gebhart/patrepeval huggingface dataset:
Effect of tilt angle of tablet on pen-based input operation based on Fitts' law (2010)

Current studies on tablets and digital pens mainly focus on the modalities of input in the field of HCI (human computer interaction). However, the effect of the changes of environmental parameters on pen-based input operation, such as tilt angle of tablet, has rarely been studied. This paper mainly investigates (1) how pen-based input operation is affected while changing tilt angle of tablet (2) at which tilt angle of tablet, can user do pen-based input operation with comfort, quickness, and accuracy. The conclusions can be got based on the results from the experiments and questionnaire. In order to compare penbased input operation among different tilt angle of tablet (0, 15, 30, 45 and 60 degrees), two experiments of 1-dimensional and 2-dimensional pointing tasks based on Fitts' law were conducted. Results show that when tilt angle of tablet is 30 degrees, it is most suitable for user to do pen-based input operation.
A Wireless-Implantable Microsystem for Continuous Blood Glucose Monitoring (2009)

A remotely powered implantable microsystem for continuous blood glucose monitoring is presented. The microsystem consists of a microfabricated glucose biosensor flip-chip bonded to a transponder chip. The transponder chip is inductively powered by an external reader with a 13.56-MHz carrier. It then measures the output signal of the glucose biosensor and transmits the measured data back to the external reader using load-shift keying (LSK). The microsystem has a volume of 32 mm(3). The procedures for the microfabrication of the glucose sensor and the assembly of the microsystem are described along with the description of the circuit blocks of the transponder chip. The transponder chip has been fabricated with the TSMC 0.18-mum CMOS process and has a total area of 1.3 x 1.3 mm(2). The chip can measure the sensor output current ranging from 1 nA to 1 muA with less than 0.3% nonlinearity error, provided that the amplitude of the received RF signal is higher than 2.6 V; the circuit consumes a total current of about 110 muA.
Regarding the Mechanism of Olefin Metathesis with Sol−Gel-Supported Ru-Based Complexes Bearing a Bidentate Carbene Ligand. Spectroscopic Evidence for Return of the Propagating Ru Carbene (2005)

Two isotopically and structurally labeled Ru-based carbenes (2-d4 and 13) have been prepared and attached to the surface of monolithic sol-gel glass. The resulting glass-supported complexes (18-dn and 19) exhibit significant catalytic activity in promoting olefin metathesis reactions and provide products of high purity. Through analysis of the derivatized glass pellets used in a sequence of catalytic ring-closing metathesis reactions mediated by various supported Ru carbenes, it is demonstrated that free Ru carbene intermediates in solution can be scavenged by support-bound styrene ether ligands prior to the onset of competing transition metal decomposition. The observations detailed herein provide rigorous evidence that the initially proposed release/return mechanism is, at least partially, operative. The present investigations shed light on a critical aspect of the mechanism of an important class of Ru-based metathesis complexes (those bearing a bidentate styrene ether ligand).
Polymer phosphorescent light-emitting devices doped with tris(2-phenylpyridine) iridium as a triplet emitter (2000)

We have fabricated phosphorescent polymer light-emitting devices with tris(2-phenylpyridine) iridium [Ir(ppy)3] as a triplet emissive dopant in poly(vinylcarbazole) (PVK) host. The device with 8% doping concentration of [Ir(ppy)3] in PVK showed the external quantum efficiency of 1.9% and the peak luminance of 2,500 cd/m2. The emission spectrum of the device exhibited no emission from PVK, indicating that the energy transfer from PVK to [Ir(ppy)3] is efficient. This work demonstrates that efficient electrophosphorescent light-emitting devices can be realized with polymers.
Surface Expression of a Protective Recombinant Pertussis Toxin S1 Subunit Fragment in Streptococcus gordonii (1999)

