Organic fertilizer improved the lead and cadmium metal tolerance of Eucalyptus camaldulensis by enhancing the uptake of potassium, phosphorus, and calcium.

Phytoremediation is a strategy for the amelioration of soil heavy metal contamination that aligns with ecological sustainability principles. Among the spectrum of phytoremediation candidates, woody plants are considered particularly adept for their substantial biomass, profound root systems, and non-participation in the food chain. This study used Eucalyptus camaldulensis-a tree species characterized for its high biomass and rapid growth rate-to assess its growth and metal uptake in mining tailings. The results were as follows: exposure to heavy metals reduced the E. camaldulensis uptake of potassium (K), phosphorus (P), and calcium (Ca). Heavy metal stress negatively affected the biomass of E. camaldulensis. Lead (Pb) primarily accumulated in the roots, while cadmium (Cd) predominantly accumulated in the stems. The application of organic fertilizers bolstered the stress tolerance of E. camaldulensis, mitigating the adverse impacts of heavy metal stress. A synergistic effect occurred when organic fertilizers were combined with bacterial fertilizers. The plant's enrichment capacity for Cd and its tolerance to Pb was augmented through the concurrent application of bacterial and organic fertilizers. Collectively, the application of organic fertilizers improved the heavy metal tolerance of E. camaldulensis by enhancing the uptake of K, P, and Ca and elevating the content of glutathione peroxidase (GPX) and gibberellin acid (GA) in roots. These findings provided nascent groundwork for breeding E. camaldulensis with enhanced heavy metal tolerance. Moreover, this proved the potentiality of E. camaldulensis for the management of heavy metal-contaminated tailings and offers a promising avenue for future environmental restoration.

Design and Antimalarial Evaluation of Polydopamine-Modified Methyl Artelinate Nanoparticles.

Targeted nanodrug delivery systems are highly anticipated for the treatment of malaria. It is known that Plasmodium can induce new permeability pathways (NPPs) on the membrane of infected red blood cells (iRBCs) for their nutrient uptake. The NPPs also enable the uptake of nanoparticles (NPs) smaller than 80 nm. Additionally, Plasmodium maintains a stable, slightly acidic, and reductive internal environment with higher glutathione (GSH) levels. Based on this knowledge, methyl artelinate (MA, a prodrug-like derivative of dihydroartemisinin) nanoparticles (MA-PCL-NPs) were developed using poly(ethylene glycol)-b-poly(ε-caprolactone) (mPEG-PCL) by a thin-film dispersion method and were further coated with polydopamine (PDA) to obtain MA-PCL@PDA-NPs with a particle size of ∼30 nm. The biomaterial PDA can be degraded in slightly acidic and reductive environments, thereby serving as triggers for drug release. MA could generate reactive oxygen species and decrease GSH levels, consequently causing parasite damage. The in vitro release experiment results indicated that the cumulative release percentage of MA from MA-PCL@PDA-NPs was considerably higher in phosphate buffer with 10 mM GSH at pH 5.5 (88.10%) than in phosphate buffer without GSH at pH 7.4 (16.98%). The green fluorescence within iRBCs of coumarin 6, the probe of NPs (C6-PCL@PDA-NPs), could be reduced significantly after adding the NPP inhibitor furosemide (p < 0.001), which demonstrated that MA-PCL@PDA-NPs could be ingested into iRBCs through NPPs. In vivo antimalarial pharmacodynamics in Plasmodium berghei K173-bearing mice showed that the inhibition ratio of MA-PCL@PDA-NPs (93.96%) was significantly higher than that of commercial artesunate injection (AS-Inj, 63.33%). The above results showed that the developed MA-PCL@PDA-NPs possessed pH-GSH dual-responsive drug release characteristics and targeting efficacy for iRBCs, leading to higher antimalarial efficacy against Plasmodium.

Inter3D: Capture of TAD Reorganization Endows Variant Patterns of Gene Transcription.

