Outer Matrix Research Articles

MiR-4729 regulates TIE1 mRNA m6A modification and angiogenesis in hemorrhoids by targeting METTL14.

BackgroundHemorrhoids are a frequently-occurring disease of the anorectal system that is often accompanied by vascular hyperplasia and edema. A METTL14-mediated RNA N-6 methyladenosine (m6A) modification can improve mRNA stability and increase its transcriptional and translational activities, closely related to the occurrence of many diseases.MethodsWestern blot, qPCR, and immunofluorescence staining were used to detect the levels of gene and protein expression. Haematoxylin and eosin staining was used for histopathological examination. RNA immunoprecipitation-PCR and RNA dot blotting were used to detect mRNA m6A modification.ResultsObvious signs of angiogenesis (CD31+/vWF+) were identified in the hemorrhoids. High levels of METTL14 expression on vascular endothelial cells (CD31+) suggested that angiogenesis was accompanied by differential modification of m6A RNA. It was subsequently found that the level of miR-4729 expression was significantly decreased in hemorrhoid tissues. The luciferase reporter enzyme assay results suggested that miR-4729 silenced its expression by targeting the 3'UTR of METTL14 mRNA. MiR-4729 overexpression in human umbilical vein endothelial cells (HUVECs) inhibited the proliferation and migration of HUVECs in vitro and vascular structure formation in the outer matrix. MiR-4729 overexpression significantly inhibited endogenous METTL14 expression in HUVECs and reduced the entire m6A RNA modification, especially the level of m6A methylation at the specific site of the 3' UTR of TIE1 mRNA. Moreover, miR-4729 overexpression significantly inhibited the molecular loop of the TIE1/VEGFA signaling pathway in HUVECs.ConclusionsOur findings confirmed that the down-regulation of miR-4729 in hemorrhoid vascular endothelial cells was one of the main reasons for vascular proliferation. The overexpression of miR-4729 in vascular endothelial cells decreased the global mRNA methylation and TIE1 mRNA 3'UTR-specific site methylation by silencing METTL14 expression, reducing TIE1 mRNA stability, down-regulating the TIE1/VEGFA signal molecular loop expression, and weakening angiogenesis ability.

MiR-140-5p in Small Extracellular Vesicles From Human Papilla Cells Stimulates Hair Growth by Promoting Proliferation of Outer Root Sheath and Hair Matrix Cells.

The application of dermal papilla cells to hair follicle (HF) regeneration has attracted a great deal of attention. However, cultured dermal papilla cells (DPCs) tend to lose their capacity to induce hair growth during passage, restricting their usefulness. Accumulating evidence indicates that DPCs regulate HF growth mainly through their unique paracrine properties, raising the possibility of therapies based on extracellular vesicles (EVs). In this study, we explored the effects of EVs from high- and low-passage human scalp follicle dermal papilla cells (DP-EVs) on activation of hair growth, and investigated the underlying mechanism. DP-EVs were isolated by ultracentrifugation and cultured with human scalp follicles, hair matrix cells (MxCs), and outer root sheath cells (ORSCs), and we found low-passage DP-EVs accelerated HF elongation and cell proliferation activation. High-throughput miRNA sequencing and bioinformatics analysis identified 100 miRNAs that were differentially expressed between low- (P3) and high- (P8) passage DP-EVs. GO and KEGG pathway analysis of 1803 overlapping target genes revealed significant enrichment in the BMP/TGF-β signaling pathways. BMP2 was identified as a hub of the overlapping genes. miR-140-5p, which was highly enriched in low-passage DP-EVs, was identified as a potential regulator of BMP2. Direct repression of BMP2 by miR-140-5p was confirmed by dual-luciferase reporter assay. Moreover, overexpression and inhibition of miR-140-5p in DP-EVs suppressed and increased expression of BMP signaling components, respectively, indicating that this miRNA plays a critical role in hair growth and cell proliferation. DP-EVs transport miR-140-5p from DPCs to epithelial cells, where it downregulates BMP2. Therefore, DPC-derived vesicular miR-140-5p represents a therapeutic target for alopecia.

