gebhart/patrepeval huggingface dataset:
A Large Accelerating Effect of Tri(tert-butyl)phosphine in the Rhodium-Catalyzed Addition of Arylboronic Acids to Aldehydes (2000)

ADVERTISEMENT RETURN TO ISSUEPREVNoteNEXTA Large Accelerating Effect of Tri(tert-butyl)phosphine in the Rhodium-Catalyzed Addition of Arylboronic Acids to AldehydesMasato Ueda and Norio MiyauraView Author Information Division of Molecular Chemistry, Graduate School of Engineering, Hokkaido University, Sapporo 060-8628, Japan Cite this: J. Org. Chem. 2000, 65, 14, 4450–4452Publication Date (Web):May 27, 2000Publication History Received10 February 2000Published online27 May 2000Published inissue 1 July 2000https://pubs.acs.org/doi/10.1021/jo000187chttps://doi.org/10.1021/jo000187cbrief-reportACS PublicationsCopyright © 2000 American Chemical SocietyRequest reuse permissionsArticle Views3326Altmetric-Citations188LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-AlertscloseSupporting Info (1)»Supporting Information Supporting Information SUBJECTS:Addition reactions,Aldehydes,Group 15 compounds,Metals,Rhodium Get e-Alerts
Promoting Reprogramming by FGF2 Reveals that the Extracellular Matrix Is a Barrier for Reprogramming Fibroblasts to Pluripotency (2013)

Leukemia inhibitory factor and bone morphogenetic protein signaling pathways play important roles in maintaining the self-renewal of mouse embryonic stem cells (ESCs). In contrast, the supplementation of fibroblast growth factor 2 (FGF2) in culture promotes mouse ESC differentiation. It has been proposed that factors that are adverse for maintaining the self-renewal of ESCs might play detrimental roles in the transcription factor-mediated reprogramming of somatic cells to pluripotency. However, recent evidence has revealed that reprogramming efficiency could be improved by FGF2, while the underlying molecular mechanism remains unknown. In this study, we dissected the roles of FGF2 in promoting mouse fibroblast reprogramming and disclosed the molecular mechanism behind this process. We used both primary induction and secondary inducible reprogramming systems and demonstrated that supplementation with FGF2 in the early phase of induced pluripotent stem cell induction could significantly increase reprogramming efficiency. Moreover, we discovered that many extracellular matrix candidate genes were significantly downregulated in fibroblasts treated with FGF2, and in particular, the synthesis of collagen could be greatly reduced by FGF2 treatment. Subsequently, we demonstrated that collagen is a barrier for reprogramming fibroblast cells to pluripotency, and the decreasing of collagen either by collagenase treatment or downregulation of collagen gene expression could significantly improve the reprogramming efficiency. Our results reveal a novel role of the extracellular matrix in mediating fibroblasts reprogramming.
Sun Grid Engine: towards creating a compute power grid (2002)

This paper provides an up-to-date overview of the Sun Grid Engine distributed resource management software and of future plans to enhance it towards and integrate it into computational grid environments. The main scope of many of today's Grid research projects is to understand and demonstrate the actual potential of networking, computing and software infrastructure for computational Grids and to build proof-of-concept middleware. This has resulted in Internet infrastructure projects like Globus (Foster and Kesselman, 1997), Legion (Chapin et al., 1999), and Punch (Kapadia and Fortes, 1999) which enable users to combine a set of distributed resources into one integrated Grid Workbench to allow users to measure nature (e.g, with microscope, telescope or particle accelerator), process the measured data according to fundamental mathematical equations (e.g. the Navier-Stokes or Maxwell equations), and provide computer simulations and animations to study and understand these complex phenomena.
Loss of the Sarcoglycan Complex and Sarcospan Leads to Muscular Dystrophy in -Sarcoglycan-Deficient Mice (1999)

