gebhart/patrepeval huggingface dataset:
DEP-on-a-Chip: Dielectrophoresis Applied to Microfluidic Platforms (2019)

Dielectric particles in a non-uniform electric field are subject to a force caused by a phenomenon called dielectrophoresis (DEP). DEP is a commonly used technique in microfluidics for particle or cell separation. In comparison with other separation methods, DEP has the unique advantage of being label-free, fast, and accurate. It has been widely applied in microfluidics for bio-molecular diagnostics and medical and polymer research. This review introduces the basic theory of DEP, its advantages compared with other separation methods, and its applications in recent years, in particular, focusing on the different electrode types integrated into microfluidic chips, fabrication techniques, and operation principles.
GaN Nanobelt-Based Strain-Gated Piezotronic Logic Devices and (2013)

Using the piezoelectric polarization charges created atthe metalGaNnanobelt (NB)interfaceunder straintomodulate transport of local charge carriers across the Schottky barrier, the piezotroniceffectisutilizedtoconvertmechanicalstimuliappliedon the wurtzite-structured GaN NB into electronic controlling signals, basedonwhichtheGaNNBstrain-gatedtransistors(SGTs)havebeen fabricated. By further assembling and integrating GaN NB SGTs, universal logic devices such as NOT, AND, OR, NAND, NOR, and XOR gates have been demonstrated for performing mechanicalelec- tricalcoupledpiezotronic logicoperations. Moreover,basicpiezotronic computationsuchasone-bitbinary addition overtheinput mechanical strains with corresponding computation results in an electrical domain by half-adder has been implemented. The strain-gated piezotronic logic devices may find applications in humanmachine interfacing, active flexible/stretchable electronics, MEMS, biomedical diagnosis/therapy, and prosthetics.
Mechanically Robust Gelatin–Alginate IPN Hydrogels by a Combination of Enzymatic and Ionic Crosslinking Approaches (2013)

In this report, novel biopolymer hydrogels composed of gelatin and alginate with an interpenetrating polymer network (IPN) structure were prepared by a combination of enzymatic and ionic crosslinking approaches. The gelation processes of the IPN hydrogels were monitored using rheological techniques. The data confirmed the formation of dual networks: one gelatin network crosslinked by transglutaminase (TG) and another alginate network crosslinked by calcium ions. The results of mechanical testing revealed that the tensile and compressive strength of the hydrogels crosslinked in the presence of both TG and calcium ions were significantly improved. Preliminary studies have also shown that the hydrogels can support cell adhesion and spreading. These mechanically robust biopolymer hydrogels prepared by such biocompatible approaches are promising for the development of tissue engineering scaffolds.
Consumption of vitamin B6 reduces colonic damage and protein expression of HSP70 and HO-1, the anti-tumor targets, in rats exposed to 1,2-dimethylhydrazine (2011)

Mounting evidence indicates that vitamin B6 is a protective factor for colon cancer. Elevations in colonic damage, cell proliferation and heat shock proteins (HSPs, molecular chaperones) have been suggested to be associated with colon carcinogenesis. This study was performed to examine the effect of dietary levels of vitamin B6 (1, 7 or 35 mg pyridoxine HCl/kg diet) for 22 weeks on colon damage, epithelial cell proliferation and expression of HSPs in rats exposed to 1,2-dimethylhydrazine (DMH). Supplemental vitamin B6 with a low vitamin B6 diet (1 mg pyridoxine HCl/kg diet) significantly reduced fecal activity of intestinal alkaline phosphatase (an index of intestinal damage) and the colonic epithelium PCNA labeling index (a marker of cell proliferation). Analysis using ELISA indicated that supplemental vitamin B6 significantly lowered protein levels of colonic HSP70 and heme oxygenase-1, HSP32 (HO-1). However, real-time RT-PCR analysis revealed that the mRNA levels of these HSPs were not decreased by supplemental vitamin B6, suggesting that the lowering effect of vitamin B6 on the colon protein expression of the HSPs is mediated by mechanisms not involving altered gene expression. This study provided evidence that dietary supplemental vitamin B6 suppresses colon damage, epithelial cell proliferation and protein expression of HSP70 and HO-1, the targets for anti-tumor agents, in rats exposed to DMH.
Algorithmic detection of semantic similarity (2005)

