Impact of Ceramic Micropillar Array and Fiber Layer Composite Structure on Kinematic and Heat Transfer Characteristics of Single Droplet Impacting a Wall.

The well-known limitations of spray cooling on high-temperature solids at the Leidenfrost temperature point have been significantly improved by a composite structure of steel micropillar arrays and insulating thin films. However, the physical mechanism of a single droplet impact on the walls of high-temperature composite structures in spray cooling remains elusive. We have experimentally studied and quantified the kinematic and thermal transfer characteristics of a single droplet impacting high-temperature micropillar arrays with fiber membrane composite structures. In particular, micropillar arrays of ceramic materials of different shapes (rectangular and cylindrical) used in this study were made using the more flexible PµSL technique, for which precision reaches the micron level. The results show that the presence and different layouts (embedded or placed on top) of the fiber layer significantly affect the spreading coefficient and thermal transfer efficiency of the droplets after impact. In terms of kinematic characteristics, unrelated to the structure of micropillar arrays, compared to structures without film, the maximum spreading coefficient of droplets significantly increased by more than 40% (43% for rectangular, 46% for cylindrical) when the fiber film was placed on top, and increased by more than 20% (20% for rectangular, 33% for cylindrical) when the fiber film was embedded. In terms of thermal transfer characteristics, at a temperature of 200 °C, the presence of the fiber layer changed the wettability of the surface of the micropillar structure, leading to a certain extension of the total evaporation time of the droplets compared to the surface of the micropillar structure without film.

LINC00511 promotes melanoma progression by targeting miR-610/NUCB2.

Long intergenic noncoding RNA 00511 (LINC00511) predicts poor prognosis in various malignancies and functions as an oncogene in distinct malignant tumors. The role of LINC00511 in melanoma progression was assessed. In our research, expression of LINC00511 in melanoma cells was detected by quantitative reverse transcription PCR. Colony formation and CCK8 assays were used to detect cell proliferation. Cell metastasis was evaluated by transwell and wound healing assays. Downstream target of LINC00511 was investigated by luciferase activity assay. As a results, LINC00511 was elevated in melanoma cells and tissues. Loss of LINC00511 decreased cell viability, reduced proliferation, invasion, and migration of melanoma. miR-610 was target of LINC00511, and miR-610 binds to 3'UTR of nucleobindin-2 (NUCB2). Inhibition of miR-610 attenuated LINC00511 deficiency-induced decrease of NUCB2 in melanoma cells. Loss of miR-610 weakened LINC00511 deficiency-induced decrease of cell viability, proliferation, invasion, and migration of melanoma. In conclusion, silence of LINC00511 reduced cell proliferation and metastasis of melanoma through down-regulation of miR-610-mediated NUCB2.

miRNA-633 and KAI1 as Potential Biomarkers of Malignant Melanoma with Gastric Cancer.

OBJECTIVE: Malignant melanoma with gastric cancer is one of the most malignant tumors. However, there have been no reports on the effects of KAI1 and miRNA-633 on the survival and prognosis of patients with malignant melanoma with gastric cancer. METHODS: Fifty patients with malignant melanoma and gastric cancer were collected from October 2017 to December 2019. The clinical parameters included clinical information, such as sex, age, tumor size, and tumor staging. RT-qPCR was used to detect the expression of KAI1 and miRNA- 633. The role of KAI1 and miRNA-633 on the overall survival of melanoma was explored by the Pearson chi-square test, Spearman-rho correlation test, Univariate and multivariate cox regression analyses, and Kaplan-Meier method. Furthermore, the bioinformatic analysis was used to verify the role of KAI1 and miRNA-633 on malignant melanoma with gastric cancer. RESULTS: The expression of KAI1 and miRNA-633 was significantly related with the tumor size and staging of tumor (p<0.05) based on the Pearson chi-square test. Spearman's correlation coefficient displayed that KAI1 was significantly correlated with the miRNA-633 (ρ=-0.439, p=0.001). The result of multivariate cox proportional regression analysis showed that KAI1 (HR =0.109, 95% CI: 0.031-0.375, p< 0.001), and miRNA-633 (HR = 13.315, 95% CI: 3.844-46.119, p<0.001) were significantly associated with overall survival. CONCLUSION: The low expression level of KAI1 and high expression of miRNA-633 are significantly correlated with the poor overall survival prognosis of malignant melanoma with gastric cancer, to provide a basis for KAI1 and miRNA-633 to become novel molecular targets for malignant melanoma with gastric cancer.

