gebhart/patrepeval huggingface dataset:
l-Dopa and Streptozotocin-induced Diabetic Nepnropathy in Rats (1990)

The purpose of the present study was to determine whether the physiological dopamine prodrug, L-dopa, could suppress streptozotocin-induced diabetic glomerular hyperfiltration, and thus prevent further evolution of the diabetic nephropathy. Male Wistar rats treated with streptozotocin (60 mg/kg, intravenously) rapidly developed hyperglycemia which was stabilized (congruent to 4 g/L) by a daily insulin injection. Within two weeks, a significant increase in glomerular filtration rate (GFR) and a rise in the filtration fraction were observed as described in the early stage of diabetic nephropathy. Increase in both GFR and in the filtration fraction were normalized by treating the rats with L-dopa (10 mg/kg, subcutaneously, twice a day for one week). The effects of L-dopa were linked to endorenal DA synthesis and to DA-1 receptor stimulation since both carbidopa and SCH 23390 suppressed them.
Abstract 16024: Effect of Tadalafil on Exercise Parameters in Young Fontan Patients (2013)

Aim: Sildenafil improves ventilatory efficiency during exercise in Fontan patients, but requires three times a day dosing. We sought to assess the effects of a long-acting phosphodiesterase-5 inhib...
Isolation and identification of methanogen-specific DNA from blanket bog peat by PCR amplification and sequence analysis (1996)

The presence of methanogenic bacteria was assessed in peat and soil cores taken from upland moors. The sampling area was largely covered by blanket bog peat together with small areas of red-brown limestone and peaty gley. A 30-cm-deep core of each soil type was taken, and DNA was extracted from 5-cm transverse sections. Purified DNA was subjected to PCR amplification with primers IAf and 1100Ar, which specifically amplify 1.1 kb of the archaeal 16S rRNA gene, and ME1 and ME2, which were designed to amplify a 0.75-kb region of the alpha-subunit gene for methyl coenzyme M reductase (MCR). Amplification with both primer pairs was obtained only with DNA extracted from the two deepest sections of the blanket bog peat core. This is consistent with the notion that anaerobiosis is required for activity and survival of the methanogen population. PCR products from both amplifications were cloned, and the resulting transformants were screened with specific oligonucleotide probes internal to the MCR or archaeal 16S rRNA PCR product. Plasmid DNA was extracted from probe-positive clones of both types and the insert was sequenced. The DNA sequences of 8 MCR clones were identical, as were those of 16 of the 17 16S rRNA clones. One clone showed marked variation from the remainder in specific regions of the sequence. From a comparison of these two different 16S rRNA sequences, an oligonucleotide was synthesized that was 100% homologous to a sequence region of the first 16 clones but had six mismatches with the variant. This probe was used to screen primary populations of PCR clones, and all of those that were probe negative were checked for the presence of inserts, which were then sequenced. By using this strategy, further novel methanogen 16S rRNA variants were identified and analyzed. The sequences recovered from the peat formed two clusters on the end of long branches within the methanogen radiation that are distinct from each other. These cannot be placed directly with sequences from any cultured taxa for which sequence information is available.
Specificity of T lymphocyte lines for peptides of myelin basic protein. (1985)

