Fluorescent chemosensors facilitate the visualization of plant health and their living environment in sustainable agriculture.

Globally, 91% of plant production encounters diverse environmental stresses that adversely affect their growth, leading to severe yield losses of 50-60%. In this case, monitoring the connection between the environment and plant health can balance population demands with environmental protection and resource distribution. Fluorescent chemosensors have shown great progress in monitoring the health and environment of plants due to their high sensitivity and biocompatibility. However, to date, no comprehensive analysis and systematic summary of fluorescent chemosensors used in monitoring the correlation between plant health and their environment have been reported. Thus, herein, we summarize the current fluorescent chemosensors ranging from their design strategies to applications in monitoring plant-environment interaction processes. First, we highlight the types of fluorescent chemosensors with design strategies to resolve the bottlenecks encountered in monitoring the health and living environment of plants. In addition, the applications of fluorescent small-molecule, nano and supramolecular chemosensors in the visualization of the health and living environment of plants are discussed. Finally, the major challenges and perspectives in this field are presented. This work will provide guidance for the design of efficient fluorescent chemosensors to monitor plant health, and then promote sustainable agricultural development.

Femtosecond laser composite manufactured double-bionic micro-nano structure for efficient photothermal anti-icing/deicing.

The solar anti-icing/deicing (SADI) strategy represents an environmentally friendly approach for removing ice efficiently. However, the extensive use of photothermal materials could negatively impact financial performance. Therefore, enhancing light utilization efficiency, especially by optimizing the design of a structure with a low content of photothermal materials, has rapidly become a focal point of research. Drawing inspiration from the antireflective micro-nano structure of compound eyes and the thermal insulating hollow structure of polar bear hair, we proposed a new strategy to design a bionic micro-nano hollow film (MNHF). The MNHF was created using a composite manufacturing process that combines femtosecond laser ablation with template transfer techniques. Both theoretical simulations and empirical tests have confirmed that this structure significantly improves photothermal conversion efficiency and thermal radiation capability. Compared to plane film, the photothermal conversion efficiency of MNHF is increased by 45.85%. Under 1.5 sun, the equilibrium temperature of MNHF can reach 73.8 °C. Moreover, even after 10 icing-deicing cycles, MNHF maintains an ultra-low ice adhesion strength of 1.8 ± 0.3 kPa. Additionally, the exceptional mechanical stability, chemical resistance, and self-cleaning capabilities of the MNHF make its practical application feasible. This innovative structure paves the way for designing cost-effective and robust surfaces for efficient photothermal anti-icing/deicing on airplane wings.

The maternal drug exposure birth cohort (DEBC) in China.

Drug exposure during pregnancy lacks global fetal safety data. The maternal drug exposure birth cohort (DEBC) study, a prospective longitudinal investigation, aims to explore the correlation of maternal drug exposure during pregnancy with pregnancy outcomes, and establish a human biospecimen biobank. Here we describe the process of establishing DEBC and show that the drug exposure rate in the first trimester of pregnant women in DEBC (n = 112,986) is 30.70%. Among the drugs used, dydrogesterone and progesterone have the highest exposure rates, which are 11.97% and 10.82%, respectively. The overall incidence of adverse pregnancy outcomes is 13.49%. Dydrogesterone exposure during the first trimester is correlated with higher incidences of stillbirth, preterm birth, low birth weight, and birth defects, along with a lower incidence of miscarriage/abortion. Due to the limitations of this cohort study, causative conclusions cannot be drawn. Further follow-up and in-depth data analysis are planned for future studies.

DNA methylation modification in Idiopathic pulmonary fibrosis.

Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and irreversible interstitial lung disease with a prognosis worse than lung cancer. It is a fatal lung disease with largely unknown etiology and pathogenesis, and no effective therapeutic drugs render its treatment largely unsuccessful. With continuous in-depth research efforts, the epigenetic mechanisms in IPF pathogenesis have been further discovered and concerned. As a widely studied mechanism of epigenetic modification, DNA methylation is primarily facilitated by DNA methyltransferases (DNMTs), resulting in the addition of a methyl group to the fifth carbon position of the cytosine base, leading to the formation of 5-methylcytosine (5-mC). Dysregulation of DNA methylation is intricately associated with the advancement of respiratory disorders. Recently, the role of DNA methylation in IPF pathogenesis has also received considerable attention. DNA methylation patterns include methylation modification and demethylation modification and regulate a range of essential biological functions through gene expression regulation. The Ten-Eleven-Translocation (TET) family of DNA dioxygenases is crucial in facilitating active DNA demethylation through the enzymatic conversion of the modified genomic base 5-mC to 5-hydroxymethylcytosine (5-hmC). TET2, a member of TET proteins, is involved in lung inflammation, and its protein expression is downregulated in the lungs and alveolar epithelial type II cells of IPF patients. This review summarizes the current knowledge of pathologic features and DNA methylation mechanisms of pulmonary fibrosis, focusing on the critical roles of abnormal DNA methylation patterns, DNMTs, and TET proteins in impacting IPF pathogenesis. Researching DNA methylation will enchance comprehension of the fundamental mechanisms involved in IPF pathology and provide novel diagnostic biomarkers and therapeutic targets for pulmonary fibrosis based on the studies involving epigenetic mechanisms.

Inflammatory status predicts prognosis in patients with gastric cancer with early pyloric stenosis who underwent radical resection: A propensity score­matching analysis.

The inflammatory status of patients is closely related to their nutritional status, and the impact of inflammatory status on patients with pyloric stenosis remains unclear. The present study aimed to investigate the impact of inflammatory status on the prognosis of patients with gastric cancer with early pyloric stenosis who underwent radical resection. A retrospective analysis included 242 patients with gastric cancer who underwent radical resection at the Affiliated Hospital of Southwest Medical University between July 2016 and December 2020. All patients were diagnosed with early pyloric stenosis. Correlation analysis was used to assess variations among different factors, and survival analysis was conducted to evaluate differences in overall survival (OS). To identify independent prognostic indicators, both univariate and multivariate Cox regression analyses were performed, addressing potential multicollinearity using Lasso analysis. Propensity score matching (PSM) was employed to eliminate potential confounding factors. Additionally, a prognostic risk model and nomogram based on inflammatory indicators were developed to comprehensively explore their impact on prognosis. Initial survival analysis revealed significant associations between neutrophil-to-lymphocyte ratio (NLR; χ2=10.522, P<0.001), systemic immune-inflammation index (SII; χ2=6.733, P=0.025), systemic inflammation response index (SIRI; χ2=15.490, P<0.001) and OS of the patients, while there was no significant survival difference among patients with different platelet-to-lymphocyte ratio (PLR; χ2=2.561, P=0.050). SIRI not only had the highest area under the curve but was also found to be an independent prognostic indicator (hazard ratio=1.851, P=0.046) in the present study. Following PSM on SIRI, a total of 174 patients were included in the subsequent analysis. Time-receiver operating characteristic and survival curves for SIRI after PSM consistently demonstrated its robust prognostic predictive capability. Furthermore, the prognostic risk model based on SIRI and the nomogram incorporating SIRI both exhibited high prognostic value. Inflammatory status was significantly associated with the prognosis of patients with gastric cancer with early pyloric stenosis who underwent radical resection. The NLR, SII and SIRI could all predict patient outcomes. Moreover, SIRI exhibited the highest prognostic value among the inflammatory indices and has been identified as an independent prognostic factor in the present study.

A novel senolytic drug for pulmonary fibrosis: BTSA1 targets apoptosis of senescent myofibroblasts by activating BAX.

