gebhart/patrepeval huggingface dataset:
The AT&T WATSON Speech Recognizer (2006)

This paper describes the AT&T WATSON real-time speech recognizer, the product of several decades of research at AT&T. The recognizer handles a wide range of vocabulary sizes and is based on continuous-density hidden Markov models for acoustic modeling and finite state networks for language modeling. The recognition network is optimized for efficient search. We identify the algorithms used for high-accuracy, real-time and low-latency recognition. We present results for small and large vocabulary tasks taken from the AT&T VoiceTone/sup /spl reg// service, showing word accuracy improvement of about 5% absolute and real-time processing speed-up by a factor between 2 and 3.
Cardiac resynchronization therapy (2004)

The first case report introducing the concept of cardiac resynchronisation therapy (CRT) was published less than 10 years ago, opening the way to the development of the first successful non-pharmacological treatment of congestive heart failure (CHF). The now routine implantation of CRT systems is applicable to multitudes of patients as adjunctive therapy in advanced CHF. This technique has transformed the traditional concepts associated with stimulation of the heart, and is now applied not only to restore an appropriate heart rate, but also to change the process of cardiac mechanical activation. Since it must be integrated within a comprehensive and multidisciplinary CHF management program, CRT has changed the practice of experts in the field of cardiac pacing. CRT in the management of CHF was ultimately validated in 2 randomised trials. MUSTIC, the first trial, compared in a single-blind, 3x3 months crossover design active versus inactive biventricular stimulation in a group of patients in sinus rhythm and another group in atrial fibrillation. Both phases of the trial were completed by 48 patients, with significant positive effects conferred by CRT on the distance walked in 6 min and on peak oxygen consumption. The number of hospitalizations for management of CHF was decreased by 2/3 (P<0.05), and 85% of patients preferred the atrio-biventricular over the inactive stimulation mode (P<0.001). These results were amply confirmed by the parallel-design MIRACLE trial. The current indications for CRT, diagnostic tools to assist in its implementation, and limitations of this new therapeutic adjunct are further discussed in this review.
Hodgkin lymphoma cells express TACI and BCMA receptors and generate survival and proliferation signals in response to BAFF and APRIL (2006)

Hodgkin lymphoma (HL) originates from the clonal expansion of malignant Hodgkin and Reed-Sternberg (HRS) cells. These B-cell-derived elements constitute less than 10% of the tumoral mass. The remaining tissue is comprised of an inflammatory infiltrate that includes myeloid cells. Myeloid cells activate B cells by producing BAFF and APRIL, which engage TACI, BCMA, and BAFF-R receptors on the B cells. Here, we studied the role of BAFF and APRIL in HL. Inflammatory and HRS cells from HL tumors expressed BAFF and APRIL. Unlike their putative germinal center B-cell precursors, HRS cells lacked BAFF-R, but expressed TACI and BCMA, a phenotype similar to that of plasmacytoid B cells. BAFF and APRIL enhanced HRS cell survival and proliferation by delivering nonredundant signals via TACI and BCMA receptors through both autocrine and paracrine pathways. These signals caused NF-kappaB activation; Bcl-2, Bcl-xL, and c-Myc up-regulation; and Bax down-regulation, and were amplified by APRIL-binding proteoglycans on HRS cells. Interruption of BAFF and APRIL signaling by TACI-Ig decoy receptor, which binds to and neutralizes BAFF and APRIL, or by small-interfering RNAs targeting BAFF, APRIL, TACI, and BCMA inhibited HRS cell accumulation in vitro and might attenuate HL expansion in vivo.
Arabidopsis intron mutations and pre‐mRNA splicing (1996)

Arabidopsis intron mutants provide and will continue to provide a valuable source of information on in vivo plant intron splicing. All of the characterized mutants discussed here contain base substitutions in either the 5' splice site :GU or 3' splice site AG: dinucleotides or broader splice site consensus sequences. Many of these mutations lead to the activation of cryptic splice sites, usually upstream or downstream of the authentic 5' and 3' splice sites respectively, often with reduced efficiency. This splicing behaviour is in agreement with detailed splicing analyses of test plant introns. However, some of the Arabidopsis mutations lead to more complex splicing patterns often involving exon skipping. These mutations illustrate the complexity of the splicing reaction (where the final splicing event reflects the characteristics such as splice site sequence, intron size and composition, and their interactions with spliceosomal components) and how single nucleotide mutations can affect the strength and balance of interactions to alter splicing patterns. The splicing patterns observed in the Arabidopsis mutants parallel those seen in mutations causing some human genetic disorders underlining the emerging similarities in mechanisms of splice site selection and intron/exon definition between plant and vertebrate systems. Analysis of the Arabidopsis intron mutations exhibiting complex splicing patterns will help to address fundamental questions in plant splicing, such as splice site selection and exon scanning. This information will be important in understanding the mechanisms by which gene expression is regulated post-transcriptionally in the ever-increasing number of alternatively spliced plant gene systems.
PROTEIN FOLDING: The Endgame (1997)

