gebhart/patrepeval huggingface dataset:
Mode-locked pulsed fiber array scalable to high power (2004)

We have developed and demonstrated a fiber amplifier based architecture capable of high peak power pulsed operation that is scalable to high average powers &gap;10 kW. Our approach uses a mode-locked master oscillator to provide the short pulse waveform and an array of fiber amplifiers to provide high efficiency power amplification using a coherently phased, wavelength multiplexed approach. The mode-locked oscillator input is decomposed into its individual modes using a grating, the individual wavelengths are then amplified in a CW format in the fiber amplifier array, recombined with a second grating, and phased to reproduce a high peak power, short pulsewidth, mode-locked output train. We report the initial demonstration of this architecture with an array of 4 fiber amplifiers. 4 modes of the master oscillator output were selected and amplified from 1 mW to 1 Watt each, followed by recombination and phasing. The phased output pulse train effectively reproduced the master oscillator pulse shape, providing a mode-locked output train of 50 psec pulses. The phase control is performed in parallel for each element of the amplifier array and is directly scalable to high average powers by increasing the power of the individual amplifiers and increasing the size of the amplifier array.
Gene Expression from Recombinant Viral Vectors in the Central Nervous System after Blood-Brain Barrier Disruption (1995)

Direct intracerebral injection of recombinant adenoviral vectors within the brain parenchyma or the ventricular system results in a limited volume of distribution of virus, as demonstrated by transgene expression. Global delivery to the central nervous system may increase the use of these vectors but only if the viral vectors can cross the blood-brain barrier and result in transduction of the underlying cells. This short-term study examines whether osmotic disruption with mannitol can result in sufficient opening of the vascular endothelium to allow for passage of replication-defective adenovirus containing the Escherichia coli beta-galactosidase gene (lacZ). Virus was injected into the carotid artery of rats after blood-brain barrier disruption with intracarotid hypertonic mannitol, and the animals were killed and analyzed after 4 days. Histochemical analysis and electron microscopy confirmed expression of the E. coli lacZ gene in the pericapillary astrocytes of the ipsilateral cerebral cortex and deep grey matter. Furthermore, the extent of gene transfer and expression correlated with the degree of barrier opening, as measured by Evans blue staining. Transgene expression was not seen in control animals that received intracarotid saline before recombinant virus injection. These data demonstrate, for the first time, that blood-brain barrier disruption can allow for the delivery of functional viral vectors to the central nervous system.
Khayyam: a second generation tunable spatial heterodyne spectrometer for broadband observation of diffuse emission line targets (2011)

We report on progress toward development of a second-generation tunable spatial heterodyne spectrometer (TSHS) at the fixed focus of the Coudé Auxiliary Telescope (CAT) in the Shane observatory at Lick Observatory (Khayyam). SHS instruments are a class of interferometric sensor capable of providing a combination of large &#233;tendue, high resolving power (R=&lambda;/d&lambda;~ 10<sup>5</sup>) and wide field of view (FOV~0.5 degree) at Optical and NUV wavelengths in a compact format. The TSHS implementation addresses the bandpass limitation of the basic SHS through controlled rotation of pilot mirrors in the interferometer. The use of a single grating as both a dispersing and beam-splitting element in the all-reflective SHS greatly relaxes the precision required in the alignment of the other optical elements relative to a more typical scanning Fourier Transform Spectrometer and allows the TSHS implementation to be accomplished with low-cost commercial rotation stages. The new design builds on a previous design originally tested in 2007, and will address several issues identified with the input beam, output imaging, and grating efficiency (Dawson and Harris, 2009). Here we will discuss the design considerations going into this new system and the initial results of the installation and testing of the TSHS and the future plans.
Raman gain in glass optical waveguides (1973)

The small signal Raman gain in a single-mode glass waveguide amplifier has been measured directly. The measured gain is in good agreement with that calculated from the Raman cross section. The cross section was determined by a comparison of the spontaneous Raman scattering of fused quartz and benzene.
Guard-band influence on orthogonal-band-multiplexed coherent optical OFDM (2008)

