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Abstract: Here, we developed a new strategy for preparation of series of in‐situ reduction bimetallic catalysts Ni‐W/SiO2 by introducing of reducing agent in the preparation process. And these catalysts were applied into the catalytic hydrogenolysis of microcrystalline cellulose and pretreated lignocellulose. The results show that the in situ reduction 15%Ni–20%W/SiO2 shows the prominent activity for microcrystalline cellulose conversion into ethylene glycol (EG), 1,2‐propylene glycol, and glycerol with the highest yield of EG at 61.30% under the experimental condition. And the relative high of EG yield (30.23%) was obtained when a combinative pretreatment technology of steam explosion (0.45 MPa) coupled with hot alkali (70 °C) was introduced to enhance the hydrogenolysis of plant lignocellulose‐based feedstocks over the in situ reduction catalyst 15%Ni–20%W/SiO2. The SEM and thermogravimetry analysis revealed that segmental lignin and hemicellulose were removed partly by hot alkali pretreatment. Meanwhile, the existence of Ni–W alloys and metal Ni particles were evidenced by X‐ray diffraction spectra. In addition, by the detailed analysis via transmission electron microscopy and X‐ray photoelectron spectroscopy, the catalytic particle size was distributed in the range of 9.3 ± 1.3 nm. [ABSTRACT FROM AUTHOR]

[Display omitted] • Novel 6-benzyloxyphthalides were synthesized. • Most compounds showed selective, competitive and reversible MAO-B inhibitory and antioxidant activities. • 8f and 14a were the outstanding representative with good in vitro multifunctional and drug-like properties. • 8f and 14a could alleviate the progress of PD in MPTP-induced mouse acute and subacute model. A series of 6-benzyloxyphthalides were designed and synthesized as potent monoamine oxidase B inhibitors with antioxidant and anti-neuroinflammatory activities. The representative compounds 8f and 14a exhibited excellent selective MAO-B inhibition activity (IC 50 = 1.33 nM, SI = 865; IC 50 = 0.02 nM, SI = 40250, respectively) and moderate antioxidant activity (0.34 and 0.36 Trolox equivalent, respectively). Further studies showed that they were competitive and quasi-reversible MAO-B inhibitors. In cellular experiments, they could significantly decrease the production of NO and TNF- α in LPS-stimulated BV-2 cells to perform their in vitro anti-neuroinflammatory activities. Moreover, BBB permeability study and the predicted physicochemical properties indicated they were suitable for the CNS. Finally, in in vivo acute and subacute MPTP-induced mice model of PD, 8f and 14a could significantly improve most behavioral disorders, restore the DA content and decrease the MDA content in the mice striatum, exhibiting better anti-PD effects than clinically used safinamide. Hence, compounds 8f and 14a are identified in our studies as prospective prototype in the research of innovative multifunctional drugs for Parkinson's disease treatment. [ABSTRACT FROM AUTHOR]

FuFang ZhenZhu TiaoZhi (FTZ) is a hospitalized traditional Chinese medicine herbal formula with documented metabolic benefits. Polycystic ovary syndrome (PCOS) characterized by ovarian dysfunction and insulin resistance represents one of the most common endocrine disorders in close association with metabolic dysfunction in premenopausal women. Aim of The Study: The present study aimed to investigate the preventive effect of FTZ on letrozole-induced experimental PCOS and its associated insulin resistance in mice. Prepubertal female mice in the experimental groups (letrozole and FTZ) received continuous infusion of letrozole (50 μg/day) for 35 days. FTZ was administrated to mice by oral gavage daily at dosage of 2.892 g/kg body weight for 5 weeks. All groups of mice were fed a high-fat diet (HFD). Ovary and adipose tissue were collected from all mice after 5 weeks and adiponectin, testosterone, estradiol, and luteinizing hormone level determined. Letrozole-induced morphological changes in the ovary, including a decreased number of corpora lutea and antral follicles, and increased cystic follicles, were significantly attenuated in FTZ-treated mice. Additionally, FTZ treatment notably reversed PCOS-related disruption of estrous status. PCOS-related insulin resistance was markedly alleviated. Mechanistically, FTZ treatment notably enhanced circulating level and transcriptional abundance of adiponectin in adipose tissue, thereby orchestrating fat-ovary crosstalk. Our data collectively demonstrate that FTZ exerted preventive benefits in an experimental model of PCOS, at least partially by potentiating the production of adiponectin from adipose tissues. This suggests that FTZ is a promising treatment for PCOS. Image 1 [ABSTRACT FROM AUTHOR]

Offspring growth requires establishing maternal behavior associated with the maternal endocrine profile. Placentae support the adaptations of the mother, producing bioactive molecules that affect maternal organs. We recently reported that placentae produce superoxide dismutase 3 (SOD3) that exerts sustained effects on the offspring liver via epigenetic modifications. Here, we demonstrate that placenta-specific Sod3 knockout (Sod3 -/- ) dams exhibited impaired maternal behavior and decreased prolactin levels. Most fibroblast growth factor (FGF)-regulated pathways were downregulated in the pituitary tissues from Sod3 -/- dams. FGF1-, FGF2-, and FGF4-induced prolactin expression and signaling via the phosphoinositide 3-kinase (PI3K)-phospholipase C-γ1 (PLCγ1)-protein kinase-Cδ (PKC)δ axis were reduced in primary pituitary cells from Sod3 -/- dams. Mechanistically, FGF1/FGF receptor (FGFR)2 expressions were inhibited by the suppression of the ten-eleven translocation (TET)/isocitrate dehydrogenase (IDH)/α-ketoglutarate pathway and DNA demethylation levels at the zinc finger and BTB domain containing 18 (ZBTB18)-targeted promoters of Fgf1/Fgfr2. Importantly, offspring from Sod3 -/- dams also showed impaired nurturing behavior to their grandoffspring. Collectively, placenta-derived SOD3 promotes maternal behavior via epigenetic programming of the FGF/FGFR-prolactin axis., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