In this study, the expression of the Bordetella pertussis S1 subunit was tested in Streptococcus gordonii, a commensal oral bacterium which has the potential to be a live oral vaccine vehicle. The DNA fragment encoding the N-terminal 179 amino acids of the S1 subunit was ligated into the middle part of spaP, the surface protein antigen P1 gene originating from Streptococcus mutans. The resulting construct, carried on the Escherichia coli-Streptococcus shuttle vector pDL276, was introduced into S. gordonii DL-1 by natural transformation. One of the transformants (RJMIII) produced a 187-kDa protein (the predicted size of the SpaP-S1 fusion protein) which was recognized by both the anti-pertussis toxin (anti-PT) and anti-SpaP antibodies, suggesting that an in-frame fusion had been made. Results from immunogold-electron microscopic studies and cellular fractionation studies showed that the fusion protein was surface localized and was mainly associated with the cell wall of RJMIII, indicating that SpaP was able to direct the fusion protein to the cell surface. A rabbit antiserum raised against heat-killed S. gordonii RJMIII recognized the native S1 subunit of PT in Western blotting and showed a weak neutralization titer to PT by the Chinese hamster ovary cell-clustering assay. BALB/c mice immunized with the heat-killed S. gordonii RJMIII were protected from the toxic effect of PT in the leukocytosis-promoting and histamine sensitization assays. In conclusion, a fragment of the S1 subunit of PT was successfully surface expressed in S. gordonii; the recombinant S1 fragment was found to be immunogenic and could induce protection against the toxic effect of PT in mice.
Adjuvants (1990)

In summary, HIV vaccine studies described have generally not been designed to measure the effect of the adjuvant or to make comparisons between adjuvants. In only one study was a head-to-head comparison made between HIV antigen alone and antigen formulated with different adjuvants. We hope that future experiments with HIV/SIV vaccine candidates will be designed to determine the relative potency and safety of different adjuvants. Unfortunately, such experiments tend to be tedious and expensive. The design of these studies will need to address a number of variables which influence the response to the vaccine, including route and schedule of immunization, genotype and species of the vaccinated subject, and intrinsic characteristics of the antigen. In addition, the immunologic endpoints should include measurement of both B and T cell function. The carrier/adjuvant/antigen formulation should be hand-tailored and then standardized so that it is manufactured reproducibly without producing different biological effects between lots, and the vaccine formulation should be stable on storage and shipping. Finally, we obviously need to identify and test the protective antigen or antigens. The best adjuvant will never correct the choice of the wrong epitope.
Cytochrome P450 active site plasticity: attenuation of imidazole binding in cytochrome P450cam by an L244A mutation (2006)

We have identified a P450(cam) mutation, L244A, that mitigates the affinity for imidazole and substituted imidazoles while maintaining a high affinity for the natural substrate camphor. The P450(cam) L244A crystal structure solved in the absence of any ligand reveals that the I-helix is displaced inwards by over 1 A in response to the cavity created by the change from leucine to alanine. Furthermore, the crystal structures of imidazole-bound P450(cam) and the 1-methylimidazole-bound P450(cam) L244A mutant reveal that the ligands have distinct binding modes in the two proteins. Whereas in wild-type P450(cam) the imidazole coordinates to the iron in an orientation roughly perpendicular to the plane of the heme, in the L244A mutant the rearranged I helix, and specifically residue Val247, forces the imidazole into an orientation almost parallel to the heme that impairs its ability to coordinate to the heme iron. As a result, the imidazole is much more weakly bound to the mutant than it is to the wild-type enzyme. Despite the constriction of the active site by the mutation, previous work with the L244A mutant has shown that it oxidizes larger substrates than the wild-type enzyme. This paradoxical situation, in which a mutation that nominally increases the active site cavity appears to decrease it, suggests that the mutation actually increases the active site maleability, allowing it to better expand to oxidize larger substrates.
[Calcium in the prevention of stress ulcer in the rat]. (1976)

Calcium gluconate, carbonate, and lactate are potent antiulcerogenic agents when administered intragastrically at pH 6.3 by sustained infusion (45 mg/kg/8 h). In intact rats, by radioimmunologically measurable serum, gastrin and calcitonin are inversely correlated, whereas gastrin and ulcer index tend to correlate directly. The findings imply a key role for thyroid-releasable endogenous calcitonin in this disorder.
Disrupting bacterial spores and cells using ultrasound applied through a solid interface (2003)