Topologically associating domain (TAD) reorganization commonly occurs in the cell nucleus and contributes to gene activation and inhibition through the separation or fusion of adjacent TADs. However, functional genes impacted by TAD alteration and the underlying mechanism of TAD reorganization regulating gene transcription remain to be fully elucidated. Here, we first developed a novel approach termed Inter3D to specifically identify genes regulated by TAD reorganization. Our study revealed that the segregation of TADs led to the disruption of intrachromosomal looping at the myosin light chain 12B (MYL12B) locus, via the meticulous reorganization of TADs mediating epigenomic landscapes within tumor cells, thereby exhibiting a significant correlation with the down-regulation of its transcriptional activity. Conversely, the fusion of TADs facilitated intrachromosomal interactions, suggesting a potential association with the activation of cytochrome P450 family 27 subfamily B member 1 (CYP27B1). Our study provides comprehensive insight into the capture of TAD rearrangement-mediated gene loci and moves toward understanding the functional role of TAD reorganization in gene transcription. The Inter3D pipeline developed in this study is freely available at https://github.com/bm2-lab/inter3D and https://ngdc.cncb.ac.cn/biocode/tool/BT7399.

Serum metabolite signature of the modified Mediterranean-DASH intervention for neurodegenerative delay (MIND) diet.

INTRODUCTION: There is a lack of biomarkers of clinically important diets, such as the Mediterranean-DASH Intervention for Neurodegenerative Delay (MIND) diet. OBJECTIVES: Our study explored serum metabolites associated with adherence to the MIND diet. METHODS: In 3,908 Atherosclerosis Risk in Communities (ARIC) study participants, we calculated a modified MIND diet score based on a 66-item self-reported food frequency questionnaire (FFQ). The modified score did not include berries and olive oil, as these items were not assessed in the FFQ. We used multivariable linear regression models in 2 subgroups of ARIC study participants and meta-analyzed results using fixed effects regression to identify significant metabolites after Bonferroni correction. We also examined associations between these metabolites and food components of the modified MIND diet. C-statistics evaluated the prediction of high modified MIND diet adherence using significant metabolites beyond participant characteristics. RESULTS: Of 360 metabolites analyzed, 27 metabolites (15 positive, 12 negative) were significantly associated with the modified MIND diet score (lipids, n = 13; amino acids, n = 5; xenobiotics, n = 3; cofactors and vitamins, n = 3; carbohydrates n = 2; nucleotide n = 1). The top 4 metabolites that improved the prediction of high dietary adherence to the modified MIND diet were 7-methylxanthine, theobromine, docosahexaenoate (DHA), and 3-carboxy-4-methyl-5-propyl-2-furanpropanoate (CMPF). CONCLUSION: Twenty-seven metabolomic markers were correlated with the modified MIND diet. The biomarkers, if further validated, could be useful to objectively assess adherence to the MIND diet.

SFRP2 modulates functional phenotype transition and energy metabolism of macrophages during diabetic wound healing.

Diabetic foot ulcer (DFU) is a serious complication of diabetes mellitus, which causes great health damage and economic burden to patients. The pathogenesis of DFU is not fully understood. We screened wound healing-related genes using bioinformatics analysis, and full-thickness skin injury mice model and cellular assays were used to explore the role of target genes in diabetic wound healing. SFRP2 was identified as a wound healing-related gene, and the expression of SFRP2 is associated with immune cell infiltration in DFU. In vivo study showed that suppression of SFRP2 delayed the wound healing process of diabetic mice, impeded angiogenesis and matrix remodeling, but did not affect wound healing process of control mice. In addition, suppression of SFRP2 increased macrophage infiltration and impeded the transition of macrophages functional phenotypes during diabetic wound healing, and affected the transcriptome signatures-related to inflammatory response and energy metabolism at the early stage of wound healing. Extracellular flux analysis (EFA) showed that suppression of SFRP2 decreased mitochondrial energy metabolism and increased glycolysis in injury-related macrophages, but impeded both glycolysis and mitochondrial energy metabolism in inflammatory macrophages. In addition, suppression of SFRP2 inhibited wnt signaling-related genes in macrophages. Treatment of AAV-SFRP2 augmented wound healing in diabetic mice and demonstrated the therapeutic potential of SFRP2. In conclusions, SFRP2 may function as a wound healing-related gene in DFU by modulating functional phenotype transition of macrophages and the balance between mitochondrial energy metabolism and glycolysis.