Background and Objective: A 6-month interval between systemic isotretinoin (ISO) and the initiation of energy-based interventions has been recommended, due to concerns about keloid formation and delayed wound healing. While this postponement goes against the current trend of early intervention for acne scarring. This systematic review evaluates the efficacy, safety, and patient satisfaction of combinations of ISO with energy-based devices (EBD)., Study Design/methods and Materials: PubMed, Embase, Web of Science, Cochrane Library, and Cochrane Central Register of Controlled Trials were comprehensively searched up to April 2023 according to PRISMA guidelines. Two independent reviewers screened the titles and abstracts to select articles. The quality of the literature was assessed for each study design., Results: A total of 16 studies addressing the efficacy and safety of energy-based modalities combined with ISO were identified, including six randomized controlled trials (RCTs), two case series, seven cohort studies, and one case report. ISO combinations with intense pulsed light (IPL), fractional ablative CO 2 laser, pulsed dye laser (PDL), non-ablative fractional laser (NAFL) and fractional microneedle radiofrequency (FMRF) have been tested for improving acne severity, acne scarring and erythema., Conclusion: The current evidence does not justify delaying the use of EBDs for patients who have recently undergone or are currently receiving ISO treatment. Evidence-based treatments such as PDL, NAFL, and FMRF etc. are suggested relatively safe and effective in treating acne and acne scarring., (© 2024 The Author(s). Journal of Cosmetic Dermatology published by Wiley Periodicals LLC.)

Efficient removal and recovery of phosphorus from aquaculture tailwater is challenging due to increasing strict water environment restrictions. This study presents a sustainable approach by using microalgae-waste-derived hydrogels/membranes for phosphorus adsorption and microalgae cultivation. Waste from Euglena gracilis (or Haematococcus pluvialis), modified with magnesium, was converted into biochars (abbreviated as MEBC or MHBC). This biochars were then combined with sodium alginate to fabricate hydrogels and with polyvinyl chloride to create membranes. Due to the almost 100 % phosphorus removal of MEBC (or MHBC) biochar, the as-obtained hydrogels/membranes demonstrated excellent phosphate adsorption, reducing total phosphorus in real aquaculture tailwater from 11 mg/L to 0. Additionally, the phosphorus-saturated hydrogel served as a phosphorus source for microalgae cultivation, while the membranes facilitated microalgae harvesting with a water flux over 40 L/m 2 /h. This study provides an eco-friendly solution for using microalgae-waste-derived materials to effectively address phosphorus removal and recovery challenges in aquaculture tailwater., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024. Published by Elsevier Ltd.)

Background: Persistent macrophage infiltration may lead to adverse consequences, such as calcifications and nodules in fat grafts. Lymphatic vessels, which transport inflammatory cells, are involved in regulating inflammatory responses. Less is known, however, about lymphatic vessels after fat grafting., Objectives: The aim of this study was to explore the regulation of fat graft survival by lymphatic vessels., Methods: A common adipose graft model was constructed to assess the processes responsible for changes in the number of lymphatic vessels in grafts. Adipose tissue samples from C57/BL6 mice and green fluorescent protein-expressing mice were cross-grafted to determine the source of lymphatic vessels. The number of lymphatic vessels in the grafts was increased by treatment with vascular endothelial growth factor C, and the effects of this increase on fat grafting were evaluated., Results: The number of lymphatic vessels was greater in postgrafted fat than in inguinal fat before transplantation, with lymphatic vessels in these grafts gradually transitioning from donor to recipient sources. Lymphatic vessels grew more slowly than blood vessels during early stages of grafting; during later stages, however, the number of blood vessels declined markedly, with more lymphatic vessels than blood vessels being observed 60 days after grafting. Vascular endothelial growth factor C treatment increased graft lymphatics and distant volume retention, while reducing fibrosis and oil sacs. Lymphatic vessels acted as drainage channels for macrophages, with the degree of sustained macrophage infiltration decreasing with increases in the number of lymphatic vessels., Conclusions: Increasing the number of lymphatic vessels is beneficial for fat graft survival, which may be related to a reduction in prolonged macrophage infiltration., (© The Author(s) 2024. Published by Oxford University Press on behalf of The Aesthetic Society. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Background: Blood perfusion in the recipient site is important for adipose tissue repair after fat grafting. It delivers host-derived macrophages derived from monocytes in bone marrow to initiate inflammatory reactions and regenerative responses. According to the ability of CXCL12, a stromal cell-derived factor, to recruit monocytes/macrophages, we studied its effect on adipose tissue repair and regeneration under ischemic and normal conditions., Methods: Each inguinal fat pad was crushed for 30 seconds with a clamp in mice (n = 35). The left inguinal vessels were divided and cut off (ischemic group), while the right inguinal vessels were kept patent (control group). Seven animals were sacrificed at 1, 3, 7, 14, and 30 days after surgery, and macrophages (Mac2 and CD206) and adipocytes (perilipin) were assessed. Levels of inflammatory factors (interleukin (IL)-1β, IL-6, and tumor necrosis factor-α) and CXCL12 were measured by quantitative PCR., Results: The number of macrophages was higher in the control group than in the ischemic group at day 3 (10.33 ± 2.40 vs. 1.33 ± 0.33, p = 0.021). The percentage of M2 macrophages was higher in the control group than in the ischemic group at day 7 (p<0.05). The levels of inflammatory factors and CXCL12 were higher in the control group than in the ischemic group at the early stage (p = 0.038)., Conclusions: Established blood perfusion leads to up-regulation of CXCL12 during adipose tissue repair and regeneration, which may increase recruitment of monocytes to damaged adipose tissue. These findings increase understanding of the cellular events involved in fat graft survival after grafting., No Level Assigned: This journal requires that authors assign a level of evidence to each submission to which Evidence-Based Medicine rankings are applicable. This excludes Review Articles, Book Reviews, and manuscripts that concern Basic Science, Animal Studies, Cadaver Studies, and Experimental Studies. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266., (© 2024. Springer Science+Business Media, LLC, part of Springer Nature and International Society of Aesthetic Plastic Surgery.)

