gebhart/patrepeval huggingface dataset:
An investigation of the effect of electrode size and electrode location on comfort during stimulation of the gastrocnemius muscle (2004)

The use of surface neuromuscular electrical stimulation (SNMES) in medicine is well established. However, discomfort has been identified as limiting the use of SNMES in these applications. This pilot study investigated the influence of various electrode sizes and their positioning on perceived pain and discomfort during neuromuscular electrical stimulation (NMES) of the gastrocnemius muscle using surface electrodes. This study formed part of a research project to develop a therapeutic device for calf muscle blood flow assist applications. Twelve healthy subjects (n=12) participated in this pilot study. Each participant attended the trial centre for testing which consisted of SNMES to four different electrode stimulation sites using two electrode sizes (round with areas 19.63 and 38.48 cm2). Comfort was assessed by asking the subjects to indicate the stimulation amplitude corresponding to the onset of discomfort (pain threshold) and the amplitude at which the discomfort became unbearable (pain tolerance). Of the four stimulation sites tested, two were deemed unsuccessful as it was very difficult to obtain a muscle contraction using these sites, while the remaining two sites elicited good muscle contraction. The most comfortable stimulation was achieved by placing the cathode electrode high on the calf, below the proximal end of the muscle heads and the anode electrode towards the end of the muscle belly and when the 19.63 cm2 electrodes were used at these sites (p=<0.001).
Simultaneous routing and buffer insertion for high performance interconnect (2002)

We present an algorithm for simultaneously finding a rectilinear Steiner tree T and buffer insertion points into T. The objective of the algorithm is to minimize a cost function (e.g., total area or power) subject to given timing constraints on the sinks of the net. An interesting side-effect of our approach is that we are able to derive an entire cost/delay tradeoff curve for added flexibility. The solutions produced by the algorithm are optimal subject to the constraint that the routing topology be induced by a permutation on the sinks of the net. We show that high quality sink permutations can be derived from a given routing structure such as the minimum spanning tree. This derivation provides an error bound on the minimum area solution induced by the permutation. The effectiveness of our algorithm is demonstrated experimentally.
A protein serologically and functionally related to the group C E3 14,700-kilodalton protein is found in multiple adenovirus serotypes (1990)

A 14.7-kilodalton protein (14.7K protein) encoded by the E3 region of group C adenoviruses has been shown to protect virus-infected fibroblasts from lysis by tumor necrosis factor (TNF) (L.R. Gooding, L.W. Elmore, A.E. Tollefson, H.A. Brady, and W.S.M. Wold, Cell 53:341-346, 1988). In this study we show that adenoviruses of other groups are also protected from TNF-induced cytolysis. Representative serotypes of groups A, B, D, and E produce a protein analogous to the 14.7K protein found in human group C adenoviruses. Deletion of this protein in group C viruses permits virus infection to induce cellular susceptibility to TNF killing. As with group C adenoviruses, cells infected with wild-type adenoviruses of other serotypes are not killed by TNF and are protected from lysis induced by TNF plus cycloheximide. However, cells are susceptible to TNF-induced lysis when infected with adenovirus type 4 mutants from which the 14.7K gene has been deleted. Although all known adenovirus serotypes infect epithelial cells, adenoviruses cause several diseases with various degrees of pathogenesis. Our findings suggest that the 14.7K protein provides a function required for the in vivo cytotoxicity of many adenoviruses independent of the site of infection or degree of pathogenesis.
Bacterial endotoxin : recognition and effector mechanisms : proceedings of the 2nd Congress of the International Endotoxin Society, Vienna, 17-20 August 1992 (1993)

