gebhart/patrepeval huggingface dataset:
Increased Phase Synchronization between Intracranial Pressure and Arterial Blood Pressure during Elevated Intracranial Pressure in Dogs (2005)

We applied the concept of "phase synchronization" from nonlinear dynamics to the complex relationship between intracranial pressure (ICP) and arterial blood pressure (ABP) signals. This method is based on multiresolution wavelet transform (MRWT) in which the signals are divided into different frequency bands. We examined ICP and ABP signals from anaesthetized dogs, exploring normal ICP and elevated ICP by 1~3 ml injection of saline into the cerebral ventricles. Phase synchronization analyses show an interesting phenomenon of phase reset from relatively uniform phase distribution to phase clustering around 0&#176; after injection. To further quantitatively measure phase synchronization, phase coherence is used to distinguish the dynamics of normal ICP and elevated ICP by saline injection. Elevated ICP exhibits higher phase coherence than that of normal ICP. The results suggest that the association between ICP and ABP may involve nonlinear mechanisms of regulation. The clinical application of this method is in investigation.
T lymphocytes from human atherosclerotic plaques recognize oxidized low density lipoprotein. (1995)

Atherosclerosis, an underlying cause of myocardial infarction, stroke, and other cardiovascular diseases, consists of focal plaques characterized by cholesterol deposition, fibrosis, and inflammation. The presence of activated T lymphocytes and macrophages and high expression of HLA class II molecules are indicative of a local immunologic activation in the atherosclerotic plaque, but the antigen(s) involved has not yet been identified. We established T-cell clones from human atherosclerotic plaques using polyclonal mitogens as stimuli and exposed the clones to potential antigens in the presence of autologous monocytes as antigen-presenting cells. Four of the 27 CD4+ clones responded to oxidized low density lipoprotein (oxLDL) by proliferation and cytokine secretion; this response was dependent on autologous antigen-presenting cells and restricted by HLA-DR. All clones that responded to oxLDL secreted interferon gamma upon activation, but only one produced interleukin 4, suggesting that the response to oxLDL results in immune activation and inflammation but may not be a strong stimulus to antibody production. No significant response to oxLDL could be detected in CD4+ T-cell clones derived from the peripheral blood of the same individuals. Together, the present data suggest that the inflammatory infiltrate in the atherosclerotic plaque is involved in a T-cell-dependent, autoimmune response to oxLDL.
Histone Deimination As a Response to Inflammatory Stimuli in Neutrophils (2008)

Posttranslational modifications, such as the deimination of arginine to citrulline by peptidyl arginine deiminase (PAD4), change protein structure and function. For autoantigens, covalent modifications represent a mechanism to sidestep tolerance and stimulate autoimmunity. To examine conditions leading to histone deimination in neutrophils, we used Abs that detect citrullines in the N terminus of histone H3. Deimination was investigated in human neutrophils and HL-60 cells differentiated into granulocytes. We observed rapid and robust H3 deimination in HL-60 cells exposed to LPS, TNF, lipoteichoic acid, f-MLP, or hydrogen peroxide, which are stimuli that activate neutrophils. Importantly, we also observed H3 deimination in human neutrophils exposed to these stimuli. Citrullinated histones were identified as components of extracellular chromatin traps (NETs) produced by degranulating neutrophils. In contrast, apoptosis proceeded without detectable H3 deimination in HL-60 cells exposed to staurosporine or camptothecin. We conclude that histone deimination in neutrophils is induced in response to inflammatory stimuli and not by treatments that induce apoptosis. Our results further suggest that deiminated histone H3, a covalently modified form of a prominent nuclear autoantigen, is released to the extracellular space as part of the neutrophil response to infections. The possible association of a modified autoantigen with microbial components could, in predisposed individuals, increase the risk of autoimmunity.
Mechanism of the Stimulatory Effect of Growth Hormone on Longitudinal Bone Growth* (1987)

