Functional connectome gradient predicts clinical symptoms of chronic insomnia disorder.

Insomnia is the second most prevalent psychiatric disorder worldwide, but the understanding of the pathophysiology of insomnia remains fragmented. In this study, we calculated the connectome gradient in 50 chronic insomnia disorder (CID) patients and 38 healthy controls (HC) to assess changes due to insomnia and utilized these gradients in a connectome-based predictive modeling (CPM) to predict clinical symptoms associated with insomnia. The results suggested that insomnia led to significant alterations in the functional gradients of some brain areas. Specifically, the gradient scores in the middle frontal gyrus, superior anterior cingulate gyrus, and right nucleus accumbens were significantly higher in the CID patients than in the HC group, whereas the scores in the middle occipital gyrus, right fusiform gyrus, and right postcentral gyrus were significantly lower than in the HC group. Further correlation analysis revealed that the right middle frontal gyrus is positively correlated with the self-rating anxiety scale (r=0.3702). Additionally, the prediction model built with functional gradients could well predict the sleep quality (r=0.5858), anxiety (r=0.6150), and depression (r=0.4022) levels of insomnia patients. This offers an objective depiction of the clinical diagnosis of insomnia, yielding a beneficial impact on the identification of effective biomarkers and the comprehension of insomnia.

Diiron Complexes with Rigid and Conjugated S-to-S Bridges for Electrocatalytic Reduction of CO2.

Electroreduction of CO2 to value-added low-carbon chemicals is a promising way for carbon neutrality and CO2 utilization. It was found that the diiron complex [(µ-bdt)Fe2(CO)6] (bdt = benzene-1,2-dithiolate) has high catalytic activity for electrocatalytic CO2 reduction. To further study the effect of the S-to-S bridge on the catalytic performances of diiron complexes for electrochemical CO2 reduction, four diiron complexes 1-4 with different rigid and conjugated S-to-S bridges were either selected or designed. The electrocatalytic studies showed that under optimal conditions, 2 with a 2,3-naphthalenedithiolato bridge exhibited the lowest catalytic onset potential (Eonset = -1.75 V vs Fc+/0), while 4 with a diphenyl-1,2-vinylidene bridge displayed the highest catalytic activity (TOFmax = 295 s-1), which is 1.5 times that of [(µ-bdt)Fe2(CO)6]. The controlled potential electrolysis experiments of 4 in 0.1 M MeOH/MeCN at -2.35 V vs Fc+/0 gave a total faradaic yield close to 100%, with selectivities of 77%, 9%, and 14% for HCOOH, CO, and H2, respectively. The mechanism for CO2 reduction was studied using density functional theory, IR spectroelectrochemistry, and electrochemical methods. The results indicate that modifying the structure of the S-to-S bridge is an effective strategy to improve the catalytic performance of diiron complexes for electrocatalytic CO2 reduction.

ZC3H13-Mediated m6A Modification Ameliorates Acute Myocardial Infarction through Preventing Inflammation, Oxidative Stress and Ferroptosis by Targeting lncRNA93358.

BACKGROUND: Acute myocardial infarction (AMI) is a life-threatening event that is associated with RNA modification and programmed cell death (PCD). This study attempted to investigate the impacts of zinc finger CCCH domain-containing protein 13 (ZC3H13)-mediated N6-methyladenosine (m6A) on ferroptosis in AMI. METHODS: The infarcted areas and cardiac function were evaluated, and the expression level of ZC3H13 was measured in AMI rats that were induced by isoproterenol. Meanwhile, oxygen glucose deprivation (OGD) in vitro model was induced to investigate the alterations on inflammation, oxidative stress and ferroptosis. The m6A modification site of lncRNA93358 modified by ZC3H13 was predicted using bioinformatics, and the interaction between ZC3H13 and lncRNA93358 was verified using the dual-luciferase reporter assays. ZC3H13 was overexpressed and lncRNA93358 was silenced to study their regulatory role in cell death, inflammation, oxidative stress and ferroptosis in AMI. RESULTS: Significant decreased expression of ZC3H13 was observed in AMI rats, with impaired cardiac function, enhanced inflammation and oxidative stress. ZC3H13 targeted the modification site GGACC of lncRNA93358 and downregulated lncRNA93358. Silencing lncRNA93358 inhibited cell death, reduced the levels of inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1ß, suppressed oxidative stress-related indicators (lactate dehydrogenase (LDH), reactive oxygen species (ROS), glutathione (GSH) and malondialdehyde (MDA), as well as downregulated ferroptosis-related acyl-CoA synthetase long chain family member 4 (ACSL4), prostaglandin-endoperoxide synthase 2 (PTGS2) and glutathione peroxidase 4 (GPX4). The effect of silencing lncRNA93358 was further enhanced by overexpression of ZC3H13. CONCLUSION: This study reveals the ZC3H13-mediated epigenetic RNA modification targeting lncRNA93358 and suggests that ZC3H13 overexpression may be a promising approach for AMI treatment.

Exact test and exact confidence interval for the Cox model.

The Cox proportional hazards model is commonly used to analyze time-to-event data in clinical trials. Standard inference procedures for the Cox model are based on asymptotic approximations and may perform poorly when there are few events in one or both treatment groups, as may be the case when the event of interest is rare or when the experimental treatment is highly efficacious. In this article, we propose an exact test of equivalence and efficacy under a proportional hazard model with treatment effect as the only fixed effect, together with an exact confidence interval that is obtained by inverting the exact test. The proposed test is based on a conditional error method originally proposed for sample size reestimation problems. In the present context, the conditional error method is used to combine information from a sequence of hypergeometric distributions, one at each observed event time. The proposed procedures are evaluated in simulation studies and illustrated using real data from an HIV prevention trial. A companion R package "ExactCox" is available for download on CRAN.

Adaptive self-supervised learning for sequential recommendation.

Sequential recommendation typically utilizes deep neural networks to mine rich information in interaction sequences. However, existing methods often face the issue of insufficient interaction data. To alleviate the sparsity issue, self-supervised learning is introduced into sequential recommendation. Despite its effectiveness, we argue that current self-supervised learning-based (i.e., SSL-based) sequential recommendation models have the following limitations: (1) using only a single self-supervised learning method, either contrastive self-supervised learning or generative self-supervised learning. (2) employing a simple data augmentation strategy in either the graph structure domain or the node feature domain. We believe that they have not fully utilized the capabilities of both self-supervised methods and have not sufficiently explored the advantages of combining graph augmentation schemes. As a result, they often fail to learn better item representations. In light of this, we propose a novel multi-task sequential recommendation framework named Adaptive Self-supervised Learning for sequential Recommendation (ASLRec). Specifically, our framework combines contrastive and generative self-supervised learning methods adaptively, simultaneously applying different perturbations at both the graph topology and node feature levels. This approach constructs diverse augmented graph views and employs multiple loss functions (including contrastive loss, generative loss, mask loss, and prediction loss) for joint training. By encompassing the capabilities of various methods, our model learns item representations across different augmented graph views to achieve better performance and effectively mitigate interaction noise and sparsity. In addition, we add a small proportion of random uniform noise to item representations, making the item representations more uniform and mitigating the inherent popularity bias in interaction records. We conduct extensive experiments on three publicly available benchmark datasets to evaluate our model. The results demonstrate that our approach achieves state-of-the-art performance compared to 14 other competitive methods: the hit rate (HR) improved by over 14.39%, and the normalized discounted cumulative gain (NDCG) increased by over 18.67%.

Loss of histone deubiquitinase Bap1 triggers anti-tumor immunity.

PURPOSE: Immunotherapy using PD-L1 blockade is effective in only a small group of cancer patients, and resistance is common. This emphasizes the importance of understanding the mechanisms of cancer immune evasion and resistance. METHODS: A genome-scale CRISPR-Cas9 screen identified Bap1 as a regulator of PD-L1 expression. To measure tumor size and survival, tumor cells were subcutaneously injected into both syngeneic WT mice and immunocompromised mice. The phenotypic and transcriptional characteristics of Bap1-deleted tumors were examined using flow cytometry, RNA-seq, and CUT&Tag-seq analysis. RESULTS: We found that loss of histone deubiquitinase Bap1 in cancer cells activates a cDC1-CD8+ T cell-dependent anti-tumor immunity. The absence of Bap1 leads to an increase in genes associated with anti-tumor immune response and a decrease in genes related to immune evasion. As a result, the tumor microenvironment becomes inflamed, with more cDC1 cells and effector CD8+ T cells, but fewer neutrophils and regulatory T cells. We also found that the elimination of Bap1-deleted tumors depends on the tumor MHCI molecule and Fas-mediated CD8+ T cell cytotoxicity. Our analysis of TCGA data further supports these findings, showing a reverse correlation between BAP1 expression and mRNA signatures of activated DCs and T-cell cytotoxicity in various human cancers. CONCLUSION: The histone deubiquitinase Bap1 could be used as a biomarker for tumor stratification and as a potential therapeutic target for cancer immunotherapies.

An adaptive cycle resilience perspective to understand the regime shifts of social-ecological system interactions over the past two millennia in the Tarim River Basin.

Socio-ecological systems (SESs) in arid regions have experienced multiple transformations throughout history due to human activities and natural forces. However, few studies have used the resilience cycle model to explain the resilience status and determinants of SESs over the past two millennia. This study proposes the adaptive cycle resilience (ACR) perspective to investigate regime shifts of socio-ecological system interactions in the Tarim River Basin (TRB) over the past two millennia. An ACR framework combining a piecewise linear regression model (PLR), ACR theory, and physical resilience models has been built to assess and quantify socio-ecological system resilience. Key indicators such as climate variability, settlement numbers, war frequency, glacier accumulation, and oasis area changes are identified and quantified to evaluate SESs adaptability and transformability. Glacier accumulation serves as a proxy for long-term climate change, while oasis area changes reflect the direct impact of human activities and environmental feedback on ecosystem productivity. Population and war indicators provide insights into social system stability and the impact of conflicts on SESs dynamics. The findings reveal that the 7th century and 1850s are critical points of regime shifts in the ACR. 200s BC-350s AD and 700s AD-900s AD are in the forward loop (r-K) period of the ACR. 350s AD-700s AD and 900s AD-1850s AD are the adaptive resilience backward loop (Ω-α) phase. Assessing the historical socio-ecological system resilience and identifying key transition points can inform proactive measures to mitigate potential regime shifts. Combining historical data with resilience theory provides a deep understanding of the ACR of SESs and their driving factors. This enriches the theoretical understanding of SESs and offers a robust case study for future resilience assessments and scenario analyses in arid regions.

Mechanistic insights on the preparation of 5-methyl-2-hexanone by hydrogenation of 5-methyl-3-hexen-2-one using Pd/Al2O3 catalysts.

5-methyl-2-hexanone is used as a versatile polymerization solvent for industrial preparation processes of bulk and fine chemicals. An efficient catalyst, Pd/γ-Al2O3, is reported for the preparation of 5-methyl-2-hexanone by selective hydrogenation of 5-methyl-3-hexen-2-one. The catalyst exhibits remarkable activity and selectivity even at atmospheric pressure and low temperature (1 atm, 80 °C). The influence weight of reaction conditions on the reaction process was obtained through the Artificial Neural Network model, which were reaction pressure, reaction temperature and liquid hourly space velocity in order. The reaction kinetics and mechanism of 5-methyl-2-hexanone preparation by hydrogenation over Pd/γ-Al2O3 catalyst were investigated. The hydrogenation reaction pathway of 5-methyl-3-hexen-2-one was obtained by using Density functional theory calculations, and the mechanism of selective hydrogenation of CC double bonds and CO double bonds was revealed. A kinetic model based on the LHHW model assumption was also proposed and compared with experimental results demonstrating good predictability.

Occurrence and potential diffusion of pine wilt disease mediated by insect vectors in China under climate change.

BACKGROUND: Pine wilt disease (PWD), a major international quarantined forest pest, causes serious ecological and economic damage to Pinus species in Asia and Europe. In China, PWD has spread northeasterly and northwesterly beyond its original northern limits. Consequently, an evaluation of the insect vector-mediated occurrence and potential diffusion of PWD is needed to identify important transmission routes and control the spread of disease. RESULTS: An optimized MaxEnt model was used to assess the current and future geographical distribution of Bursaphelenchus xylophilus and its insect vectors in China. The predicted suitable area for B. xylophilus colonization is currently 212.32 × 104 km2 and mainly concentrated in Central, East, Southwest and South China, although is anticipated to include the northwestern regions of China in the future. As for the insect vectors, Monochamus alternatus and M. saltuarius are expected to spread toward the northwest and southwest, respectively. The maximum predicted dispersion area of PWD mediated by M. alternatus, M. saltuarius and both species was 91.85 × 104, 218.76 × 104 and 29.99 × 104 km2, respectively, with potential diffusion areas being anticipated to increase in the future. Both the suitable probabilities and areas of B. xylophilus and its insect vectors were found to vary substantially along the latitudinal gradient, with the latitudinal range of these species being predicted to expand in the future. CONCLUSION: This is the first study to investigate the potential diffusion areas of PWD mediated by insect vectors in China, and our finding will provide a vital theoretical reference and empirical basis for developing more effective management strategies for the control of PWD in China. © 2024 Society of Chemical Industry.

AQP4-AS1 Can Regulate the Expression of Ferroptosis-Related Regulator ALOX15 through Competitive Binding with miR-4476 in Lung Adenocarcinoma.

Background The AQP4-AS1/miR-4476-ALOX15 regulatory axis was discovered in previous studies. We aimed to investigate the regulatory mechanism of the ferroptosis-related regulator ALOX15 by AQP4-AS1 and miR-4476 in lung adenocarcinoma (LUAD) and find new targets for clinical treatment. Methods After bioinformatics analysis, we contained one ferroptosis-related gene (FRG), namely ALOX15. MicroRNAs (miRNAs) and long noncoding RNAs were predicted by miRWalk. Furthermore, we constructed overexpressed LUAD cell lines. Real-time quantitative polymerase chain reaction and western blot were used to determine the expression of mRNA and protein, respectively. Cell Counting Kit-8 (CCK-8) and EdU assay were used to detect the cell proliferation. Double luciferase assay was used to detect the binding relationship between AQP4-AS1 and miR-4464. Results ALOX15 was the most significantly downregulated FRG compared with normal tissues. Furthermore, protein-protein interaction network analysis indicated that the AQP4-AS1-miR-4476-ALOX15 regulatory axis might be involved in the occurrence and development of LUAD and there might be direct interaction between AQP4-AS1 and miR-4476, and miR-4476 and ALOX15. Furthermore, AQP4-AS1 and ALOX15 were significantly downregulated in the LUAD tissue and cell lines, whereas miR-4476 showed the opposite results ( p < 0.001). AQP4-AS1 overexpression improved the ALOX15 expression in LUAD cell lines. CCK-8 and EdU assay revealed that overexpression of AQP4-AS1 and ALOX15 inhibited the LUAD cell proliferation. Double luciferase assay results indicated that there was a combination between AQP4-AS1 and miRNA-4476. In addition, we found that overexpressed AQP4-AS1 activates the ferroptosis in LUAD cell lines. Conclusions AQP4-AS1 can regulate the expression of ALOX15 through competitive binding with miR-4476, further activate ferroptosis and inhibit the proliferation of LUAD cells.

Revealing the Effect of the Microstructure on Potassium Storage Behavior in a Two-Dimensional Mesoporous Carbon Anode.

Hard carbon is considered as the most promising anode material for potassium-ion energy storage devices. Substantial progress has been made in exploring advanced hard carbons to solve the issues of sluggish kinetics and large volume changes caused by the large radius of K+. However, the relationship between their complicated microstructures and the K+ charge storage behavior is still not fully explored. Herein, a series of two-dimensional mesoporous carbon microcoins (2D-MCMs) with tunable microstructures in heteroatom content and graphitization degree are synthesized by a facile hard-template method and follow a temperature-controllable annealing process. It is found that high heteroatom content makes for surface-driven K+ storage behavior, which increases the capacity-contribution ratio from a high potential region, while a high graphitization degree makes for K+ intercalation behavior, which increases the capacity-contribution ratio from a low potential region. Electrochemical results from a three-electrode Swagelok cell demonstrate that a 2D-MCM anode with more capacity contribution from a low working region allows the porous carbon cathode to be operated in a much wider electrochemical window, thus storing more charge. As a result, potassium-ion capacitors based on the optimized 2D-MCM anode deliver a high energy density of 113 Wh kg-1 and an exhilarating power density of 51,000 W kg-1.

Application of spatial omics in gastric cancer.

Gastric cancer (GC), a globally prevalent and lethal malignancy, continues to be a key research focus. However, due to its considerable heterogeneity and complex pathogenesis, the treatment and diagnosis of gastric cancer still face significant challenges. With the rapid development of spatial omics technology, which provides insights into the spatial information within tumor tissues, it has emerged as a significant tool in gastric cancer research. This technology affords new insights into the pathology and molecular biology of gastric cancer for scientists. This review discusses recent advances in spatial omics technology for gastric cancer research, highlighting its applications in the tumor microenvironment (TME), tumor heterogeneity, tumor genesis and development mechanisms, and the identification of potential biomarkers and therapeutic targets. Moreover, this article highlights spatial omics' potential in precision medicine and summarizes existing challenges and future directions. It anticipates spatial omics' continuing impact on gastric cancer research, aiming to improve diagnostic and therapeutic approaches for patients. With this review, we aim to offer a comprehensive overview to scientists and clinicians in gastric cancer research, motivating further exploration and utilization of spatial omics technology. Our goal is to improve patient outcomes, including survival rates and quality of life.

Epitaxy of Monoclinic VO2 on Large-Misfit 3m Template Enabled by a Metastable Interfacial Layer.

We report the epitaxial growth of a monoclinic VO2 thin film on the CoFe2O4(111) template, assisted by an interfacial layer of the metastable orthorhombic phase. The interface between orthorhombic VO2 and CoFe2O4 is atomically sharp without noticeable interfacial diffusion. The (010)-faceted orthorhombic VO2 layer is lattice-matched to both the CoFe2O4(111) template and the monoclinic phase, although they have different surface symmetries. The occurrence of an orthorhombic VO2 thin layer significantly lowers the in-plane misfit strains of the monoclinic VO2 epilayer, along both the [100] and [001] axes. Our first-principles calculations confirm that the low-misfit orthorhombic VO2 is preferred on CoFe2O4(111) over the large-misfit monoclinic phase, at the initial growth stage. Additionally, upon increasing the film thickness to ∼8 nm, the orthorhombic phase is no longer favored, and the bulk stable monoclinic VO2 appears to minimize the free energy of the system. Moreover, we show that the metal-to-insulator transition of our VO2 epilayer can be efficiently triggered by both the temperature and Joule self-heating effect.

Recent Development of Biodegradable Occlusion Devices for Intra-Atrial Shunts.

Atrial septal defect (ASD) is the third most common type of structural congenital heart defect. Patent foramen ovale (PFO) is an anatomical anomaly in up to 25% of the general population. With the innovation of occlusion devices and improvement of transcatheter techniques, percutaneous closure has become a first-line therapeutic alternative for treatment of ASD and PFO. During the past few decades, the development of biodegradable occlusion devices has become a promising direction for transcatheter closure of ASD/PFO due to their biodegradability and improved biocompatibility. The purpose of this review is to comprehensively summarize biodegradable ASD/PFO occlusion devices, regarding device design, materials, biodegradability, and evaluation of animal or clinical experiments (if available). The current challenges and the research direction for the development of biodegradable occluders for congenital heart defects are also discussed.

miR-590-3p Overexpression Improves the Efficacy of hiPSC-CMs for Myocardial Repair.

Recent evidence demonstrates that low engraftment rates limit the efficacy of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) for cardiac repair after myocardial infarction. In this study, we attempted to overcome this limitation by enhancing the proliferative capacity of transplanted hiPSC-CMs. We found that miR-590-3p overexpression increased the proliferative capacity of hiPSC-CMs. miR-590-3p overexpression increased the number of engrafted cells and had a higher efficacy for myocardial repair than control cells. Moreover, we confirmed the safety of using miR-590-3p-overexpressing hiPSC-CMs in pig hearts. These results indicated that miR-590-3p overexpression stimulated hiPSC-CM cell cycle re-entry to induce cell proliferation and increased the therapeutic efficacy in MI.

Effect of Dynamic High-Pressure Microfluidization on the Quality of Not-from-Concentrate Cucumber Juice.

The effects of dynamic high-pressure microfluidization (DHPM at 400 MPa) and heat treatment (HT) on the microbial inactivation, quality parameters, and flavor components of not-from-concentrate (NFC) cucumber juice were investigated. Total aerobic bacteria, yeasts and molds were not detected in the 400 MPa-treated cucumber juice. Total phenolic content increased by 16.2% in the 400 MPa-treated cucumber juice compared to the control check (CK). The significant reduction in pulp particle size (volume peak decreasing from 100-1000 µm to 10-100 µm) and viscosity increased the stability of the cucumber juice while decreasing the fluid resistance during processing. HT decreased the ascorbic acid content by 25.9% (p < 0.05), while the decrease in ascorbic acid content was not significant after 400 MPa treatment. A total of 59 volatile aroma substances were identified by gas chromatography-ion mobility spectrometry (GC-IMS), and a variety of characteristic aroma substances (i.e., valeraldehyde, (E)-2-hexenal, (E)-2-nonenal, and (E,Z)-2,6-nonadienal, among others) were retained after treatment with 400 MPa. In this study, DHPM technology was innovatively applied to cucumber juice processing with the aim of providing a continuous non-thermal processing technology for the industrial production of cucumber juice. Our results provide a theoretical basis for the application of DHPM technology in cucumber juice production.

PER2 binding to PDK1 enhances the cisplatin sensitivity of oral squamous cell carcinoma through inhibition of the AKT/mTOR pathway.

Cisplatin (CDDP) is a cornerstone chemotherapeutic agent used to treat oral squamous cell carcinoma (OSCC) and many solid cancers. However, the mechanisms underlying tumor resistance to CDDP obscure the enhancement of its therapeutic efficacy. In this study, we unveil diminished expression of the biological clock gene PER2 in OSCC, negatively correlated with the expression of multidrug resistance protein 1 (MDR1) and multidrug resistance-associated protein 1 (MRP1). The overexpression of PER2 suppressed MDR1 and MRP1 expression and increased intracellular CDDP levels and DNA damage, thereby bolstering OSCC cell sensitivity to CDDP. In vivo tumorigenic assays corroborated that PER2 overexpression notably increased OSCC sensitivity to CDDP, augmenting the suppression of OSCC tumorigenesis. Co-immunoprecipitation, GST pull-down, and cycloheximide tracking assays revealed that PER2, via its C-terminal domain, bound to and diminishes PDK1 stability. The degradation of PDK1 was further dependent on the suppression of the AKT/mTOR pathway to enhance the sensitivity of OSCC cells to CDDP. Our study supports PER2 as a target for improving CDDP sensitivity in OSCC, and the combination of PER2 and CDDP is a novel strategy with potential clinical therapeutic value.

Lysine methylation modifications in tumor immunomodulation and immunotherapy: regulatory mechanisms and perspectives.

Lysine methylation is a crucial post-translational modification (PTM) that significantly impacts gene expression regulation. This modification not only influences cancer development directly but also has significant implications for the immune system. Lysine methylation modulates immune cell functions and shapes the anti-tumor immune response, highlighting its dual role in both tumor progression and immune regulation. In this review, we provide a comprehensive overview of the intrinsic role of lysine methylation in the activation and function of immune cells, detailing how these modifications affect cellular processes and signaling pathways. We delve into the mechanisms by which lysine methylation contributes to tumor immune evasion, allowing cancer cells to escape immune surveillance and thrive. Furthermore, we discuss the therapeutic potential of targeting lysine methylation in cancer immunotherapy. Emerging strategies, such as immune checkpoint inhibitors (ICIs) and chimeric antigen receptor T-cell (CAR-T) therapy, are being explored for their efficacy in modulating lysine methylation to enhance anti-tumor immune responses. By targeting these modifications, we can potentially improve the effectiveness of existing treatments and develop novel therapeutic approaches to combat cancer more effectively.

New Progress on DNA Primase Subunit Enzymes Research and Link to Cancer Development and Treatment Approaches.

In eukaryotic cells, primases are the key polymerase during DNA replication and DNA damage repair, which includes primase subunit 1 (PRIM1) and primase subunit 2 (PRIM2). Recent studies reported that the aberrant expression and activity of PRIM enzymes are closely associated with the carcinogenesis and development of various cancers. PRIM1 is overexpressed in hepatocellular carcinoma, breast cancer, and other cancers, while PRIM2 is highly expressed in lung cancer, gastrointestinal cancer, and other cancers. Further studies revealed that the knockdown of PRIM1 promoted the apoptosis of liver cancer cells, while Dihydroartemisinin (DHA) can inhibit PRIM2 expression, suppress lung cancer cell proliferation, and result in ferroptosis. The present review summarized the recent advancements in the research of the aberrant expression of PRIM1 and PRIM2 and their activity in DNA replication, DNA damage repair, and carcinogenesis. Furthermore, the strategies targeting PRIM1 or/and PRIM2 become potential therapeutic approaches in cancer treatment.

The Alarming Situation of Highly Pathogenic Avian Influenza Viruses in 2019-2023.

Avian influenza viruses (AIVs) have the potential to cause severe illness in wild birds, domestic poultry, and humans. The ongoing circulation of highly pathogenic avian influenza viruses (HPAIVs) has presented significant challenges to global poultry industry and public health in recent years. This study aimed to elucidate the circulation of HPAIVs during 2019 to 2023. Specifically, we assess the alarming global spread and continuous evolution of HPAIVs. Moreover, we discuss their transmission and prevention strategies to provide valuable references for future prevention and control measures against AIVs.