gebhart/patrepeval huggingface dataset:
ASTS: An Agile Secure Time Synchronization Protocol for Wireless Sensor Networks (2007)

Time synchronization is a crucial mechanism for wireless sensor networks, so it is a natural target of the adversaries. Errors in data aggregation and failures of other mechanisms will happen as a result of imprecise time synchronization. The well-known mu TESLA protocol can be employed to authenticate broadcast packets in secure time synchronization mechanisms. Unfortunately, nodes and base station should be loosely synchronized for mu TESLA to function. It appears to be a dilemma that time synchronization is required to achieve time synchronization. A separate synchronization mechanism is employed in some other scheme just to escape from such a dilemma. It is shown in this paper that it is NOT necessary to assist mu TESLA with any separate mechanism. Shaking off an unnecessary burden, we propose ASTS (agile secure time synchronization), a much more lightweight scheme. We build an experiment network with 32 mica2 motes to evaluate the performance of ASTS. It is shown that the synchronization error of ASTS is as low as several microseconds, matching the best possible time synchronization protocols.
Cyclosporine therapy after cardiac transplantation causes hypertension and renal vasoconstriction without sympathetic activation. (1993)

CyA therapy causes acute renal vasoconstriction without accompanying systemic hemodynamic effects. These renal effects are nonneural, not being attributable to sympathoexcitation.
MDM2 Suppresses p73 Function without Promoting p73 Degradation (1999)

The newly identified p53 homolog p73 can mimic the transcriptional activation function of p53. We investigated whether p73, like p53, participates in an autoregulatory feedback loop with MDM2. p73 bound to MDM2 both in vivo and in vitro. Wild-type but not mutant MDM2, expressed in human p53 null osteosarcoma Saos-2 cells, inhibited p73- and p53-dependent transcription driven by the MDM2 promoter-derived p53RE motif as measured in transient-transfection and chloramphenicol acetyltransferase assays and also inhibited p73-induced apoptosis in p53-null human lung adenocarcinoma H1299 cells. MDM2 did not promote the degradation of p73 but instead disrupted the interaction of p73, but not of p53, with p300/CBP by competing with p73 for binding to the p300/CBP N terminus. Both p73alpha and p73beta stimulated the expression of the endogenous MDM2 protein. Hence, MDM2 is transcriptionally activated by p73 and, in turn, negatively regulates the function of this activator through a mechanism distinct from that used for p53 inactivation.
Studies on Catalysis in Partial Oxidation of Methane to Syngas(I)──Performance and Characterization of Ni-based Catalysts (1996)

Highly active and selective Ni-based catalysts for partial oxidation of methane (POM) to syngas (CO/H,) have been studied and developed. Spectroscopic characterization by XRD, XPS, EPR, etc. demonstrated that under the POM reaction conditions, the Ni-components of the catalysts investigated were reduced and enriched on the surface to form metallic Ni0-phase. A comparative study of the first series of transition-metals showed that only Ni and Co have a high POM activity and selectivity, whereas the others (including Mn, Fe, Cu, etc. ) give mainly complete combustion products, Co, and H2O. The results favor the following viewpoints: the PoM activity is related with the rapidly changeable valence transitionmetal sites, M0/M2+ (e. g. Ni0/Ni2+ ), on the surface of the functioning catalysts;the transition-metal sites in zero-valence state seem to be responsible for the activation and dehydrogenation of methane by homolytic splitting of its C-H bonds on these sites. and the nature of rapidly changeable valence of the active sties is requisite for activation and rapid conversion of dioxygen.
Tracheal intubation using a new CCD camera‐equipped device: a report of two cases with a difficult intubation (2005)

In two patients, one with Klippel-Feil syndrome and one with fibrous dysplasia of the maxilla, no part of the larynx could be visualized by direct laryngoscopy. In both cases, the use of an intubation device equipped with a charge-coupled device camera, the endotracheal intubation device (EID), allowed smooth tracheal intubation.
TARP: A nuclear protein expressed in prostate and breast cancer cells derived from an alternate reading frame of the T cell receptor γ chain locus (2000)