AT THE beginning of this century Aschner (1) demonstrated a relationship between a factor in the pituitary and body growth. In subsequent experiments Evans and Long (2) produced supranormal growth in intact rats with administration of bovine pituitary extracts. In the 1940s a highly purified protein was isolated from bovine pituitaries (3, 4) that produced somatic growth when administered to hypophysectomized or normal rats. This protein exhibited no or small effects on the gonads and the thyroid gland and was called GH or somatotropin. The molecular structure of GH was not revealed until the beginning of the 1970s when the total amino acid sequence of GH was determined (5, 6). As early as 1923 Dott and Fraser (7) observed a decrease in epiphyseal cartilage width in cats and dogs after hypophysectomy. Dott (8) also found that treatment with extracts from the anterior pituitary lobe partially reversed this effect. Freud and co-workers (9) found that GH increased the nose-tail length in hypophysectomized rats by increasing the thickness of growth zones in the tail vertebrae, suggesting that GH increases the thickness of the growth plate by stimulating the proliferation of chondrocytes.
Conversion of Oxygen Derivatives of Hydrocarbons into Butadiene. (1945)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTConversion of Oxygen Derivatives of Hydrocarbons into Butadiene.Gustav. Egloff and George. HullaCite this: Chem. Rev. 1945, 36, 1, 63–141Publication Date (Print):February 1, 1945Publication History Published online1 May 2002Published inissue 1 February 1945https://pubs.acs.org/doi/10.1021/cr60113a002https://doi.org/10.1021/cr60113a002research-articleACS PublicationsRequest reuse permissionsArticle Views487Altmetric-Citations11LEARN 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-Alertsclose Get e-Alerts
Modulation of eDNA Release and Degradation Affects Staphylococcus aureus Biofilm Maturation (2009)

Recent studies have demonstrated a role for Staphylococcus aureus cidA-mediated cell lysis and genomic DNA release in biofilm adherence. The current study extends these findings by examining both temporal and additional genetic factors involved in the control of genomic DNA release and degradation during biofilm maturation. Cell lysis and DNA release were found to be critical for biofilm attachment during the initial stages of development and the released DNA (eDNA) remained an important matrix component during biofilm maturation. This study also revealed that an lrgAB mutant exhibits increased biofilm adherence and matrix-associated eDNA consistent with its proposed role as an inhibitor of cidA-mediated lysis. In flow-cell assays, both cid and lrg mutations had dramatic effects on biofilm maturation and tower formation. Finally, staphylococcal thermonuclease was shown to be involved in biofilm development as a nuc mutant formed a thicker biofilm containing increased levels of matrix-associated eDNA. Together, these findings suggest a model in which the opposing activities of the cid and lrg gene products control cell lysis and genomic DNA release during biofilm development, while staphylococcal thermonuclease functions to degrade the eDNA, possibly as a means to promote biofilm dispersal.
Induced pluripotent stem cells as a model for diabetes investigation (2015)

Mouse and human induced pluripotent stem cells (iPSCs) may represent a novel approach for modeling diabetes. Taking this into consideration, the aim of this study was to generate and evaluate differentiation potential of iPSCs from lep(db/db) (db/db) mice, the model of diabetes type 2 as well as from patients with Maturity Onset Diabetes of the Young 3 (HNF1A MODY). Murine iPSC colonies from both wild type and db/db mice were positive for markers of pluripotency: Oct3/4A, Nanog, SSEA1, CDy1 and alkaline phosphatase and differentiated in vitro and in vivo into cells originating from three germ layers. However, our results suggest impaired differentiation of db/db cells into endothelial progenitor-like cells expressing CD34 and Tie2 markers and their reduced angiogenic potential. Human control and HNF1A MODY reprogrammed cells also expressed pluripotency markers: OCT3/4A, SSEA4, TRA-1-60, TRA-1-81, formed embryoid bodies (EBs) and differentiated into cells of three germ layers. Additionally, insulin expressing cells were obtained from those partially reprogrammed cells with direct as well as EB-mediated differentiation method. Our findings indicate that disease-specific iPSCs may help to better understand the mechanisms responsible for defective insulin production or vascular dysfunction upon differentiation toward cell types affected by diabetes.
A putative novel role for plant defensins: a defensin from the zinc hyper‐accumulating plant, Arabidopsis halleri, confers zinc tolerance (2006)

