gebhart/patrepeval huggingface dataset:
Low temperature sinter technology die attachment for power electronic applications (2010)

New fields of high power inverter systems such like windmills, hybrid cars, hybrid trucks, and off road vehicles require new ways of power electronics integration and packaging. The requirements in size, weight, reliability, durability, ambient temperature, and environment are driving the operation temperatures of power electronics beyond the limits of today's industrial applications. In industrial power modules solder and bond wires are still the standard joining technologies of power dies. These technologies are reaching their reliability limits if die temperatures are pushed above 135°C. In this paper the authors will discuss how the environmental conditions of applications drive silicon power device selection and packaging technologies. Extreme cooling conditions and ultra high power densities require a package design that needs to work on the thermal and electrical limits of the components without making any compromise in reliability and durability. The low temperature sinter technology can extend the power and thermal cycling capabilities of modern power modules to the values that are required for industrial and automotive applications. Next to the reliability data also a proposal for a high volume manufacturing process of the low temperature sinter technology of multi chip modules will be presented.
Allium Chemistry:  Synthesis and Sigmatropic Rearrangements of Alk(en)yl 1-Propenyl Disulfide S-Oxides from Cut Onion and Garlic1 (1996)

Reduction (LiAlH4) of propyl 1-propynyl sulfide (8) to (E)-1-propenyl propyl sulfide ((E)-10), C−S cleavage (Li/NH3) to lithium (E)-1-propenethiolate (Li (E)-11), and reaction with MeSO2Cl gives (E,E)-bis(1-propenyl) disulfide ((E,E)-2); i-Bu2AlH reduction of 8 to (Z)-10 and reaction with Li/NH3 and then MeSO2Cl gives (Z,Z)-2 via Li (Z)-11. Reaction of MeSO2SR (R = Me (12a), n-Pr (12b), CH2CHCH2 (12c), CHCHMe (12d)) with K (E)-11 gives (E,Z)-2 from (Z)-12d; Li (E,Z)-11 gives alkyl (E)- and (Z)-1-propenyl disulfides (MeCHCHSSR, R = Me (3a), n-Pr (3b), CH2CHCH2 (3c)) from 12a−c, respectively. Oxidation at −60 °C of (E,E)-, (Z,Z)-, and (E,Z)-2 gives (E)-1-propenesulfinothioic acid S-(E)-1-propenyl ester ((E,E)-13, (E,E)-MeCHCHS(O)SCHCHMe) from (E,E)-2, (Z,Z)-13 from (Z,Z)-2, and ca. 2:1 (E,Z)-13)/(Z,E)-13 from (E,Z)-2. Warming (Z,Z)-13 gives (±)-(1α,2α,3β,4α,5β)-2,3-dimethyl-5,6-dithiabicyclo[2.1.1]hexane 5-oxide (1a), endo-5-methyl-exo-6-methyl-2-oxa-3,7-dithiabicyclo[2.2.1]heptane (14a), and exo-5-methyl-endo-6-methyl-2-oxa-3,7-dithiabicyclo[2.2.1]heptane (14b). Warming (E,E)-13 gives 14a and 14b; (E,Z)-13/(Z,E)-13 gives (1α,2α,3α,4α,5β)-2,3-dimethyl-5,6-dithiabicyclo[2.1.1]hexane 5-oxide (1b), exo-5-methyl-exo-6-methyl-2-oxa-3,7-dithiabicyclo[2.2.1]heptane (14c), and endo-5-methyl-endo-6-methyl-2-oxa-3,7-dithiabicyclo[2.2.1]heptane (14d). Oxidation of 3a−c gives MeCHCHSS(O)R (4) and MeCHCHS(O)SR (5). At −60 °C, m-CPBA (2 equiv) converts (E,E)-2 into (Z,Z)-d,l-2,3-dimethyl-1,4-butanedithial 1,4-dioxide (26) while (Z,Z)-2 gives meso- and d,l-26. With NaIO4, 4/5 (R = Me) gives (E)- or (Z)-12a and MeCHCHSO2SMe (6a); with m-CPBA (Z)-MeS(O)CHMeCHS+O- (25a) forms. At 85 °C 2 gives 1:1 cis- and trans-2-mercapto-3,4-dimethyl-2,3-dihydrothiophene (29).
Functional Proteomics Establishes the Interaction of SIRT7 with Chromatin Remodeling Complexes and Expands Its Role in Regulation of RNA Polymerase I Transcription (2012)

