gebhart/patrepeval huggingface dataset:
Vascular endothelial growth factor increases microvascular permeability via a Ca(2+)-dependent pathway (1997)

We tested the hypothesis that vascular endothelial growth factor (VEGF) increases microvascular permeability by increasing calcium influx into endothelial cells forming the vessel walls. We measured microvessel hydraulic conductivity (Lp) in isolated perfused MS-222-anesthetized frog mesenteric microvessels during perfusion with VEGF under conditions that attenuate calcium influx. VEGF increased Lp during a second successive perfusion in the same microvessel by 7.8-fold, which was not significantly different from that brought about by an initial application of VEGF (5.0-fold). However, under depolarizing conditions, the increase in Lp was reduced from 11.1- to 5.6-fold when depolarized to -10 mV (58 mM K+) and to 2.8-fold when depolarized to 0 mV (100 mM K+). Attenuating calcium influx by the addition of nickel ions resulted in a similar attenuation of the increase in Lp (from 13- to 2.5-fold). VEGF also increased the intracellular calcium concentration in endothelial cells of perfused microvessels as determined by measurement with fura 2. We therefore conclude that VEGF increases Lp by increasing calcium influx.
Demonstrating Quantum Error Correction that Extends the Lifetime of Quantum Information (2016)

The remarkable discovery of Quantum Error Correction (QEC), which can overcome the errors experienced by a bit of quantum information (qubit), was a critical advance that gives hope for eventually realizing practical quantum computers. In principle, a system that implements QEC can actually pass a "break-even" point and preserve quantum information for longer than the lifetime of its constituent parts. Reaching the break-even point, however, has thus far remained an outstanding and challenging goal. Several previous works have demonstrated elements of QEC in NMR, ions, nitrogen vacancy (NV) centers, photons, and superconducting transmons. However, these works primarily illustrate the signatures or scaling properties of QEC codes rather than test the capacity of the system to extend the lifetime of quantum information over time. Here we demonstrate a QEC system that reaches the break-even point by suppressing the natural errors due to energy loss for a qubit logically encoded in superpositions of coherent states, or cat states of a superconducting resonator. Moreover, the experiment implements a full QEC protocol by using real-time feedback to encode, monitor naturally occurring errors, decode, and correct. As measured by full process tomography, the enhanced lifetime of the encoded information is 320 microseconds without any post-selection. This is 20 times greater than that of the system's transmon, over twice as long as an uncorrected logical encoding, and 10% longer than the highest quality element of the system (the resonator's 0, 1 Fock states). Our results illustrate the power of novel, hardware efficient qubit encodings over traditional QEC schemes. Furthermore, they advance the field of experimental error correction from confirming the basic concepts to exploring the metrics that drive system performance and the challenges in implementing a fault-tolerant system.
Virus-specific interferon action. Protection of newborn Mx carriers against lethal infection with influenza virus. (1981)

The efficacy of interferon in antiviral protection of newborn mice differing at the Mx locus was investigated. Adult mice bearing the allele Mx exhibit a high degree of specific resistance toward lethal challenge with influenza viruses. In contrast, newborn Mx carriers are virtually as susceptible to influenza viruses as newborn mice devoid of Mx. Resistance can be abrogated by treating adult animals with anti-interferon serum. Here, we provide direct evidence of a virus-specific effect of interferon in vivo: newborn mice carrying the resistance gene Mx could be protected against lethal influenza virus infection with doses of interferon that were not protective in the absence of Mx. The efficacy of interferon towards a picornavirus (encephalomyocarditis virus) and a rhabdovirus (vesicular stomatitis virus) was independent of Mx.
High-Dose Oral Tamoxifen, a Potential Multidrug-Resistance-Reversal Agent: Phase I Trial in Combination With Vinblastine (1992)

Our study demonstrates that high-dose tamoxifen can be safely administered and that plasma concentrations that may inhibit P-glycoprotein function can be achieved.
Microfluidic bischemical analysis system (2002)

We have developed a genetic-analysis system that integrates all reactions necessary to process a sample and use a microfabricated GeneChip/sup (R)/ polynucleotide array. This system has performed a multistep assay for monitoring mutations in the HIV virus in 10 /spl mu/L reaction volumes. The microfluidic structures and thermal control methods demonstrated in this work can be generally applied to integrate other chemical and biochemical analysis systems.
Chromium-based electrocatalysts for oxygen reduction in polymer electrolyte fuel cells (1997)

