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A protocol induced by visible light for the direct insertion of α-carbonyl carbenes into the B–H bond of amine-borane adducts has been developed under conditions that are free of metal and photocatalyst. This approach provides a straightforward route to various organoboron compounds from diazo compounds and amine-borane adducts with moderate to good yields. Mechanistic investigations reveal that this photoinduced reaction proceeds through concerted carbene insertion into the B–H bond, and the photoinduced generation of free carbene from α-diazo esters may be the rate-determining step.

A simple and efficient Rh2(OAc)4/DPPM (bis(diphenylphosphanyl)methane) catalyzed regioselective 1,2-anti-Markovnikov hydrosilylation of conjugated dienes with various tertiary silanes gave homoallylic silanes in acetonitrile, which tolerate broad functional groups. Control experiments proved that no π-allyl transition metal intermediates were involved in this 1,2-anti-Markovnikov hydrosilylation. Dirhodium hydride species was observed in hydrosilylation, suggesting that a direct insertion of the terminal double bond into a Rh–H bond is involved in this reaction.

• Biodegradable contraceptive implants prepared by UV irradiation molding method. • Photo-cross-linked aliphatic polycarbonates as a matrix material. • Carrier has degradation characteristic of surface erosion mechanism. • Implants with low cytotoxicity and good biocompatibility. • Formulation has stable release kinetics and good long-acting contraceptive effects. In this study, a new class of biodegradable contraceptive implants was prepared via the UV irradiation molding method, among which, progestin levonorgestrel (LNG) was used as a model drug. Photo-cross-linked aliphatic polycarbonates (APCs), namely, poly (trimethylene carbonate-co-2,2′-dimethyltrimethylene carbonate) [P(TMC-co-DTC)] elastomers, were used as the drug delivery matrix. The results obtained from the degradation experiments carried out in Sprague-Dawley (SD) rats showed that the cross-linked elastomer had the degradation characteristics of the surface erosion degradation mechanism, with no generation of acid degradation products, and excellent form-stability, which met the performance requirements of the matrix for a long-acting sustained-release delivery system. The in vitro cytotoxicity tests and histological and immunohistochemical evaluations showed good biocompatibility and biosafety of the elastomer matrix material and contraceptive implants. Subsequently, the implant formulations were screened by in vitro release experiments, and their release kinetics were explored. Finally, in the evaluation study of the in vivo anti-fertility effect, the implants exhibited excellent dimensional stability and were degraded by a surface erosion mechanism. LNG achieved a stable and sustained release in female SD rats, maintaining a long-acting contraceptive duration of up to 4 months. The contraceptive implants obtained in this study could be used to address the limitations of currently available formulations, which required secondary surgical removal and a single means of regulating drug release kinetics. Therefore, these implants could provide a new option for birth control needs and may be of significance in reducing the incidence of induced abortion and protecting female fertility. [Display omitted] [ABSTRACT FROM AUTHOR]

Transformer structure, stacked by a sequence of encoder and decoder network layers, achieves significant development in neural machine translation. However, vanilla Transformer mainly exploits the top-layer representation, assuming the lower layers provide trivial or redundant information and thus ignoring the bottom-layer feature that is potentially valuable. In this work, we propose the Group-Transformer model (GTrans) that flexibly divides multi-layer representations of both encoder and decoder into different groups and then fuses these group features to generate target words. To corroborate the effectiveness of the proposed method, extensive experiments and analytic experiments are conducted on three bilingual translation benchmarks and three multilingual translation tasks, including the IWLST-14, IWLST-17, LDC, WMT-14, WMT-21 and OPUS-100 benchmark. Experimental and analytical results demonstrate that our model outperforms its Transformer counterparts by a consistent gain. Furthermore, it can be successfully scaled up to 60 encoder layers and 36 decoder layers.

We demonstrated a multifunctional buried interface modulation strategy by employing FBABF4 possessing simultaneously fluorinated anion and cation to manage the SnO2/perovskite interface.

