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Microbes, toxins, therapeutics and cells are often instilled into lungs of mice to model diseases and test experimental interventions. Consistent pulmonary delivery is critical for experimental power and reproducibility, but we observed variation in outcomes between handlers using different anesthetic approaches for intranasal dosing into mice. We therefore used a radiotracer to quantify lung delivery after intranasal dosing under inhalational (isoflurane) versus injectable (ketamine/xylazine) anesthesia in C57BL/6 mice. We found that ketamine/xylazine anesthesia resulted in delivery of a greater proportion (52±9%) of an intranasal dose to lungs relative to isoflurane anesthesia (30±15%). This difference in pulmonary dose delivery altered key outcomes in a model of viral pneumonia, with mice anesthetized with ketamine/xylazine for intranasal infection with influenza A virus developing worse lung pathology and more consistently losing body weight relative to control animals randomized to isoflurane anesthesia. Pulmonary dosing efficiency through oropharyngeal aspiration was not affected by anesthetic method and resulted in delivery of 63±8% of dose to lungs, and a non-surgical intratracheal dosing approach further increased lung delivery to 92±6% of dose. We conclude that anesthetic approach and dosing route can impact pulmonary dosing efficiency. These factors should be considered when planning and reporting studies involving delivery of fluids to lungs of mice.

Dendritic cells (DCs) are crucial for initiating adaptive immune responses. However, the factors that control DC positioning and homeostasis are incompletely understood. We found that type-2 conventional DCs (cDC2s) in the spleen depend on Gα 13 and adhesion G protein–coupled receptor family member-E5 (Adgre5, or CD97) for positioning in blood-exposed locations. CD97 function required its autoproteolytic cleavage. CD55 is a CD97 ligand, and cDC2 interaction with CD55-expressing red blood cells (RBCs) under shear stress conditions caused extraction of the regulatory CD97 N-terminal fragment. Deficiency in CD55-CD97 signaling led to loss of splenic cDC2s into the circulation and defective lymphocyte responses to blood-borne antigens. Thus, CD97 mechanosensing of RBCs establishes a migration and gene expression program that optimizes the antigen capture and presentation functions of splenic cDC2s.

Recipients of solid organ transplantation (SOT) rely on life-long immunosuppression (IS), which is associated with significant side effects. Extracorporeal photochemotherapy (ECP) is a safe, existing cellular therapy used to treat transplant rejection by modulating the recipient’s own blood cells. We sought to induce donor-specific hypo-responsiveness of SOT recipients by infusing ECP-treated donor leukocytes prior to transplant. To this end, we utilized major histocompatibility complex (MHC) mismatched rodent models of allogeneic cardiac, liver, and kidney transplantation to test this novel strategy. Leukocytes isolated from donor-matched spleens for ECP treatment (ECP-DL) were infused into transplant recipients seven days prior to SOT. Pre-transplant infusion of ECP-DL without additional IS was associated with prolonged graft survival in all models. This innovative approach promoted the production of tolerogenic dendritic cells and regulatory T-cells with subsequent inhibition of T-cell priming and differentiation, along with a significant reduction of donor-specific T-cells in the spleen and grafts of treated animals. This new application of donor-type ECP-treated leukocytes provides insight into the mechanisms behind ECP-induced immunoregulation and holds significant promise in the prevention of graft rejection and reduction in need of global immune suppressive therapy in patients following SOT.

