gebhart/patrepeval huggingface dataset:
Scaling of stack effect and its application for leakage reduction (2001)

Article Share on Scaling of stack effect and its application for leakage reduction Authors: Siva Narendra Microsystems Technology Laboratories, Massachusetts Institute of Technology, Cambridge, MA and Microprocessor Research Laboratories, Intel Corporation, Hillsboro, OR Microsystems Technology Laboratories, Massachusetts Institute of Technology, Cambridge, MA and Microprocessor Research Laboratories, Intel Corporation, Hillsboro, ORView Profile , Vivek De Microprocessor Research Laboratories, Intel Corporation, Hillsboro, OR Microprocessor Research Laboratories, Intel Corporation, Hillsboro, ORView Profile , Dimitri Antoniadis Microsystems Technology Laboratories, Massachusetts Institute of Technology, Cambridge, MA Microsystems Technology Laboratories, Massachusetts Institute of Technology, Cambridge, MAView Profile , Anantha Chandrakasan Microsystems Technology Laboratories, Massachusetts Institute of Technology, Cambridge, MA Microsystems Technology Laboratories, Massachusetts Institute of Technology, Cambridge, MAView Profile , Shekhar Borkar Microprocessor Research Laboratories, Intel Corporation, Hillsboro, OR Microprocessor Research Laboratories, Intel Corporation, Hillsboro, ORView Profile Authors Info & Claims ISLPED '01: Proceedings of the 2001 international symposium on Low power electronics and designAugust 2001 Pages 195–200https://doi.org/10.1145/383082.383132Online:06 August 2001Publication History 140citation1,436DownloadsMetricsTotal Citations140Total Downloads1,436Last 12 Months24Last 6 weeks3 Get Citation AlertsNew Citation Alert added!This alert has been successfully added and will be sent to:You will be notified whenever a record that you have chosen has been cited.To manage your alert preferences, click on the button below.Manage my AlertsNew Citation Alert!Please log in to your account Save to BinderSave to BinderCreate a New BinderNameCancelCreateExport CitationPublisher SiteGet Access
A Filterable Agent, Recovered from Ak Leukemic Extracts, Causing Salivary Gland Carcinomas in C3H Mice. (1953)

Summary1. Extracts prepared from livers, spleens, and lymphatic tumors of leukemic Ak mice, were centrifugated at 1400 × g (15 minutes), then 7000 × g (5 to 10 minutes), and finally passed through Selas porcelain niters. The filtered extracts were then inoculated into newborn (less than 16 hours old) C3H or C3H(f) suckling mice. 2. Of the 84 mice inoculated with fresh, filtered extracts, 9 died from leukemia, and 15 others developed bilateral epitheliomas possibly arising in the salivary glands. Of the 54 control litter-mates inoculated with heated (68°C for 30 minutes) extracts, only one developed a cervical tumor. 3. Extracts prepared from Ak leukemic cells may therefore contain 2 different agents, pathogenic for newborn C3H or C3H(f) mice: one, causing leukemia, and another salivary gland epitheliomas. These agents may differ in size. 4. It is assumed that the leukemic agent may interfere with the tumor agent preventing it from exerting its pathogenic properties on the cells of its usual Ak, carrier host, or that mice of the Ak line may be naturally resistant to the tumor agent. 5. Salivary gland tumors have not been observed in untreated mice of either the Ak, the C3H, or C3H(f) inbred lines.
Identification of CCR8 as the specific receptor for the human beta-chemokine I-309: cloning and molecular characterization of murine CCR8 as the receptor for TCA-3. (1998)

Chemokine receptor-like 1 (CKR-L1) was described recently as a putative seven-transmembrane human receptor with many of the structural features of chemokine receptors. To identify the ligand of CKR-L1, we have studied chemokine-induced calcium mobilization in 293 cells transfected with CKR-L1. Of 20 different chemokines tested, only I-309 was able to elicit a significant calcium mobilization. In addition, I-309 induced the transfectants to migrate in vitro. As expected for chemokine receptor-mediated effects, pertussis toxin, but not cholera toxin, inhibited both the calcium flux and migration of the CKR-L1 transfectants in response to I-309. All of these data support the conclusion that I-309 is a functional ligand for CKR-L1. According to the current chemokine receptor nomenclature, we have designated this gene as CCR8. The murine CCR8 (mCCR8) gene was cloned, and its predicted amino acid sequence showed a 71% identity with that of human CCR8. As human CCR8, mCCR8 is expressed in thymus. Both I-309 and its murine homologue TCA-3 were able to induce calcium mobilization in transiently transfected 293-EBNA cells expressing mCCR8. The affinity of the binding of 125I-labeled TCA-3 to mCCR8 was high (Kd approximately 2 nM); the binding was prevented completely by an excess of cold TCA-3, and only partially competed (40%) by I-309. The identification of I-309 and TCA-3 as the functional ligands for CCR8 receptors will help to unravel the role of these proteins in physiologic and pathologic situations.
Antibiotic bead chains. (1993)

