Comparative bibliometric analysis of artificial intelligence-assisted polyp diagnosis and AI-assisted digestive endoscopy: trends and growth in AI gastroenterology (2003-2023).

Introduction: Artificial intelligence is already widely utilized in gastroenterology. This study aims to comprehensively evaluate the research hotspots and development trends within the field of AI in gastroenterology by employing bibliometric techniques to scrutinize geographical distribution, authorship, affiliated institutions, keyword usage, references, and other pertinent data contained within relevant publications. Methods: This investigation compiled all pertinent publications related to artificial intelligence in the context of gastrointestinal polyps and digestive endoscopy from 2003 to 2023 within the Web of Science Core Collection database. Furthermore, the study harnessed the tools CiteSpace, VOSviewer, GraphPad Prism and Scimago Graphica for visual data analysis. The study retrieved a total of 2,394 documents in the field of AI in digestive endoscopy and 628 documents specifically related to AI in digestive tract polyps. Results: The United States and China are the primary contributors to research in both fields. Since 2019, studies on AI for digestive tract polyps have constituted approximately 25% of the total AI digestive endoscopy studies annually. Six of the top 10 most-cited studies in AI digestive endoscopy also rank among the top 10 most-cited studies in AI for gastrointestinal polyps. Additionally, the number of studies on AI-assisted polyp segmentation is growing the fastest, with significant increases in AI-assisted polyp diagnosis and real-time systems beginning after 2020. Discussion: The application of AI in gastroenterology has garnered increasing attention. As theoretical advancements in AI for gastroenterology have progressed, real-time diagnosis and detection of gastrointestinal diseases have become feasible in recent years, highlighting the promising potential of AI in this field.

Lipid metabolism reprogramming in endometrial cancer: biological functions and therapeutic implications.

BACKGROUND: Endometrial cancer is one of the major gynecological cancers, with increasing incidence and mortality in the past decades. Emerging preclinical and clinical data have indicated its close association with obesity and dyslipidemia. Metabolism reprogramming has been considered as the hallmark of cancer, to satisfy the extensive need of nutrients and energy for survival and growth. Particularly, lipid metabolism reprogramming has aroused the researchers' interest in the field of cancer, including tumorigenesis, invasiveness, metastasis, therapeutic resistance and immunity modulation, etc. But the roles of lipid metabolism reprogramming in endometrial cancer have not been fully understood. This review has summarized how lipid metabolism reprogramming induces oncogenesis and progression of endometrial cancer, including the biological functions of aberrant lipid metabolism pathway and altered transcription regulation of lipid metabolism pathway. Besides, we proposed novel therapeutic strategies of targeting lipid metabolism pathway and concentrated on its potential of sensitizing immunotherapy and hormonal therapy, to further optimize the existing treatment modalities of patients with advanced/metastatic endometrial cancer. Moreover, we expect that targeting lipid metabolism plus hormone therapy may block the endometrial malignant transformation and enrich the preventative approaches of endometrial cancer. CONCLUSION: Lipid metabolism reprogramming plays an important role in tumor initiation and cancer progression of endometrial cancer. Targeting the core enzymes and transcriptional factors of lipid metabolism pathway alone or in combination with immunotherapy/hormone treatment is expected to decrease the tumor burden and provide promising treatment opportunity for patients with advanced/metastatic endometrial cancer.

Fabrication of osmotic pump tablets utilizing semisolid extrusion three-dimensional printing technology.