Adipose tissue remodeling and plasticity are dynamically regulated by the coordinated functions of adipocytes, macrophages, and endothelial cells and extracellular matrix (ECM) that provides stiffness networks in adipose tissue component cells. Inflammation and fibrosis are crucial exogenous factors that dysregulate adipose tissue functions and drastically change the mechanical properties of the ECM. Therefore, communication among the ECM and adipose tissue component cells is necessary to understand the multifaceted functions of adipose tissues. To obtain in vivo stiffness, we used genipin as a crosslinker for collagen gels. Meanwhile, we isolated primary adipocytes, macrophages, and endothelial cells from C57BL/6J mice and incubated these cells in the differentiation media on temperature-responsive culture dishes. After the differentiation, these cell sheets were transferred onto genipin-crosslinked collagen gels with varying matrix stiffness. We found that inflammatory gene expressions were induced by hard matrix, whereas antiinflammatory gene expressions were promoted by soft matrix in all three types of cells. Interestingly, the coculture experiments of adipocytes, macrophages, and endothelial cells showed that the effects of soft or hard matrix stiffness stimulation on adipocytes were transmitted to the distant adipose tissue component cells, altering their gene expression profiles under normal matrix conditions. Finally, we identified that a hard matrix induces the secretion of CXCL13 from adipocytes, and CXCL13 is one of the important transmitters for stiffness communication with macrophages and endothelial cells. These findings provide insight into the mechanotransmission into distant cells and the application of stiffness control for chronic inflammation in adipose tissues with metabolic dysregulation., Competing Interests: Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Purpose: This study aims to explore the association of inflammatory markers such as the Systemic Immune-Inflammatory Index (SII) and LANR with the comorbidity of Chronic Obstructive Pulmonary Disease (COPD) and lung cancer., Patients and Methods: A cross-sectional analysis was conducted on the clinical data of 309 patients with COPD only and 193 patients with COPD and lung cancer who attended the First Affiliated Hospital of Anhui Medical University. Additionally, we examined autonomous risk factors that contribute to the simultaneous development of COPD and lung cancer through univariate and multivariate logistic regression analyses. This analysis resulted in the development of a nomogram model for visual representation. The effectiveness of the model was assessed using a receiver operating characteristic (ROC) curve, calibration curve, and clinical decision analysis (DCA) curve, with internal validation conducted via repeated sampling methods., Results: Multivariate analysis of clinical characteristics and inflammatory markers showed that smoking history of >60 pack-years, hemoptysis, emphysema, WBC count > 5.53 (×10^9/L), SII > 629.285, and LANR < 11.39 were significantly associated with the comorbidity of COPD and lung cancer. These factors were subsequently integrated into the nomogram model. The AUC of the model stood at 0.849 (95% CI: 0.815-0.882), demonstrating a notable improvement over the COPD-LUCSS scoring system (AUC: 0.716, 95% CI: 0.671-0.761). The DCA curve indicated a notable clinical advantage provided by the model. Additionally, patients with stage IV tumors exhibited elevated SII levels and reduced LANR levels compared to earlier stages, indicating potential prognostic significance for both markers., Conclusion: Increased levels of the inflammatory markers SII and LANR are associated with the risk of comorbidity of COPD and lung cancer., Competing Interests: The authors report no conflicts of interest in this work., (© 2024 Xu et al.)

Background: The aim was to assess the causal relationship between depression and anxiety disorders and endometrial cancer., Method: We performed two-sample Mendelian randomisation analysis using summary statistics from genome-wide association studies to assess associations of major depressive disorder, anxiety and stress-related disorders with endometrial cancer. The genome-wide association studies(GWASs) data were derived from participants of predominantly European ancestry included in the Genome-wide Association Research Collaboration. Inverse variance-weighted, MR-Egger and weighted median MR analyses were performed, together with a range of sensitivity analyses., Results: Mendelian randomisation analysis showed no statistically significant genetic responsibility effect of anxiety and stress-related disorders on any pathological type of endometrial cancer. Only the effect of major depressive disorder under the inverse variance weighting method increasing the risk of endometrial endometrial cancer (effect 0.004 p  = 0.047) and the effect of major depressive disorder under the MR-Egger method decreasing endometrial cancer of all pathology types (effect -0.691 p  = 0.015) were statistically significant. Other Mendelian randomisation analyses did not show a statistically significant effect., Conclusion: Major depressive disorder(MDD), anxiety and stress-related disorders(ASRD) are not genetically responsible for endometrial cancer. We consider that emotional disorders may affect endometrial cancer indirectly by affecting body mass index. This study provides us with new insights to better understand the aetiology of endometrial cancer and inform prevention strategies.

Aims: In patients with diabetic microvascular complications, decreased perfusion or vascular occlusion, caused by reduced vascular diameter, is a common characteristic that will lead to insufficient blood supply. Yet, the regulatory mechanism and effective treatment approach remain elusive., Methods and Results: Our initial findings revealed a notable decrease in the expression of human AQP1 in both diabetic human retina samples (49 healthy vs. 54 diabetic samples) and high-glucose-treated human retinal microvascular endothelial cells. Subsequently, our investigations unveiled a reduction in vascular diameter and compromised perfusion within zebrafish embryos subjected to high glucose treatment. Further analysis indicated a significant down-regulation of two aquaporins, aqp1a.1 and aqp8a.1, which are highly enriched in ECs and are notably responsive to hyperglycaemic conditions. Intriguingly, the loss of function of aqp1a.1 and/or aqp8a.1 resulted in a reduction of intersegmental vessel diameters, effectively mirroring the phenotype observed in the hyperglycaemic zebrafish model. The overexpression of aqp1a.1/aqp8a.1 in zebrafish ECs led to notable enlargement of microvascular diameters. Moreover, the reduced vessel diameters resulting from high-glucose treatment were effectively rescued by the overexpression of these aquaporins. Additionally, both aqp1a.1 and apq8a.1 were localized in the intracellular vacuoles in cultured ECs as well as the ECs of sprouting ISVs, and the loss of Aqps caused the reduction of those vacuoles, which was required for lumenization. Notably, while the loss of AQP1 did not impact EC differentiation from human stem cells, it significantly inhibited vascular formation in differentiated ECs., Conclusion: EC-enriched aquaporins regulate the diameter of blood vessels through an intracellular vacuole-mediated process under hyperglycaemic conditions. These findings collectively suggest that aquaporins expressed in ECs hold significant promise as potential targets for gene therapy aimed at addressing vascular perfusion defects associated with diabetes., Competing Interests: Conflict of interest: The Authors declare that there is no conflict of interest., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For commercial re-use, please contact reprints@oup.com for reprints and translation rights for reprints. All other permissions can be obtained through our RightsLink service via the Permissions link on the article page on our site—for further information please contact journals.permissions@oup.com.)