The metal tolerance of metal hyper-accumulating plants is a poorly understood mechanism. In order to unravel the molecular basis of zinc (Zn) tolerance in the Zn hyper-accumulating plant Arabidopsis halleri ssp. halleri, we carried out a functional screening of an A. halleri cDNA library in the yeast Saccharomyces cerevisiae to search for genes conferring Zn tolerance to yeast cells. The screening revealed four A. halleri defensin genes (AhPDFs), which induced Zn but not cadmium (Cd) tolerance in yeast. The expression of AhPDF1.1 under the control of the 35S promoter in A. thaliana made the transgenic plants more tolerant to Zn than wild-type plants, but did not change the tolerance to Cd, copper (Cu), cobalt (Co), iron (Fe) or sodium (Na). Thus, AhPDF1.1 is able to confer Zn tolerance both to yeast and plants. In A. halleri, defensins are constitutively accumulated at a higher level in shoots than in A. thaliana. A. halleri defensin pools are Zn-responsive, both at the mRNA and protein levels. In A. thaliana, some but not all defensin genes are induced by ZnCl2 treatment, and these genes are not induced by NaCl treatment. Defensins, found in a very large number of organisms, are known to be involved in the innate immune system but have never been found to play any role in metal physiology. Our results support the proposition that defensins could be involved in Zn tolerance in A. halleri, and that a role for plant defensins in metal physiology should be considered.
Nucleoporins Nup98 and Nup214 Participate in Nuclear Export of Human Immunodeficiency Virus Type 1 Rev (1999)

Human immunodeficiency virus type 1 (HIV-1) Rev contains a leucine-rich nuclear export signal that is essential for its nucleocytoplasmic export mediated by hCRM1. We examined the role of selected nucleoporins, which are located in peripheral structures of the nuclear pore complex and are thought to be involved in export, in Rev function in human cells. First, we found that upon actinomycin D treatment, Nup98, but not Nup214 or Nup153, is able to translocate to the cytoplasm of HeLa cells, demonstrating that Nup98 may act as a soluble factor. We further showed that Rev can recruit Nup98 and Nup214, but not Nup153, to the nucleolus. We also found that the isolated FG-containing repeat domains of Nup98 and Nup214, but not those of Nup153, competitively inhibit the Rev/RRE-mediated expression of HIV. Taken together, the recruitment of Nup98 and Nup214 by Rev and the competitive inhibition exhibited by their NP domains demonstrate direct participation of Nup98 and Nup214 in the Rev-hCRM1-mediated export.
Simulation of light intensity dependent current characteristics of polymer solar cells (2004)

An extended replacement circuit describing the current–voltage characteristics of bulk heterojunction polymer solar cells at different light bias levels is introduced and discussed. A one diode-model is expanded by an extraction model for photogenerated carriers taking into account the effective reduction of the mean distance which the charge carriers cover when sweeping the electrical bias through the fourth quadrant of the solar cell. The model properly describes the current–voltage behavior of bulk heterojunction solar cells over more than three orders in light intensity with one set of parameters.
Corner stitching for L-shaped tiles (2002)

The corner-stitching technique proposed by J.K. Ousterhout (1984) is extended for rectangular objects in interactive VLSI layout editors to L-shaped objects, thus providing added flexibility in the design of VLSI circuits. It is shown theoretically that the authors' method for handling L-shaped objects is more space-efficient than an alternative method based on a direct application of the original corner-stitching method.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Novel Fluorogenic Substrates for Imaging β-Lactamase Gene Expression (2003)

A new class of small nonfluorescent fluorogenic substrates becomes brightly fluorescent after beta-lactamase hydrolysis with up to 153-fold enhancement in the fluorescence intensity. Less than 500 fM of beta-lactamase in cell lysates can be readily detected, and beta-lactamase expression in living cells can be imaged with a red fluorescence derivative. These new fluorogenic substrates should find uses in clinical diagnostics and facilitate the applications of beta-lactamase as a biosensor.
Purification and properties of phospholipase A1 produced by Corticium centrifugum. (1979)

