Using CO2 and oxidants for in situ regeneration of permeable reactive barriers for leachate-contaminated groundwater.

Groundwater contamination near landfills is commonly caused by leachate leakage, and permeable reactive barriers (PRBs) are widely used for groundwater remediation. However, the deactivation and blockage of the reactive medium in PRBs limit their long-term effectiveness. In the current study, a new methodology was proposed for the in situ regeneration of PRB to remediate leachate-contaminated groundwater. CO2 coupled with oxidants was applied for the dispersion and regeneration of the fillers; by injecting CO2 to disperse the fillers, the permeability of the PRB was increased and the oxidants could flow evenly into the PRB. The results indicate that the optimum filler proportion was zero-valent iron (ZVI)/zeolites/activated carbon (AC) = 3:8:10 and the optimum oxidant proportion was COD/Na2S2O8/H2O2/Fe2+ = 1:5:6:5; the oxidation system of Fe2+/H2O2/S2O82- has a high oxidation efficiency and persistence. The average regeneration rate of zeolites was 72.71%, and the average regeneration rate of AC was 68.40%; the permeability of PRB also increased. This technology is effective for the remediation of landfills in China that have large contaminated areas, an uneven pollutant concentration distribution, and a long pollution duration. The purification mode of long-term adsorption and short-time in situ oxidation can be applied to the remediation of long-term high-concentration organically polluted groundwater, where pollution sources are difficult to cut off.

LncRNA LINC00466 Promotes the Progression of Breast Cancer via miR-4731-5p/EPHA2 Pathway.

BACKGROUND: Breast Cancer (BC) is a female malignancy with a high mortality rate. Novel diagnostic and prognostic biomarkers are valuable for reducing BC mortality. Our study is designed to undrape the precise role of the LINC00466/miR-4731-5p/EPHA2 axis in BC.

Arbitrary engineering of spatial caustics with 3D-printed metasurfaces.

Caustics occur in diverse physical systems, spanning the nano-scale in electron microscopy to astronomical-scale in gravitational lensing. As envelopes of rays, optical caustics result in sharp edges or extended networks. Caustics in structured light, characterized by complex-amplitude distributions, have innovated numerous applications including particle manipulation, high-resolution imaging techniques, and optical communication. However, these applications have encountered limitations due to a major challenge in engineering caustic fields with customizable propagation trajectories and in-plane intensity profiles. Here, we introduce the "compensation phase" via 3D-printed metasurfaces to shape caustic fields with curved trajectories in free space. The in-plane caustic patterns can be preserved or morphed from one structure to another during propagation. Large-scale fabrication of these metasurfaces is enabled by the fast-prototyping and cost-effective two-photon polymerization lithography. Our optical elements with the ultra-thin profile and sub-millimeter extension offer a compact solution to generating caustic structured light for beam shaping, high-resolution microscopy, and light-matter-interaction studies.

Acidic fibroblast growth factor inhibits reactive oxygen species-induced epithelial-mesenchymal transdifferentiation in vascular endothelial cells via the miR-155-5p/SIRT1/Nrf2/HO-1 pathway to promote wound healing in diabetic mice.

Background: Diabetic chronic wounds are among the most common and serious complications of diabetes and are associated with significant morbidity and mortality. Endothelial-to-mesenchymal transition (EndMT) is a specific pathological state in which endothelial cells are transformed into mesenchymal cells in response to various stimuli, such as high glucose levels and high oxidative stress. Acidic fibroblast growth factor (aFGF), which is a member of the fibroblast growth factor family, possesses strong antioxidant properties and can promote the differentiation of mesenchymal stem cells into angiogenic cells. Therefore, we investigated the role of aFGF in EndMT in diabetic wounds and analysed the underlying mechanisms. Methods: A diabetic mouse model was used to verify the effect of aFGF on wound healing, and the effect of aFGF on vascular endothelial cells in a high-glucose environment was examined in vitro. We examined the expression of miR-155-5p in a high-glucose environment and the miR-155 downstream target gene SIRT1 by luciferase reporter assays. Results: aFGF promoted wound closure and neovascularization in a mouse model of type 2 diabetes. In vitro, aFGF inhibited the production of total and mitochondrial reactive oxygen species (ROS) in vascular endothelial cells and alleviated epithelial-mesenchymal transdifferentiation in a high-glucose environment. Mechanistically, aFGF promoted the expression of SIRT1 and the downstream targets Nrf2 and HO-1 by negatively regulating miR-155-5p, thereby reducing ROS generation. Conclusions: In conclusion, our results suggest that aFGF inhibits ROS-induced epithelial-mesenchymal transdifferentiation in diabetic vascular endothelial cells via the miR-155-5p/SIRT1/Nrf2/HO-1 axis, thereby promoting wound healing.

