Chronic stress dysregulates the Hippo/YAP/14-3-3η pathway and induces mitochondrial damage in basolateral amygdala in a mouse model of depression.

Rationale: Recent evidence highlights the pivotal role of mitochondrial dysfunction in mood disorders, but the mechanism involved remains unclear. We studied whether the Hippo/YAP/14-3-3η signaling pathway mediates mitochondrial abnormalities that result in the onset of major depressive disorder (MDD) in a mouse model. Methods: The ROC algorithm was used to identify a subpopulation of mice that were exposed to chronic unpredictable mild stress (CUMS) and exhibited the most prominent depressive phenotype (Dep). Electron microscopy, biochemical assays, quantitative PCR, and immunoblotting were used to evaluate synaptic and mitochondrial changes in the basolateral amygdala (BLA). RNA sequencing was used to explore changes in the Hippo pathway and downstream target genes. In vitro pharmacological inhibition and immunoprecipitation was used to confirm YAP/14-3-3η interaction and its role in neuronal mitochondrial dysfunction. We used virus-mediated gene overexpression and knockout in YAP transgenic mice to verify the regulatory effect of the Hippo/YAP/14-3-3η pathway on depressive-like behavior. Results: Transcriptomic data identified a large number of genes and signaling pathways that were specifically altered from the BLA of Dep mice. Dep mice showed notable synaptic impairment in BLA neurons, as well as mitochondrial damage characterized by abnormal mitochondrial morphology, compromised function, impaired biogenesis, and alterations in mitochondrial marker proteins. The Hippo signaling pathway was activated in Dep mice during CUMS, and the transcriptional regulatory activity of YAP was suppressed by phosphorylation of its Ser127 site. 14-3-3η was identified as an important co-regulatory factor of the Hippo/YAP pathway, as it can respond to chronic stress and regulate cytoplasmic retention of YAP. Importantly, the integrated Hippo/YAP/14-3-3η pathway mediated neuronal mitochondrial dysfunction and depressive behavior in Dep mice. Conclusion: The integrated Hippo/YAP/14-3-3η pathway in the BLA neuron is critical in mediating depressive-like behaviors in mice, suggesting a causal role for this pathway in susceptibility to chronic stress-induced depression. This pathway therefore may present a therapeutic target against mitochondrial dysfunction and synaptic impairment in MDD.

Covalent Bond Torsion-Enabled Unique Crystal-Phase Transformation of an Organic Semiconductor for Multicolor Light-Emitting Transistors.

High-mobility and color-tunable highly emissive organic semiconductors (OSCs) are highly promising for various optoelectronic device applications and novel structure-property relationship investigations. However, such OSCs have never been reported because of the great trade-off between mobility, emission color, and emission efficiency. Here, we report a novel strategy of molecular conformation-induced unique crystalline polymorphism to realize the high mobility and color-tunable high emission in a novel OSC, 2,7-di(anthracen-2-yl) naphthalene (2,7-DAN). Interestingly, 2,7-DAN has unique crystalline polymorphism, which has an almost identical packing motif but slightly different molecular conformation enabled by the small bond rotation angle variation between anthracene and naphthalene units. More remarkably, the subtle covalent bond rotation angle change leads to a big change in color emission (from blue to green) but does not significantly modify the mobility and emission efficiency. The carrier mobility of 2,7-DAN crystals can reach up to a reliable 17 cm2 V-1 s-1, which is rare for the reported high-mobility OSCs. Based on the unique phenomenon, high-performance light-emitting transistors with blue to green emission are simultaneously demonstrated in an OSC crystal. These results open a new way for designing emerging multifunctional organic semiconductors toward next-generation advanced molecular (atomic)-scale optoelectronics devices.

α-Lipoic acid treatment regulates enzymatic browning and nutritional quality of fresh-cut pear fruit by affecting phenolic and carbohydrate metabolism.