Hydrogel microspheres have drawn great attention as functional three-dimensional (3D) microcarriers for cell attachment and growth, which have shown great potential in cell-based therapies and biomedical research. Hydrogels derived from a decellularized extracellular matrix (dECM) retain the intrinsic physical and biological cues from the native tissues, which often exhibit high bioactivity and tissue-specificity in promoting tissue regeneration. Herein, a novel two-stage temperature-controlling microfluidic system was developed which enabled production of pristine dECM hydrogel microspheres in a high-throughput manner. Porcine decellularized peripheral nerve matrix (pDNM) was used as the model raw dECM material for continuous generation of pDNM microgels without additional supporting materials or chemical crosslinking. The sizes of the microspheres were well-controlled by tuning the feed ratios of water/oil phases into the microfluidic device. The resulting pDNM microspheres (pDNM-MSs) were relatively stable, which maintained a spherical shape and a nanofibrous ultrastructure for at least 14 days. Schwann cells and PC12 cells preseeded on the pDNM-MSs not only showed excellent viability and an adhesive property, but also promoted cell extension compared to the commercially available gelatin microspheres. Moreover, primary neural stem/progenitor cells attached well to the pDNM-MSs, which further facilitated their proliferation. The successfully fabricated dECM hydrogel microspheres provided a highly bioactive microenvironment for 3D cell culture and functionalization, which showed promising potential in versatile biomedical applications.

We report a highly efficient and selective catalytic system, ABNO (9-azabicyclo-[3.3.1]nonane N-oxyl)/HNO3, for the aerobic oxidation of substituted furans to cis-2-ene-1,4-diones under mild reaction conditions using oxygen as the oxidant. The catalyst system is amenable to various substituted (mon-, di-, and tri-) furans and tolerates diverse functional groups, including cyano, nitro, naphthyl, ketone, ester, heterocycle, and even formyl groups. Based on the control and 18O-labeling experiments, the possible mechanism of the oxidation is proposed.

We report a simple and effective nickel-based catalytic system, NiCl2·6H2O/tBuOK, for the electrophilically activated hydrosilylation of terminal alkenes with primary silanes. This protocol provides excellent performance under mild reaction conditions: exclusive anti-Markovnikov selectivity, broad functional group tolerance (36 examples), and good scalability (TON = 5500). However, the secondary and tertiary silanes are not suitable. Mechanistic studies revealed that this homogeneous catalytic hydrosilylation includes an electrophilically activated Si–H bond process without the generation of nickel hydrides.

Studies have shown that the use of proangiogenic genes can improve the prognosis of ischemic stroke by promoting angiogenesis at the injury site. For example, within this study, hypoxia-inducible factor 1-α (HIF-1α) has exhibited an angiogenic effect. Our previous study reported a more stable HIF-1α mutant form (HIF-1α-AA), which was transfected into mesenchymal stem cells to provide neuroprotective effects against ischemic stroke. The safety of nonviral gene vectors has attracted researchers’ attention. This study encapsulated the HIF-1α-AA plasmid DNA into a newly synthesized effective nonviral gene vector, a hyperbranched cationic amylopectin derivative (DMAPA-Amyp) nanocarrier. In addition, a targeting strategy was applied to select the RGD peptides and bind to the designed nanocarrier as a molecule targeting endothelial cells. The targeting strategy is used to directly deliver the nanocarriers to the vascular endothelial cells of the brain peri-infarct site. This study emphasizes the targeting ability of nanocarrier and its therapeutic effect on cerebral ischemia. The results showed that RGD-DMAPA-Amyp had good biocompatibility and a high cell uptake rate, indicating that it is a safe nonviral gene vector that can be endocytosed by human cells. In rat models of ischemic stroke, compared with the nontargeted nanocarrier group, more RGD-DMAPA-Amyp nanoparticles aggregated in vascular endothelial cells of the peri-infarct region and significantly improved the recovery of neurological function. It is indicated that the RGD-modified nanomedicine promotes the recovery of nerve function more efficiently. Further study on the mechanism of RGD-DMAPA-Amyp/HIF-1α-AA in the treatment of cerebral ischemia displayed potential to significantly promote the formation of new blood vessels in vivo. Our findings suggest that the RGD-modified nonviral gene vector containing HIF-1α-AA appears to be a safe and promising therapeutic strategy for ischemic stroke gene therapy.