T lymphocyte lines specific for myelin basic protein (BP) can mediate experimental autoimmune encephalomyelitis (EAE), or can protect against the active induction of the disease. To investigate the antigenic fine specificity of guinea pig (GP) BP-specific T cell lines raised from different rat strains, and to determine whether functionally different T lymphocyte lines and clones recognized the same or different regions of the BP molecule, the proliferation responses of line cells were assessed after stimulation with purified peptides of GP-BP. Lewis rat T cell lines and clones selected for responses to whole GP-BP responded selectively to the 68-88 amino acid sequence of GP-BP, but not to the 1-37, 43-67, or 89-169 sequences. The region of GP-BP recognized by Lewis T cells was additionally defined to include the 75-80 amino acid sequence, because a T cell clone responded equally to GP and rat BP which differed by only one amino acid at position 79, but did not respond to human or bovine BP, which had a Gly-His insertion in this region. T lymphocyte lines derived from the F344 and PVG (Weizmann) rat strains shared the same selective response to peptide 68-88, but lines from BN rats responded to an epitope(s) outside of the 68-88 sequence. The functional capacity of the various T cell lines to mediate experimental autoimmune encephalomyelitis (EAE) or to induce resistance against EAE was independent of their specificity for the different GP-BP peptides; lines specific for epitope(s) within or excluded from the 68-88 sequence could be encephalitogenic depending on their strain of origin, and various lines specific for the 68-88 peptide could induce both disease and protection, disease only, or neither activity.
A single heteromeric receptor complex is sufficient to mediate biological effects of transforming growth factor-beta ligands. (1994)

Transforming growth factor beta (TGF-beta), a multifunctional cytokine that regulates a variety of biological functions, signals through a heteromeric receptor complex of the type I and type II TGF-beta receptors. The type II receptor, a transmembrane serine-threonine kinase, was cloned based on its ability to directly bind TGF-beta. Recently, a number of candidate type I TGF-beta receptors have been isolated. Although only one of these transmembrane kinases (R4) has been shown to mediate TGF-beta-dependent gene activation, others bind TGF-beta when overexpressed in COS cells. Consequently, it has been postulated that the diversity of TGF-beta responses is generated through the association of distinct type I receptors with the type II TGF-beta receptor, thus creating receptor complexes of differential signaling capacities. In contrast to this model, we demonstrate that stable expression of only the R4 type I TGF-beta receptor in a mutant cell line lacking endogenous type I TGF-beta receptor was able to complex with the endogenous type II TGF-beta receptor and restore the effects of TGF-beta on inhibition of cell proliferation and activation of specific genes, regardless of which of the three mammalian isoforms of TGF-beta was used as the ligand. Therefore, R4 acts as a fully functional type I TGF-beta receptor, and the differential effects of TGF-beta are likely mediated by a single receptor complex consisting of R4 and the type II receptor.
Automatic 3D to 2D Registration for the Photorealistic Rendering of Urban Scenes (2005)

This paper presents a novel and efficient algorithm for the 3D range to 2D image registration problem in urban scene settings. Our input is a set of unregistered 3D range scans and a set of unregistered and uncalibrated 2D images of the scene. The 3D range scans and 2D images capture real scenes in extremely high detail. A new automated algorithm calibrates each 2D image and computes an optimized transformation between the 2D images and 3D range scans. This transformation is based on a match of 3D with 2D features that maximizes an overlap criterion. Our algorithm attacks the hard 3D range to 2D image registration problem in a systematic, efficient, and automatic way. Images captured by a high-resolution 2D camera, that moves and adjusts freely, are mapped on a centimeter-accurate 3D model of the scene providing photorealistic renderings of high quality. We present results from experiments in three different urban settings.
Escape from the Acute Wolff-Chaikoff Effect Is Associated with a Decrease in Thyroid Sodium/Iodide Symporter Messenger Ribonucleic Acid and Protein1 (1999)

