gebhart/patrepeval huggingface dataset:
Cell-associated pectinolytic and cellulolytic enzymes in Rhizobium leguminosarum biovar trifolii (1992)

The involvement of Rhizobium enzymes that degrade plant cell wall polymers has long been an unresolved question about the infection process in root nodule symbiosis. Here we report the production of enzymes from Rhizobium leguminosarum bv. trifolii that degrade carboxymethyl cellulose and polypectate model substrates with sensitive methods that reliably detect the enzyme activities: a double-layer plate assay, quantitation of reducing sugars with a bicinchoninate reagent, and activity gel electrophoresis-isoelectric focusing. Both enzyme activities were (i) produced commonly by diverse wild-type strains, (ii) cell bound with at least some of the activity associated with the cell envelope, and (iii) not changed appreciably by growth in the presence of the model substrates or a flavone that activates expression of nodulation (nod) genes on the resident symbiotic plasmid (pSym). Equivalent levels of carboxymethyl cellulase activity were found in wild-type strain ANU843 and its pSym-cured derivative, ANU845, consistent with previous results of Morales et al. (V. Morales, E. Martínez-Molina, and D. Hubbell, Plant Soil 80:407-415, 1984). However, polygalacturonase activity was lower in ANU845 and was not restored to wild-type levels in the recombinant derivative of pSym- ANU845 containing the common and host-specific nod genes within a 14-kb HindIII DNA fragment of pSym from ANU843 cloned on plasmid pRt032. Activity gel electrophoresis resolved three carboxymethyl cellulase isozymes of approximately 102, 56, and 33 kDa in cell extracts from ANU843. Isoelectric focusing activity gels revealed one ANU843 polygalacturonase isozyme with a pI of approximately 7.2. These studies show that R. leguminosarum bv. trifolii produces multiple enzymes that cleave glycosidic bonds in plant cell walls and that are cell bound.
Fibrosis Is a Key Inhibitor of Lymphatic Regeneration (2009)

Soft-tissue fibrosis is associated with impairment in lymphatic regeneration and lymphatic function. These defects occur as a consequence of impaired lymphatic endothelial cell proliferation, abnormal lymphatic microarchitecture, and lymphatic fibrosis. Inhibition of fibrosis using a simple topical dressing can markedly accelerate lymphatic repair and promote regeneration of normal capillary lymphatics.
HSP70 Inhibition by the Small-Molecule 2-Phenylethynesulfonamide Impairs Protein Clearance Pathways in Tumor Cells (2011)

The evolutionarily conserved stress-inducible HSP70 molecular chaperone plays a central role in maintaining protein quality control in response to various forms of stress. Constitutively elevated HSP70 expression is a characteristic of many tumor cells and contributes to their survival. We recently identified the small-molecule 2-phenylethyenesulfonamide (PES) as a novel HSP70 inhibitor. Here, we present evidence that PES-mediated inhibition of HSP70 family proteins in tumor cells results in an impairment of the two major protein degradation systems, namely, the autophagy-lysosome system and the proteasome pathway. HSP70 family proteins work closely with the HSP90 molecular chaperone to maintain the stability and activities of their many client proteins, and PES causes a disruption in the HSP70/HSP90 chaperone system. As a consequence, many cellular proteins, including known HSP70/HSP90 substrates, accumulate in detergent-insoluble cell fractions, indicative of aggregation and functional inactivation. Overall, PES simultaneously disrupts several cancer critical survival pathways, supporting the idea of targeting HSP70 as a potential approach for cancer therapeutics.
Transforming growth factor-alpha acts as an autocrine growth factor in ovarian carcinoma cell lines. (1992)

