CNS-Native Myeloid Cells Drive Immune Suppression in the Brain Metastatic Niche through Cxcl10.

Brain metastasis (br-met) develops in an immunologically unique br-met niche. Central nervous system-native myeloid cells (CNS-myeloids) and bone-marrow-derived myeloid cells (BMDMs) cooperatively regulate brain immunity. The phenotypic heterogeneity and specific roles of these myeloid subsets in shaping the br-met niche to regulate br-met outgrowth have not been fully revealed. Applying multimodal single-cell analyses, we elucidated a heterogeneous but spatially defined CNS-myeloid response during br-met outgrowth. We found Ccr2+ BMDMs minimally influenced br-met while CNS-myeloid promoted br-met outgrowth. Additionally, br-met-associated CNS-myeloid exhibited downregulation of Cx3cr1. Cx3cr1 knockout in CNS-myeloid increased br-met incidence, leading to an enriched interferon response signature and Cxcl10 upregulation. Significantly, neutralization of Cxcl10 reduced br-met, while rCxcl10 increased br-met and recruited VISTAHi PD-L1+ CNS-myeloid to br-met lesions. Inhibiting VISTA- and PD-L1-signaling relieved immune suppression and reduced br-met burden. Our results demonstrate that loss of Cx3cr1 in CNS-myeloid triggers a Cxcl10-mediated vicious cycle, cultivating a br-met-promoting, immune-suppressive niche.

microbioTA: an atlas of the microbiome in multiple disease tissues of Homo sapiens and Mus musculus.

microbioTA (http://bio-annotation.cn/microbiota) was constructed to provide a comprehensive, user-friendly resource for the application of microbiome data from diseased tissues, helping users improve their general knowledge and deep understanding of tissue-derived microbes. Various microbes have been found to colonize cancer tissues and play important roles in cancer diagnoses and outcomes, with many studies focusing on developing better cancer-related microbiome data. However, there are currently no independent, comprehensive open resources cataloguing cancer-related microbiome data, which limits the exploration of the relationship between these microbes and cancer progression. Given this, we propose a new strategy to re-align the existing next-generation sequencing data to facilitate the mining of hidden sequence data describing the microbiome to maximize available resources. To this end, we collected 417 publicly available datasets from 25 human and 14 mouse tissues from the Gene Expression Omnibus database and use these to develop a novel pipeline to re-align microbiome sequences facilitating in-depth analyses designed to reveal the microbial profile of various cancer tissues and their healthy controls. microbioTA is a user-friendly online platform which allows users to browse, search, visualize, and download microbial abundance data from various tissues along with corresponding analysis results, aimimg at providing a reference for cancer-related microbiome research.

Premature transcription termination at the expanded GAA repeats and aberrant alternative polyadenylation contributes to the Frataxin transcriptional deficit in Friedreich's ataxia.

Frataxin deficiency in Friedreich's ataxia results from transcriptional downregulation of the FXN gene caused by expansion of the intronic trinucleotide guanine-adenine-adenine (GAA) repeats. We used multiple transcriptomic approaches to determine the molecular mechanism of transcription inhibition caused by long GAAs. We uncovered that transcription of FXN in patient cells is prematurely terminated upstream of the expanded repeats leading to the formation of a novel, truncated and stable RNA. This FXN early terminated transcript (FXN-ett) undergoes alternative, non-productive splicing and does not contribute to the synthesis of functional frataxin. The level the FXN-ett RNA directly correlates with the length of the longer of the two expanded GAA tracts. Targeting GAAs with antisense oligonucleotides or excision of the repeats eliminates the transcription impediment, diminishes expression of the aberrant FXN-ett, while increasing levels of FXN mRNA and frataxin. Non-productive transcription may represent a common phenomenon and attractive therapeutic target in diseases caused by repeat-mediated transcription aberrations.

RORα inhibits gastric cancer proliferation through attenuating G6PD and PFKFB3 induced glycolytic activity.