DNA sample processing cartridges that perform cell lysis using ultrasound require a sonication chamber with a wall, or interface, for the transfer of ultrasonic energy to the solution. The interface must present matched impedance to the transfer of energy, yet also provide a barrier to safely contain potential hazardous biological material. The use of a thin but solid polymeric interface was studied using interfaces with a range of frequency response characteristics to the ultrasonic excitation. Measurements of ultrasonically generated acoustic pressure, visual images of cavitation, and measurements of released nucleic acid from sonicated bacterial spores and cells were used to determine the parameters for optimum transfer of ultrasound. Data and theory presented show that cell lysis is a function of the natural frequency of the interface, the preload force between the interface and the ultrasonic transducer, and the amplitude of the transducer.
Software Architecture Documentation in Practice: Documenting Architectural Layers (2000)

This report represents the first milestone of a work in progress. That work is a comprehensive handbook on how to produce high-quality documentation for software architectures. The handbook, tentatively entitled Software Architecture Documentation in Practice, will be published in mid- to late-2000 by Addison Wesley Longman as a book in the SEI series on software engineering. Aimed squarely at the practitioner, the handbook is intended to fill a gap in the literature: There is a complete lack of language-independent guidance about how to actually capture an architecture in written form so that it can fulfill its purpose as a communication vehicle providing a unified design vision to all of the varied stakeholders of a development project. The theme of the work is that documenting an architecture entails documenting the set of relevant views of that architecture, and then completing the picture with documentation of information that transcends any single view. The report lays out our approach and organization for the complete book, and provides full guidance for one of the most commonly used architectural views: the layer diagram. The audience for this book is the community of practicing architects, apprentice architects, and developers who are on the receiving end of architectural documentation.
RAPID DETERMINATION OF CARBOXYHEMOGLOBIN BY ABSORBANCE DIFFERENCE BETWEEN DOUBLE WAVE LENGTH (1980)

A spectrophotometric determination of CO-Hb content was investigated on the basis of double wavelength spectrophotometry. Absorbance differences at the two wavelengths at which O2-Hb has the same absorbance reflect only the CO-Hb component because the O2-Hb component is nulled out from the mixture of O2-Hb and CO-Hb. After measurement of absorbance difference, the measuring solution was saturated with pure CO and remeasured. CO-Hb % was calculated from the ratio of the absorbance differences. Since temperature significantly influences the spectrum of hemoglobin pigment, the wavelength pair changed with temperature. For accurate measurement, it was necessary to control temperature of diluting solution before dilution. Liberation of CO fro CO-Hb was observed at more than 80% CO-Hb, and 5% and 2% liberation from 100% CO-Hb occured at 100-fold dilution with 10 mm cuvette and 20-fold dilution with 2 mm cuvette respectively. Advantages of this method are that the standard curve or equation for calculation and accurate dilution are not necessary because the interfering component is nulled out and 100% CO-Hb of the standard sample is made with the same sample; and measurement is very rapid, taking less than 2 min.
A Study of the Electrical Bio-impedance of Tumors (1993)

A new system of impedance measurement over a frequency range of 0 to 200 kHz was developed by a three-electrode method. In this study, the electrical impedances of various tumors were measured in vivo in 54 patients with breast disease (31 breast cancers, 13 fibroadenomas, and 10 fibrocystic diseases) and 57 patients with pulmonary disease (44 lung cancers, 5 metastatic pulmonary tumors, 4 pulmonary tuberculoses, and 4 organized pneumonias). On the basis of those impedance measurements and the equivalent circuits in vivo, we calculated the extracellular resistance (Re), intracellular fluid resistance (Ri), and cell membrane capacitance (Cm) in tissues, all of which were compared among the various diseases. It was found that Re and Ri were significantly higher in breast cancers than in benign tumors and normal breast tissues and that Cm was significantly lower in breast cancers than in other tissues. On the other hand, Re and Ri were significantly higher, and Cm was significantly lower, in normal lung tissues than in pulmonary masses. Re and Ri were significantly higher, and Cm was significantly lower, in malignant tumors than in organized pneumonias. The results showed that these parameters (Re, Ri, and Cm) exhibit significant differences among various tissues and tumors, suggesting possible applications in tumor diagnosis.
The ELDer project (2000)