CD34+ myeloid lineage progenitor cells are an important reservoir of latent human cytomegalovirus (HCMV), and differentiation to macrophages or dendritic cells (DCs) is known to cause reactivation of latent virus. Due to its species-specificity, murine models have been used to study mouse CMV (MCMV) latency and reactivation in vivo. While previous studies have shown that MCMV genomic DNA can be detected in the bone marrow (BM) of latently infected mice, the identity of these cells has not been defined. Therefore, we sought to identify and enrich for cellular sites of MCMV latency in the BM haematopoietic system, and to explore the potential for establishing an in vitro model for reactivation of latent MCMV. We studied the kinetics and cellular characteristics of acute infection and establishment of latency in the BM of mice. We found that while MCMV can infect a broad range of haematopoietic BM cells (BMCs), latent virus is only detectable in haematopoietic stem cells (HSCs), myeloid progenitor cells, monocytes and DC-enriched cell subsets. Using three separate approaches, MCMV reactivation was detected in association with differentiation into DC-enriched BMCs cultured in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin 4 (IL-4) followed by lipopolysaccharide (LPS) treatment. In summary, we have defined the kinetics and cellular profile of MCMV infection followed by the natural establishment of latency in vivo in the mouse BM haematopoietic system, including the haematopoietic phenotypes of cells that are permissive to acute infection, establish and harbour detectable latent virus, and can be stimulated to reactivate following DC enrichment and differentiation, followed by treatment with LPS.

Recipients of solid organ transplantation (SOT) rely on life-long immunosuppression (IS), which is associated with significant side effects. Extracorporeal photochemotherapy (ECP) is a safe, existing cellular therapy used to treat transplant rejection by modulating the recipient’s own blood cells. We sought to induce donor-specific hypo-responsiveness of SOT recipients by infusing ECP-treated donor leukocytes prior to transplant. To this end, we utilized major histocompatibility complex mismatched rodent models of allogeneic cardiac, liver, and kidney transplantation to test this novel strategy. Leukocytes isolated from donor-matched spleens for ECP treatment (ECP-DL) were infused into transplant recipients seven days prior to SOT. Pre-transplant infusion of ECP-DL without additional IS was associated with prolonged graft survival in all models. This innovative approach promoted the production of tolerogenic dendritic cells and regulatory T-cells with subsequent inhibition of T-cell priming and differentiation, along with a significant reduction of donor-specific T-cells in the spleen and grafts of treated animals. This new application of donor-type ECP-treated leukocytes provides insight into the mechanisms behind ECP-induced immunoregulation and holds significant promise in the prevention of graft rejection and reduction in need of global immune suppressive therapy in patients following SOT.

Peroxymonosulfate (PMS) was successfully adopted to remove organic pollutants in water, but it was rarely applied to soil remediation. Sulfathiazole (STZ) is a widely used sulfonamide antibiotic, while its residues have negative impacts on soil. To the best of our knowledge, this is the first attempt to apply PMS for the treatment of STZ-contaminated soil. The results showed that 4 mM PMS can degrade 96.54% of STZ in the soil within 60 min. Quenching and probe experiments revealed that singlet oxygen rather than hydroxyl radical and sulfate radical was the predominant reactive oxygen species responsible for STZ removal. The presence of Cl

Delayed graft function due to transplant ischemia/reperfusion injury adversely affects up to 50% of deceased-donor kidney transplant recipients. However, key factors contributing to the severity of ischemia/reperfusion injury remain unclear. Here, using a clinically relevant mouse model of delayed graft function, we demonstrated that donor genetic background and kidney-intrinsic MyD88/Trif-dependent innate immunity were key determinants of delayed graft function. Functional deterioration of kidney grafts directly corresponded with the duration of cold ischemia time. The graft dysfunction became irreversible after cold ischemia time exceeded six hours. When cold ischemia time reached four hours, kidney grafts displayed histological features reflective of delayed graft function seen in clinical kidney transplantation. Notably, kidneys of B6 mice exhibited significantly more severe histological and functional impairment than kidneys of C3H or BALB/c mice, regardless of recipient strains or alloreactivities. Furthermore, allografts of B6 mice also showed an upregulation of IL-6, neutrophil gelatinase-associated lipocalin, and endoplasmic reticulum stress genes, as well as an increased influx of host neutrophils and memory CD8 T-cells. In contrast, donor MyD88/Trif deficiency inhibited neutrophil influx and decreased the expression of IL-6 and endoplasmic reticulum stress genes, along with improved graft function and prolonged allograft survival. Thus, kidney-intrinsic factors involving genetic characteristics and innate immunity serve as critical determinants of the severity of delayed graft function. This preclinical murine model allows for further investigations of the mechanisms underlying delayed graft function.

