gebhart/patrepeval huggingface dataset:
Improved temperature performance of 1.31-/spl mu/m quantum dot lasers by optimized ridge waveguide design (2005)

We demonstrate the importance of the fabricated device structure for the external differential efficiency, threshold current density, and maximum operating temperature for ground state operation of a 1.31-μm quantum dot laser. The introduction of a shallow ridge etch design and selective electroplating of the gold bondpads is demonstrated to offer improved performance in comparison to a deep ridge etch design with thinner evaporated gold bondpads.
Cellular homologs of the avian erythroblastosis virus erb-A and erb-B genes are syntenic in mouse but asyntenic in man. (1984)

Avian erythroblastosis virus, a retrovirus that causes erythroblastosis and sarcomas in infected birds, possesses two host cell-derived genes [viral (v) erb-A and erb-B]. Although v-erb-B seems to be responsible for oncogenic transformation, v-erb-A might have an enhancing effect on transformation. In chickens, the natural host for avian erythroblastosis virus, cellular (c) erb-A and erb-B genes appear to be unlinked, but their chromosomal locations in other species are unknown. To ascertain the chromosomal location of c-erb genes in man and mouse, we analyzed interspecies somatic cell and microcell hybrids by Southern filter hybridization techniques using specific v-erb-A and v-erb-B probes. We found c-erb-A sequences on human chromosome 17 (17p11----qter) and located c-erb-B on human chromosome 7 (7pter----q22). In contrast, both c-erb-A and c-erb-B reside on mouse chromosome 11.
Continuous Foreign Gene Expression in Transformed Lepidopteran Insect Cells (2003)

Protocols for the isolation of recombinant baculoviruses and their use for foreign gene expression in insect cells have been described in detail in the preceding chapters (also see refs. 1–5). Generally, this approach involves the replacement of viral DNA sequences encoding the polyhedrin protein with foreign DNA sequences encoding the protein of interest. The recombinant virus is plaque-isolated, and used to infect cultured insect cells or larvae. The protein of interest will be expressed during the very late phase of infection, when polyhedrin would normally be expressed by the wild-type virus. One major advantage of baculovirus expression vectors is that they can be used to produce exceedingly large amounts of a recombinant protein. This is due to the strength of the polyhedrin promoter, which can induce the synthesis of a very large pool of mRNA for translation into large amounts of protein. A second big advantage of the baculovirus expression system is that insect cells have most of the protein-processing capabilities of higher eukaryotic cells (reviewed in ref. 6). Thus, proteins produced in recombinant baculovirusinfected cells can undergo coand posttranslational processing, resulting in an end product that is very similar, if not identical, to the native protein.
Characterization and autoradiographic localization of LHRH receptors in the rat brain (1987)

Luteinizing-hormone-releasing hormone (LHRH) is distributed in several extrahypothalamic areas, suggesting that it might act as a neurotransmitter or neuromodulator in the central nervous system. This study was undertaken to characterize and localize LHRH receptors in the rat brain by using slide-mounted frozen sections. The radioligand used was an iodinated stable LHRH agonist, [D-Ser(TBU)6, des-Gly-NH2(10)]LHRH ethylamide. It was clearly established that LHRH receptors with characteristics similar to those of pituitary LHRH receptors were present in the brain. They were found in high concentrations in the dorsal hippocampus, amygdala, septum, and subiculum and in very low amounts in the hypothalamus. Generally, a good correlation could be observed between receptor distribution and immunohistologically localized LHRH. These results strongly suggest that LHRH has multiple sites of action in the rat brain and reinforce the hypothesis that the peptide could act as a neurotransmitter/neuromodulator in the central nervous system.
Expression of integrin alpha10 is induced in malignant melanoma (2006)

Wenke, A.; Kjellman, C.; Lundgren-Akerlund, E.; Uhlmann, C.; Haass, N.; Herlyn, M.; Bosserhoff, A. Author Information
Th1 and Th17 hypercytokinemia as early host response signature in severe pandemic influenza (2009)

While infection with the nvH1N1 induces a typical innate response in both mild and severe patients, severe disease with respiratory involvement is characterized by early secretion of Th17 and Th1 cytokines usually associated with cell mediated immunity but also commonly linked to the pathogenesis of autoimmune/inflammatory diseases. The exact role of Th1 and Th17 mediators in the evolution of nvH1N1 mild and severe disease merits further investigation as to the detrimental or beneficial role these cytokines play in severe illness.
GM-CSF, via PU.1, regulates alveolar macrophage FcγR-mediated phagocytosis and the IL-18/IFN-γ–mediated molecular connection between innate and adaptive immunity in the lung (2002)