In commercial polymer electrolyte fuel cells (PEFCs), the usual catalysts are colloidal platinum or platinum nanoparticles on carbon black. Platinum is expensive and of limited supply. Many efforts have been made to replace platinum with a more common metal to perform the reaction of oxygen reduction. A catalyst for oxygen reduction in polymer electrolyte fuel cell was obtained when chromium hydroxide, Cr(OH){sub 3}, adsorbed on carbon black was pyrolyzed at 1000 degrees C in Ar containing acetonitrile vapours. X-ray diffraction showed that chromium carbide nitride was present in the catalytic material but its association with the catalytic site was not clear. Pure carbonitride must be generated by other means in order to test its intrinsic electrochemical properties for the reduction of oxygen. 14 refs., 1 tab., 8 figs.
A repetitive sequence element 3? of the human c-Ha-ras1 gene has enhancer activity (1987)

Efficient expression of the human c-Ha-ras1 gene requires sequences 3' of those specifying the polyadenylation of its transcripts. These sequences can stimulate the expression of heterologous genes in a manner largely independent of position and orientation, arguing that they possess a transcriptional enhancing activity that regulates the c-Ha-ras1 promoter. As this element is associated with a repetitive domain that is highly polymorphic, it is possible that the activity of this enhancer is variable within the human population.
Evaluating bag-of-visual-words representations in scene classification (2007)

Based on keypoints extracted as salient image patches, an image can be described as a "bag of visual words" and this representation has been used in scene classification. The choice of dimension, selection, and weighting of visual words in this representation is crucial to the classification performance but has not been thoroughly studied in previous work. Given the analogy between this representation and the bag-of-words representation of text documents, we apply techniques used in text categorization, including term weighting, stop word removal, feature selection, to generate image representations that differ in the dimension, selection, and weighting of visual words. The impact of these representation choices to scene classification is studied through extensive experiments on the TRECVID and PASCAL collection. This study provides an empirical basis for designing visual-word representations that are likely to produce superior classification performance.
Animal Models for Muscular Dystrophy Show Different Patterns of Sarcolemmal Disruption (1997)

Genetic defects in a number of components of the dystrophin-glycoprotein complex (DGC) lead to distinct forms of muscular dystrophy. However, little is known about how alterations in the DGC are manifested in the pathophysiology present in dystrophic muscle tissue. One hypothesis is that the DGC protects the sarcolemma from contraction-induced damage. Using tracer molecules, we compared sarcolemmal integrity in animal models for muscular dystrophy and in muscular dystrophy patient samples. Evans blue, a low molecular weight diazo dye, does not cross into skeletal muscle fibers in normal mice. In contrast, mdx mice, a dystrophin-deficient animal model for Duchenne muscular dystrophy, showed significant Evans blue accumulation in skeletal muscle fibers. We also studied Evans blue dispersion in transgenic mice bearing different dystrophin mutations, and we demonstrated that cytoskeletal and sarcolemmal attachment of dystrophin might be a necessary requirement to prevent serious fiber damage. The extent of dye incorporation in transgenic mice correlated with the phenotypic severity of similar dystrophin mutations in humans. We furthermore assessed Evans blue incorporation in skeletal muscle of the dystrophia muscularis (dy/dy) mouse and its milder allelic variant, the dy2J/dy2J mouse, animal models for congenital muscular dystrophy. Surprisingly, these mice, which have defects in the laminin alpha2-chain, an extracellular ligand of the DGC, showed little Evans blue accumulation in their skeletal muscles. Taken together, these results suggest that the pathogenic mechanisms in congenital muscular dystrophy are different from those in Duchenne muscular dystrophy, although the primary defects originate in two components associated with the same protein complex.
Analysis of surface atrial signals using spectral methods for time series with missing data (2007)

