Cell Gap Research Articles

Physiological response mechanism of alfalfa seedlings roots to typical explosive cyclotrimethylene trinitramine (RDX)

This study explored the physiological response mechanism of alfalfa seedlings roots to a typical explosive, cyclotrimethylenetrinitramine (RDX), so as to improve the efficiency of phytoremediation. The response of plants to different levels of RDX were analyzed from the perspectives of mineral nutrition and metabolic networks. Exposure to RDX at 10–40 mg L−1 had no significant effect on root morphology, but the plant roots significantly accumulated RDX in solution (17.6–40.9%). A 40 mg L−1 RDX exposure induced cell gap expansion and disrupted root mineral metabolism, The key response elements, P, Cu, and Mg, were significantly increased by 1.60–1.66, 1.74–1.90, and 1.85–2.50 times, respectively. The 40 mg L−1 RDX exposure also significantly disturbed root basal metabolism, resulting in a total of 197 differentially expressed metabolites (DEMs). The main response metabolites were lipids and lipid-like molecules, and the key physiological response pathways were arginine biosynthesis and aminoacyl-tRNA biosynthesis. A total of 19 DEMs in root metabolic pathways, including L-arginine, L-asparagine, and ornithine, were significantly responsive to RDX exposure. The physiological response mechanism of roots to RDX therefore involve mineral nutrition and metabolic networks and are of great significance for improving phytoremediation efficiency.

P‐12.10: Study on Optical Performance of Nomally White Reflective LCD

The optical performance of normally white reflective LCDs with various liquid crystal cell parameters and light scattering structures was investigated. The reflectivity and reflective CR both increased first and then decreased as the twist angle increased, whereas the color coordinate of white showed obvious cell gap dependency. Meanwhile, research revealed that while the light‐diffusing film had obvious advantages in terms of reflective optical performance, it could cause significant losses in transmissivity and transmissive CR, necessitating different design considerations for Full‐Reflective LCD and Trans‐Reflective LCD. Finally, the optimum design parameters were applied to our RLCD, which improved the reflectivity and CR while also achieving a better display effect of white pattern.

Performance enhancement of electrodialysis regeneration of deep eutectic solvent for liquid desiccant air conditioning systems

Despite the promising energy-saving potential of the electrodialysis regeneration technique for liquid desiccant regeneration in air conditioning systems, there are still issues that need to be resolved in electrodialysis separation systems, such as the high initial cost owing to the complexity of the cell gaps, over-limiting current, and electro-osmotic flow effects. This study utilized stereolithography (SLA) 3-D printing technology to manufacture a low-cost scalable model of an electrodialysis system. An electrodialysis system with a cell gap of 5 mm and serpentine flow feed spacers was investigated to regenerate deep eutectic solvent (DES) developed from choline chloride and ethylene glycol as a bio-friendly liquid desiccant for air conditioning systems. Ammonium chloride electrode rinsing solution with about 250 mS/cm electric conductivity was utilized to enhance the conductive properties of the system. The optimum parametric operating conditions for the system are found to be around 0.0058 m/s for the circulation flow rate, 0–4 wt.% for the concentration difference of the diluted and regenerated solutions' cells, and 6–8 V voltage supply energy input. In 60 minutes of operation, the current efficiency value of the constructed model was discovered to be as high as 65.82%. Matching the performance threshold of the commercial electrodialysis equipment described in the literature for regenerating lithium chloride conventional liquid desiccant.

Unstable oscillatory flow of non-Brownian suspensions in Hele-Shaw cells

The behavior of neutrally buoyant, non-Brownian suspensions subject to square-wave flow oscillations in Hele-Shaw cells is investigated experimentally. The velocity field across the cell gap is determined by tracking particles in a plane parallel to the main flow. The suspension develops an instability characterized by the growth of a transverse velocity component that is periodic along the main flow direction and in time. No influence of inertia on the development of the instability was observed. The characteristic onset time varies as the inverse of the oscillation amplitude with particle volume fraction dependence similar to that of the shear-induced diffusivity across the cell aperture.

CU06-1004 alleviates vascular hyperpermeability in a murine model of hereditary angioedema by protecting the endothelium.