The ELDeR (Enhanced Living through Design Research) Project, comprised of a team of designers and behavioral scientists, conducted a four-month study at a seniors community near Pittsburgh, PA. The purpose of the project was to understand the experiences of elders and their caregivers in order to: 1) study the eldercare experience from the perspective of primary stakeholders; 2) to assess the importance of psychological and social factors in the eldercare experience; and 3) to identify implications for product, interface, and interaction design and opportunities for new products and technologies. Our findings show that social, emotional, and environmental factors play a key role in the eldercare experience and the adoption and use of new products. We argue that designing eldercare technologies to address all of these factors lowers social and economic barriers to universal usability.
Small Molecule Modulation of p75 Neurotrophin Receptor Functions (2008)

Ligand-independent and/or proNGF-induced p75(NTR) signaling has emerged as a potential major contributor to a number of pathological states, including axotomy-induced death, motor neuron degeneration, neuronal degeneration in Alzheimer's disease and oligodendrocyte death following spinal cord injury. A long standing goal in the neurotrophin field has been the development of non-peptide, small molecules capable of functioning as specific ligands at neurotrophin receptors such as p75(NTR) to promote desired biological outcomes. Synthetic peptides modeled on neurotrophin protein domains have been found to bind to and activate various neurotrophin receptors, raising the possibility that active, non-peptide, small molecule ligands might also be identified; however, traditional high-throughput screening approaches have been largely ineffective in identifying such compounds. Using pharmacophores derived from the structure of loop 1 of nerve growth factor, non-peptide, small molecules that function as p75(NTR) ligands to promote survival and block proNGF-induced death have recently been identified. Small molecule p75(NTR) ligands, with high potency and specificity, may provide novel therapeutic approaches for neurodegenerative diseases, neurotrauma and other pathologic states.
VEGF increases retinal vascular ICAM-1 expression in vivo. (1999)

VEGF increases retinal vascular ICAM-1 expression. VEGF-induced increases in ICAM-1 may promote retinal leukostasis in diabetic eyes.
Lattice quantization with side information (2002)

We consider the design of lattice vector quantizers for the problem of coding Gaussian sources with uncoded side information available only at the decoder. The design of such quantizers can be reduced to the problem of finding an appropriate sublattice of a given lattice codebook. We study the performance of the resulting quantizers in the limit as the encoding rate becomes high, and we evaluate these asymptotics for three lattices of interest: the hexagonal lattice A/sub 2/, the Gosset lattice E/sub 8/, and the Leech lattice /spl Lambda//sub 24/. We also verify these asymptotics numerically, via computer simulations based on the lattice A/sub 2/. Surprisingly, the lattice E/sub 8/ achieves the best performance of all cases considered.
MUC1 Oncoprotein Blocks Glycogen Synthase Kinase 3β–Mediated Phosphorylation and Degradation of β-Catenin (2005)

Dysregulation of beta-catenin is of importance to the development of diverse human malignancies. The MUC1 oncoprotein is aberrantly overexpressed by most human carcinomas and associates with beta-catenin. However, the functional significance of the MUC1-beta-catenin interaction is not known. Here, we show that MUC1 increases beta-catenin levels in the cytoplasm and nucleus of carcinoma cells. Previous studies have shown that glycogen synthase kinase 3beta (GSK3beta) phosphorylates beta-catenin and thereby targets it for proteosomal degradation. Consistent with the up-regulation of beta-catenin levels, our results show that MUC1 blocks GSK3beta-mediated phosphorylation and degradation of beta-catenin. To further define the interaction between MUC1 and beta-catenin, we identified a serine-rich motif (SRM) in the MUC1 cytoplasmic domain that binds directly to beta-catenin Armadillo repeats. Mutation of the SRM attenuated binding of MUC1 to beta-catenin and MUC1-mediated inhibition of beta-catenin degradation. Importantly, disruption of the MUC1-beta-catenin interaction with the SRM mutant also attenuated MUC1-induced anchorage-dependent and -independent growth and delayed MUC1-mediated tumorigenicity. These findings indicate that MUC1 promotes transformation, at least in part, by blocking GSK3beta-mediated phosphorylation and thereby degradation of beta-catenin.
Synergy of interleukin 3 and tumor necrosis factor alpha in stimulating clonal growth of acute myelogenous leukemia blasts is the result of induction of secondary hematopoietic cytokines by tumor necrosis factor alpha. (1992)