BACKGROUND: Glycolysis is critical for harvesting abundant energy to maintain the tumor microenvironment in malignant tumors. Retinoic acid-related orphan receptor α (RORα) has been identified as a circadian gene. However, the association of glycolysis with RORα in regulating gastric cancer (GC) proliferation remains poorly understood. METHODS: Bioinformatic analysis and retrospective study were utilized to explore the role of RORα in cell cycle and glycolysis in GC. The mechanisms were performed in vitro and in vivo including colony formation, Cell Counting Kit-8 (CCK-8), Epithelial- mesenchymal transition (EMT) and subcutaneous tumors of mice model assays. The key drives between RORα and glycolysis were verified through western blot and chip assays. Moreover, we constructed models of high proliferation and high glucose environments to verify a negative feedback and chemoresistance through a series of functional experiments in vitro and in vivo. RESULTS: RORα was found to be involved in the cell cycle and glycolysis through a gene set enrichment analysis (GSEA) algorithm. GC patients with low RORα expression were not only associated with high circulating tumor cells (CTC) and high vascular endothelial growth factor (VEGF) levels. However, it also presented a positive correlation with the standard uptake value (SUV) level. Moreover, the SUVmax levels showed a positive linear relation with CTC and VEGF levels. In addition, RORα expression levels were associated with glucose 6 phosphate dehydrogenase (G6PD) and phosphofructokinase-2/fructose-2,6-bisphosphatase (PFKFB3) expression levels, and GC patients with low RORα and high G6PD or low RORα and high PFKFB3 expression patterns had poorest disease-free survival (DFS). Functionally, RORα deletion promoted GC proliferation and drove glycolysis in vitro and in vivo. These phenomena were reversed by the RORα activator SR1078. Moreover, RORα deletion promoted GC proliferation through attenuating G6PD and PFKFB3 induced glycolytic activity in vitro and in vivo. Mechanistically, RORα was recruited to the G6PD and PFKFB3 promoters to modulate their transcription. Next, high proliferation and high glucose inhibited RORα expression, which indicated that negative feedback exists in GC. Moreover, RORα deletion improved fluorouracil chemoresistance through inhibition of glucose uptake. CONCLUSION: RORα might be a novel biomarker and therapeutic target for GC through attenuating glycolysis.

Long-read genome sequencing reveals a novel intronic retroelement insertion in NR5A1 associated with 46,XY differences of sexual development.

Despite significant advancements in rare genetic disease diagnostics, many patients with rare genetic disease remain without a molecular diagnosis. Novel tools and methods are needed to improve the detection of disease-associated variants and understand the genetic basis of many rare diseases. Long-read genome sequencing provides improved sequencing in highly repetitive, homologous, and low-complexity regions, and improved assessment of structural variation and complex genomic rearrangements compared to short-read genome sequencing. As such, it is a promising method to explore overlooked genetic variants in rare diseases with a high suspicion of a genetic basis. We therefore applied PacBio HiFi sequencing in a large multi-generational family presenting with autosomal dominant 46,XY differences of sexual development (DSD), for whom extensive molecular testing over multiple decades had failed to identify a molecular diagnosis. This revealed a rare SINE-VNTR-Alu retroelement insertion in intron 4 of NR5A1, a gene in which loss-of-function variants are an established cause of 46,XY DSD. The insertion segregated among affected family members and was associated with loss-of-expression of alleles in cis, demonstrating a functional impact on NR5A1. This case highlights the power of long-read genome sequencing to detect genomic variants that have previously been intractable to detection by standard short-read genomic testing.

Laser patterned graphene pressure sensor with adjustable sensitivity in an ultrawide response range.

