Relationships between body image, dyadic coping and post-traumatic growth in breast cancer patients: a cross-sectional study.

Background: The diagnosis and treatment of cancer triggers not only a negative psychological response for the patient, but also a positive psychological outcome. Positive dyadic coping, as a form of coping for mental health outcomes, can maintain or reestablish internal stability between the patient and his or her spouse, resulting in positive physical and psychological changes. However, there is a paucity of research on body image, dyadic coping, and post-traumatic growth in breast cancer patients. The purpose of this study was to explore the relationship and pathways between body image, dyadic coping, and post-traumatic growth in breast cancer patients. Methods: A cross-sectional study was conducted from November 2022 to November 2023 at a tertiary care hospital in Wuxi, Jiangsu, China. This study was conducted among 154 breast cancer patients treated at the Affiliated Hospital of Jiangnan University, all of whom completed demographic and clinical information questionnaires, Body image self-rating questionnaire for breast cancer (BISQ-BC), Dyadic Coping Inventory (DCI) and Post Traumatic Growth Inventory (PTGI). A Pearson correlation analysis was used to explore the relationship between body image, dyadic coping, and post-traumatic growth. Structural equation modeling was used to analyze the path relationships among the three and to explore the mediating role of dyadic coping. Results: The level of body image was negatively correlated with post-traumatic growth (r = -0.462, p < 0.01); and the level of body image was negatively correlated with dyadic coping (r = -0.308, p < 0.01). And dyadic coping was positively associated with post-traumatic growth (r = 0.464, p < 0.01). The structural equation modeling results supported the mediation model with the following model fit indices, chi-square to degrees of freedom ratio (χ2/df = 2.05), goodness of fit index (GFI = 0.93), comparative fit index (CFI = 0.99), canonical fit index (NFI = 0.93), incremental fit index (IFI = 0.99), non-canonical fit index (TLI = 0.99) and the root mean square of the difference in approximation error (RMSEA = 0.03). Body image and dyadic coping directly affected post-traumatic growth (ß = -0.33, p < 0.05; ß = 0.43, p < 0.05). And body image indirectly influenced post-traumatic growth through dyadic coping (ß = -0.17, p < 0.05). Conclusion: Interconnections between body image, dyadic coping, and post-traumatic growth in breast cancer patients. A preliminary validation of the mediating role of dyadic coping between body image and post-traumatic growth, body image can have an impact on dyadic coping, which in turn can have an impact on post-traumatic growth. Whereby higher levels of dyadic coping in patients may also be associated with higher levels of post-traumatic growth, whereas body image disturbance may impede levels of post-traumatic growth.

S100A6 mediated epithelial-mesenchymal transition affects chemosensitivity of colorectal cancer to oxaliplatin.

PURPOSE: To investigate the mechanism by which S100 calcium-binding protein A6 (S100A6) affects colorectal cancer (CRC) cells to oxaliplatin (L-OHP) chemotherapy, and to explore new strategies for CRC treatment. METHODS: S100A6 expression was assessed in both parental and L-OHP-resistant CRC cells using western blotting, quantitative real-time polymerase chain reaction (qRT-PCR), and enzyme-linked immunosorbent assays (ELISA). Lentiviral vectors were utilized to induce the knockdown of S100A6 expression, followed by comprehensive evaluations of cell proliferation, apoptosis, and epithelial-mesenchymal transition (EMT). Additionally, RNA-seq analysis was conducted to identify genes associated with the knockdown of S100A6. RESULTS: Elevated S100A6 expression in CRC tissues correlated with an adverse prognosis in patients with CRC. Higher expression of S100A6 was also observed in L-OHP-resistant CRC cells, which showed enhanced proliferation, migration, invasion, and antiapoptotic capabilities. Notably, the knockdown of S100A6 expression resulted in decreased proliferation, increased apoptosis, and suppression of EMT and tumorigenicity in L-OHP-resistant CRC cells. Transcriptome sequencing reveals a noteworthy association between S100A6 and vimentin expression. Application of the EMT agonist, transforming growth factor ß (TGF-ß), induces EMT in CRC cells. S100A6 expression positively correlates with TGF-ß expression. TGF-ß facilitated the expression of EMT-related molecules and reduced the chemosensitivity of L-OHP in S100A6-knockdown cells. CONCLUSION: In conclusion, the knockdown of S100A6 may overcome the L-OHP resistance of CRC cells by modulating EMT.

