Hierarchical global and local auxin signals coordinate cellular interdigitation in Arabidopsis.

The development of multicellular tissues requires both local and global coordination of cell polarization, however, the mechanisms underlying their interplay are poorly understood. In Arabidopsis, leaf epidermal pavement cells (PC) develop a puzzle-piece shape locally coordinated through apoplastic auxin signaling. Here we show auxin also globally coordinates interdigitation by activating the TIR1/AFB-dependent nuclear signaling pathway. This pathway promotes a transient maximum of auxin at the cotyledon tip, which then moves across the leaf activating local PC polarization, as demonstrated by locally uncaged auxin globally rescuing defects in tir1;afb1;afb2;afb4;afb5 mutant but not in tmk1;tmk2;tmk3;tmk4 mutants. Our findings show that hierarchically integrated global and local auxin signaling systems, which respectively depend on TIR1/AFB-dependent gene transcription in the nucleus and TMK-mediated rapid activation of ROP GTPases at the cell surface, control PC interdigitation patterns in Arabidopsis cotyledons, revealing a mechanism for coordinating a local cellular process with the development of whole tissues.

Association between non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio and obstructive sleep apnea: a cross-sectional study from NHANES.

BACKGROUND: Obstructive Sleep Apnea (OSA) is a widespread sleep disturbance linked to metabolic and cardiovascular conditions. The Non-High-Density Lipoprotein Cholesterol to High-Density Lipoprotein Cholesterol Ratios (NHHR) has been proposed as being a potential biomarker to gauge cardiovascular risk. However, its relationship with OSA remains unclear. METHODS: This survey investigated the link NHHR to OSA in American citizens aged 20 and older using information collected via the National Health and Nutrition Examination Survey (NHANES) during the years 2017 to 2020. Logistic regression models with multivariable adjustments were employed to assess this relationship. Nonlinear associations were explored using smooth curve fitting, with a two-part linear regression model identifying a threshold effect. Subgroup analyses were conducted to evaluate population-specific differences. RESULTS: The survey encompassed 6763 participants, with an average age of 50.75 ± 17.32. The average NHHR stood at 2.74, accompanied by a standard deviation of 1.34, while the average frequency of OSA was 49.93%. Upon adjusting for covariates, each unit increase in NHHR may be associated with a 9% rise in OSA incidence. (95% confidence intervals 1.04-1.14; P < 0.0001). Notably, a U-shaped curve depicted the NHHR-OSA relationship, with an inflection point at 4.12. Subgroup analyses revealed consistent associations, with educational attainment and diabetes status modifying the NHHR-OSA relationship. CONCLUSION: The study highlights NHHR as a potential tool for OSA prediction, presenting avenues for advanced risk evaluation, tailored interventions, personalized treatment approaches, and preventive healthcare.

Glycerol monolaurate regulates apoptosis and inflammation by suppressing lipopolysaccharide-induced ROS production and NF-κB activation in avian macrophages.

Macrophages play a crucial role in both innate and adaptive immunity. However, their abnormal activation can lead to undesirable inflammatory reactions. This study aimed to investigate the effects of glycerol monolaurate (GML), a natural monoester known for its anti-inflammatory and immunoregulatory properties, on avian macrophages using the HD11 cell line. The results indicated that a concentration of 10 µg/mL of GML enhanced the phagocytic activity of HD11 cells (P < 0.05) without affecting cell viability (P > 0.05). GML decreased the expression of M1 macrophage polarization markers, such as CD86 and TNF-α genes (P < 0.05), while increasing the expression of M2 macrophage polarization markers, such as TGF-ß1 and IL-10 genes (P < 0.05). GML suppressed ROS production, apoptosis, and the expression of proinflammatory genes (IL-1ß and IL-6) induced by LPS (P < 0.05). GML also promoted the expression of TGF-ß1 and IL-10 (P < 0.05), both in the presence and absence of LPS exposure. Moreover, GML suppressed the gene expression of TLR4 and NF-κB p65 induced by LPS (P < 0.05), as well as the phosphorylation of NF-κB p65 (P < 0.05). In conclusion, GML exhibited regulatory effects on the polarized state of avian macrophages and demonstrated significant anti-apoptotic and anti-inflammatory properties by suppressing intracellular ROS and the NF-κB signaling pathway.