Opening remarks Alois Nowotny 1922-1992 in memoriam - Professor J. Yuzuru Homma, MD (1919-1991) introduction to Professor Otto Westphal's opening address an old-timer's reflections on endotoxin. Part 1 LPS and lipid A biosynthesis, structure and conformation: the enzymatic synthesis of lipid A, C.R.H. Raetz crystallization and molecular structure of escherichia coli Re and K-12 lipopolysaccharides, N. Kato et al modelling the three-dimensional structure of lipopolysaccharide, M. Kastowsky session summary, S. Kusumoto and P. Kosma. Part 2 Role of endotoxin in bacterial infection: genetics and the study of the virulence properties of haemophilus influenza lipopolysaccharide, D.J. Maskell and E.R. Moxon molecular mimicry and host-modification of lipo-oligosaccharides, R.E. Mandrell bactericidal and endotoxin-neutralizing activities of the bactericidal/permeability-increasing protein and its bioactive N-terminal fragment, J. Weiss et al antibacterial and antiendotoxic actions and interactions of lipopolysaccharide antibodies and complement, M. Pollack et al persistence of LPS in cells and tissues - role of LPS recognition in reaction arthritis, K. Granfors session summary, P.H. Makela and L. Hinshaw. Part 3 Interactions of endotoxin with animal cells: LPS binding proteins, LPS and CD14 mediated activation of myeloid cells, P.S. Tobias et al novel plasma proteins that mediate the interaction of LPS with CD14, S.D. Wright interrelationship of LPS, pertussis toxin and the p73 LPS receptor on lymphoreticular cells, M.-G. Lei and C.D. Morrison the 70kDa peptidoglycan/lipopolysaccharide receptor, R. Dziarski CD14 - myeloid cell surface receptor involved in bacterial lipopolysaccharide recognition, V. Bail et al lipid A binding proteins in 70Z/3 cells, T.N. Kirkland and P.S. Tobias intracellular LPS-binding proteins and peptides found in limulus hemocytes, S. Iwanaga et al session summary (part 1), R.J. Ulevitch interferon-gamma, a mediator of infection-induced sensitization towards endotoxin, A. Freudenberg et a introduction to the 70Z/3 model system, C.H. Sibley the regulation of TNF production and endotoxin mitogenicity by lipoxygenases, F.U. Schade et al the purine analog, 2-methylthio-ATP(2-MeS-ATP), protects mice from endotoxic death, P.J. Berties et al LPS mimetic effects of taxol in LPS-inducible gene expression, glucocorticoid receptor expression and tyrosine phosphorylation in murine macrophages, S.N. Vogel et al. Part 4 Prevention and therapy of endotoxicosis - new approaches.
Catabolism of aromatic biogenic amines by Pseudomonas aeruginosa PAO1 via meta cleavage of homoprotocatechuic acid (1988)

Pseudomonas aeruginosa PAO1 catabolized the aromatic amines tyramine and octopamine through 4-hydroxyphenylacetic acid and 3,4-dihydroxyphenylacetic acid (HPA). meta ring cleavage was mediated by 3,4-dihydroxyphenylacetate 2,3-dioxygenase (HPADO), producing 2-hydroxy-5-carboxymethylmuconic semialdehyde (MSA). An NAD-dependent dehydrogenase caused the disappearance of the yellow MSA product, probably forming 2-hydroxy-5-carboxymethylmuconic acid. Induction studies with extracts from mutant cells indicated that the inducer of HPADO was HPA and/or MSA. Strains PAO1.221 (tynC1) and PAO1.303 (tynD1) have chromosomal mutations causing a deficiency in the activity necessary for conversion of 4-hydroxyphenylacetic acid to HPA. Genetic analyses showed that the mutations were in different loci. Strains PAO1.197 (tynE1) and PAO1.185 (tynF1) are deficient in HPADO and the NAD-dependent dehydrogenase, respectively. Plasmid pRO1853 was constructed by cloning approximately 7.3 kilobases of PAO1 chromosomal DNA into the BamHI site of the vector plasmid pRO1614. This recombinant plasmid complemented the tynD1, tynE1, and tynF1 mutations. A putative repressor-binding site involved in the regulation of HPADO synthesis was observed for a subcloned fragment of pRO1853. This recombinant plasmid, pRO1863, failed to complement tynE1 or tynF1 but still complemented tynD1. Another construct, pRO1887, contained 9.2 kilobases of PAO1 chromosomal DNA inserted in the PstI site of the vector pRO1727. Plasmid pRO1887 complemented only the tynC1 mutation. Mapping experiments performed with the chromosome-mobilizing plasmid R68.45 located the mutations described above in a cluster at about 35 to 40 min of the PAO1 chromosome map. The mutations were linked to the proA, thr-48, lys-9015, argF10, and argG markers.
Polyhalogenoaromatic compounds. Part 42. 13C N.m.r. spectra of polyhalogeno-pyridines and -pyrimidines (1980)

B. Iddon, A. G. Mack, H. Suschitzky, J. A. Taylor and B. J. Wakefield, J. Chem. Soc., Perkin Trans. 1, 1980, 1370 DOI: 10.1039/P19800001370
A 220 mW 1 Gb/s 1024-bit rate-1/2 low density parity check code decoder (2002)