Previously, we identified the expression of a prostate-specific form of T cell receptor gamma chain (TCRgamma) mRNA in the human prostate and demonstrated that it originates from epithelial cells and not from infiltrating T lymphocytes. Here, we show that this prostate-specific transcript is also expressed in three breast cancer cell lines and breast cancer tissues. Analysis of the cDNA sequence predicts that this transcript can encode two protein products of 7 and 13 kDa, and in vitro translation experiments showed that both proteins were made. The longer ORF encodes a 13-kDa truncated version of TCRgamma, whereas the shorter alternative reading frame encodes a 7-kDa protein with five leucine residues in heptad repeats followed by a basic region. Studies with specific antibodies against each protein product revealed that both prostate and breast cancer cells contain only the 7-kDa protein, which is located in the nucleus. We have named this protein TCRgamma alternate reading frame protein (TARP). These results demonstrate that an alternative protein product is encoded by the TCRgamma locus in cells other than T lymphocytes.
High-level erythroid expression of human alpha-globin genes in transgenic mice. (1989)

The human alpha 1-globin gene was fused downstream of two erythroid-specific DNase I super-hypersensitive sites that are normally located upstream of the human beta-globin locus. This construct was injected into fertilized mouse eggs, and expression was analyzed in 16-day fetal livers and brains. All 11 fetuses that contained intact copies of the transgene expressed correctly initiated human alpha-globin mRNA in the erythroid fetal liver but not in brain. Levels of expression ranged from 4% to 337% of endogenous mouse beta-globin mRNA. A human alpha-globin construct that did not contain super-hypersensitive sites was not expressed. These results demonstrate that human beta-globin locus activation sequences can stimulate high levels of human alpha-globin gene expression in erythroid tissue of transgenic mice. The results also provide a foundation for experiments designed to coexpress human alpha- and beta-globin genes in transgenic mice and suggest a feasible approach for production of a mouse model for human sickle cell disease.
Frequent somatic deletion of the 13q12.3 locus encompassing BRCA2 in chronic lymphocytic leukemia (1996)

Chronic lymphocytic leukemia (CLL) has consistent 13q chromosomal abnormalities detected by conventional cytogenetics. Using interphase cytogenetics we show deletion of a 1-megabase 13q12.3 locus, encompassing the BRCA2 gene, in 80% of 35 CLL cases studied. Homozygous deletion of BRCA2, located within the minimal deletion consensus, was detected in a significant population of cells in 60% of the cases. Deletion of the previously described 13q14 locus (analyzed with RB1 and D13S25 probes) was seen in 63% of the cases. Homozygous deletion of RB1 was seen in one case. Seven of the cases (32%) with D13S25 deletion had a population of cells with homozygous deletion. Deletions at the 13q12 and 13q14 loci result from distinct events because they were not contiguous. These data provide evidence for the existence of a new tumor suppressor locus in B-cell CLL located at 13q12.3. BRCA2, located within the minimal deletion consensus, is a candidate for the gene whose somatic inactivation could play a role in the initiation and or progression of B-cell CLL.
ESTs reveal a multigene family for plant defensins inArabidopsis thaliana (1997)

Plant defensins, formerly named gamma-thionins, are a group of small, cysteine-rich, basic, and antimicrobial plant proteins. Random sequencing of expressed sequence tags (ESTs) in Arabidopsis thaliana has revealed several different plant defensin genes in this plant species which can be grouped into two subfamilies. We have used one EST of each subfamily to study the expression of the corresponding genes in A. thaliana. Pdf2.3 is constitutively expressed in seedlings, rosettes, flowers, and siliques and is not inducible in seedlings either by methyl jasmonate, salicylate, ethephon, and silver nitrate or by several different phytopathogenic fungi. The expression of a second gene, Pdf1.2, is in untreated plants only detectable in rosettes. In seedlings, it is inducible by methyl jasmonate, silver nitrate, and different phytopathogenic fungi, notably Fusarium oxysporum f. sp. matthiolae. The regulation of Pdf1.2 resembles that of the pathogen-inducible thionin gene Thi2.1.
Performance of Heavy Ionic Liquids with Porous Metal Electrospray Emitters (2008)

ight experiments were conducted to characterize the emitted species for each liquid and the amount of emitted current as a function of applied voltage. The results indicate that for each ionic liquid, high quality pure ions were emitted containing no observable charged droplets. Additionally, the emitters produced currents that are much higher than those reported for externally wetted needle emitters, with currents greater than 800 nA for EMI-BF4 and greater than 200 nA for heavy ionic liquids. Propulsive gures of merit including thrust and specic impulse are given and analysis shows that while the heavy ionic liquids produce more thrust per unit current than EMI-BF4, the reduction in emitted current causes actually performance to be lower than that of EMI-BF4. Preliminary time-of-ight data is also given for a mixture of two ionic liquids.
Morphological correlates of mitochondrial dysfunction in children (2000)

