Investigating the Mechanisms of Inflammation and Immune Alterations in Parkinson's Disease using Spatial Transcriptomics Techniques.

In recent years, overwhelming evidence has emphasized the crucial role of inflammation in the pathogenesis of PD. However, the exact mechanisms by which inflammation damages dopaminergic neurons in PD are still unclear. Therefore, we generated a MPTP-induced PD mouse model and performed spatial transcriptomic sequencing to provide more insight into the process of PD development at specific brain regions. Our results indicate that the pathological changes of PD are mainly manifested in the midbrain, especially in the substantia nigra region, with significant reductions in oligodendrocytes and Agt-labeled astrocytes and an increase in Gfap-labeled astrocytes. Macrophages displayed an increasing trend in the PD environment, indicating a pattern of immune modulation induced by PD. Moreover, pathway analysis revealed significant impairments in ion migration ability, abnormal Ca2+ channels, cAMP signaling, and synaptic damage in PD. Significant downregulation of Mt1 and Mt2 and upregulation of Atp1b2, Gpi1, and Cox6a1 in PD further underscored the occurrence of intense inflammation and immune alterations. On the basis of these findings, we have validated the significant accumulation of Ca2+ in the midbrain tissue in the PD environment by measuring its content. Additionally, we have demonstrated a close association between the reduction of dopaminergic neurons, represented by the midbrain region, and ferroptosis by evaluating the iron content, malondialdehyde (MDA) levels, and the protein expression of GPX4 and TH in the tissue. We propose the hypothesis that PD-related inflammation and immune changes can induce neuronal and oligodendrocyte damage through the induction of ferroptosis, thereby further accelerating the progression of PD.

Immunomodulatory Roles of IL-15 in Immune Cells and its Potential for Cancer Immunotherapy.

Interleukin-15 (IL-15) was identified in 1994 as a T-cell growth factor with the capability to mimic the functions of IL-2. IL-15 engages with the IL-15Rα subunit expressed on the surface of antigen-presenting cells (APCs) and, through a trans-presentation mechanism, activates the IL-2/IL-15Rßγ complex receptor on the surface of natural killer (NK) cells and CD8+ T cells. This interaction initiates a cascade of downstream signaling pathways, playing a pivotal role in the activation, proliferation, and anti-apoptotic processes in NK cells, CD8+ T cells, and B cells. It provides a substantial theoretical foundation and potential therapeutic targets for tumor immunotherapy. Whether through active or passive immunotherapeutic strategies, IL-15 has emerged as a critical molecule for stimulating anti-tumor cell proliferation.

Obesity-derived macrophages upregulate TNF-α to induce apoptosis in glial cell via the NF-κB/PHLPP1 axis.

Macrophages in obese adipose tissue have been shown to damage nerve fibers, however, the mechanism underlying how macrophages cause glial cell damage remains unknown. This study aimed to characterize the mechanism by which macrophages induce apoptosis in glial cell during obesity formation in mice by single-nucleus RNA sequencing (snRNA-seq). Cells obtained from paraepididymal adipose tissue in obese mice underwent snRNA-seq. Eighteen different clusters were identified, and 12 cell types were annotated, including glial cells, macrophages, and fibroblasts. There was a negative correlation between the number of glial cells and macrophages in mouse adipose tissue during the formation of obesity. The pro-apoptotic factor PHLPP1 was identified in GO Terms. The interaction between adipose tissue glial cells and macrophages was revealed via in-depth analysis, and the cell-cell communication mechanism between the TNF-α and NF-KB/PHLPP1 axes was perfected. Apoptosis of glial cell by upregulation of TNF-α via obesity-derived macrophages and activation of the NF-κB/PHLPP1 axis. We further revealed how macrophages induce apoptosis in glial cells during obesity formation, as well as different changes in the two cell populations. This study provides valuable resources and foundations for understanding the mechanistic effects of macrophages and glial cells during obesity formation, as well as diseases and potential interventions.

The mechanisms of white matter injury and immune system crosstalk in promoting the progression of Parkinson's disease: a narrative review.

