Nanoparticle-blockage-enabled rapid and reversible nanopore gating with tunable memory.

Gated protein channels act as rapid, reversible, and fully-closeable nanoscale valves to gate chemical transport across the cell membrane. Replicating or outperforming such a high-performance gating and valving function in artificial solid-state nanopores is considered an important yet unsolved challenge. Here we report a bioinspired rapid and reversible nanopore gating strategy based on controlled nanoparticle blockage. By using rigid or soft nanoparticles, we respectively achieve a trapping blockage gating mode with volatile memory where gating is realized by electrokinetically trapped nanoparticles near the pore and contact blockage gating modes with nonvolatile memory where gating is realized by a nanoparticle physically blocking the pore. This gating strategy can respond to an external voltage stimulus (∼200 mV) or pressure stimulus (∼1 atm) with response time down to milliseconds. In particular, when 1,2-diphytanoyl-sn-glycero-3-phosphocholine liposomes are used as the nanoparticles, the gating efficiency, defined as the extent of nanopore closing compared to the opening state, can reach 100%. We investigate the mechanisms for this nanoparticle-blockage-enabled nanopore gating and use it to demonstrate repeatable controlled chemical releasing via single nanopores. Because of the exceptional spatial and temporal control offered by this nanopore gating strategy, we expect it to find applications for drug delivery, biotic-abiotic interfacing, and neuromorphic computing.

The m6A modification mediated-lncRNA POU6F2-AS1 reprograms fatty acid metabolism and facilitates the growth of colorectal cancer via upregulation of FASN.

BACKGROUND: Long noncoding RNAs (lncRNAs) have emerged as key players in tumorigenesis and tumour progression. However, the biological functions and potential mechanisms of lncRNAs in colorectal cancer (CRC) are unclear. METHODS: The novel lncRNA POU6F2-AS1 was identified through bioinformatics analysis, and its expression in CRC patients was verified via qRT-PCR and FISH. In vitro and in vivo experiments, such as BODIPY staining, Oil Red O staining, triglyceride (TAG) assays, and liquid chromatography mass spectrometry (LC-MS) were subsequently performed with CRC specimens and cells to determine the clinical significance, and functional roles of POU6F2-AS1. Biotinylated RNA pull-down, RIP, Me-RIP, ChIP, and patient-derived organoid (PDO) culture assays were performed to confirm the underlying mechanism of POU6F2-AS1. RESULTS: The lncRNA POU6F2-AS1 is markedly upregulated in CRC and associated with adverse clinicopathological features and poor overall survival in CRC patients. Functionally, POU6F2-AS1 promotes the growth and lipogenesis of CRC cells both in vitro and in vivo. Mechanistically, METTL3-induced m6A modification is involved in the upregulation of POU6F2-AS1. Furthermore, upregulated POU6F2-AS1 could tether YBX1 to the FASN promoter to induce transcriptional activation, thus facilitating the growth and lipogenesis of CRC cells. CONCLUSIONS: Our data revealed that the upregulation of POU6F2-AS1 plays a critical role in CRC fatty acid metabolism and might provide a novel promising biomarker and therapeutic target for CRC.

Genetically predicted gut microbiota mediate the association between plasma lipidomics and primary sclerosing cholangitis.