Limb transplant in particular and vascularized composite allotransplant (VCA) in general have wide therapeutic promise that have been stymied by current limitations in immunosuppression and functional neuromotor recovery. Many animal models have been developed for studying unique features of VCA, but here we present a robust reproducible model of orthotopic hind limb transplant in rats designed to simultaneously investigate both aspects of current VCA limitation: immunosuppression strategies and functional neuromotor recovery. At the core of the model rests a commitment to meticulous, time-tested microsurgical techniques such as hand sewn vascular anastomoses and hand sewn neural coaptation of the femoral nerve and the sciatic nerve. This approach yields durable limb reconstructions that allow for longer lived animals capable of rehabilitation, resumption of daily activities, and functional testing. With short-term treatment of conventional immunosuppressive agents, allotransplanted animals survived up to 70 days post-transplant, and isotransplanted animals provide long lived controls beyond 200 days post-operatively. Evidence of neurologic functional recovery is present by 30 days post operatively. This model not only provides a useful platform for interrogating immunological questions unique to VCA and nerve regeneration, but also allows for in vivo testing of new therapeutic strategies specifically tailored for VCA.

Objective Active antibody-mediated rejection (aABMR), particularly late aABMR, remains a major challenge for long-term renal allograft survival. This single-center retrospective study aimed to compare clinical features between early vs late aABMR and to identify risk factors for allograft failure among patients with aABMR. Method Forty-one patients diagnosed with aABMR at our hospital were included and were divided into 2 groups: early aABMR (≤6 months; n = 10) vs late aABMR (>6 months; n = 31) based on the time from transplant to diagnosis. Their clinical and pathologic data were compared. This study was performed in compliance with the Helsinki Congress and the Declaration of Istanbul. Results Of 10 patients with early aABMR, none had allograft failure, whereas 8 of 31 patients with late aABMR had developed allograft failure at the time of follow-up (25.8%). At the time of biopsy, patients with early aABMR had higher positive grade in urine occult blood test than patients with late aABMR (P = .01); however, the late aABMR group displayed more intensive interstitial fibrosis and tubular atrophy (P = .03) and more frequent HLA-DQ-type donor-specific antibodies. Interestingly, donor-specific antibody conversion from positive to negative was not associated with C4d grade but was correlated with time from transplant to biopsy. Multivariate Cox regression analysis indicated that high levels of serum creatinine or proteinuria and concomitant T-cell-mediated rejection were independent risk factors for allograft failure in patients with aABMR. Conclusion These data not only confirm that early aABMR has better clinical outcomes than late aABMR but highlight the importance of early diagnostic biopsy and early therapeutic interventions in ABMR, particularly in patients with high levels of serum creatinine or proteinuria in the early posttransplant phase.

Subjective well-being is a comprehensive psychological indicator for measuring quality of life. Studies have found that emotional measurement methods and measurement accuracy are important for well-being-related research. Academic emotion is an emotion description in the field of education. The subjective well-being of learners in an online learning environment can be studied by analyzing academic emotions. However, in a large-scale online learning environment, it is extremely challenging to classify learners&rsquo, academic emotions quickly and accurately for specific comment aspects. This study used literature analysis and data pre-analysis to build a dimensional classification system of academic emotion aspects for students&rsquo, comments in an online learning environment, as well as to develop an aspect-oriented academic emotion automatic recognition method, including an aspect-oriented convolutional neural network (A-CNN) and an academic emotion classification algorithm based on the long short-term memory with attention mechanism (LSTM-ATT) and the attention mechanism. The experiments showed that this model can provide quick and effective identification. The A-CNN model accuracy on the test set was 89%, and the LSTM-ATT model accuracy on the test set was 71%. This research provides a new method for the measurement of large-scale online academic emotions, as well as support for research related to students&rsquo, well-being in online learning environments.

