of the epithelial marker E-cadherin and altered the expression of extracellular matrix-related proteins (collagen I, fibronectin, and PDGF-ß), which were reversed by berberine. Berberine increased RAD51 expression in BEAS-2B cells, which had been decreased by HT29 and RKO CM treatment. Conclusion: Berberine can selectively regulate the abundance of some microbiomes of lung tissue in colon cancer, improve the inflammatory response in lung tissue, and antagonize the cancerous stimulation of colon cancer cells to lung tissue cells by regulating the bronchial epithelial cell phenotype, extracellular matrix remodelling and the expression of the repair gene RAD51.

Ferroelectric Nanorods as a Polymer Interface Additive for High-Performance Garnet-Based Solid-State Batteries.

Sandwiching polymer interlayers between the electrode and solid electrolyte is considered promising in solving the interfacial issues arising from solid-solid contact in garnet-based solid-state batteries, but drawbacks including low ionic conductivity, inferior Li+ transference number, and unsatisfying mechanical property of the polymer hindered the practical application of such strategy. To solve the mentioned shortcomings of the polymer interlayer simultaneously, we introduce the ferroelectric material, BaTi2O5 (BT) nanorods, into the polymer matrix in this work. By taking full advantage of the plasticization effect and intrinsic spontaneous polarization of the introduced ferroelectric, the polymer's ionic conductivity and Li+ transference number have been significantly enhanced. The built-in electric field BT introduced also benefits the modulation of CEI components formed on the cathode particles, further enhancing the battery performance by decreasing cathode degradation. Besides, the BT nanorods' particular high aspect ratio also helps increase the mechanical property of the obtained polymer film, making it more resistant to lithium dendrite growth across the interface. Benefitting from the merits mentioned above, the assembled lithium symmetric cells using garnet SE with the BT-modified polymer interlayer exhibit stable cycling performance (no short circuit after 1000 h under RT) with low polarization voltage. The full battery employing LiFePO4 as a cathode also presents superior capacity retentions (94.6% after 200 cycles at 0.1 C and 93.4% after 400 cycles at 0.2 C). This work highlights the importance of ferroelectric materials with specific morphology in enhancing the electrochemical performance of polymer-based electrolytes, promoting the practical application of solid-state batteries.

PRMT5 facilitates angiogenesis and EMT via HIF-1α/VEGFR/Akt signaling axis in lung cancer.

Abnormal angiogenesis is a critical factor in tumor growth and metastasis, and protein arginine methyltransferase 5 (PRMT5), a prominent type II enzyme, is implicated in various human cancers. However, the precise role of PRMT5 in regulating angiogenesis to promote lung cancer cell metastasis and the underlying molecular mechanisms are not fully understood. Here, we show that PRMT5 is overexpressed in lung cancer cells and tissues, and its expression is triggered by hypoxia. Moreover, inhibiting or silencing PRMT5 disrupts the phosphorylation of the VEGFR/Akt/eNOS angiogenic signaling pathway, NOS activity, and NO production. Additionally, inhibiting PRMT5 activity reduces HIF-1α expression and stability, resulting in the down-regulation of the VEGF/VEGFR signaling pathway. Our findings indicate that PRMT5 promotes lung cancer epithelial-mesenchymal transition (EMT), which might be possibly through controlling the HIF-1α/VEGFR/Akt/eNOS signaling axis. Our study provides compelling evidence of the close association between PRMT5 and angiogenesis/EMT and highlights the potential of targeting PRMT5 activity as a promising therapeutic approach for treating lung cancer with abnormal angiogenesis.

Polycrystal Li2ZnTi3O8/C anode with lotus seedpod structure for high-performance lithium storage.

Lotus-seedpod structured Li2ZnTi3O8/C (P-LZTO) microspheres obtained by the molten salt method are reported for the first time. The received phase-pure Li2ZnTi3O8 nanoparticles are inserted into the carbon matrix homogeneously to form a Lotus-seedpod structure, as confirmed by the morphological and structural measurements. As the anode for lithium-ion batteries, the P-LZTO material demonstrates excellent electrochemical performance with a high rate capacity of 193.2 mAh g-1 at 5 A g-1 and long-term cyclic stability up to 300 cycles at 1 A g-1. After even 300 cyclings, the P-LZTO particles can maintain their morphological and structural integrity. The superior electrochemical performances have arisen from the unique structure where the polycrystalline structure is beneficial for shorting the lithium-ion diffusion path, while the well-encapsulated carbon matrix can not only enhance the electronic conductivity of the composite but also alleviate the stress anisotropy during lithiation/delithiation process, leading to well-preserved particles.