Over-release of the vasoactive peptide bradykinin (BK) due to mutation in the SERPING1 gene is the leading cause of hereditary angioedema (HAE). BK directly activates endothelial cells and increases vascular permeability by disrupting the endothelial barrier, leading to angioedema affecting face, lips, extremities, gastrointestinal tract, and larynx. Although various pharmacological treatment options for HAE became available during the last decade, they are presently limited and pose a major economic burden on patients. To identify additional therapeutic options for HAE, we evaluated the effect of CU06-1004, an endothelial dysfunction blocker, on BK-induced vascular hyperpermeability and the HAE murine model. To investigate the effect of CU06-1004 on BK-induced vascular hyperpermeability in vivo, we pre-administrated WT mice with the drug and then induced vascular leakage through intravenous injection of BK and observed vascular alternation. Then, SERPING1 deficient mice were used for a HAE murine model. For an in vitro model, the HUVEC monolayer was pre-treated with CU06-1004 and then stimulated with BK. Bradykinin disrupted the endothelial barrier and formed interendothelial cell gaps, leading to hyperpermeability in vivo and in vitro. However, CU06-1004 treatment protected the endothelial barrier by suppressing Src and myosin light chain activation via BK and alleviated hyperpermeability. Our study shows that CU06-1004 oral administration significantly reduced vascular hyperpermeability in the HAE murine model by protecting the endothelial barrier function against BK stimulation. Therefore, protecting endothelium against BK with CU06-1004 could serve as a potential prophylactic/therapeutic approach for HAE patients.

Optical efficiency modulation of vertical alignment liquid crystal displays with transparent shielding and storage electrode

A high-transmittance vertical alignment liquid crystal display (VA-LCD) using a transparent shielding and storage electrode (TSS) design is proposed. The aperture ratio of the proposed four domain TSS pixel with size of 52 × 156 μm improves approximately by 40% over the conventional pixel due to the shielding and storage metal electrode can be replaced by TSS electrode. Experimental results shown that the transmittance of TSS designed panel with 3.2 μm cell gap is 35% higher than that with conventional pixel design, whereas it is only enhanced by 21% when the cell gap is 2.6 μm. The liquid crystal dynamics simulation results revealed that both the effective birefringence and the azimuthally controlled director profile of the liquid crystal layer decreases with TSS pixel design, and these adverse impacts are magnified as the cell gap decreases. This is due to that the introduction of TSS common electrode not only weakens the vertical electric field but also affects the horizontal electric field of liquid crystal layer, which leads to a greater loss of optical efficiency under lower cell gap, resulting in the worse transmittance promotion. The proposed method is expected to be advantageously employed in enhancing transmittance of VA-LCDs for power saving.

Reversibly switching liquid crystals between three orthogonal orientation states for use in rapid-response THz phase shifters.

Liquid crystal (LC) devices for terahertz phase shifters inevitably use a thick cell gap for the required retardation, severely delaying the LC response. To improve the response, we virtually demonstrate novel LC switching between in-plane and out-of-plane for reversible switching between three orthogonal orientation states, broadening the range of continuous phase shifts. This LC switching is realized using a pair of substrates, each with two pairs of orthogonal finger-type electrodes and one grating-type electrode for in- and out-of-plane switching. An applied voltage generates an electric field that drives each switching process between the three distinct orientation states, enabling a rapid response.

Study of Camellia sinensis diploid and triploid leaf development mechanism based on transcriptome and leaf characteristics.

Polyploidization results in significant changes in the morphology and physiology of plants, with increased growth rate and genetic gains as the number of chromosomes increases. In this study, the leaf functional traits, photosynthetic characteristics, leaf cell structure and transcriptome of Camellia sinensis were analyzed. The results showed that triploid tea had a significant growth advantage over diploid tea, the leaf area was 59.81% larger, and the photosynthetic capacity was greater. The morphological structure of triploid leaves was significantly different, the xylem of the veins was more developed, the cell gap between the palisade tissue and the sponge tissue was larger and the stomata of the triploid leaves were also larger. Transcriptome sequencing analysis revealed that in triploid tea, the changes in leaf morphology and physiological characteristics were affected by the expression of certain key regulatory genes. We identified a large number of genes that may play important roles in leaf development, especially genes involved in photosynthesis, cell division, hormone synthesis and stomata development. This research will enhance our understanding of the molecular mechanism underlying tea and stomata development and provide a basis for molecular breeding of high-quality and high-yield tea varieties.