beta-Sarcoglycan, one of the subunits of the sarcoglycan complex, is a transmembranous glycoprotein which associates with dystrophin and is the molecule responsible for beta-sarcoglycanopathy, a Duchenne-like autosomal recessive muscular dystrophy. To develop an animal model of beta-sarcoglycanopathy and to clarify the role of beta-sarcoglycan in the pathogenesis of the muscle degeneration in vivo, we developed beta-sarcoglycan-deficient mice using a gene targeting technique. beta-Sarcoglycan-deficient mice (BSG(-)(/-)mice) exhibited progressive muscular dystrophy with extensive degeneration and regeneration. The BSG(-)(/-)mice also exhibited muscular hypertrophy characteristic of beta-sarcoglycanopathy. Immunohistochemical and immunoblot analyses of BSG(-)(/-)mice demonstrated that deficiency of beta-sarcoglycan also caused loss of all of the other sarcoglycans as well as of sarcospan in the sarcolemma. On the other hand, laminin-alpha2, alpha- and beta-dystroglycan and dystrophin were still present in the sarcolemma. However, the dystrophin-dystroglycan complex in BSG(-)(/-)mice was unstable compared with that in the wild-type mice. Our data suggest that loss of the sarcoglycan complex and sarcospan alone is sufficient to cause muscular dystrophy, that beta-sarcoglycan is an important protein for formation of the sarcoglycan complex associated with sarcospan and that the role of the sarcoglycan complex and sarcospan may be to strengthen the dystrophin axis connecting the basement membrane with the cytoskeleton.
Cytokine induction in HTLV‐I associated myelopathy and adult T‐cell leukemia: Alternate molecular mechanisms underlying retroviral pathogenesis (1991)

The human T-cell lymphotropic virus type I (HTLV-I) is capable of inducing a variety of host cellular genes including many of the cytokines responsible for immune regulation and osteoclast activation. This derangement in cytokine expression may contribute to the panoply of disease states associated with HTLV-I infection such as the adult T-cell leukemia (ATL) and HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP). We wished to determine if there was a correlation between the expression of an array of cytokines and the diverse clinical manifestations of ATL and HAM/TSP. Utilizing the techniques of specific mRNA amplification by the polymerase chain reaction (PCR) as well as Northern blotting, we analyzed the ex vivo mRNA expression of gamma-interferon (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and transforming growth factor-beta 1 (TGF-beta 1) in the peripheral blood of HAM/TSP and ATL patients as well as asymptomatic seropositive carriers. IFN-gamma, TNF-alpha, and IL-1 beta transcripts were up-regulated in patients with HAM/TSP and seropositive carriers when compared to their levels in ATL and normal controls. In contrast, the ATL patients constitutively expressed higher levels of TGF-beta 1 mRNA than HAM/TSP and seropositive carriers. In addition, TNF-alpha and IL-1 beta serum levels were elevated in HAM/TSP, but not in ATL patients nor seropositive carriers. However, the circulating leukemic cells from ATL patients secreted increased levels of TGF-beta 1 protein into the culture medium than T-cells derived from HAM/TSP patients. Collectively these results suggest that induction of IFN-gamma, TNF-alpha, and IL-1 beta in HAM/TSP may initiate an inflammatory cascade with subsequent events leading to immune mediated destruction of the central nervous system in these patients. Expression of osteoclast activators such as TNF-alpha and IL-1 beta is not associated with hypercalcemia in ATL. Finally, impaired cellular and humoral immune responses present in ATL, but not in HAM/TSP, may be related to elevated levels of TGF-beta 1 produced by the leukemic cells. These differences in retroviral-induced host cytokine expression in ATL and HAM/TSP suggest alternate roles in disease pathogenesis.
3D printed microfluidic devices: enablers and barriers (2016)

3D printing has the potential to significantly change the field of microfluidics. The ability to fabricate a complete microfluidic device in a single step from a computer model has obvious attractions, but it is the ability to create truly three dimensional structures that will provide new microfluidic capability that is challenging, if not impossible to make with existing approaches. This critical review covers the current state of 3D printing for microfluidics, focusing on the four most frequently used printing approaches: inkjet (i3DP), stereolithography (SLA), two photon polymerisation (2PP) and extrusion printing (focusing on fused deposition modeling). It discusses current achievements and limitations, and opportunities for advancement to reach 3D printing's full potential.
In vitro production of pig embryos: a point of view (2002)