BACKGROUND: Primary sclerosing cholangitis (PSC) is a complex disease with pathogenic mechanisms that remain to be elucidated. Previous observational studies with small sample sizes have reported associations between PSC, dyslipidemia, and gut microbiota dysbiosis. However, the causality of these associations is uncertain, and there has been no systematic analysis to date. METHODS: The datasets comprise data on PSC, 179 lipid species, and 412 gut microbiota species. PSC data (n = 14,890) were sourced from the International PSC Study Group, while the dataset pertaining to plasma lipidomics originated from a study involving 7174 Finnish individuals. Data on gut microbiota species were derived from the Dutch Microbiome Project study, which conducted a genome-wide association study involving 7738 participants. Furthermore, we employed a two-step Mendelian randomization (MR) analysis to quantify the proportion of the effect of gut microbiota-mediated lipidomics on PSC. RESULTS: Following a rigorous screening process, our MR analysis revealed a causal relationship between higher levels of gene-predicted Phosphatidylcholine (O-16:1_18:1) (PC O-16:1_18:1) and an increased risk of developing PSC (inverse variance-weighted method, odds ratio (OR) 1.30, 95% confidence interval (CI) 1.03-1.63). There is insufficient evidence to suggest that gene-predicted PSC impacts the levels of PC O-16:1_18:1 (OR 1.01, 95% CI 0.98-1.05). When incorporating gut microbiota data into the analysis, we found that Eubacterium rectale-mediated genetic prediction explains 17.59% of the variance in PC O-16:1_18:1 levels. CONCLUSION: Our study revealed a causal association between PC O-16:1_18:1 levels and PSC, with a minor portion of the effect mediated by Eubacterium rectale. This study aims to further explore the pathogenesis of PSC and identify promising therapeutic targets. For patients with PSC who lack effective treatment options, the results are encouraging.

Interleukin-25 as a Potential Biomarker in Lung Metastasis of Hepatocellular Carcinoma with HBV History in Chinese Patients: A Single Center, Case-control Study.

Background: Interleukin-25 (IL-25) has been proved to play a role in the pathogenesis and metastasis of Hepatocellular carcinoma (HCC), but the relationship between the level of IL-25 and the metastasis and prognosis of HCC is still not clear. This study aimed to investigate the expression of IL-25 and other potential biochemical indicators among healthy people, HBV-associated HCC patients without lung metastasis and HBV-associated HCC patients with lung metastasis. Methods: From September 2019 to November 2021, 33 HCC patients without lung metastasis, 37 HCC patients with lung metastasis and 29 healthy controls were included in the study. IL-25 and other commonly used biochemical markers were measured to establish predictors of overall survival (OS) and progression-free survival (PFS) after treatment. Results: The serum level of IL-25 was increased in HCC patients than healthy controls (p < 0.001) and HCC patients with lung metastasis had higher IL-25 level than HCC patients without metastasis (p = 0.035). Lung metastasis also indicated higher death rate (p < 0.001) by chi-square test, higher GGT level (p = 0.024) and higher AFP level (p = 0.049) by non-parametric test. Kaplan-Meier analysis demonstrated that IL-25 was negatively associated with PFS (p = 0.024). Multivariate Cox-regression analysis indicated IL-25 (p = 0.030) and GGT (p = 0.020) to be independent predictors of poorer PFS, while IL-25 showed no significant association with OS. Conclusion: The level of IL-25 was significantly associated with disease progression and lung metastasis of HBV-associated HCC. The high expression of IL-25 predicted high recurrence rate and death probability of HCC patients after treatment. Therefore, IL-25 may be an effective predictor of prognosis in HCC.

NIR-responsive electrospun nanofiber dressing promotes diabetic-infected wound healing with programmed combined temperature-coordinated photothermal therapy.

BACKGROUND: Diabetic wounds present significant challenges, specifically in terms of bacterial infection and delayed healing. Therefore, it is crucial to address local bacterial issues and promote accelerated wound healing. In this investigation, we utilized electrospinning to fabricate microgel/nanofiber membranes encapsulating MXene-encapsulated microgels and chitosan/gelatin polymers. RESULTS: The film dressing facilitates programmed photothermal therapy (PPT) and mild photothermal therapy (MPTT) under near-infrared (NIR), showcasing swift and extensive antibacterial and biofilm-disrupting capabilities. The PPT effect achieves prompt sterilization within 5 min at 52 °C and disperses mature biofilm within 10 min. Concurrently, by adjusting the NIR power to induce local mild heating (42 °C), the dressing stimulates fibroblast proliferation and migration, significantly enhancing vascularization. Moreover, in vivo experimentation successfully validates the film dressing, underscoring its immense potential in addressing the intricacies of diabetic wounds. CONCLUSIONS: The MXene microgel-loaded nanofiber dressing employs temperature-coordinated photothermal therapy, effectively amalgamating the advantageous features of high-temperature sterilization and low-temperature promotion of wound healing. It exhibits rapid, broad-spectrum antibacterial and biofilm-disrupting capabilities, exceptional biocompatibility, and noteworthy effects on promoting cell proliferation and vascularization. These results affirm the efficacy of our nanofiber dressing, highlighting its significant potential in addressing the challenge of diabetic wounds struggling to heal due to infection.