The last stage of protein folding, the "endgame," involves the ordering of amino acid side-chains into a well defined and closely packed configuration. We review a number of topics related to this process. We first describe how the observed packing in protein crystal structures is measured. Such measurements show that the protein interior is packed exceptionally tightly, more so than the protein surface or surrounding solvent and even more efficiently than crystals of simple organic molecules. In vitro protein folding experiments also show that the protein is close-packed in solution and that the tight packing and intercalation of side-chains is a final and essential step in the folding pathway. These experimental observations, in turn, suggest that a folded protein structure can be described as a kind of three-dimensional jigsaw puzzle and that predicting side-chain packing is possible in the sense of solving this puzzle. The major difficulty that must be overcome in predicting side-chain packing is a combinatorial "explosion" in the number of possible configurations. There has been much recent progress towards overcoming this problem, and we survey a variety of the approaches. These approaches differ principally in whether they use ab initio (physical) or more knowledge-based methods, how they divide up and search conformational space, and how they evaluate candidate configurations (using scoring functions). The accuracy of side-chain prediction depends crucially on the (assumed) positioning of the main-chain. Methods for predicting main-chain conformation are, in a sense, not as developed as that for side-chains. We conclude by surveying these methods. As with side-chain prediction, there are a great variety of approaches, which differ in how they divide up and search space and in how they score candidate conformations.
The Na+-F1F0-ATPase Operon from Acetobacterium woodii (1999)

Eight genes (<i>atpI</i>, <i>atpB</i>,<i>atpE</i> <sub>1</sub>, <i>atpE</i> <sub>2</sub>,<i>atpE</i> <sub>3</sub>, <i>atpF</i>, <i>atpH</i>, and<i>atpA</i>) upstream of and contiguous with the previously described genes <i>atpG</i>, <i>atpD</i>, and<i>atpC</i> were cloned from chromosomal DNA of<i>Acetobacterium woodii.</i> Northern blot analysis revealed that the eleven <i>atp</i> genes are transcribed as a polycistronic message. The <i>atp</i> operon encodes the Na<sup>+</sup>-F<sub>1</sub>F<sub>0</sub>-ATPase of <i>A. woodii</i>, as evident from a comparison of the biochemically derived N termini of the subunits with the amino acid sequences deduced from the DNA sequences. The molecular analysis revealed that all of the F<sub>1</sub>F<sub>0</sub>-encoding genes from <i>Escherichia coli</i> have homologs in the Na<sup>+</sup>-F<sub>1</sub>F<sub>0</sub>-ATPase operon from<i>A. woodii</i>, despite the fact that only six subunits were found in previous preparations of the enzyme from <i>A. woodii</i>. These results unequivocally prove that the Na<sup>+</sup>-ATPase from <i>A. woodii</i> is an enzyme of the F<sub>1</sub>F<sub>0</sub> class. Most interestingly, the gene encoding the proteolipid underwent quadruplication. Two gene copies (<i>atpE</i> <sub>2</sub> and <i>atpE</i> <sub>3</sub>) encode identical 8-kDa proteolipids. Two additional gene copies were fused to form the <i>atpE</i> <sub>1</sub> gene. Heterologous expression experiments as well as immunolabeling studies with native membranes revealed that <i>atpE</i> <sub>1</sub> encodes a duplicated 18-kDa proteolipid. This is the first demonstration of multiplication and fusion of proteolipid-encoding genes in F<sub>1</sub>F<sub>0</sub>-ATPase operons. Furthermore, AtpE<sub>1</sub> is the first duplicated proteolipid ever found to be encoded by an F<sub>1</sub>F<sub>0</sub>-ATPase operon.
Cayuga: A General Purpose Event Monitoring System. (2007)