N6-methyladenosine levels in peripheral blood RNA: a potential diagnostic biomarker for colorectal cancer.

BACKGROUND: N6-methyladenosine (m6A) is dysregulated in various cancers, including colorectal cancer (CRC). Herein, we assess the diagnostic potential of peripheral blood (PB) m6A levels in CRC. METHODS: We collected PB from healthy controls (HCs) and patients with CRC, analyzed PB RNA m6A levels and the expression of m6A-related demethylase genes FTO and ALKBH5, cocultured CRC cells with PB mononuclear cells (PBMCs), and constructed an MC38 cancer model. RESULTS: PB RNA m6A levels were higher in the CRC than that in HCs. The area under the curve (AUC) of m6A levels (0.886) in the CRC was significantly larger compared with carbohydrate antigen 199 (CA199; 0.666) and carcinoembryonic antigen (CEA; 0.834). The combination of CEA and CA199 with PB RNA m6A led to an increase in the AUC (0.935). Compared with HCs, the expression of FTO and ALKBH5 was decreased in the CRC. After coculturing with CRC cells, the PBMCs RNA m6A were significantly increased, whereas the expression of FTO and ALKBH5 decreased. Furthermore, m6A RNA levels in the PB of MC38 cancer models were upregulated, whereas the expression of FTO and ALKBH5 decreased. CONCLUSIONS: PB RNA m6A levels are a potential diagnostic biomarker for patients with CRC.

Rapid review: A review of methods and recommendations based on current evidence.

Rapid review (RR) could accelerate the traditional systematic review (SR) process by simplifying or omitting steps using various shortcuts. With the increasing popularity of RR, numerous shortcuts had emerged, but there was no consensus on how to choose the most appropriate ones. This study conducted a literature search in PubMed from inception to December 21, 2023, using terms such as "rapid review" "rapid assessment" "rapid systematic review" and "rapid evaluation". We also scanned the reference lists and performed citation tracking of included impact studies to obtain more included studies. We conducted a narrative synthesis of all RR approaches, shortcuts and studies assessing their effectiveness at each stage of RRs. Based on the current evidence, we provided recommendations on utilizing certain shortcuts in RRs. Ultimately, we identified 185 studies focusing on summarizing RR approaches and shortcuts, or evaluating their impact. There was relatively sufficient evidence to support the use of the following shortcuts in RRs: limiting studies to those published in English-language; conducting abbreviated database searches (e.g., only searching PubMed/MEDLINE, Embase, and CENTRAL); omitting retrieval of grey literature; restricting the search timeframe to the recent 20 years for medical intervention and the recent 15 years for reviewing diagnostic test accuracy; conducting a single screening by an experienced screener. To some extent, the above shortcuts were also applicable to SRs. This study provided a reference for future RR researchers in selecting shortcuts, and it also presented a potential research topic for methodologists.

Boosting CO2 electrocatalysis through electrical double layer regulations.

Interfacial investigation for fine-tuning microenvironment has recently emerged as a promising method to optimize the electrochemical CO2 reduction system. The electrical double layer located at the electrode-electrolyte interface presents a particularly significant impact on electrochemical reactions. However, its effect on the activity and selectivity of CO2 electrocatalysis remains poorly understood. Here, we utilized two-dimensional mica flakes, a material with a high dielectric constant, to modify the electrical double layer of Ag nanoparticles. This modification resulted in a significant enhancement of current densities for CO2 reduction and an impressive Faradaic efficiency of 98% for CO production. Our mechanistic investigations suggest that the enhancement of the electrical double layer capacitance through mica modification enriched local CO2 concentration near the reaction interface, thus facilitating CO2 electroreduction.

Development and application of Chinese medical ontology for diabetes mellitus.