Progress in research on ablation of thyroid nodules.

The incidence of thyroid nodules is rising annually. Surgical treatment is effective, but often results in significant trauma, recurrent laryngeal nerve injury, hypoparathyroidism, and other complications. Recent years have seen significant breakthroughs in thyroid nodule ablation for treating thyroid diseases, although its application remains controversial. The objective was to review the development history and current research status of thyroid nodule ablation to provide a reference for future studies. The literature on thyroid nodule ablation was reviewed, analysing its advantages and disadvantages. The therapeutic effect of thyroid nodule ablation in treating benign thyroid lesions is noteworthy, but issues such as lax treatment indications and excessive medical treatment persist. Initial success has been achieved in treating thyroid malignant lesions, particularly papillary thyroid microcarcinoma (PTMC). However, the curative effect requires further follow-up verification.

Lactate dehydrogenase B as a metabolism-related marker for immunotherapy in head and neck squamous cell carcinoma.

BACKGROUND: Head and neck squamous cell carcinoma (HNSCC) is one of the most common malignancies. Lactate dehydrogenase family genes (LDHs) play a critical role in tumor metabolism, but their functions in HNSCC have not been investigated thoroughly. Thus, we aimed to explore the value of LDHs in HNSCC. METHODS: The association between LDHs expression and mutations, methylation, copy number variations (CNVs), alternative splicing (AS) and competing endogenous RNA (ceRNA) was investigated in The Cancer Genome Atlas (TCGA). The expression level of LDHs in OSCC tissues and adjacent normal tissues was verified by qPCR. Algorithms, such as ssGSEA, ESTIMATE, xCell and TIDE were utilized to analyze the characteristics of immune infiltration. Pathway alternations were enriched by GO, GSEA and KEGG analysis. The Mantel test was employed to elucidate the correlation between metabolism and the tumor microenvironment (TME). Subsequently, MTT and colony formation assays were utilized to assess the impact of LDHB knockdown on cellular proliferation. Additionally, ATP and lactate assays were performed to examine metabolic alterations. Co-culture experiments further investigated the effect of LDHB knockdown on T cell differentiation. RESULTS: LDHs were completely analyzed in multiple databases, among which LDHB was differentially expressed in HNSCC and significantly associated with prognosis. Low LDHB expression had better clinicopathological characteristics. Downregulated LDHB expression was associated with enhanced immune cell infiltration and could influence tumor metabolism. Despite having worse cytotoxic T lymphocyte dysfunction, the LDHBlow group was predicted to respond more favorably to immune checkpoint inhibitors (ICIs) therapy. Moreover, the correlation between metabolism and TME was depicted. In vitro, LDHB knockdown resulted in inhibited cell proliferation, increased lactate levels and decreased ATP levels, while promoted the Th1 differentiation of T cells. CONCLUSIONS: Our study provided a comprehensive analysis of the LDHs and illustrated low LDHB expression could inhibit tumor cell proliferation and ATP production by influencing metabolism, with improved immune cell infiltration and better response to immunotherapy.

Exploring the connections between ER-based lipid metabolism and plasma membrane nanodomain signaling.

Recent advancements in our understanding of cell membrane dynamics have shed light on the importance of plasma membrane (PM) nanodomains in plant cell signaling. Nevertheless, many aspects of membrane nanodomains, including their regulatory mechanisms and biological functions, remain enigmatic. To address this knowledge gap, our review article proposes a novel perspective wherein signaling pathways target endoplasmic reticulum (ER)-based lipid metabolism to exert control over the formation and function of membrane nanodomains. Subsequently, these nanodomains reciprocate by influencing the localization and activity of signaling molecules at the PM. We place a specific emphasis on ER-based enzymatic reactions, given the ER's central role in membrane lipid biosynthesis and its capacity to directly impact PM lipid composition, particularly with regard to saturation levels - an essential determinant of nanodomain properties. The interplay among cell signaling, glycerolipid metabolism, and PM nanodomain may create feedforward/feedback loops that fine-tune cellular responses to developmental and environmental cues.

Efficacy and safety of intrapleural perfusion with hyperthermic chemotherapy for malignant pleural effusion: a meta-analysis.