Rational design of strong chemical coupling carbon coated N-doped C@MoS2@C nanotubes for high-performance lithium storage

1T-MoS2 is currently under intensive research, because it is a thermodynamically metastable metallic phase with a super electronic conductivity. However, the instability and finite specific capability of 1T-MoS2 hinder its application in batteries. Herein, 1T-MoS2 grown on hollow carbon fiber backbones and coated by a layer of carbon through N–S bond is synthesized by a simple hydrothermal method. N–S bond on the carbon expands the interplanar spacing of 1T-MoS2, which can accommodate more Li+ and improve electronic conductivity. Besides, the carbon coating of 1T-MoS2 grown on hollow carbon fiber backbones is a strong chemical coupling between 1T-MoS2 and the outer carbon matrix by N–S bond, providing a good stable structure on cycling. As a anode material for lithium-ion batteries, the obtained C@MoS2@C nanotubes showed a super capacity (737 mAh g−1) at high current density (2 A g−1) with long-life cycling (1200 cycles).

Solute repositioning to tune the multiple microalloying effects in an Al–Cu alloy with minor Sc, Fe and Si addition

Abstract For multicomponent Al-based alloys, one of the most valuable approaches of microstructural design is to find a path to maximize the multiple microalloying effects while overcoming their negative counterparts. In this paper, triple Sc-Fe-Si microalloying was performed in an Al–Cu alloy to assemble the co-existence of θ′-Al2Cu and Al3Sc precipitates. Besides, the mutual interactions among triple microalloying elements were utilized to maximize the positive effects on tailoring the dual precipitates, as illustrated in two goals of microstructural design: (i). As to θ′-Al2Cu plates, the multiple Sc-Fe-Si segregation at θ′-Al2Cu/matrix interface was preferentially created in the alloy before creep (as-aged condition). During subsequent high-temperature creep, such interfacial warden will be rapidly reinforced by solute repositioning, as a process of accumulating solutes diffusing from both inner θ′-Al2Cu precipitate and outer matrix to limit the interfacial migration. (ii). For Al3Sc precipitates, the beneficial Si microalloying effect on encouraging the nucleation of Sc-rich entities (precursor of Al3Sc) was successfully acquired during aging, while the detrimental Si effect on accelerating Al3Sc coarsening is generally prohibited by tuning Fe–Si synergy within Al3Sc interior. The establishments of (i) and (ii) enable the satisfactory dispersion as well as the outstanding thermal stability of dual precipitates in the current Al-Cu-Sc-Fe-Si system, leading to a good creep resistance at a high homologous temperature of 0.61Tm ~ 300 °C (where Tm is the melting temperature of the α-Al matrix).

The Effects of Grain Size and Twins Density on High Temperature Oxidation Behavior of Nickel-Based Superalloy GH738.

In the present study, surface treatment techniques such as room temperature machining (RTM) and low temperature burnishing (LTB) processing have been used to improve the microstructure of GH738 superalloy. Nano-grains and nano-twins are obtained on the top surface of RTM and LTB specimens. It is found that although the grain size of RTM and LTB specimens is almost the same, different types of nano-twins have been produced. Moreover, the effect of RTM and LTB processing on high temperature oxidation behavior of nickel-based superalloy GH738 at 700 °C is investigated. The result shows that LTB specimen has the best high temperature oxidation resistance owing to the formation of nano-grains and higher twins density, which induce to form a continuous protective Al2O3 layer at the interface between outer oxide layer and matrix. It is observed that this layer inhibits the inward diffusion of O and outward diffusion of Ti and significantly improves oxidation resistance of LTB specimen. Furthermore, the effects of nano-grains and crystal defects on the diffusion mechanism of elements are clarified during the high temperature oxidation test.