Morphological studies have traditionally played a major role in the study of adults with suspected mitochondrial diseases. Here we review their role in the investigation of paediatric patients. The morphological changes may be macroscopic, such as developmental abnormalities of the brain in pyruvate dehydrogenase deficiency, including ectopic inferior olives and the absence of corpus callosum and pyramids. Other changes are histological, such as rarefaction of the neuropil and endothelial prominence in Leigh syndrome, and spongiosis with neuronal loss and gliosis in Alpers disease. The ragged-red fibres typical of mitochondrial disease in adults are only rarely seen in skeletal muscle biopsies from children. On the other hand, dramatic ultrastructural changes involving the mitochondria may be seen in many organs, including the liver, heart and intestine. In Alpers and lethal infantile mitochondrial diseases, the hepatocytes show marked accumulation of small droplets of lipid alternating with densely packed mitochondria with pale matrix and loss of granules. These changes are associated with a marked decrease in respiratory chain enzyme activity in the liver, often without similar decrease in the skeletal muscle or fibroblasts. Enlarged mitochondria with concentric cristae are prominent in the cardiac myocytes in Barth syndrome. For the assessment of children with a suspected disorder of mitochondrial dysfunction, detailed morphological studies of the brain (at autopsy) and of biopsies (especially of the liver), including ultrastructural assessment of the mitochondria, can be a very useful preliminary investigation. The findings should then be correlated with the clinical features and used as a guide for further biochemical and molecular studies, preferably on multiple tissues.
Clinical nutrition: 4. Omega-3 fatty acids in cardiovascular care. (2002)

Case 

A 40-year-old man with a strong history of heart disease in male relatives younger than 55 years of age visits his physician for an annual checkup. He appears generally fit and well and is normotensive. His fasting lipid profile reveals cholesterol (5.4 mmol/L), low-density lipoprotein (LDL)
Mechanistic Aspects of Horseradish Peroxidase Elucidated through Single-Molecule Studies (2009)

Many individual horseradish peroxidase (HRP) molecules were isolated and observed simultaneously by fluorescence microscopy in an array of 50 000 femtoliter chambers chemically etched into the surface of a glass optical fiber bundle. The substrate turnovers of hundreds of individual HRP molecules were readily analyzed, and the large number of molecules observed provided excellent statistics. In contrast to other enzymes used for single-molecule studies, the rates of product formation in the femtoliter array were, on average, 10 times lower than in bulk solution. We attribute this phenomenon to the particular redox-reaction mechanism of HRP that involves two separate steps of product formation. HRP first oxidizes fluorogenic substrate molecules like Amplex Red to radical intermediates. Two radical molecules subsequently undergo an enzyme-independent dismutation reaction, the rate of which is decreased when confined to a femtoliter chamber resulting in less product. This two-step reaction mechanism of the widely used Amplex Red, as well as other fluorogenic substrates, is often overlooked. The mechanism not only affects single-molecule studies with HRP but also bulk reactions at low substrate turnover rates.
A NAND structured cell with a new programming technology for highly reliable 5 V-only flash EEPROM (1990)

A programming technology is proposed to improve the endurance and read retention characteristics of NAND-structured EEPROM cells programmed by Fowler-Nordheim tunneling of electrons. Erasing and writing are accomplished uniformly over the whole channel area instead of nonuniform erasing at the drain. To achieve programming over the whole channel area, a new device structure is also proposed. The high-voltage pulses can be easily generated on a chip from a single 5-V power supply because the direct current due to the avalanche breakdown does not flow. The gate length of the memory transistor is 1.0 &amp;mu;m. Using 1.0 &amp;mu;m rules, the cell size per bit is 11.7 &amp;mu;m<sup>2</sup>
Lazy snapping (2004)