A 1024 bit rate-1/2 Low Density Parity Check (LDPC) code decoder has been implemented that matches the coding gain of equivalent turbo codes. The parallel decoder architecture supports throughputs up to 1 Gb/s and convergence in the decoding algorithm translates into extremely low switching activity with power dissipation under 220 mW.
Mitochondrial dysfunction in ataxia-telangiectasia (2011)

Ataxia-telangiectasia mutated (ATM) plays a central role in DNA damage responses, and its loss leads to development of T-cell malignancies. Here, we show that ATM loss also leads to intrinsic mitochondrial abnormalities in thymocytes, including elevated reactive oxygen species, increased aberrant mitochondria, high cellular respiratory capacity, and decreased mitophagy. A fraction of ATM protein is localized in mitochondria, and it is rapidly activated by mitochondrial dysfunction. Unexpectedly, allelic loss of the autophagy regulator Beclin-1 significantly delayed tumor development in ATM-null mice. This effect was not associated with rescue of DNA damage signaling but rather with a significant reversal of the mitochondrial abnormalities. These data support a model in which ATM plays direct roles in modulating mitochondrial homeostasis and suggest that mitochondrial dysfunction and associated increases in mitochondrial reactive oxygen species contribute to the cancer-prone phenotype observed in organisms lacking ATM. Thus, ataxia-telangiectasia should be considered, at least in part, as a mitochondrial disease.
Human neutrophil lipocalin, a highly specific marker for acute exacerbation in cystic fibrosis (1999)

Cystic fibrosis (CF) is characterized by the production of abnormally thick secretions in the airways, chronic bacterial endobronchial infections and a chronic, predominantly neutrophilic inflammatory response. Therefore, myeloperoxidase (MPO) and lactoferrin are frequently used as inflammatory markers. Recently, a new protein in the neutrophil granules, human neutrophil lipocalin (HNL) has been discovered. The aim of the present study was to investigate HNL in sera of patients with CF and its relation to MPO and lactoferrin as well as to acute pulmonary exacerbation. Serum concentrations of HNL, MPO and lactoferrin were determined in 42 patients with CF and in 25 healthy subjects. Patients with CF were divided into groups with and without acute pulmonary exacerbation (APE) and also with and without colonization with Pseudomonas aeruginosa (Pa). Median serum levels of HNL (200.5 microg x L(-1)), MPO (595 microg x L(-1)) and lactoferrin (1,356.5 microg x L(-1)) were significantly increased in patients with CF compared to control subjects (57.7, 178 and 478 microg x L(-1), respectively; p<0.0001). CF patients with APE had significantly increased serum concentrations of HNL (321 versus 97.7 microg x L(-1); p<0.0001), MPO (1,125 versus 300 microg x L(-1); p<0.005) and lactoferrin (4,936 versus 980 microg x L(-1); p<0.001) compared with patients in stable clinical condition. Similarly, patients colonized with Pa had significantly higher concentrations of HNL, MPO and lactoferrin than Pa negative patients. These results indicate that in patients with cystic fibrosis, serum concentrations of human neutrophil lipocalin are markedly increased with a strong relationship to myeloperoxidase and lactoferrin. Thus, determination of serum human neutrophil lipocalin concentrations may be another useful diagnostic tool to monitor neutrophil inflammation in cystic fibrosis. The more marked difference in human neutrophil lipocalin compared with myeloperoxidase concentrations with no overlap between patients with acute pulmonary exacerbation and those in stable condition even suggests that human neutrophil lipocalin may be a more sensitive and specific discriminator.
Redesign of Retrovirus Packaging Cell Lines To Avoid Recombination Leading to Helper Virus Production (1986)

Retrovirus vectors can be made in the absence of helper virus by using retrovirus packaging cell lines. Helper-free virus is critical for a variety of gene transfer studies. The most useful packaging cell lines contain helper virus DNA from which the signal required for packaging of the viral RNA genome into virions has been deleted. However, we showed that the ability to package virus is conferred at very low frequency to cells infected with virus from these packaging cell lines, presumably by low-frequency transmission of the deleted virus genome. In addition, these packaging cell lines can interact with some retroviral vectors to yield replication-competent virus. We constructed packaging cell lines containing helper virus DNA that had several alterations in addition to deletion of the packaging signal. The new packaging cells retained the useful features of previously available lines but did not yield helper virus after introduction of any of the vectors tested, and transfer of the packaging function was not detected.
Infectious Bronchitis Virus Field Vaccination Coverage and Persistence of Arkansas-Type Viruses in Commercial Broilers (2009)

