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Magnetic field measurement technologies are extensively applied in nondestructive testing, quality inspection, and fault diagnosis of machines and equipment. Magnetic signals are highly susceptible to noise interference, and how to effectively conduct signal denoising under strong noise disturbance remains a challenge. This study designs a novel auxiliary sensor array comprising center and distributed satellite sensors for magnetic noise reconstruction and signal denoising. The signals of the center and satellite sensors are highly correlative owing to the propagation of the magnetic noise through space. An attention-based long short term memory model is designed and trained to establish the mapping relationship among the center and satellite signals. The noise of the center sensor can then be reconstructed from those of the satellite sensors in the procedure of magnetic field measurement. Finally, the denoised signal of the center sensor is obtained by subtracting the noisy signal with the reconstructed noise. The effectiveness and superiority of the proposed method are validated by experiments and compared with the conventional methods. The designed auxiliary sensor array and algorithm are easily implemented with remarkable robustness, flexibility, and scalability, thereby showing greatly potential use for magnetic signal denoising in a variety of mechatronic systems. [ABSTRACT FROM AUTHOR]

It has been challenging to measure responses of unlabeled, live whole cells. In this work, we designed a graphene-based optical biosensor with a detection depth of greater than 2 mm, a high sensitivity of 1.2 × 10 8  mV/RIU, and a fast response time of 260 ns. This novel biosensor enables fast and highly accurate label-free detection of drug responses in live cells at the cell height level, and can even sense cancer cell responses to anti-cancer drugs. Unexpected early responses to paclitaxel were observed in cancer cells using this biosensor. Two colorectal cancer cell lines, HCT116 and LoVo, were used for measurement. By combining the results from conventional biological assays, including MTT, western blot and immunofluorescence assays, these novel responses were examined in detail. This facile biosensor shows promise to be widely used as a sensor of unlabeled live cell responses for cancer therapy, anti-cancer drug screening and other cell-based research. [ABSTRACT FROM AUTHOR]

We previously reported that polyploid giant cancer cells (PGCGs) induced by CoCl2 could form through endoreduplication or cell fusion. A single PGCC formed tumors in immunodeficient mice. PGCCs are also the key contributors to the cellular atypia and associate with the malignant grade of tumors. PGCCs have the properties of cancer stem cells and produce daughter cells via asymmetric cell division. Compared with diploid cancer cells, these daughter cells express less epithelial markers and acquire mesenchymal phenotype with importance in cancer development and progression. Tumor budding is generally recognized to correlate with a high recurrence rate, lymph node metastasis, chemoresistance, and poor prognosis of colorectal cancers (CRCs) and is a good indicator to predict the metastasis and aggressiveness in CRCs. Micropapillary pattern is a special morphologic pattern and also associates with tumor metastasis and poor prognosis. There are similar morphologic features and molecular phenotypes among tumor budding, micropapillary carcinoma pattern, and PGCCs with their budding daughter cells and all of them show strong ability of tumor invasion and migration. In this review, we discuss the cancer stem cell properties of PGCCs, the molecular mechanisms of their regulation, and the relationships with tumor budding and micropapillary pattern in CRCs. [ABSTRACT FROM AUTHOR]

The real-time and label free detection abilities of surface plasmon resonance (SPR) biosensors provide a way of evaluating the influence of some genes’ expression on anti-tumor drug cytotoxicity. However, studies in this field are lacking. Connexin 43 is a tumor suppressor gene and the mechanism of its effect in cisplatin cytotoxicity is still unclear. A phase SPR biosensor was used to determine the influence of connexin 43 expression on cisplatin cytotoxicity in three cancer cell lines. The results showed that the SPR signal curves have two stages. In the first hour, the SPR signal shows dramatic changes which are related to connexin 43 expression. In the subsequent stage, the SPR signal slowly declines and is related to apoptosis. Comparison of SPR measurements from several conventional biological assays showed that connexin 43 expression can affect cellular response to cisplatin in the period of oxidative stress, and results in the cells being more sensitive to cisplatin. The conclusion is further confirmed by long-term SPR measurement results and cellular morphological changes. [ABSTRACT FROM AUTHOR]

Robot locomotion on rigid terrain or in fluids has been studied to a large extent. The locomotion dynamics on or within soft substrates such as granular material (GM) has not been fully investigated. This paper proposes a hybrid force model to simulate and evaluate the locomotion performance of a legged terrestrial robot in GM. The model incorporates an improved Resistive Force Theory (RFT) model and a failure-based model. The improved RFT model integrates the force components of individual leg elements over the curved leg portion submerged in GM at any moment during a full period of leg rotation. The failure-based model is applied in a bar drag model to yield the normal and the lateral forces of the individual RFT elements as functions of the locomotion depth and speed. The hybrid model is verified by the coincidence between the theoretical predictions and the experimental results. The hybrid model is used to analyze the effects of angular velocity and leg shape with high precision and can guide the design of the legs with any profiles. Our study reveals that the interactions between locomotor and substrate are determined by the locomotor structural characteristics, the nature of the substrate, and the control strategy. [ABSTRACT FROM AUTHOR]

In this paper, the propulsive performance of a flexible articulated caudal fin is investigated by fluid–structure interaction. The caudal fin is composed of two links which are connected by a hinge. One link is driven by pitching motion while the other one moves passively. Five cases of link flexibility are investigated, namely, the rigid–rigid case, the medium flexible–medium flexible case, the flexible–flexible case, the rigid–flexible case and the flexible–rigid case. Their fluid field and structure deformations are analysed and hydrodynamic forces are compared. It is found that the rigid–rigid caudal fin produces larger thrust force than other cases with a low-pitching frequency, while the rigid–flexible case performs better with a higher frequency. The mean thrust force increases with the frequency in our experiments, however, for the medium flexible–medium flexible case, an optimal frequency exists. Besides, the effect of the hinge stiffness is studied. It is seen that the medium flexible–medium flexible case exhibits a striking performance. When the hinge stiffness decreases, its mean thrust force increases and possesses larger amplitude while the forces of other cases decrease. These results can guide the design of flexible propeller with links and will be useful for the development of flexible underwater robots. [ABSTRACT FROM AUTHOR]

Abstract: Bone marrow is generally considered the main source of erythroid cells. Here we report that a single hypoxia-mimic chemical, CoCl2, can increase the size of fibroblasts and cancer cells and lead to formation of polyploidy giant cells (PGCs) or polyploidy giant cancer cells (PGCCs), activation of stem cell marker expression, increased growth of normal and cancer spheroid, and lead to differentiation of the fibroblasts and epithelial cells toward erythroid lineage expressing hemoglobins both in vitro and in vivo. Immunohistochemical examination demonstrated that these cells are predominantly made of embryonic hemoglobins, with various levels of fetal and adult hemoglobins. Ectopic expression of c-Myc induced the generation of nucleated erythoid cells expressing variable levels of embryonic and fetal hemoglobins. Generation of these erythroid cells can be also observed via histological examination of other cancer cell lines and human tumor samples. These data suggest that normal and solid cancer cells can directly generate erythroid cells to obtain oxygen in response to hypoxia and may explain the ineffectiveness of conventional anti-angiogenic therapies for cancer, which are directed at endothelium-dependent vessels, and offer new targets for intervention. [Copyright &y& Elsevier]