NIR-activated electrospun nanodetonator dressing enhances infected diabetic wound healing with combined photothermal and nitric oxide-based gas therapy.

Diabetic wounds pose a challenge to healing due to increased bacterial susceptibility and poor vascularization. Effective healing requires simultaneous bacterial and biofilm elimination and angiogenesis stimulation. In this study, we incorporated polyaniline (PANI) and S-Nitrosoglutathione (GSNO) into a polyvinyl alcohol, chitosan, and hydroxypropyltrimethyl ammonium chloride chitosan (PVA/CS/HTCC) matrix, creating a versatile wound dressing membrane through electrospinning. The dressing combines the advantages of photothermal antibacterial therapy and nitric oxide gas therapy, exhibiting enduring and effective bactericidal activity and biofilm disruption against methicillin-sensitive Staphylococcus aureus, methicillin-resistant Staphylococcus aureus, and Escherichia coli. Furthermore, the membrane's PTT effect and NO release exhibit significant synergistic activation, enabling a nanodetonator-like burst release of NO through NIR irradiation to disintegrate biofilms. Importantly, the nanofiber sustained a uniform release of nitric oxide, thereby catalyzing angiogenesis and advancing cellular migration. Ultimately, the employment of this membrane dressing culminated in the efficacious amelioration of diabetic-infected wounds in Sprague-Dawley rats, achieving wound closure within a concise duration of 14 days. Upon applying NIR irradiation to the PVA-CS-HTCC-PANI-GSNO nanofiber membrane, it swiftly eradicates bacteria and biofilm within 5 min, enhancing its inherent antibacterial and anti-biofilm properties through the powerful synergistic action of PTT and NO therapy. It also promotes angiogenesis, exhibits excellent biocompatibility, and is easy to use, highlighting its potential in treating diabetic wounds.

Melatonin protects zebrafish pancreatic development and physiological rhythms from sodium propionate-induced disturbances via the hypothalamic-pituitary-thyroid axis.

BACKGROUND: The widespread use of sodium propionate as a preservative in food may affect public health. We aimed to assess the effects of sodium propionate on circadian rhythms and pancreatic development in zebrafish and the possible underlying mechanisms. RESULTS: In this experiment, we analyzed the relationship between circadian rhythms and pancreatic development and then revealed the role of the thyroid endocrine system in zebrafish. The results showed that sodium propionate interfered with the rhythmic behavior of zebrafish, and altered the expression of important rhythmic genes. Experimental data revealed that pancreatic morphology and developmental genes were altered after sodium propionate exposure. Additionally, thyroid hormone levels and key gene expression associated with the hypothalamic-pituitary-thyroid axis were significantly altered. Melatonin at a concentration of 1 µmol L-1, with a mild effect on zebrafish, observably alleviated sodium propionate-induced disturbances in circadian rhythms and pancreatic development, as well as regulating the thyroid system. CONCLUSION: Melatonin, while modulating the thyroid system, significantly alleviates sodium propionate-induced circadian rhythm disturbances and pancreatic developmental disorders. We further revealed the deleterious effects of sodium propionate as well as the potential therapeutic effects of melatonin on circadian rhythm, pancreatic development and the thyroid system. © 2024 Society of Chemical Industry.