Interleukin (IL)-18 plays an important role in liver ischemia/reperfusion (I/R) injury. We have previously demonstrated that remifentanil protects against liver I/R injury by upregulating the hepatic expression of IL-18-binding protein (IL-18BP), a natural IL-18 inhibitor. The current study was performed to further clarify the effects of remifentanil on IL-18BP expression in the liver as well as investigate the underlying mechanisms. In Sprague-Dawley (SD) rats, we demonstrated that remifentanil significantly increased the expression of IL-18BP in normal rat liver tissue over a 24-h time period with maximal expression at 24 h after treatment. The upregulation of remifentanil on IL-18BP expression displayed similar trends in in vitro cellular studies, including mouse primary hepatocytes, normal human hepatocyte LO2, and mouse hepatoma cells Hep1-6. In LO2 cells, preexposure of the cells to remifentanil significantly inhibited IL-18-activated p65 NF-κB phosphorylation, and the inhibition was absent when the cells were transfected with IL-18BP siRNA, indicating the functional effects of IL-18BP induced by remifentanil. Pretreatment with actinomycin D abolished remifentanil-induced upregulation of IL-18BP mRNA, suggesting that the induction occurred at the transcriptional level. This was further supported by the luciferase reporter assay, which demonstrated that remifentanil treatment significantly increased transcription of the IL-18BP promoter. Both western blot analysis and ChIP assays showed that STAT1 and C/EBP β were activated by remifentanil. Furthermore, remifentanil failed to upregulate IL-18BP expression after silencing STAT1 or C/EBP β gene expression. These findings demonstrate that remifentanil could upregulate hepatic IL-18BP expression through transcriptional activation of the IL-18BP promoter, and STAT1 and C/EBP β are two key transcriptional factors involved in this process. In normal rats and a human hepatic cell line, the authors demonstrate that remifentanil upregulates IL-18BP expression in hepatocytes, and that the underlying mechanism involves activation of the transcription factors STAT1 and C/EBP β. These findings expand our understanding of the pharmacological effects of remifentanil and suggest its potential treatment benefits for IL-18 dysfunction-mediated hepatic diseases.

Interleukin (IL)-18 plays an important role in liver ischemia/reperfusion (I/R) injury. We have previously demonstrated that remifentanil protects against liver I/R injury by upregulating the hepatic expression of IL-18-binding protein (IL-18BP), a natural IL-18 inhibitor. The current study was performed to further clarify the effects of remifentanil on IL-18BP expression in the liver as well as investigate the underlying mechanisms. In Sprague-Dawley (SD) rats, we demonstrated that remifentanil significantly increased the expression of IL-18BP in normal rat liver tissue over a 24-h time period with maximal expression at 24 h after treatment. The upregulation of remifentanil on IL-18BP expression displayed similar trends in in vitro cellular studies, including mouse primary hepatocytes, normal human hepatocyte LO2, and mouse hepatoma cells Hep1-6. In LO2 cells, preexposure of the cells to remifentanil significantly inhibited IL-18-activated p65 NF-κB phosphorylation, and the inhibition was absent when the cells were transfected with IL-18BP siRNA, indicating the functional effects of IL-18BP induced by remifentanil. Pretreatment with actinomycin D abolished remifentanil-induced upregulation of IL-18BP mRNA, suggesting that the induction occurred at the transcriptional level. This was further supported by the luciferase reporter assay, which demonstrated that remifentanil treatment significantly increased transcription of the IL-18BP promoter. Both western blot analysis and ChIP assays showed that STAT1 and C/EBP β were activated by remifentanil. Furthermore, remifentanil failed to upregulate IL-18BP expression after silencing STAT1 or C/EBP β gene expression. These findings demonstrate that remifentanil could upregulate hepatic IL-18BP expression through transcriptional activation of the IL-18BP promoter, and STAT1 and C/EBP β are two key transcriptional factors involved in this process.