Spherical nucleic acids (SNAs) are a class of nanomaterials with a structure defined by a radial distribution of densely packed, short DNA or RNA sequences around a nanoparticle core. This structure allows SNAs to rapidly enter mammalian cells, protects the displayed oligonucleotides from nuclease degradation, and enables co-delivery of other drug cargoes. Here, we investigate the biodistribution of liposomal spherical nucleic acid (LSNA) conjugates, SNA architectures formed from liposome templates and DNA modified with hydrophobic end groups (tails). We compared linear DNA with two types of LSNAs that differ only by the affinity of the modified DNA sequence for the liposome template. We use single-stranded DNA (ssDNA) terminated with either a low-affinity cholesterol tail (CHOL-LSNA) or a high-affinity diacylglycerol lipid tail (DPPE-LSNA). Both LSNA formulations, independent of DNA conjugation, reduce the inflammatory cytokine response to intravenously administered DNA. The difference in the affinity for the liposome template significantly affects DNA biodistribution. DNA from CHOL-LSNAs accumulates in greater amounts in the lungs than DNA from DPPE-LSNAs. In contrast, DNA from DPPE-LSNAs exhibits greater accumulation in the kidneys. Flow cytometry and fluorescence microscopy of tissue sections indicate that different cell populations-immune and nonimmune-sequester the DNA depending upon the chemical makeup of the LSNA. Taken together, these data suggest that the chemical structure of the LSNAs represents an opportunity to direct the biodistribution of nucleic acids to major tissues outside of the liver.

Aim To investigate whether the parameters of machine perfusion could predict the quality of kidneys from donation after circulatory death(DCD) donors and expanded criteria donors (ECD) . Methods 58 kidneys from DCD/ECD donors were harvested in our hospital from July 2011 to August 2014. All kidneys were preserved with machine perfusion(Life Port), and parameters of machine perfusion were collected. All kidneys were biopsied before transplantation. The primary endpoints were delayed graft function(DGF), graft loss and patient death. Results After kidney transplantation, 26 patients(44.8%) had DGF. We chose 1-hour RI as a predictive parameter to predict DGF after transplant, and made the ROC curve. The ROC curve showed that 1-hour RI = 0.4 was the best cut-off point for predicting DGF after transplant. The sensitivity was 61.54% , and the specificity was 81.25%. 58 recipients were divided into two groups according to 1-hour RI of machine perfusion. 22 cases in high RI group (RI > 0.4) and 36 cases in low RI group( RI ≤0.4). DGF rate was significantly higher in the high RI group(72.7% vs. 27.8%). 1-year serum creatinine levels were also significantly higher in the high RI group(p

Paclitaxel is one of the most widely used antineoplastic drugs in the clinic. Unfortunately, the occurrence of cellular resistance has limited its efficacy and application. The ATP-binding cassette subfamily B member 1 (ABCB1/P-glycoprotein) and subfamily C member 10 (ABCC10/MRP7) are the major membrane protein transporters responsible for the efflux of paclitaxel, constituting one of the most important mechanisms of paclitaxel resistance. Here, we demonstrated that the Bruton tyrosine kinase inhibitor, ibrutinib, significantly enhanced the antitumor activity of paclitaxel by antagonizing the efflux function of ABCB1 and ABCC10 in cells overexpressing these transporters. Furthermore, we demonstrated that the ABCB1 or ABCC10 protein expression was not altered after treatment with ibrutinib for up to 72 hours using Western blot analysis. However, the ATPase activity of ABCB1 was significantly stimulated by treatment with ibrutinib. Molecular docking analysis suggested the binding conformation of ibrutinib within the large cavity of the transmembrane region of ABCB1. Importantly, ibrutinib could effectively enhance paclitaxel-induced inhibition on the growth of ABCB1- and ABCC10-overexpressing tumors in nude athymic mice. These results demonstrate that the combination of ibrutinib and paclitaxel can effectively antagonize ABCB1- or ABCC10-mediated paclitaxel resistance that could be of great clinical interest. Mol Cancer Ther; 16(6); 1021–30. ©2017 AACR.

