gebhart/patrepeval huggingface dataset:
Monosubstituted diazenes (diimides). Surprising intermediates (1971)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTMonosubstituted diazenes (diimides). Surprising intermediatesEdward M. KosowerCite this: Acc. Chem. Res. 1971, 4, 6, 193–198Publication Date (Print):June 1, 1971Publication History Published online1 May 2002Published inissue 1 June 1971https://pubs.acs.org/doi/10.1021/ar50042a001https://doi.org/10.1021/ar50042a001research-articleACS PublicationsRequest reuse permissionsArticle Views663Altmetric-Citations102LEARN 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-Alertsclose Get e-Alerts
Fusion of the MORF and CBP genes in acute myeloid leukemia with the t(10;16)(q22;p13) (2001)

The CBP gene at 16p13 fuses to MOZ and MLL as a result of the t(8;16)(p11;p13) in acute (myelo)monocytic leukemias (AML M4/M5) and the t(11;16)(q23;p13) in treatment-related AML, respectively. We show here that a novel t(10;16)(q22;p13) in a childhood AML M5a leads to a MORF-CBP chimera. RT-PCR using MORF forward and CBP reverse primers amplified a MORF-CBP fusion in which nucleotide 3103 of MORF was fused in-frame with nucleotide 284 of CBP. Nested RT-PCR with CBP forward and MORF reverse primers generated a CBP-MORF transcript in which nucleotide 283 of CBP was fused in-frame with nucleotide 3104 of MORF. Genomic analyses revealed that the breaks were close to Alu elements in intron 16 of MORF and intron 2 of CBP and that duplications had occurred near the breakpoints. A database search using MORF cDNA enabled us to construct an exon-intron map of the MORF gene. The MORF-CBP protein retains the zinc fingers, two nuclear localization signals, the histone acetyltransferase (HAT) domain, a portion of the acidic domain of MORF and the CBP protein downstream of codon 29. Thus, the part of CBP encoding the RARA-binding domain, the CREB-binding domain, the three Cys/His-rich regions, the bromodomain, the HAT domain and the Glu-rich domains is present. In the reciprocal CBP-MORF, part of the acidic domain and the C-terminal Ser- and Met-rich regions of MORF are likely to be driven by the CBP promoter. Since both fusion transcripts were present, their exact role in the leukemogenic process remains to be elucidated.
Identification of a Novel Member of the Chloride Intracellular Channel Gene Family (CLIC5) That Associates with the Actin Cytoskeleton of Placental Microvilli (2000)

The chloride intracellular channel (CLIC) gene family has been implicated in chloride ion transport within various subcellular compartments. We report here the molecular, biochemical, and cellular characterization of a new member of this gene family termed CLIC5. CLIC5 was isolated from extracts of placental microvilli as a component of a multimeric complex consisting of several known cytoskeletal proteins, including actin, ezrin, alpha-actinin, gelsolin, and IQGAP1. We cloned human cDNAs and generated antibodies specific for CLIC5, CLIC1/NCC27, and CLIC4/huH1/p64H1. CLIC5 shares 52-76% overall identity with human CLIC1, CLIC2, CLIC3, and CLIC4. Northern blot analysis showed that CLIC5 has a distinct pattern of expression compared with CLIC1 and CLIC4. Immunoblot analysis of extracts from placental tissues demonstrated that CLIC4 and CLIC5 are enriched in isolated placental microvilli, whereas CLIC1 is not. Moreover, in contrast to CLIC1 and CLIC4, CLIC5 is associated with the detergent-insoluble cytoskeletal fraction of microvilli. Indirect immunofluorescence microscopy revealed that CLIC4 and CLIC5 are concentrated within the apical region of the trophoblast, whereas CLIC1 is distributed throughout the cytoplasm. These studies suggest that CLIC1, CLIC4, and CLIC5 play distinct roles in chloride transport and that CLIC5 interacts with the cortical actin cytoskeleton in polarized epithelial cells.
Carboxy-Endcapped Conductive Polypyrrole:  Biomimetic Conducting Polymer for Cell Scaffolds and Electrodes (2006)