Colony growth of leukemic colony-forming units (L-CFU) obtained from patients with primary acute myelogenous leukemia stimulated with recombinant human interleukin 3 (rh IL-3) is significantly potentiated when recombinant human tumor necrosis factor alpha (rh TNF-alpha) is present in cultures. The costimulatory activity of tumor necrosis factor (TNF) alpha is dose dependent and maximum at TNF-alpha concentrations of 10 ng/ml. At high density, L-CFU proliferatively respond to TNF-alpha stimulation in the absence of exogenous rh IL-3. Studies of the mechanism of action of rh TNF-alpha on acute myelogenous leukemia L-CFU growth suggest that TNF-alpha acts by inducing release of growth stimulatory hematopoietic cytokines by the leukemic cells themselves, including IL-1 alpha, IL-1 beta, Granulocyte-macrophage colony-stimulating factor (CSF), granulocyte CSF, and IL-6. Treatment of L-CFU cultures, with neutralizing antibodies to IL-1 alpha, IL-1 beta, granulocyte-macrophage CSF, granulocyte CSF, and IL-6 to eliminate the endogenous source of these factors is associated with significant inhibition of the synergistic interplay of TNF-alpha and IL-3.
Effects of NO on mitochondrial function in cardiomyocytes: Pathophysiological relevance (2006)

Although the specific roles of nitric oxide (NO) in the heart in general and on cardiac mitochondria in particular remain controversial, it is now clear that both endogenous and exogenous sources of NO exert important modulatory effects on mitochondrial function. There is also growing evidence that NO can be produced within the mitochondria themselves. NO can influence respiratory activity, both through direct effects on the respiratory chain or indirectly via modulation of mitochondrial calcium accumulation. At pathological concentrations, NO can cause irreversible alterations in respiratory function and can also interact with reactive oxygen species (ROS) to form reactive nitrogen species, which may further impair mitochondrial respiration and can even lead to opening of the mitochondrial permeability transition pore and cell death. Diabetes, aging, myocardial ischemia, and heart failure have all been associated with altered ROS generation, which can alter the delicate regulatory balance of effects of NO in the mitochondria. As NO competes with oxygen at cytochrome oxidase, it can be argued that experiments exploring the roles of NO on mitochondrial respiration should be performed at physiological (i.e. relatively low) oxygen tensions. Improvements in techniques, and a gradual appreciation of the many potential pitfalls in studying mitochondrial NO, are leading to a recognition of the role of NO in the regulation of mitochondrial function in the heart in health and disease.
pH-Induced Fusion and Lysis of Phosphatidylcholine Vesicles by the Hydrophobic Polyelectrolyte Poly(2-ethylacrylic Acid) (1999)

Poly(2-ethylacrylic acid) [PEAA] was shown to induce fusion of phosphatidylcholine bilayer membranes under mildly acidic conditions. The pH-dependent destabilization and fusion of extruded large unilamellar vesicles (LUVs) by PEAA was characterized by optical density measurements, transmission electron microscopy, and lipid-mixing and contents-release assays. Reduction of either the chain length or the polymer concentration caused the fusion and contents-release events to shift to lower pH values. Release of entrapped calcein was observed at pH values approximately 1 unit higher than those found to cause membrane fusion. Decreased levels of fusion were observed when the concentration of PEAA was lower than that of the lipid; however, quantitative release of encapsulated calcein could be effected at very low polymer concentrations (∼3% w/w PEAA/lipid).