Graph-Based Pangenome of Actinidia chinensis Reveals Structural Variations Mediating Fruit Degreening.

Fruit ripening is associated with the degreening process (loss of chlorophyll) that occurs in most fruit species. Kiwifruit is one of the special species whose fruits may maintain green flesh by accumulating a large amount of chlorophyll even after ripening. However, little is known about the genetic variations related to the fruit degreening process. Here, a graph-based kiwifruit pangenome by analyzing 14 chromosome-scale haplotype-resolved genome assemblies from seven representative cultivars or lines in Actinidia chinensis is built. A total of 49,770 non-redundant gene families are identified, with core genes constituting 46.6%, and dispensable genes constituting 53.4%. A total of 84,591 non-redundant structural variations (SVs) are identified. The pangenome graph integrating both reference genome sequences and variant information facilitates the identification of SVs related to fruit color. The SV in the promoter of the AcBCM gene determines its high expression in the late developmental stage of fruits, which causes chlorophyll accumulation in the green-flesh fruits by post-translationally regulating AcSGR2, a key enzyme of chlorophyll catabolism. Taken together, a high-quality pangenome is constructed, unraveled numerous genetic variations, and identified a novel SV mediating fruit coloration and fruit quality, providing valuable information for further investigating genome evolution and domestication, QTL genes function, and genomics-assisted breeding.

Blocking the MIR155HG/miR-155 axis reduces CTGF-induced inflammatory cytokine production and α-SMA expression via upregulating AZGP1 in hypertrophic scar fibroblasts.

Hypertrophic scarring (HS) is a pathological condition characterized by excessive fibrosis and inflammation, resulting in excessive extracellular matrix formation in the skin. MIR155HG, a long non-coding RNA, is abnormally upregulated in fibrotic tissues; however, its underlying mechanism is poorly understood. Using single-cell sequencing data, we analyzed connective tissue growth factor (CTGF) expression in various cell types in HS and normal skin tissues and MIR155HG expression in clinical samples. To investigate the mechanism of fibrosis, an in vitro model using CTGF-treated hypertrophic scar fibroblasts (HSFBs) was established and qRT-PCR, western blotting and ELISA assays were performed to investigate the expression of interleukin (IL)-1ß, IL-6, and mesenchymal markers α-smooth muscle actin (α-SMA). CTGF stimulates MIR155HG level through phosphorylated STAT3 binding to the MIR155HG promoter. We analyzed the methylation of MIR155HG, assessed the levels of miR-155-5p/-3p in CTGF-treated HSFBs and identified differentially expressed genes among HS and NS samples using the Gene Expression Omnibus RNA sequencing data. The binding between miR-155-5p/-3p and AZGP1 was confirmed using a dual-luciferase assay and inflammatory cytokine production and α-SMA expression were investigated in rescue experiments. The findings revealed that CTGF elevated inflammatory cytokine production, α-SMA and MIR155HG expression in HSFBs. MIR155HG is upregulated in HS tissues due to low DNA methylation. Mechanistically, miR-155-5p/-3p was directly bound to MIR155HG 3'UTR. MIR155HG silencing inhibited cytokine production and α-SMA expression by repressing the generation of miR-155-5p/-3p in CTGF-treated HSFBs. Bioinformatics analysis and luciferase reporter assays revealed that miR-155-5p/-3p targets AZGP1. In addition, transfection with plasmids carrying AZGP1 cDNA significantly inhibited the signaling activity of miR-155-5p/-3 p-overexpressing HSFBs. Our findings highlight the importance of the MIR155HG/miR-155/AZGP1 axis in regulating cytokine production and α-SMA in HS.