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An alkoxide-catalyzed hydrosilylation of cyclic imides to isoquinolines was realized via tandem reduction and rearrangement. Using TMSOK as the catalyst and (EtO)2MeSiH as the reductant, a series of cyclic imides containing different functional groups were reduced to the corresponding 3-aryl isoquinolines in moderate to good yields. The scenario of the reaction pathway was supposed to involve the reduction of imides to ω-hydroxylactams, which underwent rearrangement in the presence of a base catalyst, and then the carbonyl reduction, followed by siloxy elimination.

To investigate the role of miRNA-15b in cardiomyocyte apoptosis after ischemia reperfusion injury in acute myocardial infarction (AMI), we conducted the AMI rat model by using left anterior descending ligation and performed hypoxia/reoxygenation experiments in H9c2 cells. MiRNA-15b was measured by quantitative reverse transcription PCR (qRT-PCR). Cardiomyocyte apoptosis was determined by terminal deoxynucleotide transferase dUTP nick end labeling staining. Synthesized miRNA-15b mimic and inhibitor were transfected into H9c2 cells by Lipofectamine regent. RNA expression of B cell lymphoma/leukemia-2 (Bcl-2) and mitogen-activated protein kinase 3 (MAPK3) was examined by qRT-PCR and their protein expression was determined by western blot. Ischemia reperfusion increased miRNA-15b expression in the ischemic rat heart and resulted more severe cardiomyocytes apoptosis. In H9c2 cells, hypoxia/reoxygenation induced increased miRNA-15b expression and augmented cardiomyocyte apoptosis observed at 24 hours after 24-hour hypoxia. Compared with the vehicle group, miRNA-15b mimic further raised miRNA-15b level and increased cardiomyocyte apoptosis, whereas miRNA-15b inhibitor suppressed miRNA-15b expression and protected cardiomyocytes from apoptosis. Although the mRNA expression of the target genes Bcl-2 and MAPK3 was not changed significantly, the protein expression of these two genes were markedly reduced after miRNA-15b mimic treatment and significantly increased after transfected with miRNA-15b inhibitors. In conclusion, miRNA-15b deteriorates cardiomyocyte apoptosis by post-transcriptionally downregulating the expression of Bcl-2 and MAPK3.

To investigate the role of miRNA-15b in cardiomyocyte apoptosis after ischemia reperfusion injury in acute myocardial infarction (AMI), we conducted the AMI rat model by using left anterior descending ligation and performed hypoxia/reoxygenation experiments in H9c2 cells. MiRNA-15b was measured by quantitative reverse transcription PCR (qRT-PCR). Cardiomyocyte apoptosis was determined by terminal deoxynucleotide transferase dUTP nick end labeling staining. Synthesized miRNA-15b mimic and inhibitor were transfected into H9c2 cells by Lipofectamine regent. RNA expression of B cell lymphoma/leukemia-2 (Bcl-2) and mitogen-activated protein kinase 3 (MAPK3) was examined by qRT-PCR and their protein expression was determined by western blot. Ischemia reperfusion increased miRNA-15b expression in the ischemic rat heart and resulted more severe cardiomyocytes apoptosis. In H9c2 cells, hypoxia/reoxygenation induced increased miRNA-15b expression and augmented cardiomyocyte apoptosis observed at 24 hours after 24-hour hypoxia. Compared with the vehicle group, miRNA-15b mimic further raised miRNA-15b level and increased cardiomyocyte apoptosis, whereas miRNA-15b inhibitor suppressed miRNA-15b expression and protected cardiomyocytes from apoptosis. Although the mRNA expression of the target genes Bcl-2 and MAPK3 was not changed significantly, the protein expression of these two genes were markedly reduced after miRNA-15b mimic treatment and significantly increased after transfected with miRNA-15b inhibitors. In conclusion, miRNA-15b deteriorates cardiomyocyte apoptosis by post-transcriptionally downregulating the expression of Bcl-2 and MAPK3.

