gebhart/patrepeval huggingface dataset:
Treatment of Human Breast Cancer Xenografts Using Natural Interferons-α and -γ Injected Singly or in Combination (1988)

Natural interferons (nIFNs) -alpha and -gamma were used to treat nude mice bearing bilateral xenografts of human breast cancer cells (MCF-7 and BT 20). The IFNs were administered singly or in combination by means of intralesional (i.l.) or intraperitoneal (i.p.) injections. In the animals treated intralesionally 1 of the 2 tumors was injected to study the local therapeutic effects, while the contralateral one was left undisturbed and used to assess systemic effects. Treatment of MCF-7 tumors with i.l. injections of nIFN-alpha and nIFN-gamma combined resulted in complete regression of the injected tumors in 8 of 20 mice treated for 2 weeks and in 10 of 10 mice of an additional group treated for 4 weeks. The corresponding contralateral tumors showed complete regression in 2 mice treated for 4 weeks and partial responses in the others. Incomplete responses were also observed when the IFNs were used singly or when they were delivered intraperitoneally. Similarly, in BT 20 xenografts the best results were obtained with i.l. injections of the 2 IFNs combined, but no complete regressions were achieved. These experiments provide further evidence for a synergistic interaction of nIFN-alpha and nIFN-gamma in vivo and indicate that the potentiated antitumoral activity is greater when these interferons are administered i.l.
ChemInform Abstract: Crystal Structure of K4(SiO4). (1991)

Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
Monolithic Integration of Carbon Nanotube Devices with Silicon MOS Technology (2003)

An integrated circuit combining single-walled carbon nanotube (SWNT) devices with n-channel metal oxide semiconductor (NMOS) field effect transistors was fabricated. SWNTs were grown, using chemical vapor deposition, from catalyst islands located on an NMOS decoder circuit. Massive arrays of nanotube devices, each addressed individually using the NMOS circuit, were rapidly characterized. The successful monolithic integration of nanotube devices and MOS transistors creates many possibilities, including electronically addressable nanotube chemical sensor arrays.
Hyperinsulinemia is associated with altered insulin receptor mRNA splicing in muscle of the spontaneously obese diabetic rhesus monkey. (1994)

The human insulin receptor has two isoforms derived from alternative splicing of exon 11 of the insulin receptor gene. The type B (containing exon 11, or exon 11+) isoform binds insulin with twofold lower affinity than the type A (lacking exon 11, or exon 11-) isoform. In efforts to resolve the controversy over whether altered splicing is involved in the development of insulin resistance and non-insulin-dependent diabetes mellitus (NIDDM), the spontaneously obese diabetic rhesus monkey, a unique model that is extraordinarily similar to human NIDDM, was used. Cross-sectional studies of insulin receptor mRNA splicing variants in vastus lateralis muscle were performed on 19 rhesus monkeys. When monkeys were divided into four groups based upon the known stages of progression to NIDDM: normal (normoglycemic/normoinsulinemic), prediabetic (normoglycemic/hyperinsulinemic), early NIDDM (hyperglycemic/hyperinsulinemic), and late NIDDM (hyperglycemic/hypoinsulinemic), both hyperinsulinemic groups had significantly higher percentages of the exon 11- mRNA splicing variant compared to the normal (74.8 +/- 1.7 vs 59.0 +/- 2.3%; P < 0.005) and late NIDDM groups (74.8 +/- 1.7 vs 64.2 +/- 3.9%; P < 0.05). Our findings provide the first direct evidence linking hyperinsulinemia to alterations in insulin receptor mRNA splicing, and suggest that alterations of insulin receptor mRNA splicing in muscle is an early molecular marker that may play an important role in NIDDM.
Anti‐CD47 antibody suppresses tumour growth and augments the effect of chemotherapy treatment in hepatocellular carcinoma (2015)

Anti-CD47 antibody treatment could complement chemotherapy which may be a promising therapeutic strategy for the treatment of HCC patients.
Efficient, one-pot syntheses of biologically active α-linked glycolipids (2007)

Per-O-silylated galactosyl iodides undergo alpha-glycosidation with fully functionalized glycolipids producing biologically relevant conjugates.
Deficiency of the p53/p63 target Perp alters mammary gland homeostasis and promotes cancer (2012)