Among mammalian sirtuins, SIRT7 is the only enzyme residing in nucleoli where ribosomal DNA is transcribed. Recent reports established that SIRT7 associates with RNA Pol I machinery and is required for rDNA transcription. Although defined by its homology to the yeast histone deacetylase Sir2, current knowledge suggests that SIRT7 itself has little to no deacetylase activity. Because only two SIRT7 interactions have been thus far described: RNA Pol I and upstream binding factor, identification of proteins and complexes associating with SIRT7 is critical to understanding its functions. Here, we present the first characterization of SIRT7 interaction networks. We have systematically investigated protein interactions of three EGFP-tagged SIRT7 constructs: wild type, a point mutation affecting rDNA transcription, and a deletion mutant lacking the predicted coiled-coil domain. A combinatorial proteomics and bioinformatics approach was used to integrate gene ontology classifications, functional protein networks, and normalized abundances of proteins co-isolated with SIRT7. The resulting refined proteomic data set confirmed SIRT7 interactions with RNA Pol I and upstream binding factor and highlighted association with factors involved in RNA Pol I- and II-dependent transcriptional processes and several nucleolus-localized chromatin remodeling complexes. Particularly enriched were members of the B-WICH complex, such as Mybbp1a, WSTF, and SNF2h. Prominent interactions were validated by a selected reaction monitoring-like approach using metabolic labeling with stable isotopes, confocal microscopy, reciprocal immunoaffinity precipitation, and co-isolation with endogenous SIRT7. To extend the current knowledge of mechanisms involved in SIRT7-dependent regulation of rDNA transcription, we showed that small interfering RNA-mediated SIRT7 knockdown leads to reduced levels of RNA Pol I protein, but not messenger RNA, which was confirmed in diverse cell types. The down-regulation of RNA Pol I protein levels placed in the context of SIRT7 interaction networks led us to propose that SIRT7 plays a crucial role in connecting the function of chromatin remodeling complexes to RNA Pol I machinery during transcription.
The expanding realm of prion phenomena in neurodegenerative disease (2009)

The aggregation of a soluble protein into insoluble, beta-sheet rich amyloid fibrils is a defining characteristic of many neurodegenerative diseases, including prion disorders. The prion protein has so far been considered unique because of its infectious nature. Recent investigations, however, suggest that other amyloid-forming proteins associated with much more common diseases, such as tau, alpha-synuclein, amyloid beta and polyglutamine proteins, while not infectious in the classical sense, share certain essential properties with prions that may explain phenotypic diversity, and patterns of spread within the nervous system. We suggest a common mechanism of pathogenesis of myriad sporadic and inherited neurodegenerative diseases based on templated conformational change.
Is there a role for Notch signalling in human breast cancer? (2003)

Aberrant Notch signalling has been observed in several human cancers, including acute T-cell lymphoblastic leukaemia and cervical cancer, and is strongly implicated in tumourigenesis. Unregulated Notch signalling in the mouse mammary gland leads to tumour formation. These results raise the possibility that Notch signalling might play a role in human breast cancer. There are currently few reports that address this question directly and this appears to be an area worthy of further investigation.
Thioflavine T interaction with synthetic Alzheimer's disease β‐amyloid peptides: Detection of amyloid aggregation in solution (1993)

Thioflavine T (ThT) associates rapidly with aggregated fibrils of the synthetic beta/A4-derived peptides beta(1-28) and beta(1-40), giving rise to a new excitation (ex) (absorption) maximum at 450 nm and enhanced emission (em) at 482 nm, as opposed to the 385 nm (ex) and 445 nm (em) of the free dye. This change is dependent on the aggregated state as monomeric or dimeric peptides do not react, and guanidine dissociation of aggregates destroys the signal. There was no effect of high salt concentrations. Binding to the beta(1-40) is of lower affinity, Kd 2 microM, while it saturates with a Kd of 0.54 microM for beta(1-28). Insulin fibrils converted to a beta-sheet conformation fluoresce intensely with ThT. A variety of polyhydroxy, polyanionic, or polycationic materials fail to interact or impede interaction with the amyloid peptides. This fluorometric technique should allow the kinetic elucidation of the amyloid fibril assembly process as well as the testing of agents that might modulate their assembly or disassembly.
High-throughput linked-pattern matching for intrusion detection systems (2005)