Development of natural polymeric microcapsules for antimicrobial drug delivery: triclosan loaded chitosan and alginate-based microcapsules

The goal of this work was the development of natural polymeric microcapsules for antimicrobial drug delivery – triclosan loaded alginate and chitosan-based microcapsules for potential coating applications in substrates such as textiles or plastics. Microcapsules containing 2.5% (w/w) or 3% (w/w) triclosan in both core and matrix were synthesized and evaluated by Fourier-transform infrared spectroscopy, scanning electron microscopy, confocal microscopy, differential scanning calorimetry, thermogravimetry, and antimicrobial activity. The microcapsules produced featured spherical and mostly irregularly-shaped surfaces composed by an alginate core in a chitosan outer matrix, as revealed by confocal microscopy, and antimicrobial activity against S. aureus and E. coli with inhibition halos up to 60 mm and 25 mm respectively, granted by a triclosan loading of 61.66%. The thermal analysis suggested that the polymers protected the active substance from temperature-induced degradation. In conclusion, these microcapsules may be applied toward antimicrobial functionalization of plastics, textiles and other materials.

Mcl-1-mediated mitochondrial fission protects against stress but impairs cardiac adaptation to exercise

Myeloid cell leukemia-1 (Mcl-1) is a structurally and functionally unique anti-apoptotic Bcl-2 protein. While elevated levels of Mcl-1 contribute to tumor cell survival and drug resistance, loss of Mcl-1 in cardiac myocytes leads to rapid mitochondrial dysfunction and heart failure development. Although Mcl-1 is an anti-apoptotic protein, previous studies indicate that its functions extend beyond regulating apoptosis. Mcl-1 is localized to both the mitochondrial outer membrane and matrix. Here, we have identified that Mcl-1 in the outer mitochondrial membrane mediates mitochondrial fission, which is independent of its anti-apoptotic function. We demonstrate that Mcl-1 interacts with Drp1 to promote mitochondrial fission in response to various challenges known to perturb mitochondria morphology. Induction of fission by Mcl-1 reduces nutrient deprivation-induced cell death and the protection is independent of its BH3 domain. Finally, cardiac-specific overexpression of Mcl-1OM, but not Mcl-1Matrix, contributes to a shift in the balance towards fission and leads to reduced exercise capacity, suggesting that a pre-existing fragmented mitochondrial network leads to decreased ability to adapt to an acute increase in workload and energy demand. Overall, these findings highlight the importance of Mcl-1 in maintaining mitochondrial health in cells.

Coating Strategy for Surface Modification of Stainless Steel Wire to Improve Interfacial Adhesion of Medical Interventional Catheters.

Poor interfacial bonding between stainless steel wire and the inner and outer layer resin matrix significantly affects the mechanical performance of braid-reinforced composite hollow fiber tube, especially torsion control. In this work, a coating of thermoplastic polyurethane (TPU) deposited on the surface of stainless steel wire greatly enhanced the mechanical performance of braid-reinforced composite hollow fiber tube. This method takes advantage of the hydrogen bonding between polyether block amide (PEBA) and thermoplastic polyurethane (TPU) for surface modification of stainless steel wire, as well as the good compatibility between PEBA and TPU. The mechanical properties of composited tubes demonstrate that the interlaminar shear strength, modulus of elasticity, and torque transmission properties were enhanced by 27.8%, 42.1%, and 41.4%, respectively. The results indicating that the interfacial adhesion between the coated stainless steel wire and the inner and outer matrix was improved. In addition, the interfacial properties of composite hollow fiber tube before and after coating was characterized by the optical microscope, and results show that the interfacial adhesion properties of the modified stainless steel wire reinforced resin matrix composites were greatly improved.

Proteomic and Metabolite Profiling Reveals Profound Structural and Metabolic Reorganization of Adipocyte Mitochondria in Obesity.