Peptidylprolyl isomerase A guides SENP5/GAU1 DNA-lncRNA triplex generation for driving tumorigenesis.

The three-stranded DNA-RNA triplex hybridization is involved in various biological processes, including gene expression regulation, DNA repair, and chromosomal stability. However, the DNA-RNA triplex mediating mechanisms underlying tumorigenesis remain to be fully elucidated. Here, we show that peptidylprolyl isomerase A (PPIA) serves as anchor to recruit GAU1 lncRNA by interacting with exon 4 of GAU1 and enhances the formation of SENP5/GAU1 DNA-lncRNA triplex. Intriguingly, TFR4 region of GAU1 exon 3 and TTS4 region of SENP5 promoter DNA constitute fragments forming the SENP5/GAU1 triplex. The SENP5/GAU1 triplex subsequently triggers the recruitment of the methyltransferase SET1A to exon 1 of GAU1, leading to the enrichment of H3K4 trimethylation and the activation of SENP5 transcription for driving the tumorigenesis of gastric cancer in vitro and in vivo. Our study reveals a mechanism of PPIA-guided SENP5/GAU1 DNA-lncRNA triplex formation in tumorigenesis and providing a concept in the dynamics of isomerase assisted DNA-RNA hybridization.

Aberrant Lipid Metabolism and Complement Activation in Age-Related Macular Degeneration.

Age-related macular degeneration (AMD) stands as a leading cause of severe visual impairment and blindness among the elderly globally. As a multifactorial disease, AMD's pathogenesis is influenced by genetic, environmental, and age-related factors, with lipid metabolism abnormalities and complement system dysregulation playing critical roles. This review delves into recent advancements in understanding the intricate interaction between these two crucial pathways, highlighting their contribution to the disease's progression through chronic inflammation, drusen formation, and retinal pigment epithelium dysfunction. Importantly, emerging evidence points to dysregulated lipid profiles, particularly alterations in high-density lipoprotein levels, oxidized lipid deposits, and intracellular lipofuscin accumulation, as exacerbating factors that enhance complement activation and subsequently amplify tissue damage in AMD. Furthermore, genetic studies have revealed significant associations between AMD and specific genes involved in lipid transport and complement regulation, shedding light on disease susceptibility and underlying mechanisms. The review further explores the clinical implications of these findings, advocating for a novel therapeutic approach that integrates lipid metabolism modulators with complement inhibitors. By concurrently targeting these pathways, the dual-targeted approach holds promise in significantly improving outcomes for AMD patients, heralding a new horizon in AMD management and treatment.

The combined predictive power of the atherogenic index of plasma and serum glycated albumin for cardiovascular events in postmenopausal patients with acute coronary syndrome after percutaneous coronary intervention.

BACKGROUND: Glycated Albumin (GA) and atherogenic index of plasma (AIP) are two important biomarkers that respectively reflect lipid and glucose levels. Previous research has revealed their roles in cardiovascular diseases (CVD) and diabetes. However, their combined predictive ability in forecasting cardiovascular events (CVE) after percutaneous coronary intervention (PCI) among postmenopausal acute coronary syndrome (ACS) patients remains insufficiently studied. METHODS: Based on the levels of AIP (AIP-L and AIP-H) and GA (GA-L and GA-H), four groups were used to categorize the patients. The CVE assessed included cardiac death, nonfatal myocardial infarction (MI) and nonfatal stroke. To evaluate the relationship between AIP, GA, and CVE, multivariate Cox regression analyses were performed. RESULTS: 98 patients (7.5%) experienced CVE during follow-up. AIP and GA were revealed as strong independent predictors of CVE through multivariate analysis (AIP: HR 3.324, 95%CI 1.732-6.365, P = 0.004; GA: HR 1.098, 95% CI 1.023-1.177, P = 0.009). In comparison to those in the initial group (AIP-L and GA-L), the fourth group (AIP-H and GA-H) of patients exhibited the greatest CVE risk (HR 2.929, 95% CI 1.206-5.117, P = 0.018). Derived from the model of baseline risk, the combination of AIP + GA significantly enhanced the AUC, meanwhile combining AIP and GA levels maximized prognostic accuracy in the baseline risk model. CONCLUSIONS: This study found that the combined measurement of AIP and GA significantly enhanced the predictive capability for CVE following PCI in postmenopausal ACS patients. By integrating these two biomarkers, it became possible to more accurately identify high-risk individuals and provided clinicians with new predictive tools for postmenopausal ACS patients in risk assessment and management.

Silencing ARL11 relieved atherosclerotic inflammation and lipid deposition via retraining JAK2/STAT1 pathway.

BACKGROUND AND AIMS: Atherosclerosis (AS), an arterial vasculature disease, is characterized by abnormal lipid accumulation and inflammatory response. ADP ribosylation factor like GTPase 11 (ARL11) is linked to multifarious processes in cells. This study aims to clarify the underlying mechanism of ARL11 in AS. METHODS: ApoE-/- mice fed with high-fat diet were used as mouse model of AS. Gene expression in AS was determined by mRNA-sequencing. ARL11 expression was detected by real-time PCR, Western blot and immunofluorescence. M1 polarization of macrophages was indicated by TNF-α and IL-6 levels as detected with ELISA, and iNOS expression determined by real-time PCR and Western blot. The role of ARL11 during AS was explored through loss-of-function analysis. RESULTS: There were 1301 upregulated and 1110 downregulated genes during AS. These differentially expressed genes (DEGs) were mainly enriched in pathways and terms which are involved in inflammation. Moreover, Arl11 was highly expressed in AS models. Downregulation of Arl11 decreased lipid deposition and atherosclerotic plaques in the aortas of AS mice, and declined inflammatory cytokines and M1 polarization of macrophages induced by IFN-γ. Furthermore, ARL11 interacted with JAK2 and p-JAK2 and modulated their degradation, thus inhibiting the activation of JAK2/STAT1 pathway. CONCLUSIONS: ARL11 promoted the development of AS via interacting with JAK2 and activating JAK2/STAT1 pathway. Thus, silencing ARL11 may prevent the process of AS and be a novel way to treat AS.

Prohibitin 2 orchestrates long noncoding RNA and gene transcription to accelerate tumorigenesis.

The spatial co-presence of aberrant long non-coding RNAs (lncRNAs) and abnormal coding genes contributes to malignancy development in various tumors. However, precise coordinated mechanisms underlying this phenomenon in tumorigenesis remains incompletely understood. Here, we show that Prohibitin 2 (PHB2) orchestrates the transcription of an oncogenic CASC15-New-Isoform 2 (CANT2) lncRNA and the coding tumor-suppressor gene CCBE1, thereby accelerating melanoma tumorigenesis. In melanoma cells, PHB2 initially accesses the open chromatin sites at the CANT2 promoter, recruiting MLL2 to augment H3K4 trimethylation and activate CANT2 transcription. Intriguingly, PHB2 further binds the activated CANT2 transcript, targeting the promoter of the tumor-suppressor gene CCBE1. This interaction recruits histone deacetylase HDAC1 to decrease H3K27 acetylation at the CCBE1 promoter and inhibit its transcription, significantly promoting tumor cell growth and metastasis both in vitro and in vivo. Our study elucidates a PHB2-mediated mechanism that orchestrates the aberrant transcription of lncRNAs and coding genes, providing an intriguing epigenetic regulatory model in tumorigenesis.

Physioxia rewires mitochondrial complex composition to protect stem cell viability.

Human induced pluripotent stem cells (hiPSCs) are an invaluable tool to study molecular mechanisms on a human background. Culturing stem cells at an oxygen level different from their microenvironmental niche impacts their viability. To understand this mechanistically, dermal skin fibroblasts of 52 probands were reprogrammed into hiPSCs, followed by either hyperoxic (20 % O2) or physioxic (5 % O2) culture and proteomic profiling. Analysis of chromosomal stability by Giemsa-banding revealed that physioxic -cultured hiPSC clones exhibited less pathological karyotypes than hyperoxic (e.g. 6 % vs. 32 % mosaicism), higher pluripotency as evidenced by higher Stage-Specific Embryonic Antigen 3 positivity, higher glucose consumption and lactate production. Global proteomic analysis demonstrated lower abundance of several subunits of NADH:ubiquinone oxidoreductase (complex I) and an underrepresentation of pathways linked to oxidative phosphorylation and cellular senescence. Accordingly, release of the pro-senescent factor IGFBP3 and ß-galactosidase staining were lower in physioxic hiPSCs. RNA- and ATAC-seq profiling revealed a distinct hypoxic transcription factor-binding footprint, amongst others higher expression of the HIF1α-regulated target NDUFA4L2 along with increased chromatin accessibility of the NDUFA4L2 gene locus. While mitochondrial DNA content did not differ between groups, physioxic hiPSCs revealed lower polarized mitochondrial membrane potential, altered mitochondrial network appearance and reduced basal respiration and electron transfer capacity. Blue-native polyacrylamide gel electrophoresis coupled to mass spectrometry of the mitochondrial complexes detected higher abundance of NDUFA4L2 and ATP5IF1 and loss of incorporation into complex IV or V, respectively. Taken together, physioxic culture of hiPSCs improved chromosomal stability, which was associated with downregulation of oxidative phosphorylation and senescence and extensive re-wiring of mitochondrial complex composition.

Surveillance and management of hepatocellular carcinoma after treatment of hepatitis C with direct-acting antiviral drugs.

Hepatitis C virus (HCV) belongs to the Flaviviridae family, and is a single-stranded RNA virus with positive polarity. It is the primary cause of hepatocellular carcinoma (HCC) worldwide. The treatment of HCV has entered a new era with the advent of direct-acting antiviral drugs (DAAs) and is associated with cure rates of more than 95 %, making HCV the only curable viral disease. The successful treatment of chronic hepatitis C has greatly reduced, but not eliminated, the risk of HCC. Certain individuals, especially those with cirrhosis already present, remain vulnerable to HCC after achieving a sustained virological response (SVR). This article systematically reviews the recent studies on the risk and mechanisms of HCC development after HCV viral cure, the screening and predictive value of biological markers, and patient surveillance. Factors such as older age, diabetes, hepatic fat accumulation, alcohol use, and lack of fibrosis reversal are linked to increased HCC risk after HCV cure. The mechanism of HCC development after DAAs treatment remains unclear, but the possible mechanisms include immune cell dysfunction during HCV infection, cytokine network imbalance, epigenetic alterations, and host factors. Several biological markers and risk prediction models have been used to monitor the risk of HCC in CHC patients who have achieved SVR, but most still require validation and standardization. The implementation of risk-stratified surveillance programs is becoming urgent from a cost-effective point of view, but the availability of validated biomarkers to predict HCC in cured patients remains an unmet clinical need. Additionally, managing CHC patients who achieve SVR is becoming a growing challenge as an increasing number of HCV patients are cured.

Deterministic Synthesis of a Two-Dimensional MAPbI3 Nanosheet and Twisted Structure with Moiré Superlattice.

The synthesis of extremely thin 2D halide perovskites and the exploration of their interlayer interactions have garnered significant attention in current research. A recent advancement we have made involves the development of a successful technique for generating ultrathin MAPbI3 nanosheets with controlled thickness and an exposed intrinsic surface. This innovative method relies on utilizing the Ruddlesden-Popper (RP) phase perovskite (BA2MAn-1PbnI3n+1) as a template. However, the precise reaction mechanism remains incompletely understood. In this work, we systematically examined the dynamic evolution of the phase conversion process, with a specific focus on the influence of inorganic slab (composed of [PbI6]4- octahedrons) numbers on regulating the thickness and quality of the resulting MAPbI3 nanosheets. Additionally, the atomic structure is directly visualized using the transmission electron microscopy (TEM) method, confirming its exceptional quality. To illustrate interfacial interactions in ultrathin structures, artificial moiré superlattices are constructed through a physical transfer approach, revealing multiple localized high-symmetry stacks within a distinctive square moiré pattern. These findings establish a novel framework for investigating the physics of interfacial interactions in ionic semiconducting crystals.

Physics-Informed Inverse Design of Programmable Metasurfaces.

Emerging reconfigurable metasurfaces offer various possibilities for programmatically manipulating electromagnetic waves across spatial, spectral, and temporal domains, showcasing great potential for enhancing terahertz applications. However, they are hindered by limited tunability, particularly evident in relatively small phase tuning over 270°, due to the design constraints with time-intensive forward design methodologies. Here, a multi-bit programmable metasurface is demonstrated capable of terahertz beam steering facilitated by a developed physics-informed inverse design (PIID) approach. Through integrating a modified coupled mode theory (MCMT) into residual neural networks, the PIID algorithm not only significantly increases the design accuracy compared to conventional neural networks but also elucidates the intricate physical relations between the geometry and the modes. Without decreasing the reflection intensity, the method achieves the enhanced phase tuning as large as 300°. Additionally, the inverse-designed programmable beam steering metasurface is experimentally validated, which is adaptable across 1-bit, 2-bit, and tri-state coding schemes, yielding a deflection angle up to 68° and broadened steering coverage. The demonstration provides a promising pathway for rapidly exploring advanced metasurface devices, with potentially great impact on communication and imaging technologies.

Comprehensive landscape of gastric cancer-targeted therapy and identification of CSNK2A1 as a potential target.

Objective: To conduct a comprehensive analysis of the landscape of gastric cancer (GC)-targeted therapy clinical trials and identify potential therapeutic targets. Methods: A systematic search and analysis of the Cochrane Central Register of Controlled Trials (CENTRAL) was performed to retrieve all GC clinical trials published up to June 30, 2022. Approved therapeutic targets for 11 common cancers were compiled and analyzed. The role of CSNK2A1 in GC was investigated using bioinformatics tools such as GEPIA, KMPLOT, SangerBox, STRING, ACLBI, and TIMER. Four gastric cancer cell lines (AGS, HGC, MGC, BGC) and one normal gastric mucosa cell line (GES-1) were utilized to assess the sensitivity to the CSNK2A1 inhibitor CX-4945. Quantitative real-time polymerase chain reaction (qPCR) was employed to quantify the cellular expression of CSNK2A1. Cellular apoptosis was evaluated using flow cytometry and Western blot analysis. Results: The failure rate of GC randomized controlled clinical trials (RCTs) was strikingly high, accounting for 74.29 % (26/35) of the trials. Among the 35 approved targets in 11 different cancers, 13 targets were rigorously evaluated and identified as potential therapeutic targets for GC. Bioinformatics analysis revealed that CSNK2A1 is closely associated with multiple biological characteristics in GC, and its increased expression correlated significantly with enhanced sensitivity to CX-4945 treatment. Flow cytometry and Western blot analysis consistently demonstrated concentration-dependent apoptosis induced by CX-4945 in GC cell lines. Conclusions: The high failure rate of GC clinical trials highlights the need for a more scientific and precise approach in target identification and clinical trial design. CSNK2A1 emerges as a promising therapeutic target for GC, and its expression level could potentially serve as a biomarker for predicting sensitivity to CX-4945 treatment. Further research is warranted to elucidate the underlying molecular mechanisms and validate the clinical significance of CSNK2A1 in GC therapy.

Photoelectrocatalytic CO2 Reduction to Formate Using a BiVO4/ZIF-8 Heterojunction.

Converting CO2 into high-value chemical fuels through green photoelectrocatalytic reaction path is considered as a potential strategy to solve energy and environmental problems. In this work, BiVO4/ZIF-8 heterojunctions are prepared by in-situ synthesis of ZIF-8 nanocrystals with unique pore structure on the surface of BiVO4. The experimental results show that the silkworm pupa-like BiVO4 is successfully combined with porous ZIF-8, and the introduction of ZIF-8 can provide more sites for CO2 capture. The optimal composite ratio of 4:1-BiVO4/ZIF-8 showed excellent CO2 reduction activity and the lowest electrochemical transport resistance. In the electrocatalytic system, 4:1-BiVO4/ZIF-8 exhibits formate Faraday efficiency of 82.60% at -1.0 V vs. RHE. Furthermore, the Faraday efficiency increases to 91.24% at - 0.9 V vs. RHE in the photoelectrocatalytic system, which is 10.8 times that of pristine BiVO4. The results show that photoelectric synergism can not only reduce energy consumption, but also improve the Faraday efficiency of formate. In addition, the current density did not decrease during 34 h electrolysis, showing long-term stability. This work highlights the importance of the construction of heterojunction to improve the performance of photoelectrocatalytic CO2 reduction.

A comprehensive analysis of the health effects associated with smoking in the largest population using UK Biobank genotypic and phenotypic data.

Background: Smoking is a widespread behavior, while the relationship between smoking and various diseases remains a topic of debate. Objective: We conducted analysis to further examine the identified associations and assess potential causal relationships. Methods: We utilized seven single nucleotide polymorphisms (SNPs) known to be linked to smoking extracting genotype data from the UK Biobank, a large-scale biomedical repository encompassing comprehensive health-related and genetic information of European descent. Phenome-wide association study (PheWAS) analysis was conducted to map the association of genetically predicted smoking status with 1,549 phenotypes. The associations identified in the PheWAS were then meticulously examined through two-sample Mendelian randomization (MR) analysis, utilizing data from the UK Biobank (n = 487,365) and the Sequencing Consortium of Alcohol and Nicotine Use (GSCAN) (n = 337,334). This approach allowed us to comprehensively characterize the links between smoking and disease patterns. Results: The PheWAS analysis produced 34 phenotypes that demonstrated significant associations with smoking (P = 0.05/1460). Importantly, sickle cell anemia and type 2 diabetes exhibited the most significant SNPs (both 85.71% significant SNPs). Furthermore, the MR analyses provided compelling evidence supporting causal associations between smoking and the risk of following diseases: obstructive chronic bronchitis (IVW: Beta = 0.48, 95% confidence interval (CI) 0.36-0.61, P = 1.62×10-13), cancer of the bronchus (IVW: Beta = 0.92, 95% CI 0.68-1.17, P = 2.02×10-13), peripheral vascular disease (IVW: Beta = 1.09, 95% CI 0.71-1.46, P = 1.63×10-8), emphysema (IVW: Beta = 1.63, 95% CI 0.90-2.36, P = 1.29×10-5), pneumococcal pneumonia (IVW: Beta = 0.30, 95% CI 0.11-0.49, P = 1.60×10-3), chronic airway obstruction (IVW: Beta = 0.83, 95% CI 0.30-1.36, P = 2.00×10-3) and type 2 diabetes (IVW: Beta = 0.53, 95% CI 0.16-0.90, P = 5.08×10-3). Conclusion: This study affirms causal relationships between smoking and obstructive chronic bronchitis, cancer of the bronchus, peripheral vascular disease, emphysema, pneumococcal pneumonia, chronic airway obstruction, type 2 diabetes, in the European population. These findings highlight the broad health impacts of smoking and support smoking cessation efforts.

Microbial community diversity analysis of kiwifruit pollen and identification of potential pathogens.

The kiwifruit industry typically uses commercial pollen for artificial pollination. However, during the collection of male flowers and pollen production, pollen can be easily contaminated by pathogenic bacteria that cause diseases such as canker and flower rot. Consequently, it is crucial to understand the structure of the pollen microbial community. This study employed Illumina high-throughput sequencing technology to analyze the fungal and bacterial composition in pollen samples from various regions in Shaanxi Province. Concurrently, potential pathogenic strains were isolated using traditional microbial isolation and cultivation techniques, and their molecular identification was performed through 16S rDNA sequence analysis. A tieback test was conducted on healthy branches to verify the pathogenicity of the strains. The results revealed a rich diversity of fungi and bacteria in kiwifruit pollen. At the phylum level, pollen fungi were mainly distributed in Ascomycota, and bacteria were mainly distributed in Proteobacteria and Firmicutes. The dominant fungal genera were Mycosphaerella, Aspergillus, and Cladosporium; the dominant bacterial genera were Weissella, Pantoea, Enterobacter, and Pseudomonas, respectively. Additionally, both Erwinia persicina and Pseudomonas fluorescens, isolated from pollen, exhibited high pathogenicity toward healthy kiwifruit branches. These findings contribute to a deeper understanding of the microbial diversity in commercial kiwifruit pollen used for mass pollination.

Valorization of barley (Hordeum vulgare L.) brans from the sustainable perspective: A comprehensive review of bioactive compounds and health benefits with emphasis on their potential applications.

Barley is an important source of sustainable diets for humans, while its brans is commonly disposed as wastes. The recycling of barley brans has become a key for facilitating the valorization of barley as a whole to achieve its sustainable development. This review summarized the value of barley brans as an excellent source of multiple functional components (phenolic compounds, ß-glucan, and arabinoxylan), which conferred extensive health benefits to barley brans mainly including antioxidant, anti-obesity and lipid-lowering, anti-diabetic, and hepatoprotective properties. The utilization of barley brans reflected a great potential for sustainable development. Exploiting of food products and edible films containing barley brans or their bioactive compounds and non-food applications (preparation of bioactive substances, laccase enzymes, and biosorbents) have been attempted for supporting the zero-waste concept and circular economy. Considering their diverse applications, effective extraction techniques of bioactive compounds from barley brans and their safety are the priority of future research.

Recovering Valuable Chemicals from Polypropylene Waste via a Mild Catalyst-Free Hydrothermal Process.

Waste polypropylene (PP) presents a significant environmental challenge, owing to its refractory nature and inert C-C backbone. In this study, we introduce a practical chemical recovery strategy from PP waste using a mild catalyst-free hydrothermal treatment (HT). The treatment converts 64.1% of the processed PP into dissolved organic products within 2 h in an air atmosphere at 160 °C. Higher temperatures increase the PP conversion efficiency. Distinct electron absorption and emission characteristics of the products are identified by spectral analysis. Fourier transform-ion cyclotron resonance-mass spectrometry (FT-ICR-MS) reveals the oxidative cracking of PP into shorter-chain homologues (10-50 carbon atoms) containing carboxylic and carbonyl groups. Density functional theory (DFT) calculations support a reaction pathway involving thermal C-H oxidation at the tertiary carbon sites in the polymer chain. The addition of 1% H2O2 further enhances the oxidation reaction to produce valuable short-chain acetic acids, enabling gram-scale recycling of both pure PP and disposable surgical masks from the real world. Techno-economic analysis (TEA) and environmental life cycle costing (E-LCC) analysis suggest that this hydrothermal oxidation recovery technology is financially viable, which shows significant potential in tackling the ongoing plastic pollution crisis and advancing plastic treatment methodologies toward a circular economy paradigm.