Subcutaneous administration of Stattic alleviates neuropathic pain by relieving inflammation in a mouse model of postherpetic neuralgia.

Stattic, a commercial inhibitor of STAT3, can drive the development of neuropathic pain. Exploring the connection between Stattic and JAK1/STAT3 signaling may facilitate the understanding of neuropathic pain caused by postherpetic neuralgia (PHN). In the current study, as crucial regulators of inflammation, STAT3 and its associated JAK1/STAT3 pathway were found to be upregulated and activated in the L4-L6 dorsal root ganglion (DRG) of mice in response to resiniferatoxin (RTX)-induced PHN, while subcutaneous administration of Stattic was found to downregulate STAT3 expression and phosphorylation in a PHN model. Stattic administration further attenuated hypersensitivity to mechanical and thermal stimuli in PHN mice, and alleviated inflammation and cell death in the L4-L6 DRG of mice. Overexpression of STAT3 via microinjection of a lentiviral-STAT3 overexpression vector reversed the abnormal decrease of STAT3 at both the mRNA and protein levels in the L4-6 DRGs of PHN mice and significantly promoted hypersensitivity to mechanical stimuli in the mice. Collectively, we found that subcutaneous static administration alleviated RTX-induced neuropathic pain by deactivating JAK1/STAT3 in mice.

Quantifying the premature mortality and economic loss from wildfire-induced PM2.5 in the contiguous U.S.

Emissions from wildfires worsen air quality and can adversely impact human health. This study utilized the fire inventory from NCAR (FINN) as wildfire emissions, and performed air quality modeling of April-October 2012, 2013, and 2014 using the U.S. Environmental Protection Agency CMAQ model under two cases: with and without wildfire emissions. This study then assessed the health impacts and economic values attributable to PM2.5 from fires. Results indicated that wildfires could lead annually to 4000 cases of premature mortality in the U.S., corresponding to $36 billion losses. Regions with high concentrations of fire-induced PM2.5 were in the west (e.g., Idaho, Montana, and northern California) and Southeast (e.g., Alabama, Georgia). Metropolitan areas located near fire sources, exhibited large health burdens, such as Los Angeles (119 premature deaths, corresponding to $1.07 billion), Atlanta (76, $0.69 billion), and Houston (65, $0.58 billion). Regions in the downwind of western fires, although experiencing relatively low values of fire-induced PM2.5, showed notable health burdens due to their large population, such as metropolitan areas of New York (86, $0.78 billion), Chicago (60, $0.54 billion), and Pittsburgh (32, $0.29 billion). Results suggest that impacts from wildfires are substantial, and to mitigate these impacts, better forest management and more resilient infrastructure would be needed.

Exogenous microbial antagonism affects the bioaugmentation of humus formation under different inoculation using Trichoderma reesei and Phanerochaete chrysosporium.

This study was aimed at exploring the effect of antagonism of Trichoderma reesei (T.r) and Phanerochaete chrysosporium (P.c) on humification during fermentation of rice (RS) and canola straw (CS). Results showed that exogeneous fungi accelerated straw degradation and enzyme activities of CMCase, xylanase and LiP. P.c inhibited the activity of LiP when co-existing with T.r beginning, it promoted the degradation of lignin and further increased the production of humus-like substances (HLS) and humic-like acid (HLA) in later fermentation when nutrients were insufficient. The HLS of RTP was 54.9 g/kg RS, higher than the other treatments, and displayed more complex structure and higher thermostability. Brucella and Bacillus were the main HLA bacterial producers. P.c was the HLA fungal producer, while T.r assisted FLA and polyphenol transformation. Therefore, RTP was recommended to advance technologies converting crop straw into humus resources.

Low-carbon emitting university campus achieved via anaerobic digestion of canteen food wastes.