The utilization of three-dimensional (3D) printing technology is prevalent in the fabrication of oral sustained release preparations; however, there is a lack of research on 3D-printed osmotic pump tablets. A 3D-printed core-shell structure bezafibrate osmotic pump tablet was developed based on the characteristics of rapid absorption and short half-life of bezafibrate, utilizing semisolid extrusion (SSE) 3D printing technology. First, the properties of different shell materials were investigated to define the composition of the shell, and ultimately, the optimal formulation was found to be ethyl cellulose:cellulose acetate:polyethylene glycol = 2:1:2. The formulation of the tablet core was defined based on the printing performance and release behavior. The formulation consisted of bezafibrate, lactis anhydrous, sodium bicarbonate, sodium alginate, polyethylene oxide and sodium dodecyl sulfate at a ratio of 400:400:300:80:50:50. The tablet was capable of achieving zero-order release. The physicochemical properties were also characterized. The pharmacokinetic data analysis indicated that there were no statistically significant differences in the pharmacokinetic parameters between the 3D-printed tablets and the reference listed drugs. There was a strong correlation between the in vitro and in vivo results for the 3D-printed tablets. The results showed that SSE printing is a practical approach for manufacturing osmotic pump tablets.

Customized surface adhesive and wettability properties of conformal electronic devices.

Conformal and body-adaptive electronics have revolutionized the way we interact with technology, ushering in a new era of wearable devices that can seamlessly integrate with our daily lives. However, the inherent mismatch between artificially synthesized materials and biological tissues (caused by irregular skin fold, skin hair, sweat, and skin grease) needs to be addressed, which can be realized using body-adaptive electronics by rational design of their surface adhesive and wettability properties. Over the past few decades, various approaches have been developed to enhance the conformability and adaptability of bioelectronics by (i) increasing flexibility and reducing device thickness, (ii) improving the adhesion and wettability between bioelectronics and biological interfaces, and (iii) refining the integration process with biological systems. Successful development of a conformal and body-adaptive electronic device requires comprehensive consideration of all three aspects. This review starts with the design strategies of conformal electronics with different surface adhesive and wettability properties. A series of conformal and body-adaptive electronics used in the human body under both dry and wet conditions are systematically discussed. Finally, the current challenges and critical perspectives are summarized, focusing on promising directions such as telemedicine, mobile health, point-of-care diagnostics, and human-machine interface applications.

Fabrication and characterization of oleic acid/sesame protein isolate/ poly (vinyl) alcohol core-shell nanofibers: Mitigating lipid oxidation by emulsion electrospinning.

Formulated oil-in-water (O/W) emulsions of oleic acid (OA) using sesame protein isolate (SPI) were processed via emulsion electrospinning with poly (vinyl) alcohol (PVA) to fabricate core-shell nanofibers for lipid oxidation prevention. The emulsion droplet size and viscosity increased as the oil volume fraction rose from 5 % to 30 %. The morphology tests and Fourier transform infrared spectroscopy (FTIR) confirmed the uniformity of nanofibers and OA encapsulation with hydrogen bonding. The thermal stability, mechanical properties, and water contact angle (WCA) of the nanofiber films improved with increased OA content. Encapsulation efficiency was 94.76 % and storage stability was maintained for 7 days in 5 % oil fraction nanofibers. The nanofibers showed lower oxidation and superior oxidative resistance to free OA, with the lowest peroxide value (POV, 2.14 mmol/L) and thiobarbituric acid-reactive substances (TBARS, 36.75 µmol/L). In conclusion, the OA/SPI/PVA (PE) core-shell nanofibers via emulsion electrospinning are efficient for fatty acid encapsulation in functional foods.

Advantages and disadvantages of various hydrogel scaffold types: A research to improve the clinical conversion rate of loaded MSCs-Exos hydrogel scaffolds.

Mesenchymal stem cell-derived exosomes(MSCs-Exos) offer promising therapeutic potential for a wide range of tissues and organs such as bone/cartilage, nerves, skin, fat, and endocrine organs. In comparison to the application of mesenchymal stem cells (MSCs), MSCs-Exos address critical challenges related to rejection reactions and ethical concerns, positioning themselves as a promising cell-free therapy. As exosomes are extracellular vesicles, their effective delivery necessitates the use of carriers. Consequently, the selection of hydrogel materials as scaffolds for exosome delivery has become a focal point of contemporary research. The diversity of hydrogel scaffolds, which can take various forms such as injectable types, dressings, microneedles, and capsules, leads to differing choices among researchers for treating diseases within the same domain. This variability in hydrogel materials poses challenges for the translation of findings into clinical practice. The review highlights the potential of hydrogel-loaded exosomes in different fields and introduces the advantages and disadvantages of different forms of hydrogel applications. It aims to provide a multifunctional and highly recognized hydrogel scaffold option for tissue regeneration at specific sites, improve clinical translation efficiency, and benefit the majority of patients.