Catheter ablation versus antiarrhythmic drug therapy for sustained ventricular tachycardia in patients with hypertrophic cardiomyopathy.

BACKGROUND: Ventricular tachycardia (VT) is the primary cause of sudden cardiac death in patients with hypertrophic cardiomyopathy (HCM). However, the strategy for VT treatment in HCM patients remains unclear. This study is aimed to compare the effectiveness of catheter ablation versus antiarrhythmic drug (AAD) therapy for sustained VT in patients with HCM. METHODS: A total of 28 HCM patients with sustained VT at 4 different centers between December 2012 and December 2021 were enrolled. Twelve underwent catheter ablation (ablation group) and sixteen received AAD therapy (AAD group). The primary outcome was VT recurrence during follow-up. RESULTS: Baseline characteristics were comparable between two groups. After a mean follow-up of 31.4 ± 17.5 months, the primary outcome occurred in 35.7% of the ablation group and 90.6% of the AAD group (hazard ratio [HR], 0.29 [95%CI, 0.10-0.89]; P = 0.021). No differences in hospital admission due to cardiovascular cause (25.0% vs. 71.0%; P = 0.138) and cardiovascular cause-related mortality/heart transplantation (9.1% vs. 50.6%; P = 0.551) were observed. However, there was a significant reduction in the composite endpoint of VT recurrence, hospital admission due to cardiovascular cause, cardiovascular cause-related mortality, or heart transplantation in ablation group as compared to that of AAD group (42.9% vs. 93.7%; HR, 0.34 [95% CI, 0.12-0.95]; P = 0.029). CONCLUSIONS: In HCM patients with sustained VT, catheter ablation reduced the VT recurrence, and the composite endpoint of VT recurrence, hospital admission due to cardiovascular cause, cardiovascular cause-related mortality, or heart transplantation as compared to AAD.

Bilateral optic nerve infiltration and leukemic retinopathy as initial signs of leukemia relapse with central nervous system involvement in an adult: a case report.

BACKGROUND: We describe a case in which bilateral optic nerve infiltration and leukemic retinopathy were the initial signs of disease relapse in a patient with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+-ALL) with central nervous system (CNS) involvement. CASE PRESENTATION: A 65-year-old Asian female with Ph+-ALL in complete remission presented at our institution with symptoms of visual disturbance, central scotoma and pain with eye movement in both eyes for a 1-month duration. Ophthalmic examination revealed remarkable optic disc swelling with multiple flame-shaped peripapillary hemorrhages, retinal venous dilation and retinal hemorrhages in both eyes. She was subsequently referred to the treating oncologist and diagnosed with Ph+-ALL relapse with multiple relapsed diseases involving the bone marrow and CNS. After intrathecal (IT) therapy, her visual acuity dramatically improved, and her leukemic infiltrates decreased. CONCLUSIONS: To the best of our knowledge, this is the first case report of ALL relapse with CNS involvement presenting as bilateral optic nerve infiltration and leukemic retinopathy in an adult. Hence, we highlight the priority and sensitivity of ophthalmic examinations, as they are noninvasive methods for detecting leukemia relapse.

Analysis of the components of Mycobacterium tuberculosis heat-resistant antigen (Mtb-HAg) and its regulation of γδ T-cell function.