Targeting SMYD2 inhibits angiogenesis and increases the efficiency of apatinib by suppressing EGFL7 in colorectal cancer.

Angiogenesis is an essential factor affecting the occurrence and development of solid tumors. SET And MYND Domain Containing 2 (SMYD2) serves as an oncogene in various cancers. However, whether SMYD2 is involved in tumor angiogenesis remains unclear. Here, we report that SMYD2 expression is associated with microvessel density in colorectal cancer (CRC) tissues. SMYD2 promotes CRC angiogenesis in vitro and in vivo. Mechanistically, SMYD2 physically interacts with HNRNPK and mediates lysine monomethylation at K422 of HNRNPK, which substantially increases RNA binding activity. HNRNPK acts by binding and stabilizing EGFL7 mRNA. As an angiogenic stimulant, EGFL7 enhances CRC angiogenesis. H3K4me3 maintained by PHF8 mediates the abnormal overexpression of SMYD2 in CRC. Moreover, targeting SMYD2 blocks CRC angiogenesis in tumor xenografts. Treatment with BAY-598, a functional inhibitor of SMYD2, can also synergize with apatinib in patient-derived xenografts. Overall, our findings reveal a new regulatory axis of CRC angiogenesis and provide a potential strategy for antiangiogenic therapy.

Decabromodiphenyl ethane affects embryonic development by interfering with nuclear F-actin in zygotes and leads to cognitive and social disorders in offspring mice.

Decabromodiphenyl ethane (DBDPE) is a novel retardant. DBDPE is used in various flammable consumer products such as electronics, building materials, textiles, and children's toys. The presence of DBDPE in humans makes it extremely urgent to assess the health effects of DBDPE exposure. Here, we used female mice as an animal model to investigate the effects of DBDPE on embryonic development and offspring health. The results showed that 50 µg/kg bw/day of DBDPE exposure did not affect spindle rotation in oocytes after fertilization, but led to a decrease of pronuclei (PN) in zygotes. Further investigation found that DBDPE interferes with the self-assembly of F-actin in PN, resulting in PN reduction, DNA damage, and reduced expression of zygotic genome activating genes, and finally leading to abnormal embryonic development. More importantly, we found that maternal DBDPE exposure did not affect the growth and development of the first generation of offspring (F1) mice, but resulted in behavioral defects in F1 mice. Female F1 mice from DBDPE-exposed mothers exhibited increased motor activity and deficits in social behavior. Both female and male F1 mice from DBDPE-exposed mothers exhibited cognitive memory impairment. These results suggest that DBDPE has developmental toxicity on embryos and has a cross-generational interference effect. It is suggested that people should pay attention to the reproductive toxicity of DBDPE. In addition, it also provides a reference for studying the origin of neurological diseases and indicates that adult diseases caused by environmental pollutants may have begun in the embryonic stage.

Hypoxia dissociates HDAC6/FOXO1 complex and aggregates them into nucleus to regulate autophagy and osteogenic differentiation.