Parkinson's disease (PD) is neurodegenerative disease in middle-aged and elderly people with some pathological mechanisms including immune disorder, neuroinflammation, white matter injury and abnormal aggregation of alpha-synuclein, etc. New research suggests that white matter injury may be important in the development of PD, but how inflammation, the immune system, and white matter damage interact to harm dopamine neurons is not yet understood. Therefore, it is particularly important to delve into the crosstalk between immune cells in the central and peripheral nervous system based on the study of white matter damage in PD. This crosstalk could not only exacerbate the pathological process of PD but may also reveal new therapeutic targets. By understanding how immune cells penetrate through the blood-brain barrier and activate inflammatory responses within the central nervous system, we can better grasp the impact of structural destruction of white matter in PD and explore how this process can be modulated to mitigate or combat disease progression. Microglia, astrocytes, oligodendrocytes and peripheral immune cells (especially T cells) play a central role in its pathological process where these immune cells produce and respond to pro-inflammatory cytokines such as tumor necrosis factor (TNF-α), interleukin-1ß(IL-1ß) and interleukin-6(IL-6), and white matter injury causes microglia to become pro-inflammatory and release inflammatory mediators, which attract more immune cells to the damaged area, increasing the inflammatory response. Moreover, white matter damage also causes dysfunction of blood-brain barrier, allows peripheral immune cells and inflammatory factors to invade the brain further, and enhances microglia activation forming a vicious circle that intensifies neuroinflammation. And these factors collectively promote the neuroinflammatory environment and neurodegeneration changes of PD. Overall, these findings not only deepen our understanding of the complexity of PD, but also provide new targets for the development of therapeutic strategies focused on inflammation and immune regulation mechanisms. In summary, this review provided the theoretical basis for clarifying the pathogenesis of PD, summarized the association between white matter damage and the immune cells in the central and peripheral nervous systems, and then emphasized their potential specific mechanisms of achieving crosstalk with further aggravating the pathological process of PD.

Single-nucleus RNA transcriptome profiling reveals murine adipose tissue endothelial cell proliferation gene networks involved in obesity development.

Endothelial cells play an important role in the metabolism of adipose tissue (AT). This study aimed to analyze the changes that adipose tissue in AT endothelial cells undergo during the development of obesity, using single-nucleus RNA sequence (snRNA-seq). Mouse paraepididymal AT cells were subjected to snRNA-seq with the 10X Genomics platform. The cell types were then clustered using t-distributed stochastic neighbor embedding and unbiased computational informatics analyses. Protein-protein interactions network was established using the STRING database and visualized using Cytoscape. The dataset was subjected to differential gene enrichment analysis. In total, 21,333 cells acquired from 24 mouse paraepididymal AT samples were analyzed using snRNA-seq. This study identified 18 distinct clusters and annotated macrophages, fibroblasts, epithelial cells, T cells, endothelial cells, stem cells, neutrophil cells, and neutrophil cell types based on representative markers. Cluster 12 was defined as endothelial cells. The proportion of endothelial cells decreased with the development of obesity. Inflammatory factors, such as Vegfa and Prdm16 were upregulated in the medium obesity group but downregulated in the obesity group. Genes, such as Prox1, Erg, Flt4, Kdr, Flt1, and Pecam1 promoted the proliferation of AT endothelial cells and maintained the internal environment of AT. This study established a reference model and general framework for studying the mechanisms, biomarkers, and therapeutic targets of endothelial cell dysfunction-related diseases at the single-cell level.

SOCS modulates JAK-STAT pathway as a novel target to mediate the occurrence of neuroinflammation: Molecular details and treatment options.

SOCS (Suppressor of Cytokine Signalling) proteins are intracellular negative regulators that primarily modulate and inhibit cytokine-mediated signal transduction, playing a crucial role in immune homeostasis and related inflammatory diseases. SOCS act as inhibitors by regulating the Janus kinase-signal transducer and activator of transcription (JAK-STAT) signaling pathway, thereby intervening in the pathogenesis of inflammation and autoimmune diseases. Recent studies have also demonstrated their involvement in central immunity and neuroinflammation, showing a dual functionality. However, the specific mechanisms of SOCS in the central nervous system remain unclear. This review thoroughly elucidates the specific mechanisms linking the SOCS-JAK-STAT pathway with the inflammatory manifestations of neurodegenerative diseases. Based on this, it proposes the theory that SOCS proteins can regulate the JAK-STAT pathway and inhibit the occurrence of neuroinflammation. Additionally, this review explores in detail the current therapeutic landscape and potential of targeting SOCS in the brain via the JAK-STAT pathway for neuroinflammation, offering insights into potential targets for the treatment of neurodegenerative diseases.

