This paper demonstrated a flexible humidity sensor based on tin dioxide/reduced graphene oxide (RGO) nanocomposite film. The humidity sensor was fabricated on a polyimide substrate with ...microelectrodes by using a facile one-step hydrothermal route. The hydrothermal synthesized SnO2 nanoparticles and SnO2/RGO hybrid nanostructures were characterized by scanning electron microscopy (SEM) and X-ray diffraction (XRD). The humidity sensing properties of the presented SnO2/RGO nano-hybrid sensor were investigated by exposing it to a broad humidity range of 11–97%RH at room temperature. Compared with traditional humidity sensors, the SnO2 modified graphene sensor demonstrated an ultrahigh sensitivity and a rapid response/recovery characteristic over a full humidity range measurement, highlighting the unique advantages of hydrothermal synthesis for sensors fabrication. Finally, the possible humidity sensing mechanism of the proposed sensor was discussed by using complex impedance spectra and bode diagrams. These observed results demonstrate that RGO modified with metal oxide is promising nanomaterials for constructing high performance humidity sensors in widespread applications.
The chromosome 8q24.21 locus, which contains the proto-oncogene c-MYC, long non-coding RNA PVT1, and microRNAs (miRs), is the most commonly amplified region in human prostate cancer. A long-range ...interaction of genetic variants with c-MYC or long non-coding PVT1 at this locus contributes to the genetic risk of prostate cancer. At this locus is a cluster of genes for six miRs (miR-1204, -1205, -1206, -1207-3p, -1207-5p, and -1208), but their functional role remains elusive. Here the copy numbers and expression levels of miRs-1204-1208 were investigated using quantitative PCR for prostate cancer cell lines and primary tumors. The data revealed that copy numbers and expression of miR-1205 were increased in both castration-resistant prostate cancer cell lines and in primary tumors. In castration-resistant prostate cancer specimens, the copy number at the miR-1205 locus correlated with the expression of miR-1205. Furthermore, functional analysis with an miR-1205 mimic, an miR-1205 inhibitor, and CRISPR/Cas9 knockout revealed that, in human prostate cancer cells, miR-1205 promoted cell proliferation and cell cycle progression and inhibited hydrogen peroxide-induced apoptosis. In these cells, miR-1205 downregulated the expression of the Egl-9 family hypoxia inducible factor 3(EGLN3) gene and targeted a site in its 3'-untranslated region to downregulate its transcriptional activity. Thus, by targeting EGLN3, miR-1205 has an oncogenic role and may contribute to the genetic risk of castration-resistant prostate cancer.
Human tubulin beta class IVa (TUBB4A) is a member of the β-tubulin family. In most normal tissues, expression of TUBB4A is little to none, but it is highly expressed in human prostate cancer. Here we ...show that high expression levels of TUBB4A are associated with aggressive prostate cancers and poor patient survival, especially for African-American men. Additionally, in prostate cancer cells, TUBB4A knockout (KO) reduces cell growth and migration but induces DNA damage through increased γH2AX and 53BP1. Furthermore, during constricted cell migration, TUBB4A interacts with MYH9 to protect the nucleus, but either TUBB4A KO or MYH9 knockdown leads to severe DNA damage and reduces the NF-κB signaling response. Also, TUBB4A KO retards tumor growth and metastasis. Functional analysis reveals that TUBB4A/GSK3β binds to the N-terminal of MYH9, and that TUBB4A KO reduces MYH9-mediated GSK3β ubiquitination and degradation, leading to decreased activation of β-catenin signaling and its relevant epithelial-mesenchymal transition. Likewise, prostate-specific deletion of Tubb4a reduces spontaneous tumor growth and metastasis via inhibition of NF-κB, cyclin D1, and c-MYC signaling activation. Our results suggest an oncogenic role of TUBB4A and provide a potentially actionable therapeutic target for prostate cancers with TUBB4A overexpression.
The tuberous sclerosis complex (TSC)-mammalian target of rapamycin (mTOR) pathway is a key regulator of cellular metabolism. We used conditional deletion of Tsc1 to address how quiescence is ...associated with the function of hematopoietic stem cells (HSCs). We demonstrate that Tsc1 deletion in the HSCs drives them from quiescence into rapid cycling, with increased mitochondrial biogenesis and elevated levels of reactive oxygen species (ROS). Importantly, this deletion dramatically reduced both hematopoiesis and self-renewal of HSCs, as revealed by serial and competitive bone marrow transplantation. In vivo treatment with an ROS antagonist restored HSC numbers and functions. These data demonstrated that the TSC-mTOR pathway maintains the quiescence and function of HSCs by repressing ROS production. The detrimental effect of up-regulated ROS in metabolically active HSCs may explain the well-documented association between quiescence and the "stemness" of HSCs.