TiO2 Nanorod-Coated Polyethylene Separator with Well-Balanced Performance for Lithium-Ion Batteries.

The thermal stability of the polyethylene (PE) separator is of utmost importance for the safety of lithium-ion batteries. Although the surface coating of PE separator with oxide nanoparticles can improve thermal stability, some serious problems still exist, such as micropore blockage, easy detaching, and introduction of excessive inert substances, which negatively affects the power density, energy density, and safety performance of the battery. In this paper, TiO2 nanorods are used to modify the surface of the PE separator, and multiple analytical techniques (e.g., SEM, DSC, EIS, and LSV) are utilized to investigate the effect of coating amount on the physicochemical properties of the PE separator. The results show that the thermal stability, mechanical properties, and electrochemical properties of the PE separator can be effectively improved via surface coating with TiO2 nanorods, but the degree of improvement is not directly proportional to the coating amount due to the fact that the forces inhibiting micropore deformation (mechanical stretching or thermal contraction) are derived from the interaction of TiO2 nanorods directly "bridging" with the microporous skeleton rather than those indirectly "glued" with the microporous skeleton. Conversely, the introduction of excessive inert coating material could reduce the ionic conductivity, increase the interfacial impedance, and lower the energy density of the battery. The experimental results show that the ceramic separator with a coating amount of ~0.6 mg/cm2 TiO2 nanorods has well-balanced performances: its thermal shrinkage rate is 4.5%, the capacity retention assembled with this separator was 57.1% under 7 C/0.2 C and 82.6% after 100 cycles, respectively. This research may provide a novel approach to overcoming the common disadvantages of current surface-coated separators.

TGF-ß1 induced deficiency of linc00261 promotes epithelial-mesenchymal-transition and stemness of hepatocellular carcinoma via modulating SMAD3.

Emerging evidence suggests that long non-coding RNAs (lncRNAs) play important roles in the metastasis and recurrence of hepatocellular carcinoma (HCC). A kinds of lncRNAs were found to be involved in regulating epithelial-mesenchymal transition (EMT) or stem-like traits in human cancers, however, the molecular mechanism and signaling pathways targeting EMT and stemness remains largely unknown. Previously, we found that linc00261 was down-regulated in HCC and associated with multiple worse clinical pathological parameters and poor prognosis. Here, we show that linc00261 was down-regulated in TGF-ß1 stimulated cells, and forced expression of linc00261 attenuated EMT and stem-like traits in HCC. Linc00261 also inhibited the tumor sphere forming in vitro and decreased the tumorigenicity in vivo. Furthermore, we revealed that linc00261 suppressed the expression and phosphorylation of SMAD3 (p-SMAD3), which could be core transcriptional modulator in TGF-ß1 signaling mediated EMT and the acquisition of stemness traits. A negative correlation between linc00261 and p-SMAD3 was determined in HCC samples. Conclusion: Our study revealed that linc00261 suppressed EMT and stem-like traits in HCC cells by inhibiting TGF-ß1/SMAD3 signaling.

Epigenetically silenced linc00261 contributes to the metastasis of hepatocellular carcinoma via inducing the deficiency of FOXA2 transcription.

