gebhart/patrepeval huggingface dataset:
New method for the introduction of a carbon-carbon triple bond at C-13 in prostaglandin synthesis. Stereocontrolled synthesis of ZK 96 480 (1988)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTNew method for the introduction of a carbon-carbon triple bond at C-13 in prostaglandin synthesis. Stereocontrolled synthesis of ZK 96 480Atsuo Takahashi and Masakatsu ShibasakiCite this: J. Org. Chem. 1988, 53, 6, 1227–1231Publication Date (Print):March 1, 1988Publication History Published online1 May 2002Published inissue 1 March 1988https://doi.org/10.1021/jo00241a020RIGHTS & PERMISSIONSArticle Views592Altmetric-Citations35LEARN 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 InReddit PDF (671 KB) Get e-Alertsclose Get e-Alerts
Mouse CD229 ligation costimulates T cell activation (176.7) (2012)

Abstract CD229 (SLAMF3) is a receptor protein primarily found on mature T cells, B cells, myeloid cells, macrophages, and thymocytes. The exact functions of this receptor remain uncertain. Data from CD229 knockout mice showed that CD229 is uniquely involved in enhancing T cell activation. However, coligation of CD229 and TCR with anti-CD229 (mAb) and anti-CD3 antibodies has been demonstrated to inhibit T cell activation. To study the functions of CD229, we expressed a soluble polyHistidine tagged protein containing the mouse CD229 extracellular domain (aa48-454) and investigated its function in purified mouse CD3+ cells in vitro. Concurrent ligation of CD229 and TCR with immobilized CD229-His protein and anti-CD3 antibody significantly enhanced cell proliferation and IFN-γ secretion in murine CD3+ splenocytes in a dose-dependent manner. Furthermore, pre-treatment of CD3+ splenocytes with polyclonal anti-CD229 antibody completely abolished co-stimulative actions of CD229-His. This suggests that CD229-His co-stimulates T cells through CD229 receptors on T cell surface. Moreover, ligation of CD229 with CD229-His in CD3+ cells led to ERK1/2 phosphorylation in response to anti-CD3 stimulation. Taken together, these results suggest that CD229 acts as a hemophilic costimulatory molecule and is able to up-regulate T-cell activation.
Comparison of various competent cell preparation methods for high efficiency DNA transformation. (1990)

Afin de determiner les conditions optimales de transformation du DNA, plusieurs souches de E. coli sont selectionnees et l'efficacite de transformation, (apres la preparation de cellules competentes) par differentes methodes est etudiee
New multimedia and telematic tools for asynchronous distance learning (2002)

New tools of modern education, connected mainly with Internet, are described in the paper. Their characteristics, principles of application were discussed in succession. Evaluation trail of their usefulness was done. Possibilities of carrying on laboratory experiments and distance designing were described. Probe to foresee directions of further development of Internet tools in the educational process was done.
Correction: Decreased Pre-existing Ad5 Capsid and Ad35 Neutralizing Antibodies Increase HIV-1 Infection Risk in the Step Trial Independent of Vaccination (2012)

Background: The Step trial raised the possibility that uncircumcised men with pre-existing Ad5 neutralizing antibodies carried an increased risk of HIV infection after vaccination. Thus, understanding Ad seropositivity in humans is important to the development of an AIDS vaccine. Here, we analyze the impact of different Ad5-specific neutralizing antibodies on immune function and clinical outcome.
The Timing of GM-CSF Expression Plasmid Administration Influences the Th1/Th2 Response Induced by an HIV-1-Specific DNA Vaccine (2000)