In this work, the analysis of atrial signals recorded during atrial fibrillation was pursued using two spectral estimators designed for series with missing data: the Lomb periodogram (LP) and the iterative singular spectrum analysis (ISSA). The main aim is to verify if subtraction of the ventricular activity might be avoided by performing spectral analysis on those ECG intervals where such activity is absent, (i.e. the T-Q intervals), at least to estimate the dominant atrial fibrillatory frequency (FF). Recordings coming from the 2004 Computers in Cardiology Termination Challenge Database were analyzed. Fibrillatory frequencies were then compared with those obtained from the analysis of the correspondent atrial signals extracted using a modified average beat subtraction (ABS) technique. We observed that the mean absolute difference was 0.42 plusmn 0.66 Hz for LP, (meanplusmnSD), and 0.39 plusmn 0.64 Hz for ISSA. We concluded that estimation of FF is feasible without applying QRS-T subtraction.
Petroleum Refining: Technology and Economics, Fifth Edition (2007)

Petroleum refiners must face billion-dollar investments in equipment in order to meet ever-changing environmental requirements. Because the design and construction of new processing units entail several years lead time, refiners are reluctant to commit these dollars for equipment that may no longer meet certain conditions when the units come on st
Enhancement and Selective Production of Phoslactomycin B, a Protein Phosphatase IIa Inhibitor, through Identification and Engineering of the Corresponding Biosynthetic Gene Cluster (2003)

Phoslactomycins (PLMs), potent and selective inhibitors of serine threonine phosphatases, are of interest for their antitumor and antiviral activity. Multiple analogs and low titers in the fermentation process have hampered the development of this class of natural products. The entire 75-kb PLM biosynthetic gene cluster of Streptomyces sp. HK-803 was cloned, sequenced, and analyzed. The loading domain and seven extension modules of the PLM polyketide synthase generate an unusual linear unsaturated polyketide chain containing both E- and Z-double bonds from a cyclohexanecarboxylic acid (CHC) primer. Hydroxylation of the CHC-derived side chain of the resulting PLM-B by PlmS2, and a subsequent esterification, produces the remaining PLM analogs. A new PCR targeting technology allowed rapid and facile allelic replacement of plmS2. The resulting mutant selectively produced the PLM-B, at 6-fold higher titers than the wild type strain. This mutant and the biosynthetic gene cluster will facilitate engineered microbial production of hybrid PLMs with improved properties.
Fast and robust multiple sequence alignment with phylogeny-aware gap placement (2012)

ProGraphMSA shows good performance and competitive execution times in various benchmarks.
Amyloid peptides incorporating a core sequence from the amyloid beta peptide and gamma amino acids: relating bioactivity to self-assembly (2011)

A series of heptapeptides comprising the core sequence Aβ(16-20), KLVFF, of the amyloid β peptide coupled with paired N-terminal γ-amino acids are investigated in terms of cytotoxicity reduction and binding to the full Aβ peptide, both pointing to inhibition of fibrillisation for selected compounds. This is related to the self-assembly capacity of the heptapeptides.
Characterization of the TGF-β1 signaling abnormalities in the Gata1low mouse model of myelofibrosis (2013)

Primary myelofibrosis (PMF) is characterized by fibrosis, ineffective hematopoiesis in marrow, and hematopoiesis in extramedullary sites and is associated with abnormal megakaryocyte (MK) development and increased transforming growth factor (TGF)-β1 release. To clarify the role of TGF-β1 in the pathogenesis of this disease, the TGF-β1 signaling pathway of marrow and spleen of the Gata1(low) mouse model of myelofibrosis (MF) was profiled and the consequences of inhibition of TGF-β1 signaling on disease manifestations determined. The expression of 20 genes in marrow and 36 genes in spleen of Gata1(low) mice was altered. David-pathway analyses identified alterations of TGF-β1, Hedgehog, and p53 signaling in marrow and spleen and of mammalian target of rapamycin (mTOR) in spleen only and predicted that these alterations would induce consequences consistent with the Gata1(low) phenotype (increased apoptosis and G1 arrest both in marrow and spleen and increased osteoblast differentiation and reduced ubiquitin-mediated proteolysis in marrow only). Inhibition of TGF-β1 signaling normalized the expression of p53-related genes, restoring hematopoiesis and MK development and reducing fibrosis, neovascularization, and osteogenesis in marrow. It also normalized p53/mTOR/Hedgehog-related genes in spleen, reducing extramedullary hematopoiesis. These data identify altered expression signatures of TGF-β1 signaling that may be responsible for MF in Gata1(low) mice and may represent additional targets for therapeutic intervention in PMF.
Control of murine hair follicle regression (catagen) by TGF‐β1 in vivo (2000)