Flexible pressure sensors have attracted wide attention because of their applications in wearable electronic, human-computer interface, and healthcare. However, it is still a challenge to design a pressure sensor with adjustable sensitivity in an ultrawide response range to satisfy the requirements of different application scenarios. Here, a laser patterned graphene pressure sensor (LPGPS) is proposed with adjustable sensitivity in an ultrawide response range based on the pre-stretched kirigami structure. Due to the out-of-plane deformation of the pre-stretched kirigami structure, the sensitivity can be easily tuned by simply modifying the pre-stretched level. As a result, it exhibits a maximum sensitivity of 0.243 kPa-1, an ultrawide range up to 1600 kPa, a low detection limit (6 Pa), a short response time (42 ms), and excellent stability with high pressure of 1200 kPa over 500 cycles. Benefiting from its high sensitivity and ultrawide response range, the proposed sensor can be applied to detect physiological and kinematic signals under different pressure intensities. Additionally, taking advantage of laser programmable patterning, it can be easily configured into an array to determine the pressure distribution. Therefore, LPGPS with adjustable sensitivity in an ultrawide response range has potential application in wearable electronic devices.

Radiation-induced exosomes promote oral squamous cell carcinoma progression via enhancing SLC1A5-glutamine metabolism.

BACKGROUND: Radiotherapy (RT) can drive cancer cells to enter a state of cellular senescence in which cells can secrete senescence-associated secretory phenotype (SASP) and produce small extracellular vesicles (sEVs) to interact with cells in the tumor microenvironment (TME). Tumor-derived sEVs that are taken up by recipient cells contribute to cancer cell metabolic plasticity, resistance to anticancer therapy, and adaptation to the TME. However, how radiation-induced sEVs support oral squamous cell carcinoma (OSCC) progression remains unclear. METHODS: Beta-galactosidase staining and SASP mRNA expression analysis were used to evaluate the senescence-associated activity of OSCC cells after irradiation. Nanoparticle tracking analysis was performed to identify radiation-induced sEVs. Liquid chromatography-tandem mass spectrometry (LC-MS) was used to explore changes in the levels of proteins in radiation-induced sEVs. Cell Counting Kit-8 and colony formation assays were performed to investigate the function of radiation-induced SASP and sEVs in vitro. A xenograft tumor model was established to investigate the functions of radiation-induced sEVs and V-9302 in vivo as well as the underlying mechanisms. Bioinformatics analysis was performed to determine the relationship between glutamine metabolism and OSCC recurrence. RESULTS: We determined that the radiation-induced SASP triggered OSCC cell proliferation. Additionally, radiation-induced sEVs exacerbated OSCC cell malignancy. LC-MS/MS and bioinformatics analyses revealed that SLC1A5, which is a cellular receptor that participates in glutamine uptake, was significantly enriched in radiation-induced sEVs. In vitro and in vivo, inhibiting SLC1A5 could block the oncogenic effects of radiation-induced sEVs in OSCC. CONCLUSION: Radiation-induced sEVs might promote the proliferation of unirradiated cancer cells by enhancing glutamine metabolism; this might be a novel molecular mechanism underlying radiation resistance in OSCC patients.

Unraveling the molecular freezing behavior of water on a calcium silicate hydrate matrix.

The hydration process of cement-based materials primarily results in the formation of calcium silicate hydrate (CSH), which is crucial in deciding how long concrete will last. This study utilizes molecular dynamics simulation technology to explore the freezing behavior of pure water solutions within various calcium silicate hydrate (CSH) matrices. The investigated matrices encompass four different Ca/Si ratios. According to the simulation, as ice crystals develop close to the surface of CSH, the CSH matrix strengthens its hydrogen and ionic interactions with water molecules, which effectively prevents water molecules from crystallizing and nucleating. Consequently, these molecules compose an unfrozen water film structure that bridges between ice crystals and the CSH matrix. The research also reveals an intriguing relationship between silica chain behavior on the Ca/Si ratio and the CSH surface. Surface flaws arise as a result of the silica chains of CSH breaking into shorter segments as the Ca/Si ratio increases. These surface defects manifest as grooves on the matrix's surface, effectively capturing and retaining specific water molecules. The CSH matrix's hydrogen bonds with water molecules are weakened as a result of this process, facilitating their participation in the crystallization process, and leading to a thinner unfrozen water film thickness with an increased Ca/Si ratio. This study contributes to a greater knowledge of the performance and dependability of cement-based products by offering molecular-level insights into the freezing actions of liquids in gel pores.