Automatic extraction of semantic information from text and links in Web pages is key to improving the quality of search results. However, the assessment of automatic semantic measures is limited by the coverage of user studies, which do not scale with the size, heterogeneity, and growth of the Web. Here we propose to leverage human-generated metadata --- namely topical directories --- to measure semantic relationships among massive numbers of pairs of Web pages or topics. The Open Directory Project classifies millions of URLs in a topical ontology, providing a rich source from which semantic relationships between Web pages can be derived. While semantic similarity measures based on taxonomies (trees) are well studied, the design of well-founded similarity measures for objects stored in the nodes of arbitrary ontologies (graphs) is an open problem. This paper defines an information-theoretic measure of semantic similarity that exploits both the hierarchical and non-hierarchical structure of an ontology. An experimental study shows that this measure improves significantly on the traditional taxonomy-based approach. This novel measure allows us to address the general question of how text and link analyses can be combined to derive measures of relevance that are in good agreement with semantic similarity. Surprisingly, the traditional use of text similarity turns out to be ineffective for relevance ranking.
Involvement of Raft Aggregates Enriched in Fas/CD95 Death-Inducing Signaling Complex in the Antileukemic Action of Edelfosine in Jurkat Cells (2009)

This work shows the involvement of DISC clusters in lipid raft aggregates as a supramolecular and physical entity responsible for the induction of apoptosis in leukemic cells by the antitumor drug edelfosine. Our data set a novel framework and paradigm in leukemia therapy, as well as in death receptor-mediated apoptosis.
Inhibition of B Cell Death Causes the Development of an IgA Nephropathy in (New Zealand White × C57BL/6)F1- bcl-2 Transgenic Mice (2004)

Little is known about the pathogenic mechanisms of IgA nephropathy, despite being the most prevalent form of glomerulonephritis in humans. We report in this study that in (New Zealand White (NZW) x C57BL/6)F(1) mice predisposed to autoimmune diseases, the expression of a human bcl-2 (hbcl-2) transgene in B cells promotes a CD4-dependent lupus-like syndrome characterized by IgG and IgA hypergammaglobulinemia, autoantibody production, and the development of a fatal glomerulonephritis. Histopathological analysis of glomerular lesions reveals that the glomerulonephritis observed in these animals resembles that of human IgA nephropathy. The overexpression of Bcl-2 in B cells selectively enhances systemic IgA immune responses to T-dependent Ags. Significantly, serum IgA purified from (NZW x C57BL/6)F(1)-hbcl-2 transgenic mice, but not from nontransgenic littermates, shows reduced levels of galactosylation and sialylation and an increased ability to deposit in the glomeruli, as observed in human patients with IgA nephropathy. Our results indicate that defects in the regulation of B lymphocyte survival associated with aberrant IgA glycosylation may be critically involved in the pathogenesis of IgA nephropathy, and that (NZW x C57BL/6)F(1)-hbcl-2 Tg mice provide a new experimental model for this form of glomerulonephritis.
Chemical synthesis of the thymidylate synthase gene. (1990)

A 978-base-pair gene that encodes thymidylate synthase (TS; 5,10-methylenetetrahydrofolate:dUMP C-methyltransferase, EC 2.1.1.45) from Lactobacillus casei has been synthesized and inserted into Escherichia coli expression vectors. The DNA sequence contains 35 unique restriction sites that are located an average of 28 base pairs apart throughout the entire length of the gene. A ribosome binding site was included 9 base pairs upstream from the translation start site and codon usage was adjusted to ensure efficient translation in E. coli. The TS gene is flanked by unique EcoRI and HindIII restriction sites that render the gene portable to any of several E. coli expression vectors. Catalytically active TS encoded by the synthetic gene is expressed in large amounts (10-20% of the soluble protein) and is indistinguishable from that isolated from L. casei. The utility of the synthetic gene for mutagenesis is demonstrated by a single experiment in which His-199 was replaced with 14 different amino acids. Analysis of the mutants by genetic complementation indicates that TS can tolerate a number of amino acid substitutions at that position and shows that His-199 is not strictly required for catalytic activity.
Transgenic mice for studies of the renin–angiotensin system in hypertension (2004)