Hepatocellular carcinoma (HCC) is one of the most common malignancies worldwide. In recent decades, long non-coding RNAs (lncRNAs) have attracted increasing attention and have been reported to play important roles in human cancers, making them ideal candidates for precise disease assessment and treatment. Our previous study found that the loss of linc00261 was significantly correlated with the malignant biological behaviors of HCC, particularly MVI, and serves as an excellent independent prognostic factor for recurrence-free survival. In this study, our in-depth research demonstrated that linc00261 inhibits epithelial-mesenchymal transition (EMT) in liver cancer cells, thereby suppressing migration, invasion, and the formation of lung metastatic lesions. Moreover, linc00261 and its neighbor gene FOXA2 were positively correlated in HCC, the gain- and loss-of-function analyses indicated that linc00261 transcriptionally promotes the expression of FOXA2. Additionally, bioinformatic analysis and rescue assays confirmed that linc00261 partially suppresses migration, invasion, and EMT by upregulating FOXA2 expression. Molecular mechanism studies showed that linc00261 transcriptionally upregulates FOXA2 in cis by recruiting SMAD3. Finally, we identified EZH2 is responsible for linc00261 transcription repression via modulating trimethylation of H3K27 at Lys27 (H3K27Me3), both EZH2 and H3K27Me3 were negatively correlated with linc00261 expression in HCC. In conclusion, these findings demonstrated a crucial role of linc00261 in HCC metastasis, and that EZH2/linc00261/FOXA2 axis might reveal potential prognostic factors and be applied as therapeutic targets for HCC metastasis.

Deficiency of pseudogene UPAT leads to hepatocellular carcinoma progression and forms a positive feedback loop with ZEB1.

Hepatocellular carcinoma (HCC) is a common disease worldwide. Accumulating reports have evidenced the internal connection between epithelial-mesenchymal transition (EMT) and cancer stem cells (CSCs), as well as their significance in metastasis and post-operative recurrence. In this study, we investigated an interesting ubiquitin-proteasome pathway associated pseudogene of AOC4, also known as UPAT, and showed that it was downregulated in 39.78% (37/93) of patients with hepatitis B virus (HBV)-related HCC. Downregulation of UPAT was associated with multiple worse clinicopathological parameters, as well as decreased recurrence-free survival (RFS). In vitro and in vivo assays found that overexpression of UPAT significantly suppressed cellular migration, invasion, EMT processes, and CSC properties. Mechanistic studies showed that UPAT promoted ZEB1 degradation via a ubiquitin-proteasome pathway and, in contrast, ZEB1 transcriptionally suppressed UPAT by binding to multiple E-box (CACCTG) elements in the promoter region. Moreover, UPAT was negatively correlated with ZEB1 protein in HCC tissues, their combined expression discriminated RFS outcomes for patients with HBV-related HCC. These data on the UPAT-ZEB1 circuit-mediated pathway will further knowledge on EMT and CSCs, and may help to develop novel therapeutic approaches for the prevention of HCC metastasis.

CaSnO3: Pr3+ phosphor for new application in temperature sensing.

CaSnO3: Pr3+ phosphor for new application in temperature sensing was investigated. CaSnO3: 0.3%Pr3+ had distorted orthorhombic perovskite structure and Pr3+ occupied Ca2+ sites due to their similar ionic radii. CaSnO3: 0.3%Pr3+ had spherical particles with mean size of 0.816 µm. The electric dipole-dipole interaction could explain the concentration quenching mechanism. The chromaticity coordinates were (0.1324, 0.3847), located in greenish-blue region and the average afterglow decay time was 60.2 s for CaSnO3: 0.15%Pr3+, which had potential applications for LED and emergency lighting. CaSnO3: 0.3%Pr3+ had the activated energy of 0.380 eV. The maximum relative temperature sensitivity for CaSnO3: 0.3%Pr3+ was 7.57% K-1 at 298 K and relative sensitivity was as high as 6722.76/T2 K-1, which was better than that of most Pr3+ doped phosphors and had potential application in temperature sensing. Moreover, the possible luminescence and long afterglow mechanisms and thermal quenching process of 3P0 level through IVCT state were proposed.

Percolation Characteristics and Fluid Movability Analysis in Tight Sandstone Oil Reservoirs.