MiR‑221 and miR‑222 regulate cell cycle progression and affect chemosensitivity in breast cancer by targeting ANXA3.

Breast malignancy remains one of the most common causes of cancer-associated mortalities among women. MicroRNA (miR)-221 and miR-222 are homologous miRs and have a substantial impact on cancer progression. In the present study, the regulatory mechanisms of miR-221/222 and its target annexin A3 (ANXA3) in breast cancer cells were investigated. Breast tissue samples were collected to evaluate the expression patterns of miR-221/222 levels in breast cancer cell lines and cancer tissues according to clinical characteristics. The levels of miR-221/222 were increased or decreased in cancer cell lines compared with normal breast cell lines according to cell line subtype. Subsequently, the changes in the progression and invasion of breast cancer cells were investigated using cell proliferation, invasion assay, gap closure and colony formation assays. Western blotting of cell cycle proteins and flow cytometry were performed to evaluate the possible pathway of miR-221/222 and ANXA3 axis. Chemosensitivity tests were performed to explore the suitability of the miR-221/222 and ANXA3 axis as a therapeutic target in breast cancer. The expression levels of miR-221/222 were associated with aggressive characteristics of breast cancer subtypes. Cell transfection assay demonstrated the regulation of breast cancer proliferation and invasiveness by miR-221/222. MiR-221/222 directly targeted the 3'-untranslated region of ANXA3 and suppressed the expression of ANXA3 at the mRNA and protein levels. In addition, miR-221/222 negatively regulated cell proliferation and the cell cycle pathway in breast cancer cells by targeting ANXA3. In combination with adriamycin, downregulation of ANXA3 may sensitize adriamycin-induced cell death to induction of persistent G2/M and G0/G1 arrest. Decreased expression of ANXA3 through increased expression of miR-221/222 reduced breast cancer progression and increased the effectiveness of the chemotherapy drug. The present results indicated the miR-221/222 and ANXA3 axis to be a possible novel therapeutic target for the treatment of breast cancer.

Sodium Butyrate Ameliorates Fluorosis-Induced Neurotoxicity by Regulating Hippocampal Glycolysis In Vivo.

Fluorosis can induce neurotoxicity. Sodium butyrate (SB), a histone deacetylase inhibitor, has important research potential in correcting glucose metabolism disorders and is widely used in a variety of neurological diseases and metabolic diseases, but it is not yet known whether it plays a role in combating fluoride-induced neurotoxicity. This study aims to evaluate the effect of SB on fluoride neurotoxicity and the possible associated mechanisms. The results of HE staining and Morris water maze showed that, in mice exposed to 100 mg/L fluoride for 3 months, the hippocampal cells arranged in loosely with large cell gaps and diminished in number. One thousand milligram per kilogram per day SB treatment improved fluoride-induced neuronal cell damage and spatial learning memory impairment. Western blot results showed that the abundance of malate dehydrogenase 2 (MDH2) and pyruvate dehydrogenase (PDH) in the hippocampus of fluorosis mice was increased, the abundance of pyruvate kinase M (PKM), lactate dehydrogenase (LDH), hexokinase (HK), phosphatidylinositol 3-kinase (PI3K), phosphorylated Akt (P-AKT), and hypoxia-inducible factor 1α (HIF-1α) was inhibited, and the content of lactate and ATP was decreased. SB treatment reversed the decreased glycolysis in the hippocampus of fluorosis mice. These results suggested that SB could ameliorate fluorosis-induced neurotoxicity, which might be linked with its function in regulating glycolysis as well as inhibition of the PI3K/AKT/HIF-1α pathway. Sodium butyrate ameliorates fluorosis-induced neurotoxicity by regulating hippocampal glycolysis in vivo (created with MedPeer (www.medpeer.cn)).