This paper presents a hardware architecture for highly efficient intrusion detection systems. In addition, a software tool for automatically generating the hardware is presented.Intrusion detection for network security is a compute-intensive application demanding high system performance. By moving both the string matching and the linking of multi-part rules to hardware, our architecture leaves the host system free for higher-level analysis. The tool automates the creation of efficient Field Programmable Gate Array architectures (FPGA). The generated hardware allows an FPGA-based system to perform deep-packet inspection of streams at up to 10 Gb/s line rates at a high level of area efficiency. Going beyond previous basic string-matching implementations that offer only single-string matching, the architecture provides support for rules requiring complex, linked (correlated-content) constructions. This allows most Snort content-linking extensions including `distance' and `within' bounding restrictions.
Genes on chromosomes 1 and 13 have significant effects on Ascaris infection (2002)

Nematode parasites show a characteristic aggregated distribution among hosts. This observation has important implications for pathogenesis, immunology, and control of these infections, but the relative roles of environment and genetics in determining these patterns have remained uncertain. This paper presents the results of the first genome scan for susceptibility to infection with roundworm (Ascaris lumbricoides). Data on 375 genetic markers were generated for each of 444 members of a genetically isolated Nepalese population, the Jirels. Ascaris worm burden as assessed by egg counts was measured in these same individuals by using the Kato Katz thick smear method. The extensive genealogical data available for the population allowed assignment of all 444 individuals to a single pedigree that contained 6,209 pairs of relatives that were informative for genetic analysis. A variance components linkage analysis resulted in the unequivocal localization of two genes (one on chromosome 1 and another on chromosome 13) with clear, significant effects on susceptibility to Ascaris infection. This is the first evidence that individual quantitative trait loci influence variation in Ascaris burden in humans.
Monoclonal antibodies to the human CSF-1 receptor (c-fms proto-oncogene product) detect epitopes on normal mononuclear phagocytes and on human myeloid leukemic blast cells (1989)

The first monoclonal antibodies (MoAbs) to epitopes in the extracellular domain of the human c-fms proto-oncogene product (receptor for the macrophage colony stimulating factor, CSF-1) were used with flow cytometric techniques to study receptor expression on normal human peripheral blood monocytes, bone marrow cells, and leukemic blasts. On normal cells CSF-1 receptors were restricted in their expression to cells of the mononuclear phagocyte lineage. CSF-1 receptors were detected on leukemic blasts from 15 (30%) of 50 children with acute myeloid leukemia, compared with four (15%) of 26 adults. By contrast, detectable CSF-1 receptors were uniformly absent on blasts from 19 children with acute lymphoblastic leukemia. CSF-1 receptors on normal monocytes and myeloid leukemia cells could be induced to downmodulate by incubation with either human recombinant CSF-1 or phorbol esters, confirming that the receptors had functional ligand- binding sites and responded to transmodulation by inducers of protein kinase C. The numbers of receptors per cell and the percentage of positive cases were highest for leukemic blasts with cytochemical and morphological features of monocytes. However, CSF-1 receptors were also detected on a subset of leukemic blast cells with features of granulocytic differentiation (FAB subtypes M1 through M3). Southern blotting analyses of DNA from 47 cases of acute myeloid leukemia demonstrated no rearrangements within the 32 kb of genomic sequences that contain CSF-1 receptor coding exons or in the 50 kb upstream of the first coding exon. Analysis of the upstream region of the c-fms locus revealed that sequences representing the terminal 112 untranslated nucleotides of c-fms mRNA map 26 kb 5′ to the first coding exon, suggesting that at least one c-fms promoter is separated from the receptor coding sequences by a very long intron. Whereas expression of the CSF-1 receptor in myeloid leukemic blasts is not restricted to cells with monocytic characteristics, the apparently aberrant pattern of receptor synthesis in a subset of cases with granulocytic features appears not to be due to chromosomal rearrangements within 50 kb upstream of sequences encoding the receptor.
Overexpression of the human insulinlike growth factor I receptor promotes ligand-dependent neoplastic transformation. (1990)