The potential of transforming growth factor-alpha (TGF-alpha) to function as an autocrine growth factor was evaluated in numerous ovarian carcinoma cell lines. All 17 lines which were examined expressed the epidermal growth factor receptor and 16 cell lines, in addition, concomitantly secreted TGF-alpha. Radioimmunoassay of processed serum-free-conditioned medium indicated TGF-alpha concentrations ranging from 16 to 197 pg/ml, or 1.5 to 95 ng/10(8) cells. 125I-TGF-alpha bound to a single class of high-affinity-binding sites on the surface of the cells. The dissociation constant for the 125I-TGF-alpha/epidermal growth factor receptor complex ranged from 0.21 to 5.3 nM with receptor numbers from 3,500 to 96,000/cell, depending upon the cell line. The growth of 8 ovarian cell lines was stimulated in a dose-dependent manner when grown in the presence of exogenous TGF-alpha. Growth in 4 of 5 cell lines capable of serum-free propagation was inhibited from 28 to 56% when cultured in medium containing a TGF-alpha-neutralizing monoclonal antibody. These results support the view that TGF-alpha is an autocrine growth factor for cell lines derived from ovarian cancers of epithelial origin and suggest a potential role for TGF-alpha in the pathogenesis or progression of the disease.
Frequency modulation detection high vacuum scanning force microscope with a self-oscillating piezoelectric cantilever (1997)

This article attempts to describe a novel high vacuum scanning force microscope (HV-SFM) using a self-oscillating piezoelectric cantilever in frequency modulation (FM) mode. Since no external deflection sensor or external vibrator is needed, the new HV-SFM is very simple and easy to handle in vacuum conditions in comparison with conventional systems using optical sensors. FM detection is used to detect the force gradient acting on the end of the piezoelectric cantilever because it gives higher response speed in vacuum conditions compared to the commonly used slope detection. The unimorph cantilever consists of a 1.0 μm thick Pb(Ti,Zr)O3 (PZT) layer on a SiO2 elastic base, which becomes self-oscillating when an ac voltage is applied to the piezoelectric layer. The 160 μm long piezoelectric cantilever has successfully been oscillated at its natural resonance frequency of 117 kHz by connecting its piezoelectric layer directly into the FM loop, which applies positive feedback to the piezoelectric charge current caused by cantilever vibration. The shift in oscillation frequency of the FM loop, or the shift of cantilever resonance frequency due to force gradient acting on the cantilever end, is measured as a SFM feedback signal. At a frequency shift of 80 Hz, the force gradient and the force acting on the cantilever tip were calculated as 0.012 N/m and 0.02 nN, respectively, from an obtained force curve. At that set point, high-resolution images of a gold film have been obtained. The constructed FM detection noncontact SFM with a self-oscillating PZT cantilever has proven to be stable and easy to handle in vacuum conditions.
Jamais chez Jean ! (Mort et résurrection) (1995)

Lys Daniel. Jamais chez Jean ! (Mort et résurrection). In: Études théologiques et religieuses, Tome 70, 1995/4. pp. 509-519.
Familial Excess Longevity in Utah Genealogies (2001)

We evaluated the influence of family history on longevity by examining longevity in a cohort of 78,994 individuals drawn from the Utah Population Database (UPDB) who were born between 1870 and 1907, and lived to at least age 65. We examined Mendelian genetic and social modes of transmission of excess longevity (the difference between observed and expected longevity) by varying weighted kinship contributions over different classes of relatives. The genetic component of the variation in excess longevity measured as heritability, h2, was approximately 0.15 (95% confidence interval [CI] 0.12-0.18). Among siblings of probands who reached the 97th percentile of excess longevity (+ 14.8 years, currently age 95 for men and 97 for women), the relative risk of recurrence (lambdas) was 2.30 (95% CI 2.08-2.56). In sibships whose relatives were in the top 15% of the distribution for familial excess longevity, the value of lambdas increased substantially, indicating that considering the longevity of distant relatives may be helpful in the selection of families in which to identify genes influencing aging and longevity.
The UCSC Genome Browser database: 2016 update (2015)

For the past 15 years, the UCSC Genome Browser (http://genome.ucsc.edu/) has served the international research community by offering an integrated platform for viewing and analyzing information from a large database of genome assemblies and their associated annotations. The UCSC Genome Browser has been under continuous development since its inception with new data sets and software features added frequently. Some release highlights of this year include new and updated genome browsers for various assemblies, including bonobo and zebrafish; new gene annotation sets; improvements to track and assembly hub support; and a new interactive tool, the "Data Integrator", for intersecting data from multiple tracks. We have greatly expanded the data sets available on the most recent human assembly, hg38/GRCh38, to include updated gene prediction sets from GENCODE, more phenotype- and disease-associated variants from ClinVar and ClinGen, more genomic regulatory data, and a new multiple genome alignment.
Conversion of ethanolamine, monomethylethanolamine and dimethylethanolamine to choline-containing compounds by neurons in culture and by the rat brain (1989)