OBJECTIVE: To evaluate the efficacy and safety of intrapleural perfusion with hyperthermic chemotherapy (IPHC) in treating malignant pleural effusion (MPE). METHODS: PubMed, Embase, Cochrane Library, Chinese National Knowledge Infrastructure (CNKI), Chinese Biomedical Literature Database (CBM), VIP Chinese Science and Technology Journal Full-text Database (VP-CSJFD), and Wanfang database were searched by computer from database establishment to January 17, 2024. Relevant randomized controlled articles with IPHC as the observational group and intrapleural perfusion chemotherapy (IPC) as the control group for MPE were included. Then, the methodological quality of the included articles was evaluated and statistically analyzed using Stata 16.0. RESULTS: Sixteen trials with 647 patients receiving IPHC and 661 patients receiving IPC were included. The meta-analysis found that MPE patients in the IPHC group had a more significant objective response rate [RR = 1.31, 95%CI (1.23, 1.38), P < 0.05] and life quality improvement rate [RR = 2.88, 95%CI (1.95, 4.24), P < 0.05] than those in the IPC group. IPHC and IPC for MPE patients had similar incidence rates of asthenia, thrombocytopenia, hepatic impairment, and leukopenia. CONCLUSION: Compared with IPC, IPHC has a higher objective response rate without significantly increasing adverse reactions. Therefore, IPHC is effective and safe. However, this study is limited by the quality of the literature. Therefore, more high-quality, multi-center, large-sample, rigorously designed randomized controlled clinical studies are still needed for verification and evaluation.

The Role of Astrocytes in Migraine with Cortical Spreading Depression: Protagonists or Bystanders? A Narrative Review.

Cortical spreading depression (CSD) is a slow wave of cortical depolarization closely associated with migraines with an aura. Previously, it was thought that CSD depolarization was mainly driven by neurons, with characteristic changes in neuronal swelling and increased extracellular potassium (K+) and glutamate. However, the role of astrocytes, a member of the neurovascular unit, in migraine with CSD has recently received increasing attention. In the early stages of CSD, astrocytes provide neurons with energy support and clear K+ and glutamate from synaptic gaps. However, in the late stages of CSD, astrocytes release large amounts of lactic acid to exacerbate hypoxia when the energy demand exceeds the astrocytes' compensatory capacity. Astrocyte endfoot swelling is a characteristic of CSD, and neurons are not similarly altered. It is primarily due to K+ influx and abnormally active calcium (Ca2+) signaling. Aquaporin 4 (AQP-4) only mediates K+ influx and has little role as an aquaporin. Astrocytes endfoot swelling causes perivascular space closure, slowing the glymphatic system flow and exacerbating neuroinflammation, leading to persistent CSD. Astrocytes are double-edged swords in migraine with CSD and may be potential targets for CSD interventions.

Magnon-Skyrmion Hybrid Quantum Systems: Tailoring Interactions via Magnons.

Coherent and dissipative interactions between different quantum systems are essential for the construction of hybrid quantum systems and the investigation of novel quantum phenomena. Here, we propose and analyze a magnon-skyrmion hybrid quantum system, consisting of a micromagnet and nearby magnetic skyrmions. We predict a strong-coupling mechanism between the magnonic mode of the micromagnet and the quantized helicity degree of freedom of the skyrmion. We show that with this hybrid setup it is possible to induce magnon-mediated nonreciprocal interactions and responses between distant skyrmion qubits or between skyrmion qubits and other quantum systems like superconducting qubits. This work provides a quantum platform for the investigation of diverse quantum effects and quantum information processing with magnetic microstructures.

Neuromuscular organoids model spinal neuromuscular pathologies in C9orf72 amyotrophic lateral sclerosis.

Hexanucleotide repeat expansions in the C9orf72 gene are the most common cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. Due to the lack of trunk neuromuscular organoids (NMOs) from ALS patients' induced pluripotent stem cells (iPSCs), an organoid system was missing to model the trunk spinal neuromuscular neurodegeneration. With the C9orf72 ALS patient-derived iPSCs and isogenic controls, we used an NMO system containing trunk spinal cord neural and peripheral muscular tissues to show that the ALS NMOs could model peripheral defects in ALS, including contraction weakness, neural denervation, and loss of Schwann cells. The neurons and astrocytes in ALS NMOs manifested the RNA foci and dipeptide repeat proteins. Acute treatment with the unfolded protein response inhibitor GSK2606414 increased the glutamatergic muscular contraction 2-fold and reduced the dipeptide repeat protein aggregation and autophagy. This study provides an organoid system for spinal neuromuscular pathologies in ALS and its application for drug testing.