University campuses of China accommodate over 30 million students and consume a large amount of fossil fuel energy, leading to high carbon emission. Implementation of bioenergy (e.g. biomethane) is one of promising ways to mitigate emission and foster low-carbon emitting campus. Biomethane potential from anaerobic digestion (AD) of food waste (FW) in 2344 universities of 353 cities of mainland China have been estimated herein. Results have shown that 1.74 million tons of FW are discharged from campus canteens annually, that can generate 195.8 million m3 biomethane and reduce 0.77 million ton CO2-eq. Wuhan, Zhengzhou, and Guangzhou are the top three cities having the most biomethane potential from campus FW, accounting up to 8.92, 7.89, and 7.28 million m3 year-1, respectively. Technical challenges and solutions have been summarized and discussed such as FW purity, accumulation of ammonia and fatty acid, foaming, and plant site selection. Low-carbon campuses are supposed to be achieved by using bioenergy, like biomethane, in appropriate ways after resolving technical and management challenges.

Identification of novel B-1 transitional progenitors by B-1 lymphocyte fate-mapping transgenic mouse model Bhlhe41 dTomato-Cre.

B-1 lymphocytes exhibit specialized roles in host defense against multiple pathogens. Despite the fact that CD19+CD93+B220lo/- B cells have been identified as B-1 progenitors, the definition for B-1 progenitors remains to be elucidated as CD19+CD93+B220+ B cells are capable to give rise to B-1 cells. Given that transcription factor Bhlhe41 is highly and preferentially expressed in B-1 cells and regulates B-1a cell development, we generated a transgenic mouse model, Bhlhe41dTomato-Cre , for fate mapping and functional analysis of B-1 cells. Bhlhe41dTomato-Cre mice efficiently traced Bhlhe41 expression, which was mainly restricted to B-1 cells in B-cell lineage. We showed an efficient and specific Cre-mediated DNA recombination in adult B-1 cells and neonatal B-1 progenitors rather than B-2 cells by flow cytometric analysis of Bhlhe41 dTomato-Cre/+ Rosa26 EYFP mice. Treatment of Bhlhe41 dTomato-Cre/+ Rosa26 iDTR mice with diphtheria toxin revealed a robust efficacy of B-1 cell depletion. Interestingly, using Bhlhe41 dTomato-Cre mice, we demonstrated that neonatal B-1 progenitors (CD19+CD93+B220lo/-) expressed Bhlhe41 and were identical to well-defined transitional B-1a progenitors (CD19+CD93+B220lo/-CD5+), which only gave rise to peritoneal B-1a cells. Moreover, we identified a novel population of neonatal splenic CD19hidTomato+B220hiCD43loCD5lo B cells, which differentiated to peritoneal B-1a and B-1b cells. Bhlhe41 deficiency impaired the balance between CD19hidTomato+B220lo/-CD5hi and CD19hidTomato+B220hiCD5lo cells. Hence, we identified neonatal CD19hidTomato+B220hiCD43loCD5lo B cells as novel transitional B-1 progenitors. Bhlhe41 dTomato-Cre/+ mouse can be used for fate mapping and functional studies of B-1 cells in host-immune responses.

Amino acid catabolism regulates hematopoietic stem cell proteostasis via a GCN2-eIF2α axis.

Hematopoietic stem cells (HSCs) adapt their metabolism to maintenance and proliferation; however, the mechanism remains incompletely understood. Here, we demonstrated that homeostatic HSCs exhibited high amino acid (AA) catabolism to reduce cellular AA levels, which activated the GCN2-eIF2α axis, a protein synthesis inhibitory checkpoint to restrain protein synthesis for maintenance. Furthermore, upon proliferation conditions, HSCs enhanced mitochondrial oxidative phosphorylation (OXPHOS) for higher energy production but decreased AA catabolism to accumulate cellular AAs, which inactivated the GCN2-eIF2α axis to increase protein synthesis and coupled with proteotoxic stress. Importantly, GCN2 deletion impaired HSC function in repopulation and regeneration. Mechanistically, GCN2 maintained proteostasis and inhibited Src-mediated AKT activation to repress mitochondrial OXPHOS in HSCs. Moreover, the glycolytic metabolite, NAD+ precursor nicotinamide riboside (NR), accelerated AA catabolism to activate GCN2 and sustain the long-term function of HSCs. Overall, our study uncovered direct links between metabolic alterations and translation control in HSCs during homeostasis and proliferation.