Abstract: Paclitaxel is commonly used to treat multiple human malignancies, but its mechanism of action is still poorly defined. Human ovarian cancer SKOV3 cells (parental SKOV3) were treated with paclitaxel (1μM) for 2days, and the morphologic changes in the cells were monitored for more than 4months. Parental SKOV3 underwent a markedly morphologic transition from the epithelial to fibroblast-like phenotype following treatment with paclitaxel; the resulting cells were designated as SKOV3-P. The SKOV3-P cells’ proliferative ability was assessed via a 3-[4,5-dimethylthiazol-2-yl]-2,5 diphenyl tetrazolium bromide (MTT) assay. The molecular characteristics of these cells were assessed via immunocytochemical staining and Western blot analysis. Their invasiveness and tumor formation ability was evaluated via wound-scratch and colony formation assays. The tumorigenicity of SKOV3-P cells was assessed in vivo after subcutaneous injection of tumor cells between injections of parental and paclitaxel-treated cells in nude mice. SKOV3-P cells have decreased the proliferation and invasion ability, decreased colony-forming ability when cultured in Matrigel and lost their tumor formation as compared with parental SKOV3 cells when injected in nude mice. SKOV3-P cells have decreased expression of E-cadherin, cytokeratin, Snail, PI3K, and P-Akt-Ser473, and increased expression of fibronectin, vimentin, Slug, P27, and PTEN. These results demonstrated that paclitaxel can inhibit tumor growth by inducing ovarian cancer epithelial cells toward a benign fibroblast-like phenotype through dysregulation of previously known pathways involved in the regulation of epithelial to mesenchymal transition (EMT), which may represent a novel mechanism for paclitaxel-induced tumor suppression. [Copyright &y& Elsevier]

Background. Gastric cancer (GC) is one of the most prevalent cancers globally. This study was designed to evaluate the potential performance of plasma SEPT9 methylation (mSEPT9) as a noninvasive biomarker for the diagnosis of GC. Methods. A total of 182 participants, i.e., 60 patients with GC, 39 with chronic superficial gastritis (CSG), 27 with chronic atrophic gastritis (CAG), 30 with gastric ulcer (GU), and 26 with gastric polys (GP), were recruited. The mSEPT9 level was measured using real-time polymerase chain reaction. Results. As a diagnostic target, mSEPT9 (1/3 algorithm) had a sensitivity of 48.33 (95% confidence interval (CI): 35.40–61.48%) and a specificity of 86.89% (95% CI: 79.28–92.09%), and mSEPT9 (2/3 algorithm) had a sensitivity of 33.33 (95% CI: 22.02–46.79%) and a specificity of 98.36% (95% CI: 93.61–99.72%). The area under the receiver operating characteristic curve (ROC) curve of mSEPT9 was 0.698 (95% CI: 0.609–0.787) for the differentiation of GC from benign gastric diseases. The effectiveness of mSEPT9 (1/3 algorithm) was superior to that of CEA, CA19-9, and CA72-4. mSEPT9 was positively correlated with T, N, M, and the clinical stage of GC. Conclusions. Plasma mSEPT9 might serve as a useful and noninvasive biomarker for the diagnosis of GC. [ABSTRACT FROM AUTHOR]

Background. RNF180 is a tumor suppressor gene involved in cell development, proliferation, and apoptosis. Methylation of RNF180 (mRNF180) leads to low expression of RNF180, which is closely related to the occurrence and development of gastric cancer (GC). This study was designed to evaluate the potential performance of plasma mRNF180 as noninvasive biomarker for the diagnosis of GC. Methods. A total of 156 participants, including 60 patients with GC, 39 with chronic superficial gastritis (CSG), 27 with chronic atrophic gastritis (CAG), and 30 with gastric ulcer (GU) were recruited for this study. Plasma mRNF180 level was measured using real-time polymerase chain reaction. Results. As a diagnostic target, mRNF180 had a sensitivity of 71.67% (95% CI: 58.36%–82.18%) and specificity of 59.38% (95% CI: 48.85%–69.14%). The area under the ROC curve value of mRNF180 was 0.731 (95% CI: 0.648%–0.813%) for differentiation of GC from benign gastric diseases (BGD). The effectiveness of mRNF180 was superior to that of CEA, CA199, and CA724. mRNF180 was positively correlated with age, tumor size, T stage, N stage, M stage, and clinical stage of patients with GC. Conclusions. Plasma mRNF180 might serve as a useful and noninvasive biomarker for the diagnosis of GC and can be used to evaluate its prognosis. [ABSTRACT FROM AUTHOR]

Abstract: In 1999, Maniotis reported that blood vessels of highly aggressive uveal melanomas are formed by tumor cells instead of endothelial cells. He termed this novel concept in tumor vascularization vasculogenic mimicry (VM). Since then, VM has been seen in several malignant tumor types such as breast cancer, liver cancer, glioma, ovarian cancer, melanoma, prostate cancer, and bidirectional differentiated malignant tumors. Laser scanning confocal angiography, electron microscopy, and three-dimensional cell culture have confirmed the existence of VM. The molecular mechanisms that underlie VM are not fully clear, but metalloproteinases via their cleavage of laminin, VE-cadherin by promoting adherence of the VM channel wall to tumor cells, tumor cell dedifferentiation, and tumor microenvironment have been shown to play a role in VM. Zhang and co-workers have proposed a three-stage phenomenon among VM channels, mosaic blood vessels, and endothelium-dependent blood vessels, wherein all three patterns participate in tumor blood supply. Therapeutic strategies that target endothelial cells have no effect on tumor cells that engage in VM. VM-targeting strategies include suppressing tyrosine kinase activity and using a knockout EphA2 gene, downregulating VE-cadherin, using antibodies against human MMPs and the laminin 5γ2 chain, and using anti-PI3K therapy. We review here the current status of research on VM; discuss molecular mechanisms of VM, factors affecting VM formation, and its clinical significance; and explore the development of novel tumor-targeted treatments that are based on the biochemical and molecular events that regulate VM. [Copyright &y& Elsevier]

Abstract: Two-dimensional electrophoresis and Matrix-assisted laser desorption ionization-time of flight-time of mass spectrometry were used to detect the differentially expressed proteins in serum of tientsin albinao 2 mice with spontaneous breast cancer, normal tientsin albinao 2 mice and tientsin albinao 1 mice. Only nuclear clusterin (n-CLU) was expressed in tientsin albinao 1. Immunohistochemistry and western blot validated that n-CLU was present in normal tientsin albinao 2 and tientsin albinao 1 mammary epithelium, and secretory clusterin expressed in the cytoplasm of normal tientsin albinao 2 mammary epithelium and spontaneous breast cancer. n-CLU may play an important role in tientsin albinao 2 spontaneous breast cancer initiation and development. [Copyright &y& Elsevier]

A social network is composed of social individuals and their relationships. In many real-world applications, such a network will evolve dynamically over time and events. A social network can be naturally viewed as a multiagent system if considering locally-interacting social individuals as autonomous agents. In this paper, we present an Autonomy-Oriented Computing (AOC) based model of a social network, and study the dynamics of the network based on this model. In the AOC model, the profile of agents, service-based interactions, and the evolution of the network are defined, and the autonomy of the agents is emphasized. The model can reveal dynamic relationships among global performance, local interaction (partner selection) strategies, and network topology. The experimental results show that the agent network forms a community with a high clustering coefficient, and the performance of the network is dynamically changing along with the formation of the network and the local interaction strategies of the agents. In this paper, the performance and topology of the agent network are analyzed, and the factors that affect the performance and evolution of the agent network are examined. [ABSTRACT FROM AUTHOR]

Background: Local recurrence after surgery and radiochemotherapy seriously affects the prognosis of locally advanced rectal cancer (LARC) patients. Studies on molecular markers related to the radiochemotherapy sensitivity of cancers have been widely carried out, which might provide valued information for clinicians to carry out individual treatment. Aim: To find potential biomarkers of tumors for predicting postoperative recurrence. Methods: In this study, LARC patients undergoing surgery and concurrent radiochemotherapy were enrolled. We focused on clinicopathological factors and PTEN, SIRT1, p-4E-BP1, and pS6 protein expression assessed by immunohistochemistry in 73 rectal cancer patients with local recurrence and 76 patients without local recurrence. Results: The expression of PTEN was higher, while the expression of p-4E-BP1 was lower in patients without local recurrence than in patients with local recurrence. Moreover, TNM stage, lymphatic vessel invasion (LVI), PTEN and p-4E-BP1 might be independent risk factors for local recurrence after LARC surgery combined with concurrent radiochemotherapy. Conclusions: This study suggests that PTEN and p-4E-BP1 might be potential biomarkers for prognostic prediction and therapeutic targets for LARC. [ABSTRACT FROM AUTHOR]