Hypertension is a polygenic and multi-factorial disorder that is extremely prevalent in western societies, and thus has received a great deal of attention by the research community. The renin-angiotensin system has a strong impact on the control of blood pressure both in the short- and long-term, making it one of the most extensively studied physiological systems. Nevertheless, despite decades of research, the specific mechanisms implicated in its action on blood pressure and electrolyte balance, as well as its integration with other cardiovascular pathways remains incomplete. The production of transgenic models either over-expressing or knocking-out specific components of the renin-angiotensin system has given us a better understanding of its role in the pathogenesis of hypertension. Moreover, our attention has recently been refocused on local tissue renin-angiotensin systems and their physiological effect on blood pressure and end-organ damage. Herein, we will review studies using genetic manipulation of animals to determine the role of the endocrine and tissue renin-angiotensin system in hypertension. We will also discuss some untraditional approaches to target the renin-angiotensin system in the kidney.
Crystallographic studies of tin(II) compounds. I. Crystal structure of tin(II) fluoride, SnF2 (1976)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTCrystallographic studies of tin(II) compounds. I. Crystal structure of tin(II) fluoride, SnF2Robert C. McDonald, Herbert H. K. Hau, and Klaas. EriksCite this: Inorg. Chem. 1976, 15, 4, 762–765Publication Date (Print):April 1, 1976Publication History Published online1 May 2002Published inissue 1 April 1976https://pubs.acs.org/doi/10.1021/ic50158a003https://doi.org/10.1021/ic50158a003research-articleACS PublicationsRequest reuse permissionsArticle Views516Altmetric-Citations66LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-AlertscloseSupporting Info (1)»Supporting Information Supporting Information Get e-Alerts
Dietary Protection Against Free Radicals: A Case for Multiple Testing to Establish Structure-activity Relationships for Antioxidant Potential of Anthocyanic Plant Species (2009)

DNA damage by reactive species is associated with susceptibility to chronic human degenerative disorders. Anthocyanins are naturally occurring antioxidants, that may prevent or reverse such damage. There is considerable interest in anthocyanic food plants as good dietary sources, with the potential for reducing susceptibility to chronic disease. While structure-activity relationships have provided guidelines on molecular structure in relation to free hydroxyl-radical scavenging, this may not cover the situation in food plants where the anthocyanins are part of a complex mixture, and may be part of complex structures, including anthocyanic vacuolar inclusions (AVIs). Additionally, new analytical methods have revealed new structures in previously-studied materials. We have compared the antioxidant activities of extracts from six anthocyanin-rich edible plants (red cabbage, red lettuce, blueberries, pansies, purple sweetpotato skin, purple sweetpotato flesh and Maori potato flesh) using three chemical assays (DPPH, TRAP and ORAC), and the in vitro Comet assay. Extracts from the flowering plant, lisianthus, were used for comparison. The extracts showed differential effects in the chemical assays, suggesting that closely related structures have different affinities to scavenge different reactive species. Integration of anthocyanins to an AVI led to more sustained radical scavenging activity as compared with the free anthocyanin. All but the red lettuce extract could reduce endogenous DNA damage in HT-29 colon cancer cells. However, while extracts from purple sweetpotato skin and flesh, Maori potato and pansies, protected cells against subsequent challenge by hydrogen peroxide at 0 degrees C, red cabbage extracts were pro-oxidant, while other extracts had no effect. When the peroxide challenge was at 37 degrees C, all of the extracts appeared pro-oxidant. Maori potato extract, consistently the weakest antioxidant in all the chemical assays, was more effective in the Comet assays. These results highlight the dangers of generalising to potential health benefits, based solely on identification of high anthocyanic content in plants, results of a single antioxidant assay and traditional approaches to structure activity relationships. Subsequent studies might usefully consider complex mixtures and a battery of assays.
Extracellular vesicles shed from gefitinib‐resistant nonsmall cell lung cancer regulate the tumor microenvironment (2014)