Magnetic α-Fe2O3/Fe3O4 Heterostructure Nanorods: Fabrication and Cytotoxicity to A549 Cells.

The magnetic α-Fe2O3/Fe3O4 heterostructure nanorods were fabricated by an alcohol-solution direct combustion method. The influence of the calcination temperature on the composition and properties of the nanorods was investigated. When the calcination temperature was not greater than 400 °C, the magnetic α-Fe2O3/Fe3O4 heterostructure nanorods were obtained, and the saturation magnetization (Ms) of the magnetic α-Fe2O3/Fe3O4 heterostructure nanorods decreased with the calcination temperature increasing from 250 °C to 400 °C; when the calcination temperature was equal or greater than 450 °C, α-Fe2O3 nanorods were obtained. In addition, the effects of nanorods' concentration, nanorods' constituent, incubation time and magnetic field on A549 cytotoxicity were investigated. The cytotoxicity of the heterostructure nanorods appeared time-dependent and concentration-dependent, and the magnetic field could enhance the cytotoxicity of nanorods to A549.

Induction of the apoptosis, degranulation and IL-13 production of human basophils by butyrate and propionate via suppression of histone deacetylation.

Allergic diseases are caused by dysregulated Th2 immune responses involving multiple effector cells including basophils. Short chain fatty acids (SCFAs), mainly acetate, propionate and butyrate, exert immunomodulatory functions via activation of its receptors GPR41 and GPR43, and inhibition of the histone deacetylases (HDACs) activity. In allergic diseases, SCFAs suppress the activity of mast cells, eosinophils and type 2 innate lymphoid cells (ILC2) but enhance the function of Th2 cells. Here, we aimed to elucidate the function of SCFAs on human basophils. Human basophils were purified from healthy donors by flow cytometric sorting. The surface proteins, apoptosis and degranulation of basophils were analyzed by flow cytometric analysis. The mRNA expression was assayed using real-time PCR. Interleukin 4 (IL-4) and IL-13 were measured by ELISA. Histone acetylation was examined by western blot. GPR41 was expressed by basophils and was enhanced by IL-3. Acetate induced intracellular calcium influx in basophils which was suppressed by blocking GPR41. Propionate and butyrate, but not acetate, induced the expression of CD69 and IL-13. In addition, propionate and butyrate enhanced IgE-mediated basophil degranulation but inhibited basophil survival and IL-4 secretion. Propionate and butyrate induced histone acetylation of basophils and suppression of HDACs activity mimicked the effects of propionate and butyrate on human basophils. Our findings demonstrate that propionate and butyrate may play a complex role in regulating basophil apoptosis, activation and degranulation via inhibiting HDACs activity. The in vivo effects of SCFAs on the regulation of basophil-associated allergic diseases need to be further explored.

Improved delivery system for celastrol-loaded magnetic Fe3O4/α-Fe2O3 heterogeneous nanorods: HIF-1α-related apoptotic effects on SMMC-7721 cell.

