Thermal Ablation Damage Analysis of CFRP Suffering from Lightning Based on Principles of Tomography

Coupled electrical–thermal finite element analysis (FEA) models are widely adopted to analyze the thermal ablation damage of carbon fiber reinforced polymer (CFRP) caused by lightning, but it is still difficult to analyze the ablation due to its complex space geometry. According to the principle of computerized tomography (CT), tomographic images of FEA models’ temperature fields with different thicknesses were obtained to calculate the mass loss and compare the damage morphology. The four areas including Area 0, Area I, Area II, and Area III; were separated from the temperature fields in terms of different vaporization and pyrolysis temperature ranges of carbon fiber (CF) and resin matrix. Ablation mass losses were calculated by pixel statistics and tomographic intervals, which were consistent with the experimental results. The maximum ablation area of unprotected CFRP was found on the tomography images of 50 μm rather than the surface by comparing tomographic images with different thickness due to the influence of the thermal radiation, but this effect was not found in CFRP protected by copper mesh. Some other phenomena, including continuous evolutions of ablation areas and the influence of the intersection angle on the direction of the ablation extension, were also discovered.     

MFC/NFC-Based Foam/Aerogel for Production of Porous Materials: Preparation,Properties and Applications

Nanofibrillated cellulose and microfibrillated cellulose are potential raw materials separated from plant fibers with a high aspect ratio and excellent mechanical properties, which can be applied in various fields (packaging, medicine, etc.). They have unique advantages in the preparation of aerogels and foams, and have attracted widespread attention in recent years. Cellulose-based porous materials have good biodegradability and biocompatibility, while high porosity and high specific surface area endow them with strong mechanical properties and liquid retention performance, which can be used in wall construction, sewage treatment and other fields. At present, the preparation method of this material has been widely reported, however, due to various process problems, the actual production has not been realized. In this paper, we summarize the existing technical problems and main solutions; in the meantime, two stable systems and several drying processes are described, and the application potential of cellulose-based porous materials in the future is described, which provides a reference for subsequent research.     

Diffusion Mechanism of Cinnamon Essential Oils Release from Calcium Alginate Based Controlled Release Films in Contact with Food Simulating Solvent

Calcium alginate based controlled release films with moderate mechanical properties were fabricated in this paper. The diffusion mechanism of these films contacting food simulating solvent (FSS) was explored in some detail. With the increase of glycerol content, the diffusion coefficient (D) values of cinnamon essential oils (CEOs) diffusing to ethanol first increased slowly (0.3–0.6 mL), then vigorously (0.6–0.9 mL), and then mildly (0.9–1.2 mL). The D values of the CEOs diffused to water are all in the order of magnitude of 10⁻¹⁰ cm²/s. The D values of CEOs diffused from films EG3 and EGC1 to aqueous ethanol altered enormously at a small moisture percentage (w = 0.3), then continuously varied vigorously, and at last altered mildly in the range of w = 0.3–1. All the results above indicate that, considering the FSS, the diffusion ability of molecules is jointly determined by the size and distribution of free volume in the system (polymer + diffusive substance + solvents), the intermolecular interaction, and the partition coefficient of the solvents. In addition, several pairs of D values, such as D_EG and D_GA, are very close to each other, indicating that different kinds of interactions between different groups may have the same effect on the diffusion ability of molecules. The correlation between D₁ and D₂ indicates that polymeric emulsifier chains also exist in the polymer-rich layer. All the findings and analysis could provide the theoretical basis and data support for further molecular dynamic simulation and could guide the design of controlled release food packaging for food protection.     

Anti-parasitic activities of specific bacterial extracellular products of Streptomyces griseus SDX-4 against Ichthyophthirius multifiliis

The ciliate Ichthyophthirius multifiliis is one of the most pathogenic parasites of fish maintained in captivity. In this study, effects of bacterial extracellular products of Streptomyces griseus SDX-4 against I. multifiliis were determined. The fermentation liquor of S. griseus was extracted successively in a separating funnel with petroleum ether, ethyl acetate, and n-butanol. In vitro assays revealed that the n-butanol extracts (NBu-E) and ethyl acetate extracts (Eto-E) of S. griseus were observed to be more effective against theronts than the other extracts with median effective concentration (EC₅₀) values of 0.86 and 12.5 mg L^?1, respectively, and significantly reduced the survival of the tomonts and the total number of theronts released by the tomonts (P?<?0.05). All encysted tomonts were killed when the concentration of NBu-E was 30.0 mg L^?1. Results of in vivo test demonstrated that the number of I. multifiliis trophonts on the grass carp treated with NBu-E was markedly lower compared to the control group at 11 days after exposed to theronts (P?<?0.05). In the control group, 100 % mortality was observed owing to heavy I. multifiliis infection at 11 days after the exposure. On the other hand, only 9.5 % mortality owing to parasite infection was recorded in the groups treated with the NBu-E (30 mg L^?1). The median lethal dose (LD₅₀) of NBu-E for grass carp was 152.4 mg L^?1. Our results indicate that n-butanol extract of S. griseus will be useful in aquaculture for controlling I. multifiliis infections.     