System for scalable event processing. We present a query language based on Cayuga Algebra for naturally expressing complex event patterns. We also describe several novel system design and implementation issues, focusing on Cayuga’s query processor, its indexing approach, how Cayuga handles simultaneous events, and its specialized garbage collector. 1.
Trehalose-6-phosphate Phosphorylase Is Part of a Novel Metabolic Pathway for Trehalose Utilization in Lactococcus lactis (2001)

Lactococcus lactis splits phosphorylated trehalose by the action of inorganic phosphate-dependent trehalose-6-phosphate phosphorylase (TrePP) in a novel catabolic pathway. TrePP was found to catalyze the reversible conversion of trehalose 6-phosphate into beta-glucose 1-phosphate and glucose 6-phosphate by measuring intermediate sugar phosphates in cell extracts from trehalose-cultivated lactococci. According to native PAGE and SDS-PAGE, TrePP was shown to be a monomeric enzyme with a molecular mass of 94 kDa. Reaction kinetics suggested that the enzyme follows a ternary complex mechanism with optimal phosphorolysis at 35 degrees C and pH 6.3. The equilibrium constants were found to be 0.026 and 0.032 at pH 6.3 and 7.0, respectively, favoring the formation of trehalose 6-phosphate. The Michaelis-Menten constants of TrePP for trehalose 6-phosphate, inorganic phosphate, beta-glucose 1-phosphate, and glucose 6-phosphate were determined to be 6, 32, 0.9, and 4 mm, respectively. The TrePP-encoding gene, designated trePP, was localized in a putative trehalose operon of L. lactis. This operon includes the gene encoding beta-phosphoglucomutase in addition to three open reading frames believed to encode a transcriptional regulator and two trehalose-specific phosphotransferase system components. The identity of trePP was confirmed by determining the N-terminal amino acid sequence of TrePP and by its overexpression in Escherichia coli and L. lactis, as well as the construction of a lactococcal trePP knockout mutant. Furthermore, both TrePP and beta-phosphoglucomutase activity were detected in Enterococcus faecalis cell extract, indicating that this bacterium exhibits the same trehalose assimilation route as L. lactis.
Randomized, double-blind, placebo-controlled trial of the oral interleukin-12/23 inhibitor apilimod mesylate for treatment of active Crohn's disease (2009)

Apilimod was well-tolerated but did not demonstrate efficacy over placebo in patients with active CD.
Adaptive agents in a persistent shout double auction (1998)

CIiff [7J has demonstrated that simple, adaptive agents are able to trade in a form of double auction marketplace, in such a way that trade prices converge towards the equilibrium price of the marketplace. However, the marketplace within which the agents trade is unrealistic. In this paper, we consider a more realiitic form of double auction marke~thepersistent shout double auction. We present agents based on the ZIP agents of (Xi [7J, but with an alternative set of heuristics for use within this auction. We demonstrate that the resulting agents achieve equilibrium signifkantly faster than ZIP agents do, maintain a more stable equilibrium, and are more robust to changes in learning rate.
IDENTIFICATION AND CHARACTERIZATION OF 22 GENES THAT AFFECT THE VULVAL CELL LINEAGES OF THE NEMATODE CAENORHABDITIS ELEGANS (1985)

Ninety-five mutants of the nematode Caenorhabditis elegans altered in the cell lineages of the vulva have been isolated on the basis of their displaying one of two phenotypes, Vulvaless or Multivulva. In Vulvaless mutants, which define 12 genes, no vulva is present. In Multivulva mutants, which define ten genes, one or more supernumerary vulva-like protrusions are located along the ventral side of the animal. A single recessive mutation is responsible for the phenotypes of most, but not all, of these strains. Fifteen of these 22 genes are represented by multiple alleles. We have shown by a variety of genetic criteria that mutations that result in a Vulvaless or Multivulva phenotype in six of the 22 genes most likely eliminate gene function. In addition, Vulvaless or Multivulva mutations in seven of the other genes most likely result in a partial reduction of gene function; the absence of the activity of any of these genes probably results in lethality or sterility. Our results suggest that we may have identified most, or all, genes of these two classes.
Gemcitabine as single-agent therapy in the management of advanced breast cancer. (2001)

