Bond strength of concrete patch repairs: an evaluation of test methods and the influence of workmanship and environment

Experiments were carried out to study the effect of workmanship and environmental conditions on bond strength for concrete patch repairs. Four repair materials, sand/cement mortar, acrylic modified cementitious mortar, SBR modified cementitious mortar, and flowing concrete, were tested with mainly three test methods (core pull-off test, patch compressive test, and patch flexural test). At the beginning of this project, slant shear tests were also carried out. In the study of the effect of workmanship, the following parameters were included: surface roughness, surface cleanliness, surface soundness, moisture condition, application method, bond coat mistiming, repair material mistiming, and curing methods. In the study of the effect of environmental conditions, four parameters were considered: high temperature curing followed by drying shrinkage, high temperature curing followed by thermal cycling, low temperature curing, and low temperature curing followed by freeze/thaw cycling. A rougher surface produces a higher bond strength, but the increase depends on individual repair material. Sand/cement mortar favours a rough surface, but polymer modified mortars are not very sensitive to surface roughness. Environmental conditions affect the bond strength development, but the effect varies with each repair material. Test results suggest that low temperature curing should be avoided for polymer modified cementitious mortars. In addition to the experimental study, theoretical analyses were carried out to evaluate the available bond test methods. The evaluation was concentrated on answering the following questions: (1) What kind of factors will influence conductinga bond test? (2) What are the response of each factor involved to a specific test method? (3) What kind of influences are crucial in ensuring the full development of the bond strength? (4) Which factors are important to achieve a durable repair? and (5) What kind of a test can be used to monitor the quality of these crucial factors? In total, about 800 tests were conducted (500 core pull-off tests, 90 patch compressive tests, 100 patch flexural tests, and 80 slant shear tests)

Cross-talk between cuproptosis and ferroptosis regulators defines the tumor microenvironment for the prediction of prognosis and therapies in lung adenocarcinoma

Cuproptosis, a newly identified form of programmed cell death, plays vital roles in tumorigenesis. However, the interconnectivity of cuproptosis and ferroptosis is poorly understood. In our study, we explored genomic alterations in 1162 lung adenocarcinoma (LUAD) samples from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) cohort to comprehensively evaluate the cuproptosis regulators. We systematically performed a pancancer genomic analysis by depicting the molecular correlations between the cuproptosis and ferroptosis regulators in 33 cancer types, indicating cross-talk between cuproptosis and ferroptosis regulators at the multiomic level. We successfully identified three distinct clusters based on cuproptosis and ferroptosis regulators, termed CuFeclusters, as well as the three distinct cuproptosis/ferroptosis gene subsets. The tumor microenvironment cell-infiltrating characteristics of three CuFeclusters were highly consistent with the three immune phenotypes of tumors. Furthermore, a CuFescore was constructed and validated to predict the cuproptosis/ferroptosis pathways in individuals and the response to chemotherapeutic drugs and immunotherapy. The CuFescore was significantly associated with the expression of miRNA and the regulation of post-transcription. Thus, our research established an applied scoring scheme, based on the regulators of cuproptosis/ferroptosis to identify LUAD patients who are candidates for immunotherapy and to predict patient sensitivity to chemotherapeutic drugs

Asymptotic Spectral-Efficiency of MIMO-CDMA Systems with Arbitrary Spatial Correlation

In this contribution, we analyze the asymptotic spectral-efficiency (ASE) of multiuser MIMO-CDMA systems, when assuming communications over flat fading channels with arbitrary spatial correlation. Our analysis is built on the operator-valued free probability theory, which is applied to obtain the limit distribution of the correlation matrix's eigenvalues, as the MIMO-CDMA systems' size tends to infinity. The spectral-efficiency (SE) performance of the MIMO-CDMA systems is investigated via both analysis and simulations. Our simulation and numerical results show that the ASE is capable of providing a good measure of the SE achieved by the corresponding realistic MIMO-CDMA systems

Sismik yüklerin azaltılmasında bazı problemler

In this contribution the asymptotic signal-to-interference-plus-noise ratio (SINR) performance of multicarrier direct-sequence code-division multiple-access systems employing time-frequency-domain spreading, i.e., of the TF/MC DS-CDMA systems, is studied, when separate minimum mean-square error multiuser detection (MMSE-MUD) is considered. The separate MMSE-MUD detects signals first in the time (T)-domain and then in the frequency (F)-domain. Based on random matrix theory, closed-form expressions for the asymptotic SINR of the TF/MC DS-CDMA systems using separate MMSE-MUD is derived, when communicating over additive white Gaussian noise (AWGN) channels. The closed-form expressions show that the asymptotic SINR performance is only depended on the T- and F-domain user load factors as well as noise variance. Hence, they are beneficial to evaluation. Furthermore, our simulation and numerical results show that in most cases the asymptotic SINR can provide a good approximation to the SINR achieved by realistic TF/MC DS-CDMA systems employing separate MMSE-MUD