Coherent optical orthogonal frequency-division multiplexing (OFDM) has recently been demonstrated beyond 100 Gb/s using orthogonal band multiplexing (OBM). OBM-OFDM gives a multitude of benefits in implementing high-speed optical OFDM transmission. We investigate the system sensitivity to the guard band of OBM-OFDM. The result suggests that when the guard band equals a multiple of the subcarrier spacing, the Q penalty practically vanishes. We also show that two OFDM bands can be demodulated simultaneously with one fast Fourier transform, owing to interband orthogonality, and its performance is almost the same as one-band detection.
An experimental investigation of model-based parameter optimisation (2009)

This work experimentally investigates model-based approaches for optimising the performance of parameterised randomised algorithms. We restrict our attention to procedures based on Gaussian process models, the most widely-studied family of models for this problem. We evaluated two approaches from the literature, and found that sequential parameter optimisation (SPO) [4] offered the most robust performance. We then investigated key design decisions within the SPO paradigm, characterising the performance consequences of each. Based on these findings, we propose a new version of SPO, dubbed SPO+, which extends SPO with a novel intensification procedure and log-transformed response values. Finally, in a domain for which performance results for other (model-free) parameter optimisation approaches are available, we demonstrate that SPO+ achieves state-of-the-art performance.
Development of Myelin Oligodendrocyte Glycoprotein Autoreactive Transgenic B Lymphocytes: Receptor Editing In Vivo After Encounter of a Self-Antigen Distinct from Myelin Oligodendrocyte Glycoprotein (2000)

We explored mechanisms involved in B cell self-tolerance against brain autoantigens in a double-transgenic mouse model carrying the Ig H-chain (introduced by gene replacement) and/or the L-chain kappa (conventional transgenic) of the mAb 8.18C5, specific for the myelin oligodendrocyte glycoprotein (MOG). Previously, we demonstrated that B cells expressing solely the MOG-specific Ig H-chain differentiate without tolerogenic censure. We show now that double-transgenic (THkappa(mog)) B cells expressing transgenic Ig H- and L-chains are subjected to receptor editing. We show that in adult mice carrying both MOG-specific Ig H- and L-chains, the frequency of MOG-binding B cells is not higher than in mice expressing solely the transgenic Ig H-chain. In fact, in THkappa(mog) double-transgenic mice, the transgenic kappa(mog) L-chain was commonly replaced by endogenous L-chains, i.e., by receptor editing. In rearrangement-deficient RAG-2(-) mice, differentiation of THkappa(mog) B cells is blocked at an immature stage (defined by the B220(low)IgM(low)IgD(-) phenotype), reflecting interaction of the autoreactive B cells with a local self-determinant. The tolerogenic structure in the bone marrow is not classical MOG, because back-crossing THkappa(mog) mice into a MOG-deficient genetic background does not lead to an increase in the proportion of MOG-binding B cells. We propose that an as yet undefined self-Ag distinct from MOG cross-reacts with the THkappa(mog) B cell receptor and induces editing of the transgenic kappa(mog) L-chain in early immature B cells without affecting the pathogenic potential of the remaining MOG-specific B cells. This phenomenon represents a particular form of chain-specific split tolerance.
Computational sprinting on a hardware/software testbed (2013)

CMOS scaling trends have led to an inflection point where thermal constraints (especially in mobile devices that employ only passive cooling) preclude sustained operation of all transistors on a chip --- a phenomenon called "dark silicon." Recent research proposed computational sprinting --- exceeding sustainable thermal limits for short intervals --- to improve responsiveness in light of the bursty computation demands of many media-rich interactive mobile applications. Computational sprinting improves responsiveness by activating reserve cores (parallel sprinting) and/or boosting frequency/voltage (frequency sprinting) to power levels that far exceed the system's sustainable cooling capabilities, relying on thermal capacitance to buffer heat. Prior work analyzed the feasibility of sprinting through modeling and simulation. In this work, we investigate sprinting using a hardware/software testbed. First, we study unabridged sprints, wherein the computation completes before temperature becomes critical, demonstrating a 6.3x responsiveness gain, and a 6% energy efficiency improvement by racing to idle. We then analyze truncated sprints, wherein our software runtime system must intervene to prevent overheating by throttling parallelism and frequency before the computation is complete. To avoid oversubscription penalties (context switching inefficiencies after a truncated parallel sprint), we develop a sprint-aware task-based parallel runtime. We find that maximal-intensity sprinting is not always best, introduce the concept of sprint pacing, and evaluate an adaptive policy for selecting sprint intensity. We report initial results using a phase change heat sink to extend maximum sprint duration. Finally, we demonstrate that a sprint-and-rest operating regime can actually outperform thermally-limited sustained execution.
Testosterone treatment to mimic hormone physiology in androgen replacement therapy (2007)