In 1948, Wolff and Chaikoff reported that organic binding of iodide in the thyroid was decreased when plasma iodide levels were elevated (acute Wolff-Chaikoff effect), and that adaptation or escape from the acute effect occurred in approximately 2 days, in the presence of continued high plasma iodide concentrations. We later demonstrated that the escape is attributable to a decrease in iodide transport into the thyroid, lowering the intrathyroidal iodine content below a critical inhibitory threshold and allowing organification of iodide to resume. We have now measured the rat thyroid sodium/iodide symporter (NIS) messenger RNA (mRNA) and protein levels, in response to both chronic and acute iodide excess, in an attempt to determine the mechanism responsible for the decreased iodide transport. Rats were given 0.05% NaI in their drinking water for 1 and 6 days in the chronic experiments, and a single 2000-microg dose of NaI i.p. in the acute experiments. Serum was collected for iodine and hormone measurements, and thyroids were frozen for subsequent measurement of NIS, TSH receptor, thyroid peroxidase (TPO), thyroglobulin, and cyclophilin mRNAs (by Northern blotting) as well as NIS protein (by Western blotting). Serum T4 and T3 concentrations were significantly decreased at 1 day in the chronic experiments and returned to normal at 6 days, and were unchanged in the acute experiments. Serum TSH levels were unchanged in both paradigms. Both NIS mRNA and protein were decreased at 1 and 6 days after chronic iodide ingestion. NIS mRNA was decreased at 6 and 24 h after acute iodide administration, whereas NIS protein was decreased only at 24 h. TPO mRNA was decreased at 6 days of chronic iodide ingestion and 24 h after acute iodide administration. There were no iodide-induced changes in TSH receptor and thyroglobulin mRNAs. These data suggest that iodide administration decreases both NIS mRNA and protein expression, by a mechanism that is likely to be, at least in part, transcriptional. Our findings support the hypothesis that the escape from the acute Wolff-Chaikoff effect is caused by a decrease in NIS, with a resultant decreased iodide transport into the thyroid. The observed decrease in TPO mRNA may contribute to the iodine-induced hypothyroidism that is common in patients with Hashimoto's thyroiditis.
PAR2 absence completely rescues inflammation and ichthyosis caused by altered CAP1/Prss8 expression in mouse skin (2011)

Altered serine protease activity is associated with skin disorders in humans and in mice. The serine protease channel-activating protease-1 (CAP1; also termed protease serine S1 family member 8 (Prss8)) is important for epidermal homeostasis and is thus indispensable for postnatal survival in mice, but its roles and effectors in skin pathology are poorly defined. In this paper, we report that transgenic expression in mouse skin of either CAP1/Prss8 (K14-CAP1/Prss8) or protease-activated receptor-2 (PAR2; Grhl3(PAR2/+)), one candidate downstream target, causes epidermal hyperplasia, ichthyosis and itching. K14-CAP1/Prss8 ectopic expression impairs epidermal barrier function and causes skin inflammation characterized by an increase in thymic stromal lymphopoietin levels and immune cell infiltrations. Strikingly, both gross and functional K14-CAP1/Prss8-induced phenotypes are completely negated when superimposed on a PAR2-null background, establishing PAR2 as a pivotal mediator of pathogenesis. Our data provide genetic evidence for PAR2 as a downstream effector of CAP1/Prss8 in a signalling cascade that may provide novel therapeutic targets for ichthyoses, pruritus and inflammatory skin diseases.
A total synthesis of phytol (1967)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTA total synthesis of phytolKikumasa Sato, Shioji Mizuno, and Masao HirayamaCite this: J. Org. Chem. 1967, 32, 1, 177–180Publication Date (Print):January 1, 1967Publication History Published online1 May 2002Published inissue 1 January 1967https://pubs.acs.org/doi/10.1021/jo01277a043https://doi.org/10.1021/jo01277a043research-articleACS PublicationsRequest reuse permissionsArticle Views608Altmetric-Citations43LEARN 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
Syndecan and tenascin expression is induced by epithelial-mesenchymal interactions in embryonic tooth mesenchyme. (1989)