Phospholipase Al, purified from the culture filtrate of Corticium centrifugum, was found to possess lysophospholipase 1 activity. The isoelectric point was pH 3.3, and the molecular weight was about 26, 800. Both enzyme activities had their pH optimum between 4.0 and 4.5 and their pH stability between 6.0 and 8.0, and were heat-unstable. Both were inhibited by p-diazobenzenesulfonic acid and N-bromosuccinimide. Although ether, 1-propanol and Triton X-100 stimulated phospholipase AI activity, these substances showed an inhibitory effect against lysophospholipase I activity. Phospholipase Al activity was almost completely inhibited by Fe2+, Fe3+ and Al3+, but the inhibition was lessened by the presence of Triton X-100. Lysophospholipase 1 activity was inhibited by Hg2+, Fe3+ and Al3+. The mode of inhibition by Fe3+ against lysophospholipase 1 activity was apparently an uncompetitive type. Phospholipase Ai hydrolyzed various phospholipids, but not triolein.
Elevated levels of 92‐kd type IV collagenase (matrix metalloproteinase 9) in giant cell arteritis (1996)

Gelatinase activity, and specifically MMP-9 levels, are substantially elevated in sera of patients with GCA. Detection of MMP-9 mRNA in the lamina media of inflamed vasculature suggests that degradation of intercellular matrix, particularly elastic fibers, may play a key role in the pathogenesis of GCA. Further studies are needed to determine if the circulating MMP-9 level could be utilized as a clinical marker of disease activity.
The candidate tumor suppressor gene, RASSF1A , from human chromosome 3p21.3 is involved in kidney tumorigenesis (2001)

Clear cell-type renal cell carcinomas (clear RCC) are characterized almost universally by loss of heterozygosity on chromosome 3p, which usually involves any combination of three regions: 3p25-p26 (harboring the VHL gene), 3p12-p14.2 (containing the FHIT gene), and 3p21-p22, implying inactivation of the resident tumor-suppressor genes (TSGs). For the 3p21-p22 region, the affected TSGs remain, at present, unknown. Recently, the RAS association family 1 gene (isoform RASSF1A), located at 3p21.3, has been identified as a candidate lung and breast TSG. In this report, we demonstrate aberrant silencing by hypermethylation of RASSF1A in both VHL-caused clear RCC tumors and clear RCC without VHL inactivation. We found hypermethylation of RASSF1A's GC-rich putative promoter region in most of analyzed samples, including 39 of 43 primary tumors (91%). The promoter was methylated partially or completely in all 18 RCC cell lines analyzed. Methylation of the GC-rich putative RASSF1A promoter region and loss of transcription of the corresponding mRNA were related causally. RASSF1A expression was reactivated after treatment with 5-aza-2'-deoxycytidine. Forced expression of RASSF1A transcripts in KRC/Y, a renal carcinoma cell line containing a normal and expressed VHL gene, suppressed growth on plastic dishes and anchorage-independent colony formation in soft agar. Mutant RASSF1A had reduced growth suppression activity significantly. These data suggest that RASSF1A is the candidate renal TSG gene for the 3p21.3 region.
A Yeast Golgi E-type ATPase with an Unusual Membrane Topology (1999)

E-type ATPases are involved in many biological processes such as modulation of neural cell activity, prevention of intravascular thrombosis, and protein glycosylation. In this study, we show that a gene of Saccharomyces cerevisiae, identified by similarity to that of animal ectoapyrase CD39, codes for a new member of the E-type ATPase family (Apy1p). Overexpression of Apy1p in yeast cells causes an increase in intracellular membrane-bound nucleoside di- and triphosphate hydrolase activity. The activity is highest with ADP as substrate and is stimulated similarly by Ca (2+), Mg(2+), and Mn(2+). The results also indicate that Apy1p is an integral membrane protein located predominantly in the Golgi compartment. Sequence analysis reveals that Apy1p contains one large NH(2)-terminal hydrophilic apyrase domain, one COOH-terminal hydrophilic domain, and two hydrophobic stretches in the central region of the polypeptide. Although no signal sequence is found at the NH(2)-terminal portion of the protein and no NH(2)-terminal cleavage of the protein is observed, demonstrated by the detection of NH(2)-terminal tagged Apy1p, the NH(2)-terminal domain of Apylp is on the luminal side of the Golgi apparatus, and the COOH-terminal hydrophilic domain binds to the cytoplasmic face of the Golgi membrane. The second hydrophobic stretch of Apy1p is the transmembrane domain. These results indicate that Apylp is a type III transmembrane protein; however, the size of the Apy1p extracytoplasmic NH(2) terminus is much larger than those of other type III transmembrane proteins, suggesting that a novel translocation mechanism is utilized.
DNA sequence of theputAgene fromSalmonella typhimurium: a bifunctional membrane-associated dehydrogenase that binds DNA (1993)

