gebhart/patrepeval huggingface dataset:
Genomic organization and chromosomal localization of the human nucleolin gene. (1990)

Nucleolin, a eukaryotic nucleolar phosphoprotein, is involved in the synthesis and maturation of ribosomes. To characterize the genomic organization and regulatory sequences of this gene, two overlapping lambda clones containing the human nucleolin gene plus flanking regions were isolated from a genomic library using human nucleolin cDNA. Southern blots of genomic DNA from human, several mammals, chicken, and yeast revealed that the nucleolin gene is well conserved across these species. The gene consists of 14 exons with 13 intervening sequences and spans approximately 11 kilobases of DNA. Analysis of the splice junctions indicated that the amino-terminal domain and the four RNA binding domains plus the nuclear localization signal are split into adjacent exons. Sequences from the 5'-flanking and the first intron contain a high content of GC residues which is consistent with nucleolin being a "housekeeping" gene. Promoter elements include an atypical TATA box (GTTA), one CCAAT box much further from the initiation site, three reverse compliments of CCAAT (ATTGG), and two pyrimidine-rich nucleotide stretches. In addition, this region and the first intron contain numerous potential Sp1, GCF, CRE-fos, GCN, AP-1, AP-2, UCE, and sequences similar to the glucocorticoid receptor binding site. The transcription start site was determined by primer extension and S1 nuclease mapping of RNA from human liver. One Kpn and three Alu repeats were found within two of the middle introns. The 3'-untranslated portion of the gene contains five homology blocks in a 100-base pair region that are highly conserved among human, mouse, and hamster genomes. Finally, we have determined that the human nucleolin gene is located on chromosome 2q12-qter and is present at one copy per haploid genome. A restriction fragment length polymorphism with EcoRI has been detected in the gene.
Pharmacological modulation of suppressor cell activity in mice with disseminated histoplasmosis (1983)

Indomethacin and cyclophosphamide (CY) were used in an attempt to modify the suppressive effects of spleen cell populations from mice with disseminated histoplasmosis at 1 week of infection. In vitro addition of indomethacin did not alter the depressed plaque-forming cell response to sheep erythrocytes of normal spleen cells cocultured with unfractionated or nylon wool-fractionated spleen cells from infected mice. Likewise, indomethacin given intraperitoneally did not enhance the subnormal in vivo plaque-forming cell response of spleen cells from infected mice. Conversely, 20 mg of CY per kg given intraperitoneally 2 days before or 6 h after the inoculation with Histoplasma capsulatum partially reversed the suppression effected by splenic T cells (nylon wool passed) in vitro, whereas 50 mg of CY per kg given intraperitoneally 6 h after the injection of H. capsulatum ablated suppressor T cell activity in vitro; neither dosage of CY altered the suppression mediated by unseparated or nylon wool-adherent spleen cells. Furthermore, the administration of 50 mg of CY per kg failed to improve the depressed footpad responses of mice infected for 1 week to sheep erythrocytes in sheep erythrocyte-sensitized mice or to histoplasmin. These findings indicate that in experimental disseminated histoplasmosis, suppression effected by splenic T cells can be alleviated by CY; however, there is a persistent immunosuppressor mechanism(s) that cannot be counteracted by either indomethacin or CY.
Increased gelatinase-A and gelatinase-B activities in malignantvs. benign breast tumors (2000)

Matrix metalloproteinases (MMP) types 2 and 9 (also known as gelatinase A and B) are thought to be causally involved in cancer invasion and metastasis. In normal as well as in malignant tissue, both these MMPs occur in multiple forms such as inactive precursors, active enzymes and enzyme-inhibitor complexes. Using newly developed quantitative activity assays, the levels of active MMP-2, total (active and activatable) MMP-2 and total MMP-9 were found to be significantly higher in breast carcinomas than in fibroadenomas. In addition, active MMP-2 and MMP-9 were detected more frequently in malignant than in benign breast carcinoma. These new quantitative activity assays are likely to be of use in studying the mechanism of action of both MMP-2 and -9, assessing their potential prognostic value in different cancers and in the design of MMP inhibitors for preventing cancer metastasis.
Improved Matching Pursuits Image Coding (2006)

