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Post-stroke cognitive impairment (PSCI) significantly affects stroke survivors. Identifying modifiable risk factors for PSCI is essential. Serum multi-trace elements are crucial for neurological function but vary in concentration among older adults. It remains unclear whether increasing multi-trace elements can reduce the incidence of PSCI. We investigated the associations between baseline serum multi-trace elements and PSCI. The Montreal Cognitive Assessment defined PSCI. We used logistic regression analyses to evaluate the association between serum multi-trace elements and PSCI. Subsequently, we assessed the associations between serum multi-trace elements and three different cognitive domains using the Kruskal–Wallis test. We further evaluated improvements in the predictive ability of serum multi-trace elements. Finally, 626 patients (mean age: 62.85 ± 7.54 years) were followed up for a median of 1.2 years. Lower concentrations of serum iron (odds ratio [OR] = 2.498, 95% confidence interval [CI]: 1.505–4.145) and zinc (OR = 2.015, 95% CI: 1.233–3.293) were associated with a higher PSCI risk. Higher concentrations of serum iron (OR = 0.368, 95% CI: 0.227–0.595) and magnesium (OR = 0.273, 95% CI: 0.164–0.454), along with lower concentrations of serum copper (OR = 0.544, 95% CI: 0.34–0.872), were significantly correlated with a lower PSCI risk. Cognitive impairments varied across multi-trace elements. Serum iron affected wider cognition, while magnesium and copper levels were strongly associated with language and executive function. Adding serum multi-trace elements to the conventional model improved PSCI risk reclassification (area under curve: 0.676–0.718). Multi-trace elements may influence PSCI progression. This study was registered with the Chinese Clinical Trial Registry (URL: https://www.chictr.org.cn/ ; unique identifier: ChiCTR1900022675).

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline and memory loss. Despite advances in understanding the pathophysiological mechanisms of AD, effective treatments remain scarce. Lithium salts, recognized as mood stabilizers in bipolar disorder, have been extensively studied for their neuroprotective effects. Several studies indicate that lithium may be a disease-modifying agent in the treatment of AD. Lithium’s neuroprotective properties in AD by acting on multiple neuropathological targets, such as reducing amyloid deposition and tau phosphorylation, enhancing autophagy, neurogenesis, and synaptic plasticity, regulating cholinergic and glucose metabolism, inhibiting neuroinflammation, oxidative stress, and apoptosis, while preserving mitochondrial function. Clinical trials have demonstrated that lithium therapy can improve cognitive function in patients with AD. In particular, meta-analyses have shown that lithium may be a more effective and safer treatment than the recently FDA-approved aducanumab for improving cognitive function in patients with AD. The affordability and therapeutic efficacy of lithium have prompted a reassessment of its use. However, the use of lithium may lead to potential side effects and safety issues, which may limit its clinical application. Currently, several new lithium formulations are undergoing clinical trials to improve safety and efficacy. This review focuses on lithium’s mechanism of action in treating AD, highlighting the latest advances in preclinical studies and clinical trials. It also explores the side effects of lithium therapy and coping strategies, offering a potential therapeutic strategy for patients with AD.

Natural products, with their extensive chemical diversity, distinctive biological activities, and vast reservoirs, provide a robust foundation for advancing cancer therapeutics. A comprehensive phytochemical investigation of the skins from Bufo bufo gargarizans afforded two new bufadienolide derivatives identified as bufalactamides A and B ( 1–2 ), along with six known compounds: argentinogenin (3) , desacetylcinobufagin ( 4 ), desacetylcinobufaginol ( 5 ), cinobufaginol ( 6 ), bufalin ( 7 ) and gamabufalin ( 8 ). The structural elucidation of these compounds was meticulously carried out by analyses of spectroscopic data (1D and 2D NMR, HR-ESIMS), and comparison with the literature data. Plausible biosynthetic pathways for the new compounds were also discussed. Moreover, the cytotoxicity of the compounds was investigated using various cancer cell lines, including lung cancer (A549), colon cancer (HCT-116), liver cancer (SK-Hep-1), and ovarian cancer (SKOV3). Our research findings indicated that compounds 3 , and 6 – 8 exhibit potent cytotoxic activity (IC 50  < 2.5 µM). In contrast, compounds 4 and 5 display moderate cytotoxic activity (IC 50  < 50 µM) while compounds 1 and 2 show no cytotoxic activity (IC 50  > 100 µM). From this data, we conducted a comprehensive analysis of the structure-activity relationships among these compounds.