To determine the coverage of infectious bronchitis virus (IBV) vaccine field boost in commercial broilers, estimate the relative amount of vaccine virus in the trachea, and follow the clearance of the vaccine, we collected approximately 100 tracheal swabs at various times postvaccination from 10 different flocks and used real-time reverse transcriptase-PCR (RT-PCR) to detect the virus. This allowed us to detect vaccine virus in as few as 3% of the birds in a flock of 20,000 birds with a 95% confidence level. We found that the number of birds positive for IBV vaccine following vaccination in the field resembled a parabolic-shaped curve that peaked around 14 days postvaccination, or it resembled a sinusoidal-type wave with a frequency of about 2 wk. The patterns did not appear to correlate with water or spray vaccination methods, nor did they correlate with the type of backpack sprayer used. The highest number of positive birds in a flock ranged from 66% to 100%. The viral genome copies in the tracheal swabs, as determined by real-time RT-PCR, ranged from 1 x 10(2.6)/ml to 1 x 10(5.2)/ml and, in most studies, had a positive correlation with the number of birds positive for vaccine virus in the flock. On the last sample day of each study, 21, 28, or 35 days postvaccination, from 12% to 66% of the birds were still positive for vaccine virus, and although different IBV vaccine types were used in each study, only Arkansas vaccine virus was identified in selected samples on those days. Arkansas vaccine virus was also the only virus identified in selected samples at 1, 3, and 5 days postvaccination, clearly indicating that Arkansas vaccine virus is persisting in the birds. Protection studies conducted on birds vaccinated with Arkansas- and Delaware-type vaccines and removed from the field at 21 days postvaccination showed complete protection against challenge with Delaware (except for one bird), whereas protection against Arkansas challenge was between 37.5% and 62.5%. Our findings show that introduction of IBV vaccines into a commercial broiler flock do not necessarily follow a seemingly logical pattern of a high number of birds infected followed by clearance from the trachea, but resembled either a parabolic curve or a sinusoidal-type wave. In addition, Arkansas vaccine viruses are clearly persisting in commercial broilers, which may be because of incomplete protection observed for that IBV type.
In vivo cloning of artificial DNA nanostructures (2008)

Mimicking nature is both a key goal and a difficult challenge for the scientific enterprise. DNA, well known as the genetic-information carrier in nature, can be replicated efficiently in living cells. Today, despite the dramatic evolution of DNA nanotechnology, a versatile method that replicates artificial DNA nanostructures with complex secondary structures remains an appealing target. Previous success in replicating DNA nanostructures enzymatically in vitro suggests that a possible solution could be cloning these nanostructures by using viruses. Here, we report a system where a single-stranded DNA nanostructure (Holliday junction or paranemic cross-over DNA) is inserted into a phagemid, transformed into XL1-Blue cells and amplified in vivo in the presence of helper phages. High copy numbers of cloned nanostructures can be obtained readily by using standard molecular biology techniques. Correct replication is verified by a number of assays including nondenaturing PAGE, Ferguson analysis, endonuclease VII digestion, and hydroxyl radical autofootprinting. The simplicity, efficiency, and fidelity of nature are fully reflected in this system. UV-induced psoralen cross-linking is used to probe the secondary structure of the inserted junction in infected cells. Our data suggest the possible formation of the immobile four-arm junction in vivo.
The interaction of beta 2‐microglobulin (β2m) with mouse class I major histocompatibility antigens and its ability to support peptide binding. A comparison of human and mouse β2m (1995)

