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Objective To explore the relationship between motor skills and cognitive self-regulation ability of 4-6 year-old children, so as to provide a basis for the demonstration of multiple values of sports. Methods 165 4-6 year-old children were selected as the research objects. The development level of motor skills was tested by Bruininks-Oseretsky Test of Motor Proficiency-2nd Edition (BOT-2), BOT-2 sensitivity subscale, Movement Assessment Battery for Children-test-2nd Edition (MABC Test-2), and MABC Test-2 throw-in motor subscale; the cognitive self-regulation level of children was evaluated by learning related cognitive self-regulation test package. Results Correlation analysis, logistic regression analysis and linear regression analysis showed that bilateral limb movement coordination, hand eye coordination, movement agility, involvement balance were positively correlated with preschool children's cognitive self-regulation ability. After using the interaction effects of month age and multiple movement skills, only bilateral limb movement coordination was significantly positively correlated with children's cognitive self-regulation ability. Boys' and girls' movement skills were positively correlated with children's cognitive self-regulation ability, with boys B =0.22.95% CI=0.08-0.36 and girls 13=0.16, 95% CI=0.04-0.29, respectively; however, there was no significant difference in the correlation between motor skills and cognitive self-regulation for different genders. Conclusion 4-6 year-old children's bilateral limb coordination skills are related to cognitive self-regulation. It is suggested that preschool sports educators should pay attention to the development and intervention of children's bilateral limb movement coordination games, and that families should develop children's coordination ability through regular parent-child sports interaction to promote the development of preschool children's cognitive self-regulation and the formation of good learning quality. [ABSTRACT FROM AUTHOR]

Abstract: Plant transpiration, a process of water movement through a plant and its evaporation from aerial parts especially leaves, consumes a large component of the total continental precipitation (≈48%) and significantly influences global water distribution and climate. To date, various chemical and/or biological explorations have been made to tune the transpiration but with uncertain environmental risks. In recent years, interfacial solar steam/vapor generation is attracting a lot of attention for achieving high energy transfer efficiency. Various optical and thermal designs at the solar absorber–water interface for potential applications in water purification, seawater desalination, and power generation appear. In this work, the concept of interfacial solar vapor generation is extended to tunable plant transpiration by showing for the first time that the transpiration efficiency can also be enhanced or suppressed through engineering the solar absorber–leaf interface. By tuning the solar absorption of membrane in direct touch with green leaf, surface temperature of green leaf will change accordingly because of photothermal effect, thus the transpiration efficiency as well as temperature and relative humidity in the surrounding environment will be tuned. This tunable transpiration by interfacial absorber‐leaf engineering can open an alternative avenue to regulate local atmospheric temperature, humidity, and eventually hydrologic cycle. [ABSTRACT FROM AUTHOR]

MiR-375 has been identified as oncogenes or tumor suppressor genes which has the potential to the development and growth of cancers. However, the limited information concerning the expression and role of miR-375 in colorectal cancer (CRC) is available. In this work, we provide evidence for a function of miR-375 in the inhibition of CRC proliferation. Here, we showed that miR-375, down-modulated in human colorectal cancer tissues compared with normal human colon tissues, including several colorectal cancer cell lines. Subsequently, using the luciferase reporter assays, we found that the KLF4 untranslated region (3′UTR) carries the direct binding site of miR-375. In terms of function in vitro, CCK-8 assay, colony formation assay, and cell cycle assay demonstrated that the overexpression of miR-375 suppressed CRC cell proliferation. Inhibition of KLF4 performed similar effects with miR-375 overexpression on CRC cells, and overexpression of KLF4 could significantly reverse the tumor suppressive effects of miR-375 on CRC cells. Furthermore, we found overexpressed miR-375 effectively repressed tumor growth via KLF4 in xenograft animal experiment. Taken together, these results illustrated that miR-375 depresses proliferation of CRC through regulating 3′UTR of KLF4 mRNA, which might be a promising therapeutic target for treating colorectal cancers. [ABSTRACT FROM AUTHOR]

Breast cancer (BC) has an extremely high global incidence rate. The Xihuang pill (XHP), a traditional Chinese formula, originates from Hongxu Wang's "Life-Saving Manual of Diagnosis and Treatment of External Diseases" written during the Qing Dynasty. In this book, XHP, was first suggested as an anticancer treatment for BC. However, the regulatory mechanism of XHP on BC requires further investigated. To assess the effects of XHP on BC and elucidate the underlying associated signaling network. The influence of XHP on cellular viability, proliferation, and apoptosis of MDA-MB-231 and BT-549 cells were examined. The ability to metastasize was evaluated using Transwell invasion and wound healing tests. Western blotting was used to examine the epithelial-mesenchymal transition (EMT) markers expression. RNA sequencing and bioinformatic analysis were utilized to investigate the regulation mechanism of XHP. A subcutaneous tumor model was developed to study the tumor-inhibitory effects of XHP or/and Doxorubicin (Dox) on BALB/c nude mice, and the EMT marker levels in tumor tissues were determined using immunohistochemical labeling. XHP demonstrated anticancer effects on BC cells by suppressing cell proliferation, inducing cellular apoptosis, and inhibiting EMT progression. XHP may regulate the EMT via the TGF-β axis, as shown by RNA sequencing and Western blotting analysis. Furthermore, the combination of XHP and Dox had a stronger therapeutic effect on BC cell proliferation, apoptosis, and metastasis in both cellular and animal models. We were the first to reveal that XHP abrogated EMT progression via modulating the TGF-β axis. Furthermore, the combination therapy of XHP and Dox presents a promising novel therapeutic candidate for BC patients. [Display omitted] • XHP suppressed malignancy-related activities in breast cancer cells by inhibiting cellular growth and the progression of epithelial-mesenchymal transition. • XHP combined with Doxorubicin enhanced chemotherapy effectiveness in vitro and in vivo. • XHP attenuated breast cancer metastasis by downregulating the TGF-β signaling pathway. [ABSTRACT FROM AUTHOR]