ECGAN-Assisted ResT-Net Based on Fuzziness for OSA Detection.

OBJECTIVE: Growing attention has been paid recently to electrocardiogram (ECG) based obstructive sleep apnea (OSA) detection, with some progresses been made on this topic. However, the lack of data, low data quality, and incomplete data labeling hinder the application of deep learning to OSA detection, which in turn affects the overall generalization capacity of the network. METHODS: To address these issues, we propose the ResT-ECGAN framework. It uses a one-dimensional generative adversarial network (ECGAN) for sample generation, and integrates it into ResTNet for OSA detection. ECGAN filters the generated ECG signals by incorporating the concept of fuzziness, effectively increasing the amount of high-quality data. ResT-Net not only alleviates the problems caused by deepening the network but also utilizes multihead attention mechanisms to parallelize sequence processing and extract more valuable OSA detection features by leveraging contextual information. RESULTS: Through extensive experiments, we verify that ECGAN can effectively improve the OSA detection performance of ResT-Net. Using only ResT-Net for detection, the accuracy on the Apnea-ECG and private databases is 0.885 and 0.837, respectively. By adding ECGAN-generated data augmentation, the accuracy is increased to 0.893 and 0.848, respectively. CONCLUSION AND SIGNIFICANCE: Comparing with the state-of-the-art deep learning methods, our method outperforms them in terms of accuracy. This study provides a new approach and solution to improve OSA detection in situations with limited labeled samples.

Huayu Qutan Recipe promotes lipophagy and cholesterol efflux through the mTORC1/TFEB/ABCA1-SCARB1 signal axis.

This study aims to investigate the mechanism of the anti-atherosclerosis effect of Huayu Qutan Recipe (HYQT) on the inhibition of foam cell formation. In vivo, the mice were randomly divided into three groups: CTRL group, MOD group and HYQT group. The HYQT group received HYQT oral administration twice a day (20.54 g/kg/d), and the plaque formation in ApoE-/- mice was observed using haematoxylin-eosin (HE) staining and oil red O (ORO) staining. The co-localization of aortic macrophages and lipid droplets (LDs) was examined using fluorescent labelling of CD11b and BODIPY fluorescence probe. In vitro, RAW 264.7 cells were exposed to 50 µg/mL ox-LDL for 48 h and then treated with HYQT for 24 h. The accumulation of LDs was evaluated using ORO and BODIPY. Cell viability was assessed using the CCK-8 assay. The co-localization of LC3b and BODIPY was detected via immunofluorescence and fluorescence probe. LysoTracker Red and BODIPY 493/503 were used as markers for lysosomes and LDs, respectively. Autophagosome formation were observed via transmission electron microscopy. The levels of LC3A/B II/LC3A/B I, p-mTOR/mTOR, p-4EBP1/4EBP1, p-P70S6K/P70S6K and TFEB protein level were examined via western blotting, while SQSTM1/p62, Beclin1, ABCA1, ABCG1 and SCARB1 were examined via qRT-PCR and western blotting. The nuclear translocation of TFEB was detected using immunofluorescence. The components of HYQT medicated serum were determined using Q-Orbitrap high-resolution MS analysis. Molecular docking was employed to identify the components of HYQT medicated serum responsible for the mTOR signalling pathway. The mechanism of taurine was illustrated. HYQT has a remarkable effect on atherosclerotic plaque formation and blood lipid level in ApoE-/- mice. HYQT decreased the co-localization of CD11b and BODIPY. HYQT (10% medicated serum) reduced the LDs accumulation in RAW 264.7 cells. HYQT and RAPA (rapamycin, a mTOR inhibitor) could promote cholesterol efflux, while chloroquine (CQ, an autophagy inhibitor) weakened the effect of HYQT. Moreover, MHY1485 (a mTOR agonist) also mitigated the effects of HYQT by reduced cholesterol efflux. qRT-PCR and WB results suggested that HYQT improved the expression of the proteins ABCA1, ABCG1 and SCARB1.HYQT regulates ABCA1 and SCARB1 protein depending on the mTORC1/TFEB signalling pathway. However, the activation of ABCG1 does not depend on this pathway. Q-Orbitrap high-resolution MS analysis results demonstrated that seven core compounds have good binding ability to the mTOR protein. Taurine may play an important role in the mechanism regulation. HYQT may reduce cardiovascular risk by promoting cholesterol efflux and degrading macrophage-derived foam cell formation. It has been observed that HYQT and ox-LDL regulate lipophagy through the mTOR/TFEB signalling pathway, rather than the mTOR/4EBP1/P70S6K pathway. Additionally, HYQT is found to regulate cholesterol efflux through the mTORC1/TFEB/ABCA1-SCARB1 signal axis, while taurine plays a significant role in lipophagy.