Tannic acid modulates intestinal barrier functions associated with intestinal morphology,antioxidative activity,and intestinal tight junction in a diquat-induced mouse model

Oxidative stress is more likely to occur in the intestine compared to other organs because it is located at the interface between an organism and its luminal environment. Tannic acid (TA) is reported to serve as an antioxidant, antimicrobial, anticarcinogenic and antimutagenic agent in various models. In the present study, we evaluated the effects of TA on body weight, intestinal morphology, antioxidative activity, and intestinal barrier in diquat-induced oxidative stress mouse model. The results showed that TA had failed to affect antioxidative enzymes in diquat-challenged mice, while the concentration of 2.5 mg kg⁻¹ to 10 mg kg⁻¹ TA had no negative effect on body weight and enhanced the colon length in mice. The dose of 2.5 mg kg⁻¹ TA ameliorated the morphological damage in the jejunum by increasing the villus height and crypt depth, activated the antioxidative pathway by decreasing jejunal protein expression of Kelch like-ECH-associated protein 1 (KEAP1) and increasing protein expression of Nuclear factor erythroid 2-related factor 2 (NRF2), and affected the intestinal barrier by inhibiting the jejunal mRNA expression of claudin and promoting mRNA expression of zonula occludens (zo-1). In conclusion, the pretreatment of TA in a mouse model of oxidative stress failed to change the antioxidative enzymes but modulated the jejunal morphology, colon length, antioxidative pathway and intestinal barrier in the diquat oxidative model.

The concentration of 2.5 mg kg⁻¹ TA can ameliorate diquat-challenged jejunal injury in mice.     

Neutrophil Dependence of Vascular Remodeling after Mycoplasma Infection of Mouse Airways

Vascular remodeling is a feature of sustained inflammation in which capillaries enlarge and acquire the phenotype of venules specialized for plasma leakage and leukocyte recruitment. We sought to determine whether neutrophils are required for vascular remodeling in the respiratory tract by using Mycoplasma pulmonis infection as a model of sustained inflammation in mice. The time course of vascular remodeling coincided with the influx of neutrophils during the first few days after infection and peaked at day 5. Depletion of neutrophils with antibody RB6-8C5 or 1A8 reduced neutrophil influx and vascular remodeling after infection by about 90%. Similarly, vascular remodeling after infection was suppressed in Cxcr2^−/− mice, in which neutrophils adhered to the endothelium of venules but did not extravasate into the tissue. Expression of the venular adhesion molecule P-selectin increased in endothelial cells from day 1 to day 3 after infection, as did expression of the Cxcr2-receptor ligands Cxcl1 and Cxcl2. Tumor necrosis factor α (TNFα) expression increased more than sixfold in the trachea of wild-type and Cxcr2^−/− mice, but intratracheal administration of TNFα did not induce vascular remodeling similar to that seen in infection. We conclude that neutrophil influx is required for remodeling of capillaries into venules in the airways of mice with Mycoplasma infection and that TNFα signaling is necessary but not sufficient for vascular remodeling.Neutrophils are key effector cells of innate immunity that rapidly arrive at sites of tissue injury to kill bacteria and interact with macrophages and other cells to orchestrate a coordinated immune cell and cytokine response to injury.^1–4 Neutrophils are involved in many inflammatory diseases of the airways and lung, including pneumonia, acute lung injury, sepsis, asthma, cystic fibrosis, bronchitis, and chronic obstructive lung disease,⁵ also contribute to tissue damage in inflammatory conditions of other organs, and play a role in arterial remodeling in atherosclerosis.⁴The signals and events that bring neutrophils to sites of inflammation are well characterized.^6–8 These include expression of endothelial cell adhesion molecules to induce rolling and firm attachment, followed by extravasation into tissues where they release cytokines and other products that can kill bacteria and promote tissue remodeling. The dominant mechanism driving neutrophil influx may be organ-specific.^9,10 Blood vessels of the microcirculation undergo numerous changes in sustained inflammation, and these include structural and functional remodeling of endothelial cells and pericytes.^11–14 Among these changes, capillaries transform into venules that support plasma leakage and leukocyte influx. The contribution of neutrophils to this remodeling is not well understood. Circumferential vessel enlargement is a prominent feature of vascular remodeling–sustained airway inflammation^15–23 and is distinct from more familiar and better-documented types of sprouting angiogenesis.²⁴We asked whether incoming neutrophils contribute to the vascular remodeling, with the thought that the initial wave of leukocyte influx could render blood vessels more efficient for leukocyte adhesion and transmigration. Although leukocyte influx is known to accompany blood vessel remodeling,^15,18,22 it is unknown whether there is a causal relationship and, if so, what is the underlying mechanism? Neutrophils are attractive candidates for contributing to vascular remodeling because they are among the first leukocytes to enter inflamed tissues^4,6,25 and can produce cytokines, growth factors, proteases, and reactive oxygen species that have profound vascular effects.^2–4,26With this background, we sought to determine whether neutrophils are essential for the vascular remodeling that occurs soon after Mycoplasma pulmonis infection, when capillaries transform into venules. In particular, we asked whether neutrophil influx coincides spatially and temporally with vascular remodeling, can vascular remodeling be prevented by neutrophil depletion, and if Cxcr2 signaling is required for the neutrophil influx that accompanies vascular remodeling?To address these questions we examined the relationship between neutrophil influx and vascular remodeling during the first week after M. pulmonis infection of the respiratory tract of mice. The approach was to compare the time course of neutrophil influx and vascular remodeling in the trachea and then determine whether the remodeling was blocked by neutrophil depletion by either of two different antineutrophil antibodies: RB6-8C5 or 1A8. We also tested whether vascular remodeling was prevented by genetic deletion of Cxcr2, which mediates the actions of the chemotactic chemokines Cxcl1 and Cxcl2, which bring neutrophils into inflamed tissues. Because previous studies have shown that vascular remodeling was inhibited by blocking tumor necrosis factor α (TNFα) signaling,¹⁹ we asked whether TNFα expression was increased in wild-type and Cxcr2^−/− mice and whether intratracheal administration of TNFα was sufficient to induce vascular remodeling similar to that seen after infection. Other studies examined the expression of the Cxcr2 ligands, Cxcl1 and Cxcl2. Together, the experiments showed that neutrophil influx was required for vascular remodeling after M. pulmonis infection, and that TNF signaling was necessary but not sufficient for vascular remodeling.