Background: Compliance with colonoscopy among elderly individuals participating in colorectal cancer (CRC) screening programs is unsatisfactory, despite a high detection rate of bowel‐related diseases. In this study, our aim was to analyze the impact of risk factors on the trends of compliance and detection rates in colonoscopy among high‐risk individuals aged 60–74. Methods: A retrospective study was conducted on the high‐risk individuals aged 60–74 participating in the 2021 CRC screening program in Tianjin, China. Logistic regression analyses, including both univariate and multivariate analyses, were performed to explore the impact of different risk factors on colonoscopy compliance among the high‐risk individuals. Besides, the study investigated the influence of various risk factors on the detection rates of bowel‐related diseases among the high‐risk individuals who underwent colonoscopy. Results: A total of 24,064 high‐risk individuals were included, and 5478 individuals received a free colonoscopy, with an overall compliance of 22.76%. Among them, the adenoma detection rate was 55.46%. Males and individuals with a positive FIT had high compliance and detection rates for CRC, advanced adenomas (AA), advanced colorectal neoplasia (ACN), and colorectal neoplasm (CN). Individuals aged 70–74 were associated with low compliance but high CRC, ACN, and CN detection rates. Individuals who reported a history of chronic constipation, bloody mucous, and CRC in first‐degree relative showed high compliance but no significantwere associated with the detection rates of CRC, AA, and CN. Conclusion: This study reported several risk factors associated with the screening behaviors for CRC. Patterns and trends in CRC, AA, ACN, and CN compliance and detection rates correlate with risk factors. [ABSTRACT FROM AUTHOR]

Background and Aim: The incidence of colorectal cancer (CRC) in individuals under 50 is increasing worldwide. We conducted an analysis of colonoscopy findings in high‐risk individuals under 50 in the CRC screening program in Tianjin, China, to determine the detection rate and risk factors of advanced adenomas (AA), advanced colorectal neoplasia (ACN), colorectal neoplasia (CN). Methods: Our study investigated individuals aged 40–49 who underwent CRC screening and completed colonoscopy, 2012–2020, while the 50–54 age group served as a control. We compared the detection rates of AA, ACN, and CN among three age groups using univariate and multivariable logistic regression analyses, and investigated the risk factors associated with AA, ACN, and CN among individuals aged 40–49. Results: We found a gradual increase in the detection rate of AA, ACN, and CN among individuals aged 40–54. The detection rates for AA (OR 0.58; 95% CI 0.41–0.81), ACN (OR 0.58; 95% CI 0.43–0.77), and CN (OR 0.64; 95% CI 0.56–0.74) were lower in individuals aged 40–44 compared to 45–49. The detection rates of AA (OR 1.08; 95% CI 0.87–1.34) and ACN (OR 1.12; 95% CI 0.93–1.35) in individuals aged 45–49 were comparable with 50–54. Besides, lifestyle factors, BMI, and FIT are not associated with the detection rates of AA, ACN, and CN among individuals aged 40–49. Conclusions: Our study reveals screening data in individuals under 50, indicating comparable detection rates of AA and ACN in individuals aged 45–49 and 50–54. These findings provide valuable data support for optimizing the optimal age to initiate screening. [ABSTRACT FROM AUTHOR]

Anomalous vascular endothelium significantly contributes to various cardiovascular diseases. VE-cadherin plays a vital role in governing the endothelial barrier. Krüppel-like factor 4(KLF4), as a transcription factor, which binds the VE-cadherin promoter and enhances its transcription. Tumor necrosis factor receptor-associated factor 7 (TRAF7) is an E3 ubiquitin ligase that has been shown to modulate the degradation of KLF4. H 2 S can covalently modify cysteine residues on proteins through S-sulfhydration, thereby influencing the structure and functionality of the target protein. However, the role of S-sulfhydration on endothelial barrier integrity remains to be comprehensively elucidated. This study aims to investigate whether protein S-sulfhydration in the endothelium regulates endothelial integrity and its underlying mechanism. In this study, we observed that protein S-sulfhydration was reduced in the endothelium during diabetes and TRAF7 was the main target. Overexpression of TRAF7-Cys327 mutant could mitigate the endothelial barrier damage by weakening TRAF7 interaction with KLF4 and reducing ubiquitination degradation of KLF4. In conclusion, our research demonstrates that H 2 S plays a pivotal role in regulating S-sulfhydration of TRAF7 at Cys327. This regulation effectively inhibits the ubiquitin-mediated degradation of KLF4, resulting in an upregulation of VE-cadherin levels. This molecular mechanism contributes to the prevention of endothelial barrier damage. [Display omitted] • H 2 S plays a pivotal role in regulating S-sulfhydration of TRAF7 at Cys327. • Transfection with TRAF7-Cys327, the S-sulfhydration level of TRAF7 significantly decreased with NaHS treatment. • S-sulfhydration of TRAF7 at Cys327 prevents KLF4 degradation. • S-sulfhydration of TRAF7 at Cys327 maintains endothelial permeability. [ABSTRACT FROM AUTHOR]

Nanoengineering the composition and morphology of functional nanoparticles endows them to perform multiple tasks and functions. An intriguing strategy for creating multifunctional nanomaterials involves the construction of core–shell nanostructures, which have enabled promising applications in biomedicine, energy, sensing, and catalysis. Here, a straightforward nanoengineering approach is presented utilizing liquid metal nanoparticles and galvanic replacement to create diverse core–shell nanostructures. Controlled nanostructures including liquid metal core‐gold nanoparticle shell (LM@Au), gold nanoparticle core‐gallium oxide shell (Au@Ga oxide), and hollow Ga oxide nanoparticles are successfully fabricated. Remarkably, these investigations reveal that LM@Au exhibits exceptional photothermal performance, achieving an impressive conversion efficiency of 65.9%, which is five times that of gold nanoparticles. By leveraging the high photothermal conversion efficiency and excellent biocompatibility of LM@Au, its promising application in hyperthermia cancer therapy is demonstrated. This simple yet powerful nanoengineering strategy opens new avenues for the controlled synthesis of complex core–shell nanostructures, advancing various fields beyond biomedicine. [ABSTRACT FROM AUTHOR]

Tumour cell dormancy is critical for metastasis and resistance to chemoradiotherapy. Polyploid giant cancer cells (PGCCs) with giant or multiple nuclei and high DNA content have the properties of cancer stem cell and single PGCCs can individually generate tumours in immunodeficient mice. PGCCs represent a dormant form of cancer cells that survive harsh tumour conditions and contribute to tumour recurrence. Hypoxic mimics, chemotherapeutics, radiation and cytotoxic traditional Chinese medicines can induce PGCCs formation through endoreduplication and/or cell fusion. After incubation, dormant PGCCs can recover from the treatment and produce daughter cells with strong proliferative, migratory and invasive abilities via asymmetric cell division. Additionally, PGCCs can resist hypoxia or chemical stress and have a distinct protein signature that involves chromatin remodelling and cell cycle regulation. Dormant PGCCs form the cellular basis for therapeutic resistance, metastatic cascade and disease recurrence. This review summarises regulatory mechanisms governing dormant cancer cells entry and exit of dormancy, which may be used by PGCCs, and potential therapeutic strategies for targeting PGCCs. [ABSTRACT FROM AUTHOR]

Over the past decade, the role of the 14–3-3 protein has received increasing interest. Seven subtypes of 14–3-3 proteins exhibit high homology; however, each subtype maintains its specificity. The 14–3-3ε protein is involved in various physiological processes, including signal transduction, cell proliferation, apoptosis, autophagy, cell cycle regulation, repolarization of cardiac action, cardiac development, intracellular electrolyte homeostasis, neurodevelopment, and innate immunity. It also plays a significant role in the development and progression of various diseases, such as cardiovascular diseases, inflammatory diseases, neurodegenerative disorders, and cancer. These immense and various involvements of 14–3-3ε in diverse processes makes it a promising target for drug development. Although extensive research has been conducted on 14–3-3 dimers, studies on 14–3-3 monomers are limited. This review aimed to provide an overview of recent reports on the molecular mechanisms involved in the regulation of binding partners by 14–3-3ε, focusing on issues that could help advance the frontiers of this field. 28PxGStmhrzzmkZE7z3ya4 Video Abstract [ABSTRACT FROM AUTHOR]