Identification of key genes for atherosclerosis in different arterial beds.

Atherosclerosis (AS) is the pathologic basis of various cardiovascular and cerebrovascular events, with a high degree of heterogeneity among different arterial beds. However, mechanistic differences between arterial beds remain unexplored. The aim of this study was to explore key genes and potential mechanistic differences between AS in different arterial beds through bioinformatics analysis. Carotid atherosclerosis (CAS), femoral atherosclerosis (FAS), infrapopliteal atherosclerosis (IPAS), abdominal aortic atherosclerosis (AAS), and AS-specific differentially expressed genes (DEGs) were screened from the GSE100927 and GSE57691 datasets. Immune infiltration analysis was used to identify AS immune cell infiltration differences. Unsupervised cluster analysis of AS samples from different regions based on macrophage polarization gene expression profiles. Weighted gene co-expression network analysis (WGCNA) was performed to identify the most relevant module genes with AS. Hub genes were then screened by LASSO regression, SVM-REF, and single-gene differential analysis, and a nomogram was constructed to predict the risk of AS development. The results showed that differential expression analysis identified 5, 4, 121, and 62 CAS, FAS, IPAS, AAS-specific DEGs, and 42 AS-common DEGs, respectively. Immune infiltration analysis demonstrated that the degree of macrophage and mast cell enrichment differed significantly in different regions of AS. The CAS, FAS, IPAS, and AAS could be distinguished into two different biologically functional and stable molecular clusters based on macrophage polarization gene expression profiles, especially for cardiomyopathy and glycolipid metabolic processes. Hub genes for 6 AS (ADAP2, CSF3R, FABP5, ITGAX, MYOC, and SPP1), 4 IPAS (CLECL1, DIO2, F2RL2, and GUCY1A2), and 3 AAS (RPL21, RPL26, and RPL10A) were obtained based on module gene, gender stratification, machine learning algorithms, and single-gene difference analysis, respectively, and these genes were effective in differentiating between different regions of AS. This study demonstrates that there are similarities and heterogeneities in the pathogenesis of AS between different arterial beds.

Effects of Salmonella Typhimurium Infection on the Gut Microbiota of Cherry Valley Meat Ducks.

Salmonella infection causes serious economic losses, threatens food safety, and is one of the most important diseases threatening meat duck farming. The gut microbiome is critical in providing resistance against colonization by exogenous microorganisms. Studying the relationship between Salmonella and gut microbiota can help us better understand the threat of the pathogenic mechanism of Salmonella and provide a more scientific theoretical basis for its prevention and treatment. This study uses Salmonella Typhimurium as the research object and Cherry Valley meat duck as the model with which to study the impact of Salmonella infection on ducks. In this field trial, 2 × 108 CFUs Salmonella Typhimurium were administered to 3-day-old ducks. After infection, duck viscera were collected to detect the colonization of Salmonella, and cecal contents were collected to analyze the changes in gut microbiota. The results show that Salmonella Typhimurium can colonize ducks three days after infection and alter the gut microbiota composition, mainly by increasing the abundance of Ruminococcaceae and Lachnospiraceae. In conclusion, Salmonella Typhimurium infection significantly alters the intestinal microbiota of ducks and poses a serious public health risk.

Successful therapy of a critically ill non-small cell lung cancer patient with compound mutations in EGFR G719X and S768I genes using furmonertinib: A case report.

