Research Progress of Single-Photon Emitters Based on Two-Dimensional Materials.

From quantum communications to quantum computing, single-photon emitters (SPEs) are essential components of numerous quantum technologies. Two-dimensional (2D) materials have especially been found to be highly attractive for the research into nanoscale light-matter interactions. In particular, localized photonic states at their surfaces have attracted great attention due to their enormous potential applications in quantum optics. Recently, SPEs have been achieved in various 2D materials, while the challenges still remain. This paper reviews the recent research progress on these SPEs based on various 2D materials, such as transition metal dichalcogenides (TMDs), hexagonal boron nitride (hBN), and twisted-angle 2D materials. Additionally, we summarized the strategies to create, position, enhance, and tune the emission wavelength of these emitters by introducing external fields into these 2D system. For example, pronounced enhancement of the SPEs' properties can be achieved by coupling with external fields, such as the plasmonic field, and by locating in optical microcavities. Finally, this paper also discusses current challenges and offers perspectives that could further stimulate scientific research in this field. These emitters, due to their unique physical properties and integration potential, are highly appealing for applications in quantum information and communication, as well as other physical and technological fields.

Epigenetic Reprogramming Potentiates ICAM1 Antibody Drug Conjugates in Preclinical Models of Melanoma.

Therapeutic benefits and underlying biomechanism(s) of antibody drug conjugates (ADC) in combination with other targeted therapeutics are largely unknown. Here, the synergy between ADC and epigenetic drug decitabine (DAC), a clinically approved DNA methylation inhibitor, in multiple preclinical models of melanoma specifically investigated. Mechanistically, the underlying biomechanisms of how DAC cooperatively worked with ICAM1 antibody conjugated DNA topoisomerase I inhibitor DXd (I1-DXd) is elucidated. DAC treatment significantly enhanced anti-tumor efficacy of I1-DXd by upregulating antigen expression, enhancing antibody internalization and potentiating tumor sensitivity by epigenetically reprogramming of melanoma. Meanwhile, I1-DXd/DAC combination also exerted regulatory effects on tumor microenvironment (TME) by enhancing tumor infiltration of innate and adaptive immune cells and improving penetration of ADCs with a boosted antitumor immunity. This study provides a rational ADC combination strategy for solid tumor treatment.

Enhance Carrier Diffusion of Monolayer MoSe2 by Interface Engineering.

Two-dimensional materials hold great potentials for beyond-CMOS (complementary metal-oxide-semiconductor) electronical and optoelectrical applications, and the development of field effect transistors (FET) with excellent performance using such materials is of particular interest. How to improve the performance of devices thus becomes an urgent issue. The performance of FETs depends greatly on the intrinsic electrical properties of the channel materials, meanwhile the device interface quality, such as extrinsic scattering of charged impurities, charge traps, and substrate surface roughness have a great influence on the performance. In this paper, the impact of the interface quality on the carrier diffusion behaviors of monolayer (ML) MoSe2 has been investigated by using an in situ ultrafast laser technique to avoid the surface contamination during device fabrication process. Two types of self-assembled monolayers (SAMs) are introduced to modify the gate dielectric surface through an interface engineering approach to obtain chemical-stable interfaces. The results showed that the transport properties of ML MoSe2 were enhanced after interface engineering, for example, the carrier mobility of ML MoSe2 was improved from ∼59.4 to ∼166.5 cm2 V-1 s-1 after the SAM modification. Meanwhile, the photocarrier dynamics of ML MoSe2 before and after interfacial engineering were also carefully studied. Our studies provide a feasible method for improving the carrier diffusion behaviors of such materials, and making them suited for application in future integrated circuit.

Tunable Photocarrier Dynamics in CuS Nanoflakes under Pressure Modulation.

