gebhart/patrepeval huggingface dataset:
Optimizing Total Migration Time in Virtual Machine Live Migration (2013)

The ability to migrate a virtual machine (VM) from one physical host to another is important in a number of cases such as power management, on-line maintenance, and load-balancing. The amount of memory used in VMs have been steadily increasing up to several gigabytes. Consequently, the time to migrate machines, the total migration time, has been increasing. The aim of this thesis is to reduce the total migration time. Previous work aimed at reducing the amount of time and disk space required for saving checkpoint images of virtual machines by excluding data from the memory that is duplicated on the disk of the VM. Other work aimed at reducing the time to restore a VM from a checkpoint by only loading a subset of data before resuming the VM and marking the other memory as invalid. These techniques have been adapted and applied to virtual machine live migration to reduce the total migration time. The implemented technique excludes sending duplicate data that exists on disk and resumes the VM before all memory has been loaded. The proposed technique has been implemented for fully virtualized guests in Xen 4.1. The results of research conducted with a number of benchmarks demonstrate that there is an average 44% reduction of the total migration time.
Software Process Recovery: Recovering Process from Artifacts (2010)

Often stakeholders, such as developers, managers, or buyers, want to find out what software development processes are being followed within a software project. Their reasons include: CMM and ISO 9000 compliance, process validation, management, acquisitions, and business intelligence. Recovering the software development processes from an existing project is expensive if one must rely upon manual inspection of artifacts and interviews of developers and their managers. Researchers have suggested live observation and instrumentation of a project to allow for more measurement, but this is costly, invasive, and also requires a live running project. Instead, we propose an after the fact analysis: software process recovery. This approach analyzes version control systems, bug trackers and mailing list archives using a variety of supervised and unsupervised techniques from machine learning, topic analysis, natural language processing and statistics. We can combine all of these methods to recover process events that we map back to software development processes like the Unified Process. We can produce diagrams called Recovered Unified Process Views (RUPV) that are similar to the Unified Process diagram, a time-line of effort per parallel discipline occurring across time. We then validate these methods using case studies of multiple open source software systems.
Action spectra for phytochrome A- and B-specific photoinduction of seed germination in Arabidopsis thaliana. (1996)

We have examined the seed germination in Arabidopsis thaliana of wild type (wt), and phytochrome A (PhyA)- and B (PhyB)-mutants in terms of incubation time and environmental light effects. Seed germination of the wt and PhyA-null mutant (phyA) was photoreversibly regulated by red and far-red lights of 10-1,000 micromol m-2 when incubated in darkness for 1-14 hr, but no germination occurred in PhyB-null mutant (phyB). When wt seeds and the phyB mutant seeds were incubated in darkness for 48 hr, they synthesized PhyA during dark incubation and germinated upon exposure to red light of 1-100 nmol m-2 and far-red light of 0.5-10 micromol m-2, whereas the phyA mutant showed no such response. The results indicate that the seed germination is regulated by PhyA and PhyB but not by other phytochromes, and the effects of PhyA and PhyB are separable in this assay. We determined action spectra separately for PhyA- and PhyB-specific induction of seed germination at Okazaki large spectrograph. Action spectra for the PhyA response show that monochromatic 300-780 nm lights of very low fluence induced the germination, and this induction was not photoreversible in the range examined. Action spectra for the PhyB response show that germination was photoreversibly regulated by alternate irradiations with light of 0.01-1 mmol m-2 at wavelengths of 540-690 nm and 695-780 nm. The present work clearly demonstrated that PhyA photoirreversibly triggers the germination upon irradiations with ultraviolet, visible and far-red light of very low fluence, while PhyB controls the photoreversible effects of low fluence.
Comparison of spray retention on synthetic superhydrophobic surface with retention on outdoor grown wheat leaves (2012)

peer reviewed
Optical coherence tomography – current and future applications (2013)

Advances in OCT technology provide for better understanding of pathogenesis, improved monitoring of progression and assistance in quantifying response to treatment modalities in diseases of the posterior segment of the eye. Further improvements in both hardware and software technologies should further advance the clinician's ability to assess and manage chorioretinal diseases.
Protease-activating Receptor-4 Induces Full Platelet Spreading on a Fibrinogen Matrix (2007)