Epidermal growth factor receptor (EGFR)-tyrosine kinase inhibitors (TKIs), including gefitinib, are the first-line treatment of choice for nonsmall cell lung cancer patients who harbor activating EGFR mutations, however, acquired resistance to EGFR-TKIs is inevitable. The main objective of this study was to identify informative protein signatures of extracellular vesicles (EV) derived from gefitinib-resistant nonsmall cell lung cancer cells using proteomics analysis. Nano-LC-MS/MS analysis identified with high confidence (false discovery rate < 0.05, fold change ≥2) 664 EV proteins enriched in PC9R cells, which are resistant to gefitinib due to EGFR T790M mutation. Computational analyses suggested components of several signal transduction mechanisms including the AKT (also PKB, protein kinase B)/mTOR (mechanistic target of rapamycin) pathway are overrepresented in EV from PC9R cells. Treatment of recipient cells with EV harvested from PC9R cells increased phosphorylation of signaling molecules, and enhanced proliferation, invasion, and drug resistance to gefitinib-induced apoptosis. Dose- and time-dependent pharmaceutical inhibition of AKT/mTOR pathway overcame drug resistance of PC9R cells and those of H1975 exhibiting EGFR T790M mutation. Our findings provide new insight into an oncogenic EV protein signature regulating tumor microenvironment, and will aid in the development of novel diagnostic strategies for prediction and assessment of gefitinib resistance.
Effects of exercise on lymphocytes and cytokines (2000)

Moderate exercise across the life span seems to increase resistance to upper respiratory tract infections, whereas repeated strenuous exercise suppresses immune function. It is premature to offer advice on nutrition to athletes in order to alter the exercise induced immunosuppression found after exercise.
Gold-catalysed intramolecular trans-allylsilylation of alkynes forming 3-allyl-1-silaindenes (2008)

3-Allyl-1-silaindenes are synthesised from alkynes having an allylsilane moiety by a gold-catalysed intramolecular trans-allylsilylation reaction.
Aberrant Splicing in the PKD2 Gene as a Cause of Polycystic Kidney Disease (1999)

It is estimated that approximately 15% of families with autosomal dominant polycystic kidney disease (ADPKD) have mutations in PKD2. Identification of these mutations is central to identifying functionally important regions of gene and to understanding the mechanisms underlying the pathogenesis of the disorder. The current study describes mutations in six type 2 ADPKD families. Two single base substitution mutations discovered in the ORF in exon 14 constitute the most COOH-terminal pathogenic variants described to date. One of these mutations is a nonsense change and the other encodes an apparent missense variant. Reverse transcription-PCR from patient lymphoblast RNA showed that, in addition, both mutations resulted in out-of-frame splice variants by activating cryptic splice sites via different mechanisms. The apparent missense variant produced such a strong splicing signal that the processed transcript from the mutant chromosome did not contain any of the normally spliced, missense product. A third mutation, a nonconservative missense change effecting a negatively charged residue in the third transmembrane span, is likely pathogenic and defines a highly conserved residue consistent with a potential channel subunit function for polycystin-2. The remaining three mutations included two frame shifts resulting from deletion of one or two bases in exons 6 and 10, respectively, and a nonsense mutation due to a single base substitution in exon 4. The study also defined a novel intragenic polymorphism in exon 1 that will be useful in analyzing "second hits" in PKD2. Finally, the study demonstrates that there are reduced levels of normal polycystin-2 protein in lymphoblast lines from PKD2-affected individuals and that truncated mutant polycystin-2 cannot be detected in patient lymphoblasts, suggesting that the latter may be unstable in at least some tissues. The mutations described will serve as critical reagents for future functional studies in PKD2.
Pathogenesis of tendinopathies: inflammation or degeneration? (2009)

The intrinsic pathogenetic mechanisms of tendinopathies are largely unknown and whether inflammation or degeneration has the prominent role is still a matter of debate. Assuming that there is a continuum from physiology to pathology, overuse may be considered as the initial disease factor; in this context, microruptures of tendon fibers occur and several molecules are expressed, some of which promote the healing process, while others, including inflammatory cytokines, act as disease mediators. Neural in-growth that accompanies the neovessels explains the occurrence of pain and triggers neurogenic-mediated inflammation. It is conceivable that inflammation and degeneration are not mutually exclusive, but work together in the pathogenesis of tendinopathies.
Inhibition of 5-lipoxygenase activating protein decreases proteinuria in diabetic rats (2003)

