gebhart/patrepeval huggingface dataset:
Transcriptional regulation of the apolipoprotein A-I gene. Species-specific expression correlates with rates of gene transcription. (1991)

Previous studies have shown that the abundance of apoA-I mRNA in liver and intestine correlates with a 2-3-fold species-specific difference in the plasma concentration of high density lipoprotein and apoA-I. In order to determine the role of gene transcription in regulating the tissue, steady state apoA-I mRNA abundance nuclear run-on assays were conducted using nuclei from two species of nonhuman primates. The transcriptional activity expressed as the ratio of apoA-I signal intensity to that for the constitutively expressed glyceraldehyde-3-phosphate dehydrogenase was calculated for seven individual animals in each of the two nonhuman primate species. The African green monkey showed a ratio of 4.18 +/- 0.35, and the cynomolgus monkey showed 2.03 +/- 0.13 (n = 7, p less than 0.004). To identify possible cis-acting elements that may be involved in transcriptional regulation of the apoA-I gene, a portion of the apoA-I regulatory region, corresponding to nucleotides -231 to +263 (where +1 is the start site of transcription), was isolated from both species using the polymerase chain reaction. The nucleotide sequence of this region was compared between monkey species, as well as with the same region from the apoA-I gene isolated from human genomic DNA. In this region, the African green monkey apoA-I gene showed 95% similarity, whereas the cynomolgus monkey showed 94% similarity to the human sequence. Although a high degree of sequence similarity was observed among all species, numerous sequence specific differences were noted in the first intron between the two primate species and between nonhuman and human primate sequences. Results from studies measuring relative promoter strength indicated that the African green monkey 5'-regulatory region had a consistently higher level of activity (1.4-3.0-fold) than the same region from the cynomolgus monkey. Interestingly, the African green monkey promoter also showed a significantly higher transcriptional activity than the human or rabbit promoter, suggesting the presence of a nonhuman primate specific cis-acting element(s) regulating apoA-I gene expression. These results demonstrate that a portion of the species-specific difference in apoA-I gene expression may be explained by sequence divergence in the 5'-regulatory region including exon/intron 1 of the apoA-I gene.
Conference record of Twenty-Sixth Asilomar Conference on Signals, Systems & Computers : October 26-28, 1992, Pacific Grove, California (1992)

Two volumes hold the papers presented at the October 1992 conference held in Pacific Grove, California. Topics covered include theoretical and applied signal processing, computers, circuits, systems, adaptive signal processing, digital storage systems, neural networks, biological signal procesing, s
Orphan Nuclear Receptors: From Gene to Function* (1999)

I. Introduction II. Nuclear Receptors: General Concepts A. Anatomy of nuclear receptors B. Mechanisms of action III. Orphan Nuclear Receptors A. Definition B. Nomenclature C. Structural and functional diversity IV. Novel Hormone Response Systems: RXR and Its Heterodimeric Partners A. RXR: rexinoids B. PPAR: multiple ligands, multiple functions C. PXR: pregnanes, xenobiotic compounds, and benzoate derivatives D. CAR (constitutive androstane receptor): androstanes and phenobarbital E. LXR: control of cholesterol metabolism by oxysterols F. FXR: bile acids receptor V. Orphans in Search of a Home A. HNF4: diabetes and possible regulation by acyl-coenzyme A (CoA) thioesters B. FTZ-F1: steroidogenesis and sexual development C. Rev-Erb: singular members of the superfamily D. ROR: neuron development and T cell selection E. TR2: the testis receptors F. TLX: forebrain development G. COUP-TF: neurogenesis, angiogenesis, and heart development H. ERR: placenta development and control of lipid metabolism I. NGFI-B: hyp...
Tumor cell invasion of three-dimensional matrices of defined composition: evidence for a specific role for heparan sulfate in rodent cell lines. (1989)