Background: Somatic mutations in epidermal growth factor receptor (EGFR) genes, such as G719X and S768I, and tyrosine kinase inhibitors (TKIs) have been confirmed to be promising for developing new targeted therapies against advanced non-small-cell lung cancer (NSCLC). The G719X and S768I mutations are uncommon and often occur in the form of compound mutations. However, the efficacy of furmonertinib in patients with these uncommon compound mutations has not yet been elucidated. Case presentation: In this study, the G719X/S768I compound mutations were detected in a critically ill NSCLC patient. This patient received furmonertinib for 14 months and successfully responded to the treatment. The present case report highlights the ideal clinical response, with ongoing follow-up. Conclusion: We report the successful treatment of a critically ill NSCLC patient carrying rare compound EGFR G719X and S768I mutations using furmonertinib. To the best of our knowledge, this is the first reported case of a successful furmonertinib treatment of compound EGFR G719X and S768I mutations. Furmonertinib, a third-generation EGFR-TKI, may be effective in controlling the EGFR G719X and S768I compound mutations in NSCLC.

Zinc glycinate alleviates LPS-induced inflammation and intestinal barrier disruption in chicken embryos by regulating zinc homeostasis and TLR4/NF-κB pathway.

The effect of an immune challenge induced by a lipopolysaccharide (LPS) exposure on systemic zinc homeostasis and the modulation of zinc glycinate (Zn-Gly) was investigated using a chicken embryo model. 160 Arbor Acres broiler fertilized eggs were randomly divided into 4 groups: CON (control group, injected with saline), LPS (LPS group, injected with 32 µg of LPS saline solution), Zn-Gly (zinc glycinate group, injected with 80 µg of zinc glycinate saline solution) and Zn-Gly+LPS (zinc glycinate and LPS group, injected with the same content of zinc glycinate and LPS saline solution). Each treatment consisted of eight replicates of five eggs each. An in ovo feeding procedure was performed at 17.5 embryonic day and samples were collected after 12 hours. The results showed that Zn-Gly attenuated the effects of LPS challenge-induced upregulation of pro-inflammatory factor interleukin 1ß (IL-1ß) level (P =0.003). The LPS challenge mediated zinc transporter proteins and metallothionein (MT) to regulate systemic zinc homeostasis, with increased expression of the jejunum zinc export gene zinc transporter protein 1 (ZnT-1) and elevated expression of the import genes divalent metal transporter 1 (DMT1), Zrt- and Irt-like protein 3 (Zip3), Zip8 and Zip14 (P < 0.05). A similar trend could be observed for the zinc transporter genes in the liver, which for ZnT-1 mitigated by Zn-Gly supplementation (P =0.01). Liver MT gene expression was downregulated in response to the LPS challenge (P =0.004). These alterations caused by LPS resulted in decreased serum and liver zinc levels and increased small intestinal, muscle and tibial zinc levels. Zn-Gly reversed the elevated expression of the liver zinc finger protein A20 induced by the LPS challenge (P =0.025), while Zn-Gly reduced the gene expression of the pro-inflammatory factors IL-1ß and IL-6, decreased toll-like receptor 4 (TLR4) and nuclear factor kappa-B p65 (NF-κB p65) (P < 0.05). Zn-Gly also alleviated the LPS-induced downregulation of the intestinal barrier gene Claudin-1. Thus, LPS exposure prompted the mobilization of zinc transporter proteins and MT to perform the remodeling of systemic zinc homeostasis, Zn-Gly participated in the regulation of zinc homeostasis and inhibited the production of pro-inflammatory factors through the TLR4/NF-κB pathway, attenuating the inflammatory response and intestinal barrier damage caused by an immune challenge.

Analysis on the change of gut microbiota and metabolome in lung transplant patients.

