Suppression or Inhibition of VEGFs on Splenic Angiosarcoma Cell with Traditional Chinese Medicine Zhi Gan Cao.

Primary splenic angiosarcoma is a very rare disease that causes the development of malignant tumors in the vascular endothelium of the splenic sinuses. Moreover, the disease maintains a very low survival rate for patients to live over 5 years, which is relatively low when compared to another splenic cancer, splenic lymphomas. The treatment options for splenic angiosarcoma narrow down to surgical removal or radiation combined with chemotherapy, but both cost a lot, so discovering potential alternative treatments may eventually increase the possible survival rate. Ginseng and Zhi Gan Cao are both common herbs in Traditional Chinese Medicine (TCM); however, the price of Ginseng is much higher than that of Zhi Gan Cao. A possible reason could be the frequent studies and researches over Ginseng's active ingredient, ginsenoside rh2 or rg3 as they are both potent cancer treatments. The reason to study Zhi Gan Cao and predict its possible potential in cancer treatment is due to the similarity between its active ingredient and the active ingredient in Ginseng, namely, ginsenoside rh2 and licorice saponins. Both TCM contain the active ingredient, triterpenoid saponin, as their main composition, and the further text will predict the possible research and results that may be taken in vitro to reveal the question of whether licorice saponin has the potential to become a major treatment for splenic angiosarcoma or not.

Luteolin and triptolide: Potential therapeutic compounds for post-stroke depression via protein STAT.

Post stroke depression (PSD) is a common neuropsychiatric complication following stroke closely associated with the immune system. The development of medications for PSD remains to be a considerable challenge due to the unclear mechanism of PSD. Multiple researches agree that the functions of gene ontology (GO) are efficient for the investigation of disease mechanisms, and DeepPurpose (DP) is extremely valuable for the mining of new drugs. However, GO terms and DP have not yet been applied to explore the pathogenesis and drug treatment of PSD. This study aimed to interpret the mechanism of PSD and discover important drug candidates targeting risk proteins, based on immune-related risk GO functions and informatics algorithms. According to the risk genes of PSD, we identified 335 immune-related risk GO functions and 37 compounds. Based on the construction of the GO function network, we found that STAT protein may be a pivot protein in underlying the mechanism of PSD. Additionally, we also established networks of Protein-Protein Interaction as well as Gene-GO function to facilitate the evaluation of key genes. Based on DP, a total of 37 candidate compounds targeting 7 key proteins were identified with a potential for the therapy of PSD. Furthermore, we noted that the mechanisms by which luteolin and triptolide acting on STAT-related GO function might involve three crucial pathways, including specifically hsa04010 (MAPK signaling pathway), hsa04151 (PI3K-Akt signaling pathway) and hsa04060 (Cytokine-cytokine receptor interaction). Thus, this study provided fresh and powerful information for the mechanism and therapeutic strategies of PSD.

Controllable and biocompatible 3D bioprinting technology for microorganisms: Fundamental, environmental applications and challenges.

3D bioprinting is a new 3D manufacturing technology, that can be used to accurately distribute and load microorganisms to form microbial active materials with multiple complex functions. Based on the 3D printing of human cells in tissue engineering, 3D bioprinting technology has been developed. Although 3D bioprinting technology is still immature, it shows great potential in the environmental field. Due to the precise programming control and multi-printing pathway, 3D bioprinting technology provides a high-throughput method based on micron-level patterning for a wide range of environmental microbiological engineering applications, which makes it an on-demand, multi-functional manufacturing technology. To date, 3D bioprinting technology has been employed in microbial fuel cells, biofilm material preparation, microbial catalysts and 4D bioprinting with time dimension functions. Nevertheless, current 3D bioprinting technology faces technical challenges in improving the mechanical properties of materials, developing specific bioinks to adapt to different strains, and exploring 4D bioprinting for intelligent applications. Hence, this review systematically analyzes the basic technical principles of 3D bioprinting, bioinks materials and their applications in the environmental field, and proposes the challenges and future prospects of 3D bioprinting in the environmental field. Combined with the current development of microbial enhancement technology in the environmental field, 3D bioprinting will be developed into an enabling platform for multifunctional microorganisms and facilitate greater control of in situ directional reactions.