Gentamicin-PMMA chains are an effective drug delivery system for local antibiotic therapy in bone and soft-tissue infections. The gentamicin concentrations at the site of infection are far higher than after systemic application of the same antibiotic and far above the minimal inhibitory concentrations of most common pathogens. Because of the very low concentrations in the serum and urine after implantation of the antibiotic bead chains, toxic side effects are not to be feared. Radical debridement with removal of all sequestrated bone fragments and removal of all alloplastic implants is mandatory before implantation of gentamicin-PMMA chains into the infected bone cavity. Primary wound closure is necessary to achieve high local concentrations. The chains can be used for temporary or permanent filling of osteomyelitic cavities. Guidelines are given for the clinical application in sequestrating osteomyelitis, infected osteosynthesis, and infected pseudarthrosis. There are distinct advantages of this new form of antibiotic therapy in chronic osteomyelitis, such as increased patient comfort by primary wound closure, no need for prolonged systemic antibiotic therapy with toxic side effects, no irrigation-suction-drainage, early ambulation, shortening of hospitalization, and reduced cost.
Molecular cloning and functional expression of rat liver cytosolic acetyl‐CoA hydrolase (2001)

A cytosolic acetyl-CoA hydrolase (CACH) was purified from rat liver to homogeneity by a new method using Triton X-100 as a stabilizer. We digested the purified enzyme with an endopeptidase and determined the N-terminal amino-acid sequences of the two proteolytic fragments. From the sequence data, we designed probes for RT-PCR, and amplified CACH cDNA from rat liver mRNA. The CACH cDNA contains a 1668-bp ORF encoding a protein of 556 amino-acid residues (62 017 Da). Recombinant expression of the cDNA in insect cells resulted in overproduction of functional acetyl-CoA hydrolase with comparable acyl-CoA chain-length specificity and Michaelis constant for acetyl-CoA to those of the native CACH. Database searching shows no homology to other known proteins, but reveals high similarities to two mouse expressed sequence tags (91% and 93% homology) and human mRNA for KIAA0707 hypothetical protein (50% homology) of unknown function.
Aggregation-prone c9FTD/ALS poly(GA) RAN-translated proteins cause neurotoxicity by inducing ER stress (2014)

The occurrence of repeat-associated non-ATG (RAN) translation, an atypical form of translation of expanded repeats that results in the synthesis of homopolymeric expansion proteins, is becoming more widely appreciated among microsatellite expansion disorders. Such disorders include amyotrophic lateral sclerosis and frontotemporal dementia caused by a hexanucleotide repeat expansion in the C9ORF72 gene (c9FTD/ALS). We and others have recently shown that this bidirectionally transcribed repeat is RAN translated, and the "c9RAN proteins" thusly produced form neuronal inclusions throughout the central nervous system of c9FTD/ALS patients. Nonetheless, the potential contribution of c9RAN proteins to disease pathogenesis remains poorly understood. In the present study, we demonstrate that poly(GA) c9RAN proteins are neurotoxic and may be implicated in the neurodegenerative processes of c9FTD/ALS. Specifically, we show that expression of poly(GA) proteins in cultured cells and primary neurons leads to the formation of soluble and insoluble high molecular weight species, as well as inclusions composed of filaments similar to those observed in c9FTD/ALS brain tissues. The expression of poly(GA) proteins is accompanied by caspase-3 activation, impaired neurite outgrowth, inhibition of proteasome activity, and evidence of endoplasmic reticulum (ER) stress. Of importance, ER stress inhibitors, salubrinal and TUDCA, provide protection against poly(GA)-induced toxicity. Taken together, our data provide compelling evidence towards establishing RAN translation as a pathogenic mechanism of c9FTD/ALS, and suggest that targeting the ER using small molecules may be a promising therapeutic approach for these devastating diseases.
Design and Synthesis of Tricyclic Imidazo[4,5- b ]pyridin-2-ones as Corticotropin-Releasing Factor-1 Antagonists (2005)

