The surface temperature rise for a semi-infinite body due to different moving heat sources is analyzed for the entire range of Peclet number using a Green’s function method. Analytical and approximate solutions of maximum and average surface temperatures are obtained for the cases of square uniform, circular uniform, and parabolic heat sources. Considering the heat partition between the two contacting bodies, solutions of interface flash temperature are presented for the general sliding contact case as well as for the case of sliding contact between two moving asperities.

Rationale: The incidence of hepatocellular carcinoma is rising worldwide. It is predicted that nearly half of the early-stage hepatocellular carcinoma (E-HCC) patients will develop recurrence. Dysregulated pH, a hallmark of E-HCC, is correlated with poor prognosis. The acidic microenvironment has been shown to promote the release of exosomes, the membrane vesicles recognized as intercellular communicators associated with tumor progression, recurrence, and metastasis. We, therefore, aimed to identify exosomes induced by acidic microenvironment that may regulate E-HCC progression and to explore their mechanisms and clinical significance in E-HCCs. Methods: miRNA microarray analysis and LASSO logistic statistic model were used to identify the main functional exosomal miRNAs. Invasion and scratch assays were performed to examine the migration and invasion of HCC cells. Immunoblotting and immunofluorescence were employed to detect the epithelial-to-mesenchymal transition (EMT) in HCC cells. Chromatin immunoprecipitation (ChIP) was used to analyze the binding of HIF-1α and HIF-2α to promoter regions of miR-21 and miR-10b. Results: The acidic microenvironment in HCC was correlated with poor prognosis of patients. Exosomes from HCC cells cultured in the acidic medium could promote cell proliferation, migration, and invasion of recipient HCC cells. We identified miR-21 and miR-10b as the most important functional miRNAs in acidic HCC-derived exosomes. Also, the acidic microenvironment triggered the activation of HIF-1α and HIF-2α and stimulated exosomal miR-21 and miR-10b expression substantially promoting HCC cell proliferation, migration, and invasion both in vivo and in vitro . In E-HCC patients, serum exosomal miR-21 and miR-10b levels were associated with advanced tumor stage and HIF-1α and HIF-2α expression and were independent prognostic factors for disease-free survival of E-HCC patients. Most importantly, we developed a nano-drug to target exosomal miR-21 and/or miR-10b and examined its therapeutic effects against HCC in vivo . Conclusion: Our findings suggested that the exosomal miR-21 and miR-10b induced by acidic microenvironment in HCC promote cancer cell proliferation and metastasis and may serve as prognostic molecular markers and therapeutic targets for HCC.

Dysregulation of non-coding RNAs, including miRNAs and lncRNAs has been reported to play vital roles in gastric cancer (GC) carcinogenesis, but the mechanism involved is largely unknown. Using the cancer genome atlas (TCGA) data set and bioinformatics analyses, we identified miR-532-5p as a potential tumor suppressor in GC, and found that lncRNA LINC01410 might be a negative regulator of miR-532-5p. We then conducted a series of in vivo and in vitro assays to explore the effect of LINC01410 on miR-532-5p-mediated GC malignancy and the underlying mechanism involved. MiR-532-5p overexpression inhibited GC metastasis and angiogenesis in vitro and in vivo, whereas miR-532-5p silencing had the opposite effect. Further study showed that miR-532-5p attenuated NF-κB signaling by directly inhibiting NCF2 expression, while miR-532-5p silencing in GC enhanced NF-κB activity. Furthermore, we demonstrated miR-532-5p down-regulation was caused by aberrantly high expression of LINC01410 in GC. Mechanistically, overexpression of LINC01410 promoted GC angiogenesis and metastasis by binding to and suppressing miR-532-5p, which resulted in up-regulation of NCF2 and sustained NF-κB pathway activation. Interestingly, NCF2 could in turn increase the promoter activity and expression of LINC01410 via NF-κB, thus forming a positive feedback loop that drives the malignant behavior of GC. Finally, high expression of LINC01410, along with low expression of miR-532-5p, was associated with poor survival outcome in GC patients. Our studies uncover a mechanism for constitutive LINC1410-miR-532-5p-NCF2-NF-κB feedback loop activation in GC, and consequently, as a potential therapeutic target in GC treatment.

A new numerical method for the analysis of elastic and elastic-plastic contacts of two rough surfaces has been developed. The method is based on a variational principle in which the real area of contact and contact pressure distribution are those which minimize the total complementary potential energy. The present variational approach guarantees the uniqueness of the solution of the contact problem and significantly reduces the computation time as compared with the conventional matrix inversion method, and thus, makes it feasible to solve 3-D contact problem with large number of contact points. The model is extended to elastic-perfectly plastic contacts. The model is used to predict contact statistics for computer generated surfaces.

A numerical method has been developed to account for the micro-meniscus effect of an ultra-thin liquid film on the static friction of rough surface contact. The classical meniscus theory of a single-sphere contact was modified to include the effect of multiple asperity contacts with a pre-existing ultra-thin liquid film during the contact of two rough surfaces. The effect of micro-meniscus formation was considered in terms of elastic - plastic deformation of rough surfaces under applied load, roughness parameters, thickness of liquid film and meniscus height. In the numerical model, elastic - plastic dry contact of rough surfaces is first analysed. In the next step, a liquid film of known mean thickness is introduced over the deformed rough surfaces. Wetted areas are determined by selecting the areas where asperities of both contacting surfaces touch the liquid. The total projected meniscus area is determined by selecting those area islands of cross cut area at a given mean meniscus height which overlap the wetted area. The meniscus force is then calculated using the meniscus equation derived from first principles of the micro-meniscus theory. Two parameters, meniscus height and liquid film thickness, are required for the analysis, which can be obtained for a given relative humidity. However, for a given liquid-film thickness, meniscus height is a function of liquid-film thickness and needs to be estimated. The present numerical method was applied to data-processing magnetic rigid disk drives to analyse the static friction during contact in the presence of an ultra-thin liquid film on one of the surfaces. Trends in numerical predictions correlate well with the measured effect of liquid films on the static friction. The analysis reveals some new insights into the `stiction' problems of disk drives.