Dynamic changes in whole genome DNA methylation, chromatin and gene expression during mouse lens differentiation

BackgroundCellular differentiation is marked by temporally and spatially coordinated gene expression regulated at multiple levels. DNA methylation represents a universal mechanism to control chromatin organization and its accessibility. Cytosine methylation of CpG dinucleotides regulates binding of methylation-sensitive DNA-binding transcription factors within regulatory regions of transcription, including promoters and distal enhancers. Ocular lens differentiation represents an advantageous model system to examine these processes as lens comprises only two cell types, the proliferating lens epithelium and postmitotic lens fiber cells all originating from the epithelium.ResultsUsing whole genome bisulfite sequencing (WGBS) and microdissected lenses, we investigated dynamics of DNA methylation and chromatin changes during mouse lens fiber and epithelium differentiation between embryos (E14.5) and newborns (P0.5). Histone H3.3 variant chromatin landscapes were also generated for both P0.5 lens epithelium and fibers by chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq). Tissue-specific features of DNA methylation patterns are demonstrated via comparative studies with embryonic stem (ES) cells and neural progenitor cells (NPCs) at Nanog, Pou5f1, Sox2, Pax6 and Six3 loci. Comparisons with ATAC-seq and RNA-seq data demonstrate that reduced methylation is associated with increased expression of fiber cell abundant genes, including crystallins, intermediate filament (Bfsp1 and Bfsp2) and gap junction proteins (Gja3 and Gja8), marked by high levels of histone H3.3 within their transcribed regions. Interestingly, Pax6-binding sites exhibited predominantly DNA hypomethylation in lens chromatin. In vitro binding of Pax6 proteins showed Pax6’s ability to interact with sites containing one or two methylated CpG dinucleotides.ConclusionsOur study has generated the first data on methylation changes between two different stages of mammalian lens development and linked these data with chromatin accessibility maps, presence of histone H3.3 and gene expression. Reduced DNA methylation correlates with expression of important genes involved in lens morphogenesis and lens fiber cell differentiation.

Improving the irradiation resistance of inverted flexible 3J solar cells by adjusting the structure

Highly efficient, flexible, and lightweight thin-film solar cells play an important role in the aerospace field. To improve the radiation resistance of GaInP/GaAs/InGaAs triple-junction inverted metamorphic (IMM3J) solar cells under intense electron irradiation in space, the back field of the top cell and band gap of the middle cell were optimized. Under 1 × 1015 e/cm2 electron irradiation, compared with the reference cell, the attenuation of the conversion efficiency of the backfield-optimized cell and bandgap-adjusted cell was reduced by 10.3 % and 2.8 %, respectively. According to the spectral response and electrical properties, the current-limiting units of the different cells before and after irradiation were analyzed. The increase in the aluminum (Al) component increased the barrier of the AGaInP back surface field, promoted the carrier absorption of the top cell, and increased the initial current of the solar cell. Optimization of the bandgap in the middle cell enables the bottom cell with a redundant current to resist irradiation attenuation. Both adjustments optimize the current-matching relationship between the sub-cells after irradiation. The decay coefficient of the minority carrier was calculated using the electrical displacement damage theory, and the lifetime decay coefficient of the minority carrier was further estimated, which indicated that the radiation resistance was improved. In addition, the mechanism of improving the radiation resistance is discussed in detail by the characteristics of carrier transport, which provides an optimal direction for improving the irradiation characteristics of solar cells in the future.

Combined Application of Exosomes and FPR2 Agonist LXA4 in Controlling Fetal Membrane Inflammation and Promoting Fetal Membrane Tissue Repair.

Preterm premature rupture of membranes (pPROM) is a common pregnancy disease closely related to inflammation. The formyl peptide receptor 2 (FPR2), a member of the G protein-coupled receptor family involved in defense responses, inflammation, and disturbances in glucose and lipid metabolism, is associated with pregnancy diseases. Lipoxin A4 (LXA4) can activate FPR2 and inhibit the inflammatory signals. Exosomes derived from mesenchymal stem cells are good materials for anti-inflammatory and tissue repair. This study aims to investigate the anti-inflammatory and tissue repair effects of the combined application of exosomes derived from human umbilical cord mesenchymal stem cells and FPR2 agonist LXA4. In this study, LPS was used to establish the inflammation model of pregnant mice and HTR8 cells, and LXA4 and exosome treatment were carried out to observe the fetal membranes' tissue repair. The scanning and transmission electron microscopy of fetal membrane tissue indicated that the structure of pPROM tissue was disordered, and the cell gap was significantly increased. The results of the inflammatory mice model suggested that LPS can cause damage to the fetal membrane structure. LXA4 combined with exosome treatment can inhibit the production of MMP2 and MMP9, and promote neovascularization by inhibiting the p38 MAPK/Nuclear factor kB p65 (NFkB) pathway in the inflammation model of HTR8 cells and pregnant mice, thus helping to control inflammation and tissue repair.