This paper reports improvements in compression of both inter- and intra-frame images by the matching pursuits (MP) algorithm. For both types of image, applying a 2D wavelet decomposition prior to MP coding is beneficial. The MP algorithm is then applied using various separable ID codebooks. MERGE coding with precision limited quantization (PLQ) is used to yield a highly embedded data stream. For inter-frames (residuals) a codebook of only 8 bases with compact footprint is found to give improved fidelity at lower complexity than previous MP methods. Great improvement is also achieved in MP coding of still images (intra-frames). Compared to JPEG 2000, lower distortion is achieved on the residual images tested, and also on intra-frames at low bit rates.
Monoclonal Antibodies Which Alter the Morphology of Cultured Chick Myogenic Cells (1982)

Two monoclonal antibodies that cause changes in the morphology of cultured myogenic cells are described. Antibody JG9 causes myoblasts to round up and causes myotubes to become thin, cable-like structures with multiple round swellings. Antibody JG22 causes both myoblasts and myotubes to become round refractile cells poorly attached to the substratum. The effects of both antibodies are reversible. Fab fragments of JG22 can cause the morphological change. A tentative identification of the antigen recognized by JG22 is made.
Self-Assembly of Discrete Cyclic Nanostructures Mediated by Transition Metals (2000)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSelf-Assembly of Discrete Cyclic Nanostructures Mediated by Transition MetalsStefan Leininger, Bogdan Olenyuk, and Peter J. StangView Author Information Department of Chemistry, 315 South 1400 East, The University of Utah, Salt Lake City, Utah 84112 Cite this: Chem. Rev. 2000, 100, 3, 853–908Publication Date (Web):February 4, 2000Publication History Received12 April 1999Published online4 February 2000Published inissue 1 March 2000https://pubs.acs.org/doi/10.1021/cr9601324https://doi.org/10.1021/cr9601324research-articleACS PublicationsCopyright © 2000 American Chemical SocietyRequest reuse permissionsArticle Views17049Altmetric-Citations3225LEARN 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 SUBJECTS:Cavities,Chemical structure,Ligands,Macrocycles,Metals Get e-Alerts
Molecular Genetics of Adult Acute Myeloid Leukemia: Prognostic and Therapeutic Implications (2011)

Molecular analyses of leukemic blasts from patients with acute myeloid leukemia (AML) have revealed a striking heterogeneity with regard to the presence of acquired gene mutations and changes in gene and microRNA expression. Multiple submicroscopic genetic alterations with prognostic significance have been discovered. Application of gene- and microRNA profiling has identified genome-wide expression signatures that separate cytogenetic and molecular subsets of patients with AML into previously unrecognized biologic and/or prognostic subgroups. These and similar future findings are likely to have a major impact on the clinical management of AML because many of the identified genetic alterations not only represent independent prognosticators, but also may constitute targets for specific therapeutic intervention. In this report, we review genetic findings in AML and discuss their clinical implications.
Depression, antidepressants, and the shrinking hippocampus (2001)

Proceedings of the National Academy of Sciences (PNAS), a peer reviewed journal of the National Academy of Sciences (NAS) - an authoritative source of high-impact, original research that broadly spans the biological, physical, and social sciences.
Gene Therapy of Murine Solid Tumors with T Cells Transduced with a Retroviral Vascular Endothelial Growth Factor–Immunotoxin Target Gene (2002)