Two-dimensional materials with a unique layered structure have attracted intense attention all around the world due to their extraordinary physical properties. Most importantly, the internal Coulomb coupling can be regulated, and thus electronic transition can be realized by manipulating the interlayer interaction effectively through adding external fields. At present, the properties of two-dimensional materials can be tuned through a variety of methods, such as adding pressure, strain, and electromagnetic fields. For optoelectronic applications, the lifetime of the photogenerated carriers is one of the most crucial parameters for the materials. Here, we demonstrate effective modulation of the optical band gap structure and photocarrier dynamics in CuS nanoflakes by applying hydrostatic pressure via a diamond anvil cell. The peak differential reflection signal shows a linear blueshift with the pressure, suggesting effective tuning of interlayer interaction inside CuS by pressure engineering. The results of transient absorption show that the photocarrier lifetime decreases significantly with pressure, suggesting that the dissociation process of the photogenerated carriers accelerates. It could be contributed to the phase transition or the decrease of the phonon vibration frequency caused by the pressure. Further, Raman spectra reveal the change of Cu-S and S-S bonds after adding pressure, indicating the possible occurrence of structural phase transition. Interestingly, all of the variation modes are reversible after releasing pressure. This work has provided an excellent sight to show the regulation of pressure on the photoelectric properties of CuS, exploring CuS to wider applications that can lead toward the realization of future excitonic and photoelectric devices modulated by high pressure.

Dual roles of HK3 in regulating the network between tumor cells and tumor-associated macrophages in neuroblastoma.

Neuroblastoma (NB) is the most common and deadliest extracranial solid tumor in children. Targeting tumor-associated macrophages (TAMs) is a strategy for attenuating tumor-promoting states. The crosstalk between cancer cells and TAMs plays a pivotal role in mediating tumor progression in NB. The overexpression of Hexokinase-3 (HK3), a pivotal enzyme in glucose metabolism, has been associated with poor prognosis in NB patients. Furthermore, it correlates with the infiltration of M2-like macrophages within NB tumors, indicating its significant involvement in tumor progression. Therefore, HK3 not only directly regulates the malignant biological behaviors of tumor cells, such as proliferation, migration, and invasion, but also recruits and polarizes M2-like macrophages through the PI3K/AKT-CXCL14 axis in neuroblastoma. The secretion of lactate and histone lactylation alterations within tumor cells accompanies this interaction. Additionally, elevated expression of HK3 in M2-TAMs was found at the same time. Modulating HK3 within M2-TAMs alters the biological behavior of tumor cells, as demonstrated by our in vitro studies. This study highlights the pivotal role of HK3 in the progression of NB malignancy and its intricate regulatory network with M2-TAMs. It establishes HK3 as a promising dual-functional biomarker and therapeutic target in combating neuroblastoma.

Unconventional Surface Doping Effect on the Spin State of an Adsorbed Magnetic Molecule.

Magnetic molecules adsorbed on two-dimensional (2D) substrates have attracted broad attention because of their potential applications in quantum device applications. Experimental observations have demonstrated substantial alteration in the spin excitation energy of iron phthalocyanine (FePc) molecules when adsorbed on nitrogen-doped graphene substrates. However, the underlying mechanism responsible for this notable change remains unclear. To shed light on this, we employ an embedding method and ab initio quantum chemistry calculations to investigate the effects of surface doping on molecular properties. Our study unveils an unconventional chemical bonding at the interface between the FePc molecule and the N-doped graphene. This bonding interaction, stronger than non-covalent interactions, significantly modifies the magnetic anisotropy energy of the adsorbed molecule, consistent with experimental observations. These findings provide valuable insights into the electronic and magnetic properties of molecules on 2D substrates, offering a promising pathway for precise manipulation of molecular spin states.

Exosomes From Human Umbilical Cord Stem Cells Suppress Macrophage-to-myofibroblast Transition, Alleviating Renal Fibrosis.

Renal fibrosis, a progressive scarring of the kidney, lacks effective treatment. Human umbilical cord mesenchymal stem cell-derived exosomes (HucMSC-Exos) hold promise for treating kidney diseases due to their anti-inflammatory properties. This study investigates their potential to lessen renal fibrosis by targeting macrophage-to-myofibroblast transformation (MMT), a key driver of fibrosis. We employed a mouse model of unilateral ureteral obstruction (UUO) and cultured cells exposed to transforming growth factor-ß (TGF-ß) to mimic MMT. HucMSC-Exos were administered to UUO mice, and their effects on kidney function and fibrosis were assessed. Additionally, RNA sequencing and cellular analysis were performed to elucidate the mechanisms by which HucMSC-Exos inhibit MMT. HucMSC-Exos treatment significantly reduced kidney damage and fibrosis in UUO mice. They downregulated markers of fibrosis (Collagen I, vimentin, alpha-smooth muscle actin) and suppressed MMT (α-SMA + F4/80 + cells). Furthermore, ARNTL, a specific molecule, emerged as a potential target of HucMSC-Exos in hindering MMT and consequently preventing fibrosis. HucMSC-Exos effectively lessen renal fibrosis by suppressing MMT, suggesting a novel therapeutic strategy for managing kidney damage and fibrosis.