Lower expression of KAI1 as a biomarker of poor survival prognosis of melanoma combined with colorectal cancer metastasis.

OBJECTIVE: This study aimed to investigate the correlation between KAI1 (CD82) and miR-633 expression and prognosis and survival time of patients with melanoma combined with colorectal cancer (CRC). METHODS: Clinical and follow-up data of melanoma and CRC patients were recorded, and the expression levels of KAI1 and miR-633 were detected. Pearson chi-square tests and Spearman correlation coefficient were used to analyze the relationship between prognosis and related parameters in these patients. Cox proportional risk regression and receiver operating characteristic curve analyses were used. RESULTS: Overall, 195 patients were included. KAI1 and miR-633 expression levels were significantly correlated with the prognosis of patients with melanoma combined with CRC. Spearman correlation analysis showed that the expression levels of KAI1 and miR-633 were significantly correlated with the prognosis of patients. Multivariate Cox regression analysis suggested that low expression levels of KAI1 and high expression levels of miR-633 indicated shorter survival time for patients. CONCLUSIONS: KAI1 expression was significantly correlated with melanoma and CRC patient prognosis. When KAI1 expression levels were low, the patient survival time was poor.

Characteristics of SP600125 Induced Tetraploid Cells in Comparison With Diploid and Tetraploid Cells of Fish.

In our previous research, SP600125 (Anthrapyrazolone) was used to induce autotetraploid of crucian carp cells (SP4N cells), and tetraploid fry was generated from the SP4N cells by somatic cell nuclear transfer technique. However, it is still unclear about biological characteristics of the SP4N cells. In this article, the cytological characteristic and gene expression profiles of the SP4N cells are investigated in comparison with the crucian carp cells (2N cells) and the tetraploid crucian carp cells (CC4N cells). The SP4N cells have tetraploid characteristics in terms of morphology and DNA ploidy levels, and their chromosome behavior is stable during the cell proliferation. The migration ability and the mtDNA copy number of SP4N cells are both lower than those in the CC4N cells and the 2N cells, but there exist giant mitochondria in the SP4N cells. The similar expression trends in the cell cycle regulation genes of the SP4N cells and 2N cells, while the corresponding expression profiles are clearly different between the SP4N cells and the CC4N cells. Moreover, the significant difference genes are associated with energy metabolism pathways among the SP4N cells, 2N cells and CC4N cells. These results can provide deeper understanding of SP600125 induction, as well as finding applications in polyploidization breeding of fish species.

ING5 inhibits cell proliferation and invasion in esophageal squamous cell carcinoma through regulation of the Akt/NF-κB/MMP-9 signaling pathway.

The inhibitor of growth 5 (ING5) is a new candidate tumor suppressor gene (TSG) of the ING family. So far, there have been many reports about its functions related to cancer development. However, the biological roles of ING5 in esophageal squamous cell carcinoma (ESCC) remain unclear. In the present study, we demonstrated that ING5 was lowly expressed in ESCC tissues and cell lines. Overexpression of ING5 inhibited ESCC cell proliferation and invasion in vitro as well as suppressed tumor growth and metastasis in vivo. We also found that overexpression of ING5 significantly decreased the levels of p-AKT, NF-κB and MMP-9 in ECA109 cells. Taken together, these findings demonstrated that ING5 inhibited cell proliferation and invasion in ESCC through regulation of the Akt/NF-κB/MMP-9 signaling pathway. Thus, ING5 might be considered a promising target for ESCC treatment.

MicroRNA-610 inhibits tumor growth of melanoma by targeting LRP6.

Accumulating evidence showed that aberrant miRNAs expression was involved in initiation and progression of melanoma. However, the investigation of different miRNAs in melanoma remain attractive. In this research, we demonstrated that miR-610 expression was decreased in melanoma tissues and cell lines. The clinical data showed that the reduced miR-610 expression was obviously associated with adverse prognostic characteristics. Furthermore, our results suggested that miR-610 had a function of prognostic indicator for 5-year predicted-survival of melanoma patients. The ectopic overexpression of miR-610 suppressed cell proliferation, cell cycle progression and promoted apoptosis while miR-610 knockdown reversed the effect in vitro and in vivo. Additionally, miR-610 could modulate LRP6 by directly interacting to its 3'-UTR. In clinical samples of melanoma, miR-610 inversely correlated with LRP6. The biological function of miR-610 on melanoma cells was abrogated by alternation of LRP6 expression. In summary, our research indexed that miR-610 had a function of tumor suppressor in regulating the proliferation, cell cycle and apoptosis of melanoma via targeting LRP6. Hence, it may represent a novel potential therapeutic target and prognostic marker for melanoma.

