Association of prenatal exposure to perfluorinated and polyfluoroalkyl substances with childhood neurodevelopment: A systematic review and meta-analysis.

BACKGROUND: Although previous studies have shown an association between prenatal exposure to perfluorinated and polyfluoroalkyl substances (PFAS) and neurodevelopmental disorders in children, the results have been inconsistent. We summarize studies on the association between prenatal PFAS exposure and neurodevelopment in children in order to better understand the relationship. OBJECTIVE: We conducted a meta-analysis of prenatal PFAS exposure and developmental outcomes associated with intellectual, executive function and behavioral difficulty in children to explore the relationship between prenatal exposure to perfluorinated and polyfluoroalkyl substances (PFAS) and neurodevelopmental disorders in children. METHODS: We searched for articles published up to August 3, 2023, included and quantified original studies on PFAS and child Intelligence Quotient (IQ), executive function and behavioral difficulty during pregnancy, and systematically summarized articles that could not be quantified. CONCLUSION: There is evidence of sex-specific relationship between PFAS exposure and children's PIQ. We found that PFOS [ß = -1.56, 95% CI = -2.96, - 0.07; exposure = per 1 ln (ng/ml) increase], PFOA [ß = -1.87, 95% CI = -3.29, - 0.46; exposure = per 1 ln (ng/ml) increase], PFHxS [ß = -2.02, 95% CI = -3.23, - 0.81; exposure = per 1 ln (ng/ml) increase] decreased performance IQ in boys, but PFOS [ß = 1.56, 95% CI = 0.06, 3.06; exposure = per 1 ln (ng/ml) increase] increased performance IQ in girls. PFAS are associated with executive function impairments in children, but not related to behavioral difficulty in children.

1,25-Dihydroxvitamin D3 attenuates the damage of human immortalised keratinocytes caused by Ultraviolet-B.

OBJECTIVE: Ultraviolet-B (UVB) radiation is an important factor in causing skin damage. The study is to explore whether 1,25-Dihydroxvitamin D3(1,25(OH)2D3) will attenuate the damage of human immortalised keratinocytes (HaCaT) cells caused by UVB and relevant underlying mechanisms. METHODS: CCK-8 was employed to determine the UVB irradiation intensity and 1,25(OH)2D3 concentration. Western blot was used to detect the expression of NF-κB, Caspase9, Caspase3, Bax, Bcl2, FADD, CytC, Beclin-1; Flowcytometry was applied to measure the production of ROS. RESULTS: The concentration of 1,25(OH)2D3 used in the study was 100 nM and the UVB irradiation intensity was 20 mJ/cm2. Compared with the HaCaT cells irradiated with UVB, the HaCaT cells that were pre-treated with 1,25(OH)2D3 had lower production of ROS, lower expression of NF-κB, Caspase9, Caspase3, Bax, FADD, CytC and Beclin-1(P < 0.05). CONCLUSION: 1,25(OH)2D3 could inhibit the development of oxidative stress and apoptosis in HaCaTs triggered by UVB. This inhibition might be achieved through the suppression of mitochondria-modulated apoptosis and autophagy. Vitamin D may be a potential UVB protective component.

Identification of C18:1-phytoceramide as the candidate lipid mediator for hydroxyurea resistance in yeast.

Recent studies showed that deletion of ISC1, the yeast homologue of the mammalian neutral sphingomyelinase, resulted in an increased sensitivity to hydroxyurea (HU). This raised an intriguing question as to whether sphingolipids are involved in pathways initiated by HU. In this study, we show that HU treatment led to a significant increase in Isc1 activity. Analysis of sphingolipid deletion mutants and pharmacological analysis pointed to a role for ceramide in mediating HU resistance. Lipid analysis revealed that HU induced increases in phytoceramides in WT cells but not in isc1Δ cells. To probe functions of specific ceramides, we developed an approach to supplement the medium with fatty acids. Oleate (C18:1) was the only fatty acid protecting isc1Δ cells from HU toxicity in a ceramide-dependent manner. Because phytoceramide activates protein phosphatases in yeast, we evaluated the role of CDC55, the regulatory subunit of ceramide-activated protein phosphatase PP2A. Overexpression of CDC55 overcame the sensitivity to HU in isc1Δ cells. However, addition of oleate did not protect the isc1Δ,cdc55Δ double mutant from HU toxicity. These results demonstrate that HU launches a lipid pathway mediated by a specific sphingolipid, C18:1-phytoceramide, produced by Isc1, which provides protection from HU by modulating Swe1 levels through the PP2A subunit Cdc55.