We report the first statistical analyses of [C ii ] and dust continuum observations in six strong O i absorber fields at the end of the reionization epoch obtained by the Atacama Large Millimeter/submillimeter Array (ALMA). Combined with one [C ii ] emitter reported in Wu et al., we detect one O i -associated [C ii ] emitter in six fields. At redshifts of O i absorbers in nondetection fields, no emitters are brighter than our detection limit within impact parameters of 50 kpc and velocity offsets between ±200 km s−1. The averaged [C ii ]-detection upper limit is <0.06 Jy km s−1(3 σ), corresponding to the [C ii ] luminosity of L [C II ]< 5.8 × 107 L ⊙ and the [C ii ]-based star formation rate of SFR[C II ]<5.5 M ⊙ yr−1. Cosmological simulations suggest that only ∼10−2.5 [C ii ] emitters around O i absorbers have comparable SFR to our detection limit. Although the detection in one out of six fields is reported, an order of magnitude number excess of emitters obtained from our ALMA observations supports that the contribution of massive galaxies that caused the metal enrichment cannot be ignored. Further, we also found 14 tentative galaxy candidates with a signal-to-noise ratio of ≈4.3 at large impact parameters (>50 kpc) and having larger outflow velocities within ±600 km s−1. If these detections are confirmed in the future, then the mechanism of pushing metals at larger distances with higher velocities needs to be further explored from the theoretical side. [ABSTRACT FROM AUTHOR]

Background: Polyploid giant cancer cells (PGCCs), a specific type of cancer stem cells (CSCs), can be induced by hypoxic microenvironments, chemical reagents, radiotherapy, and Chinese herbal medicine. Moreover, PGCCs can produce daughter cells that undergo epithelial–mesenchymal transition, which leads to cancer recurrence and disseminated metastasis. Vimentin, a mesenchymal cell marker, is highly expressed in PGCCs and their daughter cells (PDCs) and drives migratory persistence. This study explored the molecular mechanisms by which vimentin synergistically regulates PGCCs to generate daughter cells with enhanced invasive and metastatic properties. Methods: Arsenic trioxide (ATO) was used to induce the formation of PGCCs in Hct116 and LoVo cells. Immunocytochemical and immunohistochemical assays were performed to determine the subcellular localization of vimentin. Cell function assays were performed to compare the invasive metastatic abilities of the PDCs and control cells. The molecular mechanisms underlying vimentin expression and nuclear translocation were investigated by real-time polymerase chain reaction, western blotting, cell function assays, cell transfection, co-immunoprecipitation, and chromatin immunoprecipitation, followed by sequencing. Finally, animal xenograft experiments and clinical colorectal cancer samples were used to study vimentin expression in tumor tissues. Results: Daughter cells derived from PGCCs showed strong proliferative, migratory, and invasive abilities, in which vimentin was highly expressed and located in both the cytoplasm and nucleus. Vimentin undergoes small ubiquitin-like modification (SUMOylation) by interacting with SUMO1 and SUMO2/3, which are associated with nuclear translocation. P62 regulates nuclear translocation of vimentin by controlling SUMO1 and SUMO2/3 expression. In the nucleus, vimentin acts as a transcription factor that regulates CDC42, cathepsin B, and cathepsin D to promote PDC invasion and migration. Furthermore, animal experiments and human colorectal cancer specimens have confirmed the nuclear translocation of vimentin. Conclusion: P62-dependent SUMOylation of vimentin plays an important role in PDC migration and invasion. Vimentin nuclear translocation and overexpressed P62 of cancer cells may be used to predict patient prognosis, and targeting vimentin nuclear translocation may be a promising therapeutic strategy for metastatic cancers. [ABSTRACT FROM AUTHOR]

Hybrid stepper motors, which convert the input pulse train into rotating angle increments by using an open-loop control strategy, are widely used in industrial applications. The bearing is a key and vulnerable component in stepper motors, and the bearing faults affect the positioning accuracy and output torque of motors. Order analysis is an effective method in bearing fault diagnosis under varying speed conditions. The rotating angle curve is necessary for order analysis, but angle or speed sensors are not installed on hybrid stepper motors. In this article, a method of estimating the rotating angle from motor current is proposed and applied to bearing fault diagnosis. First, a variational nonlinear chirp mode decomposition method is introduced to decompose the current signal and extract a dominant mode that has a strong correlation with motor rotation. Second, the rotating angle is calculated, and the synchronous vibration signal is resampled using the rotating angle curve. Finally, the bearing fault type is identified from the envelope order spectrum of the resampled signal. The proposed method can accurately diagnose bearing faults and has potential applications in condition monitoring of stepper motors. [ABSTRACT FROM AUTHOR]

Apples and their products exemplify the recently reemphasized link between dietary fruit intake and the alleviation of human disease. Their consumption does indeed improve human health due to their high phytochemical content. To identify potentially relevant articles from clinical trials, some epidemiological studies and meta‐analyses, and in vitro and in vivo studies (cell cultures and animal models), PubMed was searched from January 1, 2012, to May 15, 2022. This review summarized the potential effects of apple and apple products (juices, puree, pomace, dried apples, extracts rich in apple bioactives and single apple bioactives) on health. Apples and apple products have protective effects against cardiovascular diseases, cancer, as well as mild cognitive impairment and promote hair growth, healing of burn wounds, improve the oral environment, prevent niacin‐induced skin flushing, promote the relief of UV‐induced skin pigmentation, and improve the symptoms of atopic dermatitis as well as cedar hay fever among others. These effects are associated with various mechanisms, such as vascular endothelial protection, blood lipids lowering, anti‐inflammatory, antioxidant, antiapoptotic, anti‐invasion, and antimetastatic effects. Meanwhile, it has provided an important reference for the application and development of medicine, nutrition, and other fields. [ABSTRACT FROM AUTHOR]

Background: Epithelial ovarian cancer is the leading cause of death from gynecologic cancer, in which serous ovarian carcinoma (SOC) is the most common histological subtype. Although PARP inhibitors (PARPi) and antiangiogenics have been accepted as maintenance treatment in SOC, response to immunotherapy of SOC patients is limited. Methods: The source of transcriptomic data of SOC was from the Cancer Genome Atlas database and Gene Expression Omnibus. The abundance scores of mesenchymal stem cells (MSC scores) were estimated for each sample by xCell. Weighted correlation network analysis is correlated the significant genes with MSC scores. Based on prognostic risk model construction with Cox regression analysis, patients with SOC were divided into low- and high-risk groups. And distribution of immune cells, immunosuppressors and pro-angiogenic factors in different risk groups was achieved by single-sample gene set enrichment analysis. The risk model of MSC scores was further validated in datasets of immune checkpoint blockade and antiangiogenic therapy. In the experiment, the mRNA expression of prognostic genes related to MSC scores was detected by real-time polymerase chain reaction, while the protein level was evaluated by immunohistochemistry. Results: Three prognostic genes (PER1, AKAP12 and MMP17) were the constituents of risk model. Patients classified as high-risk exhibited worse prognosis, presented with an immunosuppressive phenotype, and demonstrated high micro-vessel density. Additionally, these patients were insensitive to immunotherapy and would achieve a longer overall survival with antiangiogenesis treatment. The validation experiments showed that the mRNA of PER1, AKAP12, and MMP17 was highly expressed in normal ovarian epithelial cells compared to SOC cell lines and there was a positive correlation between protein levels of PER1, AKAP12 and MMP17 and metastasis in human ovarian serous tumors. Conclusion: This prognostic model established on MSC scores can predict prognosis of patients and provide the guidance for patients receiving immunotherapy and molecular targeted therapy. Because the number of prognostic genes was fewer than other signatures of SOC, it will be easily accessible on clinic. [ABSTRACT FROM AUTHOR]