Summary Peritransplant infusion of ethylene carbodiimide-fixed donor splenocytes (ECDI-SPs) induces protection of islet and cardiac allografts. However, pro-inflammatory cytokine production during the peritransplantation period may negate the effect of ECDI-SPs. Therefore, we hypothesized that blocking pro-inflammatory cytokine secretion while increasing levels of anti-inflammatory cytokines would enhance the tolerance-induced efficacy of ECDI-SPs. The objective of this study was to determine the effectiveness of using ECDI-SPs combined with a short course of α1-antitrypsin (AAT) for induction of tolerance. Using a mice cardiac transplant model, we demonstrated that ECDI-SPs + AAT effectively induced indefinite mice cardiac allograft protection in a donor-specific fashion. This effect was accompanied by modulation of cytokines through decreasing levels of pro-inflammatory cytokines (including IFN-γ, TNF-α, IL-1β, IL-6, IL-17, and IL-23) and increasing levels of anti-inflammatory cytokines (including IL-10, IL-13, and TGF-β), and by inhibition of effector T cells (Teff) and expansion of regulatory T cells (Tregs). Therefore, we concluded that combined ECDI-SPs and AAT appeared to modulate the expression of cytokines and regulate the Teff:Treg balance to create a support milieu for graft protection. Our strategy of combining ECDI-SPs and AAT provides a promising approach for inducing donor-specific transplant tolerance.

Ischemia/reperfusion injury (IRI) is inherent to all transplanted organs and is adversely associated with early renal graft function and graft longevity. Despite the progress in immunosuppressive regimens and perioperative care, no FDA-approved treatment for kidney transplant IRI is available to date. In recent years, by utilizing the modified and clinically-relevant mouse models of kidney transplantation (KTx) in which extended IRI is induced by the prolonged warm or cold ischemic time, studies have identified several potential therapeutic approaches for KTx IRI, including the hormone supplement, promoting tubular repair and regeneration, and targeting complement system, inflammation, and necroptosis. This review describes some of the lessons learned from mouse models of KTx with regard to factors that influence the severity of transplant IRI and the potential therapeutic targets.

Reactivation of latent cytomegalovirus remains an important complication after transplant. Although immunosuppression (IS) has been implicated as a primary cause, we have previously shown that the implantation response of a kidney allograft can lead to early transcriptional activation of latent murine cytomegalovirus (MCMV) genes in an immune-competent host and to MCMV reactivation and dissemination to other organs in a genetically immune-deficient recipient. We now describe a model that allows us to separately analyze the impact of the implantation effect vs that of a clinically relevant IS regimen. Treatment with IS of latently infected mice alone does not induce viral reactivation, but transplant of latently infected allogeneic kidneys combined with IS facilitates MCMV reactivation in the graft and dissemination to other organs. The IS regimen effectively dampens allo-immune inflammatory pathways and depletes recipient anti-MCMV but does not affect ischemia-reperfusion injury pathways. MCMV reactivation similar to that seen in allogeneic transplants combined with also occurs after syngeneic transplants. Thus, our data strongly suggest that while ischemia-reperfusion injury of the implanted graft is sufficient and necessary to initiate transcriptional reactivation of latent MCMV ("first hit"), IS is permissive to the first hit and facilitates dissemination to other organs ("second hit").