Insight into the mechanism of DNA methylation and miRNA-mRNA regulatory network in ischemic stroke.

BACKGROUND: Epigenetic changes, such as DNA methylation and miRNA-target gene mechanisms, have recently emerged as key provokers in Ischemic stroke (IS) onset. However, cellular and molecular events harboring these epigenetic alterations are poorly understood. Therefore, the present study aimed to explore the potential biomarkers and therapeutic targets for IS. METHODS: miRNAs, mRNAs and DNA methylation datasets of IS were derived from the GEO database and normalized by PCA sample analysis. Differentially expressed genes (DEGs) were identified, and GO and KEGG enrichment analyses were performed. The overlapped genes were utilized to construct a protein-protein interaction network (PPI). Meanwhile, differentially expressed mRNAs and miRNAs interaction pairs were obtained from the miRDB, TargetScan, miRanda, miRMap and miTarBase databases. We constructed differential miRNA-target gene regulatory networks based on mRNA-miRNA interactions. RESULTS: A total of 27 up-regulated and 15 down-regulated differential miRNAs were identified. Dataset analysis identified 1053 and 132 up-regulated and 1294 and 9068 down-regulated differentially expressed genes in the GSE16561 and GSE140275 datasets, respectively. Moreover, 9301 hypermethylated and 3356 hypomethylated differentially methylated sites were also identified. Moreover, DEGs were enriched in terms related to translation, peptide biosynthesis, gene expression, autophagy, Th1 and Th2 cell differentiation, primary immunodeficiency, oxidative phosphorylation and T cell receptor signaling pathway. MRPS9, MRPL22, MRPL32 and RPS15 were identified as hub genes. Finally, a differential miRNA-target gene regulatory network was constructed. CONCLUSIONS: RPS15, along with hsa-miR-363-3p and hsa-miR-320e have been identified in the differential DNA methylation protein interaction network and miRNA-target gene regulatory network, respectively. These findings strongly posit the differentially expressed miRNAs as potential biomarkers to improve ischemic stroke diagnosis and prognosis.

Carrier Transport Regulation of Pixel Graphene Transparent Electrodes for Active-Matrix Organic Light-Emitting Diode Display.

Integrating a graphene transparent electrode (TE) matrix with driving circuits is essential for the practical use of graphene in optoelectronics such as active-matrix organic light-emitting diode (OLED) display, however it is disabled by the transport of carriers between graphene pixels after deposition of a semiconductor functional layer caused by the atomic thickness of graphene. Here, the carrier transport regulation of a graphene TE matrix by using an insulating polyethyleneimine (PEIE) layer is reported. The PEIE forms an ultrathin uniform film (≤10 nm) to fill the gap of the graphene matrix, blocking horizontal electron transport between graphene pixels. Meanwhile, it can reduce the work function of graphene, improving the vertical electron injection through electron tunneling. This enables the fabrication of inverted OLED pixels with record high current and power efficiencies of 90.7 cd A-1 and 89.1 lm W-1 , respectively. By integrating these inverted OLED pixels with a carbon nanotube-based thin-film transistor (CNT-TFT)-driven circuit, an inch-size flexible active-matrix OLED display is demonstrated, in which all OLED pixels are independently controlled by CNT-TFTs. This research paves a way for the application of graphene-like atomically thin TE pixels in flexible optoelectronics such as displays, smart wearables, and free-form surface lighting.

Electrospinning micro-nanofibers immobilized aerobic denitrifying bacteria for efficient nitrogen removal in wastewater.