The abilities of rodent tumor cell lines; B16BL6, ND and LT dietary variants of B16BL6, +SA, RT7-4bs and RT7-4bLs to invade composite collagen I gels containing heparin, chemically modified heparins, heparan sulfate, chondroitin sulfate, hyaluronic acid, dextran, dextran sulfate, laminin and collagen IV were investigated, and compared to the invasion of plain collagen I gels. The presence of heparin or heparan sulfate most generally promoted tumor cell invasion of the gels, with more aggressive invasion being noted for the more metastatic variants examined. Of the chemically modified heparins tested, carboxyl-reduced heparin promoted matrix invasion by B16BL6 and +SA cells to the greatest degree. Hyaluronic acid marginally promoted invasion by +SA and RT7-4bs primary cells while, in these collagen I based gels laminin only promoted matrix invasion by primary +SA cells to a very limited degree. The tumor cell lines attached relatively poorly to heparan sulfate substrates compared to the other glycosaminoglycans tested, and the primary tumor cell lines also attached relatively poorly to collagen I. As expected, highly metastatic variants showed greater attachment to laminin than did their less metastatic counterparts. Apart from the negative correlation of cellular attachment to heparan sulfate substrates with invasiveness towards heparan sulfate containing gels, no other relationships emerged linking attachment rates with invasive activities for particular complex gel compositions. Our results suggest an important role for heparan sulfate, and possibly also tissue heparin, in promoting tumor cell invasion of extracellular matrices. Results from complex gels containing dextran or dextran sulfate failed to support the hypothesis that GAG sulfation is important to cellular invasion. The activity of the chemically modified heparins in promoting invasion, when present as components of these model matrices, suggests that part of the anti-metastatic activity of these compounds, when preincubated with tumor cells prior to intravenous inoculation, could result from interference with tumor cell extravasation.
Tubulyzine®, a novel tri-substituted triazine, prevents the early cell death of transplanted myogenic cells and improves transplantation success (2003)

Myoblast transplantation (MT) is a potential therapeutic approach for several muscular dystrophies. A major limiting factor is that only a low percentage of the transplanted myoblasts survives the procedure. Recent advances regarding how and when the myoblasts die indicate that events preceding actual tissue implantation and during the first days after the transplantation are crucial. Myoseverin, a recently identified tri-substituted purine, was shown to induce in vitro the fission of multinucleated myotubes and affect the expression of a variety of growth factors, and immunomodulation, extracellular matrix-remodeling, and stress response genes. Since the effects of myoseverin are consistent with the activation of pathways involved in wound healing and tissue regeneration, we have investigated whether pretreatment and co-injection of myoblasts with Tubulyzine (microtubule lysing triazine), an optimized myoseverin-like molecule recently identified from a triazine library, could reduce myoblast cell death following their transplantation and consequently improves the success of myoblast transplantation. In vitro, using annexin-V labeling, we showed that Tubulyzine (5 microM) prevents normal myoblasts from apoptosis induced by staurosporine (1 microM). In vivo, the pretreatment and co-injection of immortal and normal myoblasts with Tubulyzine reduced significantly cell death (assessed by the radio-labeled thymidine of donor DNA) and increased survival of myoblasts transplanted in Tibialis anterior (TA) muscles of mdx mice, thus giving rise to more hybrid myofibers compared to transplanted untreated cells. Our results suggest that Tubulyzine can be used as an in vivo survival factor to improve the myoblast-mediated gene transfer approach.
Comprehensive Optical Monitoring of Selective Laser Melting (2012)

The absence of on-line monitoring and process quality assurance is one of the main obstacles for wide implementation of Selective Laser Melting technology in modern manufacturing industry. Temperature monitoring in the laser impact zone are carried out by an originally developed bicolour pyrometer and CCD camera which are integrated with the optical scanning system of the PHENIX PM-100 machine. Experiments are performed with variation of basic process parameters such as powder layer thickness (0-120 m), hatch distance (60 m-1000 m), and fabrication strategy (the so-called "one-zone" and "two-zone").
Evaluating collaborative filtering recommender systems (2004)

Recommender systems have been evaluated in many, often incomparable, ways. In this article, we review the key decisions in evaluating collaborative filtering recommender systems: the user tasks being evaluated, the types of analysis and datasets being used, the ways in which prediction quality is measured, the evaluation of prediction attributes other than quality, and the user-based evaluation of the system as a whole. In addition to reviewing the evaluation strategies used by prior researchers, we present empirical results from the analysis of various accuracy metrics on one content domain where all the tested metrics collapsed roughly into three equivalence classes. Metrics within each equivalency class were strongly correlated, while metrics from different equivalency classes were uncorrelated.
Trichomonas Vaginalis Treatment Reduces Vaginal HIV-1 Shedding (2008)