OBJECTIVE: This research aimed to elucidate the molecular mechanisms underlying the periodontitis-associated bone loss, with particular emphasis on the contributory role of hypoxic microenvironment in this process. BACKGROUND: Periodontitis generally causes alveolar bone loss and is often associated with a hypoxic microenvironment, which affects bone homeostasis. However, the regulating mechanism between hypoxia and jaw metabolism remains unclear. Hypoxia triggers autophagy, which is closely related to osteogenic differentiation, but how hypoxia-induced autophagy regulates bone metabolism is unknown. HDAC6 and FOXO1 are closely related to bone metabolism and autophagy, respectively, but whether they are related to hypoxia-induced bone loss and their internal mechanisms is still unclear. METHODS: Established rat nasal obstruction model and hypoxia cell model. Immunohistochemistry was performed to detect the expression and localization of HDAC6 and FOXO1 proteins, analysis of autophagic flux and transmission electron microscopy was used to examine the autophagy level and observe the autophagosomes, co-immunoprecipitation and chromatin immunoprecipitation were preformed to investigate the interaction of HDAC6 and FOXO1. RESULTS: Hypoxia causes increased autophagy and reduced osteogenic differentiation in rat mandibles and BMSCs, and blocking autophagy can attenuate hypoxia-induced osteogenic differentiation decrease. Moreover, hypoxia dissociated the FOXO1-HDAC6 complex and accumulated them in the nucleus. Knocking down of FOXO1 or HDAC6 alleviated hypoxia-induced autophagy elevation or osteogenic differentiation reduction by binding to related genes, respectively. CONCLUSION: Hypoxia causes mandibular bone loss and autophagy elevation. Mechanically, hypoxia dissociates the FOXO1-HDAC6 complex and aggregates them in the nucleus, whereas HDAC6 decreases osteogenic differentiation and FOXO1 enhances autophagy to inhibit osteogenic differentiation.

Hypoxia caused by unilateral nasal obstruction decreases mandibular density in rats through inhibition of Cyp1a1 expression.

BACKGROUND: Oral breathing has an important impact on morphology and bone mineral density (BMD) in a mandible. This study aimed to investigate the hub genes and mechanism regulating the mandibular BMD decrease induced by nasal obstruction. METHODS: A unilateral nasal obstruction model was established in 1-week-old Wistar rats by electrocautery obstruction. BMD of the mandible was determined by micro-computed tomography. Transcriptome analysis was performed to identify differentially expressed genes (DEGs). Hub genes were identified by building protein-protein interaction network and verified by western blot. A hypoxic cell model was established in bone marrow mesenchymal stem cells (BMSCs) by using CoCl2. The expression of hypoxia-inducible factor-1α (HIF-1α), NF-kB ligand-receptor activator (RANKL), osteoprotegerin (OPG), and Cyp1a1 was detected by western blot. RESULTS: The mandibular BMD of rats in the unilateral nasal obstruction group was significantly decreased. A total of 38 DEGs were identified in nasal obstruction rats compared with normal rats. A ratio of RANKL/OPG in the mandible was elevated by nasal obstruction, while the Cyp1a1 was decreased. In vitro, the HIF-1α expression and RANKL/OPG ratio were upregulated by hypoxia while the Cyp1a1 expression was decreased. Pretreatment with Cyp1a1 activator, FICZ, could increase the expression of Cyp1a1 while attenuating the activation of HIF-1α and RANKL. CONCLUSION: Respiratory changes caused by nasal obstruction contribute to the decrease in Cyp1a1 expression in the mandible of juvenile rats, which is associated with disturbances in bone homeostasis controlled by the RANKL/OPG ratio.

Expression of spleen macrophages in a mouse model of alveolar bone resorption periodontitis.

It has been shown that macrophages can be endotoxin-tolerant under the stimulation of continuous endotoxin of Porphyromonas gingivalis. Macrophage transforms into M2-type which inhibits inflammation, and its pro-inflammatory cytokine secretion is reduced to avoid the tissue damaged by inflammation. This experiment established the corresponding animal model to explore the relative number, phenotypic proportion, and function of spleen macrophages in mice with chronic periodontitis. Twenty 16-week-old mice were randomly divided into a true ligation group (LFP group) and a pseudo-ligation group (LFC group). The periodontitis in the LFP group was induced by experimental ligation, and the LFC group was treated as a control. After 10 days of ligation, the maxilla was taken, IHC and HE staining were performed to observe the pathological changes of periodontal tissues, and IHC staining was performed to observe the RANKL/OPG ratio. Spleen mononuclear cells were isolated and counted. The ratio of M1 and M2 phenotypes was determined by fluorescence-activated cell sorting (FACS) in the spleen. The relative expression levels of macrophage-associated inflammatory cytokine TNF-a, IL-1ß and anti-inflammatory cytokine IL-10 mRNA were detected by real-time PCR. Compared with the control group (LFC:M2/M110.04%), the M2 ratio among spleen mature macrophages in the periodontitis group (LFP: M2/M135.86%) was significantly increased (P<0.01) in the spleen. The proportion of M1 macrophages was not significantly different, and the ratio of M1/M2 was significantly decreased (P<0.05) in the spleen. But the expression level of M1-type macrophage inflammatory factor TNF-a mRNA was inclined. Chronic periodontitis can up-regulate the proportion of M2 macrophages, decrease the ratio of macrophage phenotype M1/M2, and incline the expression of pro-inflammatory factor TNF-a mRNA.