Application of hydrogel microneedles in the oral cavity.

Microneedles are a transdermal drug delivery system in which the needle punctures the epithelium to deliver the drug directly to deep tissues, thus avoiding the influence of the first-pass effect of the gastrointestinal tract and minimizing the likelihood of pain induction. Hydrogel microneedles are microneedles prepared from hydrogels that have good biocompatibility, controllable mechanical properties, and controllable drug release and can be modified to achieve environmental control of drug release in vivo. The large epithelial tissue in the oral cavity is an ideal site for drug delivery via microneedles. Hydrogel microneedles can overcome mucosal hindrances to delivering drugs to deep tissues; this prevents humidity and a highly dynamic environment in the oral cavity from influencing the efficacy of the drugs and enables them to obtain better therapeutic effects. This article analyzes the materials and advantages of common hydrogel microneedles and reviews the application of hydrogel microneedles in the oral cavity.

Toll-Like Receptor 9 Aggravates Pulmonary Fibrosis by Promoting NLRP3-Mediated Pyroptosis of Alveolar Epithelial Cells.

The apoptosis-prone property of alveolar epithelial cells plays a crucial role in pulmonary fibrosis(PF), but the role of pyroptosis in it is still unclear. Toll-like receptor 9(TLR9) has been reported to play a vital role in the pathogenesis of many diseases. However, the effect of TLR9 on alveolar epithelial cells in PF has not been fully elucidated. Gene expression microarray related to Idiopathic pulmonary fibrosis(IPF) was obtained from the Gene Expression Omnibus(GEO) database. In the mouse model of bleomycin-induced PF, adeno-associated virus(AAV6) was used to interfere with TLR9 to construct TLR9 knockdown mice to study the role of TLR9 in PF, and the specific mechanism was studied by intratracheal instillation of NLR family pyrin domain containing 3(NLRP3) activator. In vitro experiments were performed using A549 cells. Bleomycin-induced pyroptosis in the lung tissue of PF mice increased, and TLR9 protein levels also increased, especially in alveolar epithelial cells. The levels of fibrosis and pyroptosis in lung tissue of TLR9 knockdown mice were improved. We found that TLR9 can bind to the NLRP3, thereby increasing the activation of the NLRP3/caspase-1 inflammasome pathway. When we use the NLRP3 activator, the levels of fibrosis and pyroptosis in lung tissue of TLR9 knockout mice can be counteracted. Pyroptosis of alveolar epithelial cells plays a vital role in PF, and TLR9 can promote NLRP3-mediated pyroptosis of alveolar epithelial cells to aggravate the progression of PF and may become a feasible target for the prevention and treatment of PF.

M-Ni-Co MOF (M=Zn, Fe, Mn) for high-performance supercapacitors by adjusting its morphology.

Metal-organic frameworks (MOF) have been wildly synthesised and studied as electrode materials for supercapacitors, and bimetallic MOF of Ni and Co has been broadly studied to enhance both specific capacitance and stability of supercapacitors. Herein, a best performance (about 320 F/g) of Ni-Co bimetallic MOF was found in a uniform preparation condition by adjusting the ratio of Ni to Co. Then tiny third metal ion was introduced, and we found that the morphology of material has a significant change on the original basis. Furthermore, certain ions (Zn, Fe, Mn) introduced make a huge improvement in capacitance based on Ni-Co MOF of 320 F/g. The result shows that Zn-Ni-Co MOF, Fe-Ni-Co MOF and Mn-Ni-Co MOF perform specific capacitance of 1135 F/g, 870 F/g and 760F/g at 1 A/g, respectively. Meanwhile, the asymmetric supercapacitor (ASC) was constructed by Zn-Ni-Co MOF as positive electrode and active carbon (AC) as negative electrode. The Zn-Ni-Co MOF//AC ASC possesses a energy density of 58 Wh/kg at a power density of 775 W/kg. This research provides a new methods to regulate the morphology of MOF and a novel viewpoint for assembling high-performance, low-price, and eco-friendly green energy storage devices.