Integrated Information for Pathogenicity and Treatment of Spiroplasma.

Spiroplasma, belonging to the class Mollicutes, is a small, helical, motile bacterium lacking a cell wall. Its host range includes insects, plants, and aquatic crustaceans. Recently, a few human cases of Spiroplasma infection have been reported. The diseases caused by Spiroplasma have brought about serious economic losses and hindered the healthy development of agriculture. The pathogenesis of Spiroplasma involves the ability to adhere, such as through the terminal structure of Spiroplasma, colonization, and invasive enzymes. However, the exact pathogenic mechanism of Spiroplasma remains a mystery. Therefore, we systematically summarize all the information about Spiroplasma in this review article. This provides a reference for future studies on virulence factors and treatment strategies of Spiroplasma.

Association between preoperative sarcopenia and prognosis of pancreatic cancer after curative-intent surgery: a updated systematic review and meta-analysis.

BACKGROUND: Sarcopenia is associated with poor outcomes in many malignancies. However, the relationship between sarcopenia and the prognosis of pancreatic cancer has not been well understood. The aim of this meta-analysis was to identify the prognostic value of preoperative sarcopenia in patients with pancreatic cancer after curative-intent surgery. METHODS: Database from PubMed, Embase, and Web of Science were searched from its inception to July 2023. The primary outcomes were overall survival (OS), progression-free survival (PFS), and the incidence of major complications. The hazard ratio (HR), odds ratio (OR), and 95% confidence intervals (CIs) were used to assess the relationship between preoperative sarcopenia and the prognosis of patients with pancreatic cancer. All statistical analyses were conducted by Review Manager 5.3 and STATA 17.0 software. RESULTS: A total of 23 retrospective studies involving 5888 patients were included in this meta-analysis. The pooled results demonstrated that sarcopenia was significantly associated with worse OS (HR = 1.53, P < 0.00001) and PFS (HR = 1.55, P < 0.00001). However, this association was not obvious in regard to the incidence of major complications (OR = 1.33, P = 0.11). CONCLUSION: Preoperative sarcopenia was preliminarily proved to be associated with the terrible prognosis of pancreatic cancer after surgery. However, this relationship needs to be further validated in more prospective studies.

Decoupling between Shockley partials and stacking faults strengthens multiprincipal element alloys.

Mechanical properties are fundamental to structural materials, where dislocations play a decisive role in describing their mechanical behavior. Although the high-yield stresses of multiprincipal element alloys (MPEAs) have received extensive attention in the last decade, the relation between their mechanistic origins remains elusive. Our multiscale study of density functional theory, atomistic simulations, and high-resolution microscopy shows that the excellent mechanical properties of MPEAs have diverse origins. The strengthening effects through Shockley partials and stacking faults can be decoupled in MPEAs, breaking the conventional wisdom that low stacking fault energies are coupled with wide partial dislocations. This study clarifies the mechanistic origins for the strengthening effects, laying the foundation for physics-informed predictive models for materials design.

Smart organic materials based on macrocycle hosts.

Innovative design of smart organic materials is of great importance for the advancement of modern technology. Macrocycle hosts, possessing cyclic skeletons, intrinsic cavities, and specific guest binding properties, have demonstrated pronounced potential for the elaborate fabrication of a variety of functional organic materials with smart stimuli-responsive characteristics. In this tutorial review, we outline the current development of smart organic materials based on macrocycle hosts as key building blocks, focusing on the design principles and functional mechanisms of the tailored systems. Three main types of macrocycle-based smart organic materials are exemplified as follows according to the distinct forms of construction patterns: (1) supramolecular polymeric materials and nanoassemblies; (2) adaptive molecular crystals; (3) smart porous organic materials. The responsive performances of macrocycle-containing smart materials in versatile aspects, including mechanically adaptive polymers, soft optoelectronic devices, data encryption, drug delivery systems, artificial transmembrane channels, crystalline-state gas adsorption/separation, and fluorescence sensing, are illustrated by discussing the representative studies as paradigms, where the roles of macrocycles in these systems are highlighted. We also provide in the conclusion part the perspectives and remaining challenges in this burgeoning field.

