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Triple-negative breast cancer (TNBC) is highly aggressive and metastatic, and has the poorest prognosis among all breast cancer subtypes. Activated β-catenin is enriched in TNBC and involved in Wnt signaling-independent metastasis. However, the underlying mechanisms of β-catenin activation in TNBC remain unknown. Here, we found that SHC4 was upregulated in TNBC and high SHC4 expression was significantly correlated with poor outcomes. Overexpression of SHC4 promoted TNBC aggressiveness in vitro and facilitated TNBC metastasis in vivo. Mechanistically, SHC4 interacted with Src and maintained its autophosphorylated activation, which activated β-catenin independent of Wnt signaling, and finally upregulated the transcription and expression of its downstream genes CD44 and MMP7. Furthermore, we determined that the PxPPxPxxxPxxP sequence on CH2 domain of SHC4 was critical for SHC4-Src binding and Src kinase activation. Overall, our results revealed the mechanism of β-catenin activation independent of Wnt signaling in TNBC, which was driven by SHC4-induced Src autophosphorylation, suggesting that SHC4 might be a potential prognostic marker and therapeutic target in TNBC. • SHC4 is upregulated in TNBC and associated with poor prognosis. • SHC4 promotes TNBC aggressiveness in vitro and facilitates TNBC metastasis in vivo. • SHC4 binds and activates Src kinase by promoting its autophosphorylation at Y419. • SHC4 PxPPxPxxxPxxP is the key sequence for activating Src kinase. • Deletion of the PxPPxPxxxPxxP sequence inhibits TNBC progression. [ABSTRACT FROM AUTHOR]

The emergence and dissemination of antibiotic-resistant bacterial pathogens have spurred the urgent need to develop novel antimicrobial agents with different mode of action. In this respect, we turned several fusogenic peptides ( FPs) derived from the hemagglutinin glycoproteins ( HAs) of IAV into potent antibacterials by replacing the negatively or neutrally charged residues of FPs with positively charged lysines. Their antibacterial activities were evaluated by testing the MICs against a panel of bacterial strains including S. aureus, S. mutans, P. aeruginosa, and E. coli. The results showed that peptides HA- FP-1, HA- FP-2-1, and HA- FP-3-1 were effective against both Gram-positive and Gram-negative bacteria with MICs ranging from 1.9 to 16.0 μ m, while the toxicities toward mammalian cells were low. In addition, the mode of action and the secondary structure of these peptides were also discussed. These data not only provide several potent peptides displaying promising potential in development as broad antimicrobial agents, but also present a useful strategy in designing new antimicrobial agents. [ABSTRACT FROM AUTHOR]

Abstract: The use of cavitational means to create transient membrane pores on living cells (i.e., sonoporation) may potentially induce a broad range of downstream bio-effects that disrupt the functioning of various organelles. Here we observed that on HL-60 leukemia cells, sonoporation may induce endoplasmic reticulum (ER) stress on a time-lapse basis and, in turn, signal the mitochondria to commit a cell toward apoptosis. Our observations were derived from in vitro ultrasound exposure experiments performed on HL-60 cells in the presence of lipid-shelled microbubbles (1:1 cell-to-bubble ratio; 1-MHz frequency; 0.45-MPa in situ peak negative pressure; 100-cycle pulse length; 1-kHz pulse repetition frequency; 60-s exposure period). Using flow cytometry, we found that sonoporated cells exhibited a progressive loss of functional ER mass over a 6-h period. Also, post-exposure Western blot assays (between 0 and 24 h) revealed various indications of post-sonoporation ER stress: (i) upregulation of ER-resident enzymes responsible for catalyzing protein folding; (ii) activation of trans-ER-membrane stress sensors; (iii) increased expression of ER-induced regulatory proteins that mediate pro-apoptotic signals to the mitochondria. These results corresponded to flow cytometry observations that depicted a progressive depolarization of a sonoporated cell’s mitochondrial outer membrane potential. They were also consistent with another Western blot assay that found, in sonoporated cells, a time-lapse increase of caspase-9 (a mitochondria-activated apoptosis initiator protein). Taken together, our findings indicate that sonoporation may upset ER homeostasis, and this may ultimately result in initiation of apoptosis. [Copyright &y& Elsevier]