The Potential Applications and Challenges of ChatGPT in the Medical Field.

ChatGPT, an AI-driven conversational large language model (LLM), has garnered significant scholarly attention since its inception, owing to its manifold applications in the realm of medical science. This study primarily examines the merits, limitations, anticipated developments, and practical applications of ChatGPT in clinical practice, healthcare, medical education, and medical research. It underscores the necessity for further research and development to enhance its performance and deployment. Moreover, future research avenues encompass ongoing enhancements and standardization of ChatGPT, mitigating its limitations, and exploring its integration and applicability in translational and personalized medicine. Reflecting the narrative nature of this review, a focused literature search was performed to identify relevant publications on ChatGPT's use in medicine. This process was aimed at gathering a broad spectrum of insights to provide a comprehensive overview of the current state and future prospects of ChatGPT in the medical domain. The objective is to aid healthcare professionals in understanding the groundbreaking advancements associated with the latest artificial intelligence tools, while also acknowledging the opportunities and challenges presented by ChatGPT.

Establishment and validation of nomograms to predict the overall survival and cancer-specific survival for non-metastatic bladder cancer patients: A large population-based cohort study and external validation.

This study aimed to develop nomograms to accurately predict the overall survival (OS) and cancer-specific survival (CSS) of non-metastatic bladder cancer (BC) patients. Clinicopathological information of 260,412 non-metastatic BC patients was downloaded from the Surveillance, Epidemiology, and End Results (SEER) database from 2000 to 2020. LASSO method and Cox proportional hazard regression analysis were utilized to discover the independent risk factors, which were used to develop nomograms. The accuracy and discrimination of models were tested by the consistency index (C-index), the area under the subject operating characteristic curve (AUC) and the calibration curve. Decision curve analysis (DCA) was used to test the clinical value of nomograms compared with the TNM staging system. Nomograms predicting OS and CSS were constructed after identifying independent prognostic factors. The C-index of the training, internal validation and external validation cohort for OS was 0.722 (95%CI: 0.720-0.724), 0.723 (95%CI: 0.721-0.725) and 0.744 (95%CI: 0.677-0.811). The C-index of the training, internal validation and external validation cohort for CSS was 0.794 (95%CI: 0.792-0.796), 0.793 (95%CI: 0.789-0.797) and 0.879 (95%CI: 0.814-0.944). The AUC and the calibration curves showed good accuracy and discriminability. The DCA showed favorable clinical potential value of nomograms. Kaplan-Meier curve and log-rank test uncovered statistically significance survival difference between high- and low-risk groups. We developed nomograms to predict OS and CSS for non-metastatic BC patients. The models have been internally and externally validated with accuracy and discrimination and can assist clinicians to make better clinical decisions.

Integrative analysis with machine learning identifies diagnostic and prognostic signatures in neuroblastoma based on differentially DNA methylated enhancers between INSS stage 4 and 4S neuroblastoma.

