Research on the Influence of Tool Surface Texture on Cutting Performance Based on Finite Element Method.

As research progresses, the surface texture tool can significantly reduce the cutting heat and cutting force. However, the tool surface texture width, depth, and spacing also have an impact on the cutting performance. Using the Taguchi method and finite element analysis, the changing laws of cutting temperature, pressure, stress distribution, and cutting force were studied. The results showed that the tool texture width had the greatest influence on the cutting performance, followed by the tool texture depth and spacing. The increase of tool texture width lead to the decrease of cutting temperature, stress distribution, and cutting force, while the effect of texture depth on cutting stress distribution was more significant. Cutting performance could be improved by optimizing the texture size and structure of the cutting tool. This research has theoretical significance for improving the cutting performance of cutting tools.

Study on the Formation Mechanism of Cutting Dead Metal Zone for Turning AISI4340 with Different Chamfering Tools.

Tools with chamfered edges are often used in high speed machining of hard materials because they provide compelling cutting toughness and reduced tool wear. Chamfered tools are also responsible for the dead metal zone (DMZ). Through numerical simulation of orthogonal cutting with AISI 4340 steel, this paper examines the mechanism of the DMZ, the cutting speed, the impacts of the chamfer angle, and the coefficient of friction on the generation of the DMZ. The analysis is based upon the Arbitrary Lagrangian-Eulerian (ALE) finite element method (FEM) for the continuous process of chip formation. The different chamfered angles, cutting speeds, and friction coefficient conditions are utilized in the simulation. The research demonstrates that a zone of trapped material called DMZ has been formed beneath the chamfer and serves as an effective cutting edge of the tool. Additionally, the dead metal zone DMZ becomes smaller while the cutting speed increases or the friction coefficient decreases. The machining forces rise with increasing chamfer angles, rise with increasing friction coefficients, and fall with increasing cutting speed in both the cutting and thrust directions. In this paper, the effect of different chamfering tools on AISI 4340 steel using carbide tools in the simulation environment is studied. It has certain reference significance for studying the formation mechanism of the dead zone of difficult-to-machine materials such as AISI4340 and improving the processing efficiency and workpiece surface quality.

Lemur tyrosine kinase 2 silencing inhibits the proliferation of gastric cancer cells by regulating GSK-3ß phosphorylation and ß-catenin nuclear translocation.

Previous studies on the mechanism of proliferation and cell cycle progression of gastric cancer cells have shown promising perspectives for the prevention and treatment of gastric cancer. The aim of the present study was to investigate the role of lemur tyrosine kinase 2 (LMTK2) in gastric cancer cell proliferation and cell cycle progression, as well as in tumor-bearing nude mouse models. The expression levels of LMTK2 were determined in gastric cancer cell lines. In addition, the effects of LMTK2 silencing or overexpression on cell proliferation were measured using Cell Counting Kit-8, BrdU and colony formation assays. Cell cycle progression was analyzed using flow cytometry and western blotting. The expression levels of proteins associated with the ß-catenin pathway were assessed using western blot analysis. A tumor-bearing nude mouse model was established by injecting gastric cancer cells, and the effect of LMTK2 knockdown or overexpression on tumor growth was examined. The expression levels of LMTK2 were found to be upregulated in all gastric cancer cell lines. Moreover, LMTK2 knockdown inhibited cell proliferation, colony formation and cell cycle progression. LMTK2 knockdown also inhibited the activation of GSK-3ß/ß-catenin signaling, as evidenced by reduced GSK-3ß phosphorylation and nuclear ß-catenin levels. LMTK2 knockdown also suppressed tumor growth, whereas overexpression accelerated this process. In conclusion, LMTK2 silencing can inhibit the proliferation of gastric cancer cells in vitro and tumor growth in vivo by regulating GSK-3ß phosphorylation and ß-catenin nuclear translocation.

Electrochemical CYFRA21-1 DNA sensor with PCR-like sensitivity based on AgNPs and cascade polymerization.