The regression phase of the hair cycle (catagen) is an apoptosis-driven process accompanied by terminal differentiation, proteolysis, and matrix remodeling. As an inhibitor of keratinocyte proliferation and inductor of keratinocyte apoptosis, transforming growth factor beta1 (TGF-beta1) has been proposed to play an important role in catagen regulation. This is suggested, for example, by maximal expression of TGF-beta1 and its receptors during late anagen and the onset of catagen of the hair cycle. We examined the potential involvement of TGF-beta1 in catagen control. We compared the first spontaneous entry of hair follicles into catagen between TGF-beta1 null mice and age-matched wild-type littermates, and assessed the effects of TGF-beta1 injection on murine anagen hair follicles in vivo. At day 18 p.p., hair follicles in TGF-beta1 -/- mice were still in early catagen, whereas hair follicles of +/+ littermates had already entered the subsequent resting phase (telogen). TGF-beta1-/- mice displayed more Ki-67-positive cells and fewer apoptotic cells than comparable catagen follicles from +/+ mice. In contrast, injection of TGF-beta1 into the back skin of mice induced premature catagen development. In addition, the number of proliferating follicle keratinocytes was reduced and the number of TUNEL + cells was increased in the TGF-beta1-treated mice compared to controls. Double visualization of TGF-beta type II receptor (TGFRII) and TUNEL reactivity revealed colocalization of apoptotic nuclei and TGFRII in catagen follicles. These data strongly support that TGF-beta1 ranks among the elusive endogenous regulators of catagen induction in vivo, possibly via the inhibition of keratinocyte proliferation and induction of apoptosis. Thus, TGF-betaRII agonists and antagonists may provide useful therapeutic tools for human hair growth disorders based on premature or retarded catagen development (effluvium, alopecia, hirsutism).
Pharmacological and initial therapeutic observations on 6-Diazo-5-Oxo-L-Norleucine (Don) in human neoplastic disease (1957)

HE structure of 6-diazo-5-oxo-~-norleucine T (DON), an antibiotic isolated from Streptomyces, is similar to that of the serine
Defining the minimal size of catalytically active primate α1,3 galactosyltransferase: structure-function studies on the recombinant truncated enzyme (1994)

The glycosylation enzyme alpha 1,3 galactosyltransferase, which synthesizes the carbohydrate Gal alpha 1-3Gal beta 1-4GlcNAc-R, is active in non-primate mammals, prosimians and New World monkeys, but not in Old World monkeys, apes and humans. In this study, we have cloned and sequenced the enzyme expressed in a New World monkey, determined the exact size of the stem region and assessed the minimal size of catalytically active alpha 1,3 galactosyltransferase (alpha 1,3GT). Various primer sets were used in the polymerase chain reaction to generate cDNAs which coded for forms of alpha 1,3GT with deletions at the N- or C-terminal domains. The cDNA was inserted into the expression vector pPROTA which contains the coding sequence for protein A, and subsequently transfected into COS cells. The soluble chimeric products (truncated enzyme and protein A) were harvested from the cell culture medium using IgG-Sepharose beads and assayed for enzymatic activity. As many as 67 amino acids could be truncated at the amino terminal region of the luminal portion of the enzyme without affecting its catalytic activity. Truncation of 68, 69 and 74 amino acids resulted in a 50, 75 and > 95% loss in the in vitro catalytic actively, respectively. Introduction of a frameshift mutation which is characteristic of apes and human alpha 1,3GT gene resulted in the complete loss of enzyme activity. Moreover, truncation of as few as three amino acids at the carboxyl end of alpha 1,3GT resulted in complete loss of the catalytic activity.(ABSTRACT TRUNCATED AT 250 WORDS)
Biodegradable Piezoelectric Force Sensor (2018)