Aeromonas salmonicida ( A . salmonicida ) is a pathogenic bacterium that causes furunculosis and poses a significant global risk, particularly in economic activities such as Atlantic salmon (Salmo salar) farming. In a previous study, we identified proteins that are significantly upregulated in kidneys of Atlantic salmon challenged with A . salmonicida . Phosphoproteomic analyses were conducted to further clarify the dynamic changes in protein phosphorylation patterns triggered by bacterial infection. To our knowledge, this is the first study to characterize phosphorylation events in proteins from A . salmonicida -infected Atlantic salmon. Overall, we identified over 5635 phosphorylation sites in 3112 proteins, and 1502 up-regulated and 77 down-regulated proteins quantified as a 1.5-fold or greater change relative to control levels. Based on the combined data from proteomic and motif analyses, we hypothesize that five prospective novel kinases (VRK3, GAK, HCK, PKCδ and RSK6) with common functions in inflammatory processes and cellular pathways to regulate apoptosis and the cytoskeleton could serve as potential biomarkers against bacterial propagation in fish. Data from STRING-based functional network analyses indicate that fga is the most central protein. Our collective findings provide new insights into protein phosphorylation patterns, which may serve as effective indicators of A . salmonicida infection in Atlantic salmon.

Despite being perennially frigid, polar oceans form an ecosystem hosting high and unique biodiversity. Various organisms show different adaptive strategies in this habitat, but how viruses adapt to this environment is largely unknown. Viruses of phyla Nucleocytoviricota and Mirusviricota are groups of eukaryote-infecting large and giant DNA viruses with genomes encoding a variety of functions. Here, by leveraging the Global Ocean Eukaryotic Viral database, we investigate the biogeography and functional repertoire of these viruses at a global scale. We first confirm the existence of an ecological barrier that clearly separates polar and nonpolar viral communities, and then demonstrate that temperature drives dramatic changes in the virus–host network at the polar–nonpolar boundary. Ancestral niche reconstruction suggests that adaptation of these viruses to polar conditions has occurred repeatedly over the course of evolution, with polar-adapted viruses in the modern ocean being scattered across their phylogeny. Numerous viral genes are specifically associated with polar adaptation, although most of their homologues are not identified as polar-adaptive genes in eukaryotes. These results suggest that giant viruses adapt to cold environments by changing their functional repertoire, and this viral evolutionary strategy is distinct from the polar adaptation strategy of their hosts. This study examines the biogeography and functional gene repertoires of marine eukaryote-infecting large and giant DNA viruses. It shows a clear divide in the viral communities between polar and nonpolar environments, with recurrent evolutionary adaptations to the polar environment likely driven by alterations of their genomic functions.

This study examined the influence mechanism of temperature on the interfacial shear strength (IFSS) between carbon fiber (CF) and epoxy resin (EP) matrices under various thermal loads using experimental and numerical simulation methods. To evaluate the change in IFSS as a function of the increase in temperature, a microbond test was performed under controlled temperature environment from 23°C to 150°C. The experimental results showed that IFSS values of CF/EP reduce significantly when the temperature reaches near glass transition temperature. To interpret the effect of thermal loads on IFSS, a thermal-mechanical coupling finite element model was used to simulate the process of fiber pull-out from EP. The results revealed that temperature dependence of IFSS is linked to modulus of the matrix as well as to the coefficients of thermal expansion of the fiber and matrix.

Liver fibrosis is a common pathological feature of chronic hepatic injury that currently lacks effective therapeutic interventions. Albiflorin (ALB), a pinane-type monoterpene derived from Paeonia lactiflora Pall, has notable anti-inflammatory and hepatoprotective effects. However, the potential role of ALB against liver fibrosis is largely unknown. In this study, we discovered that ALB significantly inhibited CCl 4 -induced liver fibrosis in mice. This was evidenced by improvements in liver and kidney function indexes, fibrosis indicators, and histopathological findings. In vitro studies also showed that ALB inhibited TGF-β1-induced LX-2 cell activation and reduced the expression of α-SMA and collagen I. Additionally, we found that ALB mitigates inflammation and ameliorates liver fibrosis by targeting the CXCL12/CXCR4 axis, as confirmed using the CXCR4 inhibitor AMD3100 in CCl 4 -treated mice. Notably, combining ALB with metformin (MET) enhanced the inhibition of liver fibrosis progression. These findings highlight that ALB exerts anti-liver fibrosis effects by targeting the CXCL12/CXCR4 axis, underscoring its potential as a standalone treatment or as an adjuvant therapy.