Image_3_Cross-talk between cuproptosis and ferroptosis regulators defines the tumor microenvironment for the prediction of prognosis and therapies in lung adenocarcinoma.tif

Cuproptosis, a newly identified form of programmed cell death, plays vital roles in tumorigenesis. However, the interconnectivity of cuproptosis and ferroptosis is poorly understood. In our study, we explored genomic alterations in 1162 lung adenocarcinoma (LUAD) samples from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) cohort to comprehensively evaluate the cuproptosis regulators. We systematically performed a pancancer genomic analysis by depicting the molecular correlations between the cuproptosis and ferroptosis regulators in 33 cancer types, indicating cross-talk between cuproptosis and ferroptosis regulators at the multiomic level. We successfully identified three distinct clusters based on cuproptosis and ferroptosis regulators, termed CuFeclusters, as well as the three distinct cuproptosis/ferroptosis gene subsets. The tumor microenvironment cell-infiltrating characteristics of three CuFeclusters were highly consistent with the three immune phenotypes of tumors. Furthermore, a CuFescore was constructed and validated to predict the cuproptosis/ferroptosis pathways in individuals and the response to chemotherapeutic drugs and immunotherapy. The CuFescore was significantly associated with the expression of miRNA and the regulation of post-transcription. Thus, our research established an applied scoring scheme, based on the regulators of cuproptosis/ferroptosis to identify LUAD patients who are candidates for immunotherapy and to predict patient sensitivity to chemotherapeutic drugs.</p

MiRNA 17 family regulates cisplatin-resistant and metastasis by targeting TGFbetaR2 in NSCLC.

MicroRNAs (miRNAs) have been proven to play crucial roles in cancer, including tumor chemotherapy resistance and metastasis of non-small-cell lung cancer (NSCLC). TGFβ signal pathway abnormality is widely found in cancer and correlates with tumor proliferation, apoptosis and metastasis. Here, miR-17, 20a, 20b were detected down-regulated in A549/DDP cells (cisplatin resistance) compared with A549 cells (cisplatin sensitive). Over-expression of miR-17, 20a, 20b can not only decrease cisplatin-resistant but also reduce migration by inhibiting epithelial-to-mesenchymal transition (EMT) in A549/DDP cells. These functions of miR-17, 20a, 20b may be caused at least in part via inhibition of TGFβ signal pathway, as miR-17, 20a, 20b are shown to directly target and repress TGF-beta receptor 2 (TGFβR2) which is an important component of TGFβ signal pathway. Consequently, our study suggests that miRNA 17 family (including miR-17, 20a, 20b) can act as TGFβR2 suppressor for reversing cisplatin-resistant and suppressing metastasis in NSCLC

miR-17, 20a, 20b regulate EMT and migration.

<p>(<b>A</b>) Morphology of A549 and A549/DDP cells with or without miRNAs treatment. (<b>B</b>) mRNA and protein expression levels of E-cadherin and Vimentin in A549 and A549/DDP cells with or without miRNAs treatment were measured by RT-PCR and Western Blotting. (<b>C</b>) Transfer cells in migration assays were detected by transwell-chamber culture systems. Bar graphs show the number of migratory cells. *P<0.05. Results were representative of three experiments.</p

miR-17, 20a, 20b target TGFβR2 by directly binding to the TGFβR2 mRNA 3′-UTR.

<p>(<b>A</b>) Site-directed mutagenesis targeting potential miR-17, 20a, 20b binding sites (MUT) on the TGFβR2 mRNA 3′-UTR-luciferase construct. (<b>B</b>) Luciferase activities significantly decreased in the WT TGFβR2 mRNA 3′-UTR-luciferase plasmid transfected A549 cells after transfection of miR-17, 20a, 20b mimics. Effect was blocked in the MUT plasmid transfected A549 cells. (<b>C</b>) By RT-PCR and Western Blotting, the expression of <i>TGFβR2</i> increased significantly in A549/DDP cells compared with A549 cells. The expression of <i>TGFβR2</i> decreased in A549/DDP cells after transfection of miR-17, 20a, 20b mimics and increased in A549 cells after transfection of miR-17, 20a, 20b inhibitors. *P<0.05. Results were representative of three experiments.</p