Layered sodium transition-metal oxides generally encounter severe capacity decay and inferior rate performance during cycling, especially at a high state of charge. Herein, defect concentration is rationally modulated to explore the impact on electrochemical behavior in NaNi 1/3 Fe 1/3 Mn 1/3 O 2 layered oxides. Bulk vacancies are increased through annealing in an oxygen-rich atmosphere, demonstrated by electron paramagnetic resonance measurement. It is found that the cathode with enriched oxygen vacancies exhibits significantly enhanced reversibility of redox reactions with a higher initial Coulombic efficiency of 90.0%. Furthermore, the reduced volume variations during the initial charge/discharge process are also confirmed by in situ X-ray diffraction. As a result, the oxygen-vacancy-rich cathode shows great cycling stability and superior rate performances. Also, full cells deliver a specific capacity of approximately 145.2 mAh g -1 at 0.5 C, with a high capacity retention of 78.3% after 100 cycles. This work presents a viable strategy for designing Na + intercalated cathodes with a high-energy density.

Type IV collagen is a major component of the extracellular matrix in adipose tissue. It is secreted during the lipogenic differentiation of mesenchymal stem cells, but its direct impact and mechanism on the differentiation of adipose-derived stem cells (ASCs) into lipids are unclear. In this study, ASCs were obtained from human liposuction samples and cultured. Lipogenic induction of ASCs was achieved using lipogenic induction medium. Immunofluorescence analysis revealed differential expression of type IV collagen during the early and late stages of adipogenic induction, displaying a distinct morphological encapsulation of ASCs. Silencing of type IV collagen using siRNA resulted in a significant decrease in adipogenic capacity, as indicated by reduced lipid droplet formation and downregulation of adipogenic-related gene transcription. Conversely, supplementation of the culture medium with synthetic type IV collagen demonstrated enhanced adipogenic induction efficiency, accompanied by upregulation of YAP/TAZ protein expression and its downstream target gene transcription. Furthermore, inhibition of the YAP/TAZ pathway using the inhibitor Blebbistatin attenuated the functionality of type IV collagen, leading to decreased lipid droplet formation and downregulation of adipocyte maturation-related gene expression. These findings highlight the crucial role of type IV collagen in promoting adipogenic differentiation of ASCs and suggest its involvement in the YAP/TAZ-mediated Hippo pathway.No Level Assigned This journal requires that authors assign a level of evidence to each submission to which Evidence-Based Medicine rankings are applicable. This excludes Review Articles, Book Reviews, and manuscripts that concern Basic Science, Animal Studies, Cadaver Studies, and Experimental Studies. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 ., (© 2024. Springer Science+Business Media, LLC, part of Springer Nature and International Society of Aesthetic Plastic Surgery.)

Photoionization is one of the most fundamental processes in light-matter interaction. Advanced attosecond photoelectron spectroscopy provides the possibility to characterize the ultrafast photoemission process in an extremely short attosecond time scale. Following scattering symmetry rules, residual ions encode ultrafast photoionization prints at the instant of electron removal forming an alternative electron emission chronoscope. Here, we experimentally illustrate the attosecond ion reconstruction of attosecond beating by interference of two-photon transition (RABBIT)-like interferometry through the development of high-resolution ion momentum detection in atomic photoionization processes. Our ion interferometry presents identical momentum- and time-dependent scattering phase shift, as we observed in photoelectron spectroscopy, and thus demonstrates that ion interferometry can be a possible alternative attosecond approach to resolve the photoionization process, without the electron homogeneity limitation.

Purpose: The previous studies that examined the effectiveness of unsupervised machine learning methods versus traditional methods in assessing dietary patterns and their association with incident hypertension showed contradictory results. Consequently, our aim is to explore the correlation between the incidence of hypertension and overall dietary patterns that were extracted using unsupervised machine learning techniques., Methods: Data were obtained from Japanese male participants enrolled in a prospective cohort study between August 2008 and August 2010. A final dataset of 447 male participants was used for analysis. Dimension reduction using uniform manifold approximation and projection (UMAP) and subsequent K-means clustering was used to derive dietary patterns. In addition, multivariable logistic regression was used to evaluate the association between dietary patterns and the incidence of hypertension., Results: We identified four dietary patterns: 'Low-protein/fiber High-sugar,' 'Dairy/vegetable-based,' 'Meat-based,' and 'Seafood and Alcohol.' Compared with 'Seafood and Alcohol' as a reference, the protective dietary patterns for hypertension were 'Dairy/vegetable-based' (OR 0.39, 95% CI 0.19-0.80, P = 0.013) and the 'Meat-based' (OR 0.37, 95% CI 0.16-0.86, P = 0.022) after adjusting for potential confounding factors, including age, body mass index, smoking, education, physical activity, dyslipidemia, and diabetes. An age-matched sensitivity analysis confirmed this finding., Conclusion: This study finds that relative to the 'Seafood and Alcohol' pattern, the 'Dairy/vegetable-based' and 'Meat-based' dietary patterns are associated with a lower risk of hypertension among men., (© 2024. The Author(s).)

Chronic nonhealing wounds significantly reduce patients' quality of life and are a major burden on healthcare systems. Over the past few decades, tissue engineering materials have emerged as a viable option for wound healing, with cell-derived extracellular matrix (CDM) showing remarkable results. The CDM's compatibility and resemblance to the natural tissue microenvironment confer distinct advantages to tissue-engineered scaffolds in wound repair. This review summarizes the current processes for CDM preparation, various cell decellularization protocols, and common characterization methods. Furthermore, it discusses the applications of CDM in wound healing, including skin defect and wound repair, angiogenesis, and engineered vessels, and offers perspectives on future developments., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this review., (Copyright © 2024 Yidan Xu et al.)