Abstract: Neuronal development is known to be a dynamic process that can be modulated by presenting guidance cues to neuronal cells. We show that ultrasound, when applied at pulsed settings and with intensities slightly greater than clinical diagnosis levels, can potentially act as a repulsive cue for modulating neuronal growth dynamics. Using differentiated Neuro-2a cells as the model, we have examined in vitro how neuronal development can change during and after exposure to 1-MHz ultrasound for different acoustic settings. Neurite retraction and cell body shrinkage were found in neuronal cells over a 10-min exposure period with 1.168 W/cm2 spatial-peak, time-averaged intensity (based on 0.84 MPa peak acoustic pressure, 100-cycle pulse duration, and 500-Hz pulse repetition frequency). These effects were found to result in instances of neuronal cell body displacement. The extent of the effects was dependent on acoustic intensity, with peak acoustic pressure being a more important contributing factor compared with pulse duration. The morphological changes were found to be non-destructive, in that post-exposure neurite outgrowth and neuritogenesis were respectively observed in neurite-bearing and neurite-less neuronal cells. Our results also showed that mechanotransduction might be involved in mediating ultrasound-neuron interactions, as the morphological changes were suppressed if stretch-activated ion channels were blocked or if calcium messenger ions were chelated. Overall, these findings suggest that ultrasound can potentially influence how neuronal cells develop through modifying their cytomechanical characteristics. [Copyright &y& Elsevier]

Abstract: Despite being a transient biophysical phenomenon, sonoporation is known to disturb the homeostasis of living cells. This work presents new evidence on how sonoporation may lead to antiproliferation effects including cell-cycle arrest and apoptosis through disrupting various cell signaling pathways. Our findings were obtained from sonoporation experiments conducted on HL-60 human promyelocytic leukemia cells (with 1% v/v microbubbles; 1 MHz ultrasound; 0.3 or 0.5MPa peak negative pressure; 10% duty cycle; 1 kHz pulse repetition frequency; 1 min exposure period). Membrane resealing in these sonoporated cells was first verified using scanning electron microscopy. Time-lapse flow cytometry analysis of cellular deoxyribonucleic acid (DNA) contents was then performed at four post-sonoporation time points (4 h, 8 h, 12 h and 24 h). Results indicate that an increasing trend in the apoptotic cell population can be observed for at least 12 h after sonoporation, whilst viable sonoporated cells are found to temporarily accumulate in the G2/M (gap-2/mitosis) phase of the cell cycle. Further analysis using western blotting reveals that sonoporation-induced apoptosis involves cleavage of poly adenosine diphosphate ribose polymerase (PARP) proteins: a pro-apoptotic hallmark related to loss of DNA repair functionality. Also, mitochondrial signaling seems to have taken part in triggering this cellular event as the expression of two complementary regulators for mitochondrial release of pro-apoptotic molecules, Bcl-2 (B-cell lymphoma 2) and Bax (Bcl-2-associated X), are seen to be imbalanced in sonoporated cells. Furthermore, sonoporation is found to induce cell-cycle arrest through perturbing the expression of various cyclin and Cdk (cyclin-dependent kinase) checkpoint proteins that play an enabling role in cell-cycle progression. These bioeffects should be taken into account when using sonoporation for therapeutic purposes. [Copyright &y& Elsevier]