Fe3O4/α-Fe2O3 heterogeneous nanorods were prepared by a rapid combustion method with α-FeOOH nanorods as precursors. Fe3O4/α-Fe2O3 heterogeneous nanorods with a saturation magnetization of 33.2 emu·g-1 were obtained using 30 mL of absolute ethanol at a calcination temperature of 300 °C. Their average length was around 140 nm, and average diameter was about 20 nm. To improve the dispersion characteristics of the Fe3O4/α-Fe2O3 heterogeneous nanorods in aqueous solution, citric acid and PEG were applied to modify the nanorod surface via the Mitsunobu reaction. The results showed that the hydrodynamic size range of Fe3O4/α-Fe2O3/CA-PEG-celastrol was 250-500 nm, the surface potential was -15 mV, and the saturation magnetization was approximately 23 emu·g-1. The drug loading capacity of Fe3O4/α-Fe2O3/CA-PEG was larger than the non-PEG modified version. Fe3O4/α-Fe2O3/CA-PEG-celastrol had slow-release characteristics and was sensitive to changes in pH. Application of a magnetic field significantly promoted the inhibition of SMMC-7721 human liver cancer cell growth after treatment with Fe3O4/α-Fe2O3/CA-PEG-celastrol. Celastrol and Fe3O4/α-Fe2O3/CA-PEG-celastrol increased the production of reactive oxygen species in SMMC-7721 cells and promoted apoptosis and apoptosis-related proteins (p53, Bax, Bcl-2) were also changed. In addition, the expression of hypoxia-inducible factor 1α (HIF-1α) was enhanced. We may conclude that celastrol-loaded magnetic Fe3O4/α-Fe2O3 heterogeneous nanorods may be applied in the chemotherapy of human cancer with good biocompatibility and delivery.

Aurka loss in CD19+ B cells promotes megakaryocytopoiesis via IL-6/STAT3 signaling-mediated thrombopoietin production.

Rationale: Aurora kinase A (Aurora-A), which is required for mitosis, is a therapeutic target in various tumors. Targeting Aurora-A led to an increase in the differentiation and polyploidization of megakaryocytes both in vivo and in vitro. However, the mechanisms involved in controlling megakaryocyte differentiation have not been fully elucidated. Methods: Conditional Aurka knockout mice were generated. B cell development, platelet development and function were subsequently examined. Proplatelet formation, in vivo response to mTPO, post-transfusion experiment, colony assay, immunofluorescence staining and quantification, and ChIP assay were conducted to gain insights into the mechanisms of Aurka loss in megakaryocytopoiesis. Results: Loss of Aurka in CD19+ B cells impaired B cell development in association with an increase in the number of platelets in peripheral blood (PB). Surprisingly, thrombopoietin (TPO) production and IL-6 were elevated in the plasma in parallel with an increase in the number of differentiated megakaryocytes in the bone marrow (BM) of Aurkaf/f;Cd19Cre/+ mice. Interestingly, compared with that of the Aurkaf/f mice, a higher number of CD19+ B cells close to megakaryocytes was observed in the BM of the Aurkaf/f;Cd19Cre/+ mice. Moreover, Aurka loss in CD19+ B cells induced signal transducer and activator of transcription-3 (STAT3) activation. Inhibition of STAT3 reduced the Tpo mRNA levels. ChIP assays revealed that STAT3 bound to the TPO promoter. Additionally, STAT3-mediated TPO transcription was an autocrine effect provoked by IL-6, at least partially. Conclusions: Deletion of Aurka in CD19+ B cells led to an increase in IL-6 production, promoting STAT3 activation, which in turn contributed to TPO transcription and megakaryocytopoiesis.

iTRAQ-Based Phosphoproteomic Analysis of Toxoplasma gondii Tachyzoites Provides Insight Into the Role of Phosphorylation for its Invasion and Egress.