Diabetic cardiomyopathy (DCM) is a serious complication of diabetes mellitus that eventually progresses to heart failure. The sarco(endo)plasmic reticulum calcium ATPase 2a (SERCA2a), an important calcium pump in cardiomyocytes, is closely related to myocardial systolic-diastolic function. In mammalian cells, hydrogen sulfide (H 2 S), as a second messenger, antioxidant, and sulfurizing agent, is involved in diverse biological processes. Despite the importance of H 2 S for protection against DCM, the mechanisms remain poorly understood. The aim of the present study was to determine whether H 2 S regulates intracellular calcium homeostasis by acting on SERCA2a to reduce cardiomyocyte apoptosis during DCM. Db/db mice were injected with NaHS for 18 weeks. Neonatal rat cardiomyocytes (NRCMs) were treated with high glucose, palmitate, oleate, and NaHS for 48 h. Compared to the NaHS-treated groups, in vivo and in vitro type 2 diabetic models both showed reduced intracellular H 2 S content, reduced cystathionine γ-lyase (CSE) expression, impaired cardiac function, decreased SERCA2a expression and decreased SERCA2a activity, reduced SUMOylation of SERCA2a, increased sentrin-specific protease 1 (SENP1) expression, and disruption of calcium homeostasis leading to activation of the mitochondrial apoptosis pathway. Compared to the NaHS-treated type 2 diabetes cellular model, overexpression of SENP1 C683A reduced the S-sulfhydration of SENP1, reduced the SUMOylation of SERCA2a, reduced the increased expression and activity of SERCA2a, and induced mitochondrial apoptosis in cardiomyocytes. These results suggested that exogenous H 2 S elevates SENP1 S-sulfhydration to increase SERCA2a SUMOylation, improve myocardial systolic-diastolic function, and decrease cardiomyocyte apoptosis in DCM. [Display omitted] • H 2 S content is reduced in diabetic cardiomyopathy. • Reduced the SUMOylation of SERCA2a in diabetic cardiomyopathy leads to decreased expression and activity of SERCA2a and imbalance in cellular calcium homeostasis. • H 2 S can S-sulfhydration the 683 cysteine site in the catalytic triad of SENP1. • Decreased S-sulfhydration of SENP1 Cys683 leads to decreased the SUMOylation of SERCA2a in diabetic cardiomyopathy. [ABSTRACT FROM AUTHOR]

We present a deep optical imaging campaign on the starburst galaxy NGC 4631 with CFHT/MegaCam. By supplementing the HST/ACS and Chandra/ACIS archival data, we search for the optical counterpart candidates of the five brightest X-ray sources in this galaxy, four of which are identified as ultraluminous X-ray sources (ULXs). The stellar environments of the X-ray sources are analyzed using the extinction-corrected color–magnitude diagrams and the isochrone models. We discover a highly asymmetric bubble nebula around X4 that exhibits different morphology in the H α and [O iii ] images. The [O iii ]/H α ratio map shows that the H α -bright bubble may be formed mainly via the shock ionization by the one-sided jet/outflow, while the more compact [O iii ] structure is photoionized by the ULX. We constrain the bubble expansion velocity and interstellar medium density with the MAPPINGS V code and hence estimate the mechanical power injected into the bubble as P w ∼ 5 × 1040 erg s−1 and the corresponding bubble age as ∼7 × 105 yr. Relativistic jets are needed to provide such a level of mechanical power with a mass-loss rate of ∼10−7 M ⊙ yr−1. Besides the accretion, the black hole spin is likely an additional energy source for the super-Eddington jet power. [ABSTRACT FROM AUTHOR]

We would like to express our gratitude to Safari, Farzad, and Noursina, Ali, for their insightful comments about our article regarding the questionnaire procedure and the assessment of symptoms, including a history of chronic constipation, chronic diarrhea, and mucous blood stools. This questionnaire has been included in national screening programs since 2007 and has been used in many cities in China.[[1], [3]] Since 2012, CRC screening in community allied third-grade class-A hospitals has been initiated in Tianjin City, China. As stated in the manuscript, only 39.41% of the screening population completed a colonoscopy within 1 month, so those with symptoms at the time of initial screening were advised to seek a definitive diagnosis promptly and were excluded from screening. [Extracted from the article]

Polyploid giant cancer cells (PGCCs) are a morphologically distinct subgroup of human tumor cells with increased nuclear size or multiple nuclei, but they are generally considered unimportant because they are presumed to be nondividing and thus nonviable. We have recently shown that these large cancer cells are not only viable but also can divide asymmetrically and yield progeny cancer cells with cancer stem-like properties via budding division. To further understand the molecular events involved in the regulation of PGCCs and the generation of their progeny cancer cells, we comparatively analyzed the proteomic profiles of PGCCs, PGCCs with budding daughter cells, and regular control cancer cells from the HEY and SKOv3 human ovarian cancer cell lines with and without CoCl2. We used a high-throughput iTRAQ-based proteomic methodology coupled with liquid chromatography-electrospray ionization tandem mass spectroscopy to determine the differentiated regulated proteins. We performed Western blotting and immunohistochemical analyses to validate the differences in the expression patterns of a variety of proteins between PGCCs or budding PGCCs and regular cancer cells identified by iTRAQ approach and also a selected group of proteins from the literature. The differentially regulated proteins included proteins involved in response to hypoxia, stem cell generation, chromatin remodeling, cell-cycle regulation, and invasion and metastasis. In particular, we found that HIF-1alpha and its known target STC1 are upregulated in PGCCs. In addition, we found that a panel of stem cell-regulating factors and epithelial-to-mesenchymal transition regulatory transcription factors were upregulated in budding PGCCs, whereas expression of the histone 1 family of nucleosomal linker proteins was consistently lower in PGCCs than in control cells. Thus, proteomic expression patterns provide valuable insight into the underlying mechanisms of PGCC formation and the relationship between PGCCs and cancer stem cells in patients with ovarian cancers. [ABSTRACT FROM AUTHOR]

Gap junctions (GJs), which are composed of connexins (Cxs), provide channels for direct information exchange between cells. Cx expression has a strong spatial specificity; however, its influence on cell behavior and information exchange between cells cannot be ignored. A variety of factors in organisms can modulate Cxs and subsequently trigger a series of responses that have important effects on cellular behavior. The expression and function of Cxs and the number and function of GJs are in dynamic change. Cxs have been characterized as tumor suppressors in the past, but recent studies have highlighted the critical roles of Cxs and GJs in cancer pathogenesis. The complex mechanism underlying Cx and GJ involvement in cancer development is a major obstacle to the evolution of therapy targeting Cxs. In this paper, we review the post-translational modifications of Cxs, the interactions of Cxs with several chaperone proteins, and the effects of Cxs and GJs on cancer. EUAGovitD21XQu5xc5u6gf Video Abstract [ABSTRACT FROM AUTHOR]

Perception of information is of critical importance for aquatic activities; however, the complex underwater situation faces unique technical challenges to address. Thus, an underwater environment‐incorporated sensing strategy, referred to as aquatic skin, has been introduced with multi‐modality sensing capacities of contact pressure, tactile mapping, depth, temperature, and salinity in a flexible architecture. Remarkably, this has been all achieved by a multi‐modality iontronic sensing principle in an all‐in‐one structural configuration, simplifying the sensor design, material preparation, device fabrication, and signal processing. Particularly, an inverse iontronic sensing mechanism, utilizing complementary elastomeric‐electrode and environmental‐electrode interfaces, is developed for contact pressure detection with exceptional resolution and hydraulic balance. Moreover, a hydrophobic ionic gel with adjustable surface morphologies has been developed as the functional sensing layer for all the units with long‐term stability. Consequently, the aquatic skin can achieve sub‐Pascal resolution of contact pressure detection (0.59 Pa), and sub‐millimeter spatial resolution of tactile mapping (522 pts cm−2) over an extended range of depths (0–40 m), while the environmental influences can be spontaneously eliminated through a self‐compensation process. The aquatic skin is applied toward several representative underwater scenes, including real‐time monitoring of vital/environmental signals, tactile recognition of creatures, and biomechanical analysis of fish swimming. [ABSTRACT FROM AUTHOR]