Electrospinning micro-nanofibers with exceptional physicochemical properties and biocompatibility are becoming popular in the medical field. These features indicate its potential application as microbial immobilized carriers in wastewater treatment. Here, aerobic denitrifying bacteria were immobilized on micro-nanofibers, which were prepared using different concentrations of polyacrylonitrile (PAN) solution (8%, 12% and 15%). The results of diameter distribution, specific surface area and average pore diameter indicated that 15% PAN micro-nanofibers with tighter surface structure were not suitable as microbial carriers. The bacterial load results showed that the cell density (OD600) and total protein of 12% PAN micro-nanofibers were 107.14% and 106.28% higher than those of 8% PAN micro-nanofibers. Subsequently, the 12% PAN micro-nanofibers were selected for aerobic denitrification under the different C/N ratios (1.5-10), and stable performance was obtained. Bacterial community analysis further manifested that the micro-nanofibers effectively immobilized bacteria and enriched bacterial structure under the high C/N ratios. Therefore, the feasibility of micro-nanofibers as microbial carriers was confirmed. This work was of great significance for promoting the application of electrospinning for microbial immobilization in wastewater treatment.

Insights into heavy metals shock on anammox systems: Cell structure-based mechanisms and new challenges.

Anaerobic ammonium oxidation (anammox) as a low-carbon and energy-saving technology, has shown unique advantages in the treatment of high ammonia wastewater. However, wastewater usually contains complex heavy metals (HMs), which pose a potential risk to the stable operation of the anammox system. This review systematically re-evaluates the HMs toxicity level from the inhibition effects and the inhibition recovery process, which can provide a new reference for engineering. From the perspective of anammox cell structure (extracellular, anammoxosome membrane, anammoxosome), the mechanism of HMs effects on cellular substances and metabolism is expounded. Furthermore, the challenges and research gaps for HMs inhibition in anammox research are also discussed. The clarification of material flow, energy flow and community succession under HMs shock will help further reveal the inhibition mechanism. The development of new recovery strategies such as bio-accelerators and bio-augmentation is conductive to breaking through the engineered limitations of HMs on anammox. This review provides a new perspective on the recognition of toxicity and mechanism of HMs in the anammox process, as well as the promotion of engineering applicability.

Preparation and luminescence properties of Ba2P2O7:Dy3+, Ce3+ phosphors.

In this paper, Ba2-x-yP2O7:xDy3+,yCe3+ phosphors are synthesized by calcining the precursor via chemical co-precipitation. The phase structure, excitation and emission spectra, thermal stability, the chromatic performance of phosphors, and energy transfer from Ce3+ to Dy3+ are studied and discussed. The results indicate the samples keep a stable crystal structure as a high-temperature σ-Ba2P2O7 phase with two different coordination of Ba2+ sites. Ba2P2O7:Dy3+ phosphors can be effectively excited by 349 nm n-UV light and emit 485 nm blue light and a relatively stronger yellow light peaking at 575 nm, corresponding to 4F9/2→6H15/2 and 4F9/2→6H13/2 transitions of Dy3+, implying that Dy3+ mainly occupies the non-inversion symmetric sites. By contrast, Ba2P2O7:Ce3+ phosphors exhibit a broadband of excitation peaking at 312 nm, and two symmetrical emission peaks at 336 nm and 359 nm from 5d1→4F5/2 and 5d1→4F7/2 transitions of Ce3+, showing Ce3+ should merely be presumed to occupy Ba1 site. After Dy3+ and Ce3+ are co-doped, Ba2P2O7:Dy3+, Ce3+ phosphors exhibit the enhanced characteristic blue and yellow emission of Dy3+ with nearly equal intensity under excitation at 323 nm, meaning Ce3+ co-doping increases the symmetry of Dy3+ site as well as the sensitizer. Simultaneously, energy transfer from Dy3+ to Ce3+ is found and discussed. The thermal stability of co-doped phosphors was characterized and briefly analyzed. The color coordinates of Ba2P2O7:Dy3+ phosphors fall in the yellow-green region near the white light, while the emission moves towards the blue-green region after the Ce3+ is co-doped.