High-risk neuroblastoma remains one of the deadliest childhood cancers. Identification of metabolic pathways that drive or maintain high-risk neuroblastoma may open new avenues of therapeutic interventions. Here, we report the isolation and propagation of neuroblastoma sphere-forming cells with self-renewal and differentiation potential from tumors of the TH-MYCNmouse, an animal model of high-risk neuroblastoma with MYCNamplification. Transcriptional profiling reveals that mouse neuroblastoma sphere-forming cells acquire a metabolic program characterized by transcriptional activation of the cholesterol and serine-glycine synthesis pathways, primarily as a result of increased expression of sterol regulatory element binding factors and Atf4, respectively. This metabolic reprogramming is recapitulated in high-risk human neuroblastomas and is prognostic for poor clinical outcome. Genetic and pharmacological inhibition of the metabolic program markedly decreases the growth and tumorigenicity of both mouse neuroblastoma sphere-forming cells and human neuroblastoma cell lines. These findings suggest a therapeutic strategy for targeting the metabolic program of high-risk neuroblastoma.

The histone lysine demethylase KDM4C is often overexpressed in cancers primarily through gene amplification. The molecular mechanisms of KDM4C action in tumorigenesis are not well defined. Here, we report that KDM4C transcriptionally activates amino acid biosynthesis and transport, leading to a significant increase in intracellular amino acid levels. Examination of the serine-glycine synthesis pathway reveals that KDM4C epigenetically activates the pathway genes under steady-state and serine deprivation conditions by removing the repressive histone modification H3 lysine 9 (H3K9) trimethylation. This action of KDM4C requires ATF4, a transcriptional master regulator of amino acid metabolism and stress responses. KDM4C activates ATF4 transcription and interacts with ATF4 to target serine pathway genes for transcriptional activation. We further present evidence for KDM4C in transcriptional coordination of amino acid metabolism and cell proliferation. These findings suggest a molecular mechanism linking KDM4C-mediated H3K9 demethylation and ATF4-mediated transactivation in reprogramming amino acid metabolism for cancer cell proliferation.

Design space exploration (DSE) is an important step before the physical level design of Field programmable gate arrays (FPGA). An optimum architecture is usually selected from the whole space. As the architecture parameters increase, the huge time cost to explore an exponentially increasing space makes this method unrealistic. We propose a novel predictive modeling approach called ECOMT to estimate the area and delay of a circuit which is mapped onto an FPGA with certain architecture. Semi-supervised model tree is adopted to model the performance with respect to architecture parameters. Combined with nonlinear programming, the area and delay model obtained can be used to guide the DSE. Experimental results show that the model trained through ECOMT has Mean relative error (MRE) below 5% compared to VTR. Meanwhile the time used to attain the model is less than 3 minutes, which reduces the time of DSE considerably.

The alkali leaching of vanadium from petroleum coke was studied in terms of the effects of several parameters. Results showed that the vanadium concentration in the residue decreased to 200 ppm under the following conditions: reaction time, 5 h; Na2CO3and NaOH concentrations, 120 and 200 g/L, respectively; H2O2, 12 ml; temperature, 383 K; and particle size, 0.09 mm to 0.106 mm. The alkali leaching kinetics of vanadium from petroleum coke was successfully described by diffusion through the gangue layer control model. The activation energy of this leaching process was found to be 7.9 kJ