Porcine embryos have become raw materials for different programmes of reproductive biotechnology and the in vitro production of embryos has some advantages over in vivo production in gene transfer programmes and for xenotransplantation. Despite this promising future, several problems limit the success of the in vitro production (IVP) of viable porcine embryos. Porcine IVP has not been fully developed because of several problems associated with different techniques, such as incomplete final maturation status after in vitro maturation, a high incidence of polyspermy after in vitro fertilization and a low development rate and poor quality of blastocysts at the end of culture. The results could be improved with studies comparing in vivo and in vitro conditions, standardization of techniques for sperm processing, testing new additives in the culture media and developing intracytoplasmic sperm injection procedures. The first objective of the present article is to summarize the main studies published on the subject. Second, we provide a guide for researchers starting work on the IVP of pig embryos, making special mention of first papers and the most recent achievements for each of the different techniques. Third, we provide suggestions for future experiments designed to improve the results of each technique.
First-Principles Characterization of the Unknown Crystal Structure and Ionic Conductivity of Li7P2S8I as a Solid Electrolyte for High-Voltage Li Ion Batteries (2016)

Using first-principles density functional theory calculations and ab initio molecular dynamics (AIMD) simulations, we demonstrate the crystal structure of the Li7P2S8I (LPSI) and Li ionic conductivity at room temperature with its atomic-level mechanism. By successively applying three rigorous conceptual approaches, we identify that the LPSI has a similar symmetry class as Li10GeP2S12 (LGPS) material and estimate the Li ionic conductivity to be 0.3 mS cm(-1) with an activation energy of 0.20 eV, similar to the experimental value of 0.63 mS cm(-1). Iodine ions provide an additional path for Li ion diffusion, but a strong Li-I attractive interaction degrades the Li ionic transport. Calculated density of states (DOS) for LPSI indicate that electrochemical instability can be substantially improved by incorporating iodine at the Li metallic anode via forming a LiI compound. Our methods propose the computational design concept for a sulfide-based solid electrolyte with heteroatom doping for high-voltage Li ion batteries.
Inducible nitric oxide synthase in vascular smooth muscle cells from prehypertensive spontaneously hypertensive rats (1996)

The inducible nitric oxide synthase (iNOS) present in vascular smooth muscle cells (VSMC) may play a role in the generation of nitric oxide (NO) in the vascular wall, regulating blood vessel tone in normotension and hypertension. In this study the effect of interleukin (IL)-1 beta, a cytokine that induces iNOS, on NO generation (measured as nitrite), cyclic guanosine monophosphate (cGMP) generation, and steady-state abundance of iNOS mRNA were examined in VSMC from 3 week old spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, during the period preceding the elevation of blood pressure. With cell density dependent variations in nitrite production eliminated, VSMC from SHR and WKY did not differ in NO generation except after prolonged incubation (30 h), when SHR cells produced less NO. However, cGMP concentrations associated with IL-1 beta stimulation were significantly smaller in SHR VSMC than in cells from WKY. IL-1 beta stimulation resulted in increased abundance of iNOS mRNA to the same extent in both WKY and SHR VSMC. Inhibitors of NOS, NG-monomethyl-L-arginine (L-NMMA) and N omega-nitro-L-arginine methyl ester (L-NAME), did not block the induction of iNOS mRNA, although nitrite production and cGMP generation were inhibited. The protein synthesis inhibitor cycloheximide and the RNA synthesis inhibitor actinomycin-D almost completely blocked the production of nitrite in cells from both strains of rats. Actinomycin-D completely blocked the induction of iNOS mRNA by IL-1 beta in cells from both strains of rats, whereas cycloheximide partially blocked its synthesis in WKY, but had no significant effect on IL-1 beta induced expression of iNOS mRNA in SHR VSMC. Thus, IL-1 beta controls iNOS gene expression at the transcriptional level, and an intermediate labile protein, whose synthesis is inhibited by cycloheximide, is required for IL-1 beta stimulated induction of iNOS mRNA transcription in WKY cells but not in SHR. We conclude that although iNOS is expressed to similar extent in VSMC of prehypertensive SHR and WKY and similar amounts of NO are initially generated, there are differences between the VSMC of SHR and WKY in the regulation of the transcription of iNOS mRNA, there is a lower sustained production of NO, and there is a reduced generation of cGMP in response to IL-1 beta stimulated NO production. These differences between VSMC from prehypertensive SHR and WKY may indicate a pathophysiological role of iNOS in early blood pressure elevation in SHR.
X-Ray crystal structure of the pentagonal bipyramidal nickel(II) complex [NiII(L)(H2O)2](BF4)2and the selective stabilisation of the nickel(I) oxidation state by a quinquedentate macrocyclic ligand (1982)