Oxidative stress in the brain-lung crosstalk: cellular and molecular perspectives.

Oxidative stress is caused by an imbalance between the production of reactive oxygen species (ROS) and the body's ability to counteract their harmful effects, playing a key role in the pathogenesis of brain and lung-related diseases. This review comprehensively examines the intricate mechanisms by which oxidative stress influences cellular and molecular pathways, contributing to neurodegenerative, cardiovascular, and respiratory disorders. Emphasizing the detrimental effects on both brain and lung health, we discuss innovative diagnostic biomarkers, such as 8-hydroxy-2'-deoxyguanosine (8-OHdG), and the potential of antioxidant therapies. For these topics, we provide insights into future research directions in the field of oxidative stress treatment, including the development of personalized treatment approaches, the discovery and validation of novel biomarkers, and the development of new drug delivery systems. This review not only provides a new perspective on understanding the role of oxidative stress in brain and lung-related diseases but also offers new insights for future clinical treatments.

Data of RNA-seq transcriptomes of gastrocnemius muscle, epididymal adipose tissue in obese rats under normoxia/hypoxic exercise environments.

Studies on the crosstalk between muscle and adipose tissue can provide beneficial help in elucidating the pathogenesis and treatment of obesity-related diseases [1]. In this data article, we performed RNA sequence analysis of mRNA isolated from epididymal adipose tissue and gastrocnemius muscle tissue in obese rats. Twenty-two samples were selected for gene expression analysis. Raw data from the Illumina Hiseq™ platform sequencer was used for differential gene expression analysis using DESeq and deposited in the GEO public repository under accession number GSE237950. With the economic development and the change of people's lifestyle, obesity has become a major public health problem that endangers global health. Obesity is a metabolic disorder caused by excessive accumulation of white adipose tissue, which can further induce metabolic syndrome such as insulin resistance, type 2 diabetes, and cardiovascular and cerebrovascular diseases. Studies have shown that altitude hypoxic exercise can not only improve muscle buffering capacity and body performance, but also reduce body weight and body fat more significantly. In many countries, it has been used as a treatment program for obesity diseases [2]. Hypoxic exercise can improve lipid metabolism, reduce blood lipid levels, inhibit fatty acid synthesis, and promote fatty acid decomposition and oxidation, which is the mechanism of hypoxic exercise to significantly reduce weight and fat. However, the mechanism of the cross-talk between muscle and fat tissue is not well understood under hypoxia exercise and normoxia exercise conditions. The data contained rat's four different states: normoxia quiet, normoxia exercise, hypoxic quiet, and hypoxic exercise. RNA-seq data will provide insights into the cross-talk between muscle and fat, and the mechanisms of fat metabolism. The data of this study have not been published and are hereby published on this platform to study the cross talk between muscle tissue and adipose tissue in rats under different oxygen content and exercise environment.

Single cell RNA-sequencing data generated from mouse adipose tissue during the development of obesity.

In recent years, the number of obesity has increased rapidly around the world, and it has become a major public health problem endangering global health [1]. Obesity is caused by excessive calorie intake over a long period of time, and high-fat diet (HFD) is one of the important predisposing factors [2], [3], [4]. Adipose tissue (AT) is an important immune and endocrine organ in the body, and plays an important role in the body [5]. Obesity leads to AT dysfunction, AT dilation and cell hypertrophy. Dysfunctional fat cells are the main source of pro-inflammatory cytokines, which aggravate low-grade systemic inflammation and further promote the development of obesity-related diseases [6], [7], [8]. However, whether AT releases pro-inflammatory cytokines in the early stages of obesity development remains unknown. The AT microenvironment is composed of a variety of cells, including fat cells, immune cells, fibroblasts, and endothelial cells. The immune microenvironment (TIME) and its metabolic imbalance can lead to the secretion or regulation of related hormones, which causes inflammation AT [9]. TIME is very important for maintaining AT homeostasis, which is crucial for the occurrence of obesity [10,11]. This data use single-cell RNA sequencing (sNuc-Seq) to analyze the characteristics of TIME changes in the mouse epididymal adipose tissue during the development of obesity, and the changes of cell types and genes in the tissue.