(NH4)2Mo3S13/MnFe2O4 hybrid with multiple active sites boosted activation of peroxymonosulfate for removal of tetracycline.

Advanced oxidation processes (AOPs) based on peroxymonosulfate (PMS) activation have attracted much attention in wastewater treatment. Here, a series of (NH4)2Mo3S13/MnFe2O4 (MSMF) composites were prepared and used as PMS activators to remove tetracycline (TC) for the first time. When the mass ratio of (NH4)2Mo3S13 to MnFe2O4 was 4.0 (MSMF4.0), the composite showed remarkable catalytic efficiency for activating PMS to remove TC. Over 93% of TC was removed in MSMF4.0/PMS system in 20 min. The aqueous •OH as well as the surface SO4•- and •OH were the primary reactive species for TC degradation in MSMF4.0/PMS system, and the comprehensive experimental results excluded the contributions of aqueous SO4•-, O2•-, and 1O2, high-valent metal-oxo species, and surface-bound PMS. The Mn(II)/Mn(III), Fe(II)/Fe(III), Mo(IV)/Mo(VI), and S2-/SOx2- all contributed to the catalytic process. MSMF4.0 also showed excellent activity and stability after five cycles and significant degradation efficiency for a variety of pollutants. This work will provide theoretical basis for applying MnFe2O4-based composites in PMS-based AOPs.

Role of COX-2/PGE2 signaling pathway in the apoptosis of rat ovarian granulosa cells induced by MEHP.

OBJECTIVE: MEHP, as the metabolite of DEHP, is a widely used environmental endocrine disruptor. Ovarian granulosa cells participate in maintaining the function of ovary and COX2/PGE2 pathway may regulate the function of granulosa cells. We aimed to explore how COX-2/PGE2 pathway affects cell apoptosis in ovarian granulosa cells caused by MEHP. METHODS: Primary rat ovarian granulosa cells were treated with MEHP (0, 200, 250, 300 and 350 µM) for 48 h. Adenovirus was used for over-expression of COX-2 gene. The cell viability was tested with CCK8 kits. The apoptosis level was tested by flow cytometry. The levels of PGE2 were tested with ELISA kits. The expression levels of COX-2/PGE2 pathway related genes, ovulation-related genes and apoptosis-related genes, were measured with RT-qPCR and Western blot. RESULTS: MEHP decreased the cell viability. After MEHP exposure, the cell apoptosis level increased. The level of PGE2 markedly decreased. The expression levels of COX-2/PGE2 pathway related genes, ovulation-related genes and anti-apoptotic genes decreased; the expression levels of pro-apoptotic genes increased. The apoptosis level was alleviated after over-expression of COX-2, and the level of PGE2 slightly increased. The expression levels of PTGER2 and PTGER4, and the levels of ovulation-related genes increased; the levels of pro-apoptotic genes decreased. CONCLUSION: MEHP can cause cell apoptosis by down-regulating the levels of ovulation-related genes via COX-2/PGE2 pathway in rat ovarian granulosa cells.

Preparation of Cod Skin Collagen Peptides/Chitosan-Based Temperature-Sensitive Gel and Its Anti-Photoaging Effect in Skin.