BACKGROUND: Mycobacterium tuberculosis heat-resistant antigen (Mtb-HAg) is a peptide antigen released from the mycobacterial cytoplasm into the supernatant of Mycobacterium tuberculosis (Mtb) attenuated H37Ra strain after autoclaving at 121 °C for 20 min. Mtb-HAg can specifically induce γδ T-cell proliferation in vitro. However, the exact composition of Mtb-HAg and the protein antigens that are responsible for its function are currently unknown. METHODS: Mtb-HAg extracted from the Mtb H37Ra strain was subjected to LC‒MS mass spectrometry. Twelve of the identified protein fractions were recombinantly expressed in Escherichia coli by genetic engineering technology using pET-28a as a plasmid and purified by Ni-NTA agarose resin to stimulate peripheral blood mononuclear cells (PBMCs) from different healthy individuals. The proliferation of γδ T cells and major γδ T-cell subset types as well as the production of TNF-α and IFN-γ were determined by flow cytometry. Their proliferating γδ T cells were isolated and purified using MACS separation columns, and Mtb H37Ra-infected THP-1 was co-cultured with isolated and purified γδ T cells to quantify Mycobacterium viability by counting CFUs. RESULTS: In this study, Mtb-HAg from the attenuated Mtb H37Ra strain was analysed by LC‒MS mass spectrometry, and a total of 564 proteins were identified. Analysis of the identified protein fractions revealed that the major protein components included heat shock proteins and Mtb-specific antigenic proteins. Recombinant expression of 10 of these proteins in by Escherichia coli genetic engineering technology was used to successfully stimulate PBMCs from different healthy individuals, but 2 of the proteins, EsxJ and EsxA, were not expressed. Flow cytometry results showed that, compared with the IL-2 control, HspX, GroEL1, and GroES specifically induced γδ T-cell expansion, with Vγ2δ2 T cells as the main subset, and the secretion of the antimicrobial cytokines TNF-α and IFN-γ. In contrast, HtpG, DnaK, GroEL2, HbhA, Mpt63, EsxB, and EsxN were unable to promote γδ T-cell proliferation and the secretion of TNF-α and IFN-γ. None of the above recombinant proteins were able to induce the secretion of TNF-α and IFN-γ by αß T cells. In addition, TNF-α, IFN-γ-producing γδ T cells inhibit the growth of intracellular Mtb. CONCLUSION: Activated γδ T cells induced by Mtb-HAg components HspX, GroES, GroEL1 to produce TNF-α, IFN-γ modulate macrophages to inhibit intracellular Mtb growth. These data lay the foundation for subsequent studies on the mechanism by which Mtb-HAg induces γδ T-cell proliferation in vitro, as well as the development of preventive and therapeutic vaccines and rapid diagnostic reagents.

Identification and expression analysis of the GLK gene family in tea plant (Camellia sinensis) and a functional study of CsGLK54 under low-temperature stress.

The Golden2-like (GLK) transcription factor family is a significant group of transcription factors in plantae. The currently available studies have shown that GLK transcription factors have been studied mainly in chloroplast growth and development, with fewer studies in abiotic stress regulation. In this study, all tea plant GLK transcription factors were identified for the first time in tea plants, and genome-wide identification, phylogenetic analysis, and thematic characterization were performed to identify 66 GLK transcription factors in tea plants. These genes are categorized into seven groups, and an amino acid sequence comparison analysis is performed. This study revealed that the structure of GLK genes in tea plants is highly conserved and that these genes are distributed across 14 chromosomes. Collinearity analysis revealed 17 pairs of genes with fragment duplications and one pair of genes with tandem duplications, and the analysis of Ka/Ks ratios indicated that most of the genes underwent negative purifying selection. Analysis of promoter cis-elements revealed that the promoters of tea plant GLK genes contain a large number of cis-acting elements related to phytohormones and stress tolerance. In addition, a large number of genes contain LTR elements, suggesting that tea plant GLK genes are involved in low-temperature stress. qRT‒PCR analysis revealed that the expression of CsGLK17, CsGLK38, CsGLK54, CsGLK11 and CsGLK60 significantly increased and that the expression of CsGLK7 and CsGLK13 decreased in response to low-temperature induction. Taken together, the results of the transcription profile analysis suggested that CsGLK54 may play an important regulatory role under low-temperature stress. The subcellular localization of CsGLK54 was in the nucleus. Furthermore, CsGLK54 positively regulated the transcription levels of the NbPOD and NbSOD genes under low-temperature stress, which led to an increase in POD and SOD enzyme activities and a decrease in MDA content. These findings provide valuable insights into the regulatory mechanism of low-temperature stress in tea plants.