The urgent unmet need of improving the outcomes of cancer patients is to develop novel treatment strategies that can reduce the systemic toxicity of chemotherapy and overcome the multiple drug resistance (MDR). Developing effective combination treatment regimens is an ideal approach to improve the efficiency of chemotherapy. Bruton's tyrosine kinase (BTK) is a key component of the B-cell receptor (BCR) signaling pathway and plays an essential role in B-cell maturation and lymphomagenesis. The development of BTK inhibitors and their application in clinic represent the major advance in the treatment of hematological malignancies. Recently, extensive studies have demonstrated that the aberrant activation of the BTK signaling pathway has been involved in MDR. Targeting the BTK signaling pathway could sensitize the cancer cells resistant to various chemotherapy drugs including paclitaxel, cisplatin, doxorubicin, proteasome inhibitors, Bcl-2 antagonists, and HDAC inhibitors. The combination treatment strategies using the BTK inhibitor, ibrutinib, and other chemotherapy agents have been proven effective in targeting resistant cell lines. Some of the combination treatment regimens are currently tested in clinical trials. In this chapter, the mechanisms, applications, as well as the efficacy of BTK inhibitors acting as sensitizing agents in cancer chemotherapy are discussed.

A digital image correlation technique with non-fixed camera is developed for deformation measurement in the field since it is difficult to fix cameras when the deformations of a large number of areas need to be measured. Multiple reference and target images of the specimen surface and a feature template are captured from different orientations and corrected before the correlation calculation. The relative positions of the specimen surface and the camera are obtained by the camera calibration method. The specimen surface is divided to several meshes to reconstruct the speckle patterns. The technique is more flexible and convenient than traditional digital image correlation method in measuring the deformation of high altitude facilities such as bridges. In order to test the accuracy of this method, the deformations of an aluminum plate under different loading forces are measured and compared to the values recorded by the tensile tester.

Transplantation tolerance is achieved when recipients are unresponsive to donor alloantigen yet mobilize against third-party antigens, including virus. After transplantation, cytomegalovirus (CMV) reactivation in latently-infected transplants reduces allograft viability. To determine if pre-tolerized recipients are resistant to viral dissemination in this setting, we transfused chemically-fixed donor splenocytes (1-ethyl-3- (3&prime, dimethyl-aminopropyl)-carbo-diimide (ECDI)-treated splenocytes (ECDIsp)) to induce donor antigen tolerance without immunosuppression. In parallel, we implanted donor islet cells to validate operational tolerance. These pre-tolerized recipients were implanted with murine CMV (MCMV) latently-infected donor kidneys (a validated model of CMV latency) to monitor graft inflammation and viral dissemination. Our results indicate that tolerance to donor islets was sustained in recipients after implantation of donor kidneys. In addition, kidney allografts implanted after ECDIsp and islet implantation exhibited low levels of fibrosis and tubulitis. In contrast, kidney cellular and innate immune infiltrates trended higher in the CMV group and exhibited increased markers of CD8+ T cell activation. Tolerance induction was unable to prevent increases in MCMV-specific CD8+ T cells or dissemination of viral IE-1 DNA. Our data suggest that latently-infected allografts are inherently more susceptible to inflammation that is associated with viral dissemination in pre-tolerized recipients. Thus, CMV latently-infected allografts require enhanced strategies to protect allograft integrity and viral spread.

A novel micro-solid phase preconcentration (μSPP) device is developed by electrochemically depositing molecularly imprinted polypyrrole (MIPPy) over carbon nanotubes (CNTs) packed inside a 22-gauge syringe needle. The ochratoxin A (OTA) template is removed with 1% triethylamine (TEA) in 20:80 v/v acetonitrile—ammonia buffer (20 mM NH4Cl/NH3, pH 9.2). This syringe needle is used to extract trace OTA in a red wine sample, and the preconcentrated OTA is eluted with 1% (v/v) TEA in 20:80 v/v acetonitrile—ammonia buffer (20 mM NH4Cl/NH3, pH 9.2). The eluate is analyzed by high performance liquid chromatography (HPLC) with fluorescence detection (FD). The results demonstrated a significantly selective enrichment of OTA at sub-ppb levels in the presence of red wine matrix components. Using a sample volume of 0.5mL red wine for preconcentration, it is possible to determine OTA down to a detection limit of 0.04 ng/mL (at 3σB) or a quantification limit of 0.10 ng/mL (at 10σB). The total MIPPy/CNTs-μSPP-HPLC-FD analysis took only 40min, including a μSPP time of 30min, elution time of 20 s, and HPLC analysis time of 10 min. This needle can be reused and hence readily adapted in an autosampler for the processing of multiple samples in series.