Background: Photoaging decreases quality of life and increases the risk of skin cancer, underscoring the urgent need to explore natural, high-efficacy, anti-skin photoaging (SP) active substances. Methods: In this study, a gel (CS/CSCPs/ß-GP gel) was prepared using chitosan (CS) and sodium ß-glycerophosphate (ß-GP) through crosslinking with small molecular CSCPs as the carried drug. We evaluated its structural characteristics and properties. The effect of CS/CSCPs/ß-GP gel on the degree of ultraviolet (UV)-induced skin aging of mice was investigated through comparative analysis of skin damage, the integrity of collagen tissues and elastic fibers, levels of reactive oxygen species (ROS) and key inflammatory factors (tumor necrosis factor [TNF]-α and interleukin [IL]-1ß, IL-6, and IL-10), and tissue expression of matrix metalloproteinase-3 (MMP-3) after repeated UV irradiation in a nude mice SP model. Results: The results showed that CS/CSCPs/ß-GP gel was successfully prepared and had the desired characteristics. Compared with CSCPs alone, the CS/CSCPs/ß-GP gel more evidently improved typical photoaging characteristics on mouse dorsal skin. It also increased the moisture content, causing the skin to become glossy and elastic. Pathological skin analysis revealed that this peptide-carrying gel can effectively inhibit epidermal thickening, reduce tissue inflammatory infiltration, suppress collagen fiber degradation, increase the collagen content, alleviate structural elastic fiber damage, and significantly inhibit abnormal MMP-3 expression. In addition, biochemical analysis showed that the CS/CSCPs/ß-GP gel can effectively inhibit the elevated expressions of ROS and key proinflammatory factors (TNF-α, IL-1ß, IL-6) in photoaging skin tissues and promote expression of the anti-inflammatory factor IL-10. Conclusion: SP can cause many clinical skin diseases, such as solar freckle-like nevus, solar keratosis, cutaneous melanoma, and squamous cell carcinoma. CSCPs are a high-efficacy anti-SP natural active substance and CS/CSCPs/ß-GP gel can synergistically enhance the CSCPs' anti-SP effect. The mechanism is likely related to the inhibited activation of ROS/nuclear transcription factor-κB signaling and the expression of downstream inflammatory factors.

PM2.5 induces the abnormal lipid metabolism and leads to atherosclerosis via Notch signaling pathway in rats.

PM2.5 can affect the lipid metabolism and cause atherosclerosis. Abnormal lipid metabolism is a sever risk factor of atherosclerosis and the underlying molecular mechanism still remains unclear. In this study, GPL16956 Agilent-045997 Arraystar human lncRNA microarray V3 (Probe Name Version) platform was used to detect the different genes of lipid metabolism between the normal arterial intima and advanced atherosclerotic plaque, which were downloaded from GEO database. A high-fat diet and vitamin D3 were administered to Wistar rats to establish the atherosclerotic model and another normal healthy 56 rats were used as the non-atherosclerotic exposure groups. The atherosclerotic rats and non-atherosclerotic rats were randomly divided into 4 PM2.5 groups (0, 1.5, 7.5, 37.5 mg/kg), respectively. The results of bioinformatics showed changes in the Notch1, Dll1, Hes1, LDLR and ABCG1 levels. PM2.5 exposure could produce damage to the physiological structure of the aorta, and aggravate atherosclerosis in rats from both non-atherosclerotic and atherosclerotic groups. With the increase of the exposure dose, the levels of TC and TG significantly increased. PM2.5 exposure significantly affected the expression levels of PPARγ, ABCA1, LDLR, CD36, SR-BI and SREBP2. PM2.5 exposure could also affect the expression levels of the Notch signaling pathways which was significantly correlated with the levels of TC and TG. The results proved that PM2.5 exposure could induce and aggravate the atherosclerosis in rats by disrupting lipid metabolism in which Notch signaling pathway may play a significant role.

Energy-Based Continuous Inverse Optimal Control.

The problem of continuous inverse optimal control (over finite time horizon) is to learn the unknown cost function over the sequence of continuous control variables from expert demonstrations. In this article, we study this fundamental problem in the framework of energy-based model (EBM), where the observed expert trajectories are assumed to be random samples from a probability density function defined as the exponential of the negative cost function up to a normalizing constant. The parameters of the cost function are learned by maximum likelihood via an "analysis by synthesis" scheme, which iterates: 1) synthesis step: sample the synthesized trajectories from the current probability density using the Langevin dynamics via backpropagation through time and 2) analysis step: update the model parameters based on the statistical difference between the synthesized trajectories and the observed trajectories. Given the fact that an efficient optimization algorithm is usually available for an optimal control problem, we also consider a convenient approximation of the above learning method, where we replace the sampling in the synthesis step by optimization. Moreover, to make the sampling or optimization more efficient, we propose to train the EBM simultaneously with a top-down trajectory generator via cooperative learning, where the trajectory generator is used to fast initialize the synthesis step of the EBM. We demonstrate the proposed methods on autonomous driving tasks and show that they can learn suitable cost functions for optimal control.