OBJECTIVE: To develop a Chinese Diabetes Mellitus Ontology (CDMO) and explore methods for constructing high-quality Chinese biomedical ontologies. MATERIALS AND METHODS: We used various data sources, including Chinese clinical practice guidelines, expert consensus, literature, and hospital information system database schema, to build the CDMO. We combined top-down and bottom-up strategies and integrated text mining and cross-lingual ontology mapping. The ontology was validated by clinical experts and ontology development tools, and its application was validated through clinical decision support and Chinese natural language medical question answering. RESULTS: The current CDMO consists of 3,752 classes, 182 fine-grained object properties with hierarchical relationships, 108 annotation properties, and over 12,000 mappings to other well-known medical ontologies in English. Based on the CDMO and clinical practice guidelines, we developed 200 rules for diabetes diagnosis, treatment, diet, and medication recommendations using the Semantic Web Rule Language. By injecting ontology knowledge, CDMO enhances the performance of the T5 model on a real-world Chinese medical question answering dataset related to diabetes. CONCLUSION: CDMO has fine-grained semantic relationships and extensive annotation information, providing a foundation for medical artificial intelligence applications in Chinese contexts, including the construction of medical knowledge graphs, clinical decision support systems, and automated medical question answering. Furthermore, the development process incorporated natural language processing and cross-lingual ontology mapping to improve the quality of the ontology and improved development efficiency. This workflow offers a methodological reference for the efficient development of other high-quality Chinese as well as non-English medical ontologies.

Exosomal miR-155-5p drives widespread macrophage M1 polarization in hypervirulent Klebsiella pneumoniae-induced acute lung injury via the MSK1/p38-MAPK axis.

BACKGROUND: Hypervirulent Klebsiella pneumoniae (hvKp) infection-induced sepsis-associated acute lung injury (ALI) has emerged as a significant clinical challenge. Increasing evidence suggests that activated inflammatory macrophages contribute to tissue damage in sepsis. However, the underlying causes of widespread macrophage activation remain unclear. METHODS: BALB/c mice were intravenously injected with inactivated hvKp (iHvKp) to observe lung tissue damage, inflammation, and M1 macrophage polarization. In vitro, activated RAW264.7 macrophage-derived exosomes (iHvKp-exo) were isolated and their role in ALI formation was investigated. RT-PCR was conducted to identify changes in exosomal miRNA. Bioinformatics analysis and dual-luciferase reporter assays were performed to validate MSK1 as a direct target of miR-155-5p. Further in vivo and in vitro experiments were conducted to explore the specific mechanisms involved. RESULTS: iHvKp successfully induced ALI in vivo and upregulated the expression of miR-155-5p. In vivo, injection of iHvKp-exo induced inflammatory tissue damage and macrophage M1 polarization. In vitro, iHvKp-exo was found to promote macrophage inflammatory response and M1 polarization through the activation of the p38-MAPK pathway. RT-PCR revealed exposure time-dependent increased levels of miR-155-5p in iHvKp-exo. Dual-luciferase reporter assays confirmed the functional role of miR-155-5p in mediating iHvKp-exo effects by targeting MSK1. Additionally, inhibition of miR-155-5p reduced M1 polarization of lung macrophages in vivo, resulting in decreased lung injury and inflammation induced by iHvKp-exo or iHvKp. CONCLUSIONS: The aforementioned results indicate that exosomal miR-155-5p drives widespread macrophage inflammation and M1 polarization in hvKp-induced ALI through the MSK1/p38-MAPK Axis.

PUFAs add fuel to Crohn's disease-associated AIEC-induced enteritis by exacerbating intestinal epithelial lipid peroxidation.

Polyunsaturated fatty acids (PUFAs) have been shown to exacerbate Crohn's disease (CD) by promoting lipid peroxidation (LPO) of intestinal epithelial cells (IECs). Dysbiosis of the gut microbiota may play a crucial role in this process. CD patients often exhibit an increased abundance of Escherichia coli (E. coli) in the gut, and the colonization of adherent-invasive E. coli (AIEC) is implicated in the initiation of intestinal inflammation in CD. However, the impact of AIEC on LPO remains unclear. In this study, we observed that AIEC colonization in the terminal ileum of CD patients was associated with decreased levels of glutathione peroxidase 4 (GPX4) and ferritin heavy chain (FTH) in the intestinal epithelium, along with elevated levels of 4-Hydroxynonenal (4-HNE). In vitro experiments demonstrated that AIEC infection reduced the levels of GPX4 and FTH, increased LPO, and induced ferroptosis in IECs. Furthermore, arachidonic acid (AA) and docosahexaenoic acid (DHA) supplementation in AIEC-infected IECs significantly aggravated LPO and ferroptosis. However, overexpression of GPX4 rescued AIEC-induced LPO and ferroptosis in IECs. Our results further confirmed that AIEC with AA supplementation, associated with excessive LPO and cell death in IECs, worsened colitis in the DSS mouse model and induced enteritis in the antibiotic cocktail pre-treatment mouse model in vivo. Moreover, treatment with ferrostatin-1, a ferroptosis inhibitor, alleviated AIEC with AA supplementation-induced enteritis in mice, accompanied by reduced LPO and cell death in IECs. Our findings suggest that AIEC, in combination with PUFA supplementation, can induce and exacerbate intestinal inflammation, primarily through increased LPO and ferroptosis in IECs.