Environmental impacts of carbon fiber production and decarbonization performance in wind turbine blades.

The application of carbon fiber in the wind power industry is of great interest in declining CO2 emissions but the carbon fiber manufacturing process is still a long way heading cleaner production. Since little to no information clarifies the dual effects from carbon fiber production to application, this study carried out a life cycle assessment (LCA) to recognize the environmental performances of polyacrylonitrile (PAN)-based carbon fiber production and explore the decarbonization effects of carbon fiber application in wind turbine blades. Based on on-site data from a leading carbon fiber production chain in China, potential environmental impacts of carbon fiber production predominantly originated from the precursor spinning stage (accounted for 13-91%). Fossil depletion (20.24 kg oil eq.), climate change (67.79 kg CO2 eq.), terrestrial ecotoxicity (165.63 kg 1,4-DCB eq.) and photochemical ozone formation (0.14 kg NOx eq.) were the four noteworthy areas to improve the sustainable development. Different scenarios in energy and advanced technology were set to explore the potential improvement of the environmental performance of carbon fiber products. Energy structure (wind power) can improve an average of 22.58% environmental benefit compared with the background scenarios. Regarding the decarbonization effects, the energy payback time and the carbon payback time were estimated to be 0.73 and 0.37 months respectively. Therefore, carbon fiber is a trustworthy material in the strategy to achieve sustainable development from a life cycle perspective.

Chip-Based Electronic System for Quantum Key Distribution.

Quantum Key Distribution (QKD) has garnered significant attention due to its unconditional security based on the fundamental principles of quantum mechanics. While QKD has been demonstrated by various groups and commercial QKD products are available, the development of a fully chip-based QKD system, aimed at reducing costs, size, and power consumption, remains a significant technological challenge. Most researchers focus on the optical aspects, leaving the integration of the electronic components largely unexplored. In this paper, we present the design of a fully integrated electrical control chip for QKD applications. The chip, fabricated using 28 nm CMOS technology, comprises five main modules: an ARM processor for digital signal processing, delay cells for timing synchronization, ADC for sampling analog signals from monitors, OPAMP for signal amplification, and DAC for generating the required voltage for phase or intensity modulators. According to the simulations, the minimum delay is 11ps, the open-loop gain of the operational amplifier is 86.2 dB, the sampling rate of the ADC reaches 50 MHz, and the DAC achieves a high rate of 100 MHz. To the best of our knowledge, this marks the first design and evaluation of a fully integrated driver chip for QKD, holding the potential to significantly enhance QKD system performance. Thus, we believe our work could inspire future investigations toward the development of more efficient and reliable QKD systems.

DC101, an anti-VEGFR2 agent, promotes high-endothelial venule formation and immune infiltration versus SAR131675 and fruquintinib.

There is an increasing interest in combining immune checkpoint inhibitors (ICIs) with anti-angiogenic drugs to enhance their anti-tumor effects. In this study, three anti-angiogenic agents, DC101 (acting on VEGFR2), SAR131675 (acting on VEGFR3), and fruquintinib (a small-molecule inhibitor acting on multiple targets) were administered to B16F1-OVA-loaded C57BL/6 mice. Immune cells infiltration in the tumor tissues, vascular normalization, and high-endothelial venule (HEV) formation were assessed to provide evidence for drug combination. Both DC101 and fruquintinib significantly slowed the melanoma growth and increased the proportion of CD3+ and CD8+ T cells infiltration compared with SAR131675, of note, the effect of DC101 was more pronounced. Moreover, DC101 and fruquintinib increased the interferon-γ and perforin levels, meanwhile, DC101 increased the granzyme B levels, whereas fruquintinib and SAR131675 did not. Only the fruquintinib-treated group showed decreased regulatory T cells infiltration. We found upregulation of PD-L1 expression in tumor cells and CD45+ immune cells in DC101-treated group as well as upregulation of PD-1 expression on CD3+ T cells. However, fruquintinib only increased PD-L1 expression in tumors. Both DC101 and fruquintinib reduced the proportion of CD31+ vessels, while DC101 increased the ratio of α-SMA +/CD31+ cells and reduced the expression of HIF-1α more than fruquintinib. Moreover, DC101 enhanced the infiltration of dendritic cells and B cells, and local HEV formation. In conclusion, our data indicate that DC101 may be a better choice for the combined clinical application of ICIs and anti-angiogenic agents.

