Improving the Corrosion Resistance of Zn-Rich Epoxy Coating with Three-Dimensional Porous Graphene.

To improve the corrosion inhibition of zinc-rich epoxy (ZRE) composite coatings and shed light on the influence of the spatial structure of graphene fillers on the coatings' performance, three-dimensional graphene (3DG) and a conventional graphene sheet (G) were used to modify the ZRE composite paint, respectively. The effect of introducing the 2D G fillers on the anti-corrosion behavior of ZRE was studied comprehensively, and its optimal content was determined to be 0.5 wt%. Interestingly, it was found that, comparing with 2D graphene sheets, the corrosion resistance of the ZRE coating could be enhanced more significantly with incorporating even less 3DG. With introducing only 0.1 wt% 3DG, the corrosion current intensity of the resulting 3DG/ZRE coating was reduced to be about 1/10 that of the G/ZRE coating with the same graphene content and 27% of that of the optimized G/ZRE. The corrosion products of the coating were analyzed with the XRD technique. The results indicated that, in contrast to neat ZRE coating, Zn5(CO3)2(OH)6 was absent from the corroded 3DG/ZRE coating, confirming its improved long-term anti-corrosion performance. The porous interconnected framework and high crystallinity of 3DG could contribute to not only its facilely mixing with epoxy resin, but also its effective incorporation into the conductive network of zinc micro-flakes, thus enhancing the corrosion resistance of its ZRE coating at a lower content. The innovative technology to improve the anti-corrosion performance of the ZRE coatings via using the 3D graphene fillers should be capable to be extended to other 2D fillers, such as MXenes.

Participation of ASK-1 in the cardiomyocyte-protective role of mechanical ventilation in a rat model of myocardial infarction.

Non-invasive positive-pressure ventilation (NIPPV) has been demonstrated to exhibit a cardioprotective function in a rat model of myocardial infarction (MI). However, the mechanism underlying NIPPV-mediated MI progression requires further investigation. We aimed to investigate the effectiveness and corresponding mechanism of NIPPV in an acute MI-induced heart failure (HF) rat model. Thirty each of healthy wild type (WT) and apoptosis signal-regulating kinase 1 (ASK-1)-deficient rats were enrolled in this study. MI models were established via anterior descending branch ligation of the left coronary artery. The corresponding data indicated that NIPPV treatment reduced the heart infarct area, myocardial fibrosis degree, and cardiac function loss in MI rats, and ameliorated apoptosis and reactive oxygen species (ROS) levels in the heart tissue. Furthermore, the expression level of ASK-1 level, a key modulator of the ROS-induced extrinsic apoptosis pathway, was upregulated in the heart tissues of MI rats, but decreased after NIPPV treatment. Meanwhile, the downstream cleavage of caspase-3, caspase-9, and PARP, alongside p38 phosphorylation and FasL expression, exhibited a similar trend to that of ASK-1 expression. The involvement of ASK-1 in NIPPV-treated MI in ASK-1-deficient rats was examined. Although MI modeling indicated that cardiac function loss was alleviated in ASK-1-deficient rats, NIPPV treatment did not confer any clear efficiency in cardiac improvement in ASK-1-knockdown rats with MI modeling. Nonetheless, NIPPV inhibited ROS-induced extrinsic apoptosis in the heart tissues of rats with MI by regulating ASK-1 expression, and subsequently ameliorated cardiac function loss and MI-dependent pathogenic changes in the heart tissue.

Toll-like receptor 4 promotes the inflammatory response in septic acute kidney injury by promoting p38 mitogen-activated protein kinase phosphorylation.

Septic acute kidney injury (AKI) contributes to the mortality and morbidity of sepsis patients. Toll-like Receptor 4 (TLR4) has prominent roles in septic AKI. This study investigated the functions of TLR4 in septic AKI. A septic AKI mouse model was established by cecal ligation and puncture surgery. Mouse kidney function and kidney tissue lesion were examined using corresponding kits and H&E staining. The in vitro cell model of septic AKI was established by lipopolysaccharide induction. Cell viability, inflammatory factor (TNF-α, IL-6, IL-4, IL-1ß, IL-18) levels, pyroptotic cell number changes, lactate dehydrogenase (LDH) activity, myeloperoxidase (MOP) concentration, and levels of pyroptosis-associated protein and MyD88, TRIF and p38 MAPK phosphorylation were determined by MTT, ELISA, FAM-FLICA Caspase-1 Detection kit, other corresponding kits, and Western blot. TLR4 was highly expressed in septic AKI mouse kidney tissues and human septic AKI cells. TLR4 knockdown alleviated kidney injury, increased cell viability, and reduced LDH activity and MPO concentration. TLR4 knockdown reduced cell pyroptosis by repressing p38 MAPK phosphorylation through MyD88/TRIF, suppressed pro-inflammatory factor (TNF-α, IL-6, IL-4, IL-1ß, IL-18) levels, promoted anti-inflammatory factor (IL-4) level, and reduced inflammatory response, thus playing a protective role in septic AKI. Briefly, TLR4 promoted the inflammatory response in septic AKI by promoting p38 MAPK phosphorylation through MyD88/TRIF.