Fresh-cut pear fruit is greatly impacted by enzymatic browning, and maintaining quality remains a challenge. This study examined the impact of exogenous α-lipoic acid (α-LA) treatment on enzymatic browning and nutritional quality of fresh-cut pears. Results revealed that 0.5 g/L α-LA treatment effectively maintained color and firmness, and inhibited the increase in microbial number. The α-LA treatment also reduced MDA and H2O2 contents, decreased PPO activity, and enhanced SOD, CAT, and PAL activities. The α-LA treatment notably upregulated phenolic metabolism-related gene expression, including PbPAL, Pb4CL, PbC4H, PbCHI and PbCHS, and then increasing total phenols and flavonoids contents. Furthermore, it also influenced carbohydrate metabolism-related gene expression, including PbSS, PbSPS, PbAI and PbNI, maintaining a high level of sucrose content. These findings indicated that α-LA treatment showed promise in reducing browning and enhancing fresh-cut pears quality, offering a potential postharvest method to prolong the lifespan and maintain nutritional quality.

Clinical outcomes of liposomal irinotecan in patients with advanced pancreatic cancer previously treated with conventional irinotecan: A meta-analysis of real-world evidence.

BACKGROUND: Pivotal clinical trials supported survival benefits of liposomal irinotecan (nal-IRI) plus fluorouracil/leucovorin in patients with pancreatic ductal adenocarcinoma (PDAC) who previously received gemcitabine-based therapy. There are concerns about the benefits of nal-IRI in patients who received FOLFIRINOX (combined fluorouracil, leucovorin, IRI, and oxaliplatin) because of potential cross-resistance to IRI. The objective of this meta-analysis was to characterize the impact of the previous receipt of IRI on the outcomes of nal-IRI regimens in patients with advanced PDAC. METHODS: Real-world studies evaluating the outcomes of nal-IRI in patients who had prior IRI exposure published up to April 2023 were searched using electronic databases. The meta-analysis was conducted using a random effects model to estimate pooled hazard ratios (HRs) and 95% confidence intervals (CIs). RESULTS: Eight studies (n = 1368 patients) were included. The pooled median progression-free survival (PFS) was 2.02 months (95% CI, 1.43-2.57 months), and the median overall survival (OS) was 4.26 months (95% CI, 3.03-5.39 months). Patients with prior IRI exposure had PFS (HR, 1.17; 95% CI, 0.94-1.47; p = .17) and OS (HR, 1.16; 95% CI, 0.95-1.42; p = .16) comparable to patients without prior IRI exposure. Likewise, patients who had progressive disease on conventional IRI had PFS (HR, 1.50; 95% CI, 0.73-3.08; p = .24) and OS (HR, 1.70; 95% CI, 0.68-4.27; p = .26) with nal-IRI comparable to patients who had no progressive disease. CONCLUSIONS: Prior IRI exposure does not affect the survival outcomes of nal-IRI regimens in patients who have advanced PDAC. The selection of later lines of chemotherapy regimens should be based on the differential safety profile, patient status, the cost of treatment, and health-related quality of life.

Air Pollution, Genetic Susceptibility, and Risk of Incident Systemic Lupus Erythematosus: A Prospective Cohort Study.

OBJECTIVE: There are few existing studies that investigate the risk of systemic lupus erythematosus (SLE) associated with long-term exposure to air pollutants. This study aimed to explore associations between long-term exposure to air pollutants and incident SLE and further evaluate interactions and joint effects of genetic risk and air pollutants. METHODS: A total of 459,815 participants were included from UK Biobank. The concentrations of air pollutants (fine particulate matter with diameter ≤2.5 µm [PM2.5], particulate matter diameter ≤10 µm [PM10], nitrogen dioxide [NO2], and nitrogen oxides [NOx]) were estimated by land-use regression model. We applied Cox proportional hazards model to explore linkages of air pollutants and incident SLE. The polygenic risk score (PRS) was used for further assessing the interactions and joint effects of genetic risk and air pollutants. RESULTS: A total of 399 patients with SLE were identified during a median follow-up of 11.77 years. There were positive associations between air pollutant exposure and incident SLE, as the adjusted hazard ratios were 1.18 (95% confidence interval [95% CI] 1.06-1.32), 1.23 (1.10-1.39), 1.27 (1.14-1.41), and 1.13 (1.03-1.23) for each interquartile range increase in PM2.5, PM10, NO2, and NOx, respectively. Moreover, participants with high genetic risk and high air pollution exposure had the highest risk of incident SLE compared with those with low genetic risk and low air pollution exposure (adjusted hazard ratio: PM2.5, 4.16 [95% CI 2.67-6.49]; PM10, 5.31 [95% CI 3.30,-8.55]; NO2, 5.61 [95% CI 3.45-9.13]; and NOx, 4.80 [95% CI 3.00-7.66]). There was a significant multiplicative interaction between NO2 and PRS. CONCLUSION: Long-term exposure to air pollutants (PM2.5, PM10, NO2, and NOx) may increase the risk of developing SLE.