Idiopathic pulmonary fibrosis is a progressive and age-related disease that results from impaired lung repair following injury. Targeting senescent myofibroblasts with senolytic drugs attenuates pulmonary fibrosis, revealing a detrimental role of these cells in pulmonary fibrosis. The mechanisms underlying the occurrence and persistence of senescent myofibroblasts in fibrotic lung tissue require further clarification. In this study, we demonstrated that senescent myofibroblasts are resistant to apoptosis by upregulating the proapoptotic protein BAX and antiapoptotic protein BCL-2 and BCL-XL, leading to BAX inactivation. We further showed that high levels of inactive BAX-mediated minority mitochondrial outer membrane permeabilization (minority MOMP) promoted DNA damage and myofibroblasts senescence after insult by a sublethal stimulus. Intervention of minority MOMP via the inhibition of caspase activity by quinolyl-valyl-O-methylaspartyl-[2,6-difluorophenoxy]-methyl ketone (QVD-OPH) or BAX knockdown significantly reduced DNA damage and ultimately delayed the progression of senescence. Moreover, the BAX activator BTSA1 selectively promoted the apoptosis of senescent myofibroblasts, as BTSA1-activated BAX converted minority MOMP to complete MOMP while not injuring other cells with low levels of BAX. Furthermore, therapeutic activation of BAX with BTSA1 effectively reduced the number of senescent myofibroblasts in the lung tissue and alleviated both reversible and irreversible pulmonary fibrosis. These findings advance the understanding of apoptosis resistance and cellular senescence mechanisms in senescent myofibroblasts in pulmonary fibrosis and demonstrate a novel senolytic drug for pulmonary fibrosis treatment.

Impact of health literacy, social support, and socioeconomic position on the serum uric acid level in asymptomatic hyperuricaemia patients in China: a structural equation model.

BACKGROUND: Hyperuricaemia (HUA) poses a significant public health challenge on a global scale. It is mostly asymptomatic hyperuricemia (AHU) with unsatisfactory recognition and control rates. The role of health literacy in influencing health outcomes is of utmost importance, and enhancing health literacy is helpful for patients in managing risk factors. Additionally, social support and socioeconomic position (SEP) have been identified as potential factors influencing health. However, the exact relationships between these factors and AHU remain unclear. This study aimed to investigate the status of health literacy among patients with AHU and explore the relationships between health literacy, social support, SEP, and serum uric acid (SUA) levels. METHODS: A cross-sectional study was conducted among 349 participants with AHU in Luzhou, China. The research instruments included a sociodemographic characteristics questionnaire, the Health Literacy Scale for Chronic Patients (HLSCP), and the Social Support Scale (SSRS). The construction of the SEP index was achieved through the application of principal component analysis. Univariate and hierarchical regression analyses were used to evaluate the associations between SEP, social support, health literacy, and SUA levels. Furthermore, structural equation modelling (SEM) was utilized to examine these associations. RESULTS: (1) Most patients exhibited low health literacy (90.18 ± 15.11), and only 44.4% possessed basic health literacy. (2) SEP was positively correlated with SUA levels (ß = 4.086, P < 0.001), and health literacy was negatively related to SUA levels (ß = -0.399, P < 0.001). There was no significant relationship between social support and SUA levels (ß = 0.051, t = 1.085). (3) Health literacy mediated the association between SEP and SUA levels (ß = -0.490, 95% CI: -0.620 to -0.382). SEP had a direct positive effect on SUA levels (ß = 0.723) and health literacy (ß = 0.696), and the total effect of SEP on SUA levels was 0.233. CONCLUSIONS: The findings indicate a low level of health literacy among patients with AHU and suggest that health literacy might play a mediating role in the relationship between SEP and SUA levels. Consequently, future initiatives are recommended to prioritize health literacy and devise appropriate intervention strategies to enhance the self-management capabilities of patients with AHU.

3D printing of interferon γ-preconditioned NSC-derived exosomes/collagen/chitosan biological scaffolds for neurological recovery after TBI.

The reconstruction of neural function and recovery of chronic damage following traumatic brain injury (TBI) remain significant clinical challenges. Exosomes derived from neural stem cells (NSCs) offer various benefits in TBI treatment. Numerous studies confirmed that appropriate preconditioning methods enhanced the targeted efficacy of exosome therapy. Interferon-gamma (IFN-γ) possesses immunomodulatory capabilities and is widely involved in neurological disorders. In this study, IFN-γ was employed for preconditioning NSCs to enhance the efficacy of exosome (IFN-Exo, IE) for TBI. miRNA sequencing revealed the potential of IFN-Exo in promoting neural differentiation and modulating inflammatory responses. Through low-temperature 3D printing, IFN-Exo was combined with collagen/chitosan (3D-CC-IE) to preserve the biological activity of the exosome. The delivery of exosomes via biomaterial scaffolds benefited the retention and therapeutic potential of exosomes, ensuring that they could exert long-term effects at the injury site. The 3D-CC-IE scaffold exhibited excellent biocompatibility and mechanical properties. Subsequently, 3D-CC-IE scaffold significantly improved impaired motor and cognitive functions after TBI in rat. Histological results showed that 3D-CC-IE scaffold markedly facilitated the reconstruction of damaged neural tissue and promoted endogenous neurogenesis. Further mechanistic validation suggested that IFN-Exo alleviated neuroinflammation by modulating the MAPK/mTOR signaling pathway. In summary, the results of this study indicated that 3D-CC-IE scaffold engaged in long-term pathophysiological processes, fostering neural function recovery after TBI, offering a promising regenerative therapy avenue.