In this work, a new method of CYFRA21-1 DNA (tDNA) detection based on electrochemically mediated atom transfer radical polymerization (e-ATRP) and surface-initiated reversible addition-fragmentation chain transfer polymerization (SI-RAFT) cascade polymerization and AgNP deposition is proposed. Firstly, the peptide nucleic acid (PNA) probe is captured on a gold electrode by Au-S bonds for specific recognition of tDNA. After hybridization, PNA/DNA strands provide high-density phosphate groups for the subsequent ATRP initiator by the identified carboxylate-Zr4+-phosphate chemistry. Then, a large number of monomers are successfully grafted from the DNA through the e-ATRP reaction. After that, the chain transfer agent of SI-RAFT and methacrylic acid (MAA) are connected by recognized carboxylate-Zr4+-carboxylate chemistry. Subsequently, through SI-RAFT, the resulting polymer introduces numerous aldehyde groups, which could deposit many AgNPs on tDNA through silver mirror reaction, causing significant amplification of the electrochemical signal. Under optimal conditions, this designed method exhibits a low detection limit of 0.487 aM. Moreover, the method enables us to detect DNA at the level of PCR-like and shows high selectivity and strong anti-interference ability in the presence of serum. It suggests that this new sensing signal amplification technology exhibits excellent potential of application in the early diagnosis of non-small cell lung cancer (NSCLC). Graphical abstract Electrochemical detection principle for CYFRA21-1 DNA based on e-ATRP and SI-RAFT signal amplification technology.

Polysaccharide-enhanced ARGET ATRP signal amplification for ultrasensitive fluorescent detection of lung cancer CYFRA 21-1 DNA.

An ultrasensitive fluorescence biosensor for detecting cytokeratin fragment antigen 21-1 (CYFRA 21-1) DNA of non-small cell lung carcinoma (NSCLC) is designed using polysaccharide and activator regenerated by electron transfer atom transfer radical polymerization (ARGET ATRP) signal amplification strategy. Thiolated peptide nucleic acid (PNA) is fixed on magnetic nanoparticles (MNPs) by a cross-linking agent and hybridized with CYFRA 21-1 DNA. Hyaluronic acid (HA) is linked to PNA/tDNA heteroduplexes in the form of carboxy-Zr4+-phosphate. Subsequently, multiple 2-bromo-2-methylpropionic acid (BMP) molecules are linked with HA to initiate ARGET ATRP reaction. Finally, a large number of fluorescein o-acrylate (FA) monomers are polymerized on the macro-initiators, and the fluorescence signal is significantly amplified. Under optimal conditions, this biosensor shows a significant linear correlation between the fluorescence intensity and logarithm of CYFRA 21-1 DNA concentration (0.1 fM to 0.1 nM), and the limit of detection is as low as 78 aM. Furthermore, the sensor has a good ability to detect CYFRA 21-1 DNA in serum samples and to recognize mismatched bases. It suggests that the strategy has broad application in early diagnosis by virtue of its high sensitivity and selectivity. Graphical abstract A novel and highly sensitive fluorescence biosensor for quantitatively detecting CYFRA 21-1 DNA via dual signal amplification of hyaluronic acid and ARGET ATRP reaction was developed. This proposed method has a low detection limit, wide detection range, high selectivity, and strong anti-interference.

CuBr2/EDTA-mediated ATRP for ultrasensitive fluorescence detection of lung cancer DNA.

In this paper, we reported a system for the ultrasensitive fluorescence detection of cytokeratin fragment antigen 21-1 DNA (CYFRA21-1 DNA) for the early diagnosis of lung cancer. The approach used electron transfer atom transfer radical polymerization (ARGET-ATRP) with ethylenediaminetetraacetic acid (EDTA) as the metal ligand. Firstly, thiolated peptide nucleic acid (PNA) was linked to aminated magnetic beads solutions (MBs) by a cross-linking agent and then hybridized with CYFRA21-1 DNA (tDNA). Subsequently, Zr4+ was introduced into the MBs by conjugating with the phosphate group of tDNA, and the initiator of ARGET-ATRP was introduced into via phosphate-Zr4+-carboxylate chemistry. Next, Cu(II)Br/EDTA was reduced to Cu(I)/EDTA by ascorbic acid (AA) to trigger ARGET-ATRP and then a large amount of fluorescein-o-acrylate (FA) molecules were grafted from the surface of the MBs, which amplified significantly the fluorescent signal. Under optimal conditions, a strong linear relationship of tDNA over the range from 0.1 fM to 1 nM (R2 = 0.9988). The limit of detection was as low as 23.8 aM (~143 molecules). The fluorescence detection based on the ARGET-ATRP strategy yielded excellent sensitivity, selectivity, outstanding anti-interference properties, and cost-effectiveness. These results indicated that this strategy has considerable potential for biological detection and early clinical diagnosis.

A Fluorescent Sensor Based on Reversible Addition-Fragmentation Chain Transfer Polymerization for the Early Diagnosis of Non-small Cell Lung Cancer.