This study provides additional support that reducing TV infection among HIV-positive women may have an impact on the prevention of HIV transmission. Reasons for the delayed treatment effect and the effect on cervical shedding need further investigation.
Muscle fiber orientation and connective tissue content in the hypertrophied human heart. (1982)

To elucidate the structural correlates of cardiac failure in myocardial tissue, muscle fiber alignment and connective tissue volume fraction were measured at multiple sites in the left ventricular free wall and in the interventricular septum of 14 human hearts. Group 1 (five hearts; 280 +/- 20 gm.) had no evidence of cardiac disease, group 2 (five hearts; 380 +/- 30 gm.) had a history of systemic hypertension without clinical heart failure, and group 3 (four hearts;; 590 +/- 40 gm.) had both left ventricular overload and congestive failure. Fiber orientations were determined by measuring fiber angle relative to the circumferential direction (helix angle). The fraction of the myocardial volume occupied by connective tissue was determined by point counting. Our results indicate a smooth transition of helix angle from epi- to endocardial surface in the normal left ventricular free wall with nearly 55 per cent of the wall occupied by circumferentially oriented fibers near the cardiac equator (latitude of largest ventricular diameter); morphologically, the interventricular septum was nearly identical with the free wall. Fiber alignment was maintained in all three groups as was the fraction of wall occupied by circumferential fibers. Connective tissue volume fraction was, however, significantly increased (p less than 0.02) in hypertrophied hearts (groups 2 and 3) as compared with normal hearts, and at two of six sites in clinically failed hearts as compared with hypertrophied but functionally compensated hearts. Thus, muscle fiber orientation is not altered in the hypertrophied pressure-overloaded left ventricle, whereas connective tissue content is increased with the increase being greatest in the failing heart.
Differential in vivo potential of endothelial progenitor cells from human umbilical cord blood and adult peripheral blood to form functional long-lasting vessels (2007)

Tissue engineering requires formation of a de novo stable vascular network. Because of their ability to proliferate, differentiate into endothelial cells, and form new vessels, blood-derived endothelial progenitor cells (EPCs) are attractive source of cells for use in engineering blood vessels. However, the durability and function of EPC-derived vessels implanted in vivo are unclear. To this end, we directly compared formation and functions of tissue-engineered blood vessels generated by peripheral blood- and umbilical cord blood-derived EPCs in a model of in vivo vasculogenesis. We found that adult peripheral blood EPCs form blood vessels that are unstable and regress within 3 weeks. In contrast, umbilical cord blood EPCs form normal-functioning blood vessels that last for more than 4 months. These vessels exhibit normal blood flow, perm-selectivity to macromolecules, and induction of leukocyte-endothelial interactions in response to cytokine activation similar to normal vessels. Thus, umbilical cord blood EPCs hold great therapeutic potential, and their use should be pursued for vascular engineering.
Lethality, DNA alkylation, and cell cycle effects of adozelesin (U-73975) on rodent and human cells. (1992)