Genome-wide identification and characterization of polycomb repressive complex 2 core components in upland cotton (Gossypium hirsutum L.).

BACKGROUND: The evolutionarily conserved Polycomb Repressive Complex 2 (PRC2) plays a vital role in epigenetic gene repression by depositing tri-methylation on lysine residue K27 of histone H3 (H3K27me3) at the target loci, thus participating in diverse biological processes. However, few reports about PRC2 are available in plant species with large and complicated genomes, like cotton. RESULTS: Here, we performed a genome-wide identification and comprehensive analysis of cotton PRC2 core components, especially in upland cotton (Gossypium hirsutum). Firstly, a total of 8 and 16 PRC2 core components were identified in diploid and tetraploid cotton species, respectively. These components were classified into four groups, E(z), Su(z)12, ESC and p55, and the members in the same group displayed good collinearity, similar gene structure and domain organization. Next, we cloned G. hirsutum PRC2 (GhPRC2) core components, and found that most of GhPRC2 proteins were localized in the nucleus, and interacted with each other to form multi-subunit complexes. Moreover, we analyzed the expression profile of GhPRC2 genes. The transcriptome data and quantitative real-time PCR (qRT-PCR) assays indicated that GhPRC2 genes were ubiquitously but differentially expressed in various tissues, with high expression levels in reproductive organs like petals, stamens and pistils. And the expressions of several GhPRC2 genes, especially E(z) group genes, were responsive to various abiotic and biotic stresses, including drought, salinity, extreme temperature, and Verticillium dahliae (Vd) infection. CONCLUSION: We identified PRC2 core components in upland cotton, and systematically investigated their classifications, phylogenetic and synteny relationships, gene structures, domain organizations, subcellular localizations, protein interactions, tissue-specific and stresses-responsive expression patterns. Our results will provide insights into the evolution and composition of cotton PRC2, and lay the foundation for further investigation of their biological functions and regulatory mechanisms.

A unique NLRC4 receptor from echinoderms mediates Vibrio phagocytosis via rearrangement of the cytoskeleton and polymerization of F-actin.

Many members of the nucleotide-binding and oligomerization domain (NACHT)- and leucine-rich-repeat-containing protein (NLR) family play crucial roles in pathogen recognition and innate immune response regulation. In our previous work, a unique and Vibrio splendidus-inducible NLRC4 receptor comprising Ig and NACHT domains was identified from the sea cucumber Apostichopus japonicus, and this receptor lacked the CARD and LRR domains that are typical of common cytoplasmic NLRs. To better understand the functional role of AjNLRC4, we confirmed that AjNLRC4 was a bona fide membrane PRR with two transmembrane structures. AjNLRC4 was able to directly bind microbes and polysaccharides via its extracellular Ig domain and agglutinate a variety of microbes in a Ca2+-dependent manner. Knockdown of AjNLRC4 by RNA interference and blockade of AjNLRC4 by antibodies in coelomocytes both could significantly inhibit the phagocytic activity and elimination of V. splendidus. Conversely, overexpression of AjNLRC4 enhanced the phagocytic activity of V. splendidus, and this effect could be specifically blocked by treatment with the actin-mediated endocytosis inhibitor cytochalasin D but not other endocytosis inhibitors. Moreover, AjNLRC4-mediated phagocytic activity was dependent on the interaction between the intracellular domain of AjNLRC4 and the ß-actin protein and further regulated the Arp2/3 complex to mediate the rearrangement of the cytoskeleton and the polymerization of F-actin. V. splendidus was found to be colocalized with lysosomes in coelomocytes, and the bacterial quantities were increased after injection of chloroquine, a lysosome inhibitor. Collectively, these results suggested that AjNLRC4 served as a novel membrane PRR in mediating coelomocyte phagocytosis and further clearing intracellular Vibrio through the AjNLRC4-ß-actin-Arp2/3 complex-lysosome pathway.