Optimization of preparation method and specificity verification of cat CD19 monoclonal antibody for disease diagnosis and treatment.

CD19 is a surface antigen on B cells that regulates B cell activation and proliferation, participating in B cell signaling. It is expressed in all B cell lineage tumor diseases, making CD19 a significant marker for detecting B cell tumor diseases and an important target for related immunotherapies. In recent years, with the deepening research on canine and feline diseases and the establishment of animal models, the demand for cat CD19 monoclonal antibodies (mAbs) has been steadily increasing. We successfully prepared cat CD19-specific monoclonal antibodies using a KLH-conjugated cat CD19 peptide as an antigen and optimized the antibody production method. The obtained monoclonal antibodies' molecular and cellular affinities were identified using CD19 peptides, eukaryotic overexpressed proteins, and peripheral blood mononuclear cells (PBMCs). The results indicate that the CD19-3H9 and CD19-8A7 monoclonal antibodies prepared in this study specifically bind to the CD19 molecule, demonstrating their suitability for use in ELISA, Western blot, and cell assays. This study successfully produced cat CD19 monoclonal antibodies with specificity and optimized the antibody preparation method, laying the foundation for the diagnosis and targeted drug combination therapy of B cell tumor diseases in both humans and pets.

Perfluorooctanoic acid (PFOA) exposure in relation to the kidneys: A review of current available literature.

Perfluorooctanoic acid is an artificial and non-degradable chemical. It is widely used due to its stable nature. It can enter the human body through food, drinking water, inhalation of household dust and contact with products containing perfluorooctanoic acid. It accumulates in the human body, causing potential harmful effects on human health. Based on the biodegradability and bioaccumulation of perfluorooctanoic acid in the human body, there are increasing concerns about the adverse effects of perfluorooctanoic acid exposure on kidneys. Research shows that kidney is the main accumulation organ of Perfluorooctanoic acid, and Perfluorooctanoic acid can cause nephrotoxicity and produce adverse effects on kidney function, but the exact mechanism is still unknown. In this review, we summarize the relationship between Perfluorooctanoic acid exposure and kidney health, evaluate risks more clearly, and provide a theoretical basis for subsequent research.

Fog scavenging of particulate matters in air pollution events: Observation and simulation in the Yangtze River Delta, China.

Stable atmospheric boundary layer is conducive to the accumulation of atmospheric pollution and the occurrence of fog, and fog has a removal effect on air pollution. In this study, we use the observation and WRF-Chem (Weather Research and Forecasting Model with Chemistry) simulation to analyze the factors affecting the removal efficiency in a continuous fog and haze episode from November 26 to 28, 2018 in Jiangsu Province, such as fog thickness and duration. The results show that the WRF-Chem simulation well reproduces the boundary layer characteristics in the stages of fog formation, development and dissipation. The atmospheric boundary layer provides favorable conditions for the maintenance of fog and air pollution. The inversion layer, with the maximum intensity of 3 °C per 100 m, creates favorable thermal conditions, and the water vapor advection is also conducive to the fog maintenance. The ground observation verifies the wet scavenging of PM2.5 during dense fog events. The scavenging effect is related to the fog duration, and the correlation is positive when the fog is just formed and negative when the fog is dissipating. The PM2.5 concentration decreases from 159 µg m-3 to 38 µg m-3 after the fog lasts for 11 h. The fog has a remarkable scavenging effect on PM2.5 in the vertical direction, due to the deposition effect of fog droplets on the pollutant particles. The PM2.5 concentration on the ground is lower than the vertical average in the fog area, and the scavenging effects during the dense fog periods on November 27 and 28 are 47.7 µg m-3 and 36.1 µg m-3, respectively. The fog duration is mostly concentrated in 3-17 h. When the duration of fog is 4-8 h, the scavenging effect on PM2.5 reaches the strongest, with an average PM2.5 concentration decrease of >70 µg m-3.