The incubation of neurons from chick embryos in primary culture with [3H]ethanolamine revealed the conversion of this base into monomethyl, dimethyl and choline derivatives, including the corresponding free bases. Labelling with [methyl-3H]monomethylethanolamine and [methyl-3H]dimethylethanolamine supported the conclusion that in chick neuron cultures, phosphoethanolamine appears to be the preferential substrate for methylation, rather than ethanolamine or phosphatidylethanolamine. The methylation of the latter two compounds, in particular that of phosphatidylethanolamine, was seemingly stopped at the level of their monomethyl derivatives. Fetal rat neurons in primary culture incubated with [3H]ethanolamine showed similar results to those observed with chick neurones. However, phosphoethanolamine and phosphatidylethanolamine and, to a lesser extent, free ethanolamine, appeared to be possible substrates for methylation reactions. The methylation of water-soluble ethanolamine compounds de novo was further confirmed by experiments performed in vivo by intraventricular injection of [3H]ethanolamine. Phosphocholine and the monomethyl and dimethyl derivatives of ethanolamine were detected in the brain 15 min after injection.
Analysis of Placement Procedures for VLSI Standard Cell Layout (1986)

This paper describes a study of placement procedures for VLSI Standard Cell Layout. The procedures studied are Simulated Annealing, Min Cut placement, and a number of improvements to Min Cut placement including a technique called Terminal Propagation which allows Min Cut to include the effect of connections to external cells. The Min Cut procedures are coupled with a Force Directed Pairwise Interchange (FDPI) algorithm for placement improvement. For the same problem these techniques produce a range of solutions with a typical standard deviation 4% for the total wire length and 3% to 4% for the routed area. The spread of results for Simulated Annealing is even larger. This distribution of results for a given algorithm implies that mean results of many placements should be used when comparing algorithms. We find that the Min Cut partitioning with simplified Terminal Propagation is the most efficient placement procedure studied.
Small volume low mechanical stress cytometry using computer-controlled Braille display microfluidics (2007)

This paper describes a micro flow cytometer system designed for efficient and non-damaging analysis of samples with small numbers of precious cells. The system utilizes actuation of Braille-display pins for micro-scale fluid manipulation and a fluorescence microscope with a CCD camera for optical detection. The microfluidic chip is fully disposable and is composed of a polydimethylsiloxane (PDMS) slab with microchannel features sealed against a thin deformable PDMS membrane. The channels are designed with diffusers to alleviate pulsatile flow behaviors inherent in pin actuator-based peristaltic pumping schemes to maximize hydrodynamic focusing of samples with minimal disturbances in the laminar streams within the channel. A funnel connected to the microfluidic channel is designed for efficient loading of samples with small number of cells and is also positioned on the chip to prevent physical damages of the samples by the squeezing actions of Braille pins during actuation. The sample loading scheme was characterized by both computational fluidic dynamics (CFD) simulation and experimental observation. A fluorescein solution was first used for flow field investigation, followed by use of fluorescence beads with known relative intensities for optical detection performance calibration. Murine myoblast cells (C2C12) were exploited to investigate cell viability for the sample loading scheme of the device. Furthermore, human promyelocytic leukemia (HL60) cells stained by hypotonic DNA staining buffer were also tested in the system for cell cycle analysis. The ability to efficiently analyze cellular samples where the number of cells is small was demonstrated by analyzing cells from a single embryoid body derived from mouse embryonic stem cells. Consequently, the designed microfluidic device reported in this paper is promising for easy-to-use, small sample size flow cytometric analysis, and has potential to be further integrated with other Braille display-based microfluidic devices to facilitate a multi-functional lab-on-a-chip for mammalian cell manipulations.
Selective targeting of human cells by a chimeric adenovirus vector containing a modified fiber protein (1997)