The single crystal X-ray structure of the pentagonal bipyramidal nickel(II) complex [NiII(L)(H2O)2](BF4)2 involving the quinquedentate macrocyclic ligand L is reported; electrochemical reduction of a series of related nickel(II) complexes [NiII(L)X2](BF4)2 yields in solution d9 nickel(I) species.
MyD88 But Not TRIF Is Essential for Osteoclastogenesis Induced by Lipopolysaccharide, Diacyl Lipopeptide, and IL-1α (2004)

Myeloid differentiation factor 88 (MyD88) plays essential roles in the signaling of the Toll/interleukin (IL)-1 receptor family. Toll-IL-1 receptor domain-containing adaptor inducing interferon-beta (TRIF)-mediated signals are involved in lipopolysaccharide (LPS)-induced MyD88-independent pathways. Using MyD88-deficient (MyD88-/-) mice and TRIF-deficient (TRIF-/-) mice, we examined roles of MyD88 and TRIF in osteoclast differentiation and function. LPS, diacyl lipopeptide, and IL-1alpha stimulated osteoclastogenesis in cocultures of osteoblasts and hemopoietic cells obtained from TRIF-/- mice, but not MyD88-/- mice. These factors stimulated receptor activator of nuclear factor-kappaB ligand mRNA expression in TRIF-/- osteoblasts, but not MyD88-/- osteoblasts. LPS stimulated IL-6 production in TRIF-/- osteoblasts, but not TRIF-/- macrophages. LPS and IL-1alpha enhanced the survival of TRIF-/- osteoclasts, but not MyD88-/- osteoclasts. Diacyl lipopeptide did not support the survival of osteoclasts because of the lack of Toll-like receptor (TLR)6 in osteoclasts. Macrophages expressed both TRIF and TRIF-related adaptor molecule (TRAM) mRNA, whereas osteoblasts and osteoclasts expressed only TRIF mRNA. Bone histomorphometry showed that MyD88-/- mice exhibited osteopenia with reduced bone resorption and formation. These results suggest that the MyD88-mediated signal is essential for the osteoclastogenesis and function induced by IL-1 and TLR ligands, and that MyD88 is physiologically involved in bone turnover.
Effects of Membrane Cation Transport on pH and Microbial Fuel Cell Performance (2006)

Due to the excellent proton conductivity of Nafion membranes in polymer electrolyte membrane fuel cells (PEMFCs), Nafion has been applied also in microbial fuel cells (MFCs). In literature, however, application of Nafion in MFCs has been associated with operational problems. Nafion transports cation species other than protons as well, and in MFCs concentrations of other cation species (Na+, K+, NH4+, Ca2+, and Mg2+) are typically 10(5) times higher than the proton concentration. The objective of this study, therefore, was to quantify membrane cation transport in an operating MFC and to evaluate the consequences of this transport for MFC application on wastewaters. We observed that during operation of an MFC mainly cation species other than protons were responsible for the transport of positive charge through the membrane, which resulted in accumulation of these cations and in increased conductivity in the cathode chamber. Furthermore, protons are consumed in the cathode reaction and, consequently, transport of cation species other than protons resulted in an increased pH in the cathode chamber and a decreased MFC performance. Membrane cation transport, therefore, needs to be considered in the development of future MFC systems.
Ash utilization with silica and metals recovery (1996)