Hydrogen sulfide (H2S), as a gasotransmitter, is involved in various pathophysiological processes. Diabetic cardiomyopathy (DCM) is a major complication of diabetes mellitus (DM), which leads to structural and functional abnormalities of the myocardium and eventually causes heart failure (HF). Systolic and diastolic dysfunction are fundamental features of heart failure. SERCA2a, as a key enzyme for calcium transport in the endoplasmic reticulum (ER), affects the process of myocardial relaxation and contraction. H2S can protect the cardiac function against diabetic hearts, however, its mechanisms are unclear. This study found that exogenous H2S affects cellular calcium transport by regulating the H2S/MuRF1/SERCA2a/cardiac contractile pathway. Our results showed that, compared with the db/db mice, exogenous H2S restored the protein expression levels of CSE and SERCA2a, and the activity of SERCA2a, while reducing cytosolic calcium concentrations and MuRF1 expression. We demonstrated that MuRF1 could interact with SERCA2a via co-immunoprecipitation. Using LC-MS/MS protein ubiquitylation analysis, we identified 147 proteins with increased ubiquitination levels, including SERCA2a, in the cardiac tissues of the db/db mice compared with NaHS-treated db/db mice. Our studies further revealed that NaHS administration modified MuRF1 S-sulfhydration and enhanced the activity and expression of SERCA2a. Under hyperglycemia and hyperlipidemia, overexpression of the MuRF1-Cys44 mutant plasmid reduced the S-sulfhydration level of MuRF1 and decreased the ubiquitination level of SERCA2a and the intracellular Ca2+ concentration. These findings suggested that H2S modulates SERCA2a ubiquitination through MuRF1 S-sulfhydration of Cys44 to prevent decreased myocardial contractility due to increased cytosolic calcium. [ABSTRACT FROM AUTHOR]

Magnetorheological fluid (MRF) has shown its great potential in the development of large mechanical devices, such as dampers, shock absorbers, rotary brakes, clutches, and prosthetic joints. Recently, more research focus has been invested on using MRF to develop soft, stretchable, and miniaturized devices with variable stiffness for realizing functionalities that cannot be achieved using solid smart materials. Here, based on liquid metal magnetoactive slurries (LMMS), a variable stiffness wire with excellent electrical conductivity is demonstrated. Without exposure to a magnetic field, the LMMS wire has an extremely low stiffness, and can be easily stretched while maintaining an excellent electrical conductivity. When applying a magnetic field, the wire becomes much stiffer and can retain its shape even under a load. The combination of properties of flexibility, high electrical conductivity, and variable stiffness of the wire is harnessed to make a flexible gripper that can grasp objects of various shapes. Moreover, by using gallium instead of its liquid metal alloys, the tunable stiffness range of the LMMS wire is significantly enhanced and can be controlled using both external magnetic fields and temperature-induced phase change. The presented LMMS wire has the potential to be applied in flexible electronics, soft robotics and so on. [ABSTRACT FROM AUTHOR]

Chondrogenesis is the formation of chondrocytes and cartilage tissues and starts with mesenchymal stem cell (MSC) recruitment and migration, condensation of progenitors, chondrocyte differentiation, and maturation. The chondrogenic differentiation of MSCs depends on co-regulation of many exogenous and endogenous factors including specific microenvironmental signals, non-coding RNAs, physical factors existed in culture condition, etc. Cancer stem cells (CSCs) exhibit self-renewal capacity, pluripotency and cellular plasticity, which have the potential to differentiate into post-mitotic and benign cells. Accumulating evidence has shown that CSCs can be induced to differentiate into various benign cells including adipocytes, fibrocytes, osteoblast, and so on. Retinoic acid has been widely used in the treatment of acute promyelocytic leukemia. Previous study confirmed that polyploid giant cancer cells, a type of cancer stem-like cells, could differentiate into adipocytes, osteocytes, and chondrocytes. In this review, we will summarize signaling pathways and cytokines in chondrogenic differentiation of MSCs. Understanding the molecular mechanism of chondrogenic differentiation of CSCs and cancer cells may provide new strategies for cancer treatment. [ABSTRACT FROM AUTHOR]

The ability to control interfacial tension electrochemically is uniquely available for liquid metals (LMs), in particular gallium‐based LM alloys. This imparts them with excellent locomotion and deformation capabilities and enables diverse applications. However, electrochemical oxidation of LM is a highly dynamic process, which often induces Marangoni instabilities that make it almost impossible to elongate LM and manipulate its morphology directly and precisely on a 2D plane without the assistance of other patterning methods. To overcome these limitations, this study investigates the use of an LM–iron (Fe) particle mixture that is capable of suppressing instabilities during the electrochemical oxidation process, thereby allowing for superelongation of the LM core of the mixture to form a thin wire that is tens of times of its original length. More importantly, the elongated LM core can be manipulated freely on a 2D plane to form complex patterns. Eliminating Marangoni instabilities also allows for the effective spreading and filling of the LM–Fe mixture into molds with complex structures and small features. Harnessing these excellent abilities, a channel‐less patterning method for fabricating elastomeric wearable sensors is demonstrated to detect motions. This study shows the potential for developing functional and flexible structures of LM with superior performance. [ABSTRACT FROM AUTHOR]

The coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) heavily burdens human health. Multiple neutralizing antibodies (nAbs) have been issued for emergency use or tested for treating infected patients in the clinic. However, SARS-CoV-2 variants of concern (VOC) carrying mutations reduce the effectiveness of nAbs by preventing neutralization. Uncoding the mutation profile and immune evasion mechanism of SARS-CoV-2 can improve the outcome of Ab-mediated therapies. In this review, we first outline the development status of anti-SARS-CoV-2 Ab drugs and provide an overview of SARS-CoV-2 variants and their prevalence. We next focus on the failure causes of anti-SARS-CoV-2 Ab drugs and rethink the design strategy for developing new Ab drugs against COVID-19. This review provides updated information for the development of therapeutic Ab drugs against SARS-CoV-2 variants. [Display omitted] • Summarize the SARS-CoV-2 variants, overview the neutralizing antibody drugs. • Clarify the failure causes of antibody drugs and mutation-caused immune evasion. • Rethink the design strategies of antibody drugs for addressing mutation challenges. [ABSTRACT FROM AUTHOR]

• A new MRE metamaterial plate with continuous programmable properties was proposed. • A real-time tunable and fast response local resonant band gap was generated. • The plane wave expansion method and the finite element method were implemented. • The vibration manipulation functionalities were experimentally verified. Metamaterial plates have attracted considerable attention due to their unprecedented elastic wave manipulation abilities. Currently, the band gap and other properties of traditional metamaterial plates are fixed, and the material parameters of most metamaterials cannot be dynamically and continuously adjusted. To address this issue, a two-dimensional (2D) magnetorheological elastomer (MRE) programmable metamaterial plate (MREPMP) with local resonance was proposed. The proposed MREPMP was composed of a thin steel plate and a periodic array of resonators, consisting of MREs and electromagnetic mass blocks. It not only has a compact structural design, but also enables real-time vibration control and programming wave manipulation by altering the amplitude of the current. The dispersion relation of the proposed MREPMP was theoretically calculated based on the plane wave expansion (PWE) method and the simulated transmissibility was numerically calculated using the finite element method in COMSOL. Subsequently, a prototype of the MREPMP was fabricated, and vibration tests were conducted to assess its programmable vibration manipulation functionalities. Two different types of defect paths were used as excitations and the corresponding real-time vibration manipulation performance was analyzed. The simulation results agree with the experimental results, showing that the MREPMP can dynamically tune the band gap and activate different waveguides through continuous online programming. This paper opens up a new idea for tunable manipulation of wave propagation. [Display omitted] [ABSTRACT FROM AUTHOR]