Comparison of Biological Characteristics of Human Umbilical Cord Wharton's Jelly-Derived Mesenchymal Stem Cells from Extremely Preterm and Term Infants.

BACKGROUND: Despite the progress in perinatal-neonatal medicine, complications of extremely preterm infants continue to constitute the major adverse outcomes in neonatal intensive care unit. Human umbilical cord Wharton's Jelly-derived mesenchymal stem cells (HUMSCs) may offer new hope for the treatment of intractable neonatal disorders. This study will explore the functional differences of HUMSCs between extremely preterm and term infants. METHODS: UMSCs from 5 extremely preterm infants(weeks of gestation: 22+5 w,24+4 w,25+3 w,26 w,28 w) and 2 term infants(39 w,39+2 w) were isolated, and mesenchymal markers, pluripotent genes, proliferation rate were analyzed. HUVECs were injured by treated with LPS and repaired by co-cultured with HUMSCs of different gestational ages. RESULTS: All HUMSCs showed fibroblast-like adherence to plastic and positively expressed surface marker of CD105,CD73 and CD90, but did not expressed CD45,CD34,CD14,CD79a and HLA-DR; HUMSCs in extremely preterm exhibited significant increase in proliferation as evidenced by CCK8, pluripotency markers OCT-4 tested by RT-PCR also showed increase. Above all, in LPS induced co-cultured inflame systerm, HUMSCs in extremely preterm were more capable to promote wound healing and tube formation in HUVEC cultures, they promoted TGFß1 expression and inhibited IL6 expression. CONCLUSIONS: Our results suggest that HUMSCs from extremely preterm infants may be more suitable as candidates in cell therapy for the preterm infants.

Mechanical ventilation reduces myocardial injury in rats with acute heart failure by inhibiting cardiomyocyte apoptosis.

OBJECTIVE: To explore the mechanism by which mechanical ventilation improves myocardial injury in rats with acute heart failure (AHF). METHODS: Thirty-six male Sprague Dawley rats were randomized into a sham group, heart failure (HF) group, and mechanical ventilation (MV) group. The AHF rat model was established by pentobarbital perfusion under right internal jugular vein monitoring. The symptoms of heart failure, changes in hemodynamic parameters, cardiac function, N-terminal pro-B-type natriuretic peptide (NT-proBNP), oxidative stress-related indicators, myocardial apoptosis index, and expression of apoptosis-related proteins were compared in an AHF rat model with or without mechanical ventilation. RESULTS: Compared to the sham group, the hemodynamics and cardiac function of MV and HF groups were markedly reduced (P<0.05), and the serum levels of NT-proBNP of MV and HF groups were elevated (P<0.05). The levels of malondialdehyde (MDA) were lowest in the sham group, followed by the MV group, and highest in the HF group. Glutathione (GSH) and superoxide dismutase (SOD) were lowest in the HF group, inermediate in MV group, and highest in the sham group (P<0.05). Mechanical ventilation improved myocardial injury and reduced apoptosis of myocardial cells in a rat model of AHF. CONCLUSION: Mechanical ventilation in the early stage of heart failure can significantly reduce the excessive occurrence of oxidative stress in rats and significantly improve apoptosis in myocardial cells in AHF rats, so as to effectively improve the symptoms of AHF and reduce the mortality of AHF rats.

Single-cell RNA sequencing reveals the potential mechanism of heterogeneity of immunomodulatory properties of foreskin and umbilical cord mesenchymal stromal cells.