Nanometer-sized semiconductor quantum dots (QDs with CdSe core and ZnS shell) and carbon nanotubes (CNTs with multi-walls) were encapsulated inside a stainless steel syringe needle by electrodeposition of polypyrrole (PPy). By cross-linking the PPy with ethylene glycol dimethacrylate (EGDMA) in the presence of ochratoxin A (OTA) as a template, molecularly imprinted polypyrrole (MIPPy) was formed on the nano-hybrid structure at an increased specific surface area. The MIPPy/CNTs/QDs-modified needle was readily adapted in an autosampler for micro-solid phase preconcentration (μSPP) of OTA from a red wine sample. After pulsed elution (PE) with 2% triethylamine (TEA), the OTA was determined by high performance liquid chromatography (HPLC) with fluorescence detection (FD). In comparison with MIPPy/CNTs, this new nano-hybrid structure of MIPPy/CNTs/QDs significantly improved the % recovery of OTA. The method, MIPPy/CNTs/QDs-μSPP-HPLC-FD, demonstrated that the MIPPy was truly a molecularly imprinted polymer (MIP) with specific recognition for OTA. All red wine matrix components could be differentially washed out, prior to accurate determination of the strongly bound OTA.

Metallic tin nanorods were synthesized by a sonochemical method employing the polyol process. In the reaction a solution of SnCl2 in ethylene glycol was exposed to high-intense ultrasound irradiation. The phase and elemental compositions, and thermal properties of the as-synthesized samples were characterized by XRD, EDX, SAED, XPS, DSC, TGA, and BET measurements. The morphologies of the products were further characterized with SEM, TEM, and HRTEM. The results show that crystallized metallic tin nanorods in diameters of 50-100 nm and in lengths of up to 3 microm were synthesized. The nanorods are encapsulated in a thin layer containing Ti and carbon compounds. On the basis of the obtained data, a possible mechanism of the formation of tin nanorods was proposed.

Semiconductor alpha-MoTe2 nanorods have been synthesized by annealing Te-seeded particles of an amorphous MoTe2 intermediate. This intermediate is prepared by a solution reaction between Mo(CO)6 and elemental Te in diphenylmethane. The as-synthesized products were characterized by structural, compositional, and morphological techniques of X-ray diffraction, selected area electron diffraction, selected area energy dispersive spectroscopy, energy dispersive X-ray analysis, X-ray photoelectron spectroscopy, transmission electron microscopy, and high-resolution transmission electron microscopy. The results of the annealing process are MoTe2 nanorods with diameters of 50-200 nm and lengths ranging from 0.1 to 3.0 microm. Here, the rodlike structure of MoTe2 is reported for the first time, and added to the list as one kind of new morphology of MoTe2 nanomaterials. A mechanism for the formation of the nanorods is proposed. The sandwich-layered structure of Te-Mo-Te and the similarity in the structure between hexagonal alpha-MoTe2 and hexagonal Te are responsible for the formation of nanorods of MoTe2.