To test early-gestation human placenta, a human trophoblast cell line, mouse eggs, preimplantation embryos, and a mouse trophoblast cell line for the expression of mRNA transcripts for stress-activated protein kinase/c-Jun N-terminal kinase (SAPKγ/JNK1, SAPKα/JNK2, and SAPKβ/JNK3).Whole RNA was isolated from the tissue sources listed above and control tissues, and reverse transcription–polymerase chain reaction (RT-PCR) was performed to assay for the qualitative and semiquantitative presence of SAPKγ/JNK1, SAPKα/JNK2, and SAPKβ/JNK3.None.None.None.The presence and magnitude of amplimer amounts in gels or gene hybridization on Affymetrix cDNA arrays of RT-PCR products of reactions for SAPKγ/JNK1, SAPKα/JNK2, and SAPKβ/JNK3.SAPKγ/JNK1 and SAPKα/JNK2 mRNA transcripts are present in early-gestation human placenta, a human trophoblast cell line, mouse eggs, preimplantation embryos, and a mouse trophoblast cell line at levels similar to positive control levels. SAPKα/JNK2 is expressed at the highest level of the three transcripts in the family. SAPKβ/JNK3 is present at levels that are 1/100–1/1,000 those of the positive control and in some cases at the apparent level of the negative control (previously measured by the less-sensitive Northern blot analysis). Analysis with an Affymetrix cDNA array suggested that SAPKα/JNK2 and 38 kDa mitogen-activated protein kinase had the highest mRNA expression measured for each of three family members.Mitotic placental trophoblast cell lines and primary conceptus/embryo samples containing early placental trophoblasts express SAPKα/JNK2 at higher levels than SAPKγ/JNK1, but not (only low background levels of) SAPKβ/JNK3 mRNA transcripts. This suggests that SAPKγ/JNK1 and SAPKα/JNK2 may be important mediators of stress-induced responses in early implanting conceptuses that could mediate embryo loss. [Copyright &y& Elsevier]

Breast cancer (BC) is a common malignancy that affects women worldwide. Although transducing beta‐like 2 (TBL2), a member of the WD40 repeat protein family, has been implicated in various intracellular signaling pathways, its precise function in BC remains unclear. The expression of TBL2 is analyzed using real‐time PCR, western blotting, and immunohistochemistry in BC patient specimens. Kaplan–Meier survival analysis is employed to assess its prognostic significance. Proteomic analysis, immunoprecipitation tests, and protein immunoblotting are employed to examine the impact of TBL2 on AKT phosphorylation activation. The findings reveal selective overexpression of TBL2 in BC, correlating significantly with various clinicopathological characteristics and poor survival outcomes in patients with BC. Through in vivo and in vitro experiments, it is observed that TBL2 suppression inhibits BC cell proliferation, while TBL2 overexpression has the opposite effect. Mechanistically, TBL2 is identified as a scaffolding protein that promotes PRMT5 and WDR77 interaction. This interaction enhances the methyltransferase activity of PRMT5, leading to increased AKT phosphorylation activation and promotion of breast cancer cell proliferation. In conclusion, this study uncovers a novel function of TBL2 in the activation of AKT by PRMT5 and suggests TBL2 as a potential therapeutic target for BC treatment. [ABSTRACT FROM AUTHOR]

This paper presents an event-triggered sliding mode fault-tolerant control method for networked control systems with actuator faults and external disturbance. First, an event-triggered scheme in the networked control systems is proposed to reduce the number of data transmission. In addition, considering the event-triggering, a sliding mode surface based on the system structure is constructed. Besides, to obtain the controller parameters that meet the H ∞ performance, the bounded real lemma in the form of linear matrix inequality is obtained using the Lyapunov functional. In addition, a sliding mode fault-tolerant control is designed to guarantee that the system can still run stably under the condition of faults and disturbances. Finally, the simulation results of gas turbine system are given to verify the feasibility of the theoretical method. [ABSTRACT FROM AUTHOR]