Solid tumor growth can be inhibited by targeting its neovasculature with vascular endothelial growth factor (VEGF)-toxin fusion proteins (FPs), but these agents have been limited by their inability to localize at the tumor site. In this study, we devised a gene therapy approach intended to deliver VEGF-toxin directly to tumor. Antigen-specific cytotoxic T lymphocytes (CTLs) served as vehicles to deliver a retroviral VEGF-toxin fusion protein to its specific leukemia cell target in vivo. A retroviral vector was constructed for gene therapy with VEGF positioned downstream of its 27-amino acid leader sequence, which promoted secretion of a catalytic immunotoxin containing either truncated diphtheria toxin or Pseudomonas exotoxin A. VEGF was chosen on the basis of the expression of VEGF receptor on endothelial cells in the tumor neovasculature. The VEGF FP was first expressed and secreted by mammalian NIH 3T3 cells. Intracellular expression of both VEGF and toxin was verified by immunofluorescence. In vitro, supernatants collected from transfected cells specifically inhibited the growth of VEGF receptor-expressing human umbilical vein endothelial cells (HUVECs), but not a control cell line. In vivo findings correlated with in vitro findings. A retroviral vector containing the target gene and a nerve growth factor receptor (NGFR) reporter gene was used to transiently transduce T15, a CD8(+) CTL line that specifically recognizes C1498, a lethal C57BL/6 myeloid tumor. Transduced T15 cells injected intravenously significantly inhibited the growth of subcutaneous tumor, whereas nontransduced controls did not. Together, these data indicate that gene therapy of T cells with retrovirus containing a VEGF-immunotoxin target gene may be a valid means of inhibiting a broad range of solid tumors dependent on angiogenesis.
Synthesis of lysogangliosides (1985)

The synthesis of gangliosides GM3, GM2, GM1, and GD1a solely lacking the fatty acid moiety, and thus called lysogangliosides in analogy to lysophospholipids, is described. Since a selective elimination of the fatty acid residue has not been achieved as yet, the gangliosides were first subjected to alkaline hydrolysis. By this procedure the fatty acyl as well as the acetyl groups of the sialic acid residue(s) were completely removed. The acetamido group of the N-acetylgalactosamine moiety of the gangliosides GM2, GM1, and GD1a was very little (congruent to 10%) hydrolyzed. In a two-phase system composed of water and ether, the selective protection of the sphingoid amino group was accomplished with a hydrophobic protective group (9-fluorenylmethoxycarbonyl). Lysogangliosides were obtained after re-N-acetylation of the sialooligosaccharide amino group(s) followed by removal of the protecting group. The overall yield was about 30%. The structures of the lysogangliosides were confirmed by chemical analysis as well as negative ion FAB mass spectrometry and 1H NMR spectroscopy. By simple re-N-acylation of lysogangliosides with any labeled fatty acid, labeled gangliosides are now obtainable that are identical with their parent gangliosides except for their labeled fatty acid residue. This has been demonstrated by the synthesis of GM1 with a [1-13C]palmitic acid moiety in its ceramide portion. If desired, double-labeled gangliosides may be obtained by use of labeled acetic anhydride in the synthesis of the lysogangliosides.
Model Study of the Sphericity Effects in Extended Atmospheres of Late-Type Stars (1978)

Abstract Spherical static models of nongray LTE atmospheres are constructed to study sphericity effects in the atmospheres of red giants and supergiants. Differential study of atmospheres of different extent but with the same effective temperature and surface gravity (A-series; Teff = 3200 K, log g = –0.5) reveals that increasing extent of the atmosphere leads to cooling of the surface layers and that this cooling strongly enhances the formation of certain molecules, such as H2O in the present case. Differential study of another series of spherical atmospheres with the same luminosity and radius but different masses (B-series; L = 6.64 × 104 L⊙, R = 600 R⊙, i.e., Teff = 3800K) shows that a distinct gravity effect appears in the T–τ relation of the spherical atmosphere, namely a decrease in the surface temperature. This gravity effect, coupled with the subsequent effects found in the A-series models, even enhances some of the molecular absorption bands, such as TiO bands in this case, and produces a noticeable variation of emergent flux Fλ as the gravity varies. These effects of the atmospheric extent in the A- and B-series are illustrated in the form of T–τ diagrams, P–τ diagrams, and Fλ–λ diagrams. The possible sphericity effects in the atmosphere of Betelgeuse are briefly discussed.
Improved Automatic Feature Selection Approach for Health Risk Prediction (2018)