The synthesis and SAR studies of tricyclic imidazo[4,5-b]pyridin-2-ones as human corticotropin-releasing factor receptor (CRF(1)) antagonists are discussed herein. Compound 16g was identified as a functional antagonist that inhibited CRF-stimulated cyclic adenosine monophosphate production and CRF-induced adrenocorticotrophic hormone release. Pharmacokinetics studies in rats showed that 16g was orally bioavailable, had good brain penetration, and had a moderate half-life. In our effort to identify CRF(1) antagonists with improved pharmacokinetics properties, 16g exhibited a favorably lower volume of distribution.
Catecholamine Response to Light in Migraine (1988)

The effect of the shift from a low to a high luminosity of the environment on the urinary excretion of norepinephrine (NE) and epinephrine (E) was studied in migraineurs (26 cases) and controls (25 cases). In the latter the shift from a low to high light exposure increased NE excretion; in contrast, in migraineurs exposure to high luminosity resulted in a depression of NE excretion and an augmentation of E excretion. The possible participation of E discharge produced by photostimulation or by other stimuli in the pathogenesis of migraine attack is discussed.
Analysis of several fluorescent detector molecules for protein microarray use (2002)

The utility of several streptavidin-linked fluorescent detector molecules was evaluated on two protein microarray platforms. Tested detector molecules included: Alexa Fluor 546; R-phycoerythrin (RPE), orange fluospheres; Cy3-containing liposomes (Large Unilamellar Vesicles, LUV) labelled with Cy3; and an RPE-antibody complex. The two array architectures tested consisted of an array of murine Fc-biotin and an array of murine IgG (the murine IgG array was probed with a biotinylated rabbit anti-murine IgG). These platforms allowed for the direct comparison of detector utility by detector recognition of array-bound biotin. All of the fluorescent detectors examined demonstrated utility on each of the array platforms. For the Fc-biotin array, detector signal intensity (background adjusted) was as follows: RPE-antibody complex > fluospheres > RPE > liposomes > Alexa 546: for the IgG array: RPE/antibody complex > RPE > fluospheres > Alexa546 > liposomes. The RPE-antibody complex fluoresced 67% and 150% more intensely than the next closest detector molecule for the Fc-biotin and the murine IgG arrays, respectively. A marked increase in background fluorescence (as compared to RPE alone) did not accompany the increase in signal intensity gained through RPE-antibody complex use (a true increase in signal:noise ratio). These results suggest that the RPE-antibody complex is superior to other molecules for fluorescent detection of analytes on protein microarrays.
Platelet C4d is highly specific for systemic lupus erythematosus (2006)

This observation suggests that platelet-bound C4d may be a useful biomarker for SLE and may be a clue to the pathogenic mechanisms responsible for the myriad thrombotic and vascular complications of lupus associated with antiphospholipid antibodies.
CMOS Image Sensors for High Speed Applications (2009)

Recent advances in deep submicron CMOS technologies and improved pixel designs have enabled CMOS-based imagers to surpass charge-coupled devices (CCD) imaging technology for mainstream applications. The parallel outputs that CMOS imagers can offer, in addition to complete camera-on-a-chip solutions due to being fabricated in standard CMOS technologies, result in compelling advantages in speed and system throughput. Since there is a practical limit on the minimum pixel size (4∼5 μm) due to limitations in the optics, CMOS technology scaling can allow for an increased number of transistors to be integrated into the pixel to improve both detection and signal processing. Such smart pixels truly show the potential of CMOS technology for imaging applications allowing CMOS imagers to achieve the image quality and global shuttering performance necessary to meet the demands of ultrahigh-speed applications. In this paper, a review of CMOS-based high-speed imager design is presented and the various implementations that target ultrahigh-speed imaging are described. This work also discusses the design, layout and simulation results of an ultrahigh acquisition rate CMOS active-pixel sensor imager that can take 8 frames at a rate of more than a billion frames per second (fps).
SPECT imaging of dopamine transporter sites in normal and MPTP-Treated rhesus monkeys. (1997)

These results demonstrate that [123I]IACFT is an excellent SPECT ligand for dopamine transporter sites that combines the critical characteristics of: (a) high striatal to cerebellar ratios, (b) high selectivity for dopamine versus 5-HT transporter sites, (c) convenient preparation at high-specific activity and radiochemical purity and (d) a striatal localization rate that is well matched to the physical t1/2 of 123I.
Metabolic syndrome with the atypical antipsychotics (2010)