Modifications on the coastal atmospheric sulfur and cloud condensation nuclei along the Eastern China seas by shipping fuel transition.

Marine fuel combustion from shipping releases SO2 and forms sulfate particles, which may alter low cloud characteristics. A series of strategies were implemented to control the sulfur content of ship fuel oil from 2018 to 2020, offering insights into the effects of the ship fuel oil transition on sulfur-related pollutants and the consequent cloud condensation nuclei (CCN) in the atmosphere. Compared to 2018 in the southeast China waters, shipping SO2 emission decreased by 78 % in 2020, resulting in a 76 % reduction in ship-related total sulfur concentration, and a decrease of 54 % in CCN number concentration under supersaturation 0.2 % (CCN0.2) contributed by shipping. The response of CCN0.2 to ship-related sulfate modification is more pronounced in relatively clean environments than polluted environments, highlighting the uneven changes in coastal CCN along the Eastern China Sea induced by the ship fuel policies. CCN can trigger the formation of cloud droplets, 2020 fuel regulation may have and will reduce the cooling radiative forcing effect with strong spatial heterogeneity. The study provides insights into the variations in coastal atmospheric sulfur-related pollutants and CCN in uneven response to changes in ship fuel oil, prompting the need for further comprehensive assessments of the climate effects resulting from potential shifts in ship fuel use in the future.

Exosomes derived from adipose tissue-derived stem cells alleviated H2O2-induced oxidative stress and endothelial-to-mesenchymal transition in human umbilical vein endothelial cells by inhibition of the mir-486-3p/Sirt6/Smad signaling pathway.

Hypertrophic scar (HS) is characterized by excessive collagen deposition and myofibroblasts activation. Endothelial-to-mesenchymal transition (EndoMT) and oxidative stress were pivotal in skin fibrosis process. Exosomes derived from adipose tissue-derived stem cells (ADSC-Exo) have the potential to attenuate EndoMT and inhibit fibrosis. The study revealed reactive oxygen species (ROS) levels were increased during EndoMT occurrence of dermal vasculature of HS. The morphology of endothelial cells exposure to H2O2, serving as an in vitro model of oxidative stress damage, transitioned from a cobblestone-like appearance to a spindle-like shape. Additionally, the levels of endothelial markers decreased in H2O2-treated endothelial cell, while the expression of fibrotic markers increased. Furthermore, H2O2 facilitated the accumulation of ROS, inhibited cell proliferation, retarded its migration and suppressed tube formation in endothelial cell. However, ADSC-Exo counteracted the biological effects induced by H2O2. Subsequently, miRNAs sequencing analysis revealed the significance of mir-486-3p in endothelial cell exposed to H2O2 and ADSC-Exo. Mir-486-3p overexpression enhanced the acceleration of EndoMT, its inhibitors represented the attenuation of EndoMT. Meanwhile, the target regulatory relationship was observed between mir-486-3p and Sirt6, whereby Sirt6 exerted its anti-EndoMT effect through Smad2/3 signaling pathway. Besides, our research had successfully demonstrated the impact of ADSC-Exo and mir-486-3p on animal models. These findings of our study collectively elucidated that ADSC-Exo effectively alleviated H2O2-induced ROS and EndoMT by inhibiting the mir-486-3p/Sirt6/Smad axis.

Elastic strain-induced amorphization in high-entropy alloys.