Engineered extracellular vesicles with polypeptide for targeted delivery of doxorubicin against EGFR­positive tumors.

Lack of effective tumor­specific delivery systems remains an unmet clinical challenge for the employment of chemotherapy using cytotoxic drugs. Extracellular vesicles (EVs) have recently been investigated for their potential as an efficient drug­delivery platform, due to their good biodistribution, biocompatibility and low immunogenicity. In the present study, the formulation of GE11 peptide­modified EVs (GE11­EVs) loaded with doxorubicin (Dox­GE11­EVs), was developed to target epidermal growth factor receptor (EGFR)­positive tumor cells. The results obtained demonstrated that GE11­EVs exhibited highly efficient targeting and drug delivery to EGFR­positive tumor cells compared with non­modified EVs. Furthermore, treatment with Dox­GE11­EVs led to a significantly inhibition of cell proliferation and increased apoptosis of EGFR­positive tumor cells compared with Dox­EVs and free Dox treatments. In addition, it was observed that treatment with either free Dox or Dox­EVs exhibited a high level of cytotoxicity to normal cells, whereas treatment with Dox­GE11­EVs had only a limited effect on cell viability of normal cells. Taken together, the findings of the present study demonstrated that the engineered Dox­GE11­EVs can treat EGFR­positive tumors more accurately and have higher safety than traditional tumor therapies.

Secondary activation on plasma-activated water by plasma-treated cotton for restoring and enhancing disinfection effect.

Plasma-activated water (PAW) is a novel antimicrobial agent with negligible toxicity and environmental burden, holding promise as an alternative to chemical disinfectants and antibiotics. In practice, liquid disinfectants are often soaked with cotton materials before further use. Rich in reducing functional groups on the surface, cotton will inevitably react with PAW, leading to the deterioration of PAW's functions. To resolve this issue, this work proposes a new concept of "secondary activation" for retaining and enhancing PAW's bioactivity, i.e., pre-treating cotton with air plasma before soaking PAW. For the first time, we find that the PAW absorbed by raw cotton completely loses its bactericidal effect, while plasma-treated cotton (PTC) restores the disinfection capacity and prolongs its effective duration. This restoration is attributed to the absorption of plasma-generated reactive species by cotton with oxidizing and nitrifying modifications on the fiber surface. Consequently, the concentrations of aqueous species in PAW increase rather than decrease after absorption by PTC. In addition, the PTC after 28-day storage can still enable PAW to achieve a bacterial reduction of ∼3 logs. This work identifies and addresses a crucial limitation in the disinfection application of PAW and elucidates the mechanism underlying PTC production and secondary activation of PAW.

Procyanidin B1 Promotes PSMC3-NRF2 Ubiquitination to Induce Ferroptosis in Glioblastoma.

NRF2 signaling is a crucial antioxidant defense mechanism against ferroptosis in tumors, and targeting NRF2 is essential for tumor therapy. However, the effectiveness of NRF2 inhibitors remains unexplored. The active ingredients of traditional Chinese medicine serve as important sources of NRF2 inhibitors. In this study, we established an intracranial glioblastoma (GBM) orthotopic model and observed the effects of procyanidin B1 on tumor growth and ferroptosis. Using protein-small-molecule docking, z-stack assay of laser confocal imaging, surface plasmon resonance assay, immunoprecipitation, mass spectrometry, and western blotting, we detected the binding between procyanidin B1 and NRF2 and the effect of PSMC3 on the ubiquitin-dependent degradation of NRF2 in GBM cells. Our results showed that procyanidin B1 acted as a novel NRF2 inhibitor to suppress GBM cell proliferation and prolonged the survival of GBM-bearing mice; it also mediated the interaction between PSMC3 and NRF2 to promote ubiquitin-dependent protein degradation of NRF2, which induced ferroptosis in GBM cells. In addition, we found that procyanidin B1 enhanced H2O2 accumulation by downregulating NRF2 during ferroptosis in GBM cells. The botanical agent procyanidin B1 induced ferroptosis and exerted anti-tumor effects through PSMC3-mediated ubiquitin-dependent degradation of NRF2 proteins, providing a potential drug candidate for adjuvant therapy in patients with GBM.