Although the involvement of protease-activating receptor PAR1 and PAR4 is well established in platelet aggregation, their role in platelet adhesion and spreading has yet to be characterized. We investigated platelet adhesion and spreading on a fibrinogen matrix after PAR1 and PAR4 stimulation in correlation with the activation of two MAPKs, ERK2 and p38. Of the two PAR-activating peptides (PAR-APs), PAR1-AP and PAR4-AP, which both induce adhesion, only PAR4-AP induced full platelet spreading. Although both PAR1-AP and PAR4-AP induced ADP secretion, which is required for platelet spreading, only PAR4-AP induced sustained Ca(2+) mobilization. In these conditions of PAR4 induction, ERK2 and p38 activation were involved in platelet spreading but not in platelet adhesion. p38 phosphorylation was dependent on ADP signaling through P2Y12, its receptor. ERK2 phosphorylation was triggered through integrin alphaIIbbeta3 outside-in signaling and was dependent on the Rho pathway. ERK2 and p38 activation induced phosphorylation of the myosin light chain and actin polymerization, respectively, necessary for cytoskeleton reorganization. These findings provide the first evidence that thrombin requires PAR4 for the full spreading response. ERK2 and p38 and sustained Ca(2+) mobilization, involved in PAR4-induced platelet spreading, contribute to the stabilization of platelet thrombi at sites of high thrombin production.
Evaluation of the Thrombolytic Effect of Tissue-Type Plasminogen Activator with Ultrasonic Irradiation: In Vitro Experiment Involving Assay of the Fibrin Degradation Products from the Clot. (1994)

Previous studies show that the combined method using thrombolytic drugs and ultrasonic irradiation enhances the effect of thrombolysis in in vitro and in vivo experiments. However, the mechanism of the clot lysis was unclear. In previous studies the evaluation of the clot lysis effect was determined by the rate of decrease in clot weight or the decrease in radioisotope-labeled fibrinogen in the clot. However, it was unclear whether or not the fibrinogen in the clot was degraded. We measured quantitatively the fibrin degradation product, D-dimer (FDP-DD), produced from clots subjected to recombinant tissue-type plasminogen activator (rt-PA, 2.0 micrograms/ml), with and without ultrasonic irradiation. Two levels of continuous ultrasound were used, 300 kHz (100 V, 0.07 W/cm2) and 1 MHz (20 V, 0.4 W/cm2). The quantity of FDP-DD produced was 1.74 times at 300 kHz and 1.80 times at 1 MHz, greater than that measured in rt-PA solution without ultrasonic irradiation; clot lysis was not observed in normal saline with ultrasonic irradiation. Our experiment clarifies that the mechanism of clot lysis when subjected to a combination of drug and ultrasound leads to degradation of fibrin, allowing a quantitative measurement of the enhancement of clot lysis. A high correlation was observed between the FDP-DD produced from the clots and the rate of decrease in clot weight.
Tumor-specific cytotoxicity and type of cell death induced by naphtho[2,3-b]furan-4,9-diones and related compounds in human tumor cell lines: relationship to electronic structure. (2009)