There is still considerable controversy concerning the issue of testosterone replacement therapy. This is because testosterone replacement therapy is not a 'risk-free' treatment and a randomized controlled trial to evaluate safety of prolonged testosterone replacement therapy is not available, nor is it likely to be in the near future. However, recent testosterone delivery systems, such as the 1% gel (Testogel, Androgel and Testim), have proven to have a good physiologic profile, allowing constant monitoring of the possible complications and prompt discontinuation in the event of adverse effects. The aim of this paper is to provide a comprehensive review of the available testosterone preparations to treat male hypogonadism, with special interest in the treatment of ageing men and late-onset hypogonadism. In addition, the experimental and clinical data on the effect of testosterone on sexual function domains is reviewed along with the indication for the combination therapy of androgens with pro-erectile drugs, for example, type 5 phosphodiesterase inhibitors.
Thermodynamic mixing of molecular states of the epidermal growth factor receptor modulates macroscopic ligand binding affinity (2000)

The epidermal growth factor receptor (EGFr), when expressed on the cell surface, has long been known to display two distinct affinities for epidermal growth factor (EGF) binding. In addition, the treatment of cells expressing the EGFr with phorbol esters has been shown to cause a loss of the high-affinity binding capacity of the receptor. In the present study, point mutations that alter acidic or phosphorylation sites have been made in an intracellular domain near Tyr-992 (residues 988-992) of the EGFr. Equilibrium (125)I-EGF binding studies demonstrate that the conversion of Tyr-992 into glutamate induces a 4-fold decrease in the EGFr apparent low-affinity dissociation constant, whereas the mutation of two acidic residues, Asp-988 and Glu-991, or the conversion of Tyr-992 into phenylalanine does not alter EGFr affinity. Phorbol ester treatment of EGFr-expressing Chinese hamster ovary cells results in a loss of high-affinity binding and an increase in the apparent low-affinity dissociation constant of the receptor, similar to the effect of a truncation mutant in which the C-terminal 190 residues are deleted. These results are examined in the context of a new model for regulation of the affinity of the EGFr for EGF in which a cytosolic particle stabilizes the high-affinity conformation of the EGFr and a rapid equilibrium exists between EGFr high-affinity and low-affinity conformations. This model demonstrates that the macroscopic affinities of the EGFr can differ from the affinities of individual EGFr molecules and provides a theoretical framework whereby the measured affinities of the EGFr are modulated by intracellular interactions.
Grundlagen der Statistik in der Betriebswirtschaft (2001)

Sie sollen die Aufgaben der Statistik und die Einteilung der statistischen Methoden kennen. Sie sollen die elementaren Grundbegriffe und die einzelnen Stufen eines planmäßigen Vorgehens bei einer statistischen Untersuchung anwenden können.
Identification of Peptides That Antagonize Formyl Peptide Receptor-Like 1-Mediated Signaling (2004)

Formyl peptide receptor-like 1 (FPRL1) is an important classical chemoattractant receptor that is expressed in phagocytic cells in the peripheral blood and brain. Recently, various novel agonists have been identified from several origins, such as host-derived molecules. Activation of FPRL1 is closely related to inflammatory responses in the host defense mechanism and neurodegenerative disorders. In the present study we identified several novel peptides by screening hexapeptide libraries that inhibit the binding of one of FPRL1's agonists (Trp-Lys-Tyr-Met-Val-D-Met-CONH(2) (WKYMVm)) to its specific receptor, FPRL1, in RBL-2H3 cells. Among the novel peptides, Trp-Arg-Trp-Trp-Trp-Trp-CONH(2) (WRWWWW (WRW(4))) showed the most potent activity in terms of inhibiting WKYMVm binding to FPRL1. We also found that WRW(4) inhibited the activation of FPRL1 by WKYMVm, resulting in the complete inhibition of the intracellular calcium increase, extracellular signal-regulated kinase activation, and chemotactic migration of cells toward WKYMVm. For the receptor specificity of WRW(4) to the FPR family, we observed that WRW(4) specifically inhibit the increase in intracellular calcium by the FPRL1 agonists MMK-1, amyloid beta42 (Abeta42) peptide, and F peptide, but not by the FPR agonist, fMLF. To investigate the effect of WRW(4) on endogenous FPRL1 ligand-induced cellular responses, we examined its effect on Abeta42 peptide in human neutrophils. Abeta42 peptide-induced superoxide generation and chemotactic migration of neutrophils were inhibited by WRW(4), which also completely inhibited the internalization of Abeta42 peptide in human macrophages. WRW(4) is the first specific FPRL1 antagonist and is expected to be useful in the study of FPRL1 signaling and in the development of drugs against FPRL1-related diseases.
Personal DLP for Facebook (2014)