Background: In plastic surgery tissue transplantation, tissue ischemia limits transplanted tissue survival. Adipose-derived stem cells (ASCs) and stromal vascular fraction (SVF) show potential for promoting angiogenesis and rescuing ischemic conditions. However, when SVF and ASC suspensions are utilized without the protection of extracellular matrix, the retention rate of transplanted cells tends to be diminished, leading to an unsatisfactory therapeutic outcome. To overcome this, adipose tissue-derived microvascular fragments (ad-MVFs) have emerged as a promising solution., Methods: We conducted enzymatic digestion on human adipose tissue to generate ad-MVFs. These fragments underwent a thorough characterization process, utilizing electron microscopy to assess their structural attributes and enabling a detailed analysis of their intricate morphology. Furthermore, our team investigated the cellular composition of these microvascular fragments, subsequently confirming their ability to enhance the viability of ischemic skin flaps., Results: The resulting product primarily comprised fragments with sizes ranging from 20 to 50 µm, and some exhibited a sophisticated network-like structure. Electron microscopy examination revealed the presence of collagen components in the product. Additionally, flow cytometry analysis indicated a substantial abundance of adipose-derived stem cells and endothelial cells within these microvascular fragments. Significantly, when tested in treating an ischemic skin flap in a nude mouse model, the product exhibited superior therapeutic efficacy compared to SVF cell suspension., Conclusion: We have successfully generated human ad-MVFs and established standardized procedures. Compared with SVF, Ad-MVFs have a better effect in the treatment of ischemic diseases., Level of Evidence Ii: This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 ., (© 2024. Springer Science+Business Media, LLC, part of Springer Nature and International Society of Aesthetic Plastic Surgery.)

Background: Culex pipiens pallens is a well-known mosquito vector for several diseases. Deltamethrin, a commonly used pyrethroid insecticide, has been frequently applied to manage adult Cx. pipiens pallens. However, mosquitoes can develop resistance to these insecticides as a result of insecticide misuse and, therefore, it is crucial to identify novel methods to control insecticide resistance. The relationship between commensal bacteria and vector resistance has been recently recognized. Bacteriophages (= phages) are effective tools by which to control insect commensal bacteria, but there have as yet been no studies using phages on adult mosquitoes. In this study, we isolated an Aeromonas phage vB AhM-LH that specifically targets resistance-associated symbiotic bacteria in mosquitoes. We investigated the impact of Aeromonas phage vB AhM-LH in an abundance of Aeromonas hydrophila in the gut of Cx. pipiens pallens and its effect on the status of deltamethrin resistance., Methods: Phages were isolated on double-layer agar plates and their biological properties analyzed. Phage morphology was observed by transmission electron microscopy (TEM) after negative staining. The phage was then introduced into the mosquito intestines via oral feeding. The inhibitory effect of Aeromonas phage vB AhM-LH on Aeromonas hydrophila in mosquito intestines was assessed through quantitative real-time PCR analysis. Deltamethrin resistance of mosquitoes was assessed using WHO bottle bioassays., Results: An Aeromonas phage vB AhM-LH was isolated from sewage and identified as belonging to the Myoviridae family in the order Caudovirales using TEM. Based on biological characteristics analysis and in vitro antibacterial experiments, Aeromonas phage vB AhM-LH was observed to exhibit excellent stability and effective bactericidal activity. Sequencing revealed that the Aeromonas phage vB AhM-LH genome comprises 43,663 bp (51.6% CG content) with 81 predicted open reading frames. No integrase-related gene was detected in the vB AH-LH genome, which marked it as a potential biological antibacterial. Finally, we found that Aeromonas phage vB AhM-LH could significantly reduce deltamethrin resistance in Cx. pipiens pallens, in both the laboratory and field settings, by decreasing the abundance of Aeromonas hydrophila in their midgut., Conclusions: Our findings demonstrate that Aeromonas phage vB AhM-LH could effectively modulate commensal bacteria Aeromonas hydrophila in adult mosquitoes, thus representing a promising strategy to mitigate mosquito vector resistance., (© 2024. The Author(s).)

Hydrogel-based flexible electronic devices serve as a next-generation bridge for human-machine interaction and find extensive applications in clinical therapy, military equipment, and wearable devices. However, the mechanical mismatch between hydrogels and human tissues, coupled with the failure of conformal interfaces, hinders the transmission of information between living organisms and flexible devices, which resulted in the instability and low fidelity of signals, especially in the acquisition of electromyographic (EMG) and electrocardiographic (ECG) signals. In this study, we designed an ion-conductive hydrogel (ICHgel) utilizing multiple physical interactions, successfully applied for human motion monitoring and the collection of epidermal physiological signals. By incorporating fumed silica (F-SiO 2 ) nanoparticles and calcium chloride into an interpenetrating network (IPN) composed of polyvinyl alcohol (PVA) and polyacrylamide (AAm)/acrylic acid (AA) chains, the ICHgel exhibited exceptional tunable stretchability (>1450% strain) and conductivity (10.58 ± 0.85 S m -1 ). Additionally, the outstanding adhesion of the ICHgel proved to be a critical factor for effective communication between epidermal tissues and flexible devices. Demonstrating its capability to acquire stable electromechanical signals, the ICHgel was attached to different parts of the human body. More importantly, as a flexible electrode, the ICHgel outperformed commercial Ag/AgCl electrodes in the collection of ECG and EMG signals. In summary, the synthesized ICHgel with its outstanding conformal interface capabilities and mechanical adaptability paves the way for enhanced human-machine interaction, fostering the development of flexible electronic devices.