BACKGROUND: Mesenchymal stromal cells (MSCs) are heterogeneous populations. Heterogeneity exists within the same tissue and between different tissues. Some studies have found enormous heterogeneity in immunomodulatory function among MSCs derived from different tissues. Moreover, the underlying mechanism of heterogeneity in immunomodulatory abilities is still unclear. METHODS: Foreskin mesenchymal stromal cells (FSMSCs) and human umbilical cord mesenchymal stromal cells (HuMSCs) were isolated and cultured until the third passage. According to the International Association for Cell Therapy standard, we confirmed the cell type. Then, FSMSCs and HuMSCs were cocultured with human peripheral blood mononuclear cells (PBMCs) stimulated by lipopolysaccharide (LPS) in vitro. Furthermore, the supernatant was sampled for an enzyme-linked immunosorbent assay to investigate the secretion of IL-1ß, IL-6, IL-10, TNF-α, and TGF-ß1. Finally, we performed single-cell RNA sequencing (scRNA-seq) of FSMSCs and HuMSCs. RESULTS: We successfully identified FSMSCs and HuMSCs as MSCs. When cocultured with LPS pretreated PBMCs, FSMSCs and HuMSCs could effectively reduced the secretion of IL-1ß and TNF-α. However, FSMSCs stimulated the PBMCs to secrete more IL-10, TGF-ß1, and IL-6. Furthermore, 4 cell subsets were identified from integrated scRNA-seq data, including proliferative MSCs (MKI67+, CD146low+, NG2+, PDGFRB-), pericytes (CD146high+, PDGFRB+, MKI67-, CD31-, CD45-, CD34-), immune MSCs (CXCL12high+, PTGIShigh+, PDGFRB+, CD146-, MKI67-) and progenitor proliferative MSCs (CXCL12low+, PTGISlow+, PDGFRB+, CD146-, MKI67-). Among them, we found that immune MSCs with strengthened transcriptional activity were similar to pericytes with regard to the degree of differentiated. Various of immune-related genes, gene sets, and regulons were also enriched in immune MSCs. Moreover, immune MSCs were determined to be close to other cell subsets in cell-cell communication analysis. Finally, we found that the proportion of immune MSCs in foreskin tissue was highest when comparing the subset compositions of MSCs derived from different tissues. CONCLUSIONS: FSMSCs show better immunomodulatory capacity than HuMSCs in vitro. Moreover, immune MSCs may play a vital role in the heterogeneity of immunoregulatory properties. This study provides new insights suggesting that immune MSCs can be isolated to exert stable immunoregulatory functions without being limited by the heterogeneity of MSCs derived from different tissues.

Seasonal Distribution, Composition, and Inventory of Plastic Debris on the Yugang Park Beach in Zhanjiang Bay, South China Sea.

Plastic debris contamination in marine environments is a global problem that poses a considerable threat to the sustainability and health of coastal ecosystems. Marine beaches, as the key zones where terrestrial plastic debris reach coastal waters, are faced with the increasing pressures of human activities. In this study, we explored the distribution, composition, and inventory of plastic debris over seasonal and tidal zones at the Yugang Park Beach (YPB) in Zhanjiang Bay, South China Sea, to provide a baseline for plastic debris on a marine beach. The results showed mean abundance of plastic debris in summer (6.00 ± 2.10 items/m2) was significantly greater than that in winter (3.75 ± 2.12 items/m2). In addition, the composition of plastic debris ranged in size mainly from 1 to 5 mm and 0.5 to 2.5 cm in winter and summer, respectively. In terms of composition, white plastic debris was the most common (81.1%), and foam was the most abundant (64.4%). Moreover, there was a significant relationship between the abundance of plastic debris and sand grain size fraction (p < 0.05), implying the abundances of microplastic debris were more easily impacted by sand grain size (>2 mm). In total inventory, there were about 1.18 × 105 and 2.95 × 105 items of plastic debris on the YPB in winter and summer, respectively. The tidal variation and human activities are responsible for the plastic debris accumulation. This study provided a method to quantify the inventory of plastic debris on a beach and could be helpful to consider regional tidal variations and critical source areas for effective plastic debris clean-up.

Sequential and Dynamic Variations of IL-6, CD18, ICAM, TNF-α, and Microstructure in the Early Stage of Diabetic Retinopathy.

OBJECTIVE: The purpose of this project is to make sequential and indepth observation of the variations of retinal microvascular, microstructure, and inflammatory mediators at the early stage of diabetic retinopathy (DR) in streptozotocin-induced diabetes mellitus (DM) rats. METHODS: DM was induced by a single intraperitoneal injection of 60 mg/kg body weight streptozotocin (STZ). The fluorescein fundus angiography, hematoxylin and eosin staining, periodic acid-Schiff staining, fluorescence imaging techniques, quantitative real-time PCR, and vascular endothelial growth factor- (VEGF-) A ELISA were performed on the 8th day, at the 4th week, 6th week, 8th week, and 10th week after DM induction, respectively. RESULTS: In this study, we observed not only the decrease of retinal ganglion cells (RGCs) and the increase of endotheliocytes to pericytes (E/P) ratio, acellular capillaries, and type IV collagen-positive strands began to occur on the 8th day after induction but the vascular permeability and new vessel buds began to appear in the diabetes group at the 8th week, while the expression of VEGF-A, VEGF mRNA, IL-6 mRNA, ICAM mRNA, and TNF-α mRNA were significantly higher in the diabetes group compared with the normal group(P < 0.01) on the 8th day after induction and maintained a high expression level throughout the 10-week observation period. However, the expression of CD18 mRNA began to increase significantly at the 4th week after induction and reached a peak at the 6th week. CONCLUSION: Our study indicated the abnormal alterations of microvessels, microstructure, and inflammatory mediators at the early stage of DR, which confirms and supplements the previous research, and also promotes an indepth understanding and exploration of the pathophysiology and underlying pathogenesis of DR.

