gebhart/patrepeval huggingface dataset:
Radon transform wave field separation for vertical seismic profiling data (1986)

Abstract The data obtained by the vertical seismic profiling (VSP) method require unique processing before interpretation. An important step is the separation of upgoing and downgoing signals by application of an f-k velocity filter and muting of the direct wave. Similarly, if the VSP section is transformed to the p-tau plane, the upgoing and downgoing wave fields become separable because they map to different p-tau quadrants according to their dips. This allows either wave field to be reconstructed by application of the inverse Radon transform after windowing in the p-tau plane.Results obtained by the Radon transform wave field separation (RTWS) method are similar to those obtained by f-k velocity filtering. However, by implementing an amplitude-ratio testing filter in the forward slant stack, the quality of the reconstructed wave field is much improved. For a specific range of p-stack values in the forward transform, this filter sorts and removes the unwanted events from the desired ones by testing their consistency in stack amplitudes.Synthetic examples of separating the upgoing wave field from a full VSP wave field by both methods are presented.
Small-Molecule Inhibitors of the Programmed Cell Death-1/Programmed Death-Ligand 1 (PD-1/PD-L1) Interaction via Transiently Induced Protein States and Dimerization of PD-L1 (2017)

Blockade of the PD-1/PD-L1 immune checkpoint pathway with monoclonal antibodies has provided significant advances in cancer treatment. The antibody-based immunotherapies carry a number of disadvantages such as the high cost of the antibodies, their limited half-life, and immunogenicity. Development of small-molecule PD-1/PD-L1 inhibitors that could overcome these drawbacks is slow because of the incomplete structural information for this pathway. The first chemical PD-1/PD-L1 inhibitors have been recently disclosed by Bristol-Myers Squibb. Here we present NMR and X-ray characterization for the two classes of these inhibitors. The X-ray structures of the PD-L1/inhibitor complexes reveal one inhibitor molecule located at the center of the PD-L1 homodimer, filling a deep hydrophobic channel-like pocket between two PD-L1 molecules. Derivatives of (2-methyl-3-biphenylyl)methanol exhibit the structures capped on one side of the channel, whereas the compounds based on [3-(2,3-dihydro-1,4-benzodioxin-6-yl)-2-methylphenyl]methanol induce an enlarged interaction interface that results in the open "face-back" tunnel through the PD-L1 dimer.
The vertical occipital fasciculus: A century of controversy resolved by in vivo measurements (2014)

The vertical occipital fasciculus (VOF) is the only major fiber bundle connecting dorsolateral and ventrolateral visual cortex. Only a handful of studies have examined the anatomy of the VOF or its role in cognition in the living human brain. Here, we trace the contentious history of the VOF, beginning with its original discovery in monkey by Wernicke (1881) and in human by Obersteiner (1888), to its disappearance from the literature, and recent reemergence a century later. We introduce an algorithm to identify the VOF in vivo using diffusion-weighted imaging and tractography, and show that the VOF can be found in every hemisphere (n = 74). Quantitative T1 measurements demonstrate that tissue properties, such as myelination, in the VOF differ from neighboring white-matter tracts. The terminations of the VOF are in consistent positions relative to cortical folding patterns in the dorsal and ventral visual streams. Recent findings demonstrate that these same anatomical locations also mark cytoarchitectonic and functional transitions in dorsal and ventral visual cortex. We conclude that the VOF is likely to serve a unique role in the communication of signals between regions on the ventral surface that are important for the perception of visual categories (e.g., words, faces, bodies, etc.) and regions on the dorsal surface involved in the control of eye movements, attention, and motion perception.
Radical oxygen (O/sup */) process for highly-reliable SiO/sub 2/ with higher film-density and smoother SiO/sub 2//Si interface (2002)

It has been clarified that the radical oxidation with the oxygen remote plasma improves the electrical reliability of the SiO/sub 2/ films, compared with the dry oxidation. By TEM observation and X-ray-scattering-reflectivity spectroscopy it was demonstrated that, in the radical oxides, planarization of the SiO/sub 2//Si[100] interface and densification of the SiO/sub 2/ films due to repairing of the SiO/sub 2/ network were realized, compared with those in the dry oxides. Moreover, it was also found that the radical oxidation can realize a reliable SiO/sub 2/ in the lower oxidation temperatures even down to 700/spl deg/C.
Desarrollo de nuevas aleaciones de aluminio y procesos de menor impacto medioambiental (2001)