Low-intensity ultrasound ameliorates brain organoid integration and rescues microcephaly deficits.

Human brain organoids represent a remarkable platform for modeling neurological disorders and a promising brain repair approach. However, the effects of physical stimulation on their development and integration remain unclear. Here, we report that low-intensity ultrasound significantly increases neural progenitor cell proliferation and neuronal maturation in cortical organoids. Histological assays and single-cell gene expression analyses reveal that low-intensity ultrasound improves the neural development in cortical organoids. Following organoid grafts transplantation into the injured somatosensory cortices of adult mice, longitudinal electrophysiological recordings and histological assays reveal that ultrasound-treated organoid grafts undergo advanced maturation. They also exhibit enhanced pain-related gamma-band activity and more disseminated projections into the host brain than the untreated groups. Finally, low-intensity ultrasound ameliorates neuropathological deficits in a microcephaly brain organoid model. Hence, low-intensity ultrasound stimulation advances the development and integration of brain organoids, providing a strategy for treating neurodevelopmental disorders and repairing cortical damage.

Long non-coding RNA LINC00930 targeting miR-6792-3p/ZBTB16 regulates the proliferation and EMT of pancreatic cancer.

Emerging evidence suggests the dysregulation of long non-coding RNAs (lncRNAs) involved in pancreatic cancer (PC). However, the function of LINC00930 in PC has not been elaborated. In this study, we found that LINC00930 was significantly down-regulated in PC cell lines and tissues, and associated with tumor size, lymphatic metastasis, TNM stage and poor prognosis. According to the bioinformatics database, the downregulation of LINC00930 was a common event in PC associated with prognosis and EMT. Overexpression of LINC00930 inhibited the aggressive cancer phenotypes including proliferation, metastasis and epithelial-mesenchymal transition (EMT) of PC in vitro and in vivo. Bioinformatics and dual-luciferase reporter assay indicated that miR-6792-3p could directly bind to LINC00930. Additionally, the Zinc finger and BTB domain containing 16 (ZBTB16) was significantly declined in PC, which was predicted to be the downstream gene of miR-6792-3p. MiR-6792-3p mimic rescued the decreased proliferation, metastasis and EMT caused by ZBTB16 in PC cells. The LINC00930/miR-6792-3p/ZBTB16 axis was associated with the malignant progression and process of PC. The relative expression of LINC00930 was negatively correlated with the expression of miR-6792-3p and was closely linked with ZBTB16 levels in PC. LINC00930 might serve as a potential prognostic biomarker and therapeutic target for PC.

ß-hydroxybutyrate alleviates neurological deficits by restoring glymphatic and inflammation after subarachnoid hemorrhage in mice.