Many active cytotoxic agents exist for breast cancer therapy, and numerous combination chemotherapy regimens are derived from them. Creating these combinations is sometimes empirically motivated by non-overlapping toxicities or the expectation of non-cross resistance. Yet, there is usually no absolute division of these aspects among cytotoxic agents, and the median survival for patients with metastatic breast cancer has not been dramatically prolonged by this approach. When the outcome of treatment is palliation rather than cure, it becomes paramount to optimize the dynamic equilibrium between chemotherapy-induced side effects and the benefits attributable to relief of cancer-related symptoms. To this end, several recent clinical trials have evaluated the novel nucleoside analog gemcitabine (Gemzar) as single-agent therapy for advanced breast cancer. This article reviews these trials.
A region of human BRCA2 containing multiple BRC repeats promotes RAD51-mediated strand exchange (2006)

Human BRCA2, a breast and ovarian cancer suppressor, binds to the DNA recombinase RAD51 through eight conserved BRC repeats, motifs of approximately 30 residues, dispersed across a large region of the protein. BRCA2 is essential for homologous recombination in vivo, but isolated BRC repeat peptides can prevent the assembly of RAD51 into active nucleoprotein filaments in vitro, suggesting a model in which BRCA2 sequesters RAD51 in undamaged cells, and promotes recombinase function after DNA damage. How BRCA2 might fulfill these dual functions is unclear. We have purified a fragment of human BRCA2 (BRCA2(BRC1-8)) with 1127 residues spanning all 8 BRC repeats but excluding the C-terminal DNA-binding domain (BRCA2(CTD)). BRCA2(BRC1-8) binds RAD51 nucleoprotein filaments in a ternary complex, indicating it may organize RAD51 on DNA. Human RAD51 is relatively ineffective in vitro at strand exchange between homologous DNA molecules unless non-physiological ions like NH4+ are present. In an ionic milieu more typical of the mammalian nucleus, BRCA2(BRCI-8) stimulates RAD51-mediated strand exchange, suggesting it may be an essential co-factor in vivo. Thus, the human BRC repeats, embedded within their surronding sequences as an eight-repeat unit, mediate homologous recombination independent of the BRCA2(CTD) through a previously unrecognized role in control of RAD51 activity.
A Novel meso -Diaminopimelate Dehydrogenase from Symbiobacterium thermophilum: Overexpression, Characterization, and Potential for d -Amino Acid Synthesis (2012)

meso-Diaminopimelate dehydrogenase (meso-DAPDH) is an NADP(+)-dependent enzyme which catalyzes the reversible oxidative deamination on the d-configuration of meso-2,6-diaminopimelate to produce l-2-amino-6-oxopimelate. In this study, the gene encoding a meso-diaminopimelate dehydrogenase from Symbiobacterium thermophilum was cloned and expressed in Escherichia coli. In addition to the native substrate meso-2,6-diaminopimelate, the purified enzyme also showed activity toward d-alanine, d-valine, and d-lysine. This enzyme catalyzed the reductive amination of 2-keto acids such as pyruvic acid to generate d-amino acids in up to 99% conversion and 99% enantiomeric excess. Since meso-diaminopimelate dehydrogenases are known to be specific to meso-2,6-diaminopimelate, this is a unique wild-type meso-diaminopimelate dehydrogenase with a more relaxed substrate specificity and potential for d-amino acid synthesis. The enzyme is the most stable meso-diaminopimelate dehydrogenase reported to now. Two amino acid residues (F146 and M152) in the substrate binding sites of S. thermophilum meso-DAPDH different from the sequences of other known meso-DAPDHs were replaced with the conserved amino acids in other meso-DAPDHs, and assay of wild-type and mutant enzyme activities revealed that F146 and M152 are not critical in determining the enzyme's substrate specificity. The high thermostability and relaxed substrate profile of S. thermophilum meso-DAPDH warrant it as an excellent starting enzyme for creating effective d-amino acid dehydrogenases by protein engineering.
Dendritic development in neocortex of children with mental defect and infantile spasms (1974)

The Golgi-Cox method was used to analyze the dendritic spread of pyramidal neurons in middle frontal gyrus of 11 patients with mental defect. Abnormalities in dendritic development were found in five profoundly retarded children at ages one to four years. Four had a history of infantile spasms and an EEG tracing characterized as “hypsarrhythmia” in addition to amentia. Histologic abnormalities included decrease in length of basal dendrites, decreased secondary branches, and—in the miost severely affected—a decrease in branches arising directly frorn the perikaryon. Horizontal and tangential branches of apical dendrites also were reduced in number and length. The method failed to detect abnormalities in frontal cortex from several older retarded individuals. The results suggest that defective growth of cortical dendrites is common in the severely retarded. Limitations of the Golgi method may account for failure to detect abnormalities in less retarded patients and in older patients.
Telomerase expression and activity are coupled with myocyte proliferation and preservation of telomeric length in the failing heart (2001)