A nanomaterial-independent and fluorescent immunoassay based on Eu-micelles for rapid and sensitive detection of fluoroquinolones in chicken.

Fluorescent nanoprobes are widely applied in innovate enzyme-linked immunosorbent assays (ELISA) for detection of fluoroquinolones (FQs) residue in foodstuffs. Nevertheless, the complicated synthesis of nanoprobes hampers their practical applications. Herein, a nanomaterial-independent and fluorescent ELISA for sensitive detection of FQs is developed using the Eu-micelles as signal probe. Non-nanostructured Eu-micelles with high quantum yield and stability are facilely synthesized through the assembly of Eu3+ and ligands. Alkaline phosphatase catalyzes hydrolysis of 4-nitrophenyl phosphate to 4-nitrophenol. The fluorescent Eu-micelles can be readily quenched by 4-nitrophenol via static quenching. The signal generation mechanism integrates well with conventional ELISA systems. The established fluorescent ELISA achieves sensitive detection of FQs with a limit of detection of 0.03 µg/kg. The validation results from LC-MS show that the fluorescent ELISA exhibits good accuracy and recoveries. Our study presents a nanomaterial-independent strategy for developing the rapid immunoassay for FQs, which holds good promise for practical applications.

Chlorella pyrenoidosa polysaccharides supplementation increases Drosophila melanogaster longevity at high temperature.

Chlorella pyrenoidos polysaccharides (CPPs) are the main active components of Chlorella pyrenoidos. They possess beneficial health properties, such as antioxidant, anti-inflammatory, and immune-enhancing. This study aims to investigate the protective function and mechanism of CPPs against high-temperature stress injury. Results showed that supplementation with 20 mg/mL CPPs significantly extended the lifespan of Drosophila melanogaster under high-temperature stress, improved its motility, and enhanced its resistance to starvation and oxidative stress. These effects were mainly attributed to the activation of Nrf2 signaling and enhanced antioxidant capacity. Additionally, it has been discovered that CPPs supplementation enhanced Drosophila resilience by preventing the disruption of the intestinal barrier and accumulation of reactive oxygen species caused by heat stress. Overall, these studies suggest that CPPs could be a useful natural therapy for preventing heat stress-induced injury.

Discovery of 7-alkoxybenzofurans as PDE4 inhibitors with hepatoprotective activity in D-GalN/LPS-induced hepatic sepsis.

Sepsis can quickly result in fatality for critically ill individuals, while liver damage can expedite the progression of sepsis, necessitating the exploration of new strategies for treating hepatic sepsis. PDE4 has been identified as a potential target for the treatment of liver damage. The scaffold hopping of lead compounds FCPR16 and Z19153 led to the discovery of a novel 7-methoxybenzofuran PDE4 inhibitor 4e, demonstrating better PDE4B (IC50 = 10.0 nM) and PDE4D (IC50 = 15.2 nM) inhibitor activity as a potential anti-hepatic sepsis drug in this study. Compared with FCPR16 and Z19153, 4e displayed improved oral bioavailability (F = 66 %) and longer half-life (t1/2 = 2.0 h) in SD rats, which means it can be more easily administered and has a longer-lasting effect. In the D-GalN/LPS-induced liver injury model, 4e exhibited excellent hepatoprotective activity against hepatic sepsis by decreasing ALT and AST levels and inflammatory infiltrating areas.

Preparation of medium- and long-chain triacylglycerols rich in n-3 polyunsaturated fatty acids by bio-imprinted lipase-catalyzed interesterification.