The human insulinlike growth factor I receptor was overexpressed in NIH 3T3 cells as well as human and rat primary fibroblast strains. The NIH 3T3 cells displayed a ligand-dependent, highly transformed phenotype. When exposed to insulinlike growth factor I or supraphysiologic levels of insulin, NIH 3T3 cells that expressed high levels of receptors formed aggregates in tissue culture dishes, colonies in soft agar, and tumors in nude mice. Expression of 1 million receptors per cell, a 40-fold increase above the base-line level, was required for anchorage-independent growth. Primary fibroblasts that expressed high levels of receptors displayed a ligand-dependent change in morphology and an increase in saturation density but did not acquire a fully transformed phenotype. The results demonstrate that when amplified, this ubiquitous growth factor receptor behaves like an oncogenic protein and is capable of promoting neoplastic growth in vivo.
Anticariogenic complexes of amorphous calcium phosphate stabilized by casein phosphopeptides: A review (1998)

Using laboratory, animal, and human in situ caries models, investigators have shown that casein phosphopeptide amorphous calcium phosphate complexes (CPP-ACP) exhibit an anticariogenic activity. The casein phosphopeptides (CPP) are produced from a tryptic digest of the milk protein casein by aggregation with calcium phosphate and purification by ultrafiltration. The CPP have a remarkable ability to stabilize calcium phosphate in solution and substantially increase the level of calcium phosphate in dental plaque. Through their multiple phosphoseryl residues, the CPP bind to forming clusters of amorphous calcium phosphate (ACP) in metastable solution, preventing their growth to the critical size required for nucleation and precipitation. The proposed mechanism of anticariogenicity for the CPP-ACP is that they localize ACP in dental plaque, which buffers the free calcium and phosphate lon activities, thereby helping to maintain a state of supersaturation with respect to tooth enamel depressing demineralization and enhancing remineralization. The CPP-ACP, unlike fluoride, can be added to sugar-containing foods and therefore have commercial potential as an additive to foods as well as to toothpastes and mouthwashes for the control of dental caries.
Protein polymer drag‐tags for DNA separations by end‐labeled free‐solution electrophoresis (2005)

We demonstrate the feasibility of end-labeled free-solution electrophoresis (ELFSE) separation of DNA using genetically engineered protein polymers as drag-tags. Protein polymers are promising candidates for ELFSE drag-tags because their sequences and lengths are controllable not only to generate monodisperse polymers with high frictional drag, but also to meet other drag-tag requirements for high-resolution separations by microchannel electrophoresis. A series of repetitive polypeptides was designed, expressed in Escherichia coli, and purified. By performing an end-on conjugation of the protein polymers to a fluorescently labeled DNA oligomer (22 bases) and analyzing the electrophoretic mobilities of the conjugate molecules by free-solution capillary electrophoresis (CE), effects of the size and charge of the protein polymer drag-tags were investigated. In addition, the electrophoretic behavior of bioconjugates comprising relatively long DNA fragments (108 and 208 bases) and attached to uncharged drag-tags was observed, by conjugating fluorescently labeled polymerase chain reaction (PCR) products to charge-neutral protein polymers, and analyzing via CE. We calculated the amount of friction generated by the various drag-tags, and estimated the potential read-lengths that could be obtained if these drag-tags were used for DNA sequencing in our current system. The results of these studies indicate that larger and uncharged drag-tags will have the best DNA-resolving capability for ELFSE separations, and that theoretically, up to 233 DNA bases could be sequenced using one of the protein polymer drag-tags we produced, which is electrostatically neutral with a chain length of 337 amino acids. We also show that denatured (unfolded) polypeptide chains impose much greater frictional drag per unit molecular weight than folded proteins, such as streptavidin, which has been used as a drag-tag before.
Phosphorylated AKT1 is associated with poor prognosis in esophageal squamous cell carcinoma (2015)

Activation of AKT1 was associated with poor prognosis in ESCC.
Via minimization for gridless layouts (1987)

This paper describes a graph theoretic algorithm which, given a particular layout, finds a layer assignment that requires the minimum number of vias. The time complexity of the algorithm is Ο(n3) where n is the number of routing segments in the given layout. Unlike previous algorithms, this algorithm does not require the layout to be grid based and places no constraints on the location of vias or the number of wires that may be joined at a single junction. The algorithm yields globally optimum results when the maximum junction degree is limited to three and has been fully implemented.
Getting Personal with Neoantigen-Based Therapeutic Cancer Vaccines (2013)

Despite years of preclinical efforts and hundreds of clinical studies, therapeutic cancer vaccines with the routine ability to limit or eliminate tumor growth in humans have been elusive. With advances in genome sequencing, it is now possible to identify a new class of tumor-specific antigens derived from mutated proteins that are present only in the tumor. These "neoantigens" should provide highly specific targets for antitumor immunity. Although many challenges remain in producing and testing neoantigen-based vaccines customized for each patient, a neoantigen vaccine offers a promising new approach to induce highly focused antitumor T cells aimed at eradicating cancer cells.
Clinical validation of a miniature nuclear probe system for continuous on-line monitoring of cardiac function and ST-segment. (1991)