The annual generation of electric power in the United States results in production of over 43 million tons of fly ash. Only about 22% of this amount is presently utilized. Neither of the used ash applications requires the recovery of metals and other valuable components (i). In the process of studying, there is another group of methods based on direct recovery of metals from ash (ii). This paper continues presentation of new technologies for ash processing with silica pre-extraction process (SP-process) and recovery of metals. Silica in ash represent about 40-65% of the total, therefore the possibility of silica recovering and converting into a wide variety of purge chemical silicate products with the predetermined properties is one of the main advantages of new technologies. For technical and economic features these perspective technologies present the third new group of methods of ash utilization (iii).
Medical Microbiology 3rd Edition (2004)

Offers a basic introduction to viruses, bacteria, fungi and parasites. This title considers the immunology of the host, looking at the complex conflicts between host and invading agent. It explores the clinical manifestations of these conflicts within a systems-based context, with a re-organised survey of microbiological diagnosis and control.
EXPRESSION OF THE DEVELOPMENTAL AND ONCOGENIC PAX2 GENE IN HUMAN PROSTATE CANCER (2001)

In the human prostate cancer cell lines LNCaP, DU145 and PC3, 27 primary prostate cancers, 10 benign prostatic hyperplasia specimens and 5 normal prostates we investigated the expression pattern of PAX2, a member of the PAX family of developmental control genes. PAX2 is expressed at high levels in developing undifferentiated cells of the urogenital system and is repressed upon terminal differentiation with no expression in normal adult cells. It is also been shown to be a proto-oncogene in mice and is expressed in human renal cell carcinoma.PAX2 expression was assessed at the RNA level by reverse transcriptase-polymerase chain reaction and Southern blot analysis using specific sets of nucleotides. The expression pattern of PAX2 was reconfirmed at the protein level by immunofluorescence in the cell lines, and by Western blot analysis in primary human prostate cancers and benign prostatic tissue.Using reverse transcription-polymerase chain reaction combined with Southern hybridization PAX2 expression was detected in 52% of primary cancers and all 3 cell lines. PAX2 expression in these samples was confirmed at a protein level using immunoblotting and immunofluorescence. PAX2 messenger RNA was not detected in any benign or normal prostatic samples. Immunoblotting of protein from benign prostatic hyperplasia samples confirmed the lack of expression of PAX2 protein.The expression of PAX2 in prostate cancer compared to nonmalignant prostates is statistically significant (Fisher's exact test p = 0.0004). These results suggest a possible role for PAX2 in prostate cancer. Although previous studies have suggested a role for PAX2 for supporting proliferation in undifferentiated cells, no correlation of PAX2 expression with Gleason score was found in prostate cancer.
In vitro analysis of the pea chloroplast 16S rRNA gene promoter. (1989)

A cloned pea chloroplast 16S rRNA gene promoter has been characterized in detail by use of a homologous in vitro transcription system that contains a highly purified chloroplast RNA polymerase. The in vivo and in vitro 16S rRNA transcriptional start site has been identified to be a T on the plus strand, 158 bases upstream of the mature 5' end of the gene. BAL 31 deletions of the 16S rRNA leader region demonstrated that the bases between -66 to +30 relative to the transcriptional start site (+1) are necessary for specific 16S transcription. Disruption of canonical TTGACA or TATAAT elements within this region caused complete transcriptional inactivation and prevented protein binding. The topological requirement for 16S transcription was examined by using a construct that synthesized a transcript from the 16S promoter and released it from a pea plastid putative terminator sequence. This minigene was relaxed in vitro with a topoisomerase I from pea chloroplast. It was shown that the 16S promoter was most active when the minigene plasmid was supercoiled.