More data have become available on the burden from metabolic complications associated with SGAs. New and effective treatment options are required in the near future to improve cardiovascular health in this susceptible population.
A Direct Microassay for Aldosterone in Plasma Extracts* (1978)

We previously described an RIA for aldosterone based on highly specific antibodies elicited with aldosterone-3,20 dioxime bovine gamma-globulin (Poulsen, K. J. Sancho, and E. Haber, Clin Immunol Immunopathol 2: 373, 1974). We now report the development of higher affinity antibodies of similar specificity that allow the direct measurement of normal aldosterone concentrations in extracts of 100 microliters plasma. The detection limit at +/- 2 SD of mean zero value was 0.2-0.3 pg. The assay was validated by 1) zero values in adrenalectomized plasma, 2) parallel displacement plots of aldosterone standards and plasma extracts, 3) 97.7 +/- 2.5% recovery of added tracer, 4) a correlation coefficient of 0.992 and a slope of 1.08 in a plot of added vs. recovered unlabeled aldosterone, 5) 10.2% interassay variation and 5.6% intraassay variation, and 6)failure of high concentrations of a variety of steroids added to plasma to perturb the measured aldosterone concentration. The simplicity of the assay results in a high degree of productivity, in that 195 plasma samples may be processed in duplicate, in addition to standard curves, in a single working day.
Cell-free extract based optimization of biomolecular circuits with droplet microfluidics (2017)

Engineering an efficient biomolecular circuit often requires time-consuming iterations of optimization. Cell-free protein expression systems allow rapid testing of biocircuits in vitro, speeding the design-build-test cycle of synthetic biology. In this paper, we combine this with droplet microfluidics to densely scan a transcription-translation biocircuit space. Our system assays millions of parameter combinations per hour, providing a detailed map of function. The ability to comprehensively map biocircuit parameter spaces allows accurate modeling to predict circuit function and identify optimal circuits and conditions.
THE mdx MOUSE SKELETAL MUSCLE MYOPATHY: I. A HISTOLOGICAL, MORPHOMETRIC AND BIOCHEMICAL INVESTIGATION (1988)

Skeletal muscle has been examined in a colony of the mdx strain of myopathic mice. Sixty-five mice from 22 to 303 days of age, showed extensive and recurrent areas of necrosis and regeneration of muscle fibres, often accompanied by active cellular infiltration. Morphometry of the soleus muscle revealed an abnormal proportion of small and large muscle fibres; over half of the muscle fibres contained 'central' (non-peripheral) nuclei. No histochemical muscle fibre-type grouping was detected. Serum activities of muscle-derived enzymes were greatly elevated in all animals and probably reflect enzyme leakage from damaged muscle fibres. Histological evidence of a cardiomyopathy was found in 13 mice. The mdx myopathy thus shows features seen in Duchenne muscular dystrophy. Mdx differs from Duchenne dystrophy principally in that it exhibits a greater degree of compensatory muscle regeneration and an absence of fibro-fatty replacement of muscle fibres.
Human CD38 (ADP-ribosyl cyclase) is a counter-receptor of CD31, an Ig superfamily member. (1998)

Human CD38 is a cell surface molecule involved in the regulation of lymphocyte adhesion to endothelial cells. This suggests that HUVEC bear a ligand(s) for CD38 on the cell surface. By means of the mAb Moon-1, which specifically inhibits CD38-mediated cell adhesion, we have identified a trans-membrane 130-kDa molecule acting as a ligand for CD38. Here, we report that the molecule recognized by the Moon-1 mAb is CD31, a member of the Ig superfamily. This conclusion is based on 1) cross-inhibition assays between Moon-1 and reference anti-CD31 mAbs; 2) sequential immunoprecipitation experiments using Moon-1 and known anti-CD31 mAbs, and 3) reactivity of the Moon-1 mAb with CD31 transfectants. Further, CD31 and CD38 cognate interactions were found to modulate heterotypic adhesion as well as to implement cytoplasmic calcium fluxes identical to those obtained by means of agonistic anti-CD38 mAbs. Other effects tested included the synthesis of messages for a panel of cytokines, markedly increased upon receptor-ligand interactions. These results suggest that the interplay between CD38 and its ligand CD31 is an important step in the regulation of cell life and of the migration of leukocytes (and CD38+ cancer cells) through the endothelial cell wall.
Intramolecular 1,3‐Dipolar Cycloaddition Reactions (1976)