Macrophage recruitment and proliferation of both small vessels (endothelium and pericytes) and fibroblast-myofibroblasts are the fundamental and provisional cellular findings in repair through granulation tissue (RTGT).Endothelium and pericytes of preexisting microvasculature may act as progenitor cells of new endothelial cells and new pericyte-fibroblast-myofibroblasts, respectively.Likewise, fibroblasts may be progenitors of themselves, and of myofibroblasts and pericytes. Moreover, all these cells may originate from circulating progenitor cells or other progenitor cells..According to this extensive cellular plasticity, this work reviews the adult stem cells (ASC) and transit- amplifying cells (TAC) related to the principal cellular components of RTGT.Moreover, we hypothesize that the perivascular region, with a heterogeneous pericyte-like cellular population, including pericytes, perivascular fibroblasts and homing cells from the bone marrow (fibrocytes and bone marrow mesenchymal cells), is the niche of progenitor cells in RTGT and the substrate of regulatory mechanisms (perivascular niche hypothesis).We also highlight RTGT as a "paracrine transitional organ" during involutive phenomena and cellular differentiation.Furthermore, we consider the combined role of both systems (ASC-TAC and RTGT) in tissue engineering and in pathological processes, such as fibrosis, organization, atherosclerosis, and tumor stroma.
Effect of calcium phosphate coating characteristics on early post-operative bone tissue ingrowth (1990)

The synthesis of model porous metal-CPC materials, and their use in one-parametric studies of bone tissue ingrowth enhancement were considered. By using the same starting calcium-deficient hydroxyapatite powder, three different coatings, CAP1, CAP2 and CAP3, were obtained of thicknesses 50 +/- 5, 75 +/- 5 and 75 +/- 5 microns, respectively. CAP1 and 2 were either the starting powder mixed in a 3:1 ratio CPC: poly(lactic acid) or the powder by itself. The CAP3 coating was the result of a thermal treatment producing a mixture of oxyhydroxyapatite, alpha- and beta-tricalcium phosphate. Orderly oriented wire mesh porous coated specimens were implanted, along with the same specimens lined with CAP 1, 2 or 3. Subsequently, the total of 156 specimens was retrieved at 2, 4 or 6 wk, and tested mechanically and processed for histomorphometry. The data produced considerable evidence for the CPC-dependent enhancement of bone tissue ingrowth in porous metals immediately after implantation. They prove that the materials processing of CPC coatings influences the resulting biological behaviour substantially. Furthermore, they support the hypothesis that ceramic dissolution is a causative factor on the bone tissue growth enhancement mechanisms.
Photoelectron spectroscopy studies of chemical vapor deposition of Ta from a TaF5 precursor on Si and SiO2 substrates (1991)

The increasing need for metallization of microelectronic structures involving deep trenches and high aspect ratio features has sparked considerable interest in chemical vapor deposition metallization schemes. In this work the results of photoemission investigations of the substrate-driven reduction of TaF5 to Ta metal on Si(111) and SiO2 substrates are reported. At moderate temperatures the reaction showed no selectivity between these two substrates, in contrast to the process with the similar molecule WF6. At 400 °C metallic Ta films could be grown on both Si and SiO2; however, x-ray photoelectron spectroscopy measurements show that the bonding of the film to Si(111) is dominated by fluorine atoms at the interface, whereas film growth on SiO2 tends to form an oxide interface with TaOF3 stoichiometry. Annealing of the deposited film to about 700 °C leads to Si diffusion to the surface which is accompanied by the release of fluorine from the film. The deposition of TaF5 on Si(111) at 250 °C results initially in a partly dissociative metallic deposition followed by a non-dissociative molecular chemisorption. Our experiments suggest the Si substrate to be reactive enough at the initial state of the deposition to break up theTaF5 molecule but that the process is quickly self-passivating.
Optic Nerve Damage in Human Glaucoma (1982)