Morphogenesis of embryonic organs is regulated by epithelial-mesenchymal interactions associating with changes in the extracellular matrix (ECM). The response of the cells to the changes in the ECM must involve integral cell surface molecules that recognize their matrix ligand and initiate transmission of signal intracellularly. We have studied the expression of the cell surface proteoglycan, syndecan, which is a matrix receptor for epithelial cells (Saunders, S., M. Jalkanen, S. O'Farrell, and M. Bernfield. J. Cell Biol. In press.), and the matrix glycoprotein, tenascin, which has been proposed to be involved in epithelial-mesenchymal interactions (Chiquet-Ehrismann, R., E. J. Mackie, C. A. Pearson, and T. Sakakura. 1986. Cell. 47:131-139) in experimental tissue recombinations of dental epithelium and mesenchyme. Our earlier studies have shown that in mouse embryos both syndecan and tenascin are intensely expressed in the condensing dental mesenchyme surrounding the epithelial bud (Thesleff, I., M. Jalkanen, S. Vainio, and M. Bernfield. 1988. Dev. Biol. 129:565-572; Thesleff, I., E. Mackie, S. Vainio, and R. Chiquet-Ehrismann. 1987. Development. 101:289-296). Analysis of rat-mouse tissue recombinants by a monoclonal antibody against the murine syndecan showed that the presumptive dental epithelium induces the expression of syndecan in the underlying mesenchyme. The expression of tenascin was induced in the dental mesenchyme in the same area as syndecan. The syndecan and tenascin positive areas increased with time of epithelial-mesenchymal contact. Other ECM molecules, laminin, type III collagen, and fibronectin, did not show a staining pattern similar to that of syndecan and tenascin. Oral epithelium from older embryos had lost its ability to induce syndecan expression but the presumptive dental epithelium induced syndecan expression even in oral mesenchyme of older embryos. Our results indicate that the expression of syndecan and tenascin in the tooth mesenchyme is regulated by epithelial-mesenchymal interactions. Because of their early appearance, syndecan and tenascin may be used to study the molecular regulation of this interaction. The similar distribution patterns of syndecan and tenascin in vivo and in vitro and their early appearance as a result of epithelial-mesenchymal interaction suggest that these molecules may be involved in the condensation and differentiation of dental mesenchymal cells.
Design for network communities (1997)

Article Free Access Share on Design for network communities Authors: Elizabeth D. Mynatt Xerox PARC Xerox PARCView Profile , Annette Adler Xerox Systems Architecture Xerox Systems ArchitectureView Profile , Mizuko Ito Stanford University & Institute for Research on Learning Stanford University & Institute for Research on LearningView Profile , Vicki L. O'Day Xerox PARC Xerox PARCView Profile Authors Info & Claims CHI '97: Proceedings of the ACM SIGCHI Conference on Human factors in computing systemsMarch 1997 Pages 210–217https://doi.org/10.1145/258549.258707Published:27 March 1997Publication History 63citation1,662DownloadsMetricsTotal Citations63Total Downloads1,662Last 12 Months52Last 6 weeks7 Get Citation AlertsNew Citation Alert added!This alert has been successfully added and will be sent to:You will be notified whenever a record that you have chosen has been cited.To manage your alert preferences, click on the button below.Manage my Alerts New Citation Alert!Please log in to your account Save to BinderSave to BinderCreate a New BinderNameCancelCreateExport CitationPublisher SiteeReaderPDF
Global Burden of Untreated Caries (2015)

We aimed to consolidate all epidemiologic data about untreated caries and subsequently generate internally consistent prevalence and incidence estimates for all countries, 20 age groups, and both sexes for 1990 and 2010. The systematic search of the literature yielded 18,311 unique citations. After screening titles and abstracts, we excluded 10,461 citations as clearly irrelevant to this systematic review, leaving 1,682 for full-text review. Furthermore, 1,373 publications were excluded following the validity assessment. Overall, 192 studies of 1,502,260 children aged 1 to 14 y in 74 countries and 186 studies of 3,265,546 individuals aged 5 y or older in 67 countries were included in separate metaregressions for untreated caries in deciduous and permanent teeth, respectively, using modeling resources from the Global Burden of Disease 2010 study. In 2010, untreated caries in permanent teeth was the most prevalent condition worldwide, affecting 2.4 billion people, and untreated caries in deciduous teeth was the 10th-most prevalent condition, affecting 621 million children worldwide. The global age-standardized prevalence and incidence of untreated caries remained static between 1990 and 2010. There is evidence that the burden of untreated caries is shifting from children to adults, with 3 peaks in prevalence at ages 6, 25, and 70 y. Also, there were considerable variations in prevalence and incidence between regions and countries. Policy makers need to be aware of a predictable increasing burden of untreated caries due to population growth and longevity and a significant decrease in the prevalence of total tooth loss throughout the world from 1990 to 2010.
Paclitaxel Enhances Antibody-dependent Cell-mediated Cytotoxicity of Trastuzumab by Rapid Recruitment of Natural Killer Cells in HER2-positive Breast Cancer (2014)