Medium and long-chain triacylglycerol (MLCT) rich in n-3 polyunsaturated fatty acids (PUFAs) were obtained in three-hour interesterification of fish oil with medium-chain triacylglycerol (MCTs), using lipase bio-imprinted with surfactant as a catalyst. Initially, for bio-imprinted lipase preparation, the interesterification reaction conditions were optimized, resulting in a lipase with 1.47 times higher catalytic activity compared to control (non-bio-imprinted). Afterwards, the reaction conditions for MLCT synthesis were optimized, using bio-imprinted lipase as a catalyst. The reaction reached equilibrium within first three hours at 70 °C temperature, 4 wt% lipase load, and molar ratio of substrate 1:1.5. Under these conditions, final product contained 18.52% MCT, 56.65% MLCT, and 24.83% long-chain triacylglycerol (LCT). To reduce the MCT content, a solvent extraction process was performed, yielding 2.42% MCT, 56.19% MLCT, and 41.39% LCT. The obtained structured lipids (SLs), enriched in n-3 PUFAs, offer significant health benefits, enhanced bioavailability, with potential applications in functional foods and nutraceuticals.

Spinal cord stimulation attenuates paclitaxel-induced gait impairment and mechanical hypersensitivity via peripheral neuroprotective mechanisms in tumor-bearing rats.

BACKGROUND: Taxanes such as paclitaxel (PTX) induce dose-dependent chemotherapy-induced peripheral neuropathy (CIPN), which is associated with debilitating chronic pain and gait impairment. Increased macrophage-related proinflammatory activities have been reported to mediate the development and maintenance of neuropathic pain. While spinal cord stimulation (SCS) has been used for a number of pain conditions, the mechanisms supporting its use for CIPN remain to be elucidated. Thus, we aimed to examine whether SCS can attenuate Schwann cell-mediated and macrophage-mediated neuroinflammation in the sciatic nerve of Rowlette Nude (RNU) rats with PTX-induced gait impairment and mechanical hypersensitivity. METHODS: Adult male tumor-bearing RNU rats were used for this study examining PTX treatment and SCS. Gait and mechanical hypersensitivity were assessed weekly. Cytokines, gene expression, macrophage infiltration and polarization, nerve morphology and Schwann cells were examined in sciatic nerves using multiplex immunoassay, bulk RNA sequencing, histochemistry and immunohistochemistry techniques. RESULTS: SCS (50 Hz, 0.2 milliseconds, 80% motor threshold) attenuated the development of mechanical hypersensitivity (20.93±0.80 vs 12.23±2.71 grams, p<0.0096) and temporal gait impairment [swing (90.41±7.03 vs 117.27±9.71%, p<0.0076), and single stance times (94.92±3.62 vs 112.75±7.27%, p<0.0245)] induced by PTX (SCS+PTX+Tumor vs Sham SCS+PTX+Tumor). SCS also attenuated the reduction in Schwann cells, myelin thickness and increased the concentration of anti-inflammatory cytokine interleukin (IL)-10. Bulk RNA sequencing revealed differential gene expression after SCS, with 607 (59.2%) genes upregulated while 418 (40.8%) genes were downregulated. Notably, genes related to anti-inflammatory cytokines and neuronal growth were upregulated, while genes related to proinflammatory-promoting genes, increased M2γ polarization and decreased macrophage infiltration and Schwann cell loss were downregulated. CONCLUSION: SCS may attenuate PTX-induced pain and temporal gait impairment, which may be partly attributed to decreases in Schwann cell loss and macrophage-mediated neuroinflammation in sciatic nerves.

NKG2A genetic deletion promotes human primary NK cell anti-tumor responses better than an anti-NKG2A monoclonal antibody.

Natural killer (NK) cells eliminate infected or cancer cells via their cytotoxic capacity. NKG2A is an inhibitory receptor on NK cells and cancer cells often overexpress its ligand HLA-E to evade NK cell surveillance. Given the successes of immune checkpoint blockade in cancer therapy, NKG2A is an interesting novel target. However, anti-NKG2A antibodies have shown limited clinical response. In the pursuit of enhancing NK cell-mediated anti-tumor responses, we devised a Cas9-based strategy to delete KLRC1, encoding NKG2A, in human primary NK cells. Our approach involved electroporation of KLRC1-targeting Cas9 ribonucleoprotein resulting in effective ablation of NKG2A expression. Compared with anti-NKG2A antibody blockade, NKG2AKO NK cells exhibited enhanced activation, reduced suppressive signaling, and elevated expression of key transcription factors. NKG2AKO NK cells overcame inhibition from HLA-E, significantly boosting NK cell activity against solid and hematologic cancer cells. We validated this efficacy across multiple cell lines, a xenograft mouse model, and primary human leukemic cells. Combining NKG2A knockout with antibody coating of tumor cells further enhanced cytotoxicity through ADCC. Thus, we provide a comprehensive comparison of inhibition of the NKG2A pathway using genetic ablation and antibodies and provide novel insight in the observed differences in molecular mechanisms, which can be translated to enhance adoptive NK cell immunotherapy.