A total of thirty-nine naphtho[2,3-b]furan-4,9-diones and related compounds were tested for their cytotoxicity against three human normal oral cells (gingival fibroblast, HGF, pulp cell, HPC, periodontal ligament fibroblast, HPLF) and four human tumor cell lines (oral squamous cell carcinoma HSC-2, HSC-3, HSC-4, promyelocytic leukemia HL-60). 2-Acetylnaphtho[2,3-b]furan-4,9-dione [1] was highly cytotoxic to both normal and tumor cells, yielding low tumor-specificity. 2-Acetyl-4,9-dimethoxynaphtho[2,3-b]furan [4], the 2-(3-furanoyl) benzoic acids [5, 6] and the 1,4-naphthoquinones [7, 8] showed much reduced cytototoxicity and low tumor-specificity. The introduction of phenoxy [18], isopropylamino [23] or 2-methylpiperidino [33] groups to the 2-position of naphtho[2,3-b]furan-4,9-dione yielded compounds that showed the greatest tumor-specificity. These compounds, at twice or four times higher concentrations than CC50, induced the activation of caspase-3, caspase-8 and caspase-9 in the HSC-2 and HL-60 cells, but not so apparently in the HSC-4 cells. However, they did not induce internucleosomal DNA fragmentation in the HSC-2 and HSC-4 cells even after 24 hours incubation and only slightly induced DNA fragmentation in the HL-60 cells. Compound [18] induced the production of annexin-positive cells, but did not induce microtubule-associated protein light chain 3 (LC3) accumulation in autophagosomes in LC3-green fluorescent protein (GFP)-transfected HSC-2 cells. These data suggested that naphtho[2,3-b]furan-4,9-diones may induce the early apoptotic marker, without induction of caspase activation and DNA fragmentation in oral squamous cell carcinoma cell lines. Quantitative structure-activity relationship (QSAR) analysis suggests the applicability of the theoretical calculations such as frontier molecular orbital, dipole moments and hydrophobicity in predicting their cytotoxic activity.
The significance of membrane changes in the safe and effective use of therapeutic and diagnostic ultrasound (1989)

The cellular changes, such as alterations in motility and the stimulation of synthesis and secretion, induced by relatively low intensities of therapeutic ultrasound (e.g. 500 mW cm-2, SAPA; 100 mW cm-2 SATA) are primarily non-thermal in origin. They appear to be associated with changes in the permeability of the cell (plasma) membrane and in the transport of ions and molecules across it, effects which have been demonstrated in cells irradiated in suspension. In epithelial tissues, both in vitro and in vivo, it has been demonstrated that not only the cellular membrane transport pathways but also the paracellular or intercellular pathways are affected. Although membrane-mediated effects can be of value therapeutically, they could produce adverse effects if they were to occur during development, for the reception and transmission by the membrane of environmental signals are involved in determination of the fate of each cell. Determination is followed by selective gene expression and differentiation, that is, by the progressive increase in structural complexity brought about by the acquisition of specialised characteristics by various cell groups. Most cells of early embryos are ionically coupled via gap junctions which provide an intercellular pathway for electrochemical signalling and the maintenance of the concentration gradients which provide the cells with positional information. Differentiation of the cells varies according to their location with respect to these gradients. Increase in the intracellular concentration of calcium ions, which has been shown to occur after exposure to therapeutic levels of ultrasound, can decrease the permeability of gap junctions and uncouple cells, in the manner which occurs when they differentiate. Ultrasonically induced increases in calcium ion concentration are thus of considerable clinical significance, since they could affect differentiation and consequently histogenesis. Modification of plasma membrane permeability and transport properties, resulting in changes in the availability and activity of second messengers such as free calcium ions, can have profound effects on cell behaviour. Calcium channels appear to be the first channels to develop in the cell membranes of embryos, and internal calcium ion concentration is known to affect the synthesis of fetal proteins. Although generally reversible at intensities of less than 500 mW cm-2, changes in membrane permeability, particularly to calcium ions, could, if prolonged, have undesirable side effects not only on embryogenesis but on late prenatal and postnatal development. It is therefore recommended that the environmental conditions, thresholds, and mechanisms involved in the production of such changes be determined, so that they can be avoided when ultrasound is used diagnostically on sensitive targets such as embryos and fetuses.
Preparation of affinity-fractionated, heparin-derived oligosaccharides and their effects on selected biological activities mediated by basic fibroblast growth factor. (1993)