Effects of microplastic exposure on the early developmental period and circadian rhythm of zebrafish (Danio rerio): A comparative study of polylactic acid and polyglycolic acid.

Polyglycolic acid (PGA) is an emerging biodegradable plastic material. Together with polylactic acid (PLA), PGA is considered a suitable alternative to conventional plastics and has been widely used in biomedical and food packaging industries. However, degradable plastics continue to face the drawbacks of harsh degradation environment and long degradation time, and may harm the environment and the human body. Therefore, our study focused on assessing the effects of degradable microplastics PGA and PLA on the development and neurobehavior of zebrafish. The results showed that PGA and PLA had little effect on 3-10 hpf embryos. However, developmental stunting was observed in a100 mg/L PGA and PLA-exposed group at 24 hpf. In addition, PGA and PLA exposure decreased the survival and hatching rates, increased wakefulness, and reduced sleep in zebrafish. This indicates that PGA and PLA may affect the circadian behavior of zebrafish by affecting the brain-derived neurotrophic factor (BDNF). Therefore, our results suggest that PGA and PLA exposure induces developmental toxicity, reduces voluntary locomotion, induces of anxiety-like behaviors, and impairs sleep/wake behaviors in zebrafish larvae. This also suggests that the potentially toxic effects of degradable plastics cannot be ignored and that the biological effects of PGA require further research.

Construction of UiO-66-NH2 decorated by MoS2 QDs as photocatalyst for rapid and effective visible-light driven Cr(VI) reduction.

The photoactive metal-organic frameworks (MOFs) are good candidates for photocatalysts, but the quick electron-hole pairs recombination has greatly restricted the photocatalytic ability of MOFs. To improve the photoactivity of MOFs, MOFs-based composite materials have been extensively studied. Here, we successfully integrated MoS2 quantum dots (QDs) with UiO-66-NH2 for the first time under hydrothermal conditions. The as-prepared MoS2 QDs/UiO-66-NH2 (MS-U) had good visible light response ability (absorption edge at 445 nm), and charge separation and transfer ability, which lays the foundation for the photocatalytic Cr(VI) reduction. Photocatalytic studies revealed that MoS2 QDs-5/UiO-66-NH2 (MS-U-5) had superior Cr(VI) reduction activity than pure MoS2 QDs and UiO-66-NH2. MS-U-5 could remove 98% Cr(VI) at pH= 2 with visible light irradiation for 20 min, which is the fastest visible light driven Cr(VI) reduction rate among the reported MOFs-based composite photocatalysts without the presence of any cocatalysts or scavengers as far as we know. Importantly, MS-U-5 could be reused at least three times. In the end, the possible electron transfer path and mechanism of Cr(VI) reduction was also investigated.

Wetting-consolidation type dust suppressant based on sugarcane bagasse as an environmental material: Preparation, characterization and dust suppression mechanism.