A number of case reports now indicate that rocuronium can induce a number of serious side effects. We hypothesized that these side effects might be mediated by the inhibition of nicotinic acetylcholine receptors (nAChRs) at superior cervical ganglion (SCG) neurons. Conventional patch clamp recordings were used to study the effects of rocuronium on nAChR currents from enzymatically dissociated rat SCG neurons. We found that ACh induced a peak transient inward current in rat SCG neurons. Additionally, rocuronium suppressed the peak ACh-evoked currents in rat SCG neurons in a concentration-dependent and competitive manner, and it increased the extent of desensitization of nAChRs. The inhibitory rate of rocuronium on nAChR currents did not change significantly at membrane potentials between −70 and −20 mV, suggesting that this inhibition was voltage independent. Lastly, rocuronium preapplication enhanced its inhibitory effect, indicating that this drug might prefer to act on the closed state of nAChR channels. In conclusion, rocuronium, at clinically relevant concentrations, directly inhibits nAChRs at the SCG by interacting with both opened and closed states. This inhibition is competitive, dose dependent, and voltage independent. Blockade of synaptic transmission in the sympathetic ganglia by rocuronium might have potentially inhibitory effects on the cardiovascular system.

The effects of parallel and angular butt designs with different gap widths on the microstructure and mechanical properties of the resultant magnesium joints in gas tungsten arc welding were investigated. The experimental results displayed that the tensile strength of the joint made with angular butt joint and 0.3 mm-wide gap reached 266 MPa, the joint fractured through the heat-affected zone or base metal during tensile testing, and the microstructure examination showed that no macropore appeared in the fusion zone. However, macropores in diameter of larger than 200 micron occurred for other joint designs, the tensile strength of the resultant joints decreased, and the joints fractured through the fusion zone during tensile testing. The fracture surfaces were examined by scanning electron microscopy and the microhardness distribution in the joints was measured by using a Vickers microhardness tester. [Copyright &y& Elsevier]

Proteolytic processing of the nuclear factor (NF)-κB2 precursor protein p100 generates the active NF-κB2 subunit p52, which in turn transcriptionally up-regulates p100 expression. p100 also functions as an IκB molecule capable of repressing p52 activity. The biological significance of this negative feedback control loop has yet to be demonstrated in vivo. Here we show that mice deficient in p100 but with constitutive expression of p52 in lymphocytes developed fatal lung inflammation characterized by diffuse alveolar damage with marked peribronchial fibrosis. In contrast, their littermates with only p100 deficiency or constitutive expression of p52 in lymphocytes developed mild lung inflammation with perivascular lymphocyte infiltration and had a normal life span. The fatal lung inflammation is associated with high-level induction of interferon-γ and its inducible inflammatory chemokines, suggesting the involvement of a T-helper-1 immune response. These findings demonstrate the physiological relevance of the NF-κB2 p100 precursor protein in limiting the potentially detrimental effects of constitutive NF-κB2 signaling in lymphocytes.

Amplification of the oncogene MYCNis a tumorigenic event in the development of a subset of neuroblastomas that commonly consist of undifferentiated or poorly differentiated neuroblasts with unfavorable clinical outcome. The cellular origin of these neuroblasts is unknown. Additionally, the cellular functions and target cells of MYCN in neuroblastoma development remain undefined. Here we examine the cell types that drive neuroblastoma development in TH-MYCNtransgenic mice, an animal model of the human disease. Neuroblastoma development in these mice begins with hyperplastic lesions in early postnatal sympathetic ganglia. We show that both hyperplasia and primary tumors are composed predominantly of highly proliferative Phox2B+neuronal progenitors. MYCN induces the expansion of these progenitors by both promoting their proliferation and preventing their differentiation. We further identify a minor population of undifferentiated nestin+cells in both hyperplastic lesions and primary tumors that may serve as precursors of Phox2B+neuronal progenitors. These findings establish the identity of neuroblasts that characterize the tumor phenotype and suggest a cellular pathway by which MYCN can promote neuroblastoma development.