Catabolism of proline is widespread in prokaryotes and in mitochondria of eukaryotic cells.In enteric bacteria, the put4 gene encodes a membrane-associated dehydrogenase (EC 1.5.99.8) that oxidizes proline to glutamate for use as the sole carbon, nitrogen or energy source (5).In addition, PutA protein also functions as the autogenous transcriptional repressor of the put operon (6, 10).The structure and function of PutA protein are interesting because it is a very large protein with multiple functions: (i) it can be isolated in both monomeric and dimeric forms (8), (ii) it has two separate enzymatic activities -proline dehydrogenase and pyrroline-5-carboxylic acid (P5C) dehydrogenase ( 8), (iii) it specifically binds put control region DNA and acts as an autogenous transcriptional repressor of the put operon (10), (iv) it binds to the cytoplasmic membrane and interacts with the electron transport chain (5), (v) it binds a number of substrates -proline, P5C, the cytoplasmic membrane, DNA, FAD, and NAD (5).In this paper we describe the complete DNA sequence of the
Selective Tethering of Ligands and Proteins to a Microfluidically Patterned Electroactive Fluid Lipid Bilayer Array (2010)

We report a new, quantitative methodology to pattern and present ligands from planar, supported, fluid lipid bilayers. By combining microfluidic lithography (microFL) with an electroactive, chemoselective interfacial reaction strategy, a number of ligands as well as protein concanavalin A were immobilized in lipid microarrays. Electroactive vesicles were generated after the spontaneous insertion of hydroquinone-tethered alkane (H(2)Q) into egg palmitoyl-oleoyl phosphatidylcholine (egg-POPC), followed by subsequent fusion to a siloxane-terminated self-assembled monolayer (SAM) on gold. An advantage of the H(2)Q system is that it can be electrochemically oxidized to the corresponding quinone (Q), followed by rapid chemoselective conjugation with oxyamine-functionalized (RONH(2)) ligands. The oxime product is also electroactive, and the reaction can be monitored and the amount of ligand bound can be quantified by electrochemistry. The bilayers were characterized by electrochemistry, fluorescence microscopy, and ellipsometry and were determined to be fluid by fluorescence recovery after photobleaching (FRAP). This strategy provides a synergistic method to pattern and present a number of ligands or biomolecules from the bilayer surface for the evaluation of enzyme or protein binding to biomembranes.
Cascade error projection: an efficient hardware learning algorithm (2002)

A new learning algorithm, termed cascade error projection (CEP), which provides efficient learning in hardware is presented. This algorithm is adapted a constructive architecture from cascade correlation and the dynamical stepsize of A/D conversion from the cascade backpropagation algorithm. The CEP technique is faster to execute, because part of the weights are deterministically obtained, and the learning of the remaining weights from the inputs to the hidden unit is performed as a single-layer perceptron learning with previously determined weights kept frozen. In addition, one can start out with zero weight values when the learning of each layer is commenced. Further, unlike cascade correlation algorithm, only a single hidden unit is added at a time. Therefore, the simplicity in hardware implementation is also achieved. In simulation, a fixed 100 epoch iterations is used for each single-layer perceptron learning. The highlight of this algorithm is that with round-off method, 5- to 8-bit parity problems can be solved with a limited synaptic resolution of only 3- to 4-bit, and the same problem with truncation technique would be solved with 5-bit or more synaptic resolution.