The origin of elemental chromium for the archaeological weapons from the pits of Qin terracotta warriors in China has been highly controversial. Although previous studies have highlighted that the chromium on the surface of weapon originated from the contamination of surrounding lacquer, the exact origin of chromium in the lacquer remains unclear. In this work, the measurement by inductively coupled plasma-mass spectrometer (ICP-MS) firstly confirmed that the elemental chromium was indeed contained in the archaeological Qin original lacquer. Nevertheless, the amount of elemental chromium in the Qin lacquer was as low as 0.0759 μg/mg, disclosing that it was impossible to artificially add extra refined chromium-containing substance to the lacquer in the preparation of the terracotta warriors. The soil from the archaeological site of Qin lacquer was found to have a chromium amount of 0.0660 μg/mg by ICP-MS. After the hygrothermal and soil-buried aging cycles for the lab-prepared lacquer, the surface and depth elemental analyses by time of flight-secondary ion mass spectrometer (TOF–SIMS) showed a gradient distribution of elemental chromium from the surface to interior of aged lacquer, indicating the migration and enrichment behavior of elemental chromium from the burial soil towards the lacquer. To explore the migration mechanism of elemental chromium, fluorescence imaging technique was employed in combination with Fourier transform infrared spectrometry (FT-IR) and X-ray photoelectron spectroscopy (XPS) characterizations. The results revealed that catechol-containing fragments were formed during hygrothermal and soil-buried aging of lacquer and consequently coordinated with chromium ions, inducing the migration of elemental chromium towards the lacquer.

NCLDVs can infect a wide range of eukaryotes, although their life cycle is less dependent on hosts compared to other viruses. However, our understanding of NCLDV-host systems is highly limited because few of these viruses have been isolated so far. Nucleocytoplasmic large DNA viruses (NCLDVs) are highly diverse and abundant in marine environments. However, the knowledge of their hosts is limited because only a few NCLDVs have been isolated so far. Taking advantage of the recent large-scale marine metagenomics census, in silico host prediction approaches are expected to fill the gap and further expand our knowledge of virus-host relationships for unknown NCLDVs. In this study, we built co-occurrence networks of NCLDVs and eukaryotic taxa to predict virus-host interactions using Tara Oceans sequencing data. Using the positive likelihood ratio to assess the performance of host prediction for NCLDVs, we benchmarked several co-occurrence approaches and demonstrated an increase in the odds ratio of predicting true positive relationships 4-fold compared to random host predictions. To further refine host predictions from high-dimensional co-occurrence networks, we developed a phylogeny-informed filtering method, Taxon Interaction Mapper, and showed it further improved the prediction performance by 12-fold. Finally, we inferred virophage-NCLDV networks to corroborate that co-occurrence approaches are effective for predicting interacting partners of NCLDVs in marine environments. IMPORTANCE NCLDVs can infect a wide range of eukaryotes, although their life cycle is less dependent on hosts compared to other viruses. However, our understanding of NCLDV-host systems is highly limited because few of these viruses have been isolated so far. Co-occurrence information has been assumed to be useful to predict virus-host interactions. In this study, we quantitatively show the effectiveness of co-occurrence inference for NCLDV host prediction. We also improve the prediction performance with a phylogeny-guided method, which leads to a concise list of candidate host lineages for three NCLDV families. Our results underpin the usage of co-occurrence approaches for the metagenomic exploration of the ecology of this diverse group of viruses.

Background Septic heart failure accounts for high mortality rates globally. With a strong reducing capacity, zero-valent iron nanoparticles (nanoFe) have been applied in many fields. However, the precise roles and mechanisms of nanoFe in septic cardiomyopathy remain unknown. Results NanoFe was prepared via the liquid-phase reduction method and functionalized with the biocompatible polymer sodium carboxymethylcellulose (CMC). We then successfully constructed a mouse model of septic myocardial injury by challenging with cecal ligation and puncture (CLP). Our findings demonstrated that nanoFe has a significant protective effect on CLP-induced septic myocardial injury. This may be achieved by attenuating inflammation and oxidative stress, improving mitochondrial function, regulating endoplasmic reticulum stress, and activating the AMPK pathway. The RNA-seq results supported the role of nanoFe treatment in regulating a transcriptional profile consistent with its role in response to sepsis. Conclusions The results provide a theoretical basis for the application strategy and combination of nanoFe in sepsis and septic myocardial injury. Graphical Abstract