With the recent advances in machines & technology, there is revolution in healthcare industry also. Thus, it gave rise to the concept of Electronic Health Record (EHR) which stores patients demographics, lab tests & results, medical history, habits etc. in electronic form. EHR is voluminous data which is difficult to store, maintain or alter. To provide extended life for people, health risk prediction model using this EHR is formulated in this work. Feature Selection is used to select only associated or relevant data from the dataset. Logistic Regression is used with improved loss functionality parameter which increases the accuracy, response time and performance of the system. Representation Learning enables formation of feature vector of the selected features thus calculating their scores. Further, risk prediction is performed by the neural network model. Deep Neural Network (DNN) is used with many hidden layers containing activation functions. Transfer learning is used to avoid re-training of the whole system every time new data enters the model. Dataset used here is of hypertension. EHR dataset is also synthetically created for analysis.
Monoclonal antibodies directed to CD20 and HLA-DR can elicit homotypic adhesion followed by lysosome-mediated cell death in human lymphoma and leukemia cells (2009)

mAbs are becoming increasingly utilized in the treatment of lymphoid disorders. Although Fc-FcgammaR interactions are thought to account for much of their therapeutic effect, this does not explain why certain mAb specificities are more potent than others. An additional effector mechanism underlying the action of some mAbs is the direct induction of cell death. Previously, we demonstrated that certain CD20-specific mAbs (which we termed type II mAbs) evoke a nonapoptotic mode of cell death that appears to be linked with the induction of homotypic adhesion. Here, we reveal that peripheral relocalization of actin is critical for the adhesion and cell death induced by both the type II CD20-specific mAb tositumomab and an HLA-DR-specific mAb in both human lymphoma cell lines and primary chronic lymphocytic leukemia cells. The cell death elicited was rapid, nonapoptotic, nonautophagic, and dependent on the integrity of plasma membrane cholesterol and activation of the V-type ATPase. This cytoplasmic cell death involved lysosomes, which swelled and then dispersed their contents, including cathepsin B, into the cytoplasm and surrounding environment. The resulting loss of plasma membrane integrity occurred independently of caspases and was not controlled by Bcl-2. These experiments provide what we believe to be new insights into the mechanisms by which 2 clinically relevant mAbs elicit cell death and show that this homotypic adhesion-related cell death occurs through a lysosome-dependent pathway.
Epidermal growth factor receptor of A431 cells. Characterization of a monoclonal anti-receptor antibody noncompetitive agonist of epidermal growth factor action. (1985)

A monoclonal antibody to the epidermal growth factor (EGF) receptor of A431 cells, denoted 2D1-IgM, was generated after fusion of immunized BALB/c mouse spleen cells with SP2/0-Ag14 myeloma cells. Specific binding of 2D1-IgM to the A431 cell-surface receptor for EGF was demonstrated by indirect immunofluorescence, immunoprecipitation, and immunoblot analysis. Scatchard analysis of 125I-EGF binding to A431 cells demonstrated that 2D1-IgM treatment did not change the number of EGF receptors, but caused an increase in the affinity of EGF receptors from a population of low affinity to a uniform population of high affinity. Like EGF, 2D1-IgM induced phosphorylation of EGF receptors and EGF receptor clustering. As in the case of EGF, a biphasic growth response with stimulation of DNA synthesis at low and inhibition at high concentrations of 2D1-IgM was evident in A431 cells. The intrinsic "EGF-like" bioactivity of 2D1-IgM was enhanced by the presence of EGF. These results suggest that the binding of 2D1-IgM to the EGF receptor at a different site from that to which EGF binds can initiate an effective EGF-like biological response; and the EGF-like biological effects of 2D1-IgM may be mediated by a population of high affinity EGF receptors which may be involved in the control of cellular growth.
Architecture and implementation of a vector/SIMD multiply-accumulate unit (2005)