The development of tight oil has started relatively late, and the flow mechanisms and fluid movability are still research spotlights. The goal of this paper is to investigate the percolation characteristics and fluid movability of the Chang 6 tight sandstone oil layer in the Upper Triassic Yanchang Formation, Ordos Basin, China. Results show that (1) at low flow velocity, the percolation curve of flow velocity vs pressure gradient is a concave-up nonlinear curve and does not pass through the origin. It is more difficult for oil flow than water flow in cores with similar permeability due to rock wettability and fluid apparent mobility. The application of back pressure makes the nonlinear stage eliminated and the percolation character improved. (2) Two-phase flow tests reveal that oil-phase permeability decreases faster in samples with lower permeability, and the coexistent flow region of oil and water is relatively narrow. The contribution of oil recovery mainly happens at the early stage. The permeability at the isotonic point reduces with the decrease of sample permeability. (3) Flow during water flooding can be roughly divided into four stages according to the injection pressure and flow change. The injection pressure experiences stages of increasing to a peak, then decreasing, and finally becoming stable, accompanied by an increase of oil production until water breaks through. (4) The pore throats of the target reservoir mainly range from 0.001 to 10 µm, and the bound water mainly distributes in pores less than 0.2 µm. The irreducible water saturation is 30-35%, and the movable fluid saturation is 65-70%, mainly distributed in pores at 0.2-10.0 µm with a maximum of 2.0 µm. The results will supplement the existing knowledge of percolation characters and fluid movability in tight sandstone oil reservoirs.

MALAT1 functions as a competing endogenous RNA to regulate SMAD5 expression by acting as a sponge for miR-142-3p in hepatocellular carcinoma.

BACKGROUND: Long non-coding RNAs are involved in the pathology of various tumors, including hepatocellular carcinoma. The expression of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is increased in numerous types of tumors and is involved in tumor cell proliferation, migration, invasion and apoptosis. MALAT1 level was reported to be upregulated in hepatocellular carcinoma tissues, but its roles and the specific molecular mechanisms are still unclear. METHODS: The expression of MALAT1 and miR-142-3p in hepatocellular carcinoma tissues, cell lines and adjacent non-tumor tissues was assessed by Q-PCR. The putative-binding sites between MALAT1 and miR-142-3p were predicted by bioinformatics analysis. The expression of MALAT1 in HepG2 and SMMC-7721 cells was knocked down by transfection with MALAT1 siRNAs. Cell viability was assessed by the Cell Counting Kit-8 (CCK-8) assay after the indicated transfection in HepG2 and SMMC-7721 cells. Cell proliferation was assessed by EdU assay, and cell apoptosis was explored by flow cytometry. The migration and invasion potency of HepG2 and SMMC-7721 cells was assessed by the cell migration assay and matrigel invasion assay. Protein level of vimentin, E-cadherin and SMAD5 were assessed by Western blot. RESULTS: Overexpressed MALAT1 acts as a competing endogenous RNA sponge for miR-142-3p in hepatocellular carcinoma. The knockdown of MALAT1 inhibited the proliferation, migration, invasion, and epithelial cell-to-mesenchymal transition (EMT), and promoted apoptosis of hepatocellular carcinoma cells via miR-142-3p. MiR-142-3p inhibited cell proliferation, migration, invasion and EMT, and promoted the cell apoptosis by targeting SMAD5 in hepatocellular carcinoma. MALAT1 promoted tumor growth by regulating the expression of miR-142-3p in vivo. CONCLUSION: MALAT1 promoted cell proliferation, migration, and invasion of hepatocellular carcinoma cells by antagonizing miR-142-3p.

Frizzled 2-induced epithelial-mesenchymal transition correlates with vasculogenic mimicry, stemness, and Hippo signaling in hepatocellular carcinoma.

Prior observation has indicated that Frizzled 2 (FZD2)-induced epithelial-mesenchymal transition (EMT) could be a key step in metastasis and early recurrence of hepatocellular carcinoma (HCC). However, the mechanism underlying tumor development and progression due to aberrant FZD2 expression is poorly defined. Here, we provide evidence that FZD2 is a driver for EMT, cancer stem cell properties, and vasculogenic mimicry (VM) in HCC. We found that FZD2 was highly expressed in two cohorts of Chinese hepatitis B virus-related HCC patients, and that high FZD2 expression was associated with poor prognosis. Concerning the mechanism, gain- and loss-of-function experiments showed the oncogenic action of FZD2 in HCC cell proliferation, apoptosis, migration, and invasion. Further investigations in vitro and in vivo suggested that FZD2 promotes the EMT process, enhances stem-like properties, and confers VM capacity to HCC cells. Notably, integrative RNA sequencing analysis of FZD2-knockdown cells indicated the enrichment of Hippo signaling pathway. Taken together, our data suggest for the first time that FZD2 could promote clinically relevant EMT, CD44+ stem-like properties, and the VM phenotype in HCC involving a potential Hippo signaling pathway-dependent mechanism, and should be considered as a promising therapeutic target for the treatment of HCC.