Abstract The intramolecular 1,3‐dipolar cycloaddition reaction of suitably functionalized 1,3‐dipoles represents a general scheme for the synthesis of novel fused ring heterocycles. Such reactions of a number of 1,3‐dipoles are summarized and the general outline and potential analogies for these reactions noted. While the immediate aim of this review is to survey and correlate published work, it is hoped that general and specific points in need of study will be revealed and will stimulate further work in this fertile field.
SpecAugment: A Simple Data Augmentation Method for Automatic Speech Recognition (2019)

We present SpecAugment, a simple data augmentation method for speech recognition. SpecAugment is applied directly to the feature inputs of a neural network (i.e., filter bank coefficients). The augmentation policy consists of warping the features, masking blocks of frequency channels, and masking blocks of time steps. We apply SpecAugment on Listen, Attend and Spell networks for end-to-end speech recognition tasks. We achieve state-of-the-art performance on the LibriSpeech 960h and Swichboard 300h tasks, outperforming all prior work. On LibriSpeech, we achieve 6.8% WER on test-other without the use of a language model, and 5.8% WER with shallow fusion with a language model. This compares to the previous state-of-the-art hybrid system of 7.5% WER. For Switchboard, we achieve 7.2%/14.6% on the Switchboard/CallHome portion of the Hub5'00 test set without the use of a language model, and 6.8%/14.1% with shallow fusion, which compares to the previous state-of-the-art hybrid system at 8.3%/17.3% WER.
SEL-10 Is an Inhibitor of Notch Signaling That Targets Notch for Ubiquitin-Mediated Protein Degradation (2001)

Notch receptors and their ligands play important roles in both normal animal development and pathogenesis. We show here that the F-box/WD40 repeat protein SEL-10 negatively regulates Notch receptor activity by targeting the intracellular domain of Notch receptors for ubiquitin-mediated protein degradation. Blocking of endogenous SEL-10 activity was done by expression of a dominant-negative form containing only the WD40 repeats. In the case of Notch1, this block leads to an increase in Notch signaling stimulated by either an activated form of the Notch1 receptor or Jagged1-induced signaling through Notch1. Expression of dominant-negative SEL-10 leads to stabilization of the intracellular domain of Notch1. The Notch4 intracellular domain bound to SEL-10, but its activity was not increased as a result of dominant-negative SEL-10 expression. SEL-10 bound Notch4 via the WD40 repeats and bound preferentially to a phosphorylated form of Notch4 in cells. We mapped the region of Notch4 essential for SEL-10 binding to the C-terminal region downstream of the ankyrin repeats. When this C-terminal fragment of Notch4 was expressed in cells, it was highly labile but could be stabilized by the expression of dominant-negative SEL-10. Ubiquitination of Notch1 and Notch4 intracellular domains in vitro was dependent on SEL-10. Although SEL-10 interacts with the intracellular domains of both Notch1 and Notch4, these proteins respond differently to interference with SEL-10 function. Thus, SEL-10 functions to promote the ubiquitination of Notch proteins; however, the fates of these proteins may differ.
Prediction of Promiscuous and High-Affinity Mutated MHC Binders (2003)

The identification of peptides in an antigenic sequence that can bind with high affinity to a wide range of MHC alleles is one of the challenges in subunit vaccine design. The mutation of natural peptides is an alternative to obtaining peptides that can bind to a wide range of MHC alleles with high affinity. A large number of experiments are typically necessary to identify mutations that define high-affinity binding peptides. Therefore there is a need to develop a computational method for detecting amino acid mutations in a peptide for making it high-affinity or promiscuous MHC binders. This report describes a high-throughput computer driven solution for the identification of promiscuous and high-affinity mutated binders of 47 MHC class I alleles by introducing mutations in an antigenic sequence. The method implements quantitative matrices for creating optimal mutations in an antigenic sequence. It has two major options: (i) prediction of promiscuous MHC binders and (ii) prediction of high-affinity binders. In case of prediction of promiscuous binders, the server allows a user to select (i) permissible mutations in a peptide; (ii) MHC alleles to whom it should bind; and (iii) positions at which mutation is allowed. In the case of prediction of high-affinity binders, the server allows users to specify the positions that should be conserved in the native protein. In both cases, the method computes the type of mutations and position of mutations in 9-mer peptides required to have the desired results. The web server MMBPred is available at www.imtech.res.in/raghava/mmbpred/.