Angiogenesis is considered a hallmark pathophysiological process in tumor development. Aberrant vasculature resulting from tumor angiogenesis plays a critical role in the development of resistance to breast cancer treatments, via exacerbation of tumor hypoxia, decreased effective drug concentrations within tumors, and immune-related mechanisms. Antiangiogenic therapy can counteract these breast cancer resistance factors by promoting tumor vascular normalization. The combination of antiangiogenic therapy with chemotherapy, targeted therapy, or immunotherapy has emerged as a promising approach for overcoming drug resistance in breast cancer. This review examines the mechanisms associated with angiogenesis and the interactions among tumor angiogenesis, the hypoxic tumor microenvironment, drug distribution, and immune mechanisms in breast cancer. Furthermore, this review provides a comprehensive summary of specific antiangiogenic drugs, and relevant studies assessing the reversal of drug resistance in breast cancer. The potential mechanisms underlying these interventions are discussed, and prospects for the clinical application of antiangiogenic therapy to overcome breast cancer treatment resistance are highlighted., Competing Interests: No potential conflicts of interest are disclosed., (Copyright: © 2024, The Authors.)

Chemotherapy remains a critical component of triple-negative breast cancer (TNBC) treatment; however, patients often develop resistance to chemotherapeutic agents. Accumulating evidence indicates that deubiquitylases (DUBs) play pivotal roles in regulating cell proliferation, differentiation, apoptosis, and tumorigenesis. Deubiquitylase OTUD1 is considered a tumor suppressor in various cancers, yet its role in doxorubicin sensitivity in breast cancer patients remains inadequately understood. In this study, we investigated the expression levels and prognostic role of OTUD1 in breast cancer. Our findings demonstrated that OTUD1 was downregulated in TNBC, and lower OTUD1 expression levels were correlated with poor prognosis. We utilized the CCK-8 cell viability assay, flow cytometric analysis, and a TNBC mouse xenograft model to examine the influence of OTUD1 on doxorubicin (DOX) chemotherapy sensitivity in vitro and in vivo. Western blot and immunohistochemistry were employed to explore the correlation between OTUD1 and P16. Our results indicated that upregulation of OTUD1 expression inhibits TNBC cell proliferation and enhances its sensitivity to doxorubicin. Additionally, rescue experiments confirmed that the chemosensitizing effect of OTUD1 overexpression could be reversed by the inhibition of P16. Therefore, our findings reveal that OTUD1 sensitizes TNBC cells to DOX by upregulating P16 expression, suggesting a potential new diagnostic biomarker and therapeutic target for the future treatment of TNBC., Competing Interests: Declaration of Competing Interest The authors declare that they have no competing interests. We confirm that neither the manuscript nor any parts of its content are currently under consideration or published in another journal. All authors have approved the manuscript and agree with its submission to pathology - research and practice., (Copyright © 2023 Elsevier GmbH. All rights reserved.)

MiR-375 has been identified as oncogenes or tumor suppressor genes which has the potential to the development and growth of cancers. However, the limited information concerning the expression and role of miR-375 in colorectal cancer (CRC) is available. In this work, we provide evidence for a function of miR-375 in the inhibition of CRC proliferation. Here, we showed that miR-375, down-modulated in human colorectal cancer tissues compared with normal human colon tissues, including several colorectal cancer cell lines. Subsequently, using the luciferase reporter assays, we found that the KLF4 untranslated region (3'UTR) carries the direct binding site of miR-375. In terms of function in vitro, CCK-8 assay, colony formation assay, and cell cycle assay demonstrated that the overexpression of miR-375 suppressed CRC cell proliferation. Inhibition of KLF4 performed similar effects with miR-375 overexpression on CRC cells, and overexpression of KLF4 could significantly reverse the tumor suppressive effects of miR-375 on CRC cells. Furthermore, we found overexpressed miR-375 effectively repressed tumor growth via KLF4 in xenograft animal experiment. Taken together, these results illustrated that miR-375 depresses proliferation of CRC through regulating 3'UTR of KLF4 mRNA, which might be a promising therapeutic target for treating colorectal cancers.