[Expression of long noncoding RNA linc00261 in hepatocellular carcinoma and its association with postoperative outcomes].

OBJECTIVE: To investigate the expression of long noncoding RNA linc00261 in hepatocellular carcinoma (HCC) and its correlation with the clinicopathological features and postoperative outcomes of the patients. METHODS: Real-time fluorescence quantitative PCR (qRT-PCR) was used to detect the expression of linc00261 in surgical specimens of HCC and adjacent tissues from 74 patients. The correlation of the expression level of linc00261 in HCC with the clinicopathological parameters of the patients was analyzed using Chi-square test. The Cox's proportional hazards regression model was used to assess the value of linc00261 in predicting the prognosis of HCC patients after operation. The expression of linc00261 was also examined in 5 HCC cell lines using qRT-PCR. The HCC cell lines MHCC-LM3 and SNU-449 were transfected with small interfering RNAs targeting linc00261 for linc00261 knockdown, and the changes in the cell proliferation, migration and invasion abilities were observed using CCK-8 assay and Transwell assay. RESULTS: The expression level of linc00261 in HCC was significantly correlated with AFP (P=0.032), tumor size (P=0.007), microscopic vascular invasion (MVI; P=0.01), and TNM stage (P=002). The patients with lowered expressions of linc00261 in HCC tissues had a significantly shortened tumor-free survival time (P < 0.05), and a lowered expression of linc00261 was identified as an independent risk factor affecting postoperative recurrence-free survival time of the patients (P < 0.05). In HCC cell lines MHCC-LM3 and SNU-449 cells, linc00261 knockdown obviously promoted the cell migration and invasion (P < 0.01) but did not significantly affect cell proliferation (P > 0.05). CONCLUSIONS: Linc00261 may serve as a new prognostic biomarker for predicting the postoperative outcomes of the patients with HCC.

Circulating Tumor Cell Phenotype Indicates Poor Survival and Recurrence After Surgery for Hepatocellular Carcinoma.

BACKGROUND: Circulating tumors cells (CTCs) may be a promising prognostic marker for patients with malignant tumors. However, there are few reports regarding its value for hepatocellular carcinoma (HCC) patients. AIMS: To investigate CTCs with epithelial and mesenchymal phenotypes as a potential prognostic biomarker for HCC patients. METHODS: Peripheral blood samples were obtained from 165 HCC patients before radical surgery. CTCs were isolated via the CanPatrol CTC enrichment technique and classified using epithelial-mesenchymal transition (EMT) markers. The relationship of CTC phenotype with clinicopathological factors and HCC recurrence in patients was analyzed. RESULTS: CTC-positive status (count ≥ 2/5 mL) was found in 70.9% of the 165 HCC patients. Increased CTC number was more common in patients with higher AFP levels, multiple tumors, advanced TNM and BCLC staging, and presence of embolus or microembolus (P < 0.05). CTCs heterogeneity was noted using EMT markers. Mesenchymal CTCs were significantly correlated with high AFP levels, multiple tumors, advanced TNM and BCLC stage, presence of embolus or microembolus, and earlier recurrence (P < 0.05). The presence of mesenchymal CTCs predicted the shortest relapse-free survival, followed by mixed phenotypic CTCs, and then epithelial CTCs (P < 0.001). CONCLUSION: CTC phenotype may serve as a prognostic indicator for HCC patients. CTCs assessment should include phenotypic identification tailored to characterize cells based on epithelial and mesenchymal markers.

[Expression of Wnt5b in patients with HBV-related hepatocellular carcinoma and its clinical significance].