The Role of Ferroptosis in the Damage of Human Proximal Tubule Epithelial Cells Caused by Perfluorooctane Sulfonate.

Perfluorooctane sulfonate (PFOS) is a typical persistent organic pollutant and environmental endocrine disruptor that has been shown to be associated with the development of many diseases; it poses a considerable threat to the ecological environment and to human health. PFOS is known to cause damage to renal cells; however, studies of PFOS-induced ferroptosis in cells have not been reported. We used the CCK-8 method to detect cell viability, flow cytometry and immunofluorescence methods to detect ROS levels and Western blot to detect ferroptosis, endoplasmic reticulum stress, antioxidant and apoptosis-related proteins. In our study, we found that PFOS could induce the onset of ferroptosis in HK-2 cells with decreased GPx4 expression and elevated ACSL4 and FTH1 expression, which are hallmarks for the development of ferroptosis. In addition, PFOS-induced ferroptosis in HK-2 cells could be reversed by Fer-1. We also found that endoplasmic reticulum stress and its mediated apoptotic mechanism and P53-mediated antioxidant mechanism are involved in the toxic damage of cells by PFOS. In this paper, we demonstrated for the first time that PFOS can induce ferroptosis in HK-2 cells. In addition, we preliminarily explored other mechanisms of cytotoxic damage by PFOS, which provides a new idea to study the toxicity of PFOS as well as the damage to the kidney and its mechanism.

Perfluorooctane Sulfonate Induces Dysfunction of Human Umbilical Vein Endothelial Cells via Ferroptosis Pathway.

(1) Background: Perfluorooctane sulfonate (PFOS) is a persistent organic pollutant, and it is receiving increasing attention regarding its human health risks due to its extensive use. Endothelial dysfunction is a mark of cardiovascular disease, but the basic mechanism of PFOS-induced endothelial dysfunction is still not fully understood. Ferroptosis is a newly defined regulatory cell death driven by cellular metabolism and iron-dependent lipid peroxidation. Although ferroptosis has been shown to be involved in the pathogenesis of cardiovascular diseases, the involvement of ferroptosis in the pathogenesis of endothelial dysfunction caused by PFOS remains unclear. (2) Purpose: To explore the role of ferroptosis in the dysfunction of endothelial cells and underlying mechanisms. (3) Methods: Human umbilical vein endothelial cells (HUVECs) were exposed to PFOS or PFOS and Fer-1. The viability, morphology change under electronic microscope, lipid-reactive oxygen species (lipid-ROS), and production of nitric oxide (NO) were determined. The expression of glutathione peroxidase 4(GPX4), ferritin heavy chain protein 1 (FTH1), heme oxygenase 1 (HO-1) and Acyl-CoA synthetase long-chain family member 4 (ACSL4) were analyzed via Western blot analysis. (4) Results: PFOS was shown to cause a decrease in viability and morphological changes of mitochondria, and well as an increase in lipid droplets. The expression of GPX4, FTH1 and HO-1 was decreased, and that of ACSL4 was increased after exposure to PFOS. In addition to the above-mentioned ferroptosis-related manifestations, there was also a reduction in NO content. (5) Conclusions: PFOS induces ferroptosis by regulating the GPX4 and ACSL4 pathways, which leads to HUVEC dysfunction.

Biogenic Selenium Nanoparticles Alleviate Intestinal Epithelial Barrier Damage through Regulating Endoplasmic Reticulum Stress-Mediated Mitophagy.