Previous studies have revealed decreased mitochondrial respiration in adipocytes of obese mice. This study aimed to identify the molecular underpinnings of altered mitochondrial metabolism in adipocytes. Untargeted proteomics of mitochondria isolated from adipocytes and metabolite profiling of adipose tissues were conducted in diet-induced obese (DIO) and lean mice. Subcutaneous and intra-abdominal adipose tissues were studied to depict depot-specific alterations. In subcutaneous adipocytes of DIO mice, changes in proteins related to mitochondrial structure and function were observed. Mitochondrial proteins of the inner and outer membrane were strongly reduced, whereas proteins of key matrix metabolic pathways were increased in the obese versus lean state, as further substantiated by metabolite profiling. A pronounced decrease in the oxidative phosphorylation (OXPHOS) enzymatic equipment and cristae density of the inner membrane was identified. In intra-abdominal adipocytes, similar systematic downregulation of the OXPHOS machinery in obesity occurred, but there was no regulation of outer membrane or matrix proteins. Protein components of the OXPHOS machinery are systematically downregulated in adipose tissues of DIO mice compared with lean mice. Loss of the mitochondrial OXPHOS capacity in adipocytes may aggravate the development of metabolic disease.

Biomineralization pathways in calcifying dinoflagellates: Uptake, storage in MgCaP-rich bodies and formation of the shell

Little is known about shell formation of calcareous dinoflagellates, despite the fact that they are one of the major calcifying organisms of the phytoplankton. Here, calcitic cyst formation in two representative members of calcareous dinoflagellates is investigated using cryo-electron microscopy (cryo-SEM and cryo-FIB-SEM) in combination with micro-Raman and infrared spectroscopy. Only calcein-AM and not calcein enters these cells, indicating active uptake of calcium and other divalent cations. Multifunctional vacuoles containing crystalline inclusions are observed, and the crystals are identified as anhydrous guanine in the β-form. The same vacuolar enclosures contain dense magnesium-, calcium-, and phosphorous-rich mineral bodies. These bodies are presumably secreted into the outer matrix where calcite forms. Calcite formation occurs via multiple independent nucleation events, and the different crystals grow with preferred orientation into a dense reticular network that forms the mature calcitic shell. We suggest a biomineralization pathway for calcareous dinoflagellates that includes (1) active uptake of calcium through the membranes, (2) deposition of Mg2+- and Ca2+-ions inside disordered MgCaP-rich mineral bodies, (3) secretion of these bodies to the inter-membrane space, and (4) Formation and growth of calcite into a dense reticulate network. This study provides new insights into calcium uptake, storage and transport in calcifying dinoflagellates. Statement of significanceLittle is known about the shell formation of calcareous dinoflagellates, despite the fact that they are one of the major calcifying organisms of the phytoplankton. We used state-of-the-art cryo-electron microscopy (cryo-SEM and cryo-FIB-SEM) in combination with micro-Raman spectroscopy to provide new insights into mineral formation in calcifying dinoflagellates.To date, intracellular crystalline calcite was assumed to be involved in calcite shell formation. Surprisingly, we identify these crystalline inclusions as anhydrous guanine suggesting that they are not involved in biomineralization. Instead, a key finding is that MgCaP-rich bodies are probably secreted into the outer matrix where the calcite shell is formed. We suggest that these bodies are an essential part of Ca-uptake, -storage and –transport and propose a new biomineralization model.

Biomineralization Pathways in Calcifying Dinoflagellates: Uptake, Storage in MgCaP-Rich Bodies and Formation of the Shell

Little is known about the formation of the shells of calcareous dinoflagellates, despite the fact that they are one of the major calcifying organisms of the phytoplankton. Here, we investigate calcitic cyst formation in two representative members from different clades of calcareous dinoflagellates using cryo-electron microscopy (cryo-SEM and cryo-FIB-SEM) in combination with micro-Raman and infrared spectroscopy.Only calcein-AM and not calcein enters these cells, indicating active uptake of calcium and other divalent cations. Multifunctional vacuoles containing crystalline inclusions are observed in both species and we identify the crystals as anhydrous guanine in the β-form. We also observe in the same vacuolar enclosures, dense magnesium, calcium and phosphorous rich mineral bodies by cryo EDX. These bodies are secreted into the outer matrix space where calcite forms. Calcite formation occurs via multiple independent nucleation events and the different crystals grow with preferred orientation into a dense reticular network that forms the calcitic cyst. The degree of atomic order of this calcite is less than that of geological calcite. We suggest a common biomineralization pathway for these two calcifying dinoflagellates: (1) Uptake of calcium and other cations through the membranes. (2) Deposition of Mg2+ and Ca2+ ions inside a disordered MgCaP-body. (3) Secretion of these bodies to the space between the outer membranes. (4) Formation and growth of calcite bodies into a dense reticulate network that forms the mature calcitic shell. This study provides new insights into calcium uptake, storage and transport in calcifying dinoflagellates.