Together, these observations demonstrate an important role for Perp in normal mammary tissue function and in mammary cancer suppression. In addition, our findings highlight the importance of desmosomes in cancer suppression and suggest the merit of evaluating Perp as a potential prognostic indicator or molecular target in breast cancer therapy.
The effects of nanostructure and composition on the hydrophobic properties of solid surfaces (2006)

Abstract The effects of nanoroughness and chemical composition on the contact and sliding angles on hydrophobic surfaces were studied theoretically and experimentally. A theoretical model based on forces developed at the contact area between a liquid drop and hydrophobic smooth or nanoroughened surface was developed and compared with the existing models, which are based on forces developed at the periphery between the drop and the solid surface. The contact area based model gives rise to an interfacial adhesion strength parameter that better describes the drop-sliding phenomenon. Consequently, relationships were derived describing the dependence between the interfacial adhesion strength of the liquid drop to the surface of a given composition, the mass of the drop, the measured contact angles and the sliding angle. For a given surface chemistry, the sliding angle on a nanometric roughened surface can be predicted based on measurements of contact angles and the sliding angle on the respective smooth surface. Various hydrophobic coatings having different surface nanoroughnesses were prepared and, subsequently, contact angles and sliding angles on them as a function of drop volume were measured. The validity of the proposed model was investigated and compared with the existing models and the proposed model demonstrated good agreement with experimental results. Keywords: NANOROUGHNESSNANOMETRICCONTACT ANGLESLIDING ANGLEHYDROPHOBIC SURFACESINTERFACIAL ADHESION STRENGTHCOATINGS
A Method for Forming Very Small Diameter Wires (1970)

Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter Facebook Reddit LinkedIn Tools Icon Tools Reprints and Permissions Cite Icon Cite Search Site Citation George E. Possin; A Method for Forming Very Small Diameter Wires. Rev. Sci. Instrum. 1 May 1970; 41 (5): 772–774. https://doi.org/10.1063/1.1684640 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAIP Publishing PortfolioReview of Scientific Instruments Search Advanced Search |Citation Search
Focal adhesion kinase: a promising target for anticancer therapy (2007)

Focal adhesion kinase (FAK) is a protein tyrosine kinase acting as an early modulator of the integrin signalling cascade, thus regulating various basic cellular functions. In transformed cells, upregulation of FAK protein expression and uncontroled signalling were held responsible for the promotion of malignant phenotypic characteristics, as well as resistance to chemotherapy and radiotherapy. Direct FAK targeting resulted in the inhibition of the malignant phenotype of cancer cells, whereas increased apoptotic rates of cancer cells, either used alone or in combination with conventional chemotherapeutic agents, radiotherapy or hormonal therapy. Furthermore, drugs used in cancer chemotherapy, besides their basic mode of action, were also shown to act through altering FAK signalling. Finally, positive results were noted by the transfection of cancer cells with fak mutants or genes that suppress FAK expression or activity, such as phosphatase and tensin homolog deleted on chromosome Ten (PTEN), ribonucleotide reductase M1 polypeptide (RRM1) and melanoma differentiation-associated gene-7 (mda-7). The purpose of this article is a comprehensive review of the existing data on the possible use of FAK targeting in anticancer therapy.
Microchimerism (2004)

Recent studies indicate cells transfer between fetus and mother during pregnancy and can persist in both decades later. The presence within one individual of a small population of cells from another genetically distinct individual is referred to as microchimerism. Naturally acquired microchimerism has recently been investigated in autoimmune diseases, including scleroderma, thyroiditis, primary biliary cirrhosis, Sjögren syndrome, systemic lupus, dermatomyositis, and neonatal lupus. Iatrogenic chimerism has been investigated in transplantation and following blood transfusion. Considering findings of naturally acquired microchimerism along with iatrogenic microchimerism suggests microchimerism can have detrimental and/or beneficial effects in both settings. Recent identification of tissue-specific microchimerism either from naturally acquired or iatrogenic microchimerism (eg, cardiac myocytes) raises the possibility that microchimerism can be a target of autoimmunity or alternatively contribute to tissue repair. Advances in this new frontier of research with varied and numerous implications for human health are summarized.
IL-1 Receptor Antagonist Serum Levels Are Increased in Human Obesity: A Possible Link to the Resistance to Leptin? (2002)