Measuring vital physiological pressures is important for monitoring health status, preventing the buildup of dangerous internal forces in impaired organs, and enabling novel approaches of using mechanical stimulation for tissue regeneration. Pressure sensors are often required to be implanted and directly integrated with native soft biological systems. Therefore, the devices should be flexible and at the same time biodegradable to avoid invasive removal surgery that can damage directly interfaced tissues. Despite recent achievements in degradable electronic devices, there is still a tremendous need to develop a force sensor which only relies on safe medical materials and requires no complex fabrication process to provide accurate information on important biophysiological forces. Here, we present a strategy for material processing, electromechanical analysis, device fabrication, and assessment of a piezoelectric Poly-l-lactide (PLLA) polymer to create a biodegradable, biocompatible piezoelectric force sensor, which only employs medical materials used commonly in Food and Drug Administration-approved implants, for the monitoring of biological forces. We show the sensor can precisely measure pressures in a wide range of 0-18 kPa and sustain a reliable performance for a period of 4 d in an aqueous environment. We also demonstrate this PLLA piezoelectric sensor can be implanted inside the abdominal cavity of a mouse to monitor the pressure of diaphragmatic contraction. This piezoelectric sensor offers an appealing alternative to present biodegradable electronic devices for the monitoring of intraorgan pressures. The sensor can be integrated with tissues and organs, forming self-sensing bionic systems to enable many exciting applications in regenerative medicine, drug delivery, and medical devices.
Mechanisms of Interactions of Factor X and Factor Xa with the Acidic Region in the Factor VIII A1 Domain (2004)

The 337-372 sequence of the factor VIIIa A1 subunit contains interactive sites for both zymogen factor X and the active enzyme, factor Xa. Solid phase binding studies indicated that factor Xa possessed a >20-fold higher affinity for the isolated A1 subunit of factor VIIIa compared with factor X. Heparin completely inhibited zero-length cross-linking of the 337-372 peptide to factor Xa but not to factor X. In the presence of calcium, factor Xa showed greater affinity for heparin than factor X. Studies using factor Xa mutants in which heparin-binding exosite residues were individually replaced by Ala showed that the R240A mutant was defective in recognition of the Lys36 cleavage site, generating the A137-372 intermediate with approximately 20% the catalytic efficiency of wild type. This defect likely resulted from an approximately 4-fold increase in Km for the A1 substrate because kcat values for the wild type and mutant were equivalent. Cleavage of the A1-A2 domain junction by factor Xa R240A was not blocked by the 337-372 peptide. Studies using mutant factor VIII where clustered acidic residues in the 337-372 segment were replaced by Ala showed that a factor VIIIa D361A/D362A/D363A mutant possessed a approximately 1.6-fold increase in Km for factor X compared with wild type. However, similar Km values were observed for recombinant factor X and R240A substrates. These results indicate that the binding regions of factor X and factor Xa for A1 domain overlap and that both utilize acidic residues 361-363. Furthermore, factor Xa but not factor X interacts with high affinity at this site via residues contained within the heparin-binding exosite of the proteinase.
Procollagen C Proteinase Enhancer 1 Genes Are Important Determinants of the Mechanical Properties and Geometry of Bone and the Ultrastructure of Connective Tissues (2005)

Procollagen C proteinases (pCPs) cleave type I to III procollagen C propeptides as a necessary step in assembling the major fibrous components of vertebrate extracellular matrix. The protein PCOLCE1 (procollagen C proteinase enhancer 1) is not a proteinase but can enhance the activity of pCPs approximately 10-fold in vitro and has reported roles in inhibiting other proteinases and in growth control. Here we have generated mice with null alleles of the PCOLCE1 gene, Pcolce, to ascertain in vivo roles. Although Pcolce-/- mice are viable and fertile, Pcolce-/- male, but not female, long bones are more massive and have altered geometries that increase resistance to loading, compared to wild type. Mechanical testing indicated inferior material properties of Pcolce-/- male long bone, apparently compensated for by the adaptive changes in bone geometry. Male and female Pcolce-/- vertebrae both appeared to compensate for inferior material properties with thickened and more numerous trabeculae and had a uniquely altered morphology in deposited mineral. Ultrastructurally, Pcolce-/- mice had profoundly abnormal collagen fibrils in both mineralized and nonmineralized tissues. In Pcolce-/- tendon, 100% of collagen fibrils had deranged morphologies, indicating marked functional effects in this tissue. Thus, PCOLCE1 is an important determinant of bone mechanical properties and geometry and of collagen fibril morphology in mammals, and the human PCOLCE1 gene is identified as a candidate for phenotypes with defects in such attributes in humans.