The intestinal barrier plays a fundamental role in body health. Intracellular redox imbalance can trigger endoplasmic reticulum stress (ERS) and mitophagy, leading to intestinal barrier damage. Our previous studies demonstrated that mitophagy is closely associated with the protective effects of biogenic selenium nanoparticles (SeNPs) on intestinal epithelial barrier function. Thus, we hypothesize that ERS and mitophagy are likely involved in the regulatory effects of SeNPs on oxidative stress-induced intestinal epithelial barrier dysfunction. The results showed that oxidative stress or ERS caused the increase of intestinal epithelial permeability. SeNPs effectively alleviated hydrogen peroxide (H2O2-)-induced structural damage of endoplasmic reticulum (ER) and mitochondria of porcine jejunal epithelial cells (IPEC-J2). SeNPs significantly decreased intracellular inositol triphosphate (IP3) and Ca2+ concentration, down-regulated inositol trisphosphate receptor (IP3R) expression level, and up-regulated ER-resident selenoproteins mRNA levels in IPEC-J2 cells exposed to H2O2. In addition, SeNPs pretreatment significantly decreased the intracellular Ca2+, IP3, IP3R, and reactive oxygen species (ROS) levels; protected the structure and function of ER and mitochondria; and effectively alleviated the increase of intestinal epithelial permeability of IPEC-J2 cells exposed to tunicamycin (TM). Moreover, SeNPs significantly inhibited the colocalization of mitochondria and lysosomes. Furthermore, compared with TM model group, SeNPs significantly inhibited the activation of PERK/eIF2α/ATF4 and AMPK/mTOR/PINK1 signaling pathway. The PERK agonist (CCT020312) and the AMPK agonist (AICAR) could reverse the protective effects of SeNPs on IPEC-J2 cells. The PERK inhibitor (GSK2656157) and the AMPK inhibitor (compound C) had a similar effect on IPEC-J2 cells as that of SeNPs. In summary, the protective effects of SeNPs on intestinal barrier dysfunction are closely associated with ERS-related PERK and mitophagy-related AMPK signaling pathway.

Adverse Effects of Perfluorooctane Sulfonate on the Liver and Relevant Mechanisms.

Perfluorooctane sulfonate (PFOS) is a persistent, widely present organic pollutant. PFOS can enter the human body through drinking water, ingestion of food, contact with utensils containing PFOS, and occupational exposure to PFOS, and can have adverse effects on human health. Increasing research shows that the liver is the major target of PFOS, and that PFOS can damage liver tissue and disrupt its function; however, the exact mechanisms remain unclear. In this study, we reviewed the adverse effects of PFOS on liver tissue and cells, as well as on liver function, to provide a reference for subsequent studies related to the toxicity of PFOS and liver injury caused by PFOS.

Dietary supplementation with biogenic selenium nanoparticles alleviate oxidative stress-induced intestinal barrier dysfunction.

Selenium (Se) is an essential micronutrient that promotes body health. Endemic Se deficiency is a major nutritional challenge worldwide. The low toxicity, high bioavailability, and unique properties of biogenic Se nanoparticles (SeNPs) allow them to be used as a therapeutic drug and Se nutritional supplement. This study was conducted to investigate the regulatory effects of dietary SeNPs supplementation on the oxidative stress-induced intestinal barrier dysfunction and its association with mitochondrial function and gut microbiota in mice. The effects of dietary SeNPs on intestinal barrier function and antioxidant capacity and its correlation with gut microbiota were further evaluated by a fecal microbiota transplantation experiment. The results showed that Se deficiency caused a redox imbalance, increased the levels of pro-inflammatory cytokines, altered the composition of the gut microbiota, and impaired mitochondrial structure and function, and intestinal barrier injury. Exogenous supplementation with biogenic SeNPs effectively alleviated diquat-induced intestinal barrier dysfunction by enhancing the antioxidant capacity, inhibiting the overproduction of reactive oxygen species (ROS), preventing the impairment of mitochondrial structure and function, regulating the immune response, maintaining intestinal microbiota homeostasis by regulating nuclear factor (erythroid-derived-2)-like 2 (Nrf2)-mediated NLR family pyrin domain containing 3 (NLRP3) signaling pathway. In addition, Se deficiency resulted in a gut microbiota phenotype that is more susceptible to diquat-induced intestinal barrier dysfunction. Supranutritional SeNPs intake can optimize the gut microbiota to protect against intestinal dysfunctions. This study demonstrates that dietary supplementation of SeNPs can prevent oxidative stress-induced intestinal barrier dysfunction through its regulation of mitochondria and gut microbiota.