Inhibition of the expression of rgs-3 alleviates propofol-induced decline in learning and memory in Caenorhabditis elegans.

BACKGROUND: Exposure to anesthesia leads to extensive neurodegeneration and long-term cognitive deficits in the developing brain. Caenorhabditis elegans also shows persistent behavioral changes during development after exposure to anesthetics. Clinical and rodent studies have confirmed that altered expression of the regulators of G protein signaling (RGS) in the nervous system is a factor contributing to neurodegenerative and psychological diseases. Evidence from preclinical studies has suggested that RGS controls drug-induced plasticity, including morphine tolerance and addiction. This study aimed to observe the effect of propofol exposure in the neurodevelopmental stage on learning and memory in the L4 stage and to study whether this effect is related to changes in rgs-3 expression. METHODS: Caenorhabditis elegans were exposed to propofol at the L1 stage, and learning and memory abilities were observed at the L4 stage. The expression of rgs-3 and the nuclear distribution of EGL-4 were determined to study the relevant mechanisms. Finally, RNA interference was performed on rgs-3-expressing cells after propofol exposure. Then, we observed their learning and memory abilities. RESULTS: Propofol time- and dose-dependently impaired the learning capacity. Propofol induced a decline in non-associative and associative long-term memory, rgs-3 upregulation, and a failure of nuclear accumulation of EGL-4/PKG in AWC neurons. Inhibition of rgs-3 could alleviate the propofol-induced changes. CONCLUSION: Inhibition of the expression of rgs-3 alleviated propofol-induced learning and memory deficits in Caenorhabditis elegans.

Di(2-ethylhexyl) phthalate induced thyroid toxicity via endoplasmic reticulum stress: In vivo and in vitro study.

Di(2-ethylhexyl) phthalate (DEHP) could induce thyroid injury but the mechanism was unclear. This study combined in vivo and in vitro experiments to clarify the mechanism. In vivo, the offspring of Sprague Dawley rats were gavaged with different doses of DEHP (5, 50, and 250 mg/[kg⋅d]) from in utero to 12 weeks-old. Transcriptome sequencing was used to detect the mRNA expression profile of the offspring's thyroids. Differentially expressed genes were identified, followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. In vitro, Nthy-ori 3-1 cells were exposed to DEHP's metabolite mono (2-ethylhexyl) phthalate (MEHP) to verify the pathway we found by KEGG analysis. The results indicated that DEHP could disorder the thyroid hormones. Compared with the offspring in control group, the mRNA levels of 656 genes were upregulated in the offspring exposed to 50 mg/(kg⋅d) DEHP. The upregulated genes were enriched in the pathway of "protein processing in the endoplasmic reticulum (ER)." It indicated that the ER stress might play significant role in the thyroid toxicity induced by DEHP. In vitro, the mitochondrial membrane potential (ΔΨm) level of cells was decreased while the reactive oxygen species level was increased after MEHP exposure. MEHP increased the intracellular Ca2+ level and induced ER stress. After ER stress was inhibited by the 4-phenylbutyric acid, the thyroid toxicity caused by MEHP was alleviated. Taken together, our results indicated that DEHP could induce thyroid toxicity by activating ER stress.

Towards understanding respiratory particle transport and deposition in the human respiratory system: Effects of physiological conditions and particle properties.