Prognosis evaluation and efficacy analysis of different treatment options for patients with visceral pleural invasion in stage IIA-IIB lung cancer.

OBJECTIVE: Controversy surrounds the treatment of visceral pleural invasion in lung cancer, and no studies have compared the efficacy of its four main treatment options (i.e., surgery, chemotherapy, targeted therapy, and immunotherapy). This study aims to compare and analyze surgery, chemotherapy, targeted therapy, and immunotherapy outcomes and explore the optimal treatment of visceral pleural invasion in lung cancer. METHODS: We searched electronic databases (i.e., Pubmed, Embase, Cochrane Library, CNKI, and Chinese Biomedical Literature Database Search) for relevant studies of treatment options for patients with visceral pleural invasion in stage IIA-IIB lung cancer. Searches times were limited to studies published between January 1, 2000 and February 20, 2021. Meta analysis was performed using RevMan 5.3 software We also downloaded original RNA transcription data about lung cancer invasion in the GEO and TCGA tumor databases, and used R 4.0.3 software to perform differential expression and co-expression gene network analyses. RESULTS: We included a total of 25 high-quality (i.e., Jadad score 4-7) studies. Meta-analysis found that surgical treatment was associated with a 3-year survival rate OR = 3.80 (95% CI 3.53, 4.09; P < 0.0001), 5-year survival rate OR = 4.10 (95% CI 3.72, 4.53; P < 0.0001), and median survival time OR = 2.71 (95% CI 2.53, 2.89; P < 0.0001). Chemotherapy was associated with a 3-year survival rate OR = 2.08 (95% CI 1.93, 2.25; P < 0.0001), 5-year survival rate OR = 1.68 (95% CI 1.49, 1.89; P < 0.0001), and median survival time OR = 1.84 (95% CI 1.66, 2.04; P < 0.0001). Targeted therapy was associated with a 3-year survival rate OR = 2.91 (95% CI 2.65, 3.19; P < 0.0001), 5-year survival rate OR = 1.83 (95% CI 1.39, 2.33; P < 0.0001), and median survival time OR = 1.76 (95% CI 1.59, 1.94; P < 0.0001). Finally, immunotherapy was associated with a 3-year survival rate OR = 1.89 (95% CI 1.73, 2.07; P < 0.0001), 5-year survival rate OR = 1.66 (95% CI 1.46, 1.88; P < 0.0001), and median survival time OR = 2.53 (95% CI 2.27, 2.82; P < 0.0001). After screening differential genes and co-expressed genes in tumor gene databases, we found that AC245595.1, ITGB1-DT and AL606489.1 may be involved in the process of lung cancer invasion, and macrophages M1 and M2, CD4+-Th1, CD8+-Th1 may participate in immune infiltration. CONCLUSIONS: In patients with visceral pleural invasion of stage IIA-IIB lung cancer, chemotherapy has shown a significant effect on improving prognosis and enhancing efficacy. However, surgical treatment did not significantly improve the overall prognosis. Therefore, the individual situation of the patient and the comprehensive benefits of the treatment program should be fully considered when developing the treatment program.

Fast, variable stiffness-induced braided coiled artificial muscles.