The invasion and egress are two key steps in lytic cycle vital to the propagation of Toxoplasma gondii infection, and phosphorylation is believed to play important roles in these processes. However, the phosphoproteome of T. gondii at these two stages has not been characterized. In this study, we profiled the phosphoproteome of tachyzoites at the stages of "just invading" (JI) and "prior to egress" (PE) based on iTRAQ quantitative analysis, in which a total of 46 phosphopeptides, 42 phosphorylation sites, and 38 phosphoproteins were detected. In the comparison of PE vs. JI, 10 phosphoproteins were detected with their phosphorylation level significantly changed, and four of them were demonstrated to be significantly down-regulated at the transcriptional level. Bioinformatic analysis of these identified phosphoproteins suggested that phosphorylation-mediated modulation of protein function was employed to regulate the pathway of toxoplasmosis and metabolism and cellular processes correlated with tachyzoite's binding, location, and metabolism, and thus play vital roles in the parasite lytic cycle. Moreover, cytoskeletal network (CN)-associated Inner Membrane Complex (IMC1, IMC4, IMC6 and IMC12), Intravascular Network (IVN)-related GRAs (GRA2, GRA3, GRA7 and GRA12), and Parasitophorous Vacuole Membrane (PVM)-localized ROP5 were shown to be enriched at the central nodes in the protein interaction network generated by bioinformatic analysis, in which the phosphorylation level of IMC4, GRA2, GRA3, and GRA12 were found to be significantly regulated. This study revealed the main cellular processes and key phosphoproteins crucial for the invasion and egress of T. gondii, which will provide new insights into the developmental biology of T. gondii in vitro and contribute to the understanding of pathogen-host interaction from the parasite perspective.

Interleukin 3-induced GITR promotes the activation of human basophils.

Human basophils regulate allergic reactions by secreting histamine, interleukin 4 (IL-4) and IL-13 through key surface receptors FcεRI as well as IL-3R, which are constitutively expressed on basophils. IL-3/IL-3R signaling axis plays key roles in regulating the development and activation of basophils. We and others have shown that IL-3-induced surface receptors e.g. ST2, IL-17RB and IL-2 receptors regulate the biology of basophils. However, the expression and function of IL-3-induced surface proteins on human basophils remain to be elucidated. We in this study aimed to identify new basophil activation regulators by transcriptomic analysis of IL-3-stimulated basophils. Gene expression microarray analysis of IL-3-treated basophils revealed 2050 differentially expressed genes, of which 323 genes encoded surface proteins including GITR. We identified that GITR was preferentially induced by IL-3 rather than anti-IgE, IL-33, fMLP and C5a. IL-3-induced GITR was suppressed by inhibitors targeting JAK2, PI3K and MEK1/2. Stimulation of IL-3-treated basophils by GITR enhanced the expression of IL-4 and IL-13. Moreover, IgE-mediated degranulation was enhanced by GITRL in the presence of IL-3. This transcriptomic analysis of IL-3-activated basophils helps to identify novel activation regulator. IL-3-induced GITR promoted the activation of basophils, adding new evidence supporting GITR as an important player in Th2-associated immune responses.

Covalent immobilization and characterization of penicillin G acylase on magnetic Fe2O3/Fe3O4 heterostructure nanoparticles prepared via a novel solution combustion and gel calcination process.

In this work, magnetic Fe2O3/Fe3O4 heterostructure nanoparticles were prepared via a novel solution combustion and gel calcination process. The glutaraldehyde was cross-linked on Fe2O3/Fe3O4 heterostructure nanoparticles decorated silica. The prepared samples were characterized by TEM, EDS, XRD, VSM, SEM, XPS, TGA/DSC, BET measurement, Raman spectroscopy, Zeta potential, HR-TEM and FT-IR. The penicillin G acylase (PGA) was covalently immobilized on magnetic Fe2O3/Fe3O4@SiO2-CHO nanocomposites via the Schiff's reaction. Variations in the observed activities as a function of immobilization time and PGA concentration have been discussed, when immobilization time and concentration of PGA were 18 h and 0.2 mg·mL-1, the activity of immobilized PGA presented optimal values of 77.8 U·L-1 and 66.2 U·L-1. The effects of pH and temperature on enzyme activity were also evaluated, the activity of PGA at the temperature of 45 °C with buffer pH of 8 arrived at the highest lever. After 12 cycles of repetitive uses, the immobilized PGA still retained around 67% of initial activity. The research results indicated that PGA immobilized on magnetic Fe2O3/Fe3O4@SiO2-CHO nanocomposites showed excellent thermal stability, pH stability, and reusability compared with free enzyme.

Immobilization and characterization of cellulase on hydroxy and aldehyde functionalized magnetic Fe2O3/Fe3O4 nanocomposites prepared via a novel rapid combustion process.