Data Loss Prevention (DLP) is a well-established security and privacy concept in enterprise environments: Enterprise DLP tools scan outgoing messages and stop unintended information flows. It may catch malicious insiders, but the main use case is avoiding data leaks due to human errors. Good DLP tools prevent careless employees from doing something they would probably regret if made aware of. Individuals using online social networks are in a very similar situation: Often they share the wrong information with the wrong people, unaware of the risks and often even unaware of the technical meaning of what they are doing. Personal DLP, introduced in this paper, extends the notion of DLP to individual users. It makes the individual users aware of risks and mistakes, and it does so based on rules explicitly set by each user, and rules derived from that users' past behavior and individual settings. Personal DLP raises awareness by explaining the risks, but the final decision is always with the user.
Miniature Ultrasonic Motor Using Shear Mode of Potassium Sodium Niobate-Based Lead-Free Piezoelectric Ceramics (2009)

A miniature piezoelectric ultrasonic motor (USM) using the shear mode of (K,Na)NbO3 (KNN)-based lead-free piezoelectric ceramics was developed. The motor can be driven in the shearing and bending vibration modes. By using the finite-element method, the motor vibration modes and driving mechanism were modeled. Both the "soft-type" (high-d USM) and "hard-type" (high-Qm USM) KNN-based lead-free piezoelectric ceramics were employed to clarify the characteristics of USMs. The experimental results reveal that the high-d USM widens the band of operational frequency in both vibration modes. In the shearing vibration mode, the high-d USM showed a revolution speed of 416 rpm, a torque of 41.5 µN m, and an efficiency of 0.6%, whereas the high-Qm USM showed the same characteristics of 313 rpm, 19.6 µN m and 1.6%, respectively. In the bending vibration mode, the characteristics of the high-Qm USM were 376 rpm, 51.4 µN m and 0.4%; however, the characters of the high-d USM deteriorated owing to the shift in resonance frequency caused by heat generation.
The Human Homolog of HAVcr-1 Codes for a Hepatitis A Virus Cellular Receptor (1998)

The hepatitis A virus cellular receptor 1 (HAVcr-1) cDNA was isolated from a cDNA expression library of African green monkey kidney (AGMK) cells by using protective monoclonal antibody (MAb) 190/4, which blocks the binding of hepatitis A virus (HAV) to AGMK cells. The HAVcr-1 cDNA codes for havcr-1, a 451-amino-acid class I integral-membrane mucin-like glycoprotein of unknown natural function. To determine the existence of a human homolog(s) of HAVcr-1 (huHAVcr-1), we used HAVcr-1-specific primers to amplify cDNAs from human liver and kidney mRNA by reverse transcription-PCR. Nucleotide sequence analysis revealed that the amplified liver and kidney huHAVcr-1 cDNAs were identical and that they coded for a 359-amino-acid glycoprotein, termed huhavcr-1, which was approximately 79% identical to havcr-1. The six Cys residues of the extracellular domain of havcr-1 and its first N-glycosylation site were conserved in huhavcr-1. However, the number of hexameric repeats of the mucin-like region was reduced from 27 in havcr-1 to 13 in huhavcr-1. In addition, 12 C-terminal amino acids in the cytoplasmic domain of huhavcr-1 were deleted. Northern blot analysis of poly(A) RNA showed that huhavcr-1 is expressed in every organ analyzed, including the liver, small intestine, colon, and spleen, and that it is expressed at higher levels in the kidney and testis. Although dog cells transfected with the huHAVcr-1 cDNA did not express the protective 190/4 epitope, they bound hepatitis A virus (HAV) and gained limited susceptibility to HAV infection. Treatment with MAb 190/4 did not protect AGMK cell transfectants expressing huhavcr-1 against HAV, suggesting that HAV infected these cells via the huhavcr-1 receptor and not the endogenously expressed havcr-1, which was blocked by MAb 190/4. Our data demonstrate that huhavcr-1 is a binding receptor for HAV and suggest that it is also a functional receptor for HAV.
Remodeling of ryanodine receptor complex causes “leaky” channels: A molecular mechanism for decreased exercise capacity (2008)