Fly ash is a common solid residue of incineration plants and poses a great environmental concern because of its toxicity upon inhalation exposure. The inhalation health impacts of fly ash is closely related to its transport and deposition in the human respiratory system which warrants significant research for health guideline setting and inhalation exposure protection. In this study, a series of fly ash transport and deposition experiments have been carried out in a bifurcation airway model by optical aerosol sampling analysis. Three types of fly ash samples of different morphologies were tested and their respiratory deposition and transport processes were compared. The deposition efficiencies were calculated and relevant transport dynamics mechanisms were discussed. The influences of physiological conditions such as breathing rate, duration, and fly ash physical properties (size, morphology, and specific surface area) were investigated. The deposition characteristics of respiratory particles containing SARS-CoV-2 has also been analyzed, which could further provide some guidance on COVID-19 prevention. The results could potentially serve as a basis for setting health guidelines and recommending personal respiratory protective equipment for fly ash handlers and people who are in the high exposure risk environment for COVID-19 transmission.

Adverse effects of PM2.5 on cardiovascular diseases.

As an air pollutant, fine particulate matter with a diameter ≤ 2.5 µm (PM2.5) can enter the body through the respiratory tract and cause adverse cardiovascular effects. Here, the effects of PM2.5 on atherosclerosis, hypertension, arrhythmia, myocardial infarction are summarized from the perspective researches of human epidemiology, animal, cell and molecule. The results of this review should be proved useful as a scientific basis for the prevention and treatment of cardiovascular disease caused by PM2.5.

The associations of urinary DEHP metabolite levels, serum thyroid hormones, and thyroid-related genes among the adolescent students from China: a cross-sectional study.

Our study aimed to investigate the associations between DEHP exposure and serum thyroid hormone levels in 347 adolescents and young adults. We measured DEHP metabolites including mono(2-ethylhexyl) phthalate (MEHP), mono(2-ethyl-5-oxohexyl) phthalate (MEOHP), mono(2-ethyl-5-hydroxyhexyl) phthalate (MEHHP), mono(2-ethyl-5-carboxypentyl) phthalate (MECPP), and mono(2-carboxymethyl)hexyl phthalate (MCMHP) in their urine. Total thyroxine (TT4), total triiodothyronine, free triiodothyronine, free thyroxine (FT4), thyroid-stimulating hormone and the mRNA levels of thyroid peroxidase (TPO), thyroglobulin (TG), sodium iodide symporter (NIS), thyroid transcription factor 1 (TTF-1), and paired box gene 8 (PAX-8) in serum were measured. The results of statistical analysis showed that urinary DEHP metabolites were generally negatively associated with TT4 levels in serum. In the males, the FT4 levels showed positive associations with urinary MEHP, MECPP, MCMHP, and ∑DEHP. The mRNA level of TG was significantly positively correlated with the levels of MECPP, MCMHP, and ∑DEHP, while the levels of TTF-1 and PAX-8 mRNA were significantly positively correlated with the levels of DEHP metabolites. Taken together, DEHP may affect the synthesis of TG by altering the normal transcription of TTF-1 and PAX-8, leading to decreased TT4 levels in Chinese adolescents.

Mechanisms of cardiovascular toxicity induced by PM2.5: a review.

An increasing number of studies have shown that exposure to particulate matter with a diameter ≤ 2.5 µm (PM2.5) could affect the onset and development of cardiovascular diseases. To explore the underlying mechanisms, the studies conducted in vitro investigations using different cell lines. In this review, we examined recently published reports cited by PubMed or Web of Science on the topic of cardiovascular toxicity induced by PM2.5 that carried the term in vitro. Here, we summarized the suggested mechanisms of PM2.5 leading to adverse effects and cardiovascular toxicity including oxidative stress; the increase of vascular endothelial permeability; the injury of vasomotor function and vascular reparative capacity in vascular endothelial cell lines; macrophage polarization and apoptosis in macrophage cell lines; and hypermethylation and apoptosis in the AC16 cell line and the related signaling pathways, which provided a new research direction of cardiovascular toxicity of PM2.5.