In this work, magnetic Fe2O3/Fe3O4 nanocomposites were prepared via a novel rapid combustion process. The silica was precipitated on the surface of Fe2O3/Fe3O4 nanocomposites. The silica-coated magnetic nanocomposites were cross-linked with glutaraldehyde, on which cellulase was covalently immobilized. The morphology, composition, and property of the prepared nanomaterials were characterized by the scanning electron microscopy (SEM), the energy dispersive spectrometry (EDS), the X-ray diffraction (XRD), the vibrating sample magnetometer (VSM), and the Fourier transform infrared (FTIR) spectroscopy. The immobilization conditions were optimized by varying operating parameters and determined to be 0.05 mL of 0.5% cellulase solution for 2 h. The catalytic stabilities of the immobilized cellulase were evaluated. The results showed that the immobilized cellulases performed higher apparent activity at pH 4.5 and exhibited good thermal stability compared with their free counterparts. The Michaelis-Menten equation showed that Km and Vmax of free cellulase were 3.46 mol·L-1 and 0.53 mol·min-1, respectively. The immobilized cellulase had higher Km and Vmax (18.99 mol·L-1 and 0.59 mol·min-1). The retained activity of the immobilized cellulase maintained over 71% of the initial activity after being used for five cycles.

Optimization on Adsorption Process of Congo Red onto Magnetic Ni0.5Cu0.5Fe2O4/SiO2 Nanocomposites and Their Adsorption Mechanism.

Magnetic Ni0.5Cu0.5Fe2O4/SiO2 nanocomposites were prepared via a solution combustion process, and were characterized by X-ray diffraction (XRD), scanning electron microscopy (SEM) and transmission electron microscopy (TEM), Energy dispersive X-ray Spectroscopy (EDX) and vibrating sample magnetometer (VSM). The magnetic Ni0.5Cu0.5Fe2O4/SiO2 nanocomposites were employed to remove Congo red (CR) from aqueous solution, and the adsorption process was optimized by response surface methodology (RSM). The optimum conditions were the silica content of 12.6 wt%, the calcination temperature of 501 °C and the pH value of 7.13. The adsorption kinetics and the adsorption isotherm of CR onto magnetic Ni0.5Cu0.5Fe2O4/SiO2 nanocomposites at room temperature were investigated, and the intraparticle diffusion kinetics model and Redlich-Peterson isotherm model fitted well the respective process.

Interleukin 2 regulates the activation of human basophils.

Basophils are important effector cells in allergic disorders and anti-parasitic immune response. A number of activators including interleukin 3 (IL-3) and IgE have been identified in the regulation of human basophils expressing mediators such as histamine and leukotriene C4 (LTC4) and cytokines, including IL-4 and IL-13. Human basophils express high levels of IL-2 receptors. However, the function of the IL-2 pathway in basophils remains unknown. Here, we identified that IL-2 induced the activation of human basophils in vitro to express a variety of inflammatory cytokines and chemokines including IL-5, IL-13, GM-CSF and CCL-17. This effect by IL-2 is confirmed by an upstream regulator analysis using Ingenuity pathway analysis. Of note, one of the top regulated cytokines, IL-5, was for the first time identified to be induced by IL-2 in human basophils rather than IL-3 or anti-IgE. Immunofluorescence analysis of skin specimens from bullous pemphigoid and eczema revealed that infiltrating basophils in skin lesions widely expressed IL-5 and GM-CSF. Together, our findings reveal IL-2 as a novel regulator of human basophils. This adds a new layer to support the importance of basophils in allergic disorders.

Bacillus subtilis Inhibits Vibrio natriegens-Induced Corrosion via Biomineralization in Seawater.