These results suggest a role for FLAP other than the activation of 5-LO, possibly in protein handling, and point to FLAP antagonists as anti-proteinuric agents.
Whence Molecular Electronics? (2004)

The drive toward yet further miniaturization of silicon-based electronics has led to a revival of efforts to build devices with molecular-scale components. The field of molecular electronics is teeming with results, rationalizations, and speculations [HN1]. Some claims may have been exaggerated, but news stories of a crisis in the field (1) are premature. Reports of passive molecular electronics devices, such as tunnel junctions and rectifiers, as well as of active devices, for example, single-molecule transistors and molecular switch tunnel junctions, have withstood scientific scrutiny. Simple molecular electronic devices usually consist of organic molecules sandwiched between conducting electrodes. According to early predictions, such devices could show electron tunneling (2) [HN2] or one-way flow of current (rectification) [HN3] through the molecule (3). In most tunneling junctions, linear alkanes are sandwiched between metal electrodes. Measurements over the past 25 years (4, 5) have largely validated McConnell's prediction (2) that the tunnel current depends exponentially on the length of the molecules between conducting electrodes [HN4]. In rectifiers, a molecule composed of an electron donor, a bridge, and an electron acceptor is extended between two electrodes (see the first figure, top panel). Experiments (6, 7) have again validated the early prediction by Aviram and Ratner (3) [HN5].
Diminished Loss of Proteoglycans and Lack of Albuminuria in Protein Kinase C-α—Deficient Diabetic Mice (2004)

Activation of protein kinase C (PKC) isoforms has been implicated in the pathogenesis of diabetic nephropathy. We showed earlier that PKC-alpha is activated in the kidneys of hyperglycemic animals. We now used PKC-alpha(-/-) mice to test the hypothesis that this PKC isoform mediates streptozotocin-induced diabetic nephropathy. We observed that renal and glomerular hypertrophy was similar in diabetic wild-type and PKC-alpha(-/-) mice. However, the development of albuminuria was almost absent in the diabetic PKC-alpha(-/-) mice. The hyperglycemia-induced downregulation of the negatively charged basement membrane heparan sulfate proteoglycan perlecan was completely prevented in the PKC-alpha(-/-) mice, compared with controls. We then asked whether transforming growth factor-beta1 (TGF-beta1) and/or vascular endothelial growth factor (VEGF) is implicated in the PKC-alpha-mediated changes in the basement membrane. The hyperglycemia-induced expression of VEGF165 and its receptor VEGF receptor II (flk-1) was ameliorated in PKC-alpha(-/-) mice, whereas expression of TGF-beta1 was not affected by the lack of PKC-alpha. Our findings indicate that two important features of diabetic nephropathy-glomerular hypertrophy and albuminuria-are differentially regulated. The glucose-induced albuminuria seems to be mediated by PKC-alpha via downregulation of proteoglycans in the basement membrane and regulation of VEGF expression. Therefore, PKC-alpha is a possible therapeutic target for the prevention of diabetic albuminuria.
Novel template requirements of N4 virion RNA polymerase. (1978)

A DNA-dependent RNA polymerase has been purified from disrupted virions of the Escherichia coli bacteriophage N4. The RNA polymerase is phage-coded and is required for class I N4 RNA synthesis, which is defined as RNA synthesized in vivo in the absence of post-infection protein synthesis. A polypeptide of molecular weight 350,000 is detected when the purified enzyme is analyzed by sodium dodecyl sulfate/polyacrylamide gel electrophoresis. N4 RNA polymerase requires denatured DNA as a template in vitro and shows a strong preference for denatured N4 DNA. With this template, transcription is asymmetric. The RNA product is complementary to only the H strand of N4 DNA. Furthermore, only class I N4 RNA is synthesized. In vivo transcription by the N4 virion RNA polymerase is inhibited by coumermycin. This result suggests that the activity of E. coli DNA gyrase, an enzyme that introduces negative supertwists into DNA, is required for N4 transcription.