Bioinformatics analysis of copper death gene in diabetic immune infiltration.

BACKGROUND: Copper plays an important role in the human body and is potentially related to the development of diabetes. The mechanism of copper death gene regulating immune infiltration in diabetes has not been studied. METHODS: Download microarray data from healthy normal and diabetic patients from the GEO database. The identification of differentially expressed genes (DEGs) was analyzed by gene enrichment. Using String online database and Cytoscape software to interact with the protein interaction network and make visual analysis. Using Wilcox analyze the correlation between the copoer death gene and diabetic mellitus. Analysis of the correlation between immune penetration cells and functions, and the difference between the diabetes group and the control group, screening the copper death gene associated with diabetes, and predicting the upper top of microRNA (miRNA) through the Funrich software. RESULTS: According to the identification of differential genes in 25 samples of GSE25724 and GSE95849 data sets, 328 differential genes were identified by consensus, including 190 up-regulated genes and 138 down-regulated genes (log2FC = 2, P < .01). KEGG results showed that neurodegeneration-multiple disease pathways were most significantly upregulated, followed by Huntington disease. According to Cytohubba, the TOP10 genes HCK, FPR1, MNDA, AQP9, TLR8, CXCR1, CSF3R, VNN2, TLR4, and CCR5 are down-regulated genes, which are mostly enriched in neutrophils. Immunoinfiltration-related heat maps show that Macrophage was strongly positively correlated with Activated dendritic cell, Mast cell, Neutrophil, and Regulatory T cell showed a strong positive correlation. Neutrophil was strongly positively correlated with Activated dendritic cell, Mast cell, and Regulatory T cell. Differential analysis of immune infiltration showed that Neutroph, Mast cell, Activated B cell, Macrophage and Eosinophil were significantly increased in the diabetic group. Central memory CD4 T cell (P < .001), Plasmacytoid dendritic cell, Immature dendritic cell, and Central memory CD8 T cell, etal were significantly decreased. DBT, SLC31A1, ATP7A, LIAS, ATP7B, PDHA1, DLST, PDHB, GCSH, LIPT1, DLD, FDX1, and DLAT genes were significantly associated with one or more cells and their functions in immune invasion. Forty-one miRNA. CONCLUSIONS: Copper death is closely related to the occurrence of diabetes. Copper death genes may play an important role in the immune infiltration of diabetes.

Striking impacts of biomass burning on PM2.5 concentrations in Northeast China through the emission inventory improvement.

Biomass burning exerts substantial influences on air quality and climate, which in turn to further aggravate air quality. The biomass burning emissions in particular of the agricultural burning may suffer large uncertainties which limits the understanding of their impact on air quality. Based on an improved emission inventory of the Visible Infrared Imaging Radiometer Suite (VIIRS) relative to commonly used Global Fire Emissions Database (GFED), we thoroughly evaluate the impact of biomass burning on air quality and climate during the episodes of November 2017 in Northeast China which is rich in agriculture burning. The results first indicate substantial underestimates in simulated PM2.5 concentrations without the inclusion of biomass burning emission inventory, based on a regional air quality model Weather Research and Forecasting model and Community Multiscale Air Quality model (WRF-CMAQ). The addition of biomass burning emissions from GFED then reduces the bias to a certain extent, which is further reduced by replacing the agricultural fires data in GFED with VIIRS. Numerical sensitivity experiments show that based on the improved emission inventory, the contribution of biomass burning emissions to PM2.5 concentrations in Northeast China reaches 32%, contrasting to 15% based on GFED, during the episode from November 1 to 7, 2017. Aerosol direct radiative effects from biomass burning are finally elucidated, which not only reduce downward surface shortwave radiation and planetary boundary layer height, but also affect the vertical distribution of air temperature, wind speed and relative humidity, favorable to the accumulation of PM2.5. During November 1-7, 2017, the mean daily PM2.5 enhancement due to aerosol radiative effects from VIIRS_G is 16 µg m-3, a few times higher than that of 2.8 µg m-3 from GFED. The study stresses the critical role of biomass burning, particularly of small fires easily missed in the traditional low-resolution satellite products, on air quality.

