PM promotes platelet activation and thrombosis via ROS/MAPKs pathway-mediated mitochondrial dysfunction.

Particulate matter (PM) has been identified as a significant risk factor for the development of cardiovascular disease. The current work combined a human panel study with animal experiments intended to investigate the effects of ambient PM on platelet function and tried to figure out the potential mechanisms. The results showed that inhaling PM caused platelet aggregation in both human subjects and mouse models, resulting in changes to both the quantity and function of platelets.

Identification of functional roles and therapeutic targets of the STAT pathway in PM-induced allergic rhinitis.

Background: Increasing evidence suggests that exposure to fine particulate matter (PM) is associated with an elevated risk of respiratory diseases. However, the precise mechanisms by which PM influences inflammatory processes in allergic rhinitis (AR) remain insufficiently understood. The STAT pathway has been identified as a critical mediator of immune and inflammatory responses, but its specific role in modulating PM-induced effects in the nasal mucosa of AR remains unclear.

Chemically Recyclable Poly(tetrathioorthocarbonate)s: Combining High Refractive Index and Abbe Number.

Polymers with high refractive index () and Abbe number () have the potential to be used in advanced optical devices. However, fabricating such materials is challenging because of the inherent trade-off between light refraction and dispersion. Herein, we present an efficient strategy for synthesizing sulfur-rich polymers with tetrathioorthocarbonate as the functional group through the alternating copolymerization of thiiranes and cyclic trithiocarbonates in a controlled fashion.

Ambient PM exposure, physical activity, and cardiovascular dysfunction: Analysis of CHARLS data and experimental study in mice.

Previous studies have confirmed ambient fine particulate matter (PM) as a major environmental risk factor for cardiovascular diseases (CVDs), yet the specific molecular pathways remain poorly understood. Furthermore, while physical activity benefits cardiovascular health, its protective effects against PM-induced damage need further explored. We aimed to investigate the relationship between long-term PM exposure, physical activity, and cardiovascular health, and explore the potential molecular mechanisms.

Combined exposure of sleep deprivation and environmental particulate matter drives aging in multiple systems.

Sleep disturbance accelerates aging, with accompanying exposure to air pollution. However, most studies ignore the combined exposure. This study aimed to investigate the combined effects of sleep deprivation and PM exposure on multi-system aging and to explore the damage mechanisms.

Effects of nasal allergens and environmental particulate matter on brainstem metabolites and the consequence of brain-spleen axis in allergic rhinitis.

Background: The growing consensus links exposure to fine particulate matter (PM) with an increased risk of respiratory diseases. However, little is known about the additional effects of particulate matter on brainstem function in allergic rhinitis (AR). Furthermore, it is unknown to what extent the PM-induced effects in the brainstem affect the inflammatory response in AR.

Chronic PM exposure disrupts intestinal barrier integrity via microbial dysbiosis-triggered TLR2/5-MyD88-NLRP3 inflammasome activation.

Background: PM, a known public health risk, is increasingly linked to intestinal disorders, however, the mechanisms of its impact are not fully understood.

Purpose: This study aimed to explore the impact of chronic PM exposure on intestinal barrier integrity and to uncover the underlying molecular mechanisms.

Methods: C57BL/6 J mice were exposed to either concentrated ambient PM (CPM) or filtered air (FA) for six months to simulate urban pollution conditions.

Closed-loop recycling of sulfur-rich polymers with tunable properties spanning thermoplastics, elastomers, and vitrimers.

The development of closed-loop recycling polymers that exhibit excellent performance is of great significance. Sulfur-rich polymers possessing excellent optical, thermal, and mechanical properties are promising candidates for chemical recycling but lack efficient synthetic strategies for achieving diverse structures. Herein, we report a universal synthetic strategy for producing polytrithiocarbonates, a class of sulfur-rich polymers, via the polycondensation of dithiols and dimethyl trithiocarbonate.

Label-free detection and quantification of ultrafine particulate matter in lung and heart of mouse and evaluation of tissue injury.

While it is known that air borne ultrafine particulate matter (PM) may pass through the pulmonary circulation of blood at the alveolar level between lung and heart and cross the air-blood barrier, the mechanism and effects are not completely clear. In this study the imaging method fluorescence lifetime imaging microscopy is adopted for visualization with high spatial resolution and quantification of ultrafine PM particles in mouse lung and heart tissues. The results showed that the median numbers of particles in lung of mice exposed to ultrafine particulate matter of diameter less than 2.

Exposure to concentrated ambient PM (CAPM) induces intestinal disturbance via inflammation and alternation of gut microbiome.

Air pollution causes a great disease burden worldwide. Recent evidences suggested that PM contributes to intestinal disease. The objective of present study was to investigate the influence of ambient PM on intestinal tissue and microbiome via whole-body inhalation exposure.

NLRP3 inflammasome is involved in ambient PM-related metabolic disorders in diabetic model mice but not in wild-type mice.

Aims: To explore the role of nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome in ambient fine particulate matter (PM)-related metabolic disorders.

Methods: In this study, the C57BL/6 and db/db mice were exposed to concentrated PM or filtered air (FA) using Shanghai Meteorological and Environmental Animal Exposure System (Shanghai-METAS) for 12 weeks. Indices of lipid metabolism, glucose metabolism, insulin sensitivity, and protein expression of NLRP3 inflammasome in visceral adipose tissue (VAT) were measured, respectively.