Background and Objectives: Spread through air spaces (STAS) is an emerging lung cancer infiltration pattern. Predicting its spread through CT scans is crucial. However, limited STAS data makes this prediction task highly challenging. Stable diffusion is capable of generating more diverse and higher-quality images compared to traditional GAN models, surpassing the dominating GAN family models in image synthesis over the past few years. To alleviate the issue of limited STAS data, we propose a method TDASD based on stable diffusion, which is able to generate high-resolution CT images of pulmonary nodules corresponding to specific nodular signs according to the medical professionals., Methods: First, we apply the stable diffusion method for fine-tuning training on publicly available lung datasets. Subsequently, we extract nodules from our hospital's lung adenocarcinoma data and apply slight rotations to the original nodule CT slices within a reasonable range before undergoing another round of fine-tuning through stable diffusion. Finally, employing DDIM and Ksample sampling methods, we generate lung adenocarcinoma nodule CT images with signs based on prompts provided by doctors. The method we propose not only safeguards patient privacy but also enhances the diversity of medical images under limited data conditions. Furthermore, our approach to generating medical images incorporates medical knowledge, resulting in images that exhibit pertinent medical features, thus holding significant value in tumor discrimination diagnostics., Results: Our TDASD method has the capability to generate medically meaningful images by optimizing input prompts based on medical descriptions provided by experts. The images generated by our method can improve the model's classification accuracy. Furthermore, Utilizing solely the data generated by our method for model training, the test results on the original real dataset reveal an accuracy rate that closely aligns with the testing accuracy achieved through training on real data., Conclusions: The method we propose not only safeguards patient privacy but also enhances the diversity of medical images under limited data conditions. Furthermore, our approach to generating medical images incorporates medical knowledge, resulting in images that exhibit pertinent medical features, thus holding significant value in tumor discrimination diagnostics., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.)

The flexible bimodal e-skin exhibits significant promise for integration into the next iteration of human-computer interactions, owing to the integration of tactile and proximity perception. However, those challenges, such as low tactile sensitivity, complex fabrication processes, and incompatibility with bimodal interactions, have restricted the widespread adoption of bimodal e-skin. Herein, a bimodal capacitive e-skin capable of simultaneous tactile and proximity sensing has been developed. The entire process eliminates intricate fabrication techniques, employing DLP-3D printing for the electrode layers and sacrificial templating for the dielectric layers, conferring high tactile sensitivity (1.672 kPa -1 ) and rapid response capability (∼30 ms) to the bimodal e-skin. Moreover, exploiting the "fringing electric field" effect inherent in parallel-plate capacitors has facilitated touchless sensing, thereby enabling static distance recognition and dynamic gesture recognition of varying materials. Interestingly, an e-skin sensing array was created to identify the positions and pressure levels of various objects of different masses. Furthermore, with the aid of machine learning techniques, an artificial neural network has been established to possess intelligent object recognition capabilities, facilitating the identification, classification, and training of various object configurations. The advantages of the bimodal e-skin render it highly promising for extensive applications in the field of next-generation human-machine interaction.

The secretion and quality control of glycosylphosphatidylinositol-anchored proteins (GPI-APs) necessitates post-attachment remodeling initiated by the evolutionarily conserved PGAP1, which deacylates the inositol in nascent GPI-APs. Impairment of PGAP1 activity leads to developmental diseases in humans and fatality and infertility in animals. Here, we present three PGAP1 structures (2.66-2.84 Å), revealing its 10-transmembrane architecture and product-enzyme interaction details. PGAP1 holds GPI-AP acyl chains in an optimally organized, guitar-shaped cavity with apparent energetic penalties from hydrophobic-hydrophilic mismatches. However, abundant glycan-mediated interactions in the lumen counterbalance these repulsions, likely conferring substrate fidelity and preventing off-target hydrolysis of bulk membrane lipids. Structural and biochemical analyses uncover a serine hydrolase-type catalysis with atypical features and imply mechanisms for substrate entrance and product release involving a drawing compass movement of GPI-APs. Our findings advance the mechanistic understanding of GPI-AP remodeling., (© 2024. The Author(s).)

Background: N6-methyladenosine (m6A) is the most frequent RNA modification in mammals, and its role in bladder cancer (BC) remains rarely revealed., Objective: To predict the value of m6A-related genes in prognosis and immunity in BC., Methods: We performed multiple omics analysis of 618 TCGA and GEO patients and used principal component analysis (PCA) to calculate the m6A score for BC patients., Results: We described the multiple omics status of 23 m6A methylation-related genes (MRGs), and four m6A clusters were identified, which showed significant differences in immune infiltration and biological pathways. Next, we intersected the differential genes among m6A clusters, and 11 survival-related genes were identified, which were used to calculate the m6A score for the patients. We found that the high-score (HS) group showed lower tumor mutation burden (TMB) and TP53 mutations and better prognosis than the low-score (LS) group. Lower immune infiltration, higher expression of PD-L1, PD-1, and CTLA4, and higher immune dysfunction and immune exclusion scores were identified in the LS group, suggesting a higher possibility of immune escape. Finally, the experimental verification shows that the m6A related genes, such as IGFBP1, plays an important role in the growth and metastasis of bladder cancer., Conclusions: These findings revealed the important roles of m6A MRGs in predicting prognosis, TMB status, TP53 mutation, immune functions and immunotherapeutic response in BC.

The epidemiological, etiological, and clinical characteristics vary greatly between pediatric (P-HCM) and adult (A-HCM) hypertrophic cardiomyopathy (HCM) patients, and the understanding of the heterogeneous pathogenesis mechanisms is insufficient to date. In this study, we aimed to comprehensively assess the respective transcriptome signatures and uncover the essential differences in gene expression patterns among A-HCM and P-HCM. The transcriptome data of adults were collected from public data (GSE89714), and novel pediatric data were first obtained by RNA sequencing from 14 P-HCM and 9 infantile donor heart samples. Our study demonstrates the common signatures of myofilament or protein synthesis and calcium ion regulation pathways in HCM. Mitochondrial function is specifically dysregulated in A-HCM, whereas the inhibition of cardiac developing networks typifies P-HCM. These findings not only distinguish the transcriptome characteristics in children and adults with HCM but also reveal the potential mechanism of the higher incidence of septal defects in P-HCM patients., Competing Interests: The authors declare no competing interests., (© 2023.)