Homogeneously sized, heparin-derived oligosaccharides were prepared from heparin following partial depolymerization with nitrous acid, reduction with sodium borohydride, and fractionation by gel permeation chromatography. The resulting pools of di-, tetra-, hexa-, octa-, and decasaccharides were sequentially applied to an affinity column of human recombinant basic fibroblast growth factor (bFGF) covalently attached to Sepharose 4B and further fractionated into subpools based on their elution from this column in response to gradients of sodium chloride. In general, pools of smaller heparin-derived oligosaccharides required relatively lower salt concentration for complete elution, and pools of larger oligosaccharides required higher salt concentration. The homogeneously sized pools and affinity-fractionated subpools of heparin-derived oligosaccharides were quantitatively assessed as inhibitors or enhancers of specific bFGF-mediated biological activities in five separate assay systems as follows: assay 1, to compete with human lymphoblastoid cells expressing syndecan (RO-12 UC cells) for binding to bFGF-coated wells (Ishihara, M., Tyrrell, D.J., Kiefer, M.C., Barr, P.J., and Swiedler, S.J. (1992) Anal. Biochem. 202, 310-315); assay 2, to inhibit 125I-bFGF binding to "low affinity sites" of adrenocortical endothelial (ACE) cells; assay 3, to inhibit bFGF-induced proliferation of ACE cells; assay 4, to support mitogenic activity of bFGF in a growth stimulation assay of chlorate-treated ACE cells; and assay 5, to enhance the in vitro interaction between 125I-bFGF and the recombinant extra-cellular domain of FGF high affinity receptor. The data derived from the five assay systems demonstrated that heparin-derived hexa- and octasaccharides inhibited the interaction between cell surface heparan sulfate proteoglycan and bFGF (assays 1 and 2) and bFGF-induced proliferation of ACE cells (assay 3) but were unable to enhance the binding of bFGF to its high affinity receptor in vitro (assay 5) or to support bFGF-induced mitogenesis in ACE cells (assay 4). These two activities required at least a decasaccharide with high affinity for bFGF.
Improved Biomaterials for Tissue Engineering Applications: Surface Modification of Polymers (2008)

Tissue engineering approaches that combine biomaterial-based scaffolds with protein delivery systems have provided a potential strategy for improved regeneration of damaged tissue. The success of polymeric scaffolds is determined by the response it elicits from the surrounding biological environment. This response is governed, to a large extent, by the surface properties of the scaffold. Surfaces of polymeric scaffolds have a significant effect on protein and cell attachment. Multiple approaches have been developed to provide micrometer to nanometer scale alterations in surface architecture of scaffolds to enable improved protein and cell interactions. Chemical modification of polymeric scaffold surfaces is one of the upcoming approaches that enables enhanced biocompatibility while providing a delivery vehicle for proteins. Similarly, physical adsorption, radiation mediated modifications, grafting, and protein modifications are other methods that have been employed successfully for alterations of surface properties of polymeric scaffolds. The goal of this review is to provide an overview of the role of surface properties /chemistry in tissue engineering and briefly discuss some of the methods of surface modification that can provide improved cell and protein interactions. It is hoped that these improved polymeric scaffolds will lead to accelerated and functional tissue regeneration.
Critical Closing Pressure Determined with a Model of Cerebrovascular Impedance (2012)

Critical closing pressure (CCP) is the arterial blood pressure (ABP) at which brain vessels collapse and cerebral blood flow (CBF) ceases. Using the concept of impedance to CBF, CCP can be expressed with brain-monitoring parameters: cerebral perfusion pressure (CPP), ABP, blood flow velocity (FV), and heart rate. The novel multiparameter method (CCPm) was compared with traditional transcranial Doppler (TCD) calculations of CCP (CCP1). Digital recordings of ABP, intracranial pressure (ICP), and TCD-based FV from previously published studies of 29 New Zealand White rabbits were reanalyzed. Overall, CCP1 and CCPm showed correlation across wide ranges of ABP, ICP, and PaCO2 (R=0.93, P<0.001). Three physiological perturbations were studied: increase in ICP (n=29) causing both CCP1 and CCPm to increase (P<0.001 for both); reduction of ABP (n=10) resulting in decrease of CCP1 (P=0.006) and CCPm (P=0.002); and controlled increase of PaCO2 (n=8) to hypercapnic levels, which decreased CCP1 and CCPm, albeit insignificantly (P=0.123 and P=0.306 respectively), caused by a spontaneous significant increase in ABP (P=0.025). Multiparameter mathematical model of critical closing pressure explains the relationship of CCP on brain-monitoring variables, allowing the estimation of CCP during cases such as hypercapnia-induced hyperemia, where traditional calculations, like CCP1, often reach negative non-physiological values.
Transgenic mouse models to study the role of the macrophage scavenger receptor class A in atherosclerosis. (2000)