LncRNA MFRL regulates the phenotypic switch of vascular smooth muscle cells to attenuate arterial remodeling by encoding a novel micropeptide MFRLP.

BACKGROUND: Arterial remodeling is a common pathophysiological change in the pathogenesis of cardiovascular diseases in which the phenotypic switch of vascular smooth muscle cells (VSMC) plays an important role. Recently, an increasing number of long non-coding RNAs(lncRNAs) have been shown to encode micropeptides that play biological roles and have great clinical transformation potential. However, the role of micropeptides encoded by lncRNAs in arterial remodeling has not been well studied and requires further exploration. METHODS AND RESULTS: Through bioinformatic analysis and experimental verification, we found that a new lncRNA, the mitochondrial function-related lncRNA (MFRL), encodes a 64-amino acid micropeptide, MFRLP. MFRL and MFRLP play important roles in the phenotypic switch of VSMC. Further experiments showed that MFRLP interacts with mitochondrial cytochrome b to reduce accumulation of reactive oxygen species, suppress mitophagy and inhibit the VSMC switch from contractile to synthetic phenotype. CONCLUSIONS: LncRNA MFRL encodes the micropeptide MFRLP, which interacts with mitochondrial cytochrome b to inhibit the VSMC switch from contractile to synthetic phenotype and improve arterial remodeling.

Impacts of organophosphate pesticide types and concentrations on aquatic bacterial communities and carbon cycling.

Organophosphorus pesticides (OPPs) are important chemical stressors in aquatic ecosystems, and they attract increasing more attentions recently. However, the impacts of different OPPs on carbon cycling remain unclear, particularly for those functional-yet-uncultivable microbes. This study investigated the change in lake aquatic microbial communities in the presence of dichlorvos, monocrotophos, omethoate and parathion. All OPPs significantly inhibited biomass (p < 0.05) and the expression of carbon cycle-related cbbLG gene (p < 0.01), and altered aquatic microbial community structure, interaction, and assembly. Variance partitioning analysis showed a stronger impact of pesticide type on microbial biomass and community structure, where pesticide concentration played more significant roles in carbon cycling. From analysis of cbbLG gene and PICRUSt2, Luteolibacter and Verrucomicrobiaceae assimilated inorganic carbon through Wood-Ljungdahl pathway, whereas it was Calvin-Benson-Bassham cycle for Cyanobium PCC-6307. This work provides a deeper insight into the behavior and mechanisms of microbial community change in aquatic system in response to OPPs, and explicitly unravels the impacts of OPPs on their carbon-cycling functions.

Device-Free Wireless Sensing for Gesture Recognition Based on Complementary CSI Amplitude and Phase.

By integrating sensing capability into wireless communication, wireless sensing technology has become a promising contactless and non-line-of-sight sensing paradigm to explore the dynamic characteristics of channel state information (CSI) for recognizing human behaviors. In this paper, we develop an effective device-free human gesture recognition (HGR) system based on WiFi wireless sensing technology in which the complementary CSI amplitude and phase of communication link are jointly exploited. To improve the quality of collected CSI, a linear transform-based data processing method is first used to eliminate the phase offset and noise and to reduce the impact of multi-path effects. Then, six different time and frequency domain features are chosen for both amplitude and phase, including the mean, variance, root mean square, interquartile range, energy entropy and power spectral entropy, and a feature selection algorithm to remove irrelevant and redundant features is proposed based on filtering and principal component analysis methods, resulting in the construction of a feature subspace to distinguish different gestures. On this basis, a support vector machine-based stacking algorithm is proposed for gesture classification based on the selected and complementary amplitude and phase features. Lastly, we conduct experiments under a practical scenario with one transmitter and receiver. The results demonstrate that the average accuracy of the proposed HGR system is 98.3% and that the F1-score is over 97%.

Comprehensive proteomic profiling of lung adenocarcinoma: development and validation of an innovative prognostic model.