Numerous regenerating tissues respond favorably to electrical stimulation, creating a need for a bioactive conducting platform for tissue engineering applications. The drive for biosensors and electrode coatings further requires control of the surface properties of promising conductive materials such as polypyrrole. Here we present carboxy-endcapped polypyrrole (PPy-alpha-COOH), a unique bioactive conducting polymer with a carboxylic acid layer, composed of a polypyrrole (PPy) surface modified with pyrrole-alpha-carboxylic acid (Py-alpha-COOH). This unique structure is simple to produce, provides a stable bioactive surface via covalent bonds, and preserves bulk properties such as electrical conductivity and mechanical integrity. The chemical structure of this polymer composite was characterized by angle-resolved X-ray photoelectron spectroscopy (XPS), which demonstrated the presence of carboxylic acid functionality on the top surface of conductive PPy. A four-point probe test was used to verify the similar conductivity of PPy-alpha-COOH compared to that of standard PPy. To demonstrate the potential to influence cellular activity, the carboxylic acid monolayer surface was grafted with the cell-adhesive Arg-Gly-Asp (RGD) motif. Human umbilical vein endothelial cells (HUVECs) cultured on RGD-modified PPy-alpha-COOH demonstrated significantly higher adhesion and spreading than on the negative controls PPy-alpha-COOH and unmodified PPy.
Aporphines 65: Chemical, microbial synthesis and characterization by gas chromatography/mass spectrometry of (R)-(−)-10-hydroxy 11-methoxy-N-n-propylnoraporphine, a potential metabolite ofN-n-propylnorapomorphine (1986)

The title compound has been synthesized by a multistep sequence from (R)(-)-morphine, and compared with the product obtained by microbial O-demethylation of (R)- and (S)-10,11-dimethoxy-N-n-propylnoraporphine (N-n-propylnorapomorphine dimethyl ether). The comparison was based on an analysis of the trifluoroacetyl derivatives of the microbial products and the synthesized compounds using gas chromatography/mass spectrometry in the electron impact mode. Examination by gas chromatography/electron impact/mass spectrometry of the trifluoroacetyl derivatives of 11-hydroxy-10-methoxyaporphine (apocodeine, 3) and 10-methoxy-11-hydroxyaporphine (isoapocodeine, 5) has revealed their excellent chromatographic resolution, and the preferential loss of the methyl group as in 3 [M-15]+ or the trifluoroacetyl group from the 10-position of the aporphine ring as in 5 [M-97]+. Characteristic fragmentations of these isomeric aporphines were used to confirm their structures and were compared with the spectra of authentic synthetic samples.
Synthesis of multiple exoproducts in Pseudomonas aeruginosa is under the control of RhlR-RhlI, another set of regulators in strain PAO1 with homology to the autoinducer-responsive LuxR-LuxI family (1995)

Mutants of Pseudomonas aeruginosa PAO1 that were deficient in the ability to produce proteases that degrade casein were detected among the survivors of chemical mutagenesis. One such mutant (PDO31) showed reduced production of elastolytic activity, beta-hemolytic activity, and pyocyanin. A 4.3-kb EcoRI fragment from a gene bank of PAO1 that complemented defects in PDO31 was found. Transposon mutagenesis and deletion derivatives of the clone were used in conjunction with complementation tests to determine the physical location of the gene of interest. Nucleotide sequence analysis revealed an open reading frame (rhlR) encoding a putative 27.6-kDa protein (RhlR) with homology to autoinducer-responsive regulators of quorum sensing systems such as LuxR of Vibrio fischeri and LasR of P. aeruginosa. Further sequence analysis downstream of rhlR revealed an independently transcribed gene (rhlI) that encodes a putative 22.2-kDa protein with homology to members of the family of autoinducer synthetases, such as LuxI of V. fischeri and LasI of P. aeruginosa. The rhlRI sequences were also recently reported by others (U.A. Ochsner and J. Reiser, Proc. Natl. Acad. Sci. USA 92: 6424-6428, 1995) as an autoinducer-mediated regulation mechanism for rhamnolipid biosurfactant synthesis in P. aeruginosa PG201. Mutants with defects in rhlR or rhlI were constructed in PAO1 by gene replacement, using clones modified by Tn501 insertion. Compared with the wild type, the rhlR and rhlI mutants both showed defects in the production of elastase, LasA protease, rhamnolipid, and pyocyanin. Transcription from the gene for elastase, as measured with a lasB-cat fusion, demonstrated that production of elastase was subject to cell density-dependent gene activation in PAO1. However, transcription of lasB-cat in the rhlI mutant, which had lost the presumptive autoinducer synthetase (predicted to activate RhlR), showed low basal activity and had lost all cell density-dependent transcription of lasB. Thus, RhlR-RhlI represent the second autoinducer-responsive regulatory mechanism found in P. aeruginosa that controls expression of multiple virulence factor exoproducts, including elastase.
Power-efficient Noise-insensitive Optical Modulation for High-sensitivity Laser Communications (2014)