Metabolic reprogramming in the tumor microenvironment: unleashing T cell stemness for enhanced cancer immunotherapy.

T cells play a pivotal role in the immune system by distinguishing between various harmful pathogens and cancerous cells within the human body and initiating an immune response. Within the tumor microenvironment (TME), immune effector T cells encounter both immunosuppressive cells and factors that hinder their functionality. Additionally, they endure robust and persistent antigenic stimulation, often leading to exhaustion and apoptosis. However, the stemness of T cells, characterized by their ability to survive and self-renew over extended periods, represents a primary target in immune checkpoint therapies such as anti-PD-1 therapy. T cell stemness encompasses specific memory T cell subsets and progenitor-exhausted T cells with stem cell-like properties. Therefore, understanding the impact of the TME on T cell stemness, including factors like K+, lactate, and H+, holds significant importance and can facilitate the mitigation of terminal T-cell depletion, the identification of potential resilient biomarkers or therapeutic targets resistant to immune checkpoint therapies, and ultimately lead to sustained anti-tumor effects. Thus, it offers a novel perspective for advancing tumor immunotherapy.

Ferroptosis increases obesity: Crosstalk between adipocytes and the neuroimmune system.

Ferroptosis requires not only the accumulation of iron ions, but also changes in many ferroptosis-related regulators, including a decrease in GPX4 and inhibition of SLC7A11 for classical ferroptosis, a deletion of FSP1 or GCH1. Surprisingly, adipose tissue (AT) in the obesity conditions is also accompanied by iron buildup, decreased GSH, and increased ROS. On the neurological side, the pro-inflammatory factor released by AT may have first caused ferroptosis in the vagus nerve by inhibiting of the NRF2-GPX4 pathway, resulting in disorders of the autonomic nervous system. On the immune side, obesity may cause M2 macrophages ferroptosis due to damage to iron-rich ATMs (MFehi) and antioxidant ATMs (Mox), and lead to Treg cells ferroptosis through reductions in NRF2, GPX4, and GCH1 levels. At the same time, the reduction in GPX4 may also trigger the ferroptosis of B1 cells. In addition, some studies have also found the role of GPX4 in neutrophil autophagy, which is also worth pondering whether there is a connection with ferroptosis. In conclusion, this review summarizes the associations between neuroimmune regulation associated with obesity and ferroptosis, and on the basis of this, highlights their potential molecular mechanisms, proposing that ferroptosis in one or more cells in a multicellular tissue changes the fate of that tissue.

Crosstalk between the CBM complex/NF-κB and MAPK/P27 signaling pathways of regulatory T cells contributes to the tumor microenvironment.

Regulatory T cells (Tregs), which execute their immunosuppressive functions by multiple mechanisms, have been verified to contribute to the tumor microenvironment (TME). Numerous studies have shown that the activation of the CBM complex/NF-κB signaling pathway results in the expression of hypoxia-inducible factor-1 (HIF-1α) and interleukin-6 (IL-6), which initiate the TME formation. HIF-1α and IL-6 promote regulatory T cells (Tregs) proliferation and migration through the MAPK/CDK4/6/Rb and STAT3/SIAH2/P27 signaling pathways, respectively. IL-6 also promotes the production of HIF-1α and enhances the self-regulation of Tregs in the process of tumor microenvironment (TME) formation. In this review, we discuss how the crosstalk between the CARMA1-BCL10-MALT1 signalosome complex (CBM complex)/NF-κB and MAPK/P27 signaling pathways contributes to the formation of the TME, which may provide evidence for potential therapeutic targets in the treatment of solid tumors.