The mechanism of immune activation induced by a plasmid-encoding GM-CSF (pGM-CSF), administered in combination with a DNA vaccine encoding the envelope of HIV, was studied. Injecting pGM-CSF i.m. into mice 3 days before DNA vaccination primarily induced a Th2 response. Simultaneous administration of the DNA vaccine plus pGM-CSF activated both a Th1 and a Th2 response. When the plasmid was injected 3 days after DNA vaccination, enhancement of Th1 immunity predominated. These results suggest that the timing of cytokine expression determines the phenotype of the resultant Th response. After 3 days of pGM-CSF injection, the increased percentages of CD11c+, CD8+ cells were observed in the regional lymph nodes. In addition, many infiltrated cells, including S-100 protein-positive cells, were found in the pGM-CSF-injected tissue. The importance of these S-100+ cells or both CD8+ and CD11c+ cells, especially that of dendritic cells (DCs), was also studied. DCs derived from bone marrow and cultured in RPMI 1640 medium containing IL-4 and GM-CSF were incubated with DNA vaccine and then transferred into naive mice. Mice receiving DCs showed strong HIV-1-specific Th2 immune responses. Our results suggest that DCs play important roles in the activation or modification of the Th2-type immune response induced by DNA vaccination.
Tec regulates platelet activation by GPVI in the absence of Btk (2003)

Abstract The Tec family kinase Btk plays an important role in the regulation of phospholipase Cγ2 (PLCγ2) downstream of the collagen receptor glycoprotein VI (GPVI) in human platelets. Platelets also express a second member of this family, Tec; however, its function has not been analyzed. To address the role of Tec, we analyzed Btk-/-, Tec-/-, and Btk/Tec double-deficient (Btk-/-/Tec-/-) platelets. Tec-/- platelets exhibit a minor reduction in aggregation to threshold concentrations of collagen or the GPVI-specific agonist collagen-related peptide (CRP), whereas responses to higher concentrations are normal. Tyrosine phosphorylation of PLCγ2 by collagen and CRP is not altered in Tec-/- platelets. However, Btk-/-/Tec-/- platelets exhibit a greater reduction in PLCγ2 phosphorylation than is seen in the absence of Btk, thus revealing an important role for Tec in this situation. Furthermore, Btk-/-/Tec-/- platelets fail to undergo an increase in Ca2+, aggregation, secretion, and spreading in response to collagen or CRP, whereas they aggregate normally to adenosine diphosphate (ADP) and spread on fibrinogen. A residual GPVI signal exists in the Btk-/-/Tec-/- platelets as CRP synergizes with ADP to mediate aggregation. These results demonstrate an essential requirement for Tec and Btk in platelet activation by GPVI and reveal a functional role for Tec in the regulation of PLCγ2 in the absence of Btk. (Blood. 2003;102: 3592-3599)
Dual Action of Double‐Stranded RNA in Inhibiting Protein Synthesis in Extracts of Interferon‐Treated Mouse L Cells (1978)

We have investigated the mechanism by which double‐stranded RNA (dsRNA) inhibits protein synthesis in cell‐free extracts prepared from mouse L cells which had been pre‐treated with purified interferon. Preincubation of such extracts for a determined period of time causes inactivation of tRNA species and hence an inhibition of protein synthesis with either Mengo RNA or poly(U,C) as mRNA. This inhibition can be overcome by addition of tRNA. We show that dsRNA inhibits the translation of Mengo RNA irrespective of the period of preincubation and that this inhibition is not overcome by tRNA. Translation of poly(U,C) is unaffected by dsRNA. Thus dsRNA does not act at the level of peptide chain elongation and does not cause inactivation of tRNA species, indicating that dsRNA inhibits protein synthesis in extracts of interferon‐treated cells by a mechanism which is different from that responsible for the inhibition observed in the absence of dsRNA. The addition of dsRNA to extracts prepared from interferon‐treated cells causes two modifications which are expected to inhibit protein synthesis. (a) An enhancement of the level of nuclease activity, causing Mengo [ 3 H]RNA to be degraded more rapidly in interferon‐treated cell extracts than control extracts, even when association of Mengo RNA with ribosomes is inhibited by the addition of pactamycin. (b) An impairment in the formation of methionyl‐tRNA · 40‐S‐ribosomal‐subunit complexes. The reduced binding of methionyl‐tRNA to 40‐S subunits can be overcome by the addition of a crude initiation factor preparation suggesting that dsRNA causes inactivation of an endogenous initiation factor(s). In the early stages of translation of Mengo RNA (10–15 min) dsRNA causes a reduction in the incorporation of [ 35 S]methionine into the N‐terminal position of polypeptides suggesting that initiation of protein synthesis is impaired, presumably as a result of the block of methionyl‐tRNA · 40‐S‐subunit complex formation. At a later stage (30–45 min) Mengo RNA is almost completely destroyed under the normal conditions of protein synthesis.
The Path from Syllabus Outcomes to Achievement in Musical Performance: Mapping the SOLO Taxonomy to Described Levels of Achievement in the NSW Higher School Certificate (2003)