The carboxyl-terminal TSP1-homology domain is the biologically active effector peptide of matricellular protein CCN5 that counteracts profibrotic CCN2

Cellular Communication Network (CCN) proteins have multi-modular structures important for their roles in cellular responses associated with organ development and tissue homeostasis. CCN2 has previously been reported to be secreted as a preproprotein that requires proteolytic activation to release its bioactive carboxyl-terminal fragment. Here, our goal was to resolve whether CCN5, a divergent member of the CCN family with converse functions relative to CCN2, releases the TSP1 homology domain as its bioactive signaling entity. The recombinant CCN5 or CCN3 TSP1 homology domains were produced in ExpiCHO-S or DG44 CHO cells as secretory fusion proteins appended to the carboxyl-terminal end of His-Halo-Sumo or amino-terminal end of human albumin, and purified from the cell culture medium. We tested these fusion proteins in various phosphokinase signaling pathways or cell physiologic assays. Fusion proteins with the CCN5 TSP1 domain inhibited key signaling pathways previously reported to be stimulated by CCN2, irrespective of fusion partner. The fusion proteins also efficiently inhibited CCN1/2-stimulated cell migration and gap closure following scratch wound of fibroblasts. Fusion protein with the CCN3 TSP1 domain inhibited these functions with similar efficacy and potency as that of the CCN5 TSP1 domain. The CCN5 TSP1 domain also recapitulated a positive regulatory function previously assigned to full-length CCN5, i.e. induction of estrogen receptor-α mRNA expression in triple negative MDA-MB-231 mammary adenocarcinoma cells and inhibited epithelial-to-mesenchymal transition and CCN2-induced mammosphere formation of MCF7 adenocarcinoma cells. In conclusion, the CCN5 TSP1 domain is the bioactive entity that confers the biologic functions of unprocessed CCN5.

An Evaluation of Surface-Active Agent Hexadecyltrimethylammonium Bromide with Vertical Self-Alignment Properties to Align Liquid Crystals for Various Cell Gap Conditions

We evaluated hexadecyltrimethylammonium bromide (HTAB) for liquid crystals (LCs) in layered ITO cells with various cell gap conditions. HTAB is a surfactant that can self-align vertically on the surface of indium tin oxide (ITO) substrates and induce homeotropic alignment of the LC molecules. For implementing RF devices with HTAB and LCs, we should consider limitations caused by the design conditions which are different from conventional liquid crystal displays such as cell gap. We quantified the concentration of HTAB ([HTAB]) that is necessary to form and maintain a sufficiently dense vertical alignment of 5CB (4-Cyano-4′-pentylbiphenyl). The required [HTAB] for full-homeotropic alignment was increased to the cell gap until it was too large to support the transfer of the surface alignment to the LC molecules, due to the weak anchoring nature of HTAB. We also showed the phase-change characteristic of the LC mixture related to [HTAB] for the design of RF devices driven by light or heat. This study may help to guide the development of new approaches to designing efficient RF devices that use LCs.

Liquid Fraction Effect on Foam Flow through a Local Obstacle.

An experimental study of quasi-two-dimensional liquid foams with varying liquid fractions is presented. Experiments are conducted in a Hele-Shaw cell with a local permeable obstacle placed in the center and filling 35, 60 and 78% of the cell gap. Foam velocity is calculated using a standard cross-correlation algorithm. Estimations of the liquid fraction of the foam are performed using a new simplified method based on a statistical analysis of foam cell structures. The pattern of the foam velocity field varies with increasing liquid fraction, responsible for significant variation of the foam's rheology. The local permeability decreases with increasing obstacle height and liquid fraction. In case of high liquid fraction (5.8×10-2), the permeability coefficient tends to zero for obstacles filling more than 78% of the cell gap.

Effect of Hele–Shaw cell gap on radial viscous fingering

The flow through a Hele–Shaw cell is an experimental prototype to study the flow through a porous medium as well as the flow in microfluidic devices. In context with porous medium flows, it is used to visualize and understand hydrodynamic instabilities like viscous fingering (VF). The gap between the plates of the cell is an important parameter affecting the flow dynamics. However, the effect of the gap on the Hele–Shaw cell flows has been minimally explored. We perform experiments to understand the effect of the gap on VF dynamics. It is observed that a minimum gap is required to observe rigorous fingering instability. The onset time of instability, as well as the width of the fingers, increases with an increment in the gap due to a decrease in the convection. The instability increases with an increase in Péclet number, but the effect of gap width on fingering patterns is evident with broader fingers observed for larger b. The results are validated by performing numerical simulations. It is further shown that the gap-averaged three-dimensional simulations using the Stokes law approach and the two-dimensional Darcy’s law result in a small gap Hele–Shaw cell.