In this paper, we present Lazy Snapping , an interactive image cutout tool. Lazy Snapping separates coarse and fine scale processing, making object specification and detailed adjustment easy . Moreover, Lazy Snapping provides instant visual feedback, snapping the cutout contour to the true object boundary efficiently despite the presence of ambiguous or low contrast edges. Instant feedback is made possible by a novel image segmentation algorithm which combines graph cut with pre-computed over-segmentation. A set of intuitive user interface (UI) tools is designed and implemented to provide flexible control and editing for the users. Usability studies indicate that Lazy Snapping provides a better user experience and produces better segmentation results than the state-of-the-art interactive image cutout tool, Magnetic Lasso in Adobe Photoshop.
Different requirements for EDS1 and NDR1 by disease resistance genes define at least two R gene-mediated signaling pathways in Arabidopsis (1998)

The Arabidopsis genes EDS1 and NDR1 were shown previously by mutational analysis to encode essential components of race-specific disease resistance. Here, we examined the relative requirements for EDS1 and NDR1 by a broad spectrum of Resistance (R) genes present in three Arabidopsis accessions (Columbia, Landsberg-erecta, and Wassilewskija). We show that there is a strong requirement for EDS1 by a subset of R loci (RPP2, RPP4, RPP5, RPP21, and RPS4), conferring resistance to the biotrophic oomycete Peronospora parasitica, and to Pseudomonas bacteria expressing the avirulence gene avrRps4. The requirement for NDR1 by these EDS1-dependent R loci is either weak or not measurable. Conversely, three NDR1-dependent R loci, RPS2, RPM1, and RPS5, operate independently of EDS1. Another RPP locus, RPP8, exhibits no strong exclusive requirement for EDS1 or NDR1 in isolate-specific resistance to P. parasitica, although resistance is compromised weakly by eds1. Similarly, resistance conditioned by two EDS1-dependent RPP genes, RPP4 and RPP5, is impaired partially by ndr1, implicating a degree of pathway cross-talk. Our results provide compelling evidence for the preferential utilization of either signaling component by particular R genes and thus define at least two disease resistance pathways. The data also suggest that strong dependence on EDS1 or NDR1 is governed by R protein structural type rather than pathogen class.
Phosphorylation of Eukaryotic Initiation Factor 4E Markedly Reduces Its Affinity for Capped mRNA (2002)

In eukaryotes, a key step in the initiation of translation is the binding of the eukaryotic initiation factor 4E (eIF4E) to the cap structure of the mRNA. Subsequent recruitment of several components, including the small ribosomal subunit, is thought to allow migration of initiation complexes and recognition of the initiation codon. Mitogens and cytokines stimulate the phosphorylation of eIF4E at Ser(209), but the functional consequences of this modification have remained a major unresolved question. Using fluorescence spectroscopy and surface plasmon resonance techniques, we show that phosphorylation of eIF4E markedly reduces its affinity for capped RNA, primarily due to an increased rate of dissociation. Variant eIF4E proteins harboring negatively charged acidic residues at position 209 also showed decreased binding to capped RNA. Furthermore, a basic residue at position 159 was shown to be essential for cap binding. Although eIF4E-binding protein 1 greatly stabilized binding of phosphorylated eIF4E to capped RNA, in the presence of eIF4E-binding protein 1 the phosphorylated form still dissociated faster compared with nonphopshorylated eIF4E. The implications of our findings for the mechanism of translation initiation are discussed.
Topogenesis of Membrane Proteins at the Endoplasmic Reticulum (2004)

Most eukaryotic membrane proteins are cotranslationally integrated into the endoplasmic reticulum membrane by the Sec61 translocation complex. They are targeted to the translocon by hydrophobic signal sequences, which induce the translocation of either their N- or their C-terminal sequence. Signal sequence orientation is largely determined by charged residues flanking the apolar sequence (the positive-inside rule), folding properties of the N-terminal segment, and the hydrophobicity of the signal. Recent in vivo experiments suggest that N-terminal signals initially insert into the translocon head-on to yield a translocated N-terminus. Driven by a local electrical potential, the signal may invert its orientation and translocate the C-terminal sequence. Increased hydrophobicity slows down inversion by stabilizing the initial bound state. In vitro cross-linking studies indicate that signals rapidly contact lipids upon entering the translocon. Together with the recent crystal structure of the homologous SecYEbeta translocation complex of Methanococcus jannaschii, which did not reveal an obvious hydrophobic binding site for signals within the pore, a model emerges in which the translocon allows the lateral partitioning of hydrophobic segments between the aqueous pore and the lipid membrane. Signals may return into the pore for reorientation until translation is terminated. Subsequent transmembrane segments in multispanning proteins behave similarly and contribute to the overall topology of the protein.
Down-regulation of the mitochondrial 3-hydroxy-3-methylglutaryl-CoA synthase gene by insulin: the role of the forkhead transcription factor FKHRL1 (2002)