We demonstrate power-efficient noise-insensitive optical waveform generation from directly modulated lasers combined with periodic time-frequency windowing. Real-time experiments with direct FPGA-driven lasers achieve near-theoretical communication performance at Gbit/s rates using flexible and scalable transceiver designs.
Effect of protein A of Staphylococcus aureus on the binding of monomeric and polymeric IgG to Fc receptor-bearing cells. (1979)

The effect of protein A of Staphylococcus aureus (SpA) on the binding of rabbit IgG to the Fc receptors of mouse lymphocytes and macrophages was found to correlate with the aggregation of the IgG ligands. After binding anti-erythrocyte IgG complexed with SpA, the cells were able to attach to and kill erythrocyte indicator cells with a higher efficiency than lymphoid cells treated with anti-erythrocyte IgG alone. The amount of anti-peroxidase IgG which can be bound to effector cells was not changed by reaction with SpA. In contrast, the binding to cells of IgG-coated erythrocytes and of anti-peroxidase IgG complexed with peroxidase was substantially reduced by reaction with SpA. The results are compatible with the presence of two distinct Fc receptors, one for cytophilic monomeric IgG and another for polymeric (antigen-complexed) IgG.
Body Size and Risk of Luminal, HER2-Overexpressing, and Triple-Negative Breast Cancer in Postmenopausal Women (2008)

Although the clinical relevance of molecular subtypes of breast cancer has been documented, little is known about risk factors for different tumor subtypes, especially the HER2-overexpressing and the triple-negative subtypes that have poor prognoses. Obesity may be differentially related to the risk of different subtypes given the various potential mechanisms underlying its association with breast cancer. We pooled two population-based case-control studies of postmenopausal breast cancer for an analysis, including 1,447 controls and 1,008 luminal (hormone receptor positive), 39 HER2-overexpressing (hormone receptor negative, HER2 positive), and 77 triple-negative (hormone receptor and HER2 negative) cases. Associations between anthropometric factors and the risk of different breast cancer subtypes were evaluated using polytomous logistic regression. Among women not currently using menopausal hormone therapy, body mass index (BMI) and weight were associated with the risk of luminal tumors [odds ratio (OR) comparing highest versus lowest quartiles, 1.7; 95% confidence interval (95% CI), 1.2-2.4 and OR, 1.7; 95% CI, 1.2-2.4, respectively] and suggestively associated with risk of triple-negative tumors (OR, 2.7; 95% CI, 1.0-7.5 and OR, 5.1; 95% CI, 1.1-23.0, respectively). Neither BMI nor weight was associated with the risk of any tumor subtype among hormone therapy users. The positive relationship between BMI and luminal tumors among postmenopausal women not using hormone therapy is well characterized in the literature. Although our sample size was limited, body size may also be related to the risk of postmenopausal triple-negative breast cancer among nonusers of hormone therapy. Given the expanding obesity epidemic, the widespread cessation of hormone therapy use, and the poor prognosis of triple-negative tumors, this novel finding merits confirmation.
Human red cell Aquaporin CHIP. II. Expression during normal fetal development and in a novel form of congenital dyserythropoietic anemia. (1994)

Channel-forming integral protein (CHIP) is the archetypal member of the Aquaporin family of water channels. Delayed CHIP expression was shown recently in perinatal rat (Smith, B. L., R. Baumgarten, S. Nielsen, D. Raben, M. L. Zeidel, and P. Agre. 1993. J. Clin. Invest. 92:2035-2041); here we delineate the human patterns. Compared with adult, second and third trimester human fetal red cells had lower CHIP/spectrin ratios (0.72 +/- 0.12, 0.94 +/- 0.22 vs 1.18 +/- 0.11) and reduced osmotic water permeability (0.029, 0.026 vs 0.037 cm/s); CHIP was already present in human renal tubules by the second trimester. A patient with a novel form of congenital dyserythropoietic anemia (CDA) with persistent embryonic and fetal globins and absent red cell CD44 protein was studied because of reduced CHIP-associated Colton antigens. Novel CDA red cells contained < 10% of the normal level of CHIP and had remarkably low osmotic water permeability (< 0.01 cm/s), but no mutation was identified in Aquaporin-1, the gene encoding CHIP. These studies demonstrate: (a) unlike rat, human CHIP expression occurs early in fetal development; (b) red cell water channels are greatly reduced in a rare phenotype; and (c) disrupted expression of red cell CHIP and CD44 suggests an approach to the molecular defect in a novel form of CDA.
Pathophysiological Role of Dopamine in the Kidney: Effects in Diabetes Mellitus and after Contralateral Nephrectomy (1995)