Angle of rotation is a key parameter in motor fault diagnosis under varying speed conditions, and is usually measured by an optical encoder. However, the use of encoders is intrusive and in many scenarios its signal is difficult to access due to technical or commercial reasons. In this study, a novel rotation angle measurement method based on stray flux analysis is proposed and applied to bearing fault diagnosis of brushless direct-current (BLDC) motors. The measurement accuracy of the proposed method is comparable to that from an encoder. The developed method is flexible, noninvasive, and nondestructive. It is easy to implement and eliminates the need for long cables and access of the motor control system. The proposed method can be extended to the diagnosis of motor electrical and drive faults. If implemented with an Internet of Things (IoT) or a hand-held device, it can further improve the reliability of sensorless motor drive systems in industrial automation so as to meet Industry 4.0 requirements. [ABSTRACT FROM AUTHOR]

Abstract: TA2 mice have a high incidence of spontaneous breast cancer without chemical stimulus. There are two proposed explanations for this phenomenon: one is gravidity and the frequency of pregnancies, and the other is related to the presence of the mouse mammary tumor virus (MMTV). MMTV is hormonally regulated and indirectly promotes tumor formation by leading to the activation of Wnt oncogenes through insertional mutagenesis. In order to clarify the relationship between estrogen, progesterone, MMTV, Wnt oncogenes and breast cancer, ovaries from virgin female TA2 mice were removed and the mice were treated with exogenous estradiol and progesterone in different patterns. This study found that the combination of exogenous estradiol and progesterone induced breast cancer formation in TA2 mice without ovaries. MMTV–LTR mRNA exhibited the highest expression in tumor tissue from the combination treatment group (CT). Mammary tissue from mice in the CT group had the highest Wnt1, Wnt5a, Wnt5b and Wnt10b mRNA expression levels. These results indicate that estradiol and progesterone act in a synergistic manner to upregulate MMTV, which subsequently induces breast cancer in TA2 mice. Various members of the Wnt gene family may play specific roles in different stages of carcinogenesis in TA2 mice. [Copyright &y& Elsevier]

Background: Hypoxia can enhance tumor cell invasion and metastasis. The cause and the molecular mechanism are still not clear. Methods: In our study, mouse melanoma B16 cells were inoculated into mouse ischemic limbs and non-ischemic controls and the engrafted melanomas were subsequently observed. Vasculogenic mimicry channels in melanoma tumors of the two groups were counted and the expression of HIF-1alpha, MMP-2, MMP-9 and VEGF was assessed by immunohistochemical staining. Formalin-fixed, paraffin-embedded tissues were used for immunohistochemical staining. Results: In the early stage of engrafted melanoma growth, the size of melanomas in ischemic limbs increased slower than in the controls. However, later there was no obvious difference in their size. Melanoma tumors in the ischemic group had more vasculogenic mimicry channels than those in the controls (P=0.039). Similarly, the expression of HIF-1alpha, MMP-2, MMP-9 and VEGF was higher in the ischemic group than in the non-ischemic controls (P=0.024, 0.047, 0.007 and 0.025, respectively). There was a positive association in melanoma cells of the ischemic group between expression of HIF-1alpha and VEGF, and also between MMP-9 and MMP-2. In the ischemic group, there was statistical significance for the correlation between HIF-1alpha and VEGF expression (r=0.456, P=0.038). Furthermore, MMP-2 expression was positively correlated with MMP-9 and VEGF expression (r=0.589 and 0.502, P=0.008 and 0.024, respectively). Conclusions: Melanoma cells in a hypoxic microenvironment increased HIF-1alpha expression and induced the formation of vasculogenic mimicry channels to acquire an adequate blood supply. On the other hand, the expression of MMP-2 and MMP-9 in tumor tissue increased to enhance the invasiveness. HIF-1alpha, MMP-2 and MMP-9 may be associated with the failure of stop-flow perfusion in some patients with melanoma. [ABSTRACT FROM AUTHOR]

An efficient data reduction algorithm is designed and implemented on an industrial Internet of Things (IIoT) node for permanent magnet synchronous motor (PMSM) bearing fault diagnosis in variable speed conditions. Leakage flux and vibration signals are, respectively, acquired by a magnetic sensor and an accelerometer on the IIoT node in a noninvasive manner. These two signals are processed and mixed on the IIoT and transmitted to a server. The received signal is separated, the cumulative rotation angle is calculated, and the vibration signal is resampled for bearing fault identification. The proposed method can reduce about 95% of the transmission data while maintaining sufficient precision in bearing fault diagnosis in comparison to a traditional method. The proposed method based on edge computing reduces the power consumption, and hence it is suitable to use on a battery-supplied IIoT node for remote PMSM condition monitoring and fault diagnosis. [ABSTRACT FROM AUTHOR]

Stretchable conductive composites (SCCs) are generally elastomer matrices filled with conductive fillers. They combine the conductivity of metals and carbon materials with the flexibility of polymers, which are attractive properties for applications such as stretchable electronics, wearable devices, and flexible sensors. Most conventional conductive composites that are filled with only one type of conductive filler face issues in mechanical and electrical properties. Recently, some studies introduced secondary fillers to create hybrid‐filler SCCs to solve these problems. The secondary fillers produce a synergistic effect with the primary fillers to enhance the electrical conductivity of the composites. They also improve the thermal conductivity and mechanical properties or impart composites with special functions like catalysis and self‐healing. Herein, the fabrication methods, stretchability enhancement strategies, and piezoresistivity of SCCs are analyzed, and their latest applications in stretchable electronics are introduced. Finally, the challenges and prospects of their development are discussed. [ABSTRACT FROM AUTHOR]

Radiation enteritis (RE) is the most common radiotherapy complication, and effective RE treatments are lacking. Resveratrol exerts beneficial effects on radiation injury. However, the effect of resveratrol in radiation-induced intestinal injury and the underlying mechanism remain unclear. Here, a C57BL/6 mouse model of RE was established and an intestinal epithelial cell line was used to evaluate the protective effects of resveratrol against radiation-induced intestinal injury and the underlying mechanisms. Resveratrol improved radiation-induced oxidative stress and cell apoptosis via upregulating antioxidant enzymes and downregulating p53 acetylation. In vivo , resveratrol-treated mice exhibited longer survival; longer villi; more intestinal crypt cells; upregulated expression of Ki67, catalase, and superoxide dismutase 2; and fewer inflammatory proteins and apoptotic cells. These protective effects were suppressed by inhibition of SIRT1. These results demonstrate that resveratrol can reduce radiation-induced intestinal injury by inhibiting oxidative stress and apoptosis via the SIRT1/FOXO3a and PI3K/AKT pathways. • Resveratrol pretreatment attenuated radiation-induced intestinal injury in mice. •Resveratrol mitigated irradiation-induced IEC-6 cell injury. •Resveratrol activated the SIRT1/FOXO3a pathway to inhibit oxidative stress. •The PI3K/AKT pathway may aid resveratrol protective effects against radiation. [ABSTRACT FROM AUTHOR]

Unlike conventional microelectromechanical systems (MEMS), machines based on gallium liquid metal alloys rely on Marangoni flows to induce motion without mechanical moving parts. Despite this advantage, currently developed liquid metal enabled robotic systems still need the locomotion of liquid metal droplets, thereby generating weak actuating forces and limiting their manoeuvrability. Here, a liquid metal engine (LME) is created to work as a jet thruster to continuously power a robot boat without the need of locomotion. In addition, the engine is electrically driven by surface tension without any mechanical moving parts. The structural design and the parameters of operation of the LME are investigated and optimized. Finally, the manipulation of the LME using a motor control unit is demonstrated for driving an untethered robot boat to realize complex locomotion with the precise control over the direction and speed. Thus, this LME could offer new opportunities for developing high‐performance liquid metal machines to power robotic systems. [ABSTRACT FROM AUTHOR]