Abstract: The pigments in Laminaria japonica was extracted with six organic solvents and analyzed in spectroscopy analysis. The extractions conditions were screened by an orthogonal test and the quantity of extracted pigments was determined spectroscopically. The results show that: (1) among the six organic solvents, acetone was the most effective one for the extraction; (2) the optimum extraction conditions were as follows: the ratio of S/M (solvent volume/ material weight) was 30 ml/g; fresh seaweed was extracted 2 times in 2 h; (3) the average total content of pigments was 1.85 mg/g (calculated with dry L. japonica).

The crystallization and melting behaviors of maleated polyethylene (MPE) and its composite with fibrous crystalline cellulose are investigated by differential scanning calorimetry. MPE exhibits a higher crystallization starting temperature, because of the interactions between maleic anhydride (MA) groups for nucleation, and lower melting and crystallization enthalpies, because of the intensive irregularity of MPE chains compared to unmaleated PE (UPE). Fibrous cellulose (FC) slightly facilitates the nucleation of MPE but causes no change in the transition enthalpies of MPE for crystallization and melting in UPE–FC and MPE–FC composites. The kinetics of crystallization show that the Avrami exponent depends on the content of MA groups and FC to a small extent and the activation energy is largely determined by the MA content, suggesting the irregularity and decreased mobility of MPE chains that is due to the interactions between the grafted MA groups in MPE and the FC composite. © 2003 Wiley Periodicals, Inc. J Appl Polym Sci 89: 3292–3300, 2003

Fibrous cellulose and maleated polyethylene (FC–MPE) composites were prepared under melt mixing by maleation of polyethylene (PE) to obtain maleic anhydride (MA) grafted PE (MPE) and successive compounding of the resultant MPE with fibrous cellulose (FC). When increasing the content of added MA to 2 wt %, the grafting efficiency of MA decreases gradually to 84% and the grafted MA chains become longer. Scanning electron microscopy (SEM) reveals strong adhesion of MPE to FC in the FC–MPE composite, which is probably due to the increased compatibility between MPE and FC, in contrast to no adhesion of unmaleated PE (UPE) to FC in the FC–UPE composite. This difference in interfacial structure between the FC–MPE and FC–UPE composites results in quite different mechanical properties for them. With an increase in the FC content to 60 wt %, the tensile strength of the FC–MPE composite increases significantly and reaches 125% that of pure PE. Furthermore, the larger Young's modulus, larger bending elastic modulus, and smaller elongation of the FC–MPE composite strongly indicate effective transfer of the high tensile strength and elasticity of FC to the MPE matrix through the strong adhesion between FC and MPE. © 2002 Wiley Periodicals, Inc. J Appl Polym Sci 84: 1971–1980, 2002; DOI 10.1002/app.10428

Induction of differentiation is a therapeutic strategy in neuroblastoma, a common pediatric cancer of the sympathetic nervous system. The homeobox protein HOXC9 is a key regulator of neuroblastoma differentiation. To gain a molecular understanding of the function of HOXC9 in promoting differentiation of neuroblastoma cells, we conducted a genome-wide analysis of the HOXC9-induced differentiation program by microarray gene expression profiling and chromatin immunoprecipitation in combination with massively parallel sequencing (ChIP-seq). Here we describe in detail the experimental system, methods, and quality control for the generation of the microarray and ChIP-seq data associated with our recent publication [1].