Parental PM exposure changes Th17/Treg cells in offspring, is associated with the elevation of blood pressure.

Epidemiological evidences have indicated that fine particulate matter (PM ) exposure is associated with the occurrence and development of hypertension. The present study aims to explore the effects of parental PM exposure on blood pressure in offspring and elucidate the potential mechanism. The parental male and female C57BL/6 mice were exposed to concentrated PM or filtered air (FA) using Shanghai Meteorological and Environmental Animal Exposure System (Shanghai-METAS) for 16 weeks.

Functional titanium dioxide nanoparticle conjugated with phthalocyanine and folic acid as a promising photosensitizer for targeted photodynamic therapy in vitro and in vivo.

Photodynamic therapy (PDT) is a promising cancer treatment that can be implemented using various agents. The conventional photosensitizer Al (III) phthalocyanine chloride tetrasulfonic acid (Pc) has limitations of selectivity in tumor targeting, low affinity to cancer cells, and low two-photon absorption. This study presents a novel photosensitizer FA-TiO-Pc, which has the TiO nanoparticle conjugated with a tumor targeting agent of folic acid (FA), and Pc.

Childhood co-exposure of cold stress and PM aggravates the susceptibility and severity of asthma in adulthood of mice.

Both cold stress and ambient fine particle particulate matter (PM ) has been reported to aggravate and induce respiratory problems like asthma, but the mechanism involved in that has not been fully understood. Therefore, the present study is to explore the mechanism involved in the increased susceptibility and severity of asthma caused by cold stress and PM exposure. Urban PM of Shanghai was concentrated to simulate a PM -polluted environment with an average concentration of 400 μg/m , where 1-month young C57BL/6J mice were exposed for 2 months under cold stress (2°C).

Fine Particulate Matter (PM) upregulates expression of Inflammasome NLRP1 ROS/NF-κB signaling in HaCaT Cells.

Skin, as the major organ of a human body, is constantly exposed to PM stimulation, which may exert specific toxic influences on the physiology of skin. This study aims to investigate the effect of PM on the formation of inflammasomes in skin cells and to explore the potential mechanism linking PM and skin inflammation. Changes in mRNA and protein levels of inflammasome-related genes were detected by real-time PCR and western blot in human immortalized epidermal cells (HaCaT) treated with PM at multiple concentrations for 24 hours.

Ambient fine particulate matter induced the elevation of blood pressure through ACE2/Ang(1-7) pathway: The evidence from urine metabolites.

Background: Exposure to ambient fine particulate matter (PM) is associated with various adverse health outcomes. Although several mechanisms have been proposed including oxidative stress and inflammatory responses, the exact mechanism is still unknown. Few studies have investigated the mechanism linking PM and blood pressure (BP).

AMPK activation ameliorates fine particulate matter-induced hepatic injury.

Both the epidemiological and animal experimental studies have reported the association between PM and respiratory, cardiovascular, and metabolic diseases. However, the study linking PM and hepatic injury is few, and the relative mechanism has not been fully elucidated. Thirty-two 6-week-old male C57BL/6 mice were exposed to filtered air (FA) or concentrated PM for 12 weeks using Shanghai Meteorological and Environmental Animal Exposure System ("Shanghai-METAS"), respectively.

Metabolomics analysis of urine from healthy wild type mice exposed to ambient PM.

Background: Ambient fine particulate matter (PM) exposure has been linked with various adverse health outcomes. However, the urine metabolomics changes impacted by PM have not been well elucidated.

Methods: The normal healthy C57BL/6 mice were exposed to concentrated ambient PM (PM) or filtered air (FA) for four weeks using "Shanghai-METAS".

PM exposure and cold stress exacerbates asthma in mice by increasing histone acetylation in IL-4 gene promoter in CD4 T cells.

Asthma is a common chronic inflammatory disease which severely reduces the quality of life in patients. Studies have demonstrated that both PM and cold stress contribute to the development of asthma. However, the combined effects of these two risking factors are unknown.

Parental PM2.5 Exposure-Promoted Development of Metabolic Syndrome in Offspring Is Associated With the Changes of Immune Microenvironment.

Parental exposure to ambient fine particulate matter (PM2.5) has been associated with some of adverse health outcomes in offspring. The association between parental PM2.

AMPK activation attenuates inflammatory response to reduce ambient PM-induced metabolic disorders in healthy and diabetic mice.

Epidemiological and experimental studies have indicated that ambient fine particulate matter (PM) exposure is associated with the occurrence and development of metabolic disorders such as obesity and type 2 diabetes mellitus (T2DM). However, the mechanism is not clear yet, and there are few studies to explore the possible prevention measure. In this study, C57BL/6 and db/db mice were exposed to concentrated PM or filtered air using Shanghai Meteorological and Environmental Animal Exposure System (Shanghai-METAS) for 12 weeks.

Fine particulate matter-induced cardiovascular injury is associated with NLRP3 inflammasome activation in Apo E mice.

Epidemiological evidences have indicated that fine particulate matter (PM) is associated with the increased risk of cardiovascular morbidity and mortality. Although several mechanisms linking PM and inflammatory responses have been widely implicated, the detailed mechanisms involving the occurrence of inflammation in PM-induced adverse effects are lacking. This study aims to investigate whether PM exposure-induced cardiovascular injury is associated with NLRP3 inflammasome activation in apolipoprotein E (Apo E) mice.