Adding paclitaxel to trastuzumab significantly enhances ADCC, with levels twice as great as with trastuzumab monotherapy, through a rapid recruitment of NK cells. This finding suggests that the combination of trastuzumab and paclitaxel has a stronger-than-expected synergistic effect in HER2-positive breast cancer.
Human SA gene locus as a candidate locus for essential hypertension. (1994)

We have recently identified a candidate gene for rat genetic hypertension by identifying an mRNA species that shows markedly higher expression in the kidneys of spontaneously hypertensive rats than in those of Wistar-Kyoto rats. By using a restriction fragment length polymorphism, we carried out cosegregation analyses between the genotype of the SA gene and blood pressure in three F2 cohorts and observed significant effects of the SA gene on blood pressure in all of those cohorts. In the present study, we have isolated a human counterpart of the rat SA gene to investigate the possible association between the human SA gene and human essential hypertension. The deduced amino acid sequence from the isolated human SA cDNA consisted of 578 amino acid residues and had slight homology to a bacterial enzyme, acetyl-coenzyme A synthase. The human gene was mapped to the human chromosome 16 with the use of a rodent/human somatic hybrid cell panel. A restriction fragment length polymorphism was found with the restriction enzyme Pst I, and the allele frequencies were compared between hypertensive and control groups. The hypertensive group consisted of 89 individuals, and the Pst I rare allele (A2 allele) frequency in this group was 0.270. The control group consisted of 81 healthy normotensive individuals whose precise clinical data were available; the A2 allele frequency in this group was 0.09. Significant differences in the frequency of the A2 allele were observed between the hypertensive and control groups (P = .0001). The present findings provide favorable evidence that the SA gene is a candidate gene for human essential hypertension and also provide a starting point for future studies.
Why do many NMDA antagonists fail, while others are safe and effective at blocking excitotoxicity associated with dementia and acute injury? (2004)

Similar to drug development programs for stroke and traumatic brain injury, programs developed for Alzheimer's disease (AD) have not been very effective in treating dementia. Recently, researchers have explored modulating excitatory synaptic neurotransmission via the N-methyl-D-aspartate receptor (NMDAR) to treat AD. However, many investigators doubt that NMDA antagonists are safe and effective for treating persons with AD because they have failed in stroke and trauma programs. This article explores the role of NMDA-mediated excitotoxicity in AD, reviews how the NMDAR functions, highlights the side effects and alternate signaling pathways that are initiated from NMDAR activation, provides examples of NMDA antagonists that do not exhibit the typical side effects, and discusses why some NMDA antagonist compounds are effective and safe in limiting cascades of excitotoxicity in dementia or acute brain injury.
Simple constrained‐optimization view of acetate overflow in E. coli (1990)

The production of acetate by aerobically growing E. coli is examined. The problem is formulated in terms of a flow network that has as its objective maximal ATP synthesis. It is found that when loads are imposed and flux constraints exist either at the level of NADH turnover rate or the activity of a key Krebs cycle enzyme, switching to acetate overflow is predicted. Moreover, the result found for the latter constraint can be shown to be formally equivalent to a correlation experimentally determined for the specific rate of acetate production by E. coli K-12.