Preparation, characterization, and in vivo evaluation of anti-inflammatory activities of selenium nanoparticles synthesized by Kluyveromyces lactis GG799.

Selenium (Se) is an essential micronutrient that has implications in human diseases, including inflammatory bowel disease (IBD), especially with respect to Se deficiencies. Recently, selenium nanoparticles (SeNPs) have attracted significant attention due to their diversity of biological activities and unique advantages including low toxicity and high biological availability. In this study, an eco-friendly, efficient and low-cost method for synthesis of SeNPs by Kluyveromyces lactis GG799 (K. lactis GG799) was established, and the SeNPs were investigated for their physicochemical properties and anti-inflammatory activities in vivo. K. lactis GG799 was able to successfully transform sodium selenite into bright-red SeNPs with particle sizes of 80 and 150 nm and the nanoparticles accumulated intracellularly. Upon isolation, the SeNPs were found to be mainly capped by proteins and polysaccharides by components analysis. Dietary supplementation with 0.6 mg kg-1 Se (in the form of biogenic SeNPs) effectively attenuated dextran sulphate sodium (DSS)-induced ulcerative colitis (UC) in mice by alleviating oxidative stress and intestinal inflammation. These findings suggested that SeNPs synthesized by K. lactis GG799 may be a promising and safe Se supplement for the prevention and treatment of IBD.

Biogenic selenium nanoparticles by Lactobacillus casei ATCC 393 alleviate the intestinal permeability, mitochondrial dysfunction and mitophagy induced by oxidative stress.

Selenium (Se) is an essential trace element. Nano-selenium has attracted great attention due to its various biological properties, especially strong antioxidant activity, high bioavailability, and low toxicity. Our previous studies demonstrated that the selenium nanoparticles (SeNPs) synthesized by Lactobacillus casei ATCC 393 (L. casei ATCC 393) alleviate hydrogen peroxide (H2O2)-induced intestinal epithelial barrier dysfunction via the mitochondrial pathway. However, the mechanism of SeNPs exerting antioxidant activity through the mitochondrial pathway remains unclear. This study was conducted to investigate the role of mitophagy in the protective effects of SeNPs on H2O2-induced porcine intestinal epithelial cells against oxidative damage. The results showed that the SeNPs synthesized by L. casei ATCC 393 had no cytotoxicity on IPEC-J2 cells and effectively antagonized the cytotoxicity of 500 µM H2O2 on IPEC-J2 cells. Moreover, SeNPs attenuated the H2O2-induced intestinal epithelial barrier dysfunction and ROS overproduction, as well as alleviated the adenosine triphosphate (ATP) level and the mitochondrial membrane potential (MMP) decrease. In addition, compared to the oxidative stress model group, pretreatment with biogenic SeNPs significantly up-regulated the expression levels of occludin and claudin-1. Moreover, when compared to the oxidative stress model group, SeNPs inhibited the phosphorylation level of the mammalian target of rapamycin (m-TOR), as well as the expression levels of Unc-51-like kinase 1(ULK1), light chain 3 (LC3)-II/LC3-I, PTEN-induced kinase 1 (PINK1) and Parkin proteins. The fluorescence colocalization images of mitochondria and lysosomes demonstrated that SeNPs significantly reduced the fusion of mitochondria and lysosomes when compared to the oxidative stress model group. These results demonstrate that the SeNPs synthesized by L. casei ATCC 393 can effectively alleviate the H2O2-induced intestinal epithelial barrier dysfunction through regulating mTOR/PINK1-mediated mitophagy.