Previous studies have shown that the gut microbiota and its metabolites are associated with the success of organ transplantation. However, the specific changes in the gut microbiota of lung transplant patients remain unclear. Hence, this study aimed to elucidate the interplay between the gut microbiota, metabolome, and lung transplantation outcomes. Using 16S metagenomics sequencing and untargeted metabolic profiling, we conducted a comprehensive analysis of gut microbial and metabolic alterations in lung transplant recipients relative to non-transplant group. Our findings revealed the predominance of Enterococcus and Streptococcus genera within the lung transplant cohort, accompanied by the significant reduction in Bacteroides, Epulopiscium, Faecalibacterium, and Prevotella abundance. In addition, a significant reduction in ATRA (all-trans retinoic acid) levels and suppression of IgA production were observed in lung transplant recipients, which were found to be closely associated with the Enterococcus genus. It was speculated that the association might have implications for the prognosis of lung transplant patients. Notably, the differences in gut microbial composition and metabolomic profiles between successful transplant recipients and those experiencing chronic rejection were not statistically significant. These novel insights shed light on the putative implications of the gut microbiota and metabolome in shaping lung transplantation outcomes, and provide a foundation for future investigations and targeted therapeutic interventions. IMPORTANCE: This study has profound implications for lung transplantation as it uncovers the important role of gut microbiota and metabolome in shaping transplantation outcomes. The identification of dominant bacterial genera, such as Enterococcus and Streptococcus, within the lung transplant cohort, along with the significant decrease in Bacteroides, Epulopiscium, Faecalibacterium, and Prevotella abundance, reveals potential microbial imbalances associated with lung transplantation. In addition, a significant reduction in ATRA (all-trans retinoic acid) levels and suppression of IgA production were observed in lung transplant recipients, which were found to be closely associated with the Enterococcus genus. It was speculated that the association might have implications for the prognosis of lung transplant patients. These findings hold immense clinical significance as they lay the groundwork for future research and targeted therapeutic interventions. Understanding the impact of the gut microbiota and metabolome on lung transplantation outcomes offers promising avenues for improving transplantation patient prognosis.

Supramolecular crystals of Mn(15-crown-5)(MnCl4)(DMF) with dielectric phase transition, high quantum yield and phase transition-induced luminescence enhancement behavior.

The supramolecular crystals, Mn(15-crown-5)(MnCl4)(DMF), (1; 15-crown-5 = 1,4,7,10,13-pentaoxacyclopentadecane), were synthesized via a self-assembly strategy under ambient conditions. Comprehensive characterization of the crystals involved microanalysis for C, H, and N elements, thermogravimetric (TG) analysis, differential scanning calorimetry (DSC) and single-crystal X-ray diffraction techniques. The results reveal that 1 undergoes a two-step thermotropic and isostructural phase transition at around 217 K and 351 K upon heating. All three phases belong to the same space group (P212121) with analogous cell parameters. These two phase transitions primarily involve the thermally activated ring rotational dynamics of the 15-crown-5 molecule, with only the transition at ca. 351 K being associated with a dielectric anomaly. 1 exhibits intense luminescence with a peak at ∼600 nm and a high quantum yield of 68%. The mechanisms underlying this intense luminescence are likely linked to low-symmetry ligand fields. Additionally, 1 displays phase transition-induced luminescence enhancement behavior, and the possible mechanism is further discussed.

Thermotropic Structure Phase Transitions and Two Types of Thermochromic Behaviors in a Bromoargentate Cluster [Pr-dabco]2Ag4Br6.

Organic-inorganic silver halide hybrids show abundant phase transitions and thermochromism. However, it is very rare that silver halides exhibit thermochromism related to thermotropic structure phase transition. Herein, a bromoargentate hybrid, [Pr-dabco]2Ag4Br6 (1) (Pr-dabco+ = 1-propyl-1,4-diazabicyclo-[2.2.2]octan-1-ium), with tetranuclear [Ag4Br6]2- clusters was prepared and characterized by microanalysis, ultraviolet-visible (UV-vis) diffuse reflectance spectroscopy, and thermogravimetric (TG) and differential scanning calorimetry (DSC) techniques. Interestingly, 1 undergoes an irreversible structure phase transition at ∼436 K in the first heating process, which is accompanied by an abrupt color change from colorless to yellow; however, a reversible color change between pale yellow and yellow is observed in the next heating-cooling cycles. Notably, DSC measurement revealed that a reversible phase transition is associated with the change in color between pale yellow and yellow, while the powder X-ray diffraction (PXRD) patterns corresponding to pale yellow and yellow phases are quite similar to each other. These observations demonstrate that thermochromism in the next heating-cooling runs is associated with a reversible structure phase transition, which perhaps concerns the disorder-order transformation of alkyl chains in the cationic ligand [Pr-dabco]+, and relevant to the anharmonic fluctuations of the Ag-Br and Ag-N bonds, a strong electron-phonon coupling effect is seen within the bromoargentate cluster.