Adozelesin (U-73975) is an extremely potent cytotoxic agent which causes 90% lethality, after 2 h exposure in vitro, of Chinese hamster ovary and lung (CHO and V79), mouse melanoma (B16), and human ovarian carcinoma (A2780) cells at 0.33, 0.19, 0.2, and 0.025 ng/ml, respectively. Under similar conditions, Adriamycin and cisplatin had 90% lethality values in CHO cells of 150 ng/ml (= 249 nM) and 6800 ng/ml (= 2266 nM), respectively. The relative drug sensitivity of the cell lines (A2780 > V79, B16, CHO) was correlated to the relative amounts of [3H]adozelesin alkylated to DNA. The greater sensitivity of A2780 was due to (a) greater DNA alkylation at different drug doses and (b) greater intrinsic sensitivity of A2780 which resulted in greater cell kill at comparable DNA alkylation. Phase specific toxicity studies show that adozelesin was least lethal to CHO cells in mitosis and very early G1. Lethality increased as cells progressed through G1 and was maximal in late G1 and early S. Mitotic cells had lower drug uptake and correspondingly less drug binding to DNA than G1 or S-phase cells. However, based on the amount of drug alkylated per micrograms of DNA, cells in M, G1, and S were equally sensitive. Therefore, the lower sensitivity of M-phase cells was due to lower drug uptake. Adozelesin had three different effects on progression of CHO, V79, B16, and A2780 through the cell cycle: (a) slowed progression through S which resulted in significantly increasing the percentage of S-phase cells. This effect was transient; (b) cell progression was blocked in G2 for a long time period; (c) the response of the cell lines to the G2 block differed. CHO and V79 cells escaped G2 block by dividing and entered the diploid DNA cycle or did not undergo cytokinesis and became tetraploid. On the contrary, B16 and A2780 cells remained blocked in G2 and did not become tetraploid. Cell progression was inhibited in a similar manner when a synchronized population of M, G1, or S-phase cells were exposed to adozelesin.
Parental bias of Ki-ras oncogenes detected in lung tumors from mouse hybrids. (1992)

A mouse strain with low lung tumor susceptibility (C3H) and a strain with high lung tumor susceptibility (A/J) were reciprocally crossed to produce C3A and AC3 F1 hybrid mice. Ki-ras oncogenes were detected in spontaneous and chemically induced lung tumors obtained from the C3A and AC3 mice. To further explore the genetics of the Ki-ras gene in mouse lung tumor susceptibility, the parental origin of Ki-ras oncogenes detected in lung tumors from the F1 hybrids was determined by a strategy based on a 37-base-pair deletion in the second intron of the A/J Ki-ras allele. Ki-ras oncogenes were derived from the A/J parent in 38 of 40 tumors obtained from C3A mice and 30 of 30 tumors from AC3 mice. The observation that the activated oncogene in hybrids originates from the susceptible parent suggests that the Ki-ras gene is directly linked to mouse lung tumor susceptibility. This finding may have implications for pulmonary adenocarcinoma development in humans, since Ki-ras oncogenes are detected in 35% of this human tumor type.
Inhibition of formation of volatile nitrosamines in fried bacon by the use of cure-solubilized .alpha.-tocopherol (1978)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTInhibition of formation of volatile nitrosamines in fried bacon by the use of cure-solubilized .alpha.-tocopherolW. Fiddler, J. W. Pensabene, E. G. Piotrowski, J. G. Phillips, J. Keating, W. J. Mergens, and H. L. NewmarkCite this: J. Agric. Food Chem. 1978, 26, 3, 653–656Publication Date (Print):May 1, 1978Publication History Published online1 May 2002Published inissue 1 May 1978https://pubs.acs.org/doi/10.1021/jf60217a046https://doi.org/10.1021/jf60217a046research-articleACS PublicationsRequest reuse permissionsArticle Views127Altmetric-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
Orphan‐receptor ligand human urotensin II: receptor localization in human tissues and comparison of vasoconstrictor responses with endothelin‐1 (2000)

We have determined the distribution of receptors for human urotensin-II (U-II) in human and rat CNS and peripheral tissues. In rat, [(125)I]-U-II binding density was highest in the abducens nucleus of brainstem (139.6+/-14 amol mm(-2)). Moderate levels were detected in dorsal horn of spinal cord and lower levels in aorta (22. 5+/-6 amol mm(-2)). In human tissues density was highest in skeletal muscle and cerebral cortex ( approximately 30 amol mm(-2)), with lower levels (<15 amol mm(-2)) in kidney cortex and left ventricle. Little binding was identified in atria, conducting system of the heart and lung parenchyma. Receptor density was less in human coronary artery smooth muscle (14.6+/-3 amol mm(-2), n=10) than rat aorta with no significant difference between normal and atherosclerotic vessels. In human skeletal muscle [(125)I]-U-II bound to a single receptor population with K(D)=0.24+/-0.17 nM and B(max)=1.97+/-1.1 fmol mg(-1) protein (n=4). U-II contracted human coronary, mammary and radial arteries, saphenous and umbilical veins with sub-nanomolar EC(50) values. U-II was 50 times more potent in arteries and <10 times more potent in veins than endothelin-1 (ET-1). The maximum response to U-II ( approximately 20% of control KCl) was significantly less than to ET-1 ( approximately 80% KCl). In contrast, in rat aorta, U-II and ET-1 were equipotent with similar maximum responses. This is the first report of high affinity receptors for [(125)I]-U-II in human CNS and peripheral tissues. This peptide produces potent, low efficacy, vasoconstriction in human arteries and veins. These data suggest a potential role for U-II in human physiology.
ME491 Melanoma-Associated Glycoprotein Family: Antigenic Identity of ME491, NKI/C-3, Neuroglandular Antigen (NGA), and CD63 Proteins (1992)