Fibrinogen is an extracellular matrix protein composed of three polypeptide chains with fibrinogen alpha (FGA), beta (FGB) and gamma (FGG). Although fibrinogen and its related fragments are involved ...in tumor angiogenesis and metastasis, their functional roles are incompatible. A recent genome-scale screening reveals that loss of
affects the acceleration of tumor growth and metastasis of lung cancer, but the mechanism remains elusive. We used CRISPR/Cas9 genome editing to knockout (KO)
in human lung adenocarcinoma (LUAD) cell lines A549 and H1299. By colony formation, transwell migration and matrix invasion assays,
KO increased cell proliferation, migration, and invasion but decreased the expressions of epithelial-mesenchymal transition marker E-cadherin and cytokeratin 5/8 in A549 and H1299 cells. However, administration of FGA inhibited cell proliferation and migration but induced apoptosis in A549 cells. Of note,
KO cells indirectly cocultured by transwells with
wild-type cells increased FGA in the culture medium, leading to decreased migration of
KO cells. Furthermore, our functional analysis identified a direct interaction of FGA with integrin α5 as well as FGA-integrin signaling that regulated the AKT-mTOR signaling pathway in A549 cells. In addition, we validated that
KO increased tumor growth and metastasis through activation of AKT signaling in an A549 xenograft model. IMPLICATIONS: These findings demonstrate that that loss of
facilities tumor growth and metastasis through the integrin-AKT signaling pathway in lung cancer.
The eHealth Literacy Scale (eHEALS) was introduced in China in 2013 as one of the most important electronic health literacy measurement instruments. After a decade of development in China, it has ...received widespread attention, although its theoretical underpinnings have been challenged, thus demanding more robust research evidence of factorial validity and multigroup measurement properties.
This study aimed to evaluate the Chinese version of the eHEALS in terms of its measurement properties.
A cross-sectional survey was conducted in a university setting in China. Item statistics were checked for response distributions and floor and ceiling effects. Internal consistency reliability was confirmed with Cronbach α, split-half reliability, Cronbach α if an item was deleted, and item-total correlation. A total of 5 representative eHEALS factor structures were examined and contrasted using confirmatory factor analysis. The study used the item-level content validity index (I-CVI) and the average of the I-CVI scores of all items on the scale to assess the content validity of the dominance model. Furthermore, the validated dominance model was subsequently used to evaluate the relevance and representation of elements in the instrument and to assess measurement invariance across genders.
A total of 972 respondents were identified, with a Cronbach α of .92, split-half reliability of 0.88, and item-total score correlation coefficients ranging from 0.715 to 0.781. Cronbach α if an item was deleted showed that all items should be retained. Acceptable content validity was supported by I-CVIs ≥0.80. The confirmatory factor analysis confirmed that the 3-factor model was acceptable. The measurement model met all relevant fit indices: average variance extracted from 0.663 to 0.680, composite reliability from 0.810 to 0.857, chi-square divided by the df of 4.768, root mean square error of approximation of 0.062, standardized root mean squared residual of 0.020, comparative fit index (CFI) of 0.987, and Tucker-Lewis index of 0.979. In addition, the scale demonstrated error variance invariance (Δnormed fit index=-0.016, Δincremental fit index=-0.012, ΔTucker-Lewis index=0.005, Δcomparative fit index=-0.012, Δrelative fit index=0.005, and Δroot mean square error of approximation=0.005).
A 3-factor model of the Chinese version of the eHEALS fits best, and our findings provide evidence for the strict measurement invariance of the instrument regarding gender.
MicroRNA-3662 (miR-3662) is minimally expressed in normal human tissues but is highly expressed in all types of cancers, including breast cancer. As determined with The Cancer Genome Atlas dataset, ...miR-3662 expression is higher in triple-negative breast cancers (TNBCs) and African American breast cancers than in other breast cancer types. However, the functional role of miR-3662 remains a topic of debate. Here, we found that inhibition or knockout of endogenous, mature miR-3662 in TNBC cells suppresses proliferation and migration in vitro and tumor growth and metastasis in vivo. Functional analysis revealed that, for TNBC cells, knockout of miR-3662 reduces the activation of Wnt/β-catenin signaling. Furthermore, using CRISPR-mediated miR-3662 activation and repression, dual-luciferase assays, and miRNA/mRNA immunoprecipitation assays, we established that HMG-box transcription factor 1 (HBP-1), a Wnt/β-catenin signaling inhibitor, is a target of miR-3662 and is most likely responsible for miR-3662-mediated TNBC cell proliferation. Our results suggest that miR-3662 has an oncogenic function in tumor progression and metastasis via an miR-3662-HBP1 axis, regulating the Wnt /β-catenin signaling pathway in TNBC cells. Since miR-3662 expression occurs a tumor-specific manner, it is a promising biomarker and therapeutic target for patients who have TNBCs with dysregulation of miR-3662, especially African Americans.