Surgical Management and Outcome of Entero-Urinary Fistula Complicating Crohn's Disease: A Single Center Study.

BACKGROUND: Entero-urinary fistulas (EUF) are a rare complication of Crohn's disease (CD), observed in 1.6 to 7.7%. The management of EUF complicating CD is challenging. We aimed to report the outcome and surgical management of EUF in CD. METHODS: A retrospective chart review was performed in all CD patients with EUF who underwent surgery in our center between January 2012 and December 2021. Patient demographics, preoperative optimization, surgical management, postoperative complications, and follow-up information were collected from a prospectively maintained database. RESULTS: A total of 74 eligible patients were identified. The median interval between CD diagnosis and EUF diagnosis was 2 (0.08-6.29) years. Patients with EUF presented with pneumaturia (75.68%), urinary tract infections (72.97%), fecaluria (66.22%), and hematuria (6.76%). Fistulae originated most commonly from the ileum (63.51%), followed by the colon (14.86%), the rectum (9.46%), the cecum (2.70%), and multiple sites (9.46%). The EUF symptoms, weight, nutritional status, laboratory results were significantly improved after preoperative optimization. The absence of EUF symptoms was observed in 42 patients after the optimization and only 9 of which required bladder repair. However, 19 of 32 patients whose symptoms did not resolve required bladder repair (P = 0.001). Only 1 patient developed a bladder leakage in the early postoperative period and 3 patients experienced recurrent bladder fistula. CONCLUSIONS: Surgical management of EUF complicating CD is effective and safe, with a low rate of postoperative complication and EUF recurrence. Preoperative optimization, which is associated with the resolution of urinary symptoms and improved surgical outcomes, should be recommended.

Exosomal transfer leads to chemoresistance through oxidative phosphorylation-mediated stemness phenotype in colorectal cancer.

Background: Recently years have seen the increasing evidence identifying that OXPHOS is involved in different processes of tumor progression and metastasis and has been proposed to be a potential therapeutical target for cancer treatment. However, the exploration in oxidative phosphorylation-mediated chemoresistance is still scarce. In our study, we identify exosomal transfer leads to chemoresistance by reprogramming metabolic phenotype in recipient cells. Methods: RNA sequencing analysis was used to screen altered targets mediating exosome transfer-induced chemoresistance. Seahorse assay allowed us to measure mitochondrial respiration. Stemness was measured by spheroids formation assay. Serum exosomes were isolated for circ_0001610 quantification. Results: The induced oxidative phosphorylation leads to more stem-like properties, which is dependent on the transfer of exosomal circ_0001610. Exosome transfer results in the removal of miR-30e-5p-mediated suppression of PGC-1a, a master of mitochondrial biogenesis and function. Consequently, increased PGC-1a reshapes cellular metabolism towards oxidative phosphorylation, leading to chemoresistance. Inhibition of OXPHOS or exosomal si-circ_0001610 increases the sensitivity of chemotherapy by decreasing cell stemness in vitro and in vivo. Conclusion: Our data suggests that exosomal circ_0001610-induced OXPHOS plays an important role in chemoresistance and supports a therapeutical potential of circ_0001610 inhibitors in the treatment of oxaliplatin-resistant colorectal cancer by manipulating cell stemness.

Multidimensional-Taylor-network-based robust optimal tracking control for MIMO nonlinear discrete-time systems.

In practical engineering, system control is indispensable. However, due to the influence of model uncertainty, speed unavailability, input nonlinearity (such as actuator dead zone/fault), and multi-input coupling, the control results are not satisfactory. In this paper, a robust optimal tracking control strategy is proposed for a class of nonlinear multi-input-multi-output discrete-time systems with unknown uncertainties. This control strategy is to minimize the cost function in the process of uncertainty processing and stabilize the closed-loop system by establishing an adaptive controlling approach based on a combination of actor MTN and critic MTN based on the Multi-dimensional Taylor Network (MTN). By using the approximation property of MTN, the optimal control signal is generated by action MTN, which is used to approach the controller, and the cost function is approximated by critic MTN, which is tuned online because the cost function cannot be obtained in hands-on experience. By designing a new cost function, the amount of calculation in the control process is reduced, and the adaptive critic design control idea is integrated into the controller design to deal with the uncertainty of the system. The simulation results verify the effectiveness of the control strategy proposed in the essay.