Malignant tumors still pose serious threats to human health due to their high morbidity and mortality. Recurrence and metastasis are the most important factors affecting patient prognosis. Chemotherapeutic drugs and radiation used to treat these tumors mainly interfere with tumor metabolism, destroy DNA integrity, and inhibit protein synthesis. The upregulation of small ubiquitin-like modifier (SUMO) is a prevalent posttranslational modification (PTM) in various cancers and plays a critical role in tumor development. The dysregulation of SUMOylation can protect cancer cells from stresses exerted by external or internal stimuli. SUMOylation is a dynamic process finely regulated by SUMOylation enzymes and proteases to maintain a balance between SUMOylation and deSUMOylation. An increasing number of studies have reported that SUMOylation imbalance may contribute to cancer development, including metastasis, angiogenesis, invasion, and proliferation. High level of SUMOylation is required for cancer cells to survive internal or external stresses. Downregulation of SUMOylation may inhibit the development of cancer, making it an important potential clinical therapeutic target. Some studies have already begun to treat tumors by inhibiting the expression of SUMOylation family members, including SUMO E1 or E2. The tumor cells become more aggressive under internal and external stresses. The prevention of tumor development, metastasis, recurrence, and radiochemotherapy resistance by attenuating SUMOylation requires further exploration. This review focused on SUMOylation in tumor cells to discuss its effects on tumor suppressor proteins and oncoproteins as well as classical tumor pathways to identify new insights for cancer clinical therapy. [ABSTRACT FROM AUTHOR]

Adipogenesis is the process through which preadipocytes differentiate into adipocytes. During this process, the preadipocytes cease to proliferate, begin to accumulate lipid droplets, and develop morphologic and biochemical characteristics of mature adipocytes. Mesenchymal stem cells (MSCs) are a type of adult stem cells known for their high plasticity and capacity to generate mesodermal and nonmesodermal tissues. Many mature cell types can be generated from MSCs, including adipocyte, osteocyte, and chondrocyte. The differentiation of stem cells into multiple mature phenotypes is at the basis for tissue regeneration and repair. Cancer stem cells (CSCs) play a very important role in tumor development and have the potential to differentiate into multiple cell lineages. Accumulating evidence has shown that cancer cells can be induced to differentiate into various benign cells, such as adipocytes, fibrocytes, osteoblast, by a variety of small molecular compounds, which may provide new strategies for cancer treatment. Recent studies have reported that tumor cells undergoing epithelial-to-mesenchymal transition can be induced to differentiate into adipocytes. In this review, molecular mechanisms, signal pathways, and the roles of various biological processes in adipose differentiation are summarized. Understanding the molecular mechanism of adipogenesis and adipose differentiation of cancer cells may contribute to cancer treatments that involve inducing differentiation into benign cells. [ABSTRACT FROM AUTHOR]

One of the most prominent features of tumor cells is uncontrolled cell proliferation caused by an abnormal cell cycle, and the abnormal expression of cell cycle-related proteins gives tumor cells their invasive, metastatic, drug-resistance, and anti-apoptotic abilities. Recently, an increasing number of cell cycle-associated proteins have become the candidate biomarkers for early diagnosis of malignant tumors and potential targets for cancer therapies. As an important cell cycle regulatory protein, Cell Division Cycle 25C (CDC25C) participates in regulating G2/M progression and in mediating DNA damage repair. CDC25C is a cyclin of the specific phosphatase family that activates the cyclin B1/CDK1 complex in cells for entering mitosis and regulates G2/M progression and plays an important role in checkpoint protein regulation in case of DNA damage, which can ensure accurate DNA information transmission to the daughter cells. The regulation of CDC25C in the cell cycle is affected by multiple signaling pathways, such as cyclin B1/CDK1, PLK1/Aurora A, ATR/CHK1, ATM/CHK2, CHK2/ERK, Wee1/Myt1, p53/Pin1, and ASK1/JNK-/38. Recently, it has evident that changes in the expression of CDC25C are closely related to tumorigenesis and tumor development and can be used as a potential target for cancer treatment. This review summarizes the role of CDC25C phosphatase in regulating cell cycle. Based on the role of CDC25 family proteins in the development of tumors, it will become a hot target for a new generation of cancer treatments. [ABSTRACT FROM AUTHOR]

Background: Our previous studies have confirmed that cobalt chloride (CoCl2) can induce the formation of polyploid giant cancer cells (PGCCs), which is the key to the heterogeneity of solid tumors. PGCC formation is closely related to the abnormal expression of cell cycle-related proteins and cell fusion. In this study, we investigated the molecular mechanism of PGCCs formation by detecting the expression of cell cycle-related proteins in mutant and wild-type p53 cancer cell lines. Methods: HEY, BT-549, SKOv3 and MDA-MB-231 cells were treated with CoCl2 and the cell cycle was detected by flow cytometry. The expression and subcellular localization of cell cycle-related proteins, kinases, and P53 were compared before and after CoCl2 treatment. Immunoprecipitation was used to analyze the interacting proteins of pCDC25C-Ser216 and pCDC25C-Ser198. The clinicopathologic significances of these cell cycle-related proteins and protein kinases expression were studied. Results: CoCl2 induced the formation of PGCCs and G2/M arrest. CDC25C, cyclin B1, and CDK1 expressions after CoCl2 treatment were lower than that in control cells. Cytoplasmic CDC25C was degraded by ubiquitin-dependent proteasome. The expression of P53 and phosphokinases including CHK1, CHK2, PLK1, and Aurora A increased after CoCl2 treatment. The expression of pCDC25C-Ser216 and pCDC25C-Ser198 depended upon the genotype of p53. The expressions of cell cycle-related proteins and kinases gradually increased with the development of ovarian cancer and breast cancer. Conclusion: CHK1, CHK2–pCDC25C-Ser216–cyclin B1–CDK1, and Aurora A–PLK1–pCDC25C-Ser198–cyclin B1–CDK1 signaling pathways may participate in the formation of PGCCs and different phosphorylation sites of CDC25C may be associated with the genotype of p53. [ABSTRACT FROM AUTHOR]

Background: To investigate the expression of long noncoding RNA (lncRNA) LINC00426 (long intergenic nonprotein coding RNA 426) in non‐small cell lung cancer (NSCLC) patients and its correlation with their prognosis. Methods: The expression of long noncoding RNA LINC00426 of non‐small cell lung cancer (NSCLC) in The Cancer Genome Atlas (TCGA) database was screened. According to the expression level of LINC00426 in tumor tissue of NSCLC patients, the patients were divided into high and low LINC00426 expression groups. The correlation between LINC00426 expression group and the prognosis of the patient was analyzed by log‐rank test. A total of 72 NSCLC patients who had undergone surgery were retrospectively included in this study. LINC00426 relative expression of tumor and normal lung tissue of the included 72 NSCLC patients were examined by real‐time quantitative PCR assay. The correlation between LINC00426 expression and the patients' clinical characteristics were also evaluated. Results: LINC00426 relative expression was not statistically different between cancer and normal tissue (P > 0.05) of NSCLC patients in the TCGA database. The amplification and deep deletion mutation of LINC00426 gene was found in 0.5% of NSCLC patients. The overall survival (OS) of the LINC00426 high expression group was significantly higher than that of the low expression group (HR = 0.81, P = 0.044), while there was no significant difference between the high and low expression group (HR = 0.97, P = 0.82) for disease‐free survival (DFS). LINC0042646 expression level was elevated in 46 cases in normal lung tissue compared to the tumor tissue of the 72 NSCLC patients. LINC0042646 expression level was significantly correlated with the clinical stage (P < 0.05). Conclusion: Long noncoding RNA LINC00426 was downregulated in the tumor tissue of NSCLC patients and correlated with poor prognosis. [ABSTRACT FROM AUTHOR]