Severely impaired pulmonary microbial clearance was observed in granulocyte-macrophage colony-stimulating factor (GM-CSF)-deficient mice. To determine mechanisms by which GM-CSF mediates lung host defense, FcgammaR-mediated phagocytosis (opsonophagocytosis) by alveolar macrophages (AMs) was assessed in GM-CSF-sufficient (GM(+/+)) and -deficient (GM(-/-)) mice and in GM(-/-) mice expressing GM-CSF only in the lungs from a surfactant protein C (SPC) promoter (SPC-GM(+/+)/GM(-/-)). Opsonophagocytosis by GM(-/-) AMs was severely impaired and was restored by pulmonary GM-CSF expression in vivo or by PU.1 expression in vitro. Defective opsonophagocytosis by GM(-/-) AMs was associated with decreased FcgammaR expression. Because interferon-gamma (IFN-gamma) augments macrophage FcgammaR levels, the role of GM-CSF/PU.1 in the regulation of AM FcgammaR expression by IFN-gamma was assessed during adenoviral lung infection. Adenoviral infection stimulated IFN-gamma production and augmented FcgammaR levels on AMs in GM-CSF-expressing but not GM(-/-) mice. However, IFN-gamma exposure ex vivo stimulated FcgammaR expression on GM(-/-) AMs. Because interleukin-18 (IL-18) and IL-12 stimulate IFN-gamma production during adenoviral infection, their role in GM-CSF/PU.1 regulation of IFN-gamma-augmented FcgammaR expression on AMs was assessed. Adenoviral infection stimulated IL-18 and IL-12 production in GM-CSF-expressing mice, but both were markedly reduced or absent in GM(-/-) mice. IL-18 expression by GM(-/-) AMs was severely impaired and was restored by pulmonary GM-CSF expression in vivo or by PU.1 expression in vitro. Pulmonary administration of IL-18 in GM(-/-) mice stimulated IFN-gamma production and restored FcgammaR expression on AMs. These results show that GM-CSF, via PU.1, regulates constitutive AM FcgammaR expression and opsonophagocytosis and is required for the IFN-gamma-dependent regulation of AM FcgammaR expression, enabling AMs to release IL-18/IL-12 during lung infection.
Genomic organization of the melanoma-associated glycoprotein MUC18: implications for the evolution of the immunoglobulin domains. (1993)

The cell surface glycoprotein MUC18, a member of the immunoglobulin superfamily and homologous to several cell adhesion molecules, is associated with tumor progression and the development of metastasis in human malignant melanoma. Immunohistochemical and Northern blot analysis revealed that expression of the antigen is restricted to advanced primary and metastatic melanomas and to cell lines of the neuroectodermal lineage. The genomic sequence encoding the cell surface antigen spans approximately 14 kb and consists of 16 exons. The organization of the gene, which is related to that of the neural cell adhesion molecule N-CAM, shows a structure where each immunoglobulin-related domain is encoded by more than one exon. Sequencing of the putative MUC18 promoter region revealed a G + C-rich promoter lacking conventional TATA and CAAT boxes. Several motifs for binding of transcription factor Sp1 are present in the regulatory region, and only a single transcription start site within a presumed initiator sequence was identified. Sequence elements which might confer melanocyte-specific expression were not detected. Instead, recognition sequences for the transcription factors CREB, AP-2, and c-Myb, as well as CArG-box motifs, were observed. These elements may contribute to the differential regulation of the MUC18 gene in normal and malignant tissues and suggest a role for this putative adhesion molecule in neural crest cells during embryonic development.
Intravenous iron in inflammatory bowel disease (2009)

The prevalence of anemia across studies on patients with inflammatory bowel disease (IBD) is high (30%). Both iron deficiency (ID) and anemia of chronic disease contribute most to the development of anemia in IBD. The prevalence of ID is even higher (45%). Anemia and ID negatively impact the patient's quality of life. Therefore, together with an adequate control of disease activity, iron replacement therapy should start as soon as anemia or ID is detected to attain a normal hemoglobin (Hb) and iron status. Many patients will respond to oral iron, but compliance may be poor, whereas intravenous (i.v.) compounds are safe, provide a faster Hb increase and iron store repletion, and presents a lower rate of treatment discontinuation. Absolute indications for i.v. iron treatment should include severe anemia, intolerance or inappropriate response to oral iron, severe intestinal disease activity, or use of an erythropoietic stimulating agent. Four different products are principally used in clinical practice, which differ in their pharmacokinetic properties and safety profiles: iron gluconate and iron sucrose (lower single doses), and iron dextran and ferric carboxymaltose (higher single doses). After the initial resolution of anemia and the repletion of iron stores, the patient's hematological and iron parameters should be carefully and periodically monitored, and maintenance iron treatment should be provided as required. New i.v. preparations that allow for giving 1000-1500 mg in a single session, thus facilitating patient management, provide an excellent tool to prevent or treat anemia and ID in this patient population, which in turn avoids allogeneic blood transfusion and improves their quality of life.
Direct measurements of interfacial contact resistance, end contact resistance, and interfacial contact layer uniformity (1983)

A four-terminal microelectronic test structure and test method are described for electrically determining the degree of uniformity of the interfacial layer in metal-semiconductor contacts and for directly measuring the interfacial contact resistance. A two-dimensional resistor network model is used to obtain the relationship between the specific contact resistance and the measured interfacial contact resistance for contacts with a uniform interfacial layer. A new six-terminal test structure is used for the direct measurement of end contact resistance and the subsequent determination of front contact resistance. A methodology is described for reducing the effects of both contact-window mask misalignment and parasitic resistance associated with these measurements. Measurement results are given for 98.5-percent Al/1.5- percent Si and 100-percent Al contacts on n-type silicon.
Single domain antibodies from llama effectively and specifically block T cell ecto‐ADP‐ribosyltransferase ART2.2 in vivo (2007)

The purpose of our study was to develop a tool for blocking the function of a specific leukocyte ecto-enzyme in vivo. ART2.2 is a toxin-related ecto-enzyme that transfers the ADP-ribose moiety from NAD onto other cell surface proteins. ART2.2 induces T cell death by activating the cytolytic P2x7 purinoceptor via ADP-ribosylation. Here, we report the generation of ART2.2-blocking single domain antibodies from an immunized llama. The variable domain of heavy-chain antibodies (VHH domain) represents the smallest known antigen-binding unit generated by adaptive immune responses. Their long CDR3 endows VHH domains with the extraordinary capacity to extend into and block molecular clefts. Following intravenous injection, the ART2.2-specific VHH domains effectively shut off the enzymatic and cytotoxic activities of ART2.2 in lymphatic organs. This blockade was highly specific (blocking ART2.2 but not the related enzymes ART1 or ART2.1), rapid (within 15 min after injection), and reversible (24 h after injection). Our findings constitute a proof of principle that opens up a new avenue for targeting leukocyte ecto-enzymes in vivo and that can serve as a model also for developing new antidotes against ADP-ribosylating toxins.
Internet Cache Protocol (ICP), version 2 (1997)

This document describes version 2 of the Internet Cache Protocol (ICPv2) as currently implemented in two World-Wide Web proxy cache packages[3,5]. ICP is a lightweight message format used for communicating among Web caches. ICP is used to exchange hints about the existence of URLs in neighbor caches. Caches exchange ICP queries and replies to gather information to use in selecting the most appropriate location from which to retrieve an object.
Retroviral-mediated gene correction for X-linked severe combined immunodeficiency (1996)

X-linked severe combined immunodeficiency (XSCID) is a lethal disease caused by a defect in the gene encoding the common gamma chain (gamma-c) of the receptor for interleukin-2 (IL-2), IL-4, IL-7, IL-9, and IL-15. Allogeneic bone marrow transplantation, the current therapy of choice for this defect, is often complicated by graft-versus-host disease and/or incomplete reconstitution of B-lymphocyte functions. Correction of the gene defect at the level of the autologous lymphohematopoietic progenitors could therefore represent an improvement in the medical management of these patients. To study the feasibility of a gene therapy approach for XSCID, a retroviral vector expressing gamma-c was used to transduce Epstein-Barr virus-transformed B-cell lines derived from patients with XSCID. After transduction, XSCID cells newly expressed gamma-c on the cell surface at levels comparable to those observed on B-cell lines obtained from normal donors. Moreover, the reconstituted gamma-c restored function to the IL-2 and IL-4 receptors as shown by signal transduction mediated by phosphorylation of the JAK1 and JAK3 members of the Janus family of tyrosine kinases and by restoration of cellular proliferation in response to IL-2.
Handbook of Semiconductor Manufacturing Technology (2010)

Overview of semiconductor devices introduction to semiconductor equipment silicon materials surface preparation ion implantation dopant diffusion oxidation silicidation rapid thermal processing overview of interconnect chemical vapourdeposition alternate interlevel dielectrics polymide dielectrics physical vapour deposition chemical-mechanical polish optical lithography photoresist materials and processing x-ray lithography electron-beam lithography photomask fabrication plasma etching equipment reliability overview of process control in-line metrology in-situ metrology yield modelling yield management electrical, physical and chemical characterization failure analysis. Appendices: glossary of manufacturing terms acronyms used in semiconductor manufacturing standards and specifications units of measure and conversion tables useful constants.
A RASTER ENGINE FOR COMPUTER GRAPHICS AND IMAGE COMPOSITION (1994)

A raster engine (RE) is designed and implemented to improve the performance of computer graphics and image composition. The RE hardware can release more than 50% CPU loads. Furthermore, if the approximated Phong method which is proposed is applied, 89% CPU operations are reduced by the RE. As the features of this design, the techniques including modified digital differential analyser (DDA), 2-level pipeline, and constant execution time for calculating cos/sup n/ /spl theta/ are proposed in RE. Three operation modes, Gouraud and Phong shading algorithm and image composition are incorporated in RE. This accelerator will be implemented by 0.8 um SPDM CMOS VLSI technology.
Virulence of Escherichia Coli in Ascending Urinary-tract Infection in Mice (1982)

The virulence of Escherichia coli strains in ascending urinary-tract infection was studied in mice drinking a 5% glucose solution; factors determining the virulence were examined. Of 33 strains, 8 (group I) infected the bladder and kidney, 10 (group II) infected only the bladder, while the remaining 15 strains (group III) did not cause infection. The adherence of group-I and group-II strains to bladder epithelial cells in vitro was inhibited by D-mannose. In group III, 13 strains barely adhered to the epithelial cells, while two strains showed an adherence unaffected by D-mannose. Most strains in groups I and II agglutinated erythrocytes of guinea-pig, chicken, and horse, and cells of Candida albicans in a mannose-sensitive manner. All strains in groups I and II had fimbriae. Virulence for the urinary tract was not directly related with O-serotype, intraperitoneal virulence, ability to grow in mouse urine, ability to ferment dulcitol, production of haemolysin, susceptibility to serum bactericidal activity, or susceptibility to antibiotics. These results suggest that the adherence of the E. coli to mouse-bladder epithelial cells in a mannose-sensitive manner plays an important role in the development of urinary-tract infection in mice and that the adherence is probably mediated by type-1 or closely related fimbriae.
Heparan Sulfate Proteoglycan Binding Properties of Adeno-Associated Virus Retargeting Mutants and Consequences for Their In Vivo Tropism (2006)

Adeno-associated virus type 2 (AAV-2) targeting vectors have been generated by insertion of ligand peptides into the viral capsid at amino acid position 587. This procedure ablates binding of heparan sulfate proteoglycan (HSPG), AAV-2's primary receptor, in some but not all mutants. Using an AAV-2 display library, we investigated molecular mechanisms responsible for this phenotype, demonstrating that peptides containing a net negative charge are prone to confer an HSPG nonbinding phenotype. Interestingly, in vivo studies correlated the inability to bind to HSPG with liver and spleen detargeting in mice after systemic application, suggesting several strategies to improve efficiency of AAV-2 retargeting to alternative tissues.
A Phase 1/2 Study of a Multiclade HIV‐1 DNA Plasmid Prime and Recombinant Adenovirus Serotype 5 Boost Vaccine in HIV‐Uninfected East Africans (RV 172) (2010)

The DNA/rAd5 vaccination regimen was safe and induced HIV type 1 multi-clade T cell responses, which were not significantly affected by titers of preexisting rAd5 neutralizing antibody. Trial Registration. ClinicalTrials.gov identifier: NCT00123968 .
Isolation of a genomic clone partially encoding human hypoxanthine phosphoribosyltransferase. (1982)

Mouse cells deficient in the enzyme hypoxanthine phosphoribosyltransferase (HPRT; EC 2.4.2.8) have been transfected with total human DNA, and cells producing human enzyme were isolated by growth in selective medium. DNA from several such cell lines has been used to generate secondary transfectants that make human HPRT. Blots of the DNA of these secondary cells have been hybridized with total human DNA probes or with cloned human Alu sequences, and one of several common bands has been cloned in pBR322. Colonies of transformed Escherichia coli containing human sequences were detected by their homology with human DNA, and subclones of resulting recombinant plasmids were prepared. Two subclones free of Alu sequences were found to contain human sequences that hybridized to human X chromosome DNA. One of these, pBR1.5, also hybridized to a single RNA band on gel blots of human and secondary transfectant cytoplasmic poly(A)+RNA but not to RNA from the parent mouse cell line. These results indicate that these clones represent human HPRT gene fragments. This has been confirmed by using pBR1.5 as a probe to isolate an authentic and expressible human HPRT cDNA clone from a library prepared by H. Okayama and P. Berg.
Properties and Anti-HIV Activity of Nicked Dumbbell Oligonucleotides (1996)

Abstract We have designed a new type of oligodeoxyribonucleotide. These oligodeoxyribonucleotides form two hairpin loop structures with base pairs (sense and antisense) in the double helical stem at the 3′ and 5′-ends (nicked dumbbell oligonucleotides). The nicked dumbbell oligonucleotides are molecules with free ends that are more resistant to exonuclease attack. Furthermore, the nicked dumbbell oligonucleotide containing phosphorothioate (P=S) bonds in the hairpin loops has increased nuclease resistance, as compared to the unmodified nicked oligonucleotide. The binding of the nicked dumbbell oligonucleotide to RNA is lower than that of a single-stranded DNA. We also describe the anti-HIV activity of nicked dumbbell oligonucleotides.
Development of robots for rehabilitation therapy: the Palo Alto VA/Stanford experience. (2001)

For over 25 years, personal assistant robots for severely disabled individuals have been in development. More recently, using robots to deliver rehabilitation therapy has been proposed. This paper summarizes the development and clinical testing of three mechatronic systems for post-stroke therapy conducted at the VA Palo Alto in collaboration with Stanford University. We describe the philosophy and experiences that guided their evolution. Unique to the Palo Alto approach is provision for bimanual, mirror-image, patient-controlled therapeutic exercise. Proof-of-concept was established with a 2-degree-of-freedom (DOF) elbow/forearm manipulator. Tests of a second-generation therapy robot producing planar forearm movements in 19 hemiplegic and control subjects confirmed the validity and reliability of interaction forces during mechanically assisted upper-limb movements. Clinical trials comparing 3-D robot-assisted therapy to traditional therapy in 21 chronic stroke subjects showed significant improvement in the Fugl-Meyer (FM) measure of motor recovery in the robot group, which exceeded improvements in the control group.
Inositol-requiring enzyme 1α is a key regulator of angiogenesis and invasion in malignant glioma (2010)

Inositol-requiring enzyme 1 (IRE1) is a proximal endoplasmic reticulum (ER) stress sensor and a central mediator of the unfolded protein response. In a human glioma model, inhibition of IRE1alpha correlated with down-regulation of prevalent proangiogenic factors such as VEGF-A, IL-1beta, IL-6, and IL-8. Significant up-regulation of antiangiogenic gene transcripts was also apparent. These transcripts encode SPARC, decorin, thrombospondin-1, and other matrix proteins functionally linked to mesenchymal differentiation and glioma invasiveness. In vivo, using both the chick chorio-allantoic membrane assay and a mouse orthotopic brain model, we observed in tumors underexpressing IRE1: (i) reduction of angiogenesis and blood perfusion, (ii) a decreased growth rate, and (iii) extensive invasiveness and blood vessel cooption. This phenotypic change was consistently associated with increased overall survival in glioma-implanted recipient mice. Ectopic expression of IL-6 in IRE1-deficient tumors restored angiogenesis and neutralized vessel cooption but did not reverse the mesenchymal/infiltrative cell phenotype. The ischemia-responsive IRE1 protein is thus identified as a key regulator of tumor neovascularization and invasiveness.