Exploring the Application of Multi-Resonant Bands Terahertz Metamaterials in the Field of Carbohydrate Films Sensing.

Terahertz spectroscopy is a powerful tool for investigating the properties and states of biological matter. Here, a systematic investigation of the interaction of THz wave with "bright mode" resonators and "dark mode" resonators has been conducted, and a simple general principle of obtaining multiple resonant bands has been developed. By manipulating the number and positions of bright mode and dark mode resonant elements in metamaterials, we realized multi-resonant bands terahertz metamaterial structures with three electromagnetic-induced transparency in four-frequency bands. Different carbohydrates in the state of dried films were selected for detection, and the results showed that the multi-resonant bands metamaterial have high response sensitivity at the resonance frequency similar to the characteristic frequency of the biomolecule. Furthermore, by increasing the biomolecule mass in a specific frequency band, the frequency shift in glucose was found to be larger than that of maltose. The frequency shift in glucose in the fourth frequency band is larger than that of the second band, whereas maltose exhibits an opposing trend, thus enabling recognition of maltose and glucose. Our findings provide new insights into the design of functional multi-resonant bands metamaterials, as well as new strategies for developing multi-band metamaterial biosensing devices.

Hydrogen Isotope Separation Using Graphene-Based Membranes in Liquid Water.

Hydrogen isotope separation has been effectively achieved electrochemically by passage of gaseous H2/D2 through graphene/Nafion composite membranes. Nevertheless, deuteron nearly does not exist in the form of gaseous D2 in nature but as liquid water. Thus, it is a more feasible way to separate and enrich deuterium from water. Herein, we have successfully transferred monolayer graphene to a rigid and porous polymer substrate, PITEM (polyimide track-etched membrane), which could avoid the swelling problem of the Nafion substrate as well as keep the integrity of graphene. Meanwhile, defects in the large area of CVD graphene could be successfully repaired by interfacial polymerization resulting in a high separation factor. Moreover, a new model was proposed for the proton transport mechanism through monolayer graphene based on the kinetic isotope effect (KIE). In this model, graphene plays a significant role in the H/D separation process by completely breaking the O-H/O-D bond, which can maximize the KIE, leading to increased H/D separation performance. This work suggests a promising application for using monolayer graphene in the industry and proposes a pronounced understanding of proton transport in graphene.

Exosomal miR-103a-3p from Crohn's Creeping Fat-Derived Adipose-Derived Stem Cells Contributes to Intestinal Fibrosis by Targeting TGFBR3 and Activating Fibroblasts.

BACKGROUND AND AIMS: Mesenteric adipose tissue hypertrophy is a hallmark of Crohn's disease [CD], and creeping fat [CF] is unique to CD. Adipose-derived stem cells [ASCs] from inflammatory tissue exhibited altered biological functions. The role of ASCs isolated from CF in intestinal fibrosis and the potential mechanism remain unclear. METHODS: ASCs were isolated from CF [CF-ASCs] and disease-unaffected mesenteric adipose tissue [Ctrl-ASCs] of patients with CD. A series of in vitro and in vivo experiments were conducted to study the effects of exosomes from CF-ASCs [CF-Exos] on intestinal fibrosis and fibroblast activation. A micro-RNA microarray analysis was performed. Western blot, luciferase assay and immunofluorescence were performed to further detect the underlying mechanisms. RESULTS: The results indicated that CF-Exos promoted intestinal fibrosis by activating fibroblasts in a dose-dependent manner. They continuously promoted progression of intestinal fibrosis even after dextran sulphate sodium withdrawal. Further analysis showed that exosomal miR-103a-3p was enriched in CF-Exos and participated in exosome-mediated fibroblast activation. TGFBR3 was identified as a target gene of miR-103a-3p. Mechanistically, CF-ASCs released exosomal miR-103a-3p and promoted fibroblast activation by targeting TGFBR3 and promoting Smad2/3 phosphorylation. We also found that the expression of miR-103a-3p in diseased intestine was positively associated with the degree of CF and fibrosis score. CONCLUSION: Our findings show that exosomal miR-103a-3p from CF-ASCs promotes intestinal fibrosis by activating fibroblasts via TGFBR3 targeting, suggesting that CF-ASCs are potential therapeutic targets for intestinal fibrosis in CD.