Quantitative results on continuity of the spectral factorization mapping

The spectral factorization mapping $F\to F^+$ puts a positive definite integrable matrix function $F$ having an integrable logarithm of the determinant in correspondence with an outer analytic matrix function $F^+$ such that $F = F^+(F^+)^*$ almost everywhere. The main question addressed here is to what extent $\|F^+ - G^+\|_{H_2}$ is controlled by $\|F-G\|_{L_1}$ and $\|\log \det F - \log\det G\|_{L_1}$.

Matrix projective cluster synchronization for arbitrarily coupled networks with different dimensional nodes via nonlinear control

SummaryRecently, many control mechanisms have been put forward to realize the cluster synchronization of networks. However, these results are derived by making very conservative assumptions on the network's nodes and its outer coupling configuration matrix, which greatly limit these results' potential applications. This paper focuses on weakening these restrictive assumptions as much as possible and further proposes nonlinear controllers for our general networks to achieve matrix projective cluster synchronization (MPCS). One outstanding characteristic of our introduced network model is that the state dimensions of the nodes in different clusters are different, which extends the case that the network is composed of identical dimensional nodes. Another distinctive characteristic is that no other restrictions are imposed on our network's outer coupling matrix except for being bounded, namely, both the outer coupling matrix and its block matrices may be time varying and nonzero‐row‐sum. Besides, the exponential MPCS (EMPCS) and asymptotic MPCS (AMPCS) are defined to make a better description of the cluster synchronization phenomena in this paper. It is worth noted that these two definitions extend the existing ones about cluster synchronization. Furthermore, by means of rigorous theoretical analysis, some nonlinear control strategies are proposed for our network to realize EMPCS or AMPCS. At last, a proper numerical example along with two control patterns is presented to demonstrate the validity and effectivity of our results in this paper.

Исследование прочности восстановленного после повреждения корпуса корабля из полимерных композиционных материалов

This paper studies the strength of the hull damaged by fire. To repair this hull, it was suggested to mould its plating on an outer matrix with asymmetric processing of the elements to be connected. Numerical investigations and experimental studies have shown that this will ensure required strength and reliability of the hull under limit design operational loads.

Macroscopic elastic moduli of spherically-symmetric-inclusion composites and the microscopic stress-strain fields

Explicit algebraic expressions of the estimates for the microscopic elastic stress-strain fields and the macroscopic elastic moduli of the (n-component) multi-coated sphere assemblage (called n-spheres) under the imposed macroscopic strains or stresses are obtained from the minimum energy principles, and the near-interaction approximations (NIAs) for certain geometric correlation parameters (in the case of macroscopically-deviatoric stress-strain states). Limiting procedures are developed to derive the respective results for the inclusion composites with surface-stress (stiff) or spring-layer (compliant) imperfect interfaces, and those with the spherically-symmetric anisotropic coating positioned between the isotropic inner inclusion and the outer matrix phases. When the volume proportion of the outermost spherical shell (the matrix) increases to be the predominant one, one obtains the respective results for the most important specific case: the dilute solutions for the complex inhomogeneities suspended in the major matrix phase, which are needed also for other effective medium approximations and microscopic fields’ analyses. The differential substitution scheme is developed to construct the initial-valued ordinary differential equations estimating the effective moduli of the inclusion composites with radially-variable-moduli coating, and those with radially-variable anisotropic-moduli coating. The equations are integrated to give explicit algebraic estimates of the moduli in a number of cases, including that with constant-anisotropic-moduli-coating.