We propose a novel, ultrasensitive and low-cost sensor using reversible addition-fragmentation chain transfer (RAFT) polymerization as a signal amplification strategy for the detection of CYFRA 21-1 DNA fragment, a tumor marker of non-small cell lung carcinoma. The peptide nucleic acid (PNA) probes were firstly immobilized on magnetic beads (MBs) to capture the CYFRA 21-1 DNA specifically. After hybridization, CPAD was tethered to the hetero duplexes through carboxylate-Zr4+-phosphate chemistry. Subsequently, a number of fluorescent tags were introduced to the heteroduplexes through RAFT polymerization, leading to an amplification of the fluorescence signal. The sensor demonstrates a low limit of detection (LOD) of 0.02 fM. It has great selectivity with respect to base mismatch DNA, and high anti-interference ability in normal human serum. Overall findings of the study suggest that proposed sensor holds enormous potential to be used as a tool for the early-stage diagnosis of lung cancers.

FBXL3 is regulated by miRNA-4735-3p and suppresses cell proliferation and migration in non-small cell lung cancer.

Non-small cell lung cancer (NSCLC) is the most common type of primary lung cancer and regarded as cancer killer. The aim of this study was to discover the detailed function and molecular mechanism of F-box and leucine rich repeat protein 3 (FBXL3) in NSCLC. In this study, the expression level of FBXL3 in NSCLC tissues and cell lines was firstly examined and identified. Moreover, the relationship between FBXL3 and the overall survival rate of NSCLC patients was analyzed by Kaplan-Meier survival curve. Functionally, MTT, colony formation assay and transwell assays were performed to determine the role of FBXL3 in regulating NSCLC cell proliferation, migration and invasion. The proliferation and migration were suppressed by overexpression of FBXL3, indicating the potential tumor suppressive role of FBXL3 in NSCLC. In addition, the dual-luciferase reporter and RNA pull-down assays revealed that miR-4735-3p was a novel upstream modulator of FBXL3. Further study showed that miR-4735-3p was upregulated in NSCLC tissues and cell lines. Finally, rescue assays and function assays revealed that miR-4735-3p exerted oncogenic function in NSCLC, and this function can be attenuated by FBXL3. Taken together, FBXL3 was regulated by miR-4735-3p and suppressed cell proliferation and invasion in non-small cell lung cancer.

Decreased Expression of miR-138-5p by lncRNA H19 in Cervical Cancer Promotes Tumor Proliferation.

MicroRNAs (miRNAs) play important roles in the carcinogenesis of cervical cancer. However, the expression and underlying mechanisms of miRNA in cervical cancer progression remain unclear. In the present study, our data showed that the expression of miR-138-5p was significantly downregulated in cervical cancer tissues, and decreased expression of miR-138-5p was correlated with advanced FIGO stage, poor differentiation, lymph node metastasis, and poor overall survival of cervical cancer patients. Function assays showed that overexpression of miR-138-5p reduced cervical cancer cell proliferation, arrested cells in the G0/G1 phase, and induced cell apoptosis in vitro. Remarkably, SIRT1 was confirmed as a direct target of miR-138-5p in cervical cancer, and miR-138-5p exerted the reduced tumor functions by suppressing SIRT1 expression. Moreover, we further identified that lncRNA H19 could act as a molecular sponge of miR-138-5p in cervical cancer progression. Taken together, these results suggested that miR-138-5p could suppress cervical cancer cell progression by targeting SIRT1.

Effect and Mechanism of Resveratrol on the Apoptosis of Lung Adenocarcinoma Cell Line A549.

Lung adenocarcinoma is the most common subtype of non-small cell lung cancer and the leading cause of cancer death worldwide. In this study, we investigated the effect of resveratrol (Res) on lung adenocarcinoma A549 cells and its potential mechanism. We found after Res treatment, the interspace of A549 cells decreased and granular material increased in the cell nucleus. These changes were remarkably correlated with the increased concentration of Res. Res induces apoptosis in A549 cells and inhibits cell proliferation in a dose-dependent manner. We further showed that after Res treatment, expression of p53, Bax, and cleaved caspase-3 protein was dramatically up-regulated, while expression of Bcl-2 and the ratio of Bcl-2/Bax were down-regulated. Our study demonstrates that Res inhibits proliferation and induces apoptosis of A549 cells through regulation of p53, Bax, Bcl-2, and cleaved caspase-3 expression.