Multiphoton light-matter interactions invoke a so-called "black box" in which the experimental observations contain the quantum interference between multiple pathways. Here, we employ polarization-controlled attosecond photoelectron metrology with a partial wave manipulator to deduce the pathway interference within this quantum 'black box" for the two-photon ionization of neon atoms. The angle-dependent and attosecond time-resolved photoelectron spectra are measured across a broad energy range. Two-photon phase shifts for each partial wave are reconstructed through the comprehensive analysis of these photoelectron spectra. We resolve the quantum interference between the degenerate p→d→p and p→s→p two-photon ionization pathways, in agreement with our theoretical simulations. Our approach thus provides an attosecond time-resolved microscope to look inside the "black box" of pathway interference in ultrafast dynamics of atoms, molecules, and condensed matter.

Many eukaryotic receptors and enzymes rely on glycosylphosphatidylinositol (GPI) anchors for membrane localization and function. The transmembrane complex GPI-T recognizes diverse proproteins at a signal peptide region that lacks consensus sequence and replaces it with GPI via a transamidation reaction. How GPI-T maintains broad specificity while preventing unintentional cleavage is unclear. Here, substrates- and products-bound human GPI-T structures identify subsite features that enable broad proprotein specificity, inform catalytic mechanism, and reveal a multilevel safeguard mechanism against its promiscuity. In the absence of proproteins, the catalytic site is invaded by a locally stabilized loop. Activation requires energetically unfavorable rearrangements that transform the autoinhibitory loop into crucial catalytic cleft elements. Enzyme-proprotein binding in the transmembrane and luminal domains respectively powers the conformational rearrangement and induces a competent cleft. GPI-T thus integrates various weak specificity regions to form strong selectivity and prevent accidental activation. These findings provide important mechanistic insights into GPI-anchored protein biogenesis., (© 2023. Springer Nature Limited.)

Lactate serves as the major glucose alternative to an energy substrate in the brain. Lactate level is increased in the fetal brain from the middle stage of gestation, indicating the involvement of lactate in brain development and neuronal differentiation. Recent reports show that lactate functions as a signaling molecule to regulate gene expression and protein stability. However, the roles of lactate signaling in neuronal cells remain unknown. Here, we showed that lactate promotes the all stages of neuronal differentiation of SH-SY5Y and Neuro2A, human and mouse neuroblastoma cell lines, characterized by increased neuronal marker expression and the rates of neurites extension. Transcriptomics revealed many lactate-responsive genes sets such as SPARCL1 in SH-SY5Y, Neuro2A, and primary embryonic mouse neuronal cells. The effects of lactate on neuronal function were mainly mediated through monocarboxylate transporters 1 (MCT1). We found that NDRG family member 3 (NDRG3), a lactate-binding protein, was highly expressed and stabilized by lactate treatment during neuronal differentiation. Combinative RNA-seq of SH-SY5Y with lactate treatment and NDRG3 knockdown shows that the promotive effects of lactate on neural differentiation are regulated through NDRG3-dependent and independent manners. Moreover, we identified TEA domain family member 1 (TEAD1) and ETS-related transcription factor 4 (ELF4) are the specific transcription factors that are regulated by both lactate and NDRG3 in neuronal differentiation. TEAD1 and ELF4 differently affect the expression of neuronal marker genes in SH-SY5Y cells. These results highlight the biological roles of extracellular and intracellular lactate as a critical signaling molecule that modifies neuronal differentiation., Competing Interests: Conflict of interest The authors declare that they have no conflicts of interest with the contents of this article., (Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved.)

Peptidylarginine deiminase 4 (PAD4), a Ca 2+ -dependent enzyme, catalyzes the conversion of arginine to citrulline and has been strongly associated with many malignant tumors. However, the molecular mechanisms of PAD4 in the development and progression of colorectal cancer (CRC) remain unclearly defined. In our study, PAD4 expression was increased in CRC tissues and cells, and was closely related to tumor size, lymph node metastasis. Moreover, the transcription factor KLF9 directly bound to PADI4 gene promoter, leading to overexpression of PAD4 in CRC cells, which augmented cell growth and migration. We revealed that PAD4 interacted with and citrullinated glycogen synthase kinase-3β (GSK3β) in CRC cells, and GSK3β Arg-344 was the dominating PAD4-citrullination site. Furthermore, IgL2 and catalytic domains of PAD4 directly bound to the kinase domain of GSK3β in CRC cells. Mechanistically, PAD4 promoted the transport of GSK3β from the cytoplasm to the nucleus, thereby increasing the ubiquitin-dependent proteasome degradation of nuclear cyclin-dependent kinase inhibitor 1 (CDKN1A). Our study is the first to reveal the details of a critical PAD4/GSK3β/CDKN1A signaling axis for CRC progression, and provides evidence that PAD4 is a potential diagnosis biomarker and therapeutic target in CRC., Competing Interests: Declaration of Competing Interest The authors declare no potential conflict of interest., (Copyright © 2022. Published by Elsevier Inc.)

Circular RNAs (circRNAs) have been reported to play essential roles in tumorigenesis and progression. This study aimed to identify dysregulated circRNAs in gastric cancer (GC) and investigate the functions and underlying mechanism of these circRNAs in GC development. Here, we identify circ&#95;CEA, a circRNA derived from the back-splicing of CEA cell adhesion molecule 5 (CEA) gene, as a novel oncogenic driver of GC. Circ&#95;CEA is significantly upregulated in GC tissues and cell lines. Circ&#95;CEA knockdown suppresses GC progression, and enhances stress-induced apoptosis in vitro and in vivo. Mechanistically, circ&#95;CEA interacts with p53 and cyclin-dependent kinases 1 (CDK1) proteins. It serves as a scaffold to enhance the association between p53 and CDK1. As a result, circ&#95;CEA promotes CDK1-mediated p53 phosphorylation at Ser315, then decreases p53 nuclear retention and suppresses its activity, leading to the downregulation of p53 target genes associated with apoptosis. These findings suggest that circ&#95;CEA protects GC cells from stress-induced apoptosis, via acting as a protein scaffold and interacting with p53 and CDK1 proteins. Combinational therapy of targeting circ&#95;CEA and chemo-drug caused more cell apoptosis, decreased tumor volume and alleviated side effect induced by chemo-drug. Therefore, targeting circ&#95;CEA might present a novel treatment strategy for GC., (© 2022. The Author(s).)