Numerous smokers are cognizant of the detrimental effects associated with this habit yet exhibit a persistent reluctance to cease their tobacco consumption. Self-exempt beliefs serve as an obstacle ...to the cessation of this addictive behavior. This research explored the impact of self-exempt beliefs on the readiness to quit smoking based on the Protection Motivation Theory (PMT) model and the mediating roles of threat appraisal and coping appraisal.
Self-exempt beliefs, PMT constructs, and the intention to quit smoking constituted the theoretical model. The questionnaires were collected from 488 Chinese adult male smokers based on snowball sampling. Exploratory Factor Analysis (EFA) was used to examine the underlying factor structure of the pre-designed self-exempt beliefs scale. The reliability, validity, path coefficients, and explanatory power of the model were calculated using Partial Least Squares Structural Equation Modeling (PLS-SEM).
The results showed that : (1) three common factors (skeptic beliefs, bulletproof beliefs, and "worth it" beliefs) with a total of 11 items were retained after EFA; (2) skeptic beliefs and "worth it" beliefs had a significantly negative effect on both threat appraisal and coping appraisal, while bulletproof beliefs did not; (3) bulletproof beliefs had a significantly positive direct impact on intention to quit, "worth it" beliefs had a significantly negative direct impact on intention, while skeptic beliefs had no significantly direct impact on intention; (4) threat appraisal and coping appraisal positively and significantly predicted cessation intention; and (5) threat appraisal and coping appraisal, as two main cognitive processes, acted as full mediations between skeptic beliefs and the intention to quit, as complementary partial mediations between "worth it" beliefs and the intention, and as non-mediation between bulletproof beliefs and the intention. Our findings suggest that efforts to undermine or "prevent" these self-exempt beliefs, particularly "worth it" and skeptic beliefs, may be an effective tactic for health communication interventions for quitting smoking.
This paper demonstrates the one-step hydrothermal synthesis of a tin dioxide (SnO
2
)-decorated reduced graphene oxide (RGO) hybrid nanocomposite, which was drop-casted on a polyimide substrate as a ...humidity sensor. The as-synthesized hybrid was characterized in terms of its nanostructural, morphological and compositional features by SEM, XRD and nitrogen sorption. The humidity sensing properties of the presented RGO/SnO
2
hybrid nanocomposite, such as repeatability, stability, response-recovery characteristics, were investigated by exposing it to a broad humidity range of 11–97% RH at room temperature. As a result, the sensor demonstrated a high sensitivity, a good repeatability, an acceptable linearity, a fast response/recovery characteristic and high long-term stability over a full humidity range measurement, indicating the unique advantages of one-step hydrothermal synthesis for sensor fabrication. The possible and proposed sensing mechanism for the sensor is mainly attributed to a humidity-induced transfer of charge carriers occuring at the interfaces and the swelling effect of RGO.
Members of the microRNA (miR)-200 family, which are involved in tumor metastasis, have potential as cancer biomarkers, but their regulatory mechanisms remain elusive.
We investigated FOXP3-inducible ...breast cancer cells, Foxp3 heterozygous Scurfy mutant (Foxp3
) female mice, and patients with breast cancer for characterization of the formation and regulation of the miR-200 family in breast cancer cells and circulation. Participants (259), including patients with breast cancer or benign breast tumors, members of breast cancer families, and healthy controls, were assessed for tumor and circulating levels of the miR-200 family.
First, we identified a FOXP3-KAT2B-miR-200c/141 axis in breast cancer cells. Second, aging Foxp3
female mice developed spontaneous breast cancers and lung metastases. Levels of miR-200c and miR-141 were lower in Foxp3
tumor cells than in normal breast epithelial cells, but plasma levels of miR-200c and miR-141 in the Foxp3
mice increased during tumor progression and metastasis. Third, in patients with breast cancer, the levels of miR-200c and 141 were lower in FOXP3
relative to those with FOXP3
breast cancer cells, especially in late-stage and metastatic cancer cells. The levels of miR-200c and miR-141 were higher in plasma from patients with metastatic breast cancer than in plasma from those with localized breast cancer, with benign breast tumors, with a family history of breast cancer, or from healthy controls. Finally, in Foxp3
mice, plasma miR-200c and miR-141 appeared to be released from tumor cells.
miR-200c and miR-141 are regulated by a FOXP3-KAT2B axis in breast cancer cells, and circulating levels of miR-200c and miR-141 are potential biomarkers for early detection of breast cancer metastases.
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