Biomimetic actuation technologies with high muscle strokes, cycle rates, and work capacities are necessary for robotic systems. We present a muscle type that operates based on changes in muscle stiffness caused by volume expansion. This muscle is created by coiling a mechanically strong braid, in which an elastomer hollow tube is adhesively attached inside. We show that the muscle reversibly contracts by 47.3% when driven by an oscillating input air pressure of 120 kilopascals at 10 Hz. It generates a maximum power density of 3.0 W/g and demonstrates a mechanical contractile efficiency of 74%. The muscle's low-pressure operation allowed for portable, thermal pneumatical actuation. Moreover, the muscle demonstrated bipolar actuation, wherein internal pressure leads to muscle length expansion if the initial muscle length is compressed and contraction if the muscle is not compressed. Modeling indicates that muscle expansion significantly alters its stiffness, which causes muscle actuation. We demonstrate the utility of BCMs for fast running and climbing robots.

DeSUMOylation of RBMX regulates exosomal sorting of cargo to promote renal tubulointerstitial fibrosis in diabetic kidney disease.

INTRODUCTION: Diabetic kidney disease (DKD) has become the primary cause of chronic renal failure in China, and renal tubulointerstitial fibrosis plays a central role in DKD progression. Urinary exosomes, which reflect kidney changes, are largely influenced by RNA-binding proteins (RBPs) in their miRNA content. OBJECTIVES: Our research aimed to determine the effect of the RNA-binding protein RBMX on exosomal miRNA in DKD. METHODS: We introduced a higher level of Rbmx into diabetic mice using an adenoassociated virus and isolated exosomes from their kidney tissue through advanced centrifugation techniques and specialized kits. We then conducted a series of tests, including qRT-PCR, Western blot, MitoSOX, ATP luminescence, coimmunoprecipitation, SUMOylation assays, RNA immunoprecipitation, and confocal microscopy. RESULTS: RBMX is found in higher levels in DKD and contributes to worsening kidney fibrosis, mitochondrial damage, and miRNA mismanagement in exosomes. It specifically binds with miR-26a, miR-23c, and miR-874 within the exosomes. This dysfunction may be linked to changes in RBMX SUMOylation. These miRNAs seem to protect against mitochondrial damage in kidney cells by targeting CERS6. CONCLUSION: DeSUMOylation of RBMX plays a crucial role in determining the makeup of miRNAs in kidney cell exosomes, impacting the protective miRNAs which regulate mitochondrial damage through their interaction with CERS6 mRNA, ultimately affecting mitochondrial health in DKD.

Association of glycemic variability and prognosis in patients with traumatic brain injury: A retrospective study from the MIMIC-IV database.

BACKGROUND: Elevated glycemic variability (GV) often occurs in intensive care unit (ICU) patients and is associated with patient prognosis. However, the association between GV and prognosis in ICU patients with traumatic brain injury (TBI) remains unclear. METHOD: Clinical data of ICU patients with TBI were obtained from the Medical Information Mart for Intensive Care (MIMIC) -IV database. The coefficient of variation (CV) was utilized to quantify GV, while the Glasgow Coma Scale (GCS) was employed to evaluate the consciousness status of TBI patients. Pearson linear correlation analysis, linear regression, COX regression and restricted cubic spline (RCS) were used to investigate the relationship between CV and consciousness impairment, as well as the risk of in-hospital mortality. RESULT: A total of 1641 ICU patients with TBI were included in the study from the MIMIC-IV database. Pearson linear correlation and restricted cubic spline (RCS) analysis results showed a negative linear relationship between CV and the last GCS (P = 0.002) with no evidence of nonlinearity (P for nonlinear = 0.733). Multivariable linear regression suggested a higher CV was associated with a lower discharge GCS [ß (95 %CI) = -1.86 (-3.08 âˆ¼ -0.65), P = 0.003]. Furthermore, multivariable COX regression indicated that CV ≥ 0.3 was a risk factor for in-hospital death in TBI patients [HR (95 %CI) = 1.74 (1.15-2.62), P = 0.003], and this result was also consistent across sensitivity and subgroup analyses. CONCLUSION: Higher GV is related to poorer consciousness outcomes and increased risk of in-hospital death in ICU patients with TBI. Additional research is needed to understand the logical relationship between GV and TBI progression.

Exploring the feasibility of preoperative tumor-bed boost, oncoplastic surgery, and adjuvant radiotherapy schedule in early-stage breast cancer: A phase II clinical trial.

BACKGROUND: Oncoplastic breast-conserving surgery (OBCS) improves satisfaction in patients who would fare otherwise sub-optimal cosmetic outcome, while brings challenge in tumor-bed identification during adjuvant radiotherapy. The ultra-hypofractionated breast radiotherapy further shortens treatment sessions from moderately hypofractionated regimens. To circumscribe the difficulty in tumor-bed contouring and the additional toxicity from larger boost volumes, we propose to move forward the boost session preoperatively from the adjuvant radiation part. Thus, the present study aims to evaluate the feasibility of a new treatment paradigm of preoperative primary-tumor boost before breast-conserving surgery (BCS) or OBCS followed by adjuvant ultra-hypofractionated whole-breast irradiation (u-WBRT) for patients with early-stage breast cancer. METHODS: There was a phase II study. Patients younger than 55 years old, with a biopsy confirmed mono-centric breast cancer, without lymph node involvement were enrolled. Preoperative primary-tumor boost was given by a single 10 Gy in 1 fraction, and BCS or OBCS was conducted within two weeks afterwards. Adjuvant u-WBRT (26 Gy/5.2 Gy/5 f) was given in 6 weeks postoperatively without any boost, after the full recovery from surgery. Surgical complications and patient-reported outcomes, as assessed via Breast-Q questionnaires, were documented. A propensity score matching approach was employed to identify a control group at a 1:1 ratio for BREAST-Q outcomes comparison. RESULTS: From May 2022 to September 2023, 36 patients were prospectively enrolled. Surgical complications were observed in 7 cases (19.4%), including 3 cases with Clavien-Dindo (CD) grade 1-2 and 4 cases with CD grade 3 complications. All but four patients (11.1%) started the planned u-WBRT within one week after the pre-defined due dates postoperatively (≤49 d). Four patients (11.1%) developed grade 2 radiodermatitis after chemotherapy initiation. Compared to the study group, the control patients reported higher scores in chest physical well-being (P=0.045) and in their attitudes towards arm swelling (P=0.01). No significant difference was detected in the other of domains (Satisfaction with Breasts, Sexual and Psychosocial Well-Being, and Adverse Effects of Radiation). With a median follow-up period of 9.8 months (2.4-18.9 mo), none had any sign of relapse. CONCLUSION: This Phase II clinical trial confirmed the technical and safety feasibility of novel radiation schedule in patients undergoing BCS or OBCS. According to the BREAST-Q questionnaire, patients who underwent novel radiation schedules reported lower satisfaction in chest physical well-being. A randomized controlled trial is necessary to further investigate these findings. Additionally, long-term follow-up is required to assess oncological outcomes.

Catalyst-Free Dearomative Allylboration of Ketones with Benzo[b]thiophenylmethyl Boronic Acids.

A novel approach to the dearomative allylboration of ketones with benzo[b]thiophenylmethyl boronic acids has been developed. By leveraging the inherent reactivity of the boronic acid unit, this process occurs under mild reaction conditions without the need for a catalyst, leading to the efficient formation of homoallylic tertiary alcohols accompanied by the construction of three-dimensional sulfur-containing alicyclic scaffolds in high yields with excellent stereoselectivities.

The HOXC10/NOD1/ERK axis drives osteolytic bone metastasis of pan-KRAS-mutant lung cancer.

While KRAS mutation is the leading cause of low survival rates in lung cancer bone metastasis patients, effective treatments are still lacking. Here, we identified homeobox C10 (HOXC10) as a lynchpin in pan-KRAS-mutant lung cancer bone metastasis. Through RNA-seq approach and patient tissue studies, we demonstrated that HOXC10 expression was dramatically increased. Genetic depletion of HOXC10 preferentially impeded cell proliferation and migration in vitro. The bioluminescence imaging and micro-CT results demonstrated that inhibition of HOXC10 significantly reduced bone metastasis of KRAS-mutant lung cancer in vivo. Mechanistically, the transcription factor HOXC10 activated NOD1/ERK signaling pathway to reprogram epithelial-mesenchymal transition (EMT) and bone microenvironment by activating the NOD1 promoter. Strikingly, inhibition of HOXC10 in combination with STAT3 inhibitor was effective against KRAS-mutant lung cancer bone metastasis by triggering ferroptosis. Taken together, these findings reveal that HOXC10 effectively alleviates pan-KRAS-mutant lung cancer with bone metastasis in the NOD1/ERK axis-dependent manner, and support further development of an effective combinatorial strategy for this kind of disease.

Myc-mediated inhibition of HIF1a degradation promotes M2 macrophage polarization and impairs CD8 T cell function through lactic acid secretion in ovarian cancer.

Ovarian cancer, the eleventh most prevalent cancer among women and a significant cause of cancer-related mortality, poses considerable challenges. While the Myc oncogene is implicated in diverse cancers, its impact on tumours expressing Myc during immune therapy processes remains enigmatic. Our study investigated Myc overexpression in a murine ovarian cancer cell line, focusing on alterations in HIF1a function. Seahorse experiments were utilized to validate metabolic shifts post-Myc overexpression. Moreover, we explored macrophage polarization and immunosuppressive potential following coculture with Myc-overexpressing tumour cells by employing Gpr132-/- mice to obtain mechanistic insights. In vivo experiments established an immune-competent tumour-bearing mouse model, and CD8 T cell, Treg, and macrophage infiltration post-Myc overexpression were evaluated via flow cytometry. Additionally, adoptive transfer of OTI CD8 T cells was conducted to investigate antigen-specific immune response variations after Myc overexpression. The findings revealed a noteworthy delay in HIF1a degradation, enhancing its functionality and promoting the classical Warburg effect upon Myc overexpression. Lactic acid secretion by Myc-overexpressing tumour cells promoted Gpr132-dependent M2 macrophage polarization, leading to the induction of macrophages capable of significantly suppressing CD8 T cell function. Remarkably, heightened macrophage infiltration in tumour microenvironments post-Myc overexpression was observed alongside impaired CD8 T cell infiltration and function. Interestingly, CD4 T-cell infiltration remained unaltered, and immune-suppressive effects were alleviated when Myc-overexpressing tumour cells were administered to Gpr132-/- mice, shedding light on potential therapeutic avenues for ovarian cancer management.

Customized Pore Creation Strategies for Hyperelastic, Robust, Insulating Multifunctional MXene Aerogels for Microwave Absorption.

The construction of heterogeneous microstructure and the selection of multicomponents have turned into a research hotspot in developing ultralight, multifunctional, high-efficiency electromagnetic wave absorbing (EMA) materials. Although aerogels are promising materials to fulfill the above requirements, the increase in functional fillers inevitably leads to the deterioration of intrinsic properties. Tuning the electromagnetic properties from the structural design point of view remains a difficult challenge. Herein, we design customized pore creation strategies via introducing sacrificial templates to optimize the conductive path and construct the discontinuous dielectric medium, increasing dielectric loss and achieving efficient microwave absorption properties. A 3D porous composite (MEM) was crafted, which encapsulated an EVA/FeCoNi (EVA/MNPs) framework with Ti3C2Tx MXene coating by employing a direct heated cross-linking and immersion method. Controllable adjustment of the conductive network inside the porous structure and regulation of the dielectric character are achieved by porosity variation. Eventually, the MEM-5 with a porosity of 66.67% realizes RLmin of -39.2 dB (2.2 mm) and can cover the entire X band. Moreover, through off-axis electronic holography and the calculation of conduction loss and polarization loss, the dielectric property is deeply investigated, and the inner mechanism of optimization is pointed out. Thanks to the inherent characteristic of EVA and the porous structure, MEM-5 showed excellent thermal insulating and superior compressibility, which can maintain 60 °C on a 90-100 °C continuous heating stage and reached a maximum compressive strength of 60.12 kPa at 50% strain. Conceivably, this work provides a facile method for the fabrication of highly efficient microwave absorbers applied under complex conditions.

Plasma Olink Proteomics Reveals Novel Biomarkers for Prediction and Diagnosis in Dilated Cardiomyopathy with Heart Failure.

In this study, we utilized the Olink Cardiovascular III panel to compare the expression levels of 92 cardiovascular-related proteins between patients with dilated cardiomyopathy combined with heart failure (DCM-HF) (n = 20) and healthy normal people (Normal) (n = 18). The top five most significant proteins, including SPP1, IGFBP7, F11R, CHI3L1, and Plaur, were selected by Olink proteomics. These proteins were further validated using ELISA in plasma samples collected from an additional cohort. ELISA validation confirmed significant increases in SPP1, IGFBP7, F11R, CHI3L1, and Plaur in DCM-HF patients compared to healthy controls. GO and KEGG analysis indicated that NT-pro BNP, SPP1, IGFBP7, F11R, CHI3L1, Plaur, BLM hydrolase, CSTB, Gal-4, CCL15, CDH5, SR-PSOX, and CCL2 were associated with DCM-HF. Correlation analysis revealed that these 13 differentially expressed proteins have strong correlations with clinical indicators such as LVEF and NT-pro BNP, etc. Additionally, in the GEO-DCM data sets, the combined diagnostic value of these five core proteins AUC values of 0.959, 0.773, and 0.803, respectively indicating the predictive value of the five core proteins for DCM-HF. Our findings suggest that these proteins may be useful biomarkers for the diagnosis and prediction of DCM-HF, and further research is prompted to explore their potential as therapeutic targets.

Targeting BRD4 to attenuate RANKL-induced osteoclast activation and bone erosion in rheumatoid arthritis.

Rheumatoid arthritis (RA) is a chronic autoimmune disease that can cause destruction of cartilage and bone's extracellular matrix. Bromodomain 4 (BRD4), as a transcriptional and epigenetic regulator, plays a key role in cancer and inflammatory diseases. While, the role of BRD4 in bone destruction in RA has not been extensively reported. Our study aimed to investigate the effect of BRD4 on the bone destruction in RA and, further, its mechanism in the pathogenesis of the disease. In this study, receiving approval from the Ethical Committee of the Affiliated Hospital of Qingdao University, we evaluated synovial tissues from patients with RA and OA for BRD4 expression through advanced techniques such as immunohistochemistry, quantitative real-time PCR (qRT-PCR), and Western blotting. We employed a collagen-induced arthritis (CIA) mouse model to assess the therapeutic efficacy of the BRD4 inhibitor JQ1 on disease progression and bone destruction, supported by detailed clinical scoring and histological examinations. Further, in vitro osteoclastogenesis assays using RAW264.7 macrophages, facilitated by TRAP staining and resorption pit assays, provided insights into the mechanistic effects of JQ1 on osteoclast function. Statistical analysis was rigorously conducted using SPSS, applying Kruskal-Wallis, one-way ANOVA, and Student's t-tests to validate the data. In our study, we found that BRD4 expression significantly increased in the synovial tissues of RA patients and the ankle joints of CIA mice, with JQ1, a BRD4 inhibitor, effectively reducing inflammation, arthritis severity (p < 0.05), and bone erosion. Treatment with JQ1 not only improved bone mass and structural integrity in CIA mice but also downregulated osteoclast-related gene expression and the RANKL/RANK signaling pathway, indicating a suppression of osteolysis. Furthermore, in vitro assays demonstrated that JQ1 markedly inhibited osteoclast differentiation and function, underscoring the pivotal role of BRD4 in osteoclastogenesis and its potential as a target for therapeutic intervention in RA-induced bone destruction. Our study concludes that targeting BRD4 with the inhibitor JQ1 significantly mitigates inflammation and bone destruction in rheumatoid arthritis, suggesting that inhibition of BRD4 may be a potential therapeutic strategy for the treatment of bone destruction in RA.