Background: Triple-negative breast cancer (TNBC) is resistant to targeted therapy with HER2 monoclonal antibodies and endocrine therapy, because it lacks the estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2). TNBC is a subtype of breast cancer with the worst prognosis and the highest mortality rate compared to other subtypes. N6-methyladenosine (m6A) modification is significant in cancer and metastasis, because it can alter gene expression and function at numerous levels, such as RNA splicing, stability, translocation, and translation. There are limited investigations into the connection between TNBC and m6A. Materials and methods: Breast cancer-related data were retrieved from the Cancer Genome Atlas (TCGA) database, and 116 triple-negative breast cancer cases were identified from the data. The GSE31519 data set, which included 68 cases of TNBC, was obtained from the Gene Expression Omnibus (GEO) database. Survival analysis was used to determine the prognosis of distinct m6A types based on their m6A group, gene group, and m6A score. To investigate the potential mechanism, GO and KEGG analyses were performed on the differentially expressed genes. Results: The expression of m6A-related genes and their impact on prognosis in TNBC patients were studied. According to the findings, m6A was crucial in determining the prognosis of TNBC patients, and the major m6A-linked genes in this process were YTHDF2, RBM15B, IGFBP3, and WTAP. YTHDF2, RBM15B and IGFBP3 are associated with poor prognosis, while WTAP is associated with good prognosis. By cluster analysis, the gene cluster and the m6A cluster were beneficial in predicting the prognosis of TNBC patients. The m6A score based on m6A and gene clusters was more effective in predicting the prognosis of TNBC patients. Furthermore, the tumor microenvironment may play an important role in the process of m6A, influencing TNBC prognosis. Conclusions: N6-adenylic acid methylation (m6A) was important in altering the prognosis of TNBC patients, and the key m6A-associated genes in this process were YTHDF2, RBM15B, IGFBP3, and WTAP. Furthermore, the comprehensive typing based on m6A and gene clusters was useful in predicting TNBC patients' prognosis, showing potential as valuable evaluating tools for TNBC. [ABSTRACT FROM AUTHOR]

Highlights: [•] Sonoporation reduced polyunsaturated fatty acids and cholesterol of Jurkat cells. [•] Sonoporation showed delayed apoptosis in Jurkat cells. [•] Sonoporation of Jurkat cells increased oxidized lipid products. [•] Generation of oxidized lipid products are non-enzyme dependent. [•] Sonoporation elevated antioxidant enzyme activity. [ABSTRACT FROM AUTHOR]

Background: Host immunity plays an important role in tumor development and treatment. Tumor‐infiltrating lymphocytes (TILs) have been proven to predict the efficacy of neoadjuvant therapy (NAT) in breast cancer (BC) patients, but their application is limited due to various reasons. This study aims to explore the relationship between peripheral blood lymphocytes (PBLs) subsets distribution and the efficacy of NAT. Methods: Between December 2017 and March 2021, a total of 116 BC patients appropriate for NAT in Sun Yat‐Sen University cancer center were enrolled, pre‐NAC baseline blood samples were taken for further flow cytometry analysis to quantitatively evaluate the PBLs subsets distribution, and corresponding clinical information including pathological complete response (pCR) rate of NAT response were recorded. Results: Baseline CD3+ T cells(OR 1.11, 1.03–1.21, p = 0.011), CD8+ T cells (OR 1.09, 1.02–1.18, p = 0.015), and NK cells (OR 0.91, 0.83–0.98, p = 0.028) in PBLs subgroup distribution were independent predictors of pCR in BC patients receiving NAT, in which CD8+ T cells had the highest predictive ability (AUC = 0.76). Compared with some previous prediction indicators, its prediction ability has been improved to some extent. Conclusion: Peripheral baseline CD3+ T cells, CD8+ T cells, and NK cells were independent predictors of pCR in BC patients receiving NAT, in which CD8+ T cells had the highest predictive ability. Therefore, it can provide newly non‐invasive, relatively accurate and easily accessible predictors for corresponding patients, and help clinicians better understand tumor immunity. [ABSTRACT FROM AUTHOR]