Normal physiological responses to carbohydrate shortages cause the liver to increase the production of ketone bodies from the acetyl-CoA generated from fatty acid oxidation. This allows the use of ketone bodies for energy, thereby preserving the limited glucose for use by the brain. This adaptative response is switched off by insulin rapidly inhibiting the expression of the mitochondrial 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase (HMGCS2) gene, which is a key control site of ketogenesis. We decided to investigate the molecular mechanism of this inhibition. In the present study, we show that FKHRL1, a member of the forkhead in rhabdosarcoma (FKHR) subclass of the Fox family of transcription factors, stimulates transcription from transfected 3-hydroxy-3-methylglutaryl-CoA synthase promoter-luciferase reporter constructs, and that this stimulation is repressed by insulin. An FKHRL1-responsive sequence AAAAATA, located 211 bp upstream of the HMGCS2 gene transcription start site, was identified by deletion analysis. It binds FKHRL1 in vivo and in vitro and confers FKHRL1 responsiveness on homologous and heterologous promoters. If it is mutated, it partially blocks the effect of insulin in HepG2 cells, both in the absence and presence of overexpressed FKHRL1. These results suggest that FKHRL1 contributes to the regulation of HMGCS2 gene expression by insulin.
Antibiotic interaction and diffusion through alginate and exopolysaccharide of cystic fibrosis-derived Pseudomonas aeruginosa (1988)

The interaction of five anti-pseudomonas antibiotics with both commercial and pseudomonas alginates was studied by investigation of their binding and diffusion characteristics. The two sources of alginate were qualitatively but not quantitatively similar in these respects. Unlike the beta-lactams, gentamicin and tobramycin bound avidly to both sources of alginate and, when the alginate gel to antibiotic ratio was high, the aminoglycosides exhibited diffusion coefficients which were approximately 20% of the beta-lactam values. At much lower ratios of alginate to antibiotic the aminoglycosides caused precipitation in the alginate with apparent disruption of the gel structure, and ultimately penetrated the gel at a faster rate than the beta-lactams. The strong aminoglycoside binding to alginate was reduced, but not eliminated by the presence of physiological concentrations of salts.
N-(4-hydroxyphenyl) retinamide is cytotoxic to melanoma cellsInVitro through induction of programmed cell death (1999)

Melanoma is a highly malignant and increasingly common tumour. Since metastatic melanoma remains incurable, new treatment approaches are needed. Previously, we reported that the synthetic retinoid N-(4-hydroxyphenyl)retinamide (fenretinide, HPR) induces apoptosis in neuroblastoma cells, sharing a neuroectodermal origin with melanoma cells. Since no data exist thus far on the effects of HPR on human melanoma tumours, our purpose was to investigate the in vitro modulation of cell growth and apoptosis by HPR in melanoma cells. Ten human melanoma cell lines were exposed in vitro to increasing concentrations of HPR. Dose-dependent growth inhibition and cytotoxicity were observed. According to cytofluorimetric analysis, propidium iodide staining and TUNEL assay, HPR-treated melanoma cells were shown to undergo apoptosis. However, IC50 values ranged from 5 to 28 microM, while IC90 values were between 10 and 45 microM. These last concentrations are approximately 10-fold higher than those achievable in patients given oral HPR. To explore the potential of new delivery strategies, HPR was loaded at high concentrations into immunoliposomes directed to disialoganglioside GD2, a tumour-specific antigen extensively expressed by neuroectoderma-derived tumours. Treatment of melanoma cells for a short time (2 hr) with HPR-containing immunoliposomes followed by culture in drug-free medium gave rise to apoptosis of target cells, whereas cells treated for 2 hr with equivalent concentrations of the free drug survived. The efficacy of immunoliposomal HPR was strongly dependent on the density of GD2 expression in the different cell lines.