The number and distribution of human optic nerve axons were compared with clinical measurements available the same eyes, including visual acuity, disc appearance, and visual field studies. Definite loss of axons occurs prior to reproducible visual field defects in some patients suspected of having glaucoma. In glaucoma, the superior and inferior poles of the nerve lose nerve fibers at a selectively greater rate, leading to an hourglass-shaped atrophy. Cavernous degeneration of the retrobulbar optic nerve is rarely observed in chronic glaucoma. The pattern of atrophy in examples of toxic amblyopia, ischemic optic neuropathy and chronic papilledema differ from that of glaucoma, suggesting different mechanisms of damage in these conditions.
Directed Synthesis of the Triangular Mixed-Metal Cluster H2RhRe2Cp*(CO)9: Ligand Fluxionality and Facile Cluster Fragmentation in the Presence of CO, Halogenated Solvents, and Thiols (2009)

The reaction of H2Re2(CO)8 (1) with Cp*Rh(CO)2 (2) in refluxing hexane affords the mixed-metal clusters H2RhRe2Cp*(CO)9 (4, major product), HRh2ReCp*2(CO)6 (5), and HRhRe3Cp*(CO)14 (6). 4 and 5 are electron-precise 48e clusters and display triangular metallic cores, while 6 contains 64 valence electrons and exhibits a spiked-triangular core having a pendant Re(CO)5 moiety. Heating 1 with Cp*2Rh2(CO)2 (3) gives 4 and 5 as the principal products, in addition to H2Rh2Re2Cp*2(CO)8 (7) in low yield. Cluster 7 possesses 60e and contains a tetrametallic core with two face-capping CO and hydride groups. Heating 4 under CO leads to cluster fragmentation and formation of Re2(CO)10 and 2 in essentially quantitative yield, as assessed by IR spectroscopy. The kinetics for the fragmentation of 4 in toluene under CO have been investigated over the temperature range 325−349 K by UV−vis spectroscopy. On the basis of the first-order rate constants and the Eyring activation parameters (ΔH⧧ = 25.0(8) kcal/mol; ΔS⧧ = −2.6(3) eu), a rate-limiting step involving a polyhedral opening of 4 is supported. 4 is thermally and photochemically sensitive, and reactions conducted in the presence of chlorinated solvents furnish the face-shared bioctahedral compound Cp*Rh(μ-Cl)3Re(CO)3 (8). Heating 4 and H2S in benzene at ca. 60 °C furnishes the 48e triangular cluster S2Rh3Cp*(CO)4 (9), which contains two Rh(CO)2 moieties and two face-capping sulfide groups. The reaction of 4 with p-methylbenzenethiol gives the sulfido-bridged dimer Cp*Rh(μ-SC6H4Me-p)3Re(CO)3 (11). The dinuclear compounds Cp*Rh(μ-Cl)(μ-SC6H4Me-p)2Re(CO)3 (10) and 11 are formed when 8 is allowed to react with p-methylbenzenethiol. Treatment of 8 and 10 with excess p-methylbenzenethiol yields 11 at elevated temperature in toluene. Compounds 4−11 have been isolated and fully characterized by IR and NMR spectroscopy and by X-ray crystallography. The reactivity displayed by 4 is contrasted with that of the known indenyl-substituted cluster H2Re2Ir(η5-ind)(CO)9 prepared earlier by Shapley and co-workers.
Sequences for controlling laser excitation with femtosecond three-pulse four-wave mixing (1999)

Three-pulse four-wave mixing (FWM) is used here to study and control laser excitation processes. For general laser excitation processes, after a molecule interacts resonantly with a laser pulse, the molecule has a probability of being in the ground or in the excited state. Control over this process depends on the phase and amplitude of the electric fields that interact with the molecular system. Here we show how three-pulse FWM can be used to control the excitation of iodine molecules. Depending on the time delay between the first two pulses, the observed signal reflects the dynamics of the ground or excited state. A theoretical formalism based on the density matrix formulation is presented and solved for a four-level system. Experiments are found to be in excellent agreement with the theory. The influence of linear chirp on three-pulse FWM experiments is explored. Spectrally dispersed three-pulse FWM is found to be extremely useful for studying the effect of chirp on laser excitation of molecular systems. Experimental demonstrations of these effects are included.
Fenretinide-induced apoptosis of human head and neck squamous carcinoma cell lines☆☆☆★★★ (1998)