The adenovirus fiber protein is responsible for attachment of the virion to unidentified cell surface receptors. There are at least two distinct adenovirus fiber receptors which interact with the group B (Ad3) and group C (Ad5) adenoviruses. We have previously shown by using expressed adenovirus fiber proteins that it is possible to change the specificity of the fiber protein by exchanging the head domain with another serotype which recognizes a different receptor (S. C. Stevenson et al., J. Virol. 69:2850-2857, 1995). A chimeric fiber cDNA containing the Ad3 fiber head domain fused to the Ad5 fiber tail and shaft was incorporated into the genome of an adenovirus vector with E1 and E3 deleted encoding beta-galactosidase to generate Av9LacZ4, an adenovirus particle which contains a chimeric fiber protein. Western blot analysis of the chimeric fiber vector confirmed expression of the chimeric fiber protein and its association with the adenovirus capsid. Transduction experiments with fiber protein competitors demonstrated the altered receptor tropism of the chimeric fiber vector compared to that of the parental Av1LacZ4 vector. Transduction of a panel of human cell lines with the chimeric and parental vectors provided evidence for a different cellular distribution of the Ad5 and Ad3 receptors. Three cell lines (THP-1, MRC-5, and FaDu) were more efficiently transduced by the vector containing the Ad3 fiber head than by the Ad5 fiber vector. In contrast, human coronary artery endothelial cells were transduced more readily with the vector containing the Ad5 fiber than with the chimeric fiber vector. HeLa and human umbilical vein endothelial cells were transduced at equivalent levels compared with human diploid fibroblasts, which were refractory to transduction with both vectors. These results provide evidence for the differential expression of the Ad5 and Ad3 receptors on human cell lines derived from clinically relevant target tissues. Furthermore, we show that exchange of the fiber head domain is a viable approach to the production of adenovirus vectors with cell-type-selective transduction properties. It may be possible to extend this approach to the use of ligands for a range of different cellular receptors in order to target gene transfer to specific cell types at the level of transduction.
Targeted correction of a major histocompatibility class II E alpha gene by DNA microinjected into mouse eggs. (1989)

DNA molecules containing the 5' end of a functional major histocompatibility class II E alpha gene were injected into mouse eggs bearing E alpha genes with 630-base-pair (bp) deletions encompassing the promoter and first exon. The deletion was corrected by homologous recombination in 1 of about 500 transgenic mice that incorporated the injected DNA. The corrected E alpha gene was transmitted to progeny, which were bred to homozygosity. Southern blot analysis, polymerase chain reaction amplification of the DNA spanning the deletion, and sequence analysis revealed that the corrected allele resembles the wild-type E alpha gene. At sites of single-base-pair polymorphisms, there was apparently random conversion to either the donor or recipient sequence. In addition, many point mutations were introduced. mRNAs were produced from the corrected allele in a tissue-specific manner, but their sizes were different from the wild-type allele, and they did not produce detectable E alpha protein. This experiment demonstrates the feasibility of targeting foreign DNA to a gene that is completely inactive in fertilized mouse eggs.
Immunological Aspects of Experimental Allergic Encephalomyelitis and Multiple Sclerosis (1995)

Multiple sclerosis (MS) is the most frequent, demyelinating disease of the central nervous system (CNS) in Northern Europeans and North Americans. Despite intensive research its etiology is still unknown, but a T cell-mediated autoimmune pathogenesis is likely to be responsible for the demyelination. This hypothesis is based both on findings in MS patients and studies of an experimental animal model for demyelinating diseases, experimental allergic encephalomyelitis (EAE). Experiments in EAE have not only demonstrated which myelin antigens are able to induce the demyelinating process but also have determined the characteristics of encephalitogenic T cells, that is, their fine specificity, major histocompatibility complex (MHC) restriction, lymphokine secretion, activation requirements, and T cell receptor (TCR) usage. Based on these findings, highly specific and efficient immune interventions have been designed in EAE and have raised hopes that similar approaches could modulate the disease process in MS. Although the examination of the myelin-specific T cell response in MS patients has shown parallels to EAE, this remains an area of intensive research because a number of questions remain. This review summarizes the important lessons from EAE, examines recent findings in MS, and discusses current concepts about how the disease process develops and which steps might be taken to modulate it.
Growth factors are released by mechanically wounded endothelial cells. (1989)