Abstract: The interaction between ultrasound pulses and microbubbles is known to generate acoustic cavitation that may puncture biological cells. This work presents new experimental findings on the bioeffects of ultrasound-microbubble mediated cavitation in plant cells with emphasis on direct observations of morphological impact and analysis of viability trends in tobacco BY-2 cells that are widely studied in higher plant physiology. The tobacco cell suspensions were exposed to 1 MHz ultrasound pulses in the presence of 1% v/v microbubbles (10% duty cycle; 1 kHz pulse repetition frequency; 70 mm between probe and cells; 1-min exposure time). Few bioeffects were observed at low peak negative pressures (<0.4 MPa) where stable cavitation presumably occurred. In contrast, at 0.9 MPa peak negative pressure (with more inertial cavitation activities according to our passive cavitation detection results), random pores were found on tobacco cell wall (observed via scanning electron microscopy) and enhanced exogenous uptake into the cytoplasm was evident (noted in our fluorescein isothiocyanate dextran uptake analysis). Also, instant lysis was observed in 23.4% of cells (found using trypan blue staining) and programmed cell death was seen in 23.3% of population after 12 h (determined by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling [TUNEL]). These bioeffects generally correspond in trend with those for mammalian cells. This raises the possibility of developing ultrasound-microbubble mediated cavitation into a targeted gene transfection paradigm for plant cells and, conversely, adopting plant cells as experimental test-beds for sonoporation-based gene therapy in mammalian cells. [Copyright &y& Elsevier]

Triple‐negative breast cancer (TNBC) is fast‐growing and highly metastatic with the poorest prognosis among the breast cancer subtypes. Inactivation of glycogen synthase kinase 3 beta (GSK3β) plays a vital role in the aggressiveness of TNBC; however, the underlying mechanism for sustained GSK3β inhibition remains largely unknown. Here, we find that protein phosphatase 1 regulatory inhibitor subunit 14C (PPP1R14C) is upregulated in TNBC and relevant to poor prognosis in patients. Overexpression of PPP1R14C facilitates cell proliferation and the aggressive phenotype of TNBC cells, whereas the depletion of PPP1R14C elicits opposite effects. Moreover, PPP1R14C is phosphorylated and activated by protein kinase C iota (PRKCI) at Thr73. p‐PPP1R14C then represses Ser/Thr protein phosphatase type 1 (PP1) to retain GSK3β phosphorylation at high levels. Furthermore, p‐PPP1R14C recruits E3 ligase, TRIM25, toward the ubiquitylation and degradation of non‐phosphorylated GSK3β. Importantly, the blockade of PPP1R14C phosphorylation inhibits xenograft tumorigenesis and lung metastasis of TNBC cells. These findings provide a novel mechanism for sustained GSK3β inactivation in TNBC and suggest that PPP1R14C might be a potential therapeutic target. [ABSTRACT FROM AUTHOR]

Recent studies suggest that desmoid tumors can be managed more conservatively rather than undergoing wide surgical resection (SR). Ultrasound-guided vacuum-assisted biopsy (UGVAB) is a minimally invasive technique. This retrospective study aimed to compare the outcome in patients with breast desmoid tumor (BDT) who received UGVAB alone versus SR. The pathology database was searched for patients diagnosed with BDT ≤ 3 cm from 2007 to 2019. All patients underwent breast ultrasound examination and were then performed UGVAB alone or local SR. The Kaplan–Meier method with a log-rank test was used as a univariate analysis to compare the relapse-free survival (RFS) rates between UGVAB and SR groups. Cox regression analysis was used for multivariate analysis. A total of 39 patients were included. The median follow-up was 41 mo (range, 5-110 mo). The incidence of tumor recurrence was 23.1% (9/39). The 3-y cumulative RFS was 83.1% and 95.8% in the UGVAB and SR group, respectively, which was not significantly different between the two groups (P = 0.131, log-rank test). Multivariate analysis also revealed that treatment strategy (UGVAB versus SR) was not associated with an increased risk of relapse events (P = 0.274). Small desmoid tumors (≤3 cm) after UGVAB alone did not have a significantly compromised RFS compared with those who underwent SR. UGVAB may be an alternative and relatively conservative method for the diagnosis and local control of BDT with a smaller size. A prospective, randomized study with large sample size is needed to confirm this observation. • The treatment of breast desmoid tumors can be more conservatively. • Radical surgery may result in complication in some patients. • Ultrasound-guided vacuum-assisted biopsy is widely used in breast benign tumors. • Ultrasound-guided vacuum-assisted biopsy is an option for breast desmoid tumor patient. [ABSTRACT FROM AUTHOR]