Our results indicate that the data obtained in studies of these three melanoma antigens may be pooled, and we propose that the molecule recognized by these reagents be classified as CD63.
Oral insulin treatment suppresses virus-induced antigen-specific destruction of beta cells and prevents autoimmune diabetes in transgenic mice. (1996)

Oral administration of self-antigens has been proposed as a therapy to prevent and treat autoimmune diseases. Here we report that oral treatment with insulin prevents virus-induced insulin-dependent diabetes mellitus (IDDM) in a transgenic (tg) mouse model. Such mice express the viral nucleoprotein (NP) of lymphocytic choriomeningitis virus (LCMV) under control of the rat insulin promoter in their pancreatic beta cells and < 2% spontaneously develop diabetes. However, 2 mo after challenge with LCMV, IDDM occurs in > 95% of tg mice but not in controls. Oral treatment with 1 mg of insulin twice per week for 2 mo starting either 1 wk before or 10 d after initiating LCMV infection prevents IDDM in > 50% of the tg mice (observation time 8 mo). Thus, insulin therapy is effective in preventing progression to overt IDDM in prediabetic tg mice with ongoing islet infiltration. Oral administration of insulin does not affect the generation of LCMV-NP-specific anti-self cytotoxic T lymphocytes nor the infiltration of lymphocytes into the pancreas. However, less beta cells are destroyed in insulin-treated mice, upregulation of MHC class I and II molecules does not occur, and antiviral (self) cytotoxic T lymphocytes are not found in the islets, events present in tg mice developing IDDM. The majority of lymphocytes in the islets of insulin-treated tg mice without IDDM produces IL-4, IL-10, and TGF-beta. In contrast, lymphocytes from islets of tg mice developing IDDM mainly make gamma-IFN.
Binding of complement subcomponent C1q to Streptococcus pyogenes: evidence for interactions with the M5 and FcRA76 proteins (2006)

Binding of C1q, the first component of the complement system, to some human pathogens has been earlier reported. In the present study, direct binding of C1q to group A streptococci (GAS) of various serotypes as well as some other Gram-positive and Gram-negative species was demonstrated. The interaction between C1q and GAS was investigated more in detail. In hot neutral extracts of a number of GAS strains two components of 64 and 52 kDa, respectively, bound C1q; alkaline and SDS extracts yielded the 52 kDa component as the main C1q-binding substance. Trypsin treatment of the SDS extracts of two GAS strains suggested the C1q-binding component(s) to be of protein nature. C1q-binding material purified from the SDS extract of an avirulent strain, type T27, was separated in 12% SDS-PAGE and probed in Western blot with human C1q and fibrinogen, conjugated to horse radish peroxidase (HRP) as well as rabbit IgG antibodies complexed to HRP (PAP system). The 52 kDa component was non-reactive with fibrinogen or rabbit IgG. However, C1q-binding components purified from the alkaline extracts of two M-positive strains revealed strong binding of either fibrinogen (type M5) or both fibrinogen and rabbit IgG (type M76); the molecular mass of these components. 55 kDa and 43-40 kDa, respectively, was in agreement with the reported molecular mass of the M5 and FcRA76 proteins. Our findings suggest that C1q may interact with GAS through certain M-family proteins as well as by a so far unidentified surface factor of protein nature occurring in most GAS strains. The involvement of M-family proteins, regarded as virulence factors of these organisms, may suggest the interaction of GAS with C1q as biologically important.