The cotton pectin methyl esterase gene GhPME21 functions in microspore development and fertility in Gossypium hirsutum L.

Pectin widely exists in higher plants' cell walls and intercellular space of higher plants and plays an indispensable role in plant growth and development. We identified 55 differentially expressed genes related to pectin degradation by transcriptomic analysis in the male sterile mutant, ms1. A gene encoding pectin methylesterase (GhPME21) was found to be predominantly expressed in the developing stamens of cotton but was significantly down-regulated in ms1 stamens. The tapetal layer of GhPME21 interfered lines (GhPME21i) was significantly thickened compared to that of WT at the early stage; anther compartment morphology of GhPME21i lines was abnormal, and the microspore wall was broken at the middle stage; Alexander staining showed that the pollen grains of GhPME21i lines differed greatly in volume at the late stage. The mature pollen surfaces of GhPME21i lines were deposited with discontinuous and broken sheets and prickles viewed under SEM. Fewer pollen tubes were observed to germinate in vitro in GhPME21i lines, while tiny of those in vivo were found to elongate to the ovary. The seeds harvested from GhPME21i lines as pollination donors were dry and hollow. The changes of phenotypes in GhPME21i lines at various stages illustrated that the GhPME21 gene played a vital role in the development of cotton stamens and controlled plant fertility by affecting stamen development, pollen germination, and pollen tube elongation. The findings of this study laid the groundwork for further research into the molecular mechanisms of PMEs involved in microspore formation and the creation of cotton male sterility materials.

Crohn's disease-associated AIEC inhibiting intestinal epithelial cell-derived exosomal let-7b expression regulates macrophage polarization to exacerbate intestinal fibrosis.

The interaction between adherent-invasive Escherichia coli (AIEC) and intestinal macrophages is implicated in the pathogenesis of Crohn's disease (CD). However, its role in intestinal fibrogenesis and the underlying molecular mechanisms are poorly understood. In addition, miRNAs such as let-7b may participate in AIEC-macrophage interactions. In this study, we identified that the colonization of AIEC in the ileum was associated with enhanced intestinal fibrosis and reduced let-7b expression by enrolling a prospective cohort of CD patients undergoing ileocolectomy. Besides, AIEC-infected IL-10-/- mice presented more severe intestinal fibrosis and could be improved by exogenous let-7b. Mechanistically, intestinal macrophages were found to be the main target of let-7b. Transferring let-7b-overexpressing macrophages to AIEC-infected IL-10-/- mice significantly alleviated intestinal fibrosis. In vitro, AIEC suppressed exosomal let-7b derived from intestinal epithelial cells (IECs), instead of the direct inhibition of let-7b in macrophages, to promote macrophages to a fibrotic phenotype. Finally, TGFßR1 was identified as one target of let-7b that regulates macrophage polarization. Overall, the results of our work indicate that AIEC is associated with enhanced intestinal fibrosis in CD. AIEC could inhibit exosomal let-7b from IECs to promote intestinal macrophages to a fibrotic phenotype and then contributed to fibrogenesis. Thus, anti-AIEC or let-7b therapy may serve as novel therapeutic approaches to ameliorate intestinal fibrosis.

What is the context?Adherent-invasive Escherichia coli (AIEC) plays an important role in the pathogenesis of Crohn's disease (CD) and has a strong association with intestinal fibrosis in animal models. However, how these bacteria contribute to intestinal fibrosis in CD patients is still unclear.The plasticity of macrophages is crucial in immune tolerance and tissue repair in the gastrointestinal tract, and the abnormal interaction between macrophages and gut bacteria triggers the fibrogenesis in the intestine.The association between the miRNA let-7b and fibrosis process has been widely reported in many tissues, except the intestine.What is new?AIEC colonization in the terminal ileum is associated with severe intestinal fibrosis in CD patients and the let-7b plays an anti-fibrotic role in intestinal fibrosis.Intestinal macrophages are the key modulator of AIEC-induced fibrosis and can be promoted to an antifibrotic phenotype through let-7b-targeted TGFßR1 inhibition.AIEC suppresses intestinal epithelial cell-derived exosomal let-7b to promote intestinal macrophages to a fibrotic phenotype, rather than a direct effect on macrophage regulation.What is the impact? Anti-AIEC and let-7b therapy may serve as potential therapeutic strategies to reduce intestinal fibrosis in CD in the future.