Background: Although both circular RNAs (circRNAs) and autophagy are associated with the function of breast cancer (BC), whether circRNAs regulate BC progression via autophagy remains unknown. In this study, we aim to explore the regulatory mechanisms and the clinical significance of autophagy-associated circRNAs in BC. Methods: Autophagy associated circRNAs were screened by circRNAs deep sequencing and validated by qRT-PCR in BC tissues with high- and low- autophagic level. The biological function of autophagy associated circRNAs were assessed by plate colony formation, cell viability, transwells, flow cytometry and orthotopic animal models. For mechanistic study, RNA immunoprecipitation, circRNAs pull-down, Dual luciferase report assay, Western Blot, Immunofluorescence and Immunohistochemical staining were performed. Results: An autophagy associated circRNA circCDYL was elevated by 3.2 folds in BC tissues as compared with the adjacent non-cancerous tissues, and circCDYL promoted autophagic level in BC cells via the miR-1275-ATG7/ULK1 axis; Moreover, circCDYL enhanced the malignant progression of BC cells in vitro and in vivo. Clinically, increased circCDYL in the tumor tissues and serum of BC patients was associated with higher tumor burden, shorter survival and poorer clinical response to therapy. Conclusions: circCDYL promotes BC progression via the miR-1275-ATG7/ULK1-autophagic axis and circCDYL could act as a potential prognostic and predictive molecule for breast cancer patients. [ABSTRACT FROM AUTHOR]

Purpose: Glutamine (Gln) is essential for the proliferation of most cancer cells, making it an appealing target for cancer therapy. However, the role of Gln in gastric cancer (GC) metabolism is unknown and Gln-targeted therapy against GC remains scarce. The aim of this study was to investigate the relevance of Gln in GC growth and targeting.Methods: Expression of Gln transporter ASCT2 and glutamine synthetase (GS) in the parental and molecularly engineered GC cells or in human GC specimens was determined by RT-PCR and western blot analysis or immunohistochemistry. Cell proliferation and survival was assessed by CCK-8 assay and colony formation assay. Intracellular Gln content was measured by a HPLC system. Effects of ASCT2 and/or GS inhibitor on tumor growth were investigated in xenograft models.Results: A significant heterogeneity of GC cells was observed with respect to their response to the treatment of ASCT2 inhibitor benzylserine (BenSer). Gln deprivation did not affect the BenSer-resistant cell growth due to endogenous GS expression, whose inhibition remarkably reduced cell proliferation. The differential in vitro sensitivity correlated with overall intracellular Gln content. Combined therapy with both ASCT2 and GS inhibitors produced a greater therapeutic efficacy than the treatment of either inhibitor alone. Furthermore, 77% human GC tissues were found to express moderate and high levels of ASCT2, 12% of which also co-expressed relatively high levels of GS.Conclusion: Gln mediates GC growth and the therapeutic efficacy of Gln-targeted treatment relies on distinct ASCT2 and GS expression pattern in specific gastric cancer groups. [ABSTRACT FROM AUTHOR]