Both insulin-dependent diabetes mellitus (IDDM) and unilateral nephrectomy (UNX) are associated with an increase in the glomerular filtration rate. Glomerular hyperfiltration has been linked to intraglomerular hypertension in both conditions, although it has only been linked to the development of nephropathy in diabetes. In this study, we examined the possibility of preventing diabetic nephropathy through early dopamine (DA) prodrugs treatment and we also investigated the participation of endogenous DA in the acute functional adaptation of the remaining kidney after UNX. In an animal model of IDDM (steptozotocin-treated Wistar rats), the early increase in the glomerular filtration rate was prevented by treatment with DA prodrugs (L-dopa or gludopa), an effect which was mimicked by fenoldopam (a D1 agonist) and suppressed by carbidopa and SCH 23390 (a D1 antagonist). An increase in endorenal DA synthesis and the subsequent stimulation of vascular D1 receptors appears to prevent early glomerular hyperfiltration in diabetic rats. However, in a long-term study lasting more than one year, streptozotocin-diabetic Wistar rats (unlike to diabetic Munich Wistar rats) failed to develop overt nephropathy characterized by albuminuria and systemic hypertension. During long-term treatment of diabetic rats with L-dopa, the renal availability of DA was diminished. The acute adaptation of the remaining kidney to UNX took the form of an early transient pressor effect with a moderate increase in the glomerular filtration rate and renal blood flow, and a marked decrease in tubular sodium reabsorption. SCH 23390 suppressed the hemodynamic and tubular responses to UNX, suggesting that endogenous DA plays a key role.
Ezrin has a COOH-terminal actin-binding site that is conserved in the ezrin protein family. (1994)

Ezrin, previously also known as cytovillin, p81, and 80K, is a cytoplasmic protein enriched in microvilli and other cell surface structures. Ezrin is postulated to have a membrane-cytoskeleton linker role. Recent findings have also revealed that the NH2-terminal domain of ezrin is associated with the plasma membrane and the COOH-terminal domain with the cytoskeleton (Algrain, M., O. Turunen, A. Vaheri, D. Louvard, and M. Arpin. 1993. J. Cell Biol. 120: 129-139). Using bacterially expressed fragments of ezrin we now demonstrate that ezrin has an actin-binding capability. We used glutathione-S-transferase fusion proteins of truncated ezrin in affinity chromatography to bind actin from the cell extract or purified rabbit muscle actin. We detected a binding site for filamentous actin that was localized to the COOH-terminal 34 amino acids of ezrin. No binding of monomeric actin was detected in the assay. The region corresponding to the COOH-terminal actin-binding site in ezrin is highly conserved in moesin, actin-capping protein radixin and EM10 protein of E. multilocularis, but not in merlin/schwannomin. Consequently, this site is a potential actin-binding site also in the other members of the protein family. Furthermore, the actin-binding site in ezrin shows sequence homology to the actin-binding site in the COOH terminus of the beta subunit of the actin-capping protein CapZ and one of the potential actin-binding sites in myosin heavy chain. The actin-binding capability of ezrin supports its proposed role as a membrane-cytoskeleton linker.
Paramagnetic polymerized liposomes as new recirculating MR contrast agents (1995)