Hyperintensities of middle frontal gyrus in patients with diabetic optic neuropathy: a dynamic amplitude of low-frequency fluctuation study.

Diabetic optic neuropathy (DON) is a diverse complication of diabetes and its pathogenesis has not been fully elucidated. The purpose of this study was to explore dynamic cerebral activity changes in DON patients using dynamic amplitude of low-frequency fluctuation (dALFF). In total, 22 DON patients and 22 healthy controls were enrolled. The dALFF approach was used in all participants to investigate dynamic intrinsic brain activity differences between the two groups. Compared with HCs, DON patients exhibited significantly increased dALFF variability in the right middle frontal gyrus (P < 0.01). Conversely, DON patients exhibited obviously decreased dALFF variability in the right precuneus (P < 0.01). We also found that there were significant negative correlations between HADS scores and dALFF values of the right middle frontal gyrus in the DON patients (r = -0.6404, P <0.01 for anxiety and r = -0.6346, P <0.01 for depression; HADS, Hospital Anxiety and Depression Scale). Abnormal variability of dALFF was observed in specific areas of the cerebrum in DON patients, which may contribute to distinguishing patients with DON from HCs and a better understanding of DON, hyperintensities of right middle frontal gyrus may be potential diagnostic marker for DON.

White Matter Hyperintensities of Bilateral Lenticular Putamen in Patients with Proliferative Diabetic Retinopathy: A Voxel-based Morphometric Study.

OBJECTIVE: To explore the changes in gray matter volume (GMV) and white matter volume (WMV) in proliferative diabetic retinopathy (PDR) patients using voxel-based morphometry (VBM). PARTICIPANTS AND METHODS: In total, 15 patients (10 males, 5 females) with PDR were enrolled to the patient group and 15 healthy controls (10 males, 5 females) to the control group, matched for age, sex, handedness, and education status. All individuals underwent voxel-based morphometry scans. GMV and WMV were compared between the two groups. RESULTS: GMV in bilateral superior temporal gyrus, sixth area of left cerebellum, left middle temporal gyrus, left orbital inferior frontal gyrus and left middle cingulum gyrus and WMV in left thalamus and left precuneus were significantly lower in patients than controls (P<0.01). Conversely, WMV was significantly higher in bilateral lenticular putamen of patients than controls (P<0.01). CONCLUSION: Abnormal GMV and WMV in many specific areas of the cerebrum provide new insights for exploration of the occurrence and development of DR and its pathophysiology.

Effect of intravitreal injection of ranibizumab on retinal ganglion cells and microvessels in the early stage of diabetic retinopathy in rats with streptozotocin-induced diabetes.

The aim of the present study was to investigate the effect of intravitreal injection of ranibizumab on retinal ganglion cells and microvessels at the early stage of diabetic retinopathy (DR) in rats with streptozotocin-induced diabetes mellitus (DM). DM was induced by a single intraperitoneal injection of 60 mg/kg body weight streptozotocin. A total of 80 diabetic rats were randomly assigned to four treatment groups (n=20 in each group) and were treated with an oculus dexter intravitreal injection of ranibizumab. Groups A and B were injected with ranibizumab two and four weeks after DM-induction, respectively, while groups a and b (controls) were injected with phosphate-buffered saline at the same time points. In addition, 20 normal rats were assigned to group N (blank control; without intraocular injection). Vitreous humors were isolated for vascular endothelial growth factor (VEGF)-A ELISA and retinas were obtained for hematoxylin and eosin staining, periodic acid-Schiff staining and fluorescence imaging techniques at six and eight weeks after the onset of DM. At six and eight weeks, a significantly increased in retinal ganglion cells (RGCs) was observed in group A compared with group a (P<0.01), and in group B compared with group b (P<0.01). In addition, there was a significant difference in the RGC level between groups A and B at six weeks after DM induction (P<0.01), but not at eight weeks (P>0.05). VEGF-A concentrations in rat vitreous humors were significantly lower in groups A and B compared with groups a and b at six and eight weeks after DM induction (P<0.01). Furthermore, the ratio of endotheliocytes to pericytes in groups A and B was significantly lower compared with groups a and b at six and eight weeks (P<0.05). Furthermore, it was also demonstrated that type IV collagen-positive strands were not present in group A during the eight-week observation period, which was significantly different from groups a, b and B (P<0.01). In conclusion, intravitreal injection of ranibizumab at a very early stage of DR in streptozotocin-induced DM rats slowed the progression of DR by reducing vascular regression or damage and maintaining RGC numbers, as well as reducing VEGF-A concentrations.