The Role of Vasoactive Intestinal Peptide and Mast Cells in the Regulatory Effect of Lactobacillus casei ATCC 393 on Intestinal Mucosal Immune Barrier.

Vasoactive intestinal peptide (VIP) plays an important role in the neuro-endocrine-immune system. Mast cells (MCs) are important immune effector cells. This study was conducted to investigate the protective effect of L. casei ATCC 393 on Enterotoxigenic Escherichia coli (ETEC) K88-induced intestinal mucosal immune barrier injury and its association with VIP/MC signaling by in vitro experiments in cultures of porcine mucosal mast cells (PMMCs) and in vivo experiments using VIP receptor antagonist (aVIP) drug. The results showed that compared with the ETEC K88 and lipopolysaccharides (LPS)-induced model groups, VIP pretreatment significantly inhibited the activation of MCs and the release of ß-hexosaminidase (ß-hex), histamine and tryptase. Pretreatment with aVIP abolished the protective effect of L. casei ATCC 393 on ETEC K88-induced intestinal mucosal immune barrier dysfunction in C57BL/6 mice. Also, with the blocking of VIP signal transduction, the ETEC K88 infection increased serum inflammatory cytokines, and the numbers of degranulated MCs in ileum, which were decreased by administration of L. casei ATCC 393. In addition, VIP mediated the regulatory effect of L. casei ATCC 393 on intestinal microbiota in mice. These findings suggested that VIP may mediate the protective effect of L.casei ATCC 393 on intestinal mucosal immune barrier dysfunction via MCs.

Lactobacillus casei ATCC 393 and it's metabolites alleviate dextran sulphate sodium-induced ulcerative colitis in mice through the NLRP3-(Caspase-1)/IL-1ß pathway.

Inflammatory bowel disease (IBD) represents a broad group of intestinal disorders, including ulcerative colitis (UC) and Crohn's disease (CD). Probiotics are increasingly being recognized as a means of treatment for people suffering from IBD. Our previous studies demonstrated that Lactobacillus casei ATCC 393 (L. casei ATCC 393) effectively alleviated enterotoxigenic Escherichia coli K88-induced intestinal barrier dysfunction. This study was conducted to investigate the protective effects of L. casei ATCC 393 and its metabolites on dextran sulfate sodium (DSS)-induced UC in C57BL/6 mice and the potential mechanism of these effects. The results showed that oral administration of L. casei ATCC 393 and its metabolites both effectively reversed the DSS-induced weight loss, and the reduction in the disease activity index (DAI), colon length, and villus height of colon tissue in mice. Compared to the DSS-induced model group, L. casei ATCC 393 and its metabolites significantly inhibited the infiltration of immune cells into the intestinal mucosa, decreased the production of pro-inflammatory factors, and increased the expression of anti-inflammatory factors in the serum and colon tissue, increased the expression levels of occludin, ZO-1, and claudin-1, and reduced the expression of nucleotide binding oligomeric domain-like receptor protein 3 (NLRP3), cysteine proteinase-1 (Caspase-1), IL-1ß, and IL-18. In addition, L. casei ATCC 393 and its metabolites effectively improved DSS-induced gut microbiota dysbiosis. These results suggested that L. casei ATCC 393 and its metabolites alleviated the DSS-induced ulcerative inflammatory response in C57BL/6 mice through the NLRP3-(Caspase-1)/IL-1ß signaling pathway.

Optimized design parameters for CRISPR Cas9 and Cas12a homology-directed repair.