Elastic stability is the basis for understanding structural responses to external stimuli in crystalline solids, including melting, incipient plasticity and fracture. In this work, elastic stability is investigated in a series of high-entropy alloys (HEAs) using in situ mechanical tests and atomic-resolution characterization in transmission electron microscopy. Under tensile loading, the HEA lattices are observed to undergo a sudden loss of ordering as the elastic strain reached ∽ 10%. Such elastic strain-induced amorphization stands in intrinsic contrast to previously reported dislocation-mediated elastic instability and defect accumulation-mediated amorphization, introducing a form of elastic instability. Together with the first principle calculations and atomic-resolution chemical mapping, we identify that the elastic strain-induced amorphization is closely related to the depressed dislocation nucleation due to the local atomic environment inhomogeneity of HEAs. Our findings provide insights for the understanding of the fundamental nature of physical mechanical phenomena like elastic instability and incipient plasticity.

PTPRO inhibits LPS-induced apoptosis in alveolar epithelial cells.

Acute lung injury (ALI) and its severe manifestation, acute respiratory distress syndrome (ARDS), represent critical clinical syndromes with multifactorial origins, notably stemming from sepsis within intensive care units (ICUs). Despite their high mortality rates, no selective cure is available beside ventilation support. Apoptosis plays a complex and pivotal role in the pathophysiology of acute lung injury. Excessive apoptosis of alveolar epithelial and microvascular endothelial cells can lead to disruption of lung epithelial barrier integrity, impairing the body's ability to exchange blood and gas. At the same time, apoptosis of damaged or dysfunctional cells, including endothelial and epithelial cells, can help maintain tissue integrity and accelerate recovery from organ pro-inflammatory stress. The balance between pro-survival and pro-apoptotic signals in lung injury determines patient outcomes, making the modulation of apoptosis an area of intense research in the quest for more effective therapies. Here we found that protein tyrosine phosphatase receptor type O (PTPRO), a poorly understood receptor-like protein tyrosine phosphatase, is consistently upregulated in multiple tissue types of mice under septic conditions and in the lung alveolar epithelial cells. PTPRO reduction by its selective short-interfering RNA (siRNA) leads to excessive apoptosis in lung alveolar epithelial cells without affecting cell proliferation. Consistently PTPRO overexpression by a DNA construct attenuates apoptotic signaling induced by LPS. These effects of PTPTO on cellular apoptosis are dependent on an ErbB2/PI3K/Akt/NFκB signaling pathway. Here we revealed a novel regulatory pathway of cellular apoptosis by PTPRO in lung alveolar epithelial cells during sepsis.

Tolerance threshold of a pelagic species in China to total dissolved gas supersaturation: from the perspective of survival characteristics and swimming ability.

Total dissolved gas (TDG) supersaturation downstream of dams can occur in the Yangtze River basin and is known to cause stress and even death in fish. Consequently, it is important to establish tolerance thresholds of endemic fish to protect local aquatic resources. We conducted experiments to assess survival characteristics and swimming ability of bighead carp, an important commercial fish dwelling in the Yangtze River, to evaluate its tolerance threshold to TDG supersaturation. The typical external symptoms of gas bubble trauma (GBT) were observed and the time when the fish lost equilibrium and died were recorded. The results showed that the mortality occurred when TDG level exceeded 125%, with obvious symptoms such as exophthalmos and bubbles on the head. The interval between loss of equilibrium and mortality decreased with an increase in TDG level. Neither exposure time nor TDG level significantly affected the critical swimming speed (Ucrit) of fish exposed to non-lethal exposure (110%, 120% and 125% TDG) over a 7 day period. Significant reductions in Ucrit were found under 130% and 135% TDG conditions when the exposure lasted 52.0 h and 42.9 h, respectively. The Ucrit also significantly decreased after exposure of 1.6 h under 140% TDG condition. Moreover, after exposure to 140% TDG for 39.2 h, 135% TDG for 56.5 h and 130% TDG for 95.9 h, bighead carp were transferred into air saturated water to recover for 24 h or 48 h; however, swimming performance remained impaired. The results of this study indicate that 125% TDG was the highest TDG level where limited mortality was observed and the swimming ability was not impaired, showing that 125% TDG can be set as the tolerance threshold of this species to guide the operation of dams in the Yangtze River Basin.