Several in vivo studies have been performed on the role of the macrophage scavenger receptor class A (SR-A) in atherosclerosis using SR-A knockout mice. The results indicate both an antiatherogenic and a proatherogenic role of SR-A, depending on the nature of the animal model serving as the athero-susceptible background. To study the role of SR-A in a different model, we generated a transgenic mouse model with high level expression of the human SR-A gene using a 180 Kb yeast artificial chromosome (MSR1 transgenic mice). These mice show increased expression of SR-A according to the natural expression pattern. The MSR1 transgenic mice were crossed onto a low-density lipoprotein receptor deficient background and were fed a high fat diet for 10 weeks. After this period, the size of the atherosclerotic lesions in the proximal aorta was measured. Surprisingly, atherosclerosis was significantly reduced in the MSR1 transgenic mice. In a second study, the effect of SR-A was examined in APOE-3 Leiden mice providing a different athero-susceptible background. To exclude nonmacrophage effects, bone marrow was transplanted from MSR1 mice and wild-type littermates to APOE-3 Leiden transgenic mice. After 8 weeks on a high fat diet, atherosclerosis in the mice that had received MSR1 bone marrow was reduced compared with mice that had received wild-type bone marrow. This difference reached statistical significance when individual cholesterol exposure of the mice was taken into account. Both experiments indicated an antiatherogenic role of the SR-A. This observation cannot be explained easily by SR-A function in foam cell formation because in MSR1 macrophages in vitro foam cell formation is increased. Alternatively, however, SR-A may affect the activation of macrophages. Hence the response to lipopolysaccharide was measured in MSR1-transgenic macrophages. These macrophages showed a reduction in their activation in response to lipopolysaccharide, as measured by nitric oxide production. These data show that an elevated level of SR-A expression reduces atherosclerosis, potentially by modifying the response of macrophages to activation signals in the plaque.
The primary structure of ornithine aminotransferase (1986)

Tentative assignments of functional residues in rat liver mitochondrial ornithine aminotransferase have recently been made using the amino acid sequence deduced from a cDNA clone [(1985) J.Biol.Chem. 260, 12993-12997]. Partial sequences obtained using the pure mature protein demonstrate that one of these assignments, that of Lys 292 as the residue that binds the coenzyme pyridoxal phosphate, is correct. However, the identification of the Glu 34-Gln 35 bond as the site of post-translational proteolysis is in error. This cleavage occurs instead at Ala 25-Thr 26.
Primary Structure of Human Plasma Glutathione Peroxidase Deduced from eDNA Sequences1 (1990)

Human plasma glutathione peroxidase (GSHPx) has been shown to be a selenium-containing enzyme immunologically distinct from cellular GSHPx. Oligonucleotide probes, based on the partial amino acid sequence of plasma GSHPx, were synthesized and used to screen a human placenta cDNA library. Nucleotide sequence analysis of the obtained clones revealed that GSHPx consisted of a 678-base pair open reading frame coding for a 226-amino acid polypeptide with a Mr of 25,389. About 50% of the deduced amino acid sequence was confirmed by partial amino acid sequencing of the peptides in a lysine endopeptidase-digest of the purified enzyme. The amino acid sequence exhibited only 44% homology with that of human cellular GSHPx. Northern blot analysis revealed a single transcript of 2.2 kilobases in the poly(A)+ RNA fractions of human placenta and HepG2 (a human hepatic cell line), but not that of human liver and endothelial cells.
Integrating a medical database and advisory system (1991)

A system is described which incorporates the use of a diagnostic and treatment advice expert system into the routine information-handling functions of a surgical breast clinic. The main focus of the system is on identification and management of non-malignant breast disease. The advisor is linked with a clinical database which is used to hold summary case notes, and from which reports forming the basis for audit of case-mix and resource utilization can be produced. The system uses backward chaining of extended production rules and a relational database, and runs on a desktop microcomputer.