BACKGROUND: Squamous cell carcinoma of the head and neck (HNSCC) has a high incidence of recurrence and associated second primary malignancy. The retinoid 13-cis-retinoic acid has been shown to be effective as both a chemopreventive and chemotherapeutic agent for HNSCC, but often with treatment-limiting toxicity. The synthetic retinoid fenretinide (N-(4-hydroxyphenyl)retinamide) (HPR) has significant antiproliferative activity against a number of animal and human malignancies and has been used in clinical trials as a chemopreventive agent in patients with breast and prostate cancer and oral leukoplakia. HPR has been shown to have a toxicity profile lower than that for other retinoids used in clinical trials. PURPOSE: The aim of this study was to investigate the effect of HPR on the growth of HNSCC cell lines in vitro. METHODS: Four HNSCC cell lines (JHU-011-SCC, JHU-020-SCC, JHU-022-SCC, and FaDu) were treated with a range of concentrations of HPR for various times. After HPR exposure, cell viability was determined by tetrazolium dye (MTT) colorimetric assay, comparing cell survival with that of untreated control cells. HPR-induced apoptosis was determined by flow-cytometric deoxyribonucleic acid cell-cycle analysis, ultrastructural analysis with electron microscopy, and deoxyribonucleic acid fragmentation detected by gel electrophoresis. RESULTS: HPR caused significant growth inhibition in three of the four HNSCC cell lines in a dose- and time-dependent fashion. In two cell lines (JHU-011-SCC, JHU-020-SCC) a significant antiproliferative effect was achieved between 1 and 2.5 μmol/L HPR after 72 hours of treatment. By deoxyribonucleic acid cell-cycle analysis, electron microscopy, and gel electrophoresis, HPR was shown to induce apoptosis in the JHU-011-SCC and JHU-020-SCC cell lines, but not in the FaDu cell line, which was insensitive to the growth inhibitory effect of HPR. CONCLUSIONS: This study has demonstrated that HPR reduces cell viability in HNSCC cells in vitro at clinically relevant doses, with the growth inhibition occurring through the induction of apoptosis. (Otolaryngol Head Neck Surg 1998;118:464-71.)
Highly sensitive Hall magnetic sensor microsystem in CMOS technology (2002)

A highly sensitive magnetic sensor microsystem based on a Hall device is presented. This microsystem consists of a Hall device improved by an integrated magnetic concentrator and new circuit architecture for the signal processing. It provides an amplification of the sensor signal with a resolution better than 30 /spl mu/V and a periodic offset cancellation while the output of the microsystem is available in continuous time. This microsystem features an overall magnetic gain of 420 V/T.
Activated Cdc42-associated kinase Ack1 promotes prostate cancer progression via androgen receptor tyrosine phosphorylation (2007)

Activation of the androgen receptor (AR) may play a role in androgen-independent progression of prostate cancer. Multiple mechanisms of AR activation, including stimulation by tyrosine kinases, have been postulated. We and others have recently shown involvement of activated Cdc42-associated tyrosine kinase Ack1 in advanced human prostate cancer. Here we provide the molecular basis for interplay between Ack1 and AR in prostate cancer cells. Activated Ack1 promoted androgen-independent growth of LNCaP and LAPC-4 prostate xenograft tumors, AR recruitment to the androgen-responsive enhancer, and androgen-inducible gene expression in the absence of androgen. Heregulin-stimulated HER2 activation induced Ack1 activation and AR tyrosine phosphorylation. Ack1 knockdown inhibited heregulin-dependent AR tyrosine phosphorylation, AR reporter activity, androgen-stimulated gene expression, and AR recruitment. Ack1 was recruited to the androgen-responsive enhancers after androgen and heregulin stimulation. In 8 of 18 primary androgen-independent prostate tumor samples, tyrosine-phosphorylated AR protein was detected and correlated with the detection of tyrosine-phosphorylated Ack1. Neither was elevated in androgen-dependent tumors or benign prostate samples. Activated Ack1 phosphorylated AR protein at Tyr-267 and Tyr-363, both located within the transactivation domain. Mutation of Tyr-267 completely abrogated and mutation of Tyr-363 reduced Ack1-induced AR reporter activation and recruitment of AR to the androgen-responsive enhancer. Expression of AR point mutants inhibited Ack1-driven xenograft tumor growth. Thus, Ack1 activated by surface signals or oncogenic mechanisms may directly enhance AR transcriptional function and promote androgen-independent progression of prostate cancer. Targeting the Ack1 kinase may be a potential therapeutic strategy in prostate cancer.
Cachexia (2000)