Background: Lung adenocarcinoma (LUAD), a global leading cause of cancer deaths, remains inadequately addressed by current protein biomarkers. Our study focuses on developing a protein-based risk signature for improved prognosis of LUAD. Methods: We employed the least absolute shrinkage and selection operator (LASSO)-COX algorithm on The Cancer Genome Atlas database to construct a prognostic model incorporating six proteins (CD49B, UQCRC2, SMAD1, FOXM1, CD38, and KAP1). The model's performance was assessed using principal component, Kaplan-Meier (KM), and receiver operating characteristic (ROC) analysis, indicating strong predictive capability. The model stratifies LUAD patients into distinct risk groups, with further analysis revealing its potential as an independent prognostic factor. Additionally, we developed a predictive nomogram integrating clinicopathologic factors, aimed at assisting clinicians in survival prediction. Gene set enrichment analysis (GSEA) and examination of the tumor immune microenvironment were conducted, highlighting metabolic pathways in high-risk genes and immune-related pathways in low-risk genes, indicating varied immunotherapy sensitivity. Validation through immunohistochemistry from the Human Protein Atlas (HPA) database and immunofluorescence staining of clinical samples was performed, particularly focusing on CD38 expression. Results: Our six-protein model (CD49B, UQCRC2, SMAD1, FOXM1, CD38, KAP1) effectively categorized LUAD patients into high and low-risk groups, confirmed by principal component, KM, and ROC analyses. The model showed high predictive accuracy, with distinct survival differences between risk groups. Notably, CD38, traditionally seen as protective, was paradoxically associated with poor prognosis in LUAD, a finding supported by immunohistochemistry and immunofluorescence data. GSEA revealed that high-risk genes are enriched in metabolic pathways, while low-risk genes align with immune-related pathways, suggesting better immunotherapy response in the latter group. Conclusions: This study presented a novel prognostic protein model for LUAD, highlighting the CD38 expression paradox and enhancing our understanding of protein roles in lung cancer progression. It offered new clinical tools for prognosis prediction and provided assistance for future lung cancer pathogenesis research.

Association of residential greenness with incident pneumonia: A prospective cohort study.

Residential greenness is considered beneficial to human health, and its association with respiratory function has been found in previous studies. However, its link with pneumonia remains unclear. To explore the association of residential greenness with incident pneumonia, we conducted a prospective cohort study based on participants of the UK Biobank, followed from 2006 to 2010 to the end of 2019. Residential greenness was measured by Normalized Difference Vegetation Index (NDVI) within 500 m and 1000 m buffer. Cox proportional hazard models were conducted to assess the association, and restricted cubic spline models were also constructed to estimate their exposure-response relationship. Results demonstrate that residential greenness was negatively related to the risk of incident pneumonia. An interquartile (IQR) increase in NDVI 500-m buffer was associated with 4 % [HR (95 % CI) =0.96 (0.94, 0.97), P < 0.001] lower risk of incident pneumonia. Compared to the lowest greenness quartile (Q1), the highest quartile (Q4) had a lower risk of incident pneumonia, with the HR (95 % CI) estimated to be 0.91 (0.87, 0.95) (P values <0.001). Analyses based on NDVI 1000-m buffer obtained similar results. Furthermore, a significant effect of modifications by age and income on the linkage between residential greenness and incident pneumonia was found. These findings propose a potential effective prevention of incident pneumonia and provide the scientific basis for promoting the construction of residential greenness.

Comprehensive pan­cancer analysis of MTDH for human tumor prognosis and as an immunological biomarker including breast and kidney cancer.

Metadherin (MTDH), initially discovered in primary astrocytes of the human fetus through rapid subtraction hybridization and labeled as astrocyte elevated gene-1, represents a widely recognized oncogene present in multiple types of cancers. However, the role of MTDH in different types of cancer remains unclear. To address this, a comprehensive analysis of MTDH across various types of cancers was conducted by utilizing multiple databases such as The Cancer Genome Atlas. The present analysis discovered that MTDH exhibits differential expression in different types of cancer and is associated with important factors including tumor mutational burden and microsatellite instability. These findings highlighted the significance of MTDH in the tumor microenvironment and its involvement in the development of immune cells in specific cancers. Furthermore, the results of the present study indicated that the expression of MTDH is strongly correlated with clinical prognosis, mutations and immune cell infiltration. MTDH could serve as a potential indicator of patient prognosis and potentially play a role in modulating the immune system. Given its potential as a novel immunological checkpoint, MTDH may be a viable target for tumor immunotherapy.