CRISPR-Cas proteins are RNA-guided nucleases used to introduce double-stranded breaks (DSBs) at targeted genomic loci. DSBs are repaired by endogenous cellular pathways such as non-homologous end joining (NHEJ) and homology-directed repair (HDR). Providing an exogenous DNA template during repair allows for the intentional, precise incorporation of a desired mutation via the HDR pathway. However, rates of repair by HDR are often slow compared to the more rapid but less accurate NHEJ-mediated repair. Here, we describe comprehensive design considerations and optimized methods for highly efficient HDR using single-stranded oligodeoxynucleotide (ssODN) donor templates for several CRISPR-Cas systems including S.p. Cas9, S.p. Cas9 D10A nickase, and A.s. Cas12a delivered as ribonucleoprotein (RNP) complexes. Features relating to guide RNA selection, donor strand preference, and incorporation of blocking mutations in the donor template to prevent re-cleavage were investigated and were implemented in a novel online tool for HDR donor template design. These findings allow for high frequencies of precise repair utilizing HDR in multiple mammalian cell lines. Tool availability: https://www.idtdna.com/HDR.

Estimation of radiative forcing and heating rate based on vertical observation of black carbon in Nanjing, China.

Owing to a lack of vertical observations, the impacts of black carbon (BC) on radiative forcing (RF) have typically been analyzed using ground observations and assumed profiles. In this study, a UAV platform was used to measure high-resolution in-situ vertical profiles of BC, fine particles (PM2.5), and relevant meteorological parameters in the boundary layer (BL). Further, a series of calculations using actual vertical profiles of BC were conducted to determine its impact on RF and heating rate (HR). The results show that the vertical distributions of BC were strongly affected by atmospheric thermodynamics and transport. Moreover. Three main types of profiles were revealed: Type I, Type II, Type III, which correspond to homogenous profiles (HO), negative gradient profiles (NG), and positive gradient profiles (PG), respectively. Types I and II were related to the diurnal evolution of the BL, and Type III was caused by surrounding emissions from high stacks and regional transport. There were no obvious differences in RF calculated for HO profiles and corresponding surface BC concentrations, unlike for NG and PG profiles. RF values calculated using surface BC concentrations led to an overestimate of 13.2 W m-2 (27.5%, surface) and 18.2 W m-2 (33.4%, atmosphere) compared to those calculated using actual NG profiles, and an underestimate of approximately 15.4 W m-2 (35.0%, surface) and 16.1 W m-2 (29.9%, atmosphere) compared to those calculated using actual PG profiles. In addition, the vertical distributions of BC HR exhibited clear sensitivity to BC profile types. Daytime PG profiles resulted in a positive vertical gradient of HR, which may strengthen temperature inversion at high altitudes. These findings indicate that calculations that use BC surface concentrations and ignore the vertical distribution of BC will lead to substantial uncertainties in the effects of BC on RF and HR.

Stable and transport indices applied to winter air pollution over the Yangtze River Delta, China.

Previous studies have developed a stable weather index (SWI) based on meteorological elements that adequately represent PM2.5 pollution over the North China Plain (NCP). However, the SWI performs poorly over the Yangtze River Delta (YRD) region because air pollution over this region is affected not only by stagnant weather (STAG) but also by transport (TRANS). For example, air pollutants can be transported from the NCP to the YRD by cold fronts. In this study, an obliquely rotated principal component analysis in the T-model is applied to classify the synoptic patterns of winter weather over the YRD region from 2013 to 2018. Among the four identified synoptic patterns, two of which cause TRANS, one pattern is most likely to cause STAG, and one pattern can lead to either STAG or TRANS depending on the location of high pressure around Shandong province. Due to the large contribution (63%) of TRANS to the total PM2.5 pollution events, a transport pollution index (TPI) is constructed to describe the transport features of PM2.5 pollution over the YRD region. Our results show that, when considering the SWI alone, the correlation coefficients between the SWI and ln(PM2.5) range from 0.50 to 0.57 in the main cities of the YRD. Excitingly, when considering both the TPI and SWI (TPI+SWI), the correlation coefficients increase significantly to 0.63-0.78, suggesting that TPI+SWI better reflects the wintertime PM2.5 pollution level over the YRD region. In addition, satisfactory performance in validation also suggests that TPI+SWI can increase the accuracy of evaluating and forecasting of PM2.5 pollution episodes over regions downstream of source emissions.