A new, miniature cesium iodide/photodiode nuclear probe (the "Cardioscint") has been developed for continuous on-line measurement of left ventricular function and the ST-segment. Ejection fraction (EF) measurements in 77 patients were compared with gated equilibrium radionuclide ventriculograms. The probe was positioned over the left ventricle by first using a blind positioning algorithm and then by using the gamma camera. Background was measured both manually and automatically. There was good correlation between probe (positioned blind) and gamma camera EF with both manual (r = 0.80, n = 65) and automatic (r = 0.78, n = 66) backgrounds. Use of the gamma camera did not significantly alter the results. Correlation between the probe stroke counts and thermodilution-derived stroke index during atrial pacing in six subjects was also satisfactory (r = 0.69, n = 102). Thus, the Cardioscint is able to provide a reliable estimate of EF and can track rapid changes in cardiac volumes.
E1A induces phosphorylation of the retinoblastoma protein independently of direct physical association between the E1A and retinoblastoma products. (1991)

We have studied the initial effects of adenovirus E1A expression on the retinoblastoma (RB) gene product in normal quiescent cells. Although binding of the E1A products to pRB could, in theory, make pRB phosphorylation unnecessary for cell cycle progression, we have found that the 12S wild-type E1A product is capable of inducing phosphorylation of pRB in normal quiescent cells. The induction of pRB phosphorylation correlates with E1A-mediated induction of p34cdc2 expression and kinase activity, consistent with the possibility that p34cdc2 is a pRB kinase. Expression of simian virus 40 T antigen induces similar effects. Induction of pRB phosphorylation is independent of the pRB binding activity of the E1A products; E1A domain 2 mutants do not bind detectable levels of pRB but remain competent to induce pRB phosphorylation and to activate cdc2 protein kinase expression and activity. Although the kinetics of induction are slower, domain 2 mutants induce wild-type levels of pRB phosphorylation and host cell DNA synthesis and yet fail to induce cell proliferation. These results imply that direct physical interaction between the RB and E1A products does not play a required role in the early stages of E1A-mediated cell cycle induction and that pRB phosphorylation is not, of itself, sufficient to allow quiescent cells to divide. These results suggest that the E1A products do not need to bind pRB in order to stimulate resting cells to enter the cell cycle. Indeed, a more important role of the RB binding activity of the E1A products may be to prevent dividing cells from returning to G0.
ChemInform Abstract: Fluorine and Trifluoromethyl Substituted Anilines: Site Selective Metalation and Electrophilic Substitution. (1992)

Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
A 60 $\mu$W 60 nV/$\surd$Hz Readout Front-End for Portable Biopotential Acquisition Systems (2007)

<para xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"> There is a growing demand for low-power, small-size and ambulatory biopotential acquisition systems. A crucial and important block of this acquisition system is the analog readout front-end. We have implemented a low-power and low-noise readout front-end with configurable characteristics for Electroencephalogram (EEG), Electrocardiogram (ECG), and Electromyogram (EMG) signals. Key to its performance is the new AC-coupled chopped instrumentation amplifier (ACCIA), which uses a low power current feedback instrumentation amplifier (IA). Thus, while chopping filters the 1/f noise of CMOS transistors and increases the CMRR, AC coupling is capable of rejecting differential electrode offset (DEO) up to <formula formulatype="inline"><tex>${\pm}$</tex></formula>50 mV from conventional Ag/AgCl electrodes. The ACCIA achieves 120 dB CMRR and 57 nV/<formula formulatype="inline"><tex>$\surd$</tex></formula>Hz input-referred voltage noise density, while consuming 11.1 <formula formulatype="inline"><tex>$\mu$</tex> </formula>A from a 3 V supply. The chopping spike filter (CSF) stage filters the chopping spikes generated by the input chopper of ACCIA and the digitally controllable variable gain stage is used to set the gain and the bandwidth of the front-end. The front-end is implemented in a 0.5 <formula formulatype="inline"> <tex>$\mu$</tex></formula>m CMOS process. Total current consumption is 20 <formula formulatype="inline"><tex>$\mu$</tex></formula>A from 3V. </para>