Prevalence of Clostridium difficile Infection in the Hematopoietic Transplantation Setting: Update of Systematic Review and Meta-Analysis.

Hematopoietic stem cell transplant (HSCT) recipients are vulnerable to Clostridium difficile infection (CDI) due to risk factors such as immunosuppression, antimicrobial use, and frequent hospitalization. We systematically searched PubMed and Embase to screen relevant studies from April 2014 to November 2021. A meta-analysis was performed to identify the association between CDI and hematopoietic transplantation based on the standard mean difference and 95% confidence intervals (CIs). Among the 431 retrieved citations, we obtained 43 eligible articles, which included 15,911 HSCT patients at risk. The overall estimated prevalence of CDI was 13.2%. The prevalence of CDI among the 10,685 allogeneic transplantation patients (15.3%) was significantly higher than that among the 3,840 autologous HSCT recipients (9.2%). Different incidence rates of CDI diagnosis over the last 7 years were found worldwide, of which North America (14.1%) was significantly higher than Europe (10.7%) but not significantly different from the prevalence among Asia (11.6%). Notably, we found that the estimated prevalence of CDI diagnosed by polymerase chain reaction (PCR) (17.7%) was significantly higher than that diagnosed by enzyme immunoassay (11.5%), indicating a significant discrepancy in the incidence rate of CDI owing to differences in the sensibility and specificity of the detection methods. Recurrence of CDI was found in approximately 15% of the initial patients with CDI. Furthermore, 20.3% of CDI cases were severe. CDI was found to be a common complication among HSCT recipients, displaying an evident increase in the morbidity of infection.

Roles of ERRα and TGF-ß signaling in stemness enhancement induced by 1 µM bisphenol A exposure via human neural stem cells.

Bisphenol A (BPA) is a common industrial chemical widely used to produce various plastics and is known to impair neural stem cells (NSCs). However, the effects of low-dose BPA exposure on the stemness maintenance and differentiation fate of NSCs remain unclear in the infant brain. The present study demonstrated that 1 µM BPA promoted human NSC proliferation and stemness, without significantly increasing apoptosis. The Chip-seq experiments demonstrated that both the cell cycle and the TGF-ß signaling pathway were accelerated after treatment with 1 µM BPA. Subsequently, estrogen-related receptor α (ERRα) gene knockout cell lines were constructed using CRISPR/Cas9. Further western blotting and chromatin immunoprecipitation-PCR experiments demonstrated that BPA maintained cell stemness by binding to an EERα receptor and activating the TGF-ß1 signaling pathway, including the downstream factors Aurora kinases B and Id2. In conclusion, the stemness of NSCs could be maintained by BPA at 1 µM through the activation of the ERRα and TGF-ß1 signaling pathways and could restrain the differentiation of NSCs into neurons. The present research further clarified the mechanism of BPA toxicity on NSCs from the novel perspective of ERRα and TGF-ß1 signaling pathways regulated by BPA and provided insights into potential novel methods of prevention and therapy for neurogenic diseases.

Air stagnation in China: Spatiotemporal variability and differing impact on PM2.5 and O3 during 2013-2018.

In recent years, winter PM2.5 and summer O3 pollution which often occurred with air stagnation condition has become a major concern in China. Thus, it is imperative to understand the air stagnation distribution in China and elucidate its impact on air pollution. In this study, three air stagnation indices were calculated according to atmospheric thermal and dynamics parameters using ERA5 data. Two improved indices were more suitable in China, and they displayed similar characteristics: most of the air stagnant days were found in winter, and seasonal distributions showed substantial regional heterogeneity. During stagnation events, flat west or northwest winds at 500 hPa and high pressure at surface dominated, with high relative humidity (RH) and temperature (T), weak winds in most regions. The pollutants concentrations on stagnant days were higher than those on non-stagnant days in most studied areas, with the largest difference of the 90th percentiles of maximum daily 8-h average (MDA8) O3 up to 62.2 µg m-3 in Pearl River Delta (PRD) and PM2.5 up to 95.8 µg m-3 in North China Plain (NCP). During the evolution of stagnation events, the MDA8 O3 concentrations showed a significant increase (6.0 µg m-3 day-1) in PRD and a slight rise in other regions; the PM2.5 concentrations and the frequency of extreme PM2.5 days increased, especially in NCP. Furthermore, O3 was simultaneously controlled by temperature and stagnation except for Xinjiang (XJ), with the average growth rate of 19.5 µg m-3 every 3 °C at 19 °C-31 °C. PM2.5 was dominated by RH and stagnation in northern China while mainly controlled by stagnation in southern China. Notably, the extremes of summer O3 (winter PM2.5) pollution was most associated with air stagnation and T at 25 °C-31 °C (air stagnation and RH >50%). The results are expected to provide important reference information for air pollution control in China.