BACKGROUND: Both glymphatic system dysfunction and inflammatory response aggravate neurological dysfunction after subarachnoid hemorrhage (SAH). Studies have shown that ß-hydroxybutyrate (BHB) may mitigate painful diabetic neuropathy (PDN) by upregulating SNTA1 expression and reinstating AQP4 polarity. However, the potential of BHB to ameliorate glymphatic system function and inflammatory response in SAH mice remains uncertain. METHODS: The SAH models were constructed by injection of arterial blood into cisterna Magana. Three groups of C57 mice were randomly assigned: Sham, SAH, and BHB. All mice were subjected to neurological function assessment, western blot, immunofluorescence double staining, and RNA-seq. Glymphatic system function was examined with tracer and immunofluorescence double staining, and the differential genes were examined with RNA-seq. In addition, the expression of related inflammation was detected. RESULTS: Compared with the SAH group, BHB reinstated AQP4 polarization by upregulating SNTA1 protein to enhance the glymphatic system. According to RNA-seq, the different genes were primarily connected to microglia activation, astrocytes, and inflammation. Western blot and immunofluorescence further confirmed that the related inflammatory protein expression levels were upregulated. BHB attenuated neuroinflammation after SAH. Ultimately, it can mitigate the neurological deficits in SAH mice. CONCLUSION: The study reveals a novel mechanism that BHB treatment mitigates neurologic impairment in SAH mice. We propose that BHB may play a neuroprotective effect by enhancing glymphatic system function and attenuating neuroinflammatory subarachnoid hemorrhage.

Racial and Ethnic Characteristics and Outcomes of Patients Diagnosed with CLL/SLL in the USA.

INTRODUCTION: This study was designed to compare outcomes among patients by race and ethnicity in the post-covalent Bruton tyrosine kinase inhibitor (cBTKi) treatment era. METHODS: A nationwide electronic health record (EHR)-derived de-identified database was utilized that included patients diagnosed with CLL from 2013 to 2022 who received systemic therapy for their disease. Use of cBTKi therapy, time to next treatment or death (TTNT-D), and overall survival (OS) were compared by race in unadjusted (Kaplan-Meier method) and adjusted analyses (Cox proportional hazards regression). RESULTS: This study included 4,572 White (71.8%) and 558 Black (8.8%) patients with CLL; 270 were Hispanic or Latino (4.2%). Patients who were Black were significantly younger, more were female, had later stage disease, were of lower socioeconomic status (SES), and were more likely to have unmutated immunoglobulin heavy chain gene (IGHV) and to have received cBTKi therapy than White patients (all p ≤ 0.002). SES was also significantly different by ethnicity. TTNT-D and OS were not different by race in either unadjusted or adjusted analyses (all p > 0.05). CONCLUSION: In unadjusted and adjusted analyses, TTNT-D and OS were not different by race. These data did not identify racial healthcare disparities in the era following the introduction of cBTKi therapy despite differences in baseline characteristics.

Global prevalence of major depressive disorder in LGBTQ+ samples: A systematic review and meta-analysis of epidemiological studies.

BACKGROUND: LGBTQ+ populations have been reported to have higher rates of depression compared with their heterosexual peers. Such data provided us the impetus to conduct a meta-analysis on the worldwide prevalence of major depressive disorder (MDD) in LGBTQ+ populations and moderating factors that contributed to differences in prevalence estimates between studies. METHODS: A systematic literature search was performed in major international (PubMed, PsycINFO, Web of Science, EMBASE) and Chinese (Chinese Nation Knowledge Infrastructure (CNKI) and WANFANG) databases from dates of inception to 10 December 2021. RESULTS: 48 articles comprising 4,616,903 individuals were included in the meta-analysis. The overall prevalence of MDD was 32.2 % (95%CI: 30.8-33.6 %, I2 = 99.6 %, τ2 = 0.284). MDD prevalence was higher in the LGBTQ+ samples from the United States than other countries, though the difference was not significant in moderator analyses. Moderator analyses indicated point and lifetime prevalence of MDD were significantly higher than estimates based on the past year (Q = 6.270, p = 0.043). Furthermore, studies that relied on convenience sampling had a higher prevalence of MDD than those based on other sampling methods (Q = 8.159, p = 0.017). In meta-regression analyses, mean age (B = 0.03, z = 9.54, p < 0.001) and study quality assessment score (B = 0.24, z = 67.64, p < 0.001) were positively associated with pooled prevalence of MDD while mediation data of year of study (B = -0.08, z = -72.55, p < 0.001) and sample size (B = -1.46, z = -37.83, p < 0.001) were negatively associated with pooled prevalence of MDD in LGBTQ+ samples. CONCLUSIONS: MDD is common among in LGBTQ+ individuals. Considering the negative consequences MDD has on daily life and well-being, appropriate prevention and treatment measures should be provided to vulnerable members of these populations. The findings of this meta-analysis could facilitate identifying at-risk subgroups, developing relevant health policy for LGBTQ+ individuals and allocating health resources from an intersectionality perspective.