Hypoxic ASCs-derived Exosomes Attenuate Colitis by Regulating Macrophage Polarization via miR-216a-5p/HMGB1 Axis.

BACKGROUND: Exosomes derived from mesenchymal stem cells have shown therapeutic effects for colitis. As a more clinically accessible resource, the therapeutic potential of exosomes from adipose-derived stem cells (ASCs) has not been fully elucidated, and whether hypoxia precondition could improve the therapeutic effect of ASC-derived exosomes in colitis remains elusive. METHODS: In this study, exosomes were derived from ASCs under normoxia (NExos) and hypoxia (HExos) and were identified by detecting their morphology, size distribution, and exosome surface markers. The concentration of inflammation-related cytokines was detected by ELISA, and macrophage phenotype-related genes were determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR), western blot, and immunofluorescence. A miRNA microarray sequencing analysis was conducted to confirm the differentially expressed miRNAs. Dextran sulfate sodium-induced colitis was employed as an in vivo assay. RESULTS: Administration of NExos alleviated inflammation by modulating the balance of macrophages both in cellular assays and in vivo experiments, and HExos showed higher therapeutic efficiency than NExos. The miR-216a-5p in HExos was significantly enriched and promoted macrophage M2 polarization through transfer to macrophages by exosomes. The miR-216a-5p was confirmed to target the 3'-UTR of HMGB1. Mechanistically, hypoxia-induced ASCs release miR-216a-5p in an exosomal way that induced macrophage M2 polarization by regulating the HMGB1/TLR4/NF-κB signaling pathway. CONCLUSIONS: Exosomal miR-216a-5p released from hypoxia-prime ASCs showed higher therapeutic efficiency than NExos in experimental colitis by promoting the M2 macrophage phenotype, which indicated that hypoxia prime may represent a promising approach to optimizing the function of ASC-derived exosomes.

Exosomal miR-216a-5p released from hypoxia-prime ASCs showed higher therapeutic efficiency than NExos in experimental colitis by promoting the M2 macrophage phenotype, which indicated that hypoxia prime may represent a promising approach to optimize the function of ASC-derived exosomes.

Nonvolatile chirality switching in terahertz chalcogenide metasurfaces.

Actively controlling the polarization states of terahertz (THz) waves is essential for polarization-sensitive spectroscopy, which has various applications in anisotropy imaging, noncontact Hall measurement, and vibrational circular dichroism. In the THz regime, the lack of a polarization modulator hinders the development of this spectroscopy. We theoretically and experimentally demonstrate that conjugated bilayer chiral metamaterials (CMMs) integrated with Ge2Sb2Te5 (GST225) active components can achieve nonvolatile and continuously tunable optical activity in the THz region. A THz time-domain spectroscopic system was used to characterize the device, showing a tunable ellipticity (from ‒36° to 0°) and rotation of the plane polarization (from 32° to 0°) at approximately 0.73 THz by varying the GST225 state from amorphous (AM) to crystalline (CR). Moreover, a continuously tunable chiroptical response was experimentally observed by partially crystallizing the GST225, which can create intermediate states, having regions of both AM and CR states. Note that the GST225 has an advantage of nonvolatility over the other active elements and does not require any energy to retain its structural state. Our work allows the development of THz metadevices capable of actively manipulating the polarization of THz waves and may find applications for dynamically tunable THz circular polarizers and polarization modulators for THz emissions.

Software Defined Radio-Based Wireless Sensing System.

In this paper, we investigate the application of using software-defined radio (SDR) and surface acoustic wave (SAW) device for wireless measurement of the response of in situ sensors. SDR uses software to realize different communication functions. After collecting the magnitude and phase of the response at discrete frequencies, we apply inverse Fourier transform to analyze the time domain responses which, in turn, allows for monitoring the changes of the response of the in situ sensor. We employ microwave signal flow graph concepts to improve the quality of the received signals. Comparing the normalized results obtained by SDR with those obtained from a commercial vector network analyzer (VNA), we demonstrate that the results are sufficiently close, and the SDR-based experiments can provide satisfactory measurement of the in-situ sensors. The objective is to eventually employ this wireless measurement system for soil nutrient sensing.