During exercise, defects in calcium (Ca2+) release have been proposed to impair muscle function. Here, we show that during exercise in mice and humans, the major Ca2+ release channel required for excitation-contraction coupling (ECC) in skeletal muscle, the ryanodine receptor (RyR1), is progressively PKA-hyperphosphorylated, S-nitrosylated, and depleted of the phosphodiesterase PDE4D3 and the RyR1 stabilizing subunit calstabin1 (FKBP12), resulting in "leaky" channels that cause decreased exercise tolerance in mice. Mice with skeletal muscle-specific calstabin1 deletion or PDE4D deficiency exhibited significantly impaired exercise capacity. A small molecule (S107) that prevents depletion of calstabin1 from the RyR1 complex improved force generation and exercise capacity, reduced Ca2+-dependent neutral protease calpain activity and plasma creatine kinase levels. Taken together, these data suggest a possible mechanism by which Ca2+ leak via calstabin1-depleted RyR1 channels leads to defective Ca2+ signaling, muscle damage, and impaired exercise capacity.
Electrical signatures of single-stranded DNA with single base mutations in a nanopore capacitor (2006)

In this paper, we evaluate the magnitude of the electrical signals produced by DNA translocation through a 1 nm diameter nanopore in a capacitor membrane with a numerical multi-scale approach, and assess the possibility of resolving individual nucleotides as well as their types in the absence of conformational disorder. We show that the maximum recorded voltage caused by the DNA translocation is about 35 mV, while the maximum voltage signal due to the DNA backbone is about 30 mV, and the maximum voltage of a DNA base is about 8 mV. Signals from individual nucleotides can be identified in the recorded voltage traces, suggesting a 1 nm diameter pore in a capacitor can be used to accurately count the number of nucleotides in a DNA strand. Furthermore, we study the effect of a single base substitution on the voltage trace, and calculate the differences among the voltage traces due to a single base mutation for the sequences C3AC7, C3CC7, C3GC7 and C3TC7. The calculated voltage differences are in the 5–10 mV range. The calculated maximum voltage caused by the translocation of individual bases varies from 2 to 9 mV, which is experimentally detectable.
Practical filtering for efficient ray-traced directional occlusion (2011)

Ambient occlusion and directional (spherical harmonic) occlusion have become a staple of production rendering because they capture many visually important qualities of global illumination while being reusable across multiple artistic lighting iterations. However, ray-traced solutions for hemispherical occlusion require many rays per shading point (typically 256-1024) due to the full hemispherical angular domain. Moreover, each ray can be expensive in scenes with moderate to high geometric complexity. However, many nearby rays sample similar areas, and the final occlusion result is often low frequency. We give a frequency analysis of shadow light fields using distant illumination with a general BRDF and normal mapping, allowing us to share ray information even among complex receivers. We also present a new rotationally-invariant filter that easily handles samples spread over a large angular domain. Our method can deliver 4x speed up for scenes that are computationally bound by ray tracing costs.
DNA marker haplotype association with pancreatic sufficiency in cystic fibrosis. (1989)

Patients with cystic fibrosis (CF) generally suffer from chronic obstructive lung disease, pancreatic insufficiency (PI), and a number of other exocrine malfunctions. Approximately 15% of CF patients are, however, pancreatic sufficient. To investigate whether the two clinical subgroups, PI and pancreatic sufficiency (PS), are caused by different CF mutant alleles, we have performed linkage disequilibrium and haplotype association analysis with three DNA markers that are tightly linked to the CF locus. The study showed that the allelic and haplotype distributions for these RFLPs are significantly different between the two groups. The data suggest that most of the CF-PI patients are probably descendants of a single mutational event at the CF locus and that the CF-PS patients resulted from multiple, different mutations. While final interpretation of these data awaits molecular cloning of the CF gene, the information on haplotype association in CF may be useful in genetic counseling and disease prognosis, in identifying the gene itself, and in defining the mutations.