This paper examines the path from syllabus outcomes through to the criteria used for assessing musical performances. It uses, as a case study, the Music 2 and Music Extension syllabuses as developed by the Board of Studies (NSW) and the subsequent examination of the performance component of the Higher School Certificate, the NSW public examinations conducted at the end of schooling. The SOLO (Structure of the Observed Learning Outcome) Taxonomy (Biggs and Collis, 1982) has been proposed as a tool for educators to described levels of achievement in musical performance (McPherson 2001, 2002). The marking criteria and guidelines used to assess musical performances in the Music 2 and Music Extension examinations are discussed and comparisons made to previous descriptions of musical performances using the SOLO Taxonomy.
Deferasirox Reduces Iron Overload in a Murine Model of Juvenile Hemochromatosis. (2006)

Abstract Introduction: Targeted disruption of the hemojuvelin gene in mice (HJV−/−) has recently been reported to cause markedly increased liver, pancreas and heart iron deposition, and act as a model for juvenile hemochromatosis (Niederkofler et al. 2005, Huang et al. 2005). Deferasirox, a novel tridentate oral iron chelator, is effective in the treatment of patients with transfusional iron overload and it has not been investigated in primary iron overload. We sought to examine spontaneous iron loading and the effect of deferasirox on the removal of iron in HJV−/− mice with iron overload. Methods: Inductively-Coupled Plasma Optical Emission Spectrometry (ICP-OES, measurement of elemental iron) determinations in liver, heart, spleen and pancreas were performed at week 8 (study start), 14, 20 and 28 in HJV −/− and wild-type (wt) mice (n=6–8), subsequent to MRI measurements in heart and liver. Starting at week 20 three groups of HJV−/− animals received daily 0 (vehicle), 30 or 100 mg/kg deferasirox, control wt-mice remained untreated. Iron loading was observed up to 28 weeks (including vehicle group) and the effects of deferasirox were assessed by comparing the 28-week groups. MRI R2* measurements were performed using a 4.7T MR imager. For the myocardial and hepatic R2* assessments single-slice, ECG gated gradient-echo images and single-slice transversal gradient-echo images were acquired, respectively. Results: Iron loading of the liver and the heart was 21- and 5-fold higher in HJV−/− than in wt mice. Conspicuously, pancreas showed the most extreme difference in iron load (34-fold). Visual inspection of the time courses of iron loading between week 8 and 28 suggest a delayed loading of the heart and pancreas as compared with liver. Effects of deferasirox on organ iron load were modest at 30 mg/kg but quite pronounced in liver and heart at 100 mg/kg. This may seem contradictory to data from human studies, which show effects between 20 and 30 mg/kg in iron overload, but may be explained by the approximately 6–9 times lower exposure of deferasirox in mice. At 100 mg/kg deferasirox, liver iron was reduced by 63% and heart iron by 41% as compared with the (HJV−/−)-vehicle treated group. Pancreas showed a clear trend to lower levels at the 100 mg/kg dose. Contrary to liver, heart and pancreas, iron burden of the spleen was lower in HJV−/− as compared to wt mice. This behavior is expected because the same (enhanced) iron efflux mechanism that allows iron to enter the circulation from enterocytes is also in place in reticuloendothelial cells. MRI R2* values are more variable than organ iron concentrations determined by ICP-OES. However, the profiles of the time courses of R2* of liver and heart in HJV−/− mice were similar to the time courses of liver and heart iron as determined by ICP-OES, underlining the correlation between R2* values and organ iron. Conclusion: Deferasirox significantly reduced liver and heart iron in the hemojuvelin knock-out mouse and showed a trend to improvement of pancreatic iron load within 8 weeks of treatment. Figure Figure
Location of cis-acting regulatory sequences in the human T-cell leukemia virus type I long terminal repeat. (1985)