INTRODUCTION: Accumulating evidence demonstrates that aberrant methylation of enhancers is crucial in gene expression profiles across several cancers. However, the latent effect of differently expressed enhancers between INSS stage 4S and 4 neuroblastoma (NB) remains elusive. METHODS: We utilized the transcriptome and methylation data of stage 4S and 4 NB patients to perform Enhancer Linking by Methylation/Expression Relationships (ELMER) analysis, discovering a differently expressed motif within 67 enhancers between stage 4S and 4 NB. Harnessing the 67 motif genes, we established the INSS stage related signature (ISRS) by amalgamating 12 and 10 distinct machine learning (ML) algorithms across 113 and 101 ML combinations to precisely diagnose stage 4 NB among all NB patients and to predict the prognosis of NB patients. Based on risk scores calculated by prognostic ISRS, patients were categorized into high and low-risk groups according to median risk score. We conducted comprehensive comparisons between two risk groups, in terms of clinical applications, immune microenvironment, somatic mutations, immunotherapy, chemotherapy and single-cell analysis. Ultimately, we empirically validated the differential expressions of two ISRS model genes, CAMTA2 and FOXD1, through immunochemistry staining. RESULTS: Through leave-one-out cross-validation, in both feature selection and model construction, we selected the random forest algorithm to diagnose stage 4 NB, and Enet algorithm to develop prognostic ISRS, due to their highest average C-index across five NB cohorts. After validations, the ISRS demonstrated a stable predictive capability, outperforming the previously published NB signatures and several clinic variables. We stratified NB patients into high and low-risk group based on median risk score, which showed the low-risk group with a superior survival outcome, an abundant immune infiltration, a decreased mutation landscape, and an enhanced sensitivity to immunotherapy. Single-cell analysis between two risk groups reveals biologically cellular variations underlying ISRS. Finally, we verified the significantly higher protein levels of CAMTA2 and FOXD1 in stage 4S NB, as well as their protective prognosis value in NB. CONCLUSION: Based on multi-omics data and ML algorithms, we successfully developed the ISRS to enable accurate diagnosis and prognostic stratification in NB, which shed light on molecular mechanisms of spontaneous regression and clinical utilization of ISRS.

One-stage posterior transpedicular debridement, hemi-interbody and unilateral-posterior bone grafting, and instrumentation for the treatment of thoracic spinal tuberculosis: a retrospective study.

PURPOSE: To investigate the clinical efficacy and feasibility of the surgical treatment of thoracic spinal tuberculosis using one-stage posterior instrumentation, transpedicular debridement, and hemi-interbody and unilateral posterior bone grafting. METHODS: Fifty-six patients with thoracic spinal tuberculosis who underwent surgery performed by a single surgeon between September 2009 and August 2020 were enrolled in this study. Based on data from the erythrocyte sedimentation rate (ESR), Visual Analog Scale (VAS), and Cobb angle before surgery, after surgery, and at the most recent follow-up, clinical effectiveness was assessed using statistical analysis. The variables investigated included operating time, blood loss, complications, neurological function, and hemi-interbody fusion. RESULTS: None of the patients experienced significant surgery-associated complications. At the last follow-up, 23 of the 25 patients (92%) with neurological impairment showed improvement. The thoracic kyphotic angle was significantly decreased from 24.1 ± 9.9° to 13.4 ± 8.6° after operation (P < 0.05), and the angle was 14.44 ± 8.8° at final follow-up (P < 0.05). The Visual Analog Scale significantly decreased from 6.7 ± 1.4 preoperatively to 2.3 ± 0.8 postoperatively (P < 0.05) and finally to 1.2 ± 0.7 at the last follow-up (P < 0.05). Bone fusion was confirmed in 56 patients at 3-6 months postoperatively. CONCLUSIONS: One-stage posterior transpedicular debridement, hemi-interbody and unilateral posterior bone grafting, and instrumentation are effective and feasible treatment methods for thoracic spinal tuberculosis.

Doxycycline hydrochloride inhibits the progress of malignant rhabdoid tumor of kidney by targeting MMP17 and MMP1 through PI3K-Akt signaling pathway.

OBJECTIVE: To identify therapeutic targets for malignant rhabdoid tumors of kidney (MRTK) and to investigate the effects and underlying mechanism of doxycycline hydrochloride on these tumors. METHODS: Gene expression and clinical data of MRTK were retrieved from the TARGET database. Differentially expressed genes (DEGs) and prognostic-related genes (PRGs) were selected through a combination of statistical analyses. The functional roles of MMP17 and MMP1 were elucidated through RNA overexpression and intervention experiments. Furthermore, in vitro and in vivo studies provided evidence for the inhibitory effect of doxycycline hydrochloride on MRTK. Additionally, transcriptome sequencing was employed to investigate the underlying molecular mechanisms. RESULTS: 3507 DEGs and 690 PRGs in MRTK were identified. Among these, we focused on 41 highly expressed genes associated with poor prognosis and revealed their involvement in extracellular matrix regulatory pathways. Notably, MMP17 and MMP1 stood out as particularly influential genes. When these genes were knocked out, a significant inhibition of proliferation, invasion and migration was observed in G401 cells. Furthermore, our study explored the impact of the matrix metalloproteinase inhibitor, doxycycline hydrochloride, on the malignant progression of G401 both in vitro and in vivo. Combined with sequencing data, the results indicated that doxycycline hydrochloride effectively inhibited MRTK progression, due to its ability to suppress the expression of MMP17 and MMP1 through the PI3K-Akt signaling pathway. CONCLUSION: Doxycycline hydrochloride inhibits the expression of MMP17 and MMP1 through the PI3K-Akt signaling pathway, thereby inhibiting the malignant progression of MRTK in vivo and in vitro.