Swimming ability of Schizothoracinae fishes in Yarlung Zangbo River of China.

The Yarlung Zangbo River is a river with abundant hydropower resources but fragile biodiversity in China. As an important benchmark for both research and ecological management, there is still a lack of knowledge about the swimming ability of fishes in the Yarlung Zangbo River. The induced flow velocity (Uind), critical swimming speed (Ucrit), and burst swimming speed (Uburst) of five Schizothoracinae species were tested in this study. Relative swimming ability related to body length and body shape was calculated. The results indicated that the average absolute swimming speeds (Uind-a, Ucrit-a, and Uburst-a) of all the experimental fish were 10.20 ± 0.01, 57.58 ± 3.28, and 69.54 ± 2.94 cm/s, respectively, and the corresponding relative Uind, Ucrit, and Uburst related to body length (Uind-l, Ucrit-l, Uburst-l) were 1.15 ± 0.07, 5.04 ± 0.26, and 7.23 ± 0.28 BL/s, respectively. Moreover, relative Uind, Ucrit, and Uburst related to body shape (Uind-s, Ucrit-s, and Uburst-s) were 0.80 ± 0.13, 2.49 ± 0.51, and 4.32 ± 0.57 cm-2/s, respectively. No significantly differences in relative swimming speeds existed among five species. Only Oxygymnocypris stewartii was significantly weaker in Uburst-s than Schizothorax o'connori. The body shape showed a stronger relationship with swimming speed than the body length did. Schizothoracinae fish in the Yarlung Zangbo River basin are less sensitive to the water flow and performed weaker Ucrit and Uburst compared to those in the Yangtze River basin, indicating that Schizothoracinae fish in the Yarlung Zangbo River may be more susceptible to threats from environmental changes. The paper enriched the research on the swimming ability of Schizothoracinae fishes and provided efficient data for the fish conservation in the Yarlung Zangbo River.

Multi-Scale Masked Autoencoders for Cross-Session Emotion Recognition.

Affective brain-computer interfaces (aBCIs) have garnered widespread applications, with remarkable advancements in utilizing electroencephalogram (EEG) technology for emotion recognition. However, the time-consuming process of annotating EEG data, inherent individual differences, non-stationary characteristics of EEG data, and noise artifacts in EEG data collection pose formidable challenges in developing subject-specific cross-session emotion recognition models. To simultaneously address these challenges, we propose a unified pre-training framework based on multi-scale masked autoencoders (MSMAE), which utilizes large-scale unlabeled EEG signals from multiple subjects and sessions to extract noise-robust, subject-invariant, and temporal-invariant features. We subsequently fine-tune the obtained generalized features with only a small amount of labeled data from a specific subject for personalization and enable cross-session emotion recognition. Our framework emphasizes: 1) Multi-scale representation to capture diverse aspects of EEG signals, obtaining comprehensive information; 2) An improved masking mechanism for robust channel-level representation learning, addressing missing channel issues while preserving inter-channel relationships; and 3) Invariance learning for regional correlations in spatial-level representation, minimizing inter-subject and inter-session variances. Under these elaborate designs, the proposed MSMAE exhibits a remarkable ability to decode emotional states from a different session of EEG data during the testing phase. Extensive experiments conducted on the two publicly available datasets, i.e., SEED and SEED-IV, demonstrate that the proposed MSMAE consistently achieves stable results and outperforms competitive baseline methods in cross-session emotion recognition.

Acute lung injury: a view from the perspective of necroptosis.