We have recently shown that human monocytic cells express functional leptin receptors and that leptin is capable of inducing the expression and secretion of the IL-1 receptor antagonist (IL-1Ra). Although IL-1Ra has anti-inflammatory and possibly anti-atherogenic properties, it has also been shown to antagonize the action of leptin at the hypothalamic level in rodents, thereby inducing leptin resistance. We have therefore examined whether IL-1Ra levels are increased in human hyperleptinemic conditions, such as obesity. To this end, we measured serum IL-1Ra levels in 20 morbidly obese nondiabetic subjects [body mass index (BMI), 45 +/- 6 kg/m(2); serum leptin, 52 +/- 20 ng/ml] as well as in 10 age- and sex-matched lean controls (BMI, 22 +/- 2 kg/m(2); serum leptin, 7 +/- 4 ng/ml). Serum IL-1Ra concentrations proved to be elevated 6.5-fold in the obese subjects, and they were positively correlated in a linear manner with the leptin levels (r(2) = 0.34; P = 0.01), although lean body mass (LBM) and the insulin resistance index were even better predictors of IL-1Ra levels (r(2) = 0.45 and 0.58, respectively; P < 0.01). Six months after 15 of the 20 obese subjects had undergone bypass surgery for their morbid obesity, their mean BMI and leptin levels decreased to 33 +/- 7 kg/m(2) and 18 plus minus 12 ng/ml, respectively. This change in leptin concentrations was associated with a significant reduction in IL-1Ra levels (P < 0.02). However, there was a better correlation between the decrease in IL-1Ra level and the change in LBM than with the reduction in leptin levels, indicating that leptin is not the sole determinant of circulating IL-1Ra in obesity. In summary, we demonstrate that IL-1Ra levels are highly elevated in human obesity and that its concentrations decrease after weight loss from bypass surgery. However, LBM and insulin resistance are better predictors of serum IL-1Ra concentrations than are leptin levels, suggesting that additional metabolic factors control the secretion of this cytokine antagonist. Although the immunological consequences of this alteration remain unknown, it is tempting to speculate that the obesity-related increase in IL-1Ra might contribute to the central resistance to leptin in obese patients, similar to the inhibition of the hypothalamic signaling of leptin by IL-1Ra in rodents.
Glycoprotein gIII of pseudorabies virus is multifunctional (1988)

One of the major glycoproteins of pseudorabies virus, gIII, is nonessential for growth in cell culture. Mutants defective in gIII, however, consistently yield lower titers of infectious virus (3- to 20-fold) than does wild-type virus. The interactions of gIII- mutants with their host cells were compared with those of wild-type virus in an attempt to uncover the functions of gIII. We show that gIII plays a major role in the stable adsorption of the virus to its host cell; in the absence of gIII, the rate of adsorption is reduced and adsorption is easily reversed by washing. Thus, adsorption of pseudorabies virus can be said to occur in at least the following two ways: (i) a gIII-mediated rapid adsorption or (ii) a slower and more labile adsorption that is independent of gIII. After virions have been complexed with monoclonal antibodies against gIII (but not some monoclonal antibodies against other glycoproteins), both modes of adsorption were inhibited. Glycoprotein gIII affects virus stability and virus release, as well as adsorption. The effect on virus release is marked when the virus is defective in additional functions. Thus, although we found no obvious difference in the release of virus from gIII- or wild-type virus-infected rabbit kidney cells, release of a gIII-/gI- double mutant from the cells occurred less readily than did release of a gI- mutant. The gIII-/gI- and gIII- mutants, however, adsorbed to cells at a similar rate, indicating that the effects of gIII on adsorption and virus release constitute separate functions. The Bartha vaccine strain of pseudorabies virus has a defective gIII gene and is released poorly from rabbit kidney cells. After the resident Bartha gIII gene was replaced by the gIII gene of wild-type virus, virus release was enhanced considerably. Since inactivation of gIII in wild-type pseudorabies virus did not significantly affect virus release, the Bartha strain must be defective in another function which, in conjunction with gIII, significantly affects virus release. These results indicate again that gIII affects virus release in conjunction with other functions. Also, although the Bartha strain was functionally defective in virus release, it adsorbed to cells as well as wild-type virus did, showing that the effects of gIII on virus adsorption and release constitute separate functions. We conclude that gIII is a multifunctional glycoprotein.
Embryonal long terminal repeat-binding protein is a murine homolog of FTZ-F1, a member of the steroid receptor superfamily. (1992)