MicroRNA138 regulates keratin 17 protein expression to affect HaCaT cell proliferation and apoptosis by targeting hTERT in psoriasis vulgaris.

The purpose of this study is to explore the how microRNA-138 (miR-138) affects the expression of keratin 17 (K17) and psoriasis development. Twenty-eight skin lesions from patients with psoriasis vulgaris and twenty-four normal skin tissues from healthy controls were collected. The HaCaT cells were assigned into blank, negative control (NC), miR-138 mimic, miR-138 inhibitor, hTERT siRNA and miR-138 inhibitor+hTERT siRNA groups. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the miR-138 expression. The hTERT and K17 protein expression were testified by Western Blotting. MTT assay, flow cytometry with PI single staining and Annexin V/PI double staining were performed to detect the cell proliferation activity, cell cycle and apoptosis, respectively. Compared with the healthy skin, the expression of miR-138 decreased in the psoriatic skin, but hTERT and K17 protein expressions increased. The miR-138 mimic and hTERT siRNA groups showed significantly decreased hTERT and K17 protein expressions, inhibited cell proliferation, increased number of cells at G1 phase and elevated apoptosis rate in comparison to the rest three groups. The hTERT and K17 protein expressions in the miR-138 inhibitor group were up-regulated with promoted cell proliferation and reduced apoptosis rate as compared with the other four groups. In the miR-138 inhibitor+hTERT siRNA group, the hTERT and K17 protein expressions, cell proliferation and apoptosis were intermediate between the miR-138 inhibitor and hTERT siRNA groups. These findings indicated that the expression of miR-138 was lower in the psoriatic skin, which was negatively correlated to K17 expression. MiR-138 may regulate K17 protein expression to affect HaCaT cell proliferation and apoptosis by targeting hTERT gene.

Significance of interstitial tumor-associated macrophages in the progression of lung adenocarcinoma.

Stepwise progression from adenocarcinoma in situ (AIS) and minimally invasive adenocarcinoma (MIA) to lepidic predominant adenocarcinoma (LPA) was proposed by various scholars. Interstitial tumor-associated macrophages (TAMs) and various potential chemokines involved in the progression from AIS/MIA to LPA were hypothesized. In the present study, immunohistochemistry or immunofluorescent double staining was used to detect the expression of the TAMs marker cluster of differentiation (CD) 68, tumor-derived colony-stimulating factor (CSF)-1, interleukin (IL)-6, matrix metalloproteinase (MMP)-2, E-cadherin and Snail in lung adenocarcinoma specimens, including AIS/MIA, LPA and other types. It was observed that infiltrating TAMs were negatively associated with the prognosis of patients, and that the infiltration degree of interstitial TAMs was higher in LPA than that in AIS/MIA. In addition, E-cadherin, Snail and MMP-2 expression were significantly correlated with the infiltration degree of TAMs. Survival analysis revealed that co-expression of CD68, CSF-1 and IL-6 was an independent prognostic factor. Stratified analysis demonstrated that, in AIS/MIA patients, there was a statistically significant difference between the number of TAMs (TAMs ≤25 and TAMs >25) in the CD68+CSF-1+IL-6+ group compared with other groups (including CD68+CSF-1-IL-6-, CD68+CSF-1+IL-6-, CD68+CSF-1-IL-6+ and CD68- groups). By contrast, in patients with TAMs >25 and in patients with positive CD68, CSF-1 and IL-6 expression, the survival rates were not significantly different between AIS/MIA and LPA. These results suggested that co-expression of TAMs marker CD68, CSF-1 and IL-6 may be a valuable independent prognostic predictor in lung adenocarcinoma. TAMs may facilitate AIS/MIA progression to LPA, which may be closely associated with the induction of the epithelial-mesenchymal transition.