The location of cis-acting regulatory regions within the long terminal repeat (LTR) of the human T-cell leukemia virus type I (HTLV-1) was determined. The sequences present between nucleotides -350 and -55 (cap site +1) contain an enhancer element that is active in lymphoid and nonlymphoid cell lines. The sequences located near the "TATA" and RNA initiation sites contain a promoter, the activity of which can be augmented by homologous and heterologous enhancer elements. A region responsive to trans-acting transcription factors present in HTLV-I- and HTLV type II-infected cells is located between nucleotides -159 and +315. HTLV-I LTR deletion mutants respond in a similar manner both to the trans-acting factors present in infected cells and to the tat protein encoded by the x-lor region of the genome, thus providing further evidence that the tat protein mediates transcriptional trans-activation of the LTR in HTLV-infected cells.
A covalent linkage between daunorubicin and proteins that is stable in serum and reversible by lysosomal hydrolases, as required for a lysosomotropic drug-carrier conjugate: in vitro and in vivo studies. (1982)

Daunorubicin (DNR) has been conjugated to succinylated serum albumin by an amide bond joining the amino group of the drug and a carboxyl side chain of the protein either directly or with the intercalation of a peptide spacer arm varying from one to four amino acids. During in vitro incubation with lysosomal hydrolases, intact DNR could be released extensively only from conjugates prepared with a tri- or tetrapeptide spacer arm. These latter conjugates remained very stable in the presence of serum. When tested in vivo against the intraperitoneal form of L1210 leukemia, the conjugates in which DNR was linked to serum albumin directly or via one amino acid were completely inactive but the conjugate with a dipeptide spacer arm was not more active than free DNR. In parallel with the in vitro studies, the best therapeutic results were obtained with the conjugates formed with tri- and tetrapeptidic spacer arms; they were much more active than DNR, inducing a high percentage of long-term survivors. Thus, use of a tri- or tetrapeptide spacer arm is essential to obtain DNR-protein conjugates that remain stable in serum and from which DNR can be released through the action of lysosomal hydrolases. The in vivo results suggest, moreover, that these conjugates are endocytosed by L1210 cells and that DNR is released intracellularly after digestion by lysosomal enzymes. This conjugation method can be applied to other drugs possessing a free amino group and to various potential carriers, such as antibodies, polypeptide hormones, and glycoproteins, that have amino or carboxyl side chains.
Reliable Transient Promoter Assay Using Fluorescein-di-β-D-galactopyranoside Substrate (1990)

The promoter region of the mouse myelin proteolipid protein (PLP) gene was cloned into a promoter testing vector, pIP111. The pIP111 vector is a promoterless derivative of pCH110 (SV40 early region promoter-lacZ) and contains the Escherichia coli lpp transcription terminator sequence at the 5' end of the cloning site. The newly constructed PLP-lacZ fusion plasmid (pWP) was transfected into PLP-nonproducing NIH-3T3 fibroblasts or PLP-producing C6 cells. When the measured beta-galactosidase activity in the pWP-transfected cells was normalized to the pCH110-transfected cells (an appropriate control if the SV40 early region promoter functions constitutively in various cell lines), the results suggested that the promoter region of the PLP gene contains the information necessary for initiation of transcription in a C6 cell-specific manner. However, the beta-galactosidase produced in viable cells was also detected by fluorescein-di-beta-D-galactopyranoside (FDG) treatment followed by image analysis using inverted fluorescent microscopy, which allowed the transfection efficiency to be calculated, and the beta-galactosidase activity obtained by the regular ONPG method was normalized with the value obtained. This procedure indicated that the promoter region of the PLP gene did not show C6-specific expression, because the SV40 early-region promoter was 10 times more active in NIH-3T3 cells than in C6 cells. Thus, the standard experiment gave misleading results. As our detection method is simple and can be used to analyze the promoter activity in a single cell, many applications should be possible.(ABSTRACT TRUNCATED AT 250 WORDS)
Invited Review: Role of insulin in translational control of protein synthesis in skeletal muscle by amino acids or exercise (2002)