The role and even the existence of myocyte proliferation in the adult heart remain controversial. Documentation of cell cycle regulators, DNA synthesis, and mitotic images has not modified the view that myocardial growth can only occur from hypertrophy of an irreplaceable population of differentiated myocytes. To improve understanding the biology of the heart and obtain supportive evidence of myocyte replication, three indices of cell proliferation were analyzed in dogs affected by a progressive deterioration of cardiac performance and dilated cardiomyopathy. The magnitude of cycling myocytes was evaluated by the expression of Ki67 in nuclei. Ki67 labeling of left ventricular myocytes increased 5-fold, 12-fold, and 17-fold with the onset of moderate and severe ventricular dysfunction and overt failure, respectively. Telomerase activity in vivo is present only in multiplying cells; this enzyme increased 2.4-fold and 3.1-fold in the decompensated heart, preserving telomeric length in myocytes. The contribution of cycling myocytes to telomerase activity was determined by the colocalization of Ki67 and telomerase in myocyte nuclei. More than 50% of Ki67-positive cells expressed telomerase in the overloaded myocardium, suggesting that these myocytes were the morphological counterpart of the biochemical assay of enzyme activity. Moreover, we report that 20--30% of canine myocytes were telomerase competent, and this value was not changed by cardiac failure. In conclusion, the enhanced expression of Ki67 and telomerase activity, in combination with Ki67-telomerase labeling of myocyte nuclei, support the notion that myocyte proliferation contributes to cardiac hypertrophy of the diseased heart.
A Flexible Method for Multi-Material Decomposition of Dual-Energy CT Images (2013)

The ability of dual-energy computed-tomographic (CT) systems to determine the concentration of constituent materials in a mixture, known as material decomposition, is the basis for many of dual-energy CT's clinical applications. However, the complex composition of tissues and organs in the human body poses a challenge for many material decomposition methods, which assume the presence of only two, or at most three, materials in the mixture. We developed a flexible, model-based method that extends dual-energy CT's core material decomposition capability to handle more complex situations, in which it is necessary to disambiguate among and quantify the concentration of a larger number of materials. The proposed method, named multi-material decomposition (MMD), was used to develop two image analysis algorithms. The first was virtual unenhancement (VUE), which digitally removes the effect of contrast agents from contrast-enhanced dual-energy CT exams. VUE has the ability to reduce patient dose and improve clinical workflow, and can be used in a number of clinical applications such as CT urography and CT angiography. The second algorithm developed was liver-fat quantification (LFQ), which accurately quantifies the fat concentration in the liver from dual-energy CT exams. LFQ can form the basis of a clinical application targeting the diagnosis and treatment of fatty liver disease. Using image data collected from a cohort consisting of 50 patients and from phantoms, the application of MMD to VUE and LFQ yielded quantitatively accurate results when compared against gold standards. Furthermore, consistent results were obtained across all phases of imaging (contrast-free and contrast-enhanced). This is of particular importance since most clinical protocols for abdominal imaging with CT call for multi-phase imaging. We conclude that MMD can successfully form the basis of a number of dual-energy CT image analysis algorithms, and has the potential to improve the clinical utility of dual-energy CT in disease management.
Effects of Xenon on In Vitro and In Vivo Models of Neuronal Injury (2002)

Xenon, when coadministered with the injurious agent, exerts a concentration-dependent neuroprotective effect at concentrations below which anesthesia is produced in rodents. Unlike either nitrous oxide or ketamine (other anesthetics with NMDA antagonist properties), xenon is devoid of both neurotoxicity and clinically significant adverse hemodynamic properties. Studies are proposed to determine whether xenon can be used as a neuroprotectant in certain clinical settings.
Binary Optics Technology: The Theory and Design of Multi-Level Diffractive Optical Elements (1989)

Abstract : Multi-level diffractive phase have the potential to significantly improved the performance of many conventional lens systems. The theory, design and fabrication of these diffractive profiles are described in detail. Basic examples illustrate the potential usefulness, as well as the limitations, of these elements. Keywords: Binary optics; Diffractive optical elements.