A series of early metal-promoted Ru-, Pd-, Pt-, and Rh-doped mesoporous tantalum oxide catalysts were synthesized using a variety of dopant ratios and dopant precursors, and the effects of these parameters on the catalytic activity of NH3 synthesis from H2 and N2 were explored. Previous studies on this system supported an unprecedented mechanism in which N-N cleavage occurred at the Ta sites rather than on Ru. The results of the present study showed, for all systems, that Ba is a better promoter than Cs or La and that the nitrate is a superior precursor for Ba than the isopropoxide or the hydroxide. 15N-labeling studies showed that residual nitrate functions as the major ammonia source in the first hour but that it does not account for the ammonia produced after the nitrate is completely consumed. Ru3(CO)12 proved to be a better Ru precursor than RuCl(3).3H2O, and an almost linear increase in activity with increasing Ru loading level was observed at 350 degrees C (623 K). However, at 175 degrees C (448 K), the increase in Ru had no effect on the reaction rate. Pd functioned with comparable rates to Ru, while Pt and Rh functioned far less efficiently. The surprising activities for the Pd-doped catalysts, coupled with XPS evidence for low-valent Ta in this catalyst system, support a mechanism in which cleavage of the N-N triple bond occurs on Ta rather than the precious metal because the Ea value for N-N cleavage on Pd is 2.5 times greater than that for Ru, and the 9.3 kJ mol-1 Ea value measured previously for the Ru system suggests that N-N cleavage cannot occur at the Ru surface.

Soybean hull peroxidase (SHP) was crystallised from an enzyme solution with low purity by a simple method. The enzyme solution was purified by cooperation salting out of acetone and ammonium sulphate, and lumpy crystals were obtained with the size of about 40 x 30 mum when ammonium sulphate was quickly added to the enzyme solution. The crystal was examined and confirmed to be an SHP crystal by the method of activity test. The result shows that, though the purity of the enzyme solution was not high, crystals could be formed when the enzyme solution rapidly reached to a degree of supersaturation, which was different from the traditional methods of protein crystallisation. Additionally, a purification method of acetone and ammonium sulphate fractional salting out was also studied, in which the procedure was simplified, and a satisfactory purification effect was obtained.

A biotransformation process was developed for the production of (S)-ketoprofen by enantioselective hydrolysis of racemic ketoprofen ester using the mutant Trichosporon laibacchii strain CBS 5791. A satisfactory result was obtained, in which the E was 82.5, with an ee of 0.94 and a conversion of 0.47 under the optimum hydrolysis conditions [E is enantiomeric ratio, E=ln[1-X(1+ee)]/ln[1-X(1-ee)]; ee is enantiomeric excess, ee=(CS-CR)/(CS+CR): temperature of hydrolysis was 23 degrees C]. The medium used in biotransformation was a mixture of growth broth and biotransformation broth at a ratio of 1:9, the concentration of Tween 80 was 15 g/l, the time of hydrolysis, 72 h. These results are promising for further scale-up. Tween 80 significantly improved lipase enantioselectivity and activity at the optimum concentration.

A simple sonication route to decorate multi-walled carbon nanotubes (MWCNTs) with crystalline tin nanoparticles is reported. The sonication process results in a uniform decoration of nanoparticles over the entire outer surface of the nanotubes. Acid-treated MWCNTs were exposed to ultrasonic radiation in a solution of SnCl2 in ethylene glycol under an N2 atmosphere. The products were characterized by X-ray powder diffraction measurements, differential scanning calorimetry, transmission electron microscopy, and high-resolution transmission electron microscopy. The decoration is composed of metallic tin nanocrystals of size less than 5 nm. This technique is suggested as a general versatile method for decorating carbon nanotubes with other nanoparticles.

A novel two-step approach to the synthesis of nanotubes of a transition metal dichalcogenide is reported. The synthesis combines a sonochemical reaction and an annealing process. MoTe2 nanotubes have been synthesized by calcining amorphous nanoparticles of MoTe2 which were sonochemically synthesized by reacting Te with Mo(CO)6 in decalin. The as-synthesized product was characterized by the structural, compositional and morphological techniques of XRD, SAED, SAEDS, EDX, TEM and HRTEM. The results show that the two-step process leads to MoTe2 nanotubes whose outer diameters are 20–60 nm and their lengths range from 100 to 500 nm. This method has potential for the synthesis of nanotubes of other transition metal dichalcogenides.