Microbial species from multiple maternal body sites shape the developing giant panda (Ailuropoda melanoleuca) cub gut microbiome.

The gut microbiome of the giant panda (Ailuropoda melanoleuca) plays a vital role in nutrient acquisition from its specialized bamboo diet. Giant panda cubs harbour significantly different gut microbiota during their growth and development when feeding on milk before switching to bamboo. The fetal gut is sterile, and following birth, mother-to-infant microbial transmission has been implicated as a seeding source for the infant gut microbiota. Details of this transmission in giant pandas remain unclear. In this study, faecal samples were collected from seven panda mother-cub pairs when the cubs were 4-16 months old. Additional samples from the cubs' diet, soil and drinking water, and multiple body sites of the mothers were collected. Bacterial 16S rRNA gene sequencing and shotgun metagenomic sequencing were performed to determine the source and potential transmission routes of the cub gut microbiome. Source tracking analysis showed that maternal vagina, milk and faeces were the primary contributory sources of microbes, shaping the cub gut microbiome. Bacterial species from maternal faeces persisted the longest in the cub gut. Bacterial species in the diet contributed to the microbial community. Metagenomics analysis indicated that the predicted metabolic pathways of the gut microbiome also varied at different growth stages. Gut colonization with bacteria from various body sites of the mothers provides a foundational microbial community that is beneficial in fulfilling the evolving dietary needs of the cubs. This study suggests that mother-to-cub transmission is indispensable in shaping the gut microbiome of the developing panda cub.

Reactions of Thorium Oxide Clusters with Water: The Effects of Oxygen Content.

Thorium oxide has many important applications in industry. In this article, theoretical calculations have been carried out to explore the hydrolysis reactions of the ThOn (n=1-3) clusters. The reaction mechanisms of the O-deficient ThO and the O-rich ThO3 are compared with the stoichiometric ThO2 . The theoretical results show good agreement with the prior experiments. It is shown that the hydrolysis mainly occurred on the singlet potential surface. The overall reactions consist of two hydrolysis steps which are all favourable in energy. The effects of oxygen content on the hydrolysis are elucidated. Interestingly, among them, the peroxo group O2 2- in ThO3 is converted to the HOO- ligand, behaving like the terminal O2- in the hydrolysis which is transformed into the HO- groups. In addition, natural bond orbital (NBO) analyses were employed to further understand the bonding of the pertinent species and to interpret the differences in hydrolysis.

An Emerging Role of Extracellular Traps in Chronic Rhinosinusitis.

PURPOSE OF REVIEW: Chronic rhinosinusitis (CRS) is a complicated, heterogeneous disease likely caused by inflammatory and infectious factors. There is clear evidence that innate immune cells, including neutrophils and eosinophils, play a significant role in CRS. Multiple immune cells, including neutrophils and eosinophils, have been shown to release chromatin and granular proteins into the extracellular space in response to triggering extracellular traps (ETs). The formation of ETs remains controversial due to their critical function during pathogen clearance while being associated with harmful inflammatory illnesses. This article summarizes recent research on neutrophil extracellular traps (NETs) and eosinophil extracellular traps (EETs) and their possible significance in the pathophysiology of CRS. RECENT FINDINGS: A novel type of programmed cell death called ETosis, which releases ETs, has been proposed by recent study. Significantly more NETs are presented in nasal polyps, and its granule proteins LL-37 induce NETs production in CRS with nasal polyps (CRSwNP) patients. Similar to NETs, developed in the tissue of nasal polyps, primarily in subepithelial regions with epithelial barrier defects, and are associated with linked to elevated tissue levels of IL-5 and S. aureus colonization. This article provides a comprehensive overview of NETs and EETs, as well as an in-depth understanding of the functions of these ETs in CRS.