This work presents 64-bit fixed-point vector multiply-accumulator (MAC) architecture capable of supporting multiple precisions. The vector MAC can perform one 64/spl times/64, two 32/spl times/32, four 16/spl times/16, or eight 8/spl times/8 bit signed/unsigned multiply using essentially the same hardware as a scalar 64-bit MAC and with only a small increase in delay. The scalar MAC architecture is "vectorized" by inserting mode-dependent multiplexing into the partial product generation and by inserting mode-dependent kills in the carry chain of the reduction tree and the final carry-propagate adder. This is an example of "shared segmentation" in which the existing scalar structure is segmented and then shared between vector modes. The vector MAC is area efficient and can be fully pipelined, which makes it suitable for high-performance processors and, possibly, dynamically reconfigurable processors. The "shared segmentation" method is compared to an alternative method, referred to as the "shared subtree" method, by implementing vector MAC designs using two different technologies and three different vector widths.
Inhibition of fibronectin receptor function by antibodies against baby hamster kidney cell wheat germ agglutinin receptors. (1982)

Previous studies suggest that the baby hamster kidney (BHK) cell fibronectin receptor is also a wheat germ agglutinin receptor (WGA-R). To analyze this possibility further, IgG and Fab fragments of antibodies produced against a BHK cell WGA-R preparation were tested to determine their effects on cell adhesion mediated by fibronectin, wheat germ agglutinin, concanavalin A, and polycationic ferritin. The WGA-R preparation was isolated by octylglucoside extraction of BHK cells followed by chromatography of the extract on WGA-agarose. The antibodies against the WGA-R preparation reacted primarily with polypeptides of molecular weights 48, 61, 83, 105, 120, 165, 210, and 230 kilodaltons (kdaltons). It was concluded that the antibodies interfered with BHK cell fibronectin receptors on the basis of the ability of anti-WGA-R IgG or Fab fragments to (a) inhibit cell spreading on fibronectin-coated substrata; (b) cause rounding and detachment of cells previously spread on fibronectin-coated substrata; and (c) inhibit binding of fibronectin-coated latex beads to the cells. Antibody activity was blocked by treatment of anti-WGA-R with the WGA-R preparation or by absorption of anti-WGA-R with intact BHK cells. The antibodies also appeared to prevent coupling of ligand-receptor complexes (involving concanavalin A or polycationic ferritin) with the cytoskeleton. Finally, cell rounding and detachment caused by the antibodies were found to require metabolic energy since it did not occur in the presence of azide or at 4 degrees C.
Regulation of 2-Oxoglutarate (α-Ketoglutarate) Dehydrogenase Stability by the RING Finger Ubiquitin Ligase Siah (2004)

The 2-oxoglutarate dehydrogenase complex (OGHDC) (also known as the alpha-ketoglutarate dehydrogenase complex) is a rate-limiting enzyme in the mitochondrial Krebs cycle. Here we report that the RING finger ubiquitin-protein isopeptide ligase Siah2 binds to and targets OGDHC-E2 for ubiquitination-dependent degradation. OGDHC-E2 expression and activity are elevated in Siah2(-/-) cells compared with Siah2(+)(/)(+) cells. Deletion of the mitochondrial targeting sequence of OGDHC-E2 results in its cytoplasmic localization and rapid proteasome-dependent degradation in Siah2(+)(/)(+) but not in Siah2(-/-) cells. Significantly, because of its overexpression or disruption of the mitochondrial membrane potential, the release of OGDHC-E2 from mitochondria to the cytoplasm also results in its concomitant degradation. The role of the Siah family of ligases in the regulation of OGDHC-E2 stability is expected to take place under pathological conditions in which the levels of OGDHC-E2 are altered.