Efficacy and late kidney effects of nephron-sparing surgery in the management of unilateral Wilms tumor: a systematic review and meta-analysis.

To evaluate the efficiency and long-term renal function of nephron sparing surgery (NSS) in unilateral WT patients compared with radical nephrectomy (RN). The review was performed following Cochrane Handbook guidelines and Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). We searched five databases (Pubmed, Embase, Scopus, Web of Science and Cochrane) for studies reporting the efficiency and late renal function of NSS and/or RN on February 10, 2023. Comparative studies were evaluated by Risk of Bias in Non-randomized Studies of Interventions (ROBINS-I) and RoB 2.0. Assessed outcomes included survival rate, relapse rate, eGFR, renal dysfunction and hypertension. 26 studies involving 10322 unilateral WT cases underwent RN and 657 unilateral WT cases underwent NSS were enrolled. Overall effect estimates demonstrated that NSS significantly increased eGFR at follow-up (SMD, 0.38; 95% CI 0.05-0.72; p = 0.025) compared to that at diagnosis, and RN did not significantly decrease eGFR at follow-up (SMD, - 0.33; 95% CI - 0.77-0.11; p = 0.142) compared to that at diagnosis. Moreover, no significant difference was found in outcomes of survivability (OR, 1.38; 95% CI 0.82-2.32; p = 0.226), recurrence (OR, 0.62; 95% CI 0.34-1.12; p = 0.114), eGFR at follow-up (SMD, 0.16; 95% CI - 0.36-0.69; p = 0.538), renal dysfunction (OR, 0.36; 95% CI 0.07-1.73; p = 0.200) and hypertension (OR, 0.17; 95% CI 0.03-1.10; p = 0.063). Current evidence suggests that NSS is safe and effective for unilateral WT patients, because it causes better renal function and similar oncological outcomes compared with RN. Future efforts to conduct more high-quality studies and explore sources of heterogeneity is recommended.

The PI3K-AKT-mTOR signaling pathway mediates the cytoskeletal remodeling and epithelial-mesenchymal transition in bladder outlet obstruction.

Objective: Partial bladder outlet obstruction(pBOO) is the most common cause of lower urinary tract symptoms (LUTS) and significantly affects the quality of life. Long-term pBOO can cause changes in bladder structure and function, referred to as bladder remodeling. The pathogenesis of pBOO-induced bladder remodeling has yet to be fully understood, so effective treatment options are lacking. Our study aimed to explore how pBOO-induced bladder remodeling brings new strategies for treating pBOO. Methods: A rat model of pBOO was established by partial ligation of the bladder neck, and the morphological changes and fibrosis changes in the bladder tissues were detected by H&E and Masson trichrome staining. Furthermore, EMT(epithelial-mesenchymal transition) related indicators and related pathway changes were further examined after TGF- ß treatment of urothelial cells SV-HUC-1. Finally, the above indicators were tested again after using the PI3K inhibitor. Subsequently, RNA sequencing of bladder tissues to identify differential genes and related pathways enrichment and validated by immunofluorescence and western blotting analysis. Results: The pBOO animal model was successfully established by partially ligating the bladder neck. H&E staining showed significant changes in the bladder structure, and Masson trichrome staining showed significantly increased collagen fibers. RNA sequencing results significantly enriched in the cytoskeleton, epithelial-mesenchymal transformation, and the PI3K-AKT-mTOR signaling pathway. Immunofluorescence and western blotting revealed EMT and cytoskeletal remodeling in SV-HUC-1 cells after induction of TGF- ß and in the pBOO bladder tissues. The western blotting showed significant activation of the PI3K-AKT-mTOR signaling pathway in SV-HUC-1 cells after induction of TGF-ß and in pBOO bladder tissues. Furthermore, EMT and cytoskeletal damage were partially reversed after PI3K pathway inhibition using PI3K inhibitors. Conclusions: In the pBOO rat model, the activation of the PI3K-AKT-mTOR signaling pathway can mediate the cytoskeletal remodeling and the EMT to induce fibrosis in the bladder tissues. PI3K inhibitors partially reversed EMT and cytoskeletal damage.