We describe a well-tolerated blood pool contrast agent with extended recirculatory half-life based on paramagnetic polymerized liposomes (PPLs). PPLs were constructed from a new type of polymerizable lipid molecule that has a derivative of gadopentetate dimeglumine as the hydrophilic head group and diacetylene groups in the hydrophobic acyl chains, which cross-link when irradiated with ultraviolet (UV) light. Biodistribution, blood pool half-life, and MR image enhancement were determined for PPLs composed of 10% of the gadopentetate dimeglumine lipid and 90% of ditricosadiynoyl tricosadiynayl phosphatidylcholine (DAPC) at a dose of 0.015 mmol Gd+3/kg in rats. In T1-weighed MR images (TR/TE = 400/18 msec), an average signal enhancement of 34% in the kidneys and 20% in the liver was observed, which persisted for at least 90 minutes after administration of the PPLs. Biodistribution studies using radiolabeled PPLs confirmed that 80% of the injected dose remained in the blood pool after 2 hours. The half-life of elimination from the blood pool was 19 hours. The preparation was well tolerated in rats and produced similar MR contrast enhancement of the blood pool as produced by other liposome contrast agents. However, the half-life of PPL elimination from the blood pool was prolonged relative to other liposome systems.
AUGUSTUS: a web server for gene finding in eukaryotes (2004)

We present a www server for AUGUSTUS, a novel software program for ab initio gene prediction in eukaryotic genomic sequences. Our method is based on a generalized Hidden Markov Model with a new method for modeling the intron length distribution. This method allows approximation of the true intron length distribution more accurately than do existing programs. For genomic sequence data from human and Drosophila melanogaster, the accuracy of AUGUSTUS is superior to existing gene-finding approaches. The advantage of our program becomes apparent especially for larger input sequences containing more than one gene. The server is available at http://augustus.gobics.de.
Abstract 34: A MET x MET bispecific antibody that induces receptor degradation potently inhibits the growth of MET-addicted tumor xenografts (2017)

Abstract Aberrant regulation of MET receptor tyrosine kinase signaling is associated with development and progression of various human tumors. Elevated MET signaling during tumorigenesis results from MET amplification, mutation or up-regulation of the ligand, HGF. MET amplification is thought to be a key driver of oncogenesis in non-small cell lung cancers (NSCLC) and oesophagogastric malignancies. In addition, mutations resulting in exon 14 deletion of MET have been described as oncogenic drivers in a subset of NSCLC. Both preclinical and recent clinical results indicate that tumors harboring these genetic alterations respond to MET inhibitors, validating MET as a cancer driver. We have developed a novel bispecific antibody that binds to two distinct epitopes on MET. The METxMET bispecific antibody blocks HGF binding and exhibits very low agonist activity (much weaker than either of its parental antibodies). Furthermore, the METxMET bispecific antibody effectively promotes MET degradation, thereby inhibiting ligand-independent signaling in MET-amplified tumor cells. The METxMET bispecific antibody exhibits strong anti-tumor efficacy in xenograft models harboring MET genetic alterations, either completely inhibiting tumor growth (EBC1 MET-amplified NSCLC) or promoting substantial tumor regression (SNU5 MET-amplified gastric cancer, Hs746T MET-amplified/MET exon 14 skip gastric cancer). Analysis of lysates from SNU5 tumors treated with the METxMET bispecific antibody confirms its ability to effectively promote MET degradation in vivo. Finally, the METxMET bispecific antibody strongly inhibits the growth of a glioblastoma xenograft model (U118) driven by autocrine HGF signaling. In summary, we have generated a novel METxMET bispecific antibody that potently inhibits the growth of MET-dependent tumor xenografts. Our data suggest that antibody-mediated MET degradation may be an effective clinical strategy in tumors harboring MET genetic alterations. Citation Format: John DaSilva. A MET x MET bispecific antibody that induces receptor degradation potently inhibits the growth of MET-addicted tumor xenografts [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 34. doi:10.1158/1538-7445.AM2017-34
Object-to-object color transfer: Optimal flows and SMSP transformations (2010)

Given a source object and a target object, we consider the problem of transferring the “color scheme” of the source to the target, while at the same time maintaining the target's original look and feel. This is a challenging problem due to the fact that the source and target may each consist of multiple colors, each of which comes in multiple shades. We propose a two stage solution to this problem. (1) A discrete color flow is computed from the target histogram to the source histogram; this flow is computed as the solution to a convex optimization problem, whose global optimum may be found. (2) The discrete flow is turned into a continuous color transformation, which can be written as a convex sum of Stretch-Minimizing Structure-Preserving (SMSP) transformations. These SMSP transformations, which are computed based on the color flow, are affine transformations with desirable theoretical properties. The effectiveness of this two stage algorithm is validated in a series of experiments.