The marine bacterium, Vibrio natriegens, grows quickly in a marine environment and can significantly accelerate the corrosion of steel materials. Here, we present an approach to inhibit V. natriegens-induced corrosion by biomineralization. The corrosion of steel is mitigated in seawater via the formation of a biomineralized film induced by Bacillus subtilis. The film is composed of extracellular polymeric substances (EPS) and calcite, exhibiting stable anti-corrosion activity. The microbial diversity and medium chemistry tests demonstrated that the inhibition of V. natriegens growth by B. subtilis was essential for the formation of the biomineralized film.

The air quality and health impacts of projected long-haul truck and rail freight transportation in the United States in 2050.

Diesel emissions from freight transportation activities are a key threat to public health. This study examined the air quality and public health impacts of projected freight-related emissions in 2050 over the continental United States. Three emission scenarios were considered: (1) a projected business-as-usual socioeconomic growth with freight fleet turnover and stringent emission control (CTR); (2) the application of a carbon pricing climate policy (PO); and (3) further technology improvements to eliminate high-emitting conditions in the truck fleet (NS). The PO and NS cases are superimposed on the CTR case. Using a WRF-SMOKE-CMAQ-BenMAP modeling framework, we quantified the impacts of diesel fine particulate matter (PM2.5) emissions change on air quality, health, and economic benefits. In the CTR case, we simulate a widespread reduction of PM2.5 concentrations, between 0.5 and 1.5 µg m-3, comparing to a base year of 2011. This translates into health benefits of 3600 (95% CI: 2400-4800) prevented premature deaths, corresponding to $38 (95% CI: $3.5-$100) billion. Compared to CTR case, the PO case can obtain ~9% more health benefits nationally, however, climate policy also affects the health outcomes regionally due to transition of demand from truck to rail; regions with fewer trucks could gain in health benefits, while regions with added rail freight may potentially experience a loss in health benefits due to air quality degradation. The NS case provides substantial additional benefits (~20%). These results support that a combination of continuous adoption of stringent emission standards and strong improvements in vehicle technology are necessary, as well as rewarding, to meet the sustainable freight and community health goals. States and metropolitan areas with high population density and usually high freight demand and emissions can take more immediate actions, such as accelerating vehicle technology improvements and removing high-emitting trucks, to improve air quality and health benefits.

Image restoration and color fusion of digital microscopes.

Traditional microscopes do not meet a wide field of view and high resolution at the same time. We propose a method for image restoration and color fusion of digital microscopes. It combines a single high-resolution gray scale hologram with a low-resolution color image to obtain a high-resolution color image. Specifically, the high-resolution gray scale image is obtained by reconstructing three different height holograms using a wavelet-based method, and the color information is obtained using a portable cell phone microscope. The subsequent calibration and blending of colors ultimately results in a high-resolution, wide-field color map that can be of great help in the study of pathology or biomedicine. This method breaks the rule that the large field of view and high resolution of a traditional microscope cannot be simultaneously satisfied, which can realize a more comprehensive observation of the shape and details of the slice.

A Facile Solution Combustion and Gel Calcination Process for the Preparation of Magnetic MnFe2O4 Nanoparticles.

A facile solution combustion and gel calcination process for the preparation of magnetic MnFe²O4 nanoparticles was introduced. The experimental results showed that the volume of absolute alcohol and the calcination temperature were two key factors to grain size, crystallinity and magnetic properties of MnFe²O4 nanoparticles. With the volume of absolute alcohol increasing from 15 to 100 mL, the average grain size of MnFe²O4 nanoparticles calcined at 400 °C for 2 h increased from 13.4 nm to 36.0 nm, and the saturation magnetization (Ms) value of MnFe²O4 nanoparticles increased from 1.2 emu/g to 105.5 emu/g; while, with the calcination temperature increasing from 400 °C to 800 °C, the average grain size increased from 13.4 nm to 32.9 nm, and the saturation magnetization value increased from 1.2 emu/g to 15.3 emu/g. The specific surface area of MnFe²O4 nanoparticles calcined at 400 °C for 2 h with absolute alcohol of 30 mL was measured, which was large of 49.6 m²/g.