OBJECTIVE: To investigate the expression of Wnt5b in hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) tissues and its correlation with the clinicopathological parameters. METHODS: Quantitative real-time polymerase chain reaction (qRT-PCR) and immunohistochemical staining were employed to measure Wnt5b mRNA and protein expressions in two groups of HBV-related HCC patients (100 cases in each) selected from a cohort of 289 cases with HBV-related HCC using simple random sampling method. The correlation of Wnt5b expression with the clinicopathological parameters and the prognosis of HCC patients was analyzed. RESULTS: Wnt5b mRNA expression was significantly higher in HCC tissues than that of adjacent noncancerous tissues in 65.0% (65/100) of the cases, and the positivity rate of Wnt5b protein was significantly higher in HCC tissues than that of adjacent noncancerous tissues (58.0% vs 22.0%, P<0.05). Wnt5b expression was significantly correlated with the tumor size (P<0.05), tumor number (P<0.01, only at the protein level), tumor differentiation (P<0.01, only at the protein level), TNM stage (P<0.05), BCLC stage (P<0.05), metastasis (P<0.05) and recurrence (P<0.01). The patients with up-regulated Wnt5b mRNA and protein had a shorter relapse-free survival (P<0.01). CONCLUSION: s Up-regulated Wnt5b might contribute to the progression of HBV-related HCC and predicts a poor prognosis.

Loss of tumor suppressor miR-126 contributes to the development of hepatitis B virus-related hepatocellular carcinoma metastasis through the upregulation of ADAM9.

Hepatocellular carcinoma is the most common histological type of primary liver cancer, which represents the second leading cause of cancer-related mortality. MiR-126 was reported to be downregulated in hepatocellular carcinoma tissues, compared with its levels in noncancerous tissues. However, baseline miR-126 expression levels in hepatitis B virus-related hepatocellular carcinoma patients who did not undergo pre-operational treatment remains unknown since hepatitis B virus infection and pre-operational transcatheter arterial chemoembolization were shown to upregulate miR-126 expression. Here, we demonstrated that miR-126 is generally downregulated in a homogeneous population of pre-operational treatment-naïve hepatitis B virus-related hepatocellular carcinoma patients (84.0%, 84/100), and its expression is significantly associated with pre-operational alpha-fetoprotein levels ( p < 0.05), microvascular invasion ( p < 0.05), tumor metastasis ( p < 0.05), as well as early recurrence (12 months after surgery; p < 0.01). Furthermore, the results of our study revealed that miR-126 is negatively correlated with ADAM9 expression in hepatitis B virus-related hepatocellular carcinoma patients. Overexpression of miR-126 was shown to attenuate ADAM9 expression in hepatocellular carcinoma cells, which subsequently inhibits cell migration and invasion in vitro. In addition, Cox proportional hazards regression model analysis showed that ADAM9 levels, tumor number, microvascular invasion, and tumor metastasis rate represent independent prognostic factors for shorter recurrence-free survival. In conclusion, we demonstrated that the loss of tumor suppressor miR-126 in hepatitis B virus-related hepatocellular carcinoma cells contributes to the development of metastases through the upregulated expression of its target gene, ADAM9. MiR-126-ADAM9 pathway-based therapeutic targeting may represent a novel approach for the inhibition of hepatitis B virus-related hepatocellular carcinoma metastases.

[Expressions and clinical significances of TSLC1 and 4.1B in non-small cell lung cancer].

BACKGROUND: Tumor suppressor in lung cancer-1 (TSLC1) belongs to immunoglobulin superfamily of cell adhesion molecule and differentially expressed in adenocarcinoma of the lung (4.1B)belongs to NF2/ERM/4.1 protein superfamily. They may suppress carcinogenesis via construction of the adjacent cell adhesion stability. The aim of this study is to detect the expressions of TSLC1 and 4.1B in non-small cell lung cancer and the clinical pathological significances. METHODS: The expressions of TSLC1 and 4.1B were detected by RT-PCR in 52 cases of non-small cell lung cancer and corresponding adjacent cancer lung tissues RESULTS: The expressions of TSLC1 and 4.1B in cancer tissues were significantly lower than that in adjacent cancer lung tissues (0.349 ± 0.008 vs 0.555 ± 0.010; 0.209 ± 0.040 vs 0.721 ± 0.071) (P < 0.01). The expressions of TSLC1 and 4.1B showed a significant correlation with cancer differentiation and TNM staging (P < 0.05), but not with gender, age and pathological type (P > 0.05). The expressions of TSLC1 and 4.1B were positively correlated (r=0.471, P < 0.001). CONCLUSIONS: Down-regulated expressions of TSLC1 and 4.1B in non-small cell lung cancer, both may participate in a cascade of non-small cell lung cancer occurrence and development. TSLC1 and 4.1B are promising targets for non-small cell lung cancer diagnosis and treatment.