Growth factors may be required at sites of mechanical injury and normal wear and tear in vivo, suggesting that the direct action of mechanical forces on cells could lead to growth factor release. Scraping of cells from the tissue culture substratum at 37 degrees C was used to test this possibility. We show that scraping closely mimics in vitro both the transient plasma membrane wounds observed in cells subject to mechanical forces in vivo (McNeil, P. L., and S. Ito. 1989. Gastroenterology. 96:1238-1248) and the transient plasma membrane wounds shown here to occur in endothelial cells under normal culturing conditions. Scraping of endothelial cells from the culturing substratum released into the culture medium a potent growth-promoting activity for Swiss 3T3 fibroblasts. Growth-promoting activity was released rapidly (within 5 min) after scraping but was not subsequently degraded by the endothelial cells for at least 24 h thereafter. A greater quantity of growth-promoting activity was released by cells scraped 4 h after plating than by those scraped 4 or 7 d afterwards. Thus release is not due to scraping-induced disruption of extracellular matrix. Release was only partially cold inhibitable, was poorly correlated with the level of cell death induced by scraping, and did not occur when cells were killed with metabolic poisons. These results suggest that mechanical disruption of plasma membrane, either transient or permanent, is the essential event leading to release. A basic fibroblast growth factor-like molecule and not platelet-derived growth factor appears to be partially responsible for the growth-promoting activity. We conclude that one biologically relevant route of release of basic fibroblast growth factor, a molecule which lacks the signal peptide sequence for transport into the endoplasmic reticulum, could be directly through mechanically induced membrane disruptions of endothelial cells growing in vivo and in vitro.
Role of CFTR in Autosomal Recessive Polycystic Kidney Disease (2001)

An extensive body of in vitro data implicates epithelial chloride secretion, mediated through cystic fibrosis transmembrane conductance regulator (CFTR) protein, in generating or maintaining fluid filled cysts in MDCK cells and in human autosomal dominant polycystic kidney disease (ADPKD). In contrast, few studies have addressed the pathophysiology of fluid secretion in cyst formation and enlargement in autosomal recessive polycystic kidney disease (ARPKD). Murine models of targeted disruptions or deletions of specific genes have created opportunities to examine the role of individual gene products in normal development and/or disease pathophysiology. The creation of a murine model of CF, which lacks functional CFTR protein, provides the opportunity to determine whether CFTR activity is required for renal cyst formation in vivo. Therefore, this study sought to determine whether renal cyst formation could be prevented by genetic complementation of the BPK murine model of ARPKD with the CFTR knockout mouse. The results of this study reveal that in animals that are homozygous for the cystic gene (bpk), the lack of functional CFTR protein on the apical surface of cystic epithelium does not provide protection against cyst growth and subsequent decline in renal function. Double mutant mice (bpk -/-; cftr -/-) developed massively enlarged kidneys and died, on average, 7 d earlier than cystic, non-CF mice (bpk -/-; cftr +/+/-). This suggests fundamental differences in the mechanisms of transtubular fluid secretion in animal models of ARPKD compared with ADPKD.
Demographic prediction based on user's browsing behavior (2007)

Demographic information plays an important role in personalized web applications. However, it is usually not easy to obtain this kind of personal data such as age and gender. In this paper, we made a first approach to predict users' gender and age from their Web browsing behaviors, in which the Webpage view information is treated as a hidden variable to propagate demographic information between different users. There are three main steps in our approach: First, learning from the Webpage click-though data, Webpages are associated with users' (known) age and gender tendency through a discriminative model; Second, users' (unknown) age and gender are predicted from the demographic information of the associated Webpages through a Bayesian framework; Third, based on the fact that Webpages visited by similar users may be associated with similar demographic tendency, and users with similar demographic information would visit similar Webpages, a smoothing component is employed to overcome the data sparseness of web click-though log. Experiments are conducted on a real web click-through log to demonstrate the effectiveness of the proposed approach. The experimental results show that the proposed algorithm can achieve up to 30.4% improvements on gender prediction and 50.3% on age prediction in terms of macro F1, compared to baseline algorithms.