Protein synthesis in skeletal muscle is modulated in response to a variety of stimuli. Two stimuli receiving a great deal of recent attention are increased amino acid availability and exercise. Both of these effectors stimulate protein synthesis in part through activation of translation initiation. However, the full response of translation initiation and protein synthesis to either effector is not observed in the absence of a minimal concentration of insulin. The combination of insulin and either increased amino acid availability or endurance exercise stimulates translation initiation and protein synthesis in part through activation of the ribosomal protein S6 protein kinase S6K1 as well as through enhanced association of eukaryotic initiation factor eIF4G with eIF4E, an event that promotes binding of mRNA to the ribosome. In contrast, insulin in combination with resistance exercise stimulates translation initiation and protein synthesis through enhanced activity of a guanine nucleotide exchange protein referred to as eIF2B. In both cases, the amount of insulin required for the effects is low, and a concentration of the hormone that approximates that observed in fasting animals is sufficient for maximal stimulation. This review summarizes the results of a number of recent studies that have helped to establish our present understanding of the interactions of insulin, amino acids, and exercise in the regulation of protein synthesis in skeletal muscle.
Variable-rate coding for meteor-burst communications (1989)

The performance of variable-rate Reed-Solomon error-control coding for meteor-burst communications is considered. The code rate is allowed to vary from codeword to codeword within each packet, and the optimum number of codewords per packet and optimum rates for the codewords are determined as a function of the length of the message and the decay rate for the meteor trail. The resulting performance is compared to that obtained from, fixed-rate coding. Of central importance is the derivation of tractable expressions for the probability of correct decoding for bounded-distance decoding on a memoryless channel with a time-varying symbol error probability. A throughout measure is developed that is based on the probability distribution of the initial signal-to-noise ratio.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Inflammatory mechanisms in Alzheimer's disease: inhibition of beta-amyloid-stimulated proinflammatory responses and neurotoxicity by PPARgamma agonists. (2000)

Alzheimer's disease (AD) is characterized by the extracellular deposition of beta-amyloid fibrils within the brain and the subsequent association and phenotypic activation of microglial cells associated with the amyloid plaque. The activated microglia mount a complex local proinflammatory response with the secretion of a diverse range of inflammatory products. Nonsteroidal anti-inflammatory drugs (NSAIDs) are efficacious in reducing the incidence and risk of AD and significantly delaying disease progression. A recently appreciated target of NSAIDs is the ligand-activated nuclear receptor peroxisome proliferator-activated receptor gamma (PPARgamma). PPARgamma is a DNA-binding transcription factor whose transcriptional regulatory actions are activated after agonist binding. We report that NSAIDs, drugs of the thiazolidinedione class, and the natural ligand prostaglandin J2 act as agonists for PPARgamma and inhibit the beta-amyloid-stimulated secretion of proinflammatory products by microglia and monocytes responsible for neurotoxicity and astrocyte activation. The activation of PPARgamma also arrested the differentiation of monocytes into activated macrophages. PPARgamma agonists were shown to inhibit the beta-amyloid-stimulated expression of the cytokine genes interleukin-6 and tumor necrosis factor alpha. Furthermore, PPARgamma agonists inhibited the expression of cyclooxygenase-2. These data provide direct evidence that PPARgamma plays a critical role in regulating the inflammatory responses of microglia and monocytes to beta-amyloid. We argue that the efficacy of NSAIDs in the treatment of AD may be a consequence of their actions on PPARgamma rather than on their canonical targets the cyclooxygenases. Importantly, the efficacy of these agents in inhibiting a broad range of inflammatory responses suggests PPARgamma agonists may provide a novel therapeutic approach to AD.