Coal mines generate a lot of dust during production and transportation, which not only damages the health of personnel, but also causes environmental pollution. Based on the problems of low extraction efficiency of cellulose matrix and low economy of existing dust suppressants for biomass materials, this paper uses bagasse extracted cellulose from sugar production waste as a matrix and adds polyvinyl alcohol and polyacrylamide as monomers to prepare a wetting-crusting type highly efficient environmental protection dust suppressant for coal mine production and transportation process. The dust suppression effect of the product was analyzed by the performance tests of dust suppression efficiency, consolidation layer strength and permeability. The dust suppression rate of the product prepared in this paper remained above 90% at the simulated wind speed of 10 m/s, the consolidation layer strength of 42.3 KPa was much higher than that of the pure water solution, and the average permeation rate within 30 min was greater than that of the surfactant solution. It is proved that the dust suppressant prepared in this paper has good dust suppression effect, high consolidated layer strength and good permeability, and the product prepared in this paper using environmentally friendly biomass raw materials has good degradability, and the mechanism of the dust suppressant is illustrated by MS simulation. The biomass dust suppressant can meet the requirements of dust suppression in the process of coal mining and transportation and is non-toxic and environmentally friendly.

Study on MICP dust suppression technology in open pit coal mine: Preparation and mechanism of microbial dust suppression material.

With the recent increases in energy demands, the dust hazards of coal mining caused by transportation, loading and unloading and other processes are becoming increasingly serious. To control dust in open pit coal mines more environmentally friendly and efficiently, and to promote the use and development of non-in situ high-yield urease microorganisms for dust suppression in coal mines, Bacillus pasteurii was selected for dust suppression experiments in this article. Additionally, the growth of microorganisms in the coal dust microenvironment was simulated, and the effect of microbial mineralization products on the calorific value of upper coal dust was further studied. Our findings indicated that Bacillus pasteurii induced dust suppression by forming a calcite precipitate with non-uniform particle size to coal dust cementation. Moreover, after a single spray, the wind erosion resistance efficiency was 84% when the wind speed was set at 10 m/s. The growth of microorganisms and urease activity in the coal dust leachate were largely equal to those in the control group, reaching a peak at approximately 24 h, that the maximum growth quantity of OD600 was about 1.5, and the maximum urease activity was 11 mmol·L-1·min-1. The difference between the peak heat release rate of mixed coal dust and pure coal was only 4.82 kW/m2, which would not affect the value of coal products. Non in-situ Bacillus pasteurii can be growth metabolized normally in the microenvironment of coal dust. Finally, the mechanism of coal dust suppression by mineralization of microbial bacterial solution to form calcium carbonate was described by a reaction equation, which is important for further application and development of microbial dust suppressants.

Asymmetric Entanglement-Assisted Quantum MDS Codes Constructed from Constacyclic Codes.

Due to the asymmetry of quantum errors, phase-shift errors are more likely to occur than qubit-flip errors. Consequently, there is a need to develop asymmetric quantum error-correcting (QEC) codes that can safeguard quantum information transmitted through asymmetric channels. Currently, a significant body of literature has investigated the construction of asymmetric QEC codes. However, the asymmetry of most QEC codes identified in the literature is limited by the dual-containing condition within the Calderbank-Shor-Steane (CSS) framework. This limitation restricts the exploration of their full potential in terms of asymmetry. In order to enhance the asymmetry of asymmetric QEC codes, we utilize entanglement-assisted technology and exploit the algebraic structure of cyclotomic cosets of constacyclic codes to achieve this goal. In this paper, we generalize the decomposition method of the defining set for constacyclic codes and apply it to count the number of pre-shared entangled states in order to construct four new classes of asymmetric entanglement-assisted quantum maximal-distance separable (EAQMDS) codes that satisfy the asymmetric entanglement-assisted quantum Singleton bound. Compared with the codes existing in the literature, the lengths of the constructed EAQMDS codes and the number of pre-shared entangled states are more general, and the codes constructed in this paper have greater asymmetry.

PDRG1 promotes the proliferation and migration of GBM cells by the MEK/ERK/CD44 pathway.