Attosecond chronoscopy is central to the understanding of ultrafast electron dynamics in matter from gas to the condensed phase with attosecond temporal resolution. It has, however, not yet been possible to determine the timing of individual partial waves, and steering their contribution has been a substantial challenge. Here, we develop a polarization-skewed attosecond chronoscopy serving as a partial wave meter to reveal the role of each partial wave from the angle-resolved photoionization phase shifts in rare gas atoms. We steer the relative ratio between different partial waves and realize a magnetic-sublevel-resolved atomic phase shift measurement. Our experimental observations are well supported by time-dependent R-matrix numerical simulations and analytical soft-photon approximation analysis. The symmetry-resolved, partial-wave analysis identifies the transition rate and phase shift property in the attosecond photoelectron emission dynamics. Our findings provide critical insights into the ubiquitous attosecond optical timer and the underlying attosecond photoionization dynamics., (© 2022. The Author(s).)

Eukaryotic cells are coated with an abundance of glycosylphosphatidylinositol anchor proteins (GPI-APs) that play crucial roles in fertilization, neurogenesis, and immunity. The removal of a hydrophobic signal peptide and covalent attachment of GPI at the new carboxyl terminus are catalyzed by an endoplasmic reticulum membrane GPI transamidase complex (GPI-T) conserved among all eukaryotes. Here, we report the cryo-electron microscopy (cryo-EM) structure of the human GPI-T at a global 2.53-Å resolution, revealing an equimolar heteropentameric assembly. Structure-based mutagenesis suggests a legumain-like mechanism for the recognition and cleavage of proprotein substrates, and an endogenous GPI in the structure defines a composite cavity for the lipid substrate. This elongated active site, stemming from the membrane and spanning an additional ~22-Å space toward the catalytic dyad, is structurally suited for both substrates which feature an amphipathic pattern that matches this geometry. Our work presents an important step towards the mechanistic understanding of GPI-AP biosynthesis., (© 2022. The Author(s).)

Background: Circular RNA (circRNA), a subclass of non-coding RNA, plays a critical role in cancer tumorigenesis and metastasis. It has been suggested that circRNA acts as a microRNA sponge or a scaffold to interact with protein complexes; however, its full range of functions remains elusive. Recently, some circRNAs have been found to have coding potential., Methods: To investigate the role of circRNAs in gastric cancer (GC), parallel sequencing was performed using five paired GC samples. Differentially expressed circAXIN1 was proposed to encode a novel protein. FLAG-tagged circRNA overexpression plasmid construction, immunoblotting, mass spectrometry, and luciferase reporter analyses were applied to confirm the coding potential of circAXIN1. Gain- and loss-of-function studies were conducted to study the oncogenic role of circAXIN1 and AXIN1-295aa on the proliferation, migration, invasion, and metastasis of GC cells in vitro and in vivo. The competitive interaction between AXIN1-295aa and adenomatous polyposis coli (APC) was investigated by immunoprecipitation analyses. Wnt signaling activity was observed using a Top/Fopflash assay, real-time quantitative RT-PCR, immunoblotting, immunofluorescence staining, and chromatin immunoprecipitation., Results: CircAXIN1 is highly expressed in GC tissues compared with its expression in paired adjacent normal gastric tissues. CircAXIN1 encodes a 295 amino acid (aa) novel protein, which was named AXIN1-295aa. CircAXIN1 overexpression enhances the cell proliferation, migration, and invasion of GC cells, while the knockdown of circAXIN1 inhibits the malignant behaviors of GC cells in vitro and in vivo. Mechanistically, AXIN1-295aa competitively interacts with APC, leading to dysfunction of the "destruction complex" of the Wnt pathway. Released β-catenin translocates to the nucleus and binds to the TCF consensus site on the promoter, inducing downstream gene expression., Conclusion: CircAXIN1 encodes a novel protein, AXIN1-295aa. AXIN1-295aa functions as an oncogenic protein, activating the Wnt signaling pathway to promote GC tumorigenesis and progression, suggesting a potential therapeutic target for GC., (© 2021. The Author(s).)

Cardiac hypertrophy is a common pathological alteration in heart disease, which has been reported to be connected with serine/threonine protein phosphatases that control the dephosphorylation of a variety of cardiac proteins. Herein, we generated protein phosphatase type 2A knockout expressing a tamoxifen-inducible Cre recombinase protein fused to two mutant estrogen-receptor ligand-binding domains (MerCreMer) under the control of the a-myosin heavy chain promoter. Cardiac function of mice was determined by echocardiography. Decrease in PP2A activity leads to increased cardiomyocyte hypertrophy and fibrosis. Loss of PP2ACα leads to the heart failure, including the changes of EF, FS, LV, ANP and BNP. On the molecular level, knockout mice shows increased expression of B55a and B56e at 60 days after tamoxifen injection. Additionally, the regulation of the Akt/GSK3β/β-catenin pathway is severely disturbed in knockout mice. In conclusion, cardiomyocyte specific deletion of PP2A gene causes the cardiac hypertrophy. We will use the knockout mice to generate a type of cardiomyocyte hypertrophy mouse model with myocardial fibrosis.

Objective: To report the clinical data of a case of iron-refractory iron deficiency anemia (IRIDA), so as to improve the understanding of IRIDA., Methods: The IRIDA patient's hematological characteristics were summarized and analyzed. The hepcidin levels were tested by ELISA kit. The TMPRSS6 gene was amplified by PCR reaction and its mutation was analyzed by sequencing. The effect of TMPRSS6 gene mutation on TMPRSS6 protein tertiary structure was predicted by Swiss-Model., Results: The patient was characterized by typical microcytic hypochromic anemia, low transferrin saturation, more reduction of intracellular iron than exocellular iron. The plasma hepcidin level was 213.77 μg/L which was significantly higher than that of IDA patients [5.19(3.31-12.02) μg/L]. The patient also carried a homozygous missense mutation of K253E in exon 7 of TMPRSS6., Conclusion: In children and younger IDA patients with no reason for iron deficiency but unresponsiveness to routine iron treatment, the diagnosis of IRIDA needs to be considered. Serum hepcidin level and TMPRSS6 gene mutation should be detected.