Biogenic selenium nanoparticles synthesized by Lactobacillus casei ATCC 393 alleviate diquat-induced intestinal barrier dysfunction in C57BL/6 mice through their antioxidant activity.

Selenium (Se) as an essential micronutrient plays a crucial role in human health. Biogenic selenium nanoparticles (SeNPs) possess attractive biological properties, biocompatibility, stability and low-toxicity. This study was aimed to investigate the protective effect of biogenic SeNPs of size 50-80 nm synthesized by Lactobacillus casei ATCC 393 (L. casei ATCC 393) on diquat-induced intestinal barrier dysfunction in C57BL/6 mice and the intrinsic mechanisms. Our results showed that oral administration of SeNPs significantly inhibited the increase of the serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), diamine oxidase (DAO) and d-lactic acid (d-LA) levels induced by diquat, and increased the total superoxide dismutase (T-SOD), thioredoxin reductase (TrxR) and glutathione peroxidase (GSH-Px) activities in serum and jejunum. Moreover, SeNPs increased the number of goblet cells, decreased the production of reactive oxygen species (ROS), maintained the mitochondrial functions, and improved the expression levels of occludin and claudin-1 in jejunum compared to the diquat-induced oxidative stress model group. In addition, SeNPs activated the nuclear factor (erythroid-derived-2)-like 2 (Nrf2), and improved the protein levels of heme oxygenase (HO)-1 and NADPH dehydrogenase (NQO)-1 compared to other treatment groups. These results suggested that biogenic SeNPs synthesized by L. casei ATCC 393 can protect the intestinal barrier function against oxidative damage via Nrf2-mediated signaling pathway.

Lactobacillus casei ATCC 393 alleviates Enterotoxigenic Escherichia coli K88-induced intestinal barrier dysfunction via TLRs/mast cells pathway.

AIMS: Mast cells play a crucial role in gastrointestinal physiology and pathophysiology. This study was conducted to investigate the role of mast cells (MCs) in the protective effect of Lactobacillus casei ATCC 393 (L. casei ATCC 393) on intestinal barrier function. MAIN METHODS: The regulatory effect of L. casei ATCC 393 on intestinal barrier dysfunction and MCs activation induced by Enterotoxigenic Escherichia coli K88 (ETEC K88) were evaluated by porcine mucosal mast cells (PMMCs)-porcine jejunal epithelial cells (IPEC-J2)-L. casei ATCC 393 co-culture experiments in vitro and MCs stabilizer drug experiment in vivo. KEY FINDINGS: Results showed that L. casei ATCC 393 pretreatment effectively alleviated the reduction of cell viability and increase of permeability in ETEC K88-infected IPEC-J2 cells. L. casei ATCC 393 pretreatment inhibited the increase of proinflammatory cytokines and some other MCs mediators, and decrease of anti-inflammatory cytokines in ETEC K88-infected PMMCs. Cromolyn sodium or L. casei ATCC 393 prevented ETEC K88-induced increase of intestinal epithelial cell permeability in IPEC-J2 cells when co-cultivation with PMMCs. Furthermore, cromolyn sodium or L. casei ATCC 393 pretreatment attenuated ETEC K88-induced increase of MCs mediators, mast cell proteases (MCPs) and carboxypeptidase A3 (CPA3) mRNA levels, and down-regulation of tight junction proteins, Toll-like receptor 2 and 4 (TLR2 and TLR4) expression levels in mice challenged by ETEC K88. SIGNIFICANCE: These results indicated that intestinal barrier dysfunction caused by ETEC K88 was mediated by intestinal mast cell activation which can be prevented by L. casei ATCC 393 via TLRs signaling pathway.