Cachexia represents the clinical consequence of a chronic, systemic inflammatory response, and its manifestations differ considerably from those of starvation. Although cachexia is classically associated with chronic infections and malignant conditions, some of its elements have been identified in a wide variety of chronic diseases and in aging persons. Cachexia has repeatedly been associated with adverse clinical outcomes. The changes seen in cachexia are multidimensional and highly coordinated. Most obvious is a redistribution of the body's protein content, with preferential depletion of skeletal muscle and an increase in the synthesis of proteins involved in the response to tissue injury-the so-called acute-phase response. The physiologic, metabolic, and behavioral changes of cachexia are tightly regulated by cytokines, which signal the synthesis of acute-phase proteins as well as changes in intermediary metabolism that provide substrate and energy. The metabolic adaptations, notably the increase in the rate of protein degradation, limit the ability of hypercaloric feeding to reverse the depletion of lean mass. Recent studies have demonstrated the ability of anabolic and anticatabolic agents to mitigate the loss of skeletal muscle and to improve clinical outcomes in selected circumstances. Preclinical initiatives target the cytokine regulation of protein metabolism. It should be stressed that metabolic manipulation in cachexia could have positive or negative clinical effects, which must be distinguished through appropriate clinical trials.
Identification and functional characterization of two distinct epitopes on the human T cell surface protein Tp50. (1983)

The structural and functional domains of Tp50, the human T lymphocyte surface protein associated with the E rosette receptor, were probed with the use of two murine monoclonal antibodies. Lysostripping, immune precipitation, and competitive binding experiments demonstrated that antibodies 9.6 and 35.1 bind to Tp50 epitopes in close proximity. In functional studies, both antibodies caused a similar degree of antigenic modulation, inhibited T cell proliferative responses, and inhibited cytotoxic T lymphocyte function without affecting cells that mediate antibody-dependent cell-mediated cytotoxicity. The antibodies were strikingly different, however, in that antibody 9.6 inhibited E rosette formation and natural killer cell-mediated lysis, whereas antibody 35.1 did not. These results could not be ascribed to differences in antibody class or binding characteristics, because Scatchard analysis demonstrated that these two IgG2a antibodies have comparable avidity and that T cells bind each antibody in equivalent amounts. The differential binding of antibodies 9.6 and 35.1 to T cells from nonhuman primates further supports the interpretation that the differences between the antibodies in their effects on E rosette formation and natural killer function stem from the fact that they bind to distinct epitopes of Tp50. The implications of these findings for understanding the functions of Tp50 molecules are discussed.
Self-Sterility in Sweetgum (1964)

Abstract ( Liquidambar styraciflua L.) trees in Florida and North Carolina yielded an average of 46 seeds per fruit after cross-pollination but only 2 seeds per fruit after self-pollination. Post-pollination cytological analysis of pistillate infloresences from two of the North Carolina trees revealed that self-fertilized ovules aborted before they reached the cellular endosperm stage. This means that outbreeding due to wind-pollination is reinforced by self-sterility. The possible relation of the breeding system to population variation is discussed.
The nuclear hormone receptor coactivator SRC-1 is a specific target of p300. (1996)

p300 and its family member, CREB-binding protein (CBP), function as key transcriptional coactivators by virtue of their interaction with the activated forms of certain transcription factors. In a search for additional cellular targets of p300/CBP, a protein-protein cloning strategy, surprisingly identified SRC-1, a coactivator involved in nuclear hormone receptor transcriptional activity, as a p300/CBP interactive protein. p300 and SRC-1 interact, specifically, in vitro and they also form complexes in vivo. Moreover, we show that SRC-1 encodes a new member of the basic helix-loop-helix-PAS domain family and that it physically interacts with the retinoic acid receptor in response to hormone binding. Together, these results implicate p300 as a component of the retinoic acid signaling pathway, operating, in part, through specific interaction with a nuclear hormone receptor coactivator, SRC-1.