Role of Regulatory T Cells in Intracerebral Hemorrhage.

Intracerebral hemorrhage (ICH) is a common cerebrovascular disease that can lead to severe neurological dysfunction in surviving patients, resulting in a heavy burden on patients and their families. When ICH occurs, the blood‒brain barrier is disrupted, thereby promoting immune cell migration into damaged brain tissue. As important immunosuppressive T cells, regulatory T (Treg) cells are involved in the maintenance of immune homeostasis and the suppression of immune responses after ICH. Treg cells mitigate brain tissue damage after ICH in a variety of ways, such as inhibiting the neuroinflammatory response, protecting against blood‒brain barrier damage, reducing oxidative stress damage and promoting nerve repair. In this review, we discuss the changes in Treg cells in ICH clinical patients and experimental animals, the mechanisms by which Treg cells regulate ICH and treatments targeting Treg cells in ICH, aiming to support new therapeutic strategies for clinical treatment.

The Polysaccharides from Pinellia ternata and Their Derivatives: Preparation, Structure Characteristics, and Activities in Vitro.

Three polysaccharides, PTC, PTH, and PTB, were extracted from Pinellia ternata using three different extraction conditions: room temperature water, hot water, and 2 % Na2CO3 solution. PTC and PTH were composed of rhamnose, glucose, galactose, mannose, glucuronic acid, galacturonic acid, and arabinose, which combine to form complex structures. PTB was composed solely of glucose and rhamnose. Further analysis indicated that PTC and PTB exhibited triple-helix structures. PTC showed the highest scavenging capacity against DPPH, superoxide anion, and hydroxyl radicals, with half maximal inhibitory concentrations (IC50) of 1004.1, 1584.1, and 1584.1 µg/mL, respectively. Additionally, PTC, PTH, and PTB were subjected to sulfation, phosphorylation, and selenization, resulting in the production of nine derivates. The distinctive absorptive bands of these derivates were determined through infrared spectroscopy. Selenized and sulfated derivates have shown significant antitumor and immunoenhancing properties. Our findings revealed that at 400 µg/mL, the inhibition rate of selenated PTB on HeLa cells was 54.2 % and that on HepG2 cells was 43.1 %. Additionally, selenized PTC displayed significant immunoenhancing activity, with a proliferation rate of 63.7 % at 400 µg/mL in RAW264.7 cells. These results provide valuable evidence supporting the consideration of polysaccharides from Pinellia ternata as a potential candidate for the development of antineoplastic drugs.

Brownification increases the abundance of microorganisms related to carbon and nitrogen cycling in shallow lakes.

Brownification in aquatic ecosystems under global change has attracted attention. The composition and quantity of dissolved organic matter transported from various land use types to lakes differ significantly, causing varying ecological effects of lake brownification by region. Bacterial communities make a significant contribution to the material cycle of ecosystems and are sensitive to environmental changes. In this study, a series of mesocosm systems were used to simulate forest lakes and urban lakes with different degrees of brownification, and a high-throughput amplicon sequencing technique was used to explore the changes in the composition, structure, and function of bacterial communities in shallow lakes undergoing brownification. Principal coordinate analysis (PCoA) and Jensen‒Shannon distance typing analysis both indicated significant differences in bacterial communities between forest lakes and urban lakes. The α diversity of bacterial communities in urban lakes increased with the degree of brownification. However, whether forest lakes or urban lakes, brownification increased the abundance of carbon cycling-related bacterial phyla (Proteobacteria, Poribacteria, and Chloroflexi) and nitrogen cycling-related bacterial genera (Microbacteriaceae, Limnohabitans, Comamonadaceae, Bacillus, and Rhizobiales_Incertae_Sedis). Additionally, the carbon and nitrogen cycling functions of bacterial communities in forest lakes are dominant, while those in urban lakes are dominated by functions related to light. Our study has preliminarily revealed that lake brownification promotes the growth of carbon and nitrogen cycling microorganisms, providing a new paradigm for understanding the response of lake ecosystems in different catchment areas to environmental changes and the carbon and nitrogen cycling processes in shallow lake ecosystems.