P53 and DNA damage-regulated gene1 (PDRG1) is overexpressed in diverse carcinomas. Here, we discover that PDRG1 is overexpressed in glioblastoma multiforme (GBM). However, the clinical significance, biological role, and underlying molecular mechanisms of PDRG1 in GBM remain unclear. PDRG1 was aberrantly overexpressed in glioma, especially prevalent in GBM, and correlated with poor clinicopathologic features of glioma. The risk score, operational feature curve analysis, Kaplan-Meier curve, and univariate and multivariate Cox regression analysis indicated that PDRG1 was an independent prognostic indicator and significantly correlates with disease progression of glioma. A prognostic nomogram was constructed to predict the survival risk of individual patients. The function and pathway enrichment analysis of PDRG1 in The Cancer Genome Atlas cohort was performed. PDRG1 knockdown significantly inhibited the migration and proliferation of GBM cells in vitro and in vivo. Transcriptome sequencing analysis of PDRG1 knockdown U-118 MG(U118) cells indicated that biological regulation adhesion, growth and death, cell motility, cell adhesion molecular and proteoglycans in cancer were significantly enriched. Importantly, we found that the expression of adhesion molecule cluster of differentiation 44 (CD44) was regulated by PDRG1 in GBM. We found that PDRG1 promoted the migration and proliferation of GBM cells via the mitogen-activated protein kinase kinase (MEK)/extracellular regulated protein kinase (ERK)/CD44 pathway. Our findings provide proof that PDRG1 upregulation predicts progression and poor prognosis in human gliomas, especially in isocitrate dehydrogenase (IDH) wt glioma patients. The study provides new evidence that PDRG1 regulates the expression of CD44 in GBM cells and might promote the migration and proliferation via the MEK/ERK/CD44pathway. PDRG1 might be a novel diagnostic indicator and promising therapeutic target for GBM.

Association between chronic obstructive pulmonary disease and periodontitis: The common role of innate immune cells?

Innate immune cells are of broad interest in a variety of diseases. These cells include neutrophils, macrophages, dendritic cells and mast cells, etc. Innate immune cells are often mentioned in inflammatory diseases as the first line of defense against pathogens' invasion. As chronic obstructive pulmonary disease and periodontitis are inflammatory diseases, innate immune cells play an important role in the development of both diseases. COPD and periodontitis are common epidemic diseases with a very high prevalence, thus affecting a large number of people and also reducing the quality of life of patients. In addition, epidemiological studies suggested a link between the two, creating a co-morbid burden, but the mechanism of the link is yet to be explained. This article discusses the possible mechanism of the link between the two diseases in terms of innate immune cells and discusses possible future targeted therapies that could alleviate the burden on patients.

One-step hydrothermal synthesis of WS2 quantum dots as fluorescent sensor for sensitive and selective recognition of hemoglobin and cardiac biomarker myoglobin.

Transition metal dichalcogenide (TMD) dots exhibit excellent photoluminescence performance due to the quantum confinement effect and edge effect, and are extensively applied in electronic and optical devices, sensors, catalysis, and bioimaging. In this work, WS2 quantum dots (WS2 QDs) were prepared under a simple one-step hydrothermal method by optimizing the reaction conditions, and a quantum yield of 11.23% was achieved. The as-prepared WS2 QDs possess good photo-bleaching resistance, salt tolerance, and pH stability. The fluorescence investigations showed that the WS2 QDs acted as a highly efficient fluorescent sensor to detect hemoglobin (Hb) and cardiac biomarker myoglobin (Myo). The linear range was 1-600 µg/mL for Hb and 0.01-120 µg/mL for Myo, with detection limits as low as 260 and 7.6 ng/mL, respectively. Importantly, the WS2 QDs were used to determine the Hb/Myo content in human blood/serum samples, with satisfactory results, indicating that this technique holds promise for application in clinical diagnosis associated with Hb/Myo levels. To the best of our knowledge, this is the first example of TMD QDs without any modification as a fluorescent sensor for detecting Hb and Myo simultaneously.