Transepidermal UV radiation of scalp skin exvivo induces hair follicle damage that is alleviated by the topical treatment with caffeine.

ObjectivesAlthough the effect of ultraviolet radiation (UVR) on human skin has been extensively studied, very little is known on how UVR impacts on hair follicle (HF) homeostasis. Here, we investigated how solar spectrum UVR that hits the human skin surface impacts on HF biology, and whether any detrimental effects can be mitigated by a widely used cosmetic and nutraceutical ingredient, caffeine.MethodsHuman scalp skin with terminal HFs was irradiated transepidermally ex vivo using either 10 J/cm2 UVA (340–440 nm) + 20 mJ/cm2 UVB (290–320 nm) (low dose) or 50 J/cm2 UVA + 50 mJ/cm2 UVB (high dose) and organ‐cultured under serum‐free conditions for 1 or 3 days. 0.1% caffeine (5.15 mmol/L) was topically applied for 3 days prior to UV exposure with 40 J/cm2 UVA + 40 mJ/cm2 UVB and for 3 days after UVR. The effects on various toxicity and vitality read‐out parameters were measured in defined skin and HF compartments.ResultsConsistent with previous results, transepidermal UVR exerted skin cytotoxicity and epidermal damage. Treatment with high and/or low UVA+UVB doses also induced oxidative DNA damage and cytotoxicity in human HFs. In addition, it decreased proliferation and promoted apoptosis of HF outer root sheath (ORS) and hair matrix (HM) keratinocytes, stimulated catagen development, differentially regulated the expression of HF growth factors, and induced perifollicular mast cell degranulation. UVR‐mediated HF damage was more severe after irradiation with high UVR dose and reached also proximal HF compartments. The topical application of 0.1% caffeine did not induce skin or HF cytotoxicity and stimulated the expression of IGF‐1 in the proximal HF ORS. However, it promoted keratinocyte apoptosis in selected HF compartments. Moreover, caffeine provided protection towards UVR‐mediated HF cytotoxicity and dystrophy, keratinocyte apoptosis, and tendential up‐regulation of the catagen‐promoting growth factor.ConclusionOur study highlights the clinical relevance of our scalp UV irradiation ex vivo assay and provides the first evidence that transepidermal UV radiation negatively affects important human HF functions. This suggests that it is a sensible prophylactic strategy to integrate agents such as caffeine that can act as HF photoprotectants into sun‐protective cosmeceutical and nutraceutical formulations.

Expression Pattern and Role of Klotho in Human Hair Follicles.

BackgroundKlotho protein plays a pivotal role in aging regulation. However, it is unclear whether klotho is expressed in human hair follicles and is correlated with hair growth.ObjectiveThe purpose of this study was to determine the expression pattern and role of klotho in human hair follicles.MethodsWe examined the klotho expression patterns in human hair follicles from young and aged donors. Furthermore, we examined the functional roles of klotho on human hair growth using klotho siRNA and klotho recombinant protein.ResultsInterestingly, klotho was expressed in human hair follicles at both gene and protein levels. In hair follicles, prominent klotho expression was mainly observed in the outermost regions of the outer root sheath and hair bulb matrix cells. Quantification of klotho protein expression in young and aged donors showed that klotho expression decreased with aging. In human hair follicle organ culture, klotho silencing promoted premature catagen induction and inhibited human hair growth. Otherwise, klotho protein prolonged human hair growth.ConclusionThese results indicate that klotho might be an important regulatory factor for human hair growth and hair cycle change.