Non-mass breast lesions on ultrasound (US) are areas without an associated mass. The purpose of this study was to evaluate whether combining B-mode US with color Doppler US and strain elastography (SE) improves US differentiation between benign and malignant non-mass breast lesions and the decision for biopsy. In this prospective study, three different radiologists analyzed the US images of 77 non-mass lesions independently and recorded Breast Imaging Reporting and Data System (BI-RADS) categories for four data sets. The image characteristics and BI-RADS categories of the four data sets were analyzed by another radiologist. The final diagnosis was made on the basis of pathologic findings. Values for area under the receiver operating curve (AUC), sensitivity, specificity and accuracy were compared among the data sets. The AUC of B-mode US combined with both color Doppler US and SE was greater than that of B-mode US alone (0.666 vs. 0.828) (p = 0.011). The specificity of making the decision for biopsy increased from 6.5% to 38.7% when B-mode US was combined with color Doppler and SE, without a statistically significant change in sensitivity (p < 0.001). Combined use of color Doppler and SE could improve the diagnostic value of B-mode US in distinguishing benign from malignant non-mass breast lesions and the specificity of making the decision for biopsy of non-mass breast lesions. [ABSTRACT FROM AUTHOR]

Background: Gastric cancer (GC) accounts for the fourth most occurring malignancy and the third major cause of cancer death. Identifying novel molecular signaling pathways participating in gastric tumorigenesis and progression is pivotal for rational design of targeted therapies to improve advanced GC outcome. Recently, the endoplasmic reticulum (ER) protein 29 (ERp29) has been shown to inversely associate with primary tumor development and function as a tumor suppressor in breast cancer. However, the role of ERp29 in GC patients' prognosis and its function in GC progression is unknown.Methods: Clinical importance of ERp29 in the prognosis of GC patients was assessed by examining its expression in 148 GC tumor samples and correlation with clinicopathological characteristics and survival of the patients. The function and underlying mechanisms of ERp29 in GC growth, invasion and metastasis were explored both in vitro and in vivo.Results: Downregulation of ERp29 was commonly found in GC tissues and highly correlated with more aggressive phenotypes and poorer prognosis. Functional assays demonstrated that knockdown of ERp29 increased GC cell migration and invasion and promoted metastasis. Conversely, ectopic overexpression of ERp29 produced opposite effects. Mechanistic studies revealed that loss of ERp29 induced an epithelial-to-mesenchymal transition (EMT) in the GC cells through activation of PI3K/Akt pathway signaling.Conclusion: These findings suggest that downregulation of ERp29 is probably one of the key molecular mechanisms responsible for the development and progression of GC. [ABSTRACT FROM AUTHOR]

The high humidity response of the sol–gel-synthesized ZnFe 2 O 4 films was discovered, which was characterized through the relative humidity (RH) influence on the electric parameters of capacitance, impedance and resistance. As the RH increased from 30% to 90%, both the impedance and resistance of the ZnFe 2 O 4 films, decreased by ∼2–3 orders of magnitude. This might be due to the physical adsorption and polarization of water molecules on the ZnFe 2 O 4 surface. The high humidity response of ZnFe 2 O 4 films has potential application in humidity sensitive devices. [ABSTRACT FROM AUTHOR]

Abstract: Disrupting plasma membrane integrity would inevitably promote anomalous ion fluxes across the membrane and thereby upset the trans-membranous potential. In this article, we report new findings on how sonoporation as a physical membrane perforation strategy would lead to different forms of plasma membrane potential disruption. Our investigation was conducted with a customized fluorescence imaging platform that enabled live monitoring of plasma membrane potential in relation to individual sonoporation events triggered on HeLa cervical cancer cells. Sonovue microbubbles were used as sonoporation agents (added at a 4:3 cell-to-bubble ratio), and they were activated by 1-MHz pulsed ultrasound with 0.35-MPa peak negative pressure, 20-cycle pulse duration, 20-Hz pulse repetition frequency and 1-s total exposure duration. Results indicate that the plasma membrane potential response was heterogeneous among sonoporated cells: (i) membrane potential of irreversibly sonoporated cells was permanently depolarized; (ii) reversibly sonoporated cells exhibited either transient or sustained membrane depolarization; (iii) intact cells adjacent to sonoporated ones underwent transitory membrane depolarization. These findings effectively serve to substantiate the causal relationship between sonoporation and plasma membrane potential. [Copyright &y& Elsevier]