Acrylate copolymers containing hydrophobic monomers (methyl methacrylate, butyl acrylate, styrene, or divinyl benzene) and hydrophilic monomer (acrylic acid) were synthesized by solution polymerization, and neutralized to form the soap-free hydrosol. The waterborne coating was prepared from the hydrosol crosslinked by M(NH3)²⁺4 (M²⁺ was Zn²⁺ , Cu²⁺, Ni²⁺ or Co²⁺). ¹³C-NMR analysis was used to identify the copolymer. The result of GPC showed that the molecular weight of the copolymer was within the range of thermosetting resin for coating. The factors affecting the crosslinking degree of the coating films were studied by DSC and gravimetric analysis. The results indicated that the appropriate crosslinking agent was Zn(NH3)²⁺4, and the optimum curing condition was heating at 80°C for 30 min. © 1999 John Wiley & Sons, Inc. J Appl Polym Sci 74: 91–96, 1999

Abstract: BSD/I18N project is established for the purpose of internationalizing the 4.3BSD UNIX systems. Its tasks are to provide an internationalized application software development environment, support the 4.3BSD commands/utilities with multi-language processing, and build a complete English and Japanese user environments without excluding other languages like Chinese and Korean.

Perovskite solar cells (PSCs) have attracted tremendous interest because of their rushing improvement in power conversion efficiency (PCE) from the initial 3.8% to the most recently certified 25.2%. Despite the high efficiency of photovoltaic prospects, organic-inorganic hybrid perovskite materials with the requisite organic components are very sensitive and heterolytic under heat and humidity conditions. One of the promising methods to prepare inorganic perovskite solar cells (I–PSCs) by completely replacing the A-site organic cations in ABX3structure has developed rapidly due to their excellent thermal and environmental stability. However, the phase instability of inorganic perovskite, especially for α‐CsPbI3, has been the bottleneck hindering their development in ambient conditions. Doping with new components is regarded as an effective method to assist the formation of high‐quality and stable inorganic perovskite films. The Gold-Schmidt tolerance factor toptimization or the intramolecular interaction between perovskite precursors with the new components has a substantial influence on the crystallization kinetics and the structural stability, while simultaneously offering the enhanced carrier transport characteristics and surface tension. Here, we systematically summarize the most recent research progress of inorganic perovskite and discuss strategies to overcome the phase instability from the perspective of doping for the first time. We also outlined the doped system of perovskite derivatives and summarized the application of the doped inorganic perovskite for photovoltaic application. Finally, we focus on prospecting the challenges and future research directions to achieve super-stable inorganic perovskites and their photovoltaics.

Ball milling of crystalline cellulose with maleated polyethylene (MPE) yields a novel composite with ester bonds formed by reaction of the hydroxy groups of the cellulose with the maleic anhydride groups of MPE; the composite exhibits much improved toughness and ductility compared with the product formed by melt-mixing, probably because of the formation of an interphase of MPE chains bonded on cellulose particles.

Local anesthetics have been extensively employed to treat postoperative pain, but they generally suffer from short acting duration and potential neurotoxicity under high local concentrations, which require the controlled and sustained releasing patterns of treatment drugs. In this work, it is reported, for the first time, the construction of hollow mesoporous organosilica nanoparticles (HMONs)‐based nanoplatforms for localized delivery and controlled/sustained release of loaded ropivacaine for local anesthetics, which can be repeatedly triggered by either external ultrasound irradiation or acidity triggering to release the payload, causing on‐demand and long‐lasting analgesia. Based on the in vivo mouse model of incision pain, the controlled and sustained release of ropivacaine achieves more than six hours of continuous analgesia, which is almost three times longer as compared to single free ropivacaine injection. The low neurotoxicity and high biocompatibility of HMONs for nanoparticle‐enabled analgesia are also demonstrated both in vitro and in vivo. This designed/constructed HMONs‐based nanoplatform provides a potential methodology for clinical pain management via on‐demand and long‐lasting pain relief. A unique dual stimuli‐responsive (ultrasound and acidity) hollow mesoporous organosilica nanoparticles (HMONs)‐based nanoplatforms, ropivacaine@HMONs,are engineered for achieving on‐demand and long‐lasting pain relief, which are demonstrated by the in vivo mouse model of incision pain. The low neurotoxicity and high biocompatibility of HMONs for nanoparticle‐enabled analgesia are also demonstrated both in vitro and in vivo.