BACKGROUND: ALI/ARDS is a syndrome of acute onset characterized by progressive hypoxemia and noncardiogenic pulmonary edema as the primary clinical manifestations. Necroptosis is a form of programmed cell necrosis that is precisely regulated by molecular signals. This process is characterized by organelle swelling and membrane rupture, is highly immunogenic, involves extensive crosstalk with various cellular stress mechanisms, and is significantly implicated in the onset and progression of ALI/ARDS. METHODS: The current body of literature on necroptosis and ALI/ARDS was thoroughly reviewed. Initially, an overview of the molecular mechanism of necroptosis was provided, followed by an examination of its interactions with apoptosis, pyroptosis, autophagy, ferroptosis, PANOptosis, and NETosis. Subsequently, the involvement of necroptosis in various stages of ALI/ARDS progression was delineated. Lastly, drugs targeting necroptosis, biomarkers, and current obstacles were presented. CONCLUSION: Necroptosis plays an important role in the progression of ALI/ARDS. However, since ALI/ARDS is a clinical syndrome caused by a variety of mechanisms, we emphasize that while focusing on necroptosis, it may be more beneficial to treat ALI/ARDS by collaborating with other mechanisms.

Immune responses induced by Mycobacterium tuberculosis heat-resistant antigen (Mtb-HAg) upon co-administration with Bacillus Calmette-Guérin in mice.

OBJECTIVES: To preliminarily assess the immunogenicity of Mtb-HAg in mice and the synergistic effect provided by HAg when co-immunised with BCG. METHODS: Mice were randomly grouped for different immunisations and then spleens were aseptically removed and lymphocytes were extracted for immediate detection of cytokines transcript levels and stimulation index(SI), cytokine secretion and multifunctional antigen-specific T cells were detected after incubation for different times. RESULTS: HAg extracted from active Mtb is a group of mixed polypeptides with molecular weights of (10-14) kDa. It can significantly stimulate lymphocytes proliferation and increase SI. Injection of HAg alone and in combination with BCG induced significantly higher numbers of multifunctional antigen-specific T cells including CD4+ IFN-γ+, CD4+ IL-2+, CD8+ IFN-γ+, and CD8+ IL-2+ cells than that in BCG-treated mice. Co-immunisation induced the secretion of higher levels of IFN-γ, TNF-α, IL-2 and IL-4 and increased their mRNA expression levels. Significant increases in the transcription levels of IL-10, IL-12 and IL-17 were observed in the co-immunised group with the assistance of HAg. CONCLUSION: We demonstrated that HAg has favourable immunogenicity, triggers a stronger Th1-type immune response and proposed the hypothesis that HAg can be used as a BCG booster to further enhance the benefits of BCG.

Fungal community diversity and their contribution to nitrogen cycling in in-situ aerated landfills: Insights from field and laboratory studies.

The application of in-situ aeration technology in landfills has been reported to promote fungal growth, but the community diversity and function of fungi in the aerated landfill system remain unknown. This study firstly investigated an in-situ aerated remediation landfill site to characterize the fungal community diversity in refuse. And to further reveal the fungal involvement in the nitrogen cycling system, laboratory-scale simulated aerated landfill reactors were then constructed. The results in the aerated landfill site showed a significant correlation between fungal community structure and ammonia nitrogen content in the refuse. Dominant fungi in the fungal community included commonly found environmental fungi such as Fusarium, Aspergillus, Gibberella, as well as unique fungi in the aerated system like Chaetomium. In the laboratory-scale aerated landfill simulation experiments, the fungal system was constructed using bacterial inhibitor, and nitrogen balance analysis confirmed the significant role of fungal nitrification in the nitrogen cycling process. When ammonia nitrogen was not readily available, fungi converted organic nitrogen to nitrate, serving as the main nitrification mechanism in the system, with a contribution rate ranging from 62.71 % to 100 % of total nitrification. However, when ammonia nitrogen was present in the system, autotrophic nitrification became the main mechanism, and the contribution of fungal nitrification to total nitrification was only 15.96 %. Additionally, fungi were capable of directly utilizing nitrite for nitrate production with a rate of 4.65 mg L-1 d-1. This research article contributes to the understanding of the importance of fungi in the aerated landfill systems, filling a gap in knowledge.