Spatiotemporal linear stability of viscoelastic Saffman–Taylor flows

The temporal and spatiotemporal linear stability analyses of a displaced Oldroyd-B fluid with the mean flow in a horizontally aligned, square, Hele–Shaw cell are reported to identify the regions of topological transition of the advancing interface. The viscosity of the displacing fluid is negligible in comparison to the displaced fluid. While all the inertial terms in the model are retained, the interface is assumed to evolve on a slow timescale compared with the timescale of the perturbation (or the so-called “quasi-stationary” approximation). The parameters governing stability are the Reynolds number Re=b2ρU012η2L, the elasticity number E=12λ(1−ν)η2ρb2, and the ratio of the solvent to the polymer solution viscosity ν=ηsη2, where b,L,U0,ρ,λ are the cell gap, the cell length (or width), the mean flow velocity, the density of the driven fluid, and the polymer relaxation time, respectively. Reasonably good agreement on the relative finger width data computed with our model and the experimental data in the Stokes and the inertial Newtonian regime is found. In the asymptotic limit E(1−ν)≪1, the critical Reynolds number, Rec, diverges as Rec∼[E(1−ν)]−5/3 and the critical wavenumber, αc, increases as αc∼[E(1−ν)]−2/3. In a confined domain, the temporal stability analysis indicates (a) the destabilizing influence of the inertial terms, (b) the destabilizing impact of the finite boundaries near the wall, and (c) the stabilizing impact of elasticity until a critical Reynolds number. The Briggs idea of analytic continuation is deployed to classify regions of absolute and convective instabilities as well as the evanescent modes. The phase diagram reveals the presence of an absolutely unstable region at high values of Reynolds and elasticity number, confirming the role of fluid inertia in triggering a pinch-off.

40.2: A Polarization‐independent Liquid Crystal Device with large Phase Retardation

A polarization-independent liquid crystal (LC) device for large optical phase depth is demonstrated. Using LC layer with the twist angle of 180°, the parallel rubbing LC device shows good polarization-independence. A phase modulator with a 180° twist LC layer and cell gap of 12um was fabricated whose polarization dependence can be lowered to 0.1% for 8.7π phase retardation at 532nm. The proposed LC phase modulator shows great potential for optical communication and imaging systems.

Endoplasmic reticulum stress-controlled autophagic pathway promotes polystyrene microplastics-induced myocardial dysplasia in birds

In complex ecosystems, birds are generally long-lived and occupy high trophic positions, making them good bioindicators for monitoring environmental contaminants. The effects of microplastics (MPs) on myocardial development in bird is currently unknown. Chicks, as a high trophic level terrestrial bird, may be more affected by MPs exposure and. Therefore, we established an in vivo model of chicks exposed to different concentrations of polystyrene microplastics (PS-MPs) and selected 12-day-old chicken embryos in vitro to extract primary cardiomyocytes to further investigate the potential molecular mechanisms of the effect of PS-MPs on myocardial development in birds. Histopathological observations revealed that the PS-MPs treated exhibited loose and irregular myocardial arrangement, large cell gaps and broken myocardial fiber bundles. More mechanistically, TnnT2, Nkx2-5, Gata4, TBX5 and ACTN2 were down-regulated, endoplasmic reticulum (ER) stress markers GRP78, PERK, eIF2α, IRE1, ATF4, ATF6 and CHOP were overexpressed, autophagy-related genes LC3, ATG5, Beclin1 and P62 were down-expressed after PS-MPs exposure, and the addition of 4PBA effectively deregulated the above aberrant expression. Hence, our report indicated that PS-MPs induced myocardial dysplasia in birds is mainly attributed to the ER stress-mediated autophagic pathway. This provided data supporting the protection of birds from the health risks of MPs pollution. More critically, the study of cardiac developmental toxicity in birds may help to better explain or solve the problem of MPs pollution in complex ecosystems.