Identification of genes influencing formation of the Type III Brush Hair in Yangtze River Delta white goats by differential display of mRNA.

Yangtze River Delta white goat is an exclusive indigenous Chinese goat breeds that can produce Brush Hair specialized in making valuable writing brush. The high-grade (Type III) Brush Hair is conical coarse hair but with a tip, which only grows in the cervical carina and back regions of Yangtze River Delta white goats. Screening of genes influencing the formation of Type III Brush Hair was conducted using differential display of mRNA technique in skin including the hair follicles of different goat groups and the differential bands were identified using reverse Northern dot blot, and the positive bands were subsequently cloned and sequenced. The results showed that 20 differentially displayed bands were obtained, seven of which were identified positive as expressed in skin. Three of these seven cDNAs were homologous to certain sequences from GenBank and the other four were respectively homologous to CKLF-like MARVEL transmembrane domain containing 3 (CMTM3), S100 calcium binding protein A4 (S100A4), protein kinase inhibitor gamma (PKIG) and fibulin 1-D. The study would provide a new view to elucidate their roles in hair growth and hair follicle cycle and increase our understanding of the formation of Type III Brush Hair.

Construction of bilayered tissue-engineered skin with human amniotic mesenchymal cells and human amniotic epithelial cells.

Human amniotic mesenchymal cells (hAMCs) and human amniotic epithelial cells (hAECs) have attracted increasing attention in recent years as a possible reserve of stem cells that may be useful for clinical application in regenerative medicine. The object of this study was to establish a new model for reconstruction of bilayered tissue-engineered (TE) skin with hAMCs and hAECs (amniotic cells TE skin, AC-TE skin). We studied these two types of cells and confirmed that they possessed the properties of stem cells. Mesenchymal-epidermal interactions are responsible for organogenesis. On the basis of this mechanism, we modified the constructing methods of traditional TE skin (TE skin with human fibroblasts and keratinocytes) and then established a new bilayered TE skin-AC-TE skin. Histological and immunochemical methods were carried out to assess AC-TE skin. The results showed that AC-TE skin was similar in morphology to human skin which had stratified epidermis and underlying dermis. AC-TE skin expressed proliferative cells marker Ki67 and epithelial stem cells marker K19; moreover, the constructed AC-TE skin could successfully repair full thickness skin defects on athymic mice. Our findings suggest that AC-TE skin is a useful skin equivalent which has good application prospects in regenerative medicine.

High levels of ß-catenin signaling reduce osteogenic differentiation of stem cells in inflammatory microenvironments through inhibition of the noncanonical Wnt pathway.

Periodontal ligament stem cells (PDLSCs), a new population of mesenchymal stem cells (MSCs), have been isolated from the periodontal ligament (PDL). The capacity of multipotency and self-renewal makes them an excellent cell source for bone regeneration and repair. However, their bone-regeneration ability could be awakened in inflammatory microenvironments, which may be the result of changes in their differentiation potential. Recently, genetic evidences has shown that the Wnt pathway plays an important role in bone homeostasis. In this study we have determined the specific role of ß-catenin in osteogenic differentiation of PDLSCs obtained from inflammatory microenvironments (P-PDLSCs). The inflammatory microenvironment, while inhibiting osteogenic differentiation potential, promotes proliferation of MSCs. A higher the level of ß-catenin in P-PDLSCs than in H-PDLSCs (PDLSCs obtained from a healthy microenvironment) resulted in the same disparity in canonical Wnt signaling pathway activation between each cell type. Here we show that activation of ß-catenin suppresses the noncanonical Wnt/Ca(2+) pathway, leading to increased proliferation but reduced osteogenic differentiation of P-PDLSCs. Downregulation of the levels of ß-catenin by treatment with dickkopf-1 (DKK-1) leads to activation of the noncanonical Wnt/Ca(2+) pathway, which, in turn, results in the promotion of osteogenic differentiation in P-PDLSCs. Interestingly, ß-catenin can affect both the canonical Wnt/ß-catenin pathway and the noncanonical Wnt/Ca(2+) pathway. Our data indicate that ß-catenin plays a central role in regulating osteogenic differentiation of MSCs in inflammatory microenvironments. Given the important role of Wnt signaling in osteogenic differentiation, it is possible that agents that can modify this pathway may be of value in bone regeneration by MSCs in chronic inflammatory microenvironments.