Mass and number concentration distribution of marine aerosol in the Western Pacific and the influence of continental transport.

We quantify for the first time marine aerosol properties and their differences in the offshore and remote ocean in the mid-latitude South Asian waters, low-latitude South Asian waters, and equatorial waters of the Western Pacific Ocean, based on shipboard cruise observations conducted by the Western Pacific Ocean Scientific Observation Network in winter 2018, and further investigate the effects of long-range transport of continental aerosols on the marine environment. During the overall observation period, the average number concentration of particle matter which aerodynamic diameters<2.5 µm (PM2.5N) was 35.1 ± 87.4 cm-3 and the mass concentration (PM2.5M) was 12.3 ± 9.1 µg/m3. The PM2.5N and PM2.5M during the continental air mass transport period were 7.2 and 1.3 times higher than those during the non-transport period (109.2 ± 169.3 cm-3, 15.9 ± 14.9 µg/m3), respectively. Excluding transport period, the average PM2.5N and PM2.5M are reduced by 120% and 7%. Coarse mode particle number concentration (PM2.5-10N) and mass concentration (PM2.5-10M) are not significantly influenced by continental air masses (only a reduction of 7% and 2%). The variation of marine aerosol concentrations in different latitudes zones is greatly influenced by continental aerosol transport. The offshore PM2.5M/PM10M was 30%, 21%, and 22% in the mid-latitude sea of South Asia, a low-latitude sea of South Asia, and the equatorial sea, respectively. In comparison, in the remote ocean, the distribution ratio of PM2.5M/PM10M tended to be steady (22%-23%), and the background characteristics of marine aerosols were clearly represented. The aerosol concentration decreases with the increase of wind speed during the transport period, and the wind speed reflects the scavenging effect on aerosol. In the non-transport period, the wind speed at the sea surface promotes the generation of marine aerosols, and the impact in wind speed is strongest in the PM2.5-PM5 particle size range.

Vertical evolution of black and brown carbon during pollution events over North China Plain.

The vertical distribution of carbonaceous aerosol impacts climate change, air quality and human health, but there is a lack of in-situ vertical observations of black (BC) and brown carbon (BrC). Thus, the characteristic of vertical profiles of BC concentration, particle number concentration (PNC), O3 concentration and optical absorption of BC and BrC were observed in a suburban site over North China Plain, where heavy pollution of PM2.5 and O3 always occurred in winter and summer, respectively. In winter, during a heavy pollution episode, the BC and PNC was near uniformly distributed within mixing layer (ML) (15.2 ± 6.7 µg m-3 and 678 ± 227 p cm-3, respectively) and decreased with altitude above the ML. The BC heating rate reached about 0.13 K h-1 during the heaviest pollution day. In summer, the BC concentration (2.9 ± 1.3 µg m-3) in ML during the middle O3 pollution events was higher than that (1.7 ± 0.6 µg m-3) during the light O3 pollution. The light absorption coefficients of BC at 880 nm and BrC at 375 nm measured in the early morning were lower than that in the daytime, and the contribution of BrC to total light absorption of carbonaceous aerosols was in the range of 27-47%. In addition, BC was effectively transported to high altitude than BrC in the daytime. The light absorption of secondary BrC in the daytime was higher 10-20% than that in the early morning. Simultaneously, the contribution of secondary BrC to the total BrC light absorption at 375 nm was range from 32% to 68% within 1000 m.