The function of major histocompatibility complex (MHC) class I molecules is to sample peptides derived from intracellular proteins and to present these peptides to CD8+ cytotoxic T lymphocytes. In this paper, biochemical assays addressing MHC class I binding of both peptide and beta 2-microglobulin (beta 2m) have been used to examine the assembly of the trimolecular MHC class I/beta 2m/peptide complex. Recombinant human beta 2m and mouse beta 2ma have been generated to compare the binding of the two beta 2m to mouse class I. It is frequently assumed that human beta 2m binds to mouse class I heavy chain with a much higher affinity than mouse beta 2m itself. We find that human beta 2m only binds to mouse class I heavy chain with slightly (about 3-fold) higher affinity than mouse beta 2m. In addition, we compared the effect of the two beta 2m upon peptide binding to mouse class I. The ability of human beta 2m to support peptide binding correlated well with its ability to saturate mouse class I heavy chains. Surprisingly, mouse beta 2m only facilitated peptide binding when mouse beta 2m was used in excess (about 20-fold) of what was needed to saturate the class I heavy chains. The inefficiency of mouse beta 2m to support peptide binding could not be attributed to a reduced affinity of mouse beta 2m/MHC class I complexes for peptides or to a reduction in the fraction of mouse beta 2m/MHC class I molecules participating in peptide binding. We have previously shown that only a minor fraction of class I molecules are involved in peptide binding, whereas most of class I molecules are involved in beta 2m binding. We propose that mouse beta 2m interacts with the minor peptide binding (i.e. the "empty") fraction with a lower affinity than human beta 2m does, whereas mouse and human beta 2m interact with the major peptide-occupied fraction with almost similar affinities. This would explain why mouse beta 2m is less efficient than human beta 2m in generating the peptide binding moiety, and identifies the empty MHC class I heavy chain as the molecule that binds human beta 2m preferentially.
DNA-Binding Proteins (1983)

The structures of three proteins that regulate gene expression have been determined recently and suggest how these proteins may bind to their specific recognition sites on the DNA. One protein (Cro) is a repressor of gene expression, the second (CAP) usually stimulates gene expression, and the third (lambda repressor) can act as either a repressor or an activator. The three proteins contain a substructure consisting of two consecutive alpha helices that is virtually identical in each case. Structural and amino acid sequence comparisons suggest that this bihelical fold occurs in a number of proteins that regulate gene expression, and is an intrinsic part of the DNA-protein recognition event. The modes of repression and activation by Cro and lambda repressor are understood reasonably well, but the mode of action of CAP is still unclear.
Transfection of the Escherichia coli nth Gene into Radiosensitive Chinese Hamster Cells: Effects on Sensitivity to Radiation, Hydrogen Peroxide, and Bleomycin Sulfate (1992)

The Escherichia coli nth gene encodes endonuclease III, which catalyses the glycolytic removal of various oxidized thymine residues from DNA. A truncated version of nth, with the prokaryotic regulatory sequences removed, was ligated into the retrovirus-based vector pZipneoSV(X)1 and transfected into the radiosensitive Chinese hamster ovary cell line, xrs7. Following selection with G418, two clones (x7nth1 and x7nth6) were shown by Southern analysis to contain the nth gene. No substantial difference in gamma-ray sensitivity was detected between xrs7, clones x7nth1 and x7nth6, and the parent vector transfected clone (x7neo1). However, clones containing the nth gene were more resistant to hydrogen peroxide cytotoxicity [D0's for x7nth1 and x7nth6 were 0.072 microgram/ml (4 microM) and 0.046 microgram/ml, respectively, compared with D0's of 0.034 and 0.027 microgram/ml for xrs7 and x7neo1, respectively] but markedly more sensitive to bleomycin sulfate cytotoxicity than xrs7 and x7neo1 (e.g., 1D0's for x7nth6 and xrs7 were 0.05 and 0.12 microgram/ml, while 2D0's for x7nth1 and xrs7 were 0.35 and 0.48 microgram/ml, respectively). Alterations in sensitivity to hydrogen peroxide and bleomycin sulfate could not be explained by differences in the distribution of the cell-cycle phases and growth rate of nth-containing clones and control cell lines. These results are consistent with the hypothesis that modified thymine lesions are potentially cytotoxic. Hence, when cells incur a high level of endonuclease III-repairable damage relative to strand breakage, such as after treatment with hydrogen peroxide, increased repair capacity increases survival. Gamma radiation produces a lower level of endonuclease III-repairable damage relative to all the other types of lesions produced; hence increased repair capacity has no measurable effect on cell survival. The increased sensitivity of x7nth1 and x7nth6 to bleomycin sulfate toxicity may indicate that, when thymine damage and single-strand breaks are in close proximity on opposite strands of the DNA, endonuclease III, which incises DNA at the site of damaged residues, can increase the number of double-strand breaks and hence decrease the level of cell survival.