The embryonal long terminal repeat-binding protein, ELP, is present in undifferentiated mouse embryonal carcinoma cells. It binds to and suppresses transcription of the Moloney leukemia virus long terminal repeat in undifferentiated murine embryonal carcinoma cells. We report here that ELP is a mouse homolog of Drosophila FTZ-F1, which positively regulates transcription of the fushi tarazu gene in blastoderm-stage embryos of the fly. As members of the steroid receptor superfamily, ELP and FTZ-F1 have both DNA binding and putative ligand binding domains which are well conserved between the two. ELP and FTZ-F1 function in cells in the extremely early stage of development. A high degree of conservation between the two transcription factors during the evolution of these species indicates the importance of their functions in early-stage embryogenesis. In addition, the sequence elements they recognize do not contain repeat units, in contrast to other steroid receptors, which usually bind to either palindromic or direct repeat sequences.
Dendritic cells as a major source of macrophage-derived chemokine/CCL22in vitro andin vivo (2001)

Macrophage-derived chemokine (MDC)/CCL22 is a CC chemokine active on dendritic cells (DC), NK cells and Th2 lymphocytes. The present study was aimed at comprehensively investigating MDC production in vitro and in vivo. DC were the most potent producers of MDC among leukocytes tested. Endothelial cells did not produce MDC under a variety of conditions. Signals that induce maturation (lipopolysaccharide, IL-1, TNF, CD40 ligand, recognition of bacteria and yeast) dramatically augmented MDC production, and dexamethasone and vitamin D3 blocked it. Prostaglandin E(2), which blocked the acquisition of IL-12 production and the capacity to promote Th1 generation, did not affect MDC production. Using mass spectrometry-based techniques, DC supernatants were found to contain N-terminally truncated forms of MDC [MDC(3-69), MDC(5-69) and MD(C7-69)] as well as the full-length molecule. In vivo, CD1a(+), CD83(+), MDC(+) DC were found in reactive lymph nodes, and in Langerhans' cell histiocytosis. Skin lesions of atopic dermatitis patients showed that CD1a(+) or CD1b(+) DC, and DC with a CD83(+) phenotype were responsible for MDC production in this Th2-oriented disorder. Thus, DC are the predominant source of MDC in vitro and in vivo under a variety of experimental and clinical conditions. Processing of MDC to MDC(3-69) and shorter forms which do not recognize CCR4 is likely to represent a feedback mechanism of negative regulation.
Graphene optical modulator (2011)

Data communications have been growing at a speed even faster than Moore's Law, with a 44-fold increase expected within the next 10 years. Data Transfer on such scale would have to recruit optical communication technology and inspire new designs of light sources, modulators, and photodetectors. An ideal optical modulator will require high modulation speed, small device footprint and large operating bandwidth. Silicon modulators based on free carrier plasma dispersion effect and compound semiconductors utilizing direct bandgap transition have seen rapid improvement over the past decade. One of the key limitations for using silicon as modulator material is its weak refractive index change, which limits the footprint of silicon Mach-Zehnder interferometer modulators to millimeters. Other approaches such as silicon microring modulators reduce the operation wavelength range to around 100 pm and are highly sensitive to typical fabrication tolerances and temperature fluctuations. Growing large, high quality wafers of compound semiconductors, and integrating them on silicon or other substrates is expensive, which also restricts their commercialization. In this work, we demonstrate that graphene can be used as the active media for electroabsorption modulators. By tuning the Fermi energy level of the graphene layer, we induced changes in the absorption coefficient of graphene at communication wavelength and achieve a modