Mechanism of Yi-Qi-Bu-Shen Recipe for the Treatment of Diabetic Nephropathy Complicated with Cognitive Dysfunction Based on Network Pharmacology and Experimental Validation.

Context: Diabetic nephropathy (DN) and cognitive dysfunction (CD) are common complications of diabetes. Yi-Qi-Bu-Shen Recipe (YQBS) can effectively reduce blood glucose, improve insulin resistance, and delay the progression of diabetic complications. The underlying mechanisms of its effects need to be further studied. Objective: This study elucidates the mechanism of YQBS in DN with CD through network pharmacology and experimental validation. Materials and Methods: Protein-protein interaction, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed. Male Sprague-Dawley (SD) rats were divided into 6 groups: model, YQBS (2, 4, 8 g/kg), positive control (metformin, 200 mg/kg), and control; the DN model was established by high sugar and high fat diet combined with intraperitoneal streptozotocin injection. After the DN model was established, the rats were gavaged for 10 weeks. Serum, kidneys, and hippocampus tissues were collected to measure the expression levels of TLR4, NF-κB, TNF-α, and IL-6. Results: The network pharmacology analysis showed that quercetin and kaempferol were the main active components of YQBS. TNF and IL-6 were the key targets, and TLR4/NF-κB pathway was crucial to YQBS in treating DN complicated with CD. Experimental validation showed that the intervention of YQBS can reduce TNF-α and IL-6 in serum, and also significantly decreases the protein expression of TLR4 and NF-κB. Conclusion: YQBS exerts anti-inflammatory effects on DN with CD through TLR4/NF-κB pathway. This study provides a biological basis for the scientific usage of YQBS in inflammation diseases and supplies experimental evidence for future traditional Chinese medicine development.

Damage to the behavior and physiological functions of Apis mellifera (Hymenoptera: Apidae) by monocrotaline via the modulation of tryptophan metabolism and the corazonin receptor.

Monocrotaline (MCT) is a toxic pyrrolizidine alkaloid found in plants of the Crotalaria genus. As primary pollinators of Crotalaria plants, honeybees come into contact with this harmful substance. However, limited research has been conducted on the effects of MCT on Apis mellifera, particularly the risks of long-term exposure to sublethal concentrations. Through evaluating the proboscis extension reflex (PER) ability, analyzing the honeybee brain transcriptome, and analyzing the honeybee hemolymph metabolome, we discovered that sublethal concentrations of MCT impair the olfactory and memory capabilities of honeybees by affecting tryptophan (Trp) metabolism. Furthermore, MCT upregulates the expression of the corazonin receptor (CrzR) gene in the honeybee brain, which elevates reactive oxygen species (ROS) levels in the brain while reducing glucose levels in the hemolymph, consequently shortening the honeybees' lifespan. Our findings regarding the multifaceted impact of MCT on honeybees lay the foundation for exploring its toxicological pathways and management in honeybee populations.

Multilevel Printed Wearable Radio-Frequency Intelligent Identification Platform for Object Recognition.

As a noncontact target recognition technique, radio-frequency identification (RFID) technology demonstrates attractive potential in constructing human-machine interaction (HMI) systems. However, the current development of RFID technologies in HMI systems is hampered by critical challenges in manufacturing high-performance RFID readers with superior flexibility and wearing comfort. Hence, we propose a multilevel printing strategy to overcome the difficulties in manufacturing high-performance large-scale microwave systems. Compared to traditional processes, the RFID system fabricated by the hybrid additive manufacturing technique exhibits equivalent electromagnetic performance and has obvious advantages in terms of manufacturing cost and environmental friendliness. A printed reconfigurable antenna with intelligent radiation mode is seamlessly integrated with the reader circuit via a "one-step" printing technology. Additionally, through chemical doping and artificial intelligence (AI) prediction, we have developed a modified polydimethylsiloxane (PDMS) encapsulation to miniaturize the system volume and enhance reliability. Electromagnetic and mechanical measurements demonstrated that our flexible RFID platform offers superior reliability and stability during long-term daily use. The RFID platform possesses exceptional capabilities in target positioning and accurate identification, demonstrating unique potential in noncontact sensing and recognition, which are highly demanded by flexible and wearable HMI systems.

Boosting the Activation of Molecular Oxygen and the Degradation of Rhodamine B in Polar-Functional-Group-Modified g-C3N4.

Molecular oxygen activation often suffers from high energy consumption and low efficiency. Developing eco-friendly and effective photocatalysts remains a key challenge for advancing green molecular oxygen activation. Herein, graphitic carbon nitride (g-C3N4) with abundant hydroxyl groups (HCN) was synthesized to investigate the relationship between these polar groups and molecular oxygen activation. The advantage of the hydroxyl group modification of g-C3N4 included narrower interlayer distances, a larger specific surface area and improved hydrophilicity. Various photoelectronic measurements revealed that the introduced hydroxyl groups reduced the charge transfer resistance of HCN, resulting in accelerated charge separation and migration kinetics. Therefore, the optimal HCN-90 showed the highest activity for Rhodamine B photodegradation with a reaction time of 30 min and an apparent rate constant of 0.125 min-1, surpassing most other g-C3N4 composites. This enhanced activity was attributed to the adjusted band structure achieved through polar functional group modification. The modification of polar functional groups could alter the energy band structure of photocatalysts, narrow band gap, enhance visible-light absorption, and improve photogenerated carrier separation efficiency. This work highlights the significant potential of polar functional groups in tuning the structure of g-C3N4 to enhance efficient molecular oxygen activation.

Lactic acid: The culprit behind the immunosuppressive microenvironment in hepatocellular carcinoma.

As a solid tumor with high glycolytic activity, hepatocellular carcinoma (HCC) produces excess lactic acid and increases extracellular acidity, thus forming a unique immunosuppressive microenvironment. L-lactate dehydrogenase (LDH) and monocarboxylate transporters (MCTs) play a very important role in glycolysis. LDH is the key enzyme for lactic acid (LA) production, and MCT is responsible for the cellular import and export of LA. The synergistic effect of the two promotes the formation of an extracellular acidic microenvironment. In the acidic microenvironment of HCC, LA can not only promote the proliferation, survival, transport and angiogenesis of tumor cells but also have a strong impact on immune cells, ultimately leading to an inhibitory immune microenvironment. This article reviews the role of LA in HCC, especially its effect on immune cells, summarizes the progress of LDH and MCT-related drugs, and highlights the potential of immunotherapy targeting lactate combined with HCC.

Alterations in serum metabolomics during the first seizure and after effective control of epilepsy.

The existing diagnostic methods of epilepsy have great limitations, and more reliable and less difficult diagnostic methods are needed. We collected serum samples of adult patients with first-diagnosed epilepsy (EPs) and seizure control patients (EPRs) for non-targeted metabolomics detection and found that they were both significantly altered, with increased expression of nicotine addiction, linoleic acid metabolism, purine metabolism, and other metabolic pathways. The diagnostic model based on 4 differential metabolites achieved a diagnostic efficiency of 99.4% in the training cohort and 100% in the validation cohort. In addition, the association analysis of oral flora, serum metabolism, and clinical indicators also provided a new angle to analyze the mechanism of epilepsy. In conclusion, this study characterized the serum metabolic characteristics of EPs and EPRs and the changes before and after epilepsy control based on a large cohort, demonstrating the potential of metabolites as non-invasive diagnostic tools for epilepsy.

Efficacy and safety of Tianqi Pingchan Granule, a compound Chinese herbal medicine, for levodopa-induced dyskinesia in Parkinson's disease: A randomized double-blind placebo-controlled trial.

BACKGROUND: Patients with Parkinson's disease (PD) undergoing long-term levodopa therapy are prone to develop levodopa-induced dyskinesia (LID). Amantadine is the main drug recommended for the treatment of LID by current guidelines, but it is far from meeting clinical needs. Tianqi Pingchan Granule (TPG), a compound Chinese herbal medicine, has been developed to relieve symptom of LID. OBJECTIVE: This randomized controlled trial evaluated the efficacy and safety of the combination of TPG and amantadine for LID. DESIGN, SETTING, PARTICIPANTS AND INTERVENTIONS: This is a randomized double-blind placebo-controlled trial, conducted from January 2020 to August 2021 at 6 sites in Jiangsu, Zhejiang and Shanghai, China. One hundred PD patients with ≥ 0.5 h of LID were randomly assigned to either the TPG plus amantadine group (TPG group) or the placebo plus amantadine group (placebo group), and treated for a period of 12 weeks. To ensure unbiased results, all study participants, investigators and sponsors were unaware of group allocations. Additionally, the data analysts remained blinded until the analysis was finalized. MAIN OUTCOME MEASURES: The primary outcome was assessed using the Unified Dyskinesia Rating Scale (UDysRS) (Range 0-104). The key secondary end point was improvement of motor and non-motor symptoms. Safety analyses included all enrolled patients. RESULTS: One hundred patients were enrolled and randomized into the two treatment groups. The changes in UDysRS at week 12 were -11.02 for the TPG group and -4.19 for the placebo group (treatment difference -6.83 [-10.53 to -3.12]; P = 0.0004). Adverse events were reported for 2 of 50 patients (4.0%) in each of the groups. CONCLUSION: This study indicated that a 12-week treatment of amantadine plus TPG effectively reduced UDysRS scores and was well tolerated, demonstrating the efficacy and safety of TPG for the treatment of LID in PD. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT04173832. PLEASE CITE THIS ARTICLE AS: Zhang Y, Zhu XB, Zhao Y, Cui GY, Li WT, Yuan CX, Huang JP, Wan Y, Wu N, Song L, Zhao JH, Liang Y, Xu CY, Liu MJ, Gao C, Chen XX, Liu ZG. Efficacy and safety of Tianqi Pingchan Granule, a compound Chinese herbal medicine, for levodopa-induced dyskinesia in Parkinson's disease: A randomized double-blind placebo-controlled trial. J Integr Med. 2024; 22(5): 545-551.

HPTRMF: Collaborative Matrix Factorization-Based Prediction Method for LncRNA-Disease Associations Using High-Order Perturbation and Flexible Trifactor Regularization.

Existing matrix factorization methods face challenges, including the cold start problem and global nonlinear data loss during similarity learning, particularly in predicting associations between long noncoding RNAs (LncRNAs) and diseases. To overcome these issues, we introduce HPTRMF, a matrix factorization approach incorporating high-order perturbation and flexible trifactor regularization. HPTRMF constructs a high-order correlation matrix utilizing the known association matrix, leveraging high-order perturbation to effectively address the cold start problem caused by data sparsity. Additionally, HPTRMF incorporates a flexible trifactor regularization term to capture similarity information on LncRNAs and diseases, enabling the effective handling of global nonlinear data loss by capturing such data in the similarity matrix. Experimental results demonstrate the superiority of HPTRMF over nine state-of-the-art algorithms in Leave-One-Out Cross-Validation (LOOCV) and Five-Fold Cross-Validation (5-Fold CV) on three data sets.HPTRMF and data sets are available in https://github.com/Llvvvv/HPTRMF.

Astrocyte-TREM2 alleviates brain injury by regulating reactive astrocyte states following ischemic stroke.

Triggering receptor expressed on myeloid cells 2 (TREM2) has been shown to confer strong neuroprotective effects in acute ischemic stroke (AIS). However, as the vast majority of research findings to date are based on its functions in microglia, the precise role of TREM2 in astrocytes after AIS is unknown. Here, both loss- and gain-of-function experiments were employed to investigate how astrocytic TREM2 influences the pathogenesis of AIS in vivo and in vitro. Our results demonstrated that cerebral ischemia triggered induction of TREM2 expression on reactive astrocytes following AIS. In addition, astrocyte-specific TREM2 knockout mice exhibited much greater brain injury than TREM2 flox/flox controls following AIS, as evidenced by increased cerebral infarct volume, neuronal apoptosis and neurological deficit, which was associated with an increased expression of pro-inflammatory molecule complement component 3 (C3) on reactive astrocytes and activation of microglia/macrophages but decreased expression of S100 calcium binding protein A10 (S100A10) and arginase1 (Arg1) on reactive astrocytes. Mechanistic analyses revealed that astrocytic TREM2 alleviated brain injury by inhibiting detrimental actions of reactive astrocytes but promoting their neuro- and glioprotective actions via the kruppel-like transcription factor-4-nuclear factor-κB axis. Together, this study provides novel evidence for a critical protective role of astrocyte-derived TREM2 in AIS and highlights a potential therapeutic target for the treatment of AIS.

Extracellular vesicles and endothelial dysfunction in infectious diseases.

Cardiovascular diseases (CVDs) remain the leading cause of mortality and morbidity globally. Studies have shown that infections especially bacteraemia and sepsis are associated with increased risks for endothelial dysfunction and related CVDs including atherosclerosis. Extracellular vesicles (EVs) are small, sealed membrane-derived structures that are released into body fluids and blood from cells and/or microbes and are critically involved in a variety of important cell functions and disease development, including intercellular communications, immune responses and inflammation. It is known that EVs-mediated mechanism(s) is important in the development of endothelial dysfunction in infections with a diverse spectrum of microorganisms including Escherichia coli, Candida albicans, SARS-CoV-2 (the virus for COVID-19) and Helicobacter pylori. H. pylori infection is one of the most common infections globally. During H. pylori infection, EVs can carry H. pylori components, such as lipopolysaccharide, cytotoxin-associated gene A, or vacuolating cytotoxin A, and transfer these substances into endothelial cells, triggering inflammatory responses and endothelial dysfunction. This review is to illustrate the important role of EVs in the pathogenesis of infectious diseases, and the development of endothelial dysfunction in infectious diseases especially H. pylori infection, and to discuss the potential mechanisms and clinical implications.

SARS-CoV-2: pathogenesis, therapeutics, variants, and vaccines.

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), emerged in December 2019 with staggering economic fallout and human suffering. The unique structure of SARS-CoV-2 and its underlying pathogenic mechanism were responsible for the global pandemic. In addition to the direct damage caused by the virus, SARS-CoV-2 triggers an abnormal immune response leading to a cytokine storm, culminating in acute respiratory distress syndrome and other fatal diseases that pose a significant challenge to clinicians. Therefore, potential treatments should focus not only on eliminating the virus but also on alleviating or controlling acute immune/inflammatory responses. Current management strategies for COVID-19 include preventative measures and supportive care, while the role of the host immune/inflammatory response in disease progression has largely been overlooked. Understanding the interaction between SARS-CoV-2 and its receptors, as well as the underlying pathogenesis, has proven to be helpful for disease prevention, early recognition of disease progression, vaccine development, and interventions aimed at reducing immunopathology have been shown to reduce adverse clinical outcomes and improve prognosis. Moreover, several key mutations in the SARS-CoV-2 genome sequence result in an enhanced binding affinity to the host cell receptor, or produce immune escape, leading to either increased virus transmissibility or virulence of variants that carry these mutations. This review characterizes the structural features of SARS-CoV-2, its variants, and their interaction with the immune system, emphasizing the role of dysfunctional immune responses and cytokine storm in disease progression. Additionally, potential therapeutic options are reviewed, providing critical insights into disease management, exploring effective approaches to deal with the public health crises caused by SARS-CoV-2.

Inhibiting AGTR1 reduces AML burden and protects the heart from cardiotoxicity in mouse models.

Clinical treatment of acute myeloid leukemia (AML) largely relies on intensive chemotherapy. However, the application of chemotherapy is often hindered by cardiotoxicity. Patient sequence data revealed that angiotensin II receptor type 1 (AGTR1) is a shared target between AML and cardiovascular disease (CVD). We found that inhibiting AGTR1 sensitized AML to chemotherapy and protected the heart against chemotherapy-induced cardiotoxicity in a human AML cell-transplanted mouse model. These effects were regulated by the AGTR1-Notch1 axis in AML cells and cardiomyocytes from mice. In mouse cardiomyocytes, AGTR1 was hyperactivated by AML and chemotherapy. AML leukemogenesis increased the expression of the angiotensin-converting enzyme and led to increased production of angiotensin II, the ligand of AGTR1, in an MLL-AF9-driven AML mouse model. In this model, the AGTR1-Notch1 axis regulated a variety of genes involved with cell stemness and chemotherapy resistance. AML cell stemness was reduced after Agtr1a deletion in the mouse AML cell transplant model. Mechanistically, Agtr1a deletion decreased γ-secretase formation, which is required for transmembrane Notch1 cleavage and release of the Notch1 intracellular domain into the nucleus. Using multiomics, we identified AGTR1-Notch1 signaling downstream genes and found decreased binding between these gene sequences with Notch1 and chromatin enhancers, as well as increased binding with silencers. These findings describe an AML/CVD association that may be used to improve AML treatment.

Achievements, challenges, and perspectives in the design of polymer binders for advanced lithium-ion batteries.

Energy storage devices with high power and energy density are in demand owing to the rapidly growing population, and lithium-ion batteries (LIBs) are promising rechargeable energy storage devices. However, there are many issues associated with the development of electrode materials with a high theoretical capacity, which need to be addressed before their commercialization. Extensive research has focused on the modification and structural design of electrode materials, which are usually expensive and sophisticated. Besides, polymer binders are pivotal components for maintaining the structural integrity and stability of electrodes in LIBs. Polyvinylidene difluoride (PVDF) is a commercial binder with superior electrochemical stability, but its poor adhesion, insufficient mechanical properties, and low electronic and ionic conductivity hinder its wide application as a high-capacity electrode material. In this review, we highlight the recent progress in developing different polymeric materials (based on natural polymers and synthetic non-conductive and electronically conductive polymers) as binders for the anodes and cathodes in LIBs. The influence of the mechanical, adhesion, and self-healing properties as well as electronic and ionic conductivity of polymers on the capacity, capacity retention, rate performance and cycling life of batteries is discussed. Firstly, we analyze the failure mechanisms of binders based on the operation principle of lithium-ion batteries, introducing two models of "interface failure" and "degradation failure". More importantly, we propose several binder parameters applicable to most lithium-ion batteries and systematically consider and summarize the relationships between the chemical structure and properties of the binder at the molecular level. Subsequently, we select silicon and sulfur active electrode materials as examples to discuss the design principles of the binder from a molecular structure point of view. Finally, we present our perspectives on the development directions of binders for next-generation high-energy-density lithium-ion batteries. We hope that this review will guide researchers in the further design of novel efficient binders for lithium-ion batteries at the molecular level, especially for high energy density electrode materials.

GLP-1 receptor agonists and myocardial metabolism in atrial fibrillation.

Atrial fibrillation (AF) is the most common cardiac arrhythmia. Many medical conditions, including hypertension, diabetes, obesity, sleep apnea, and heart failure (HF), increase the risk for AF. Cardiomyocytes have unique metabolic characteristics to maintain adenosine triphosphate production. Significant changes occur in myocardial metabolism in AF. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have been used to control blood glucose fluctuations and weight in the treatment of type 2 diabetes mellitus (T2DM) and obesity. GLP-1RAs have also been shown to reduce oxidative stress, inflammation, autonomic nervous system modulation, and mitochondrial function. This article reviews the changes in metabolic characteristics in cardiomyocytes in AF. Although the clinical trial outcomes are unsatisfactory, the findings demonstrate that GLP-1 RAs can improve myocardial metabolism in the presence of various risk factors, lowering the incidence of AF.

Oxidized Low-Density Lipoprotein Decreases the Survival of Bone Marrow Stem Cells via Inhibition of Bcl-2 Expression.

Therapy with mesenchymal stem cells (MSCs) is considered an attractive strategy for the repair or regeneration of damaged tissues. However, low survival of MSCs limits their applications clinically. Oxidized low-density lipoprotein (ox-LDL) is significantly increased in patients with hyperlipidemia and decreases the survival of MSCs. Bcl-2 is critically involved in important cell functions, including cell membrane integrity and cell survival. The present study was designed to test the hypothesis that ox-LDL attenuates the survival of MSCs through suppression of Bcl-2 expression. Bone marrow MSCs from C57BL/6 mice were cultured with ox-LDL at different concentrations (0-140 µg/mL) for 24 h with native LDL as control. Ox-LDL treatment substantially decreased the survival of MSCs dose-dependently and enhanced the release of intracellular lactate dehydrogenase (LDH) in association with a significant decrease in Bcl-2 protein level without change in BAX protein expression in MSCs. Bcl-2 overexpression effectively protected MSCs against ox-LDL-induced damages with preserved cell numbers without significant increase in LDH release. Treatment with N-acetylcysteine (NAC) (1 mM) effectively preserved Bcl-2 protein expression in MSCs and significantly attenuated ox-LDL-induced decrease of cell number and increase in the release of intracellular LDH. These data indicated that ox-LDL treatment resulted in a significant damage of cell membrane and dramatically decreased the survival of MSCs dose-dependently through inhibition of Bcl-2 expression. NAC treatment significantly protected MSCs against the damage of cell membrane by ox-LDL and promoted the survival of MSCs in association with preserved Bcl-2 expression.

Decreased resting-state functional connectivity and brain network abnormalities in the prefrontal cortex of elderly patients with Parkinson's disease accompanied by depressive symptoms.

This study aimed to explore the brain network characteristics in elderly patients with Parkinson's disease (PD) with depressive symptoms. Thirty elderly PD patients with depressive symptoms (PD-D) and 26 matched PD patients without depressive symptoms (PD-NOD) were recruited based on HAMD-24 with a cut-off of 7. The resting-state functional connectivity (RSFC) was conducted by 53-channel functional near-infrared spectroscopy (fNIRS). There were no statistically significant differences in MMSE scores, disease duration, Hoehn-Yahr stage, daily levodopa equivalent dose, and MDS-UPDRS III between the two groups. However, compared to the PD-NOD group, the PD-D group showed significantly higher MDS-UPDRS II, HAMA-14, and HAMD-24. The interhemispheric FC strength and the FC strength between the left dorsolateral prefrontal cortex (DLPFC-L) and the left frontal polar area (FPA-L) was significantly lower in the PD-D group (FDR p < 0.05). As for graph theoretic metrics, the PD-D group had significantly lower degree centrality (aDc) and node efficiency (aNe) in the DLPFC-L and the FPA-L (FDR, p < 0.05), as well as decreased global efficiency (aEg). Pearson correlation analysis indicated moderate negative correlations between HAMD-24 scores and the interhemispheric FC strength, FC between DLPFC-L and FPA-L, aEg, aDc in FPA-L, aNe in DLPFC-L and FPA-L. In conclusion, PD-D patients show decreased integration and efficiency in their brain networks. Furthermore, RSFC between DLPFC-L and FPA-L regions is negatively correlated with depressive symptoms. These findings propose that targeting DLPFC-L and FPA-L regions via non-invasive brain stimulation may be a potential intervention for alleviating depressive symptoms in elderly PD patients.

Association of dietary selenium intake and all-cause mortality of Parkinson's disease and its interaction with blood cadmium level: a retrospective cohort study.

BACKGROUND: Parkinson's disease (PD) is a slowly progressive neurodegenerating disease that may eventually lead to disabling condition and pose a threat to the health of aging populations. This study aimed to explore the association of two potential risk factors, selenium and cadmium, with the prognosis of Parkinson's disease as well as their interaction effect. METHODS: Data were obtained from the National Health and Nutrition Examination Survey (NHANES) 2005-2006 to 2015-2016 and National Death Index (NDI). Participants were classified as Parkinson's patients by self-reported anti-Parkinson medications usage. Cox regression models and restricted cubic spline models were applied to evaluate the association between PD mortality and selenium intake level as well as blood cadmium level. Subgroup analysis was also conducted to explore the interaction between them. RESULTS: A total of 184 individuals were included. In full adjusted cox regression model (adjusted for age, gender, race, hypertension, pesticide exposure, smoking status and caffeine intake), compared with participants with low selenium intake, those with normal selenium intake level were significantly associated with less risk of death (95%CI: 0.18-0.76, P = 0.005) while no significant association was found between low selenium intake group and high selenium group (95%CI: 0.16-1.20, P = 0.112). Restricted cubic spline model indicated a nonlinear relationship between selenium intake and PD mortality (P for nonlinearity = 0.050). The association between PD mortality and blood cadmium level was not significant (95%CI: 0.19-5.57, P = 0.112). However, the interaction term of selenium intake and blood cadmium showed significance in the cox model (P for interaction = 0.048). Subgroup analysis showed that the significant protective effect of selenium intake existed in populations with high blood cadmium but not in populations with low blood cadmium. CONCLUSION: Moderate increase of selenium intake had a protective effect on PD mortality especially in high blood cadmium populations.

Impact of greening trends on biogenic volatile organic compound emissions in China from 1985 to 2022: Contributions of afforestation projects.

The rapid expansion of green areas in China has enhanced carbon sinks, but it also presents challenges regarding increased biogenic volatile organic compound (BVOC) emissions. This study examines the impact of greening trends on BVOC emissions in China from 1985 to 2001 and from 2001 to 2022, focusing on evaluating long-term trends in BVOC emissions within eight afforestation project areas during these two periods. Emission factors for 62 dominant tree species and provincial Plant Functional Types were updated. The BVOC emission inventories were developed for China at a spatial resolution of 27 km × 27 km using the Model of Emissions of Gases and Aerosols from Nature. The national BVOC emissions in 2018 were estimated at 54.24 Tg, with isoprene, monoterpenes, sesquiterpenes, and other BVOC contributing 26.94 Tg, 2.29 Tg, 0.44 Tg, and 24.57 Tg, respectively. Over the past 37 years, BVOC emissions experienced a slow growth rate of 1.7 % (0.79 Tg) during 1985-2001, followed by a significant increase of 12 % (6 Tg) from 2001 to 2022. BVOC emissions in the eight afforestation project areas increased by 2 % and 20 % during the two periods. From 2001 to 2022, at the regional scale, the Shelterbelt program for the middle reaches of the Yellow River area exhibited the largest rate of increase (43 %) in BVOC emissions. The Shelterbelt program for the upper and middle reaches of the Yangtze River made the most largest contribution (45 %) to the national increase in BVOC emissions. Afforestation projects have shifted towards planting more broadleaf trees than needleleaf trees from 2001 to 2022, and there also showed a change from herbaceous plants to broadleaf trees. These trends have led to higher average emission factors for vegetation, resulting in increased BVOC emissions. It underscores the importance of considering BVOC emissions when evaluating afforestation initiatives, emphasizing the need to balancing ecological benefits with potential atmospheric consequences.

Effects of abamectin nanocapsules on bees through host physiology, immune function, and gut microbiome.

Pesticide usage is a common practice to increase crop yields. Nevertheless, the existence of pesticide residues in the surrounding environment presents a significant hazard to pollinators, specifically the potential undisclosed dangers related to emerging nanopesticides. This study examines the impact of abamectin nanocapsules (AbaNCs), created through electrostatic self-assembly, as an insecticide on honey bees. It was determined that AbaNCs upregulated detoxification genes, including CYP450, as well as antioxidant and immune genes in honey bees. Furthermore, AbaNCs affected the activity of crucial enzymes such as superoxide dismutase (SOD). Although no apparent damage was observed in bee gut tissue, AbaNCs significantly decreased digestive enzyme activity. Microbiome sequencing revealed that AbaNCs disrupted gut microbiome, resulting in a reduction of beneficial bacteria such as Bifidobacterium and Lactobacillus. Additionally, these changes in the gut microbiome were associated with decreased activity of digestive enzymes, including lipase. This study enhances our understanding of the impact of nanopesticides on pollinating insects. Through the revelation of the consequences arising from the utilization of abamectin nanocapsules, we have identified potential stress factors faced by these pollinators, enabling the implementation of improved protective measures.