Livestock greenhouse gas emission and mitigation potential in China.

Livestock is an important source of greenhouse gas emissions (GHGE) in China. Understanding the greenhouse gas (GHG) emission trends and reduction strategies in livestock is crucial for promoting low-carbon transformation of the livestock sector (LS) and achieving the goal of "carbon peak and carbon neutralization". First, based on the life cycle assessment and IPCC coefficient methods, we calculated the GHGE of the LS in 31 provinces of China from 2000 to 2020 and identified the temporal and spatial evolution of GHG emission intensity. The LMDI method was then used to analyze the influence of efficiency, structure, economy, and population size on GHGE. Finally, the STIRPAT model was used to simulate the future evolution trend of the LS emissions under the SSPs scenario. The results revealed that the GHGE in the life cycle of livestock production decreased from 535.47 Mt carbon dioxide equivalent (CO2e) in 2000 to 532.18 Mt CO2e in 2020, and the main source was CH4 emissions from enteric fermentation of livestock. Economic and efficiency factors markedly influenced the changes in GHGE from the LS in China. Further, economic factors contributed >40% to the increase in GHGE in most provinces. Under the SSP1, SSP2, and SSP4 scenarios, livestock production can achieve the carbon peak target in 2030. Under the baseline scenario (SSP2), the GHGE of China's LS in 2030 and 2060 are expected to be 491.48 Mt CO2e and 352.11 Mt CO2e, respectively. The focus of mitigation measures for livestock production in the future is to optimize the production structure of the LS, promote the low-carbon transformation of the energy structure of livestock feeding, and establish an efficient and intensive management model. In addition, we focus on emission reduction in key areas, such as Northeast and Northwest China, while optimizing diet and reducing food waste from the consumer side.

Activation of the p53 signaling pathway by piRNA-MW557525 overexpression induces a G0/G1 phase arrest thus inhibiting neuroblastoma growth.

BACKGROUND: Neuroblastoma (NB) is the most common extracranial malignant solid tumor in children. Due to drug resistance to radiotherapy and chemotherapy, mainly due to the existence of cancer stem cells (CSCs), some children still have a poor prognosis. Therefore, researchers have focused their attention on CSCs. Our research group successfully constructed cancer stem cell-like cells named Piwil2-iCSCs by reprogramming human preputial fibroblasts (FBs) with the PIWIL2 gene in the early stage, and Piwil2-iCSCs were confirmed to induce the formation of embryonic tumors. PiRNAs, noncoding small RNAs that interact with PIWI proteins, play important roles in a variety of tumors. Therefore, our study aimed to explore the role of differentially expressed (DE) piRNAs derived from sequencing of Piwil2-iCSCs in NB. METHODS: The DE piRNAs in Piwil2-iCSCs were screened using high-throughput sequencing and further verified in NB tissues and cells. An unknown piRNA, named piRNA-MW557525, showed obvious downregulation in NB. Thus we studied the effect of piRNA-MW557525 on the biological behavior of NB through in vitro and in vivo experiments. On this basis, we successfully constructed a stably transfected NB cell line overexpressing piRNA-MW557525 and performed transcriptome sequencing to further explore the mechanism of piRNA-MW557525 in NB. RESULTS: In vitro, piRNA-MW557525 inhibited NB cell proliferation, migration and invasion and induced apoptosis; in vivo, piRNA-MW557525 significantly reduced the volume and weight of tumors and inhibited their proliferation, migration and invasion. piRNA-MW557525 overexpression induced G0/G1 phase arrest in NB cells via activation of the P53-P21-CDK2-Cyclin E signaling pathway thus inhibiting NB growth. CONCLUSIONS: Our findings show that piRNA-MW557525 functions as a tumor suppressor gene in NB and may serve as an innovative biomarker and possible therapeutic target for NB.