Changes in the mitochondrial proteome in human hepatocytes in response to alpha-amanitin hepatotoxicity

Amanitin-induced apoptosis is proposed to have a significant effect on the pathogenesis of liver damage. However, few reports have focused on proteome changes induced by α-amanitin (α-AMA). Here, we evaluated changes in mitochondrial proteins of hepatocytes in response to 2 μM α-AMA, a concentration at which α-AMA-induced cell damage could be rescued at cellular level by common clinical drugs. We found 56 proteins were differentially expressed in an α-AMA-treated group. Among them, 38 proteins were downregulated and 18 were upregulated. Downregulated functional proteins included importer TOMM40, respiratory chain component cytochrome C, and metabolic enzymes of citrate acid cycle such as malate dehydrogenase, which localize on the mitochondrial outer membrane, inner membrane and matrix respectively. Immunoblot analysis showed that α-AMA decreased mitochondrial import receptor subunit TOMM40 and cytochrome c accompanied by an increase in the cytosol although their total protein levels were not affected significantly. The mitochondrial membrane potential was also destroyed by α-AMA and was restored by the clinical drug silibinin. Immunofluorescence suggested that mitochondrial morphology did not change. Taken together, our results provide further insights into the toxic mechanism of α-AMA on hepatocytes.

Impact of eosinophil-peroxidase (EPX) deficiency on eosinophil structure and function in mouse airways.

Eosinophil peroxidase (EPX) is a major constituent of the large cytoplasmic granules of both human and mouse eosinophilic leukocytes. Human EPX deficiency is a rare, autosomal-recessive disorder limited to the eosinophil lineage. Our intent was to explore the impact of EPX gene deletion on eosinophil content, structure, and function. In response to repetitive intranasal challenge with a filtrate of the allergen, Alternaria alternata, we found significantly fewer eosinophils peripherally and in the respiratory tracts of EPX-/- mice compared to wild-type controls; furthermore, both the major population (Gr1-/lo ) and the smaller population of Gr1hi eosinophils from EPX-/- mice displayed lower median fluorescence intensities (MFIs) for Siglec F. Quantitative evaluation of transmission electron micrographs of lung eosinophils confirmed the relative reduction in granule outer matrix volume in cells from the EPX-/- mice, a finding analogous to that observed in human EPX deficiency. Despite the reduced size of the granule matrix, the cytokine content of eosinophils isolated from allergen-challenged EPX-/- and wild-type mice were largely comparable to one another, although the EPX-/- eosinophils contained reduced concentrations of IL-3. Other distinguishing features of lung eosinophils from allergen-challenged EPX-/- mice included a reduced fraction of surface TLR4+ cells and reduced MFI for NOD1. Interestingly, the EPX gene deletion had no impact on eosinophil-mediated clearance of gram-negative Haemophilus influenzae from the airways. As such, although no clinical findings have been associated with human EPX deficiency, our findings suggest that further evaluation for alterations in eosinophil structure and function may be warranted.

Fenton-like degradation of sulfamethoxazole using Fe-based magnetic nanoparticles embedded into mesoporous carbon hybrid as an efficient catalyst

Fe-based magnetic nanoparticles (NPs) embedded into mesoporous carbon hybrid (Fe@MesoC) was successfully fabricated from Fe-based metal-organic framework (MIL-100(Fe)) through a pyrolysis method, which was for the first time proposed as a novel Fenton-like catalyst for the degradation of sulfamethoxazole (SMX). The catalytic activity of Fe@MesoC was systematically evaluated on the basis of several reaction parameters including initial pH, initial H2O2 concentration and temperature. Under the optimal conditions, the Fe@MesoC composite demonstrated a superior catalytic activity for decomposing SMX in the presence of H2O2, and it accomplished 100% SMX and 54.5% total organic carbon (TOC) conversion within 120 min. Such outstanding performance can be explained by the excellent enrichment ability of the outer mesoporous carbon matrix, the abundant active sites of the inner Fe-based NPs, as well as the possible synergistic effect between the two components. Moreover, the facile electrons transfer from Fe0 to iron oxide in the inner Fe-based NPs could facilitate the reduction of Fe3+ to Fe2+ ( represents the iron species anchored to the surface of the catalyst) and further improve the generation of hydroxyl radicals. With the high structural stability and saturation magnetization, the Fe@MesoC composite can be easily recycled for three subsequent runs without significant activity loss. The possible catalytic mechanism and degradation pathways for SMX degradation induced by hydroxyl radicals in Fe@MesoC/H2O2 Fenton-like system were also tentatively proposed.