Molecular beacon-based detection of circulating microRNA-containing extracellular vesicle as an α-synucleinopathy biomarker.

Early and precise diagnosis of α-synucleinopathies is challenging but critical. In this study, we developed a molecular beacon-based assay to evaluate microRNA-containing extracellular vesicles (EVs) in plasma. We recruited 1203 participants including healthy controls (HCs) and patients with isolated REM sleep behavior disorder (iRBD), α-synucleinopathies, or non-α-synucleinopathies from eight centers across China. Plasma miR-44438-containing EV levels were significantly increased in α-synucleinopathies, including those in the prodromal stage (e.g., iRBD), compared to both non-α-synucleinopathy patients and HCs. However, there are no significant differences between Parkinson's disease (PD) and multiple system atrophy. The miR-44438-containing EV levels negatively correlated with age and the Hoehn and Yahr stage of PD patients, suggesting a potential association with disease progression. Furthermore, a longitudinal analysis over 16.3 months demonstrated a significant decline in miR-44438-containing EV levels in patients with PD. These results highlight the potential of plasma miR-44438-containing EV as a biomarker for early detection and progress monitoring of α-synucleinopathies.

Abnormal mitochondrial iron metabolism damages alveolar type II epithelial cells involved in bleomycin-induced pulmonary fibrosis.

Rationale: Pulmonary fibrosis is a chronic progressive lung disease with limited therapeutic options. We previously revealed that there is iron deposition in alveolar epithelial type II cell (AECII) in pulmonary fibrosis, which can be prevented by the iron chelator deferoxamine. However, iron in the cytoplasm and the mitochondria has two relatively independent roles and regulatory systems. In this study, we aimed to investigate the role of mitochondrial iron deposition in AECII injury and pulmonary fibrosis, and to find potential therapeutic strategies. Methods: BLM-treated mice, MLE-12 cells, and primary AECII were employed to establish the mouse pulmonary fibrosis model and epithelial cells injury model, respectively. Mitochondrial transplantation, siRNA and plasmid transfection, western blotting (WB), quantitative real-time polymerase chain reaction (RT-qPCR), polymerase chain reaction (PCR), immunofluorescence, immunoprecipitation (IP), MitoSOX staining, JC-1 staining, oxygen consumption rate (OCR) measurement, and Cell Counting Kit-8 (CCK8) assay were utilized to elucidate the role of mitochondrial iron deposition in cell and lung fibrosis and determine its mechanism. Results: This study showed that prominent mitochondrial iron deposition occurs within AECII in bleomycin (BLM)-induced pulmonary fibrosis mouse model and in BLM-treated MLE-12 epithelial cells. Further, the study revealed that healthy mitochondria rescue BLM-damaged AECII mitochondrial iron deposition and cell damage loss. Mitoferrin-2 (MFRN2) is the main transporter that regulates mitochondrial iron metabolism by transferring cytosolic iron into mitochondria, which is upregulated in BLM-treated MLE-12 epithelial cells. Direct overexpression of MFRN2 causes mitochondrial iron deposition and cell damage. In this study, decreased ubiquitination of the ubiquitin ligase F-box/LRR-repeat protein 5 (FBXL5) degraded iron-reactive element-binding protein 2 (IREB2) and promoted MFRN2 expression as well as mitochondrial iron deposition in damaged AECII. Activation of the prostaglandin E2 receptor EP4 subtype (EP4) receptor signaling pathway counteracted mitochondrial iron deposition by downregulating IREB2-MFRN2 signaling through upregulation of FBXL5. This intervention not only reduced mitochondrial iron content but also preserved mitochondrial function and protected against AECII damage after BLM treatment. Conclusion: Our findings highlight the unexplored roles, mechanisms, and regulatory approaches of abnormal mitochondrial iron metabolism of AECII in pulmonary fibrosis. Therefore, this study deepens the understanding of the mechanisms underlying pulmonary fibrosis and offers a promising strategy for developing effective therapeutic interventions using the EP4 receptor activator.

Preparation of hyperbranched hydrophobic nano-silica and its superior needling-effect in PDMS defoam agent.

Hydrophobic nano silica powder is a kind of important synergist to silicone defoaming agents. The large pore volume and branched chain conformation of silica nanoparticles present superior effects on defoaming properties. However, silica nanoparticles synthesized by liquid phase easily aggregate and pore collapse because of their high surface activity and polarity, leading to poorer dispersity and limited practicability. In this paper, a novel hydrophobic silica with a hyperbranched structure was designed through in-situ modifying method with hexamethyldisilazane (HMDS) and polydimethylsiloxane (PDMS) in the liquid phase. The trimethylsilanol generated by HMDS hydrolysis reacts quickly with the highly active hydroxyl groups on the silica, causing the surface properties of the nanoparticles to transform from polar to non-polar properties. The steric hindrance of the trimethyl silicon and the reduction of the surface polarity effectively prevent silica pores from collapsing and maintain the macropore structures to realize the hyperbranched silica. At the same time, the -Si (CH3)2- from PDMS endowed the hyperbranched silica with excellent hydrophobicity. When applied in the defoaming agent, the hydrophobicity of silica contributes to dewetting the foams, and the hyperbranched spatial structures play an enhanced needling effect. Therefore, this hydrophobic hyperbranched silica exhibited a surprising defoaming effect, which significantly reduced the defoaming time from 464.4 s to less than 2 s, superior to commercial defoaming silica (155.3 s). The defoaming efficiency reached 100 % within 2 s of the end of the shaking, and the defoamer antifoaming ability was improved to reach 27.5 min, which was 77 % higher than that of commercial defoamer.

Unveiling cancer dormancy: Intrinsic mechanisms and extrinsic forces.

Tumor cells disseminate in various distant organs at early stages of cancer progression. These disseminated tumor cells (DTCs) can stay dormant/quiescent without causing patient symptoms for years or decades. These dormant tumor cells survive despite curative treatments by entering growth arrest, escaping immune surveillance, and/or developing drug resistance. However, these dormant cells can reactivate to proliferate, causing metastatic progression and/or relapse, posing a threat to patients' survival. It's unclear how cancer cells maintain dormancy and what triggers their reactivation. What are better approaches to prevent metastatic progression and relapse through harnessing cancer dormancy? To answer these remaining questions, we reviewed the studies of tumor dormancy and reactivation in various types of cancer using different model systems, including the brief history of dormancy studies, the intrinsic characteristics of dormant cells, and the external cues at the cellular and molecular levels. Furthermore, we discussed future directions in the field and the strategies for manipulating dormancy to prevent metastatic progression and recurrence.

Androgen receptor splice variants drive castration-resistant prostate cancer metastasis by activating distinct transcriptional programs.

One critical mechanism through which prostate cancer (PCa) adapts to treatments targeting androgen receptor (AR) signaling is the emergence of ligand-binding domain-truncated and constitutively active AR splice variants, particularly AR-V7. While AR-V7 has been intensively studied, its ability to activate distinct biological functions compared with the full-length AR (AR-FL), and its role in regulating the metastatic progression of castration-resistant PCa (CRPC), remain unclear. Our study found that, under castrated conditions, AR-V7 strongly induced osteoblastic bone lesions, a response not observed with AR-FL overexpression. Through combined ChIP-seq, ATAC-seq, and RNA-seq analyses, we demonstrated that AR-V7 uniquely accesses the androgen-responsive elements in compact chromatin regions, activating a distinct transcription program. This program was highly enriched for genes involved in epithelial-mesenchymal transition and metastasis. Notably, we discovered that SOX9, a critical metastasis driver gene, was a direct target and downstream effector of AR-V7. Its protein expression was dramatically upregulated in AR-V7-induced bone lesions. Moreover, we found that Ser81 phosphorylation enhanced AR-V7's pro-metastasis function by selectively altering its specific transcription program. Blocking this phosphorylation with CDK9 inhibitors impaired the AR-V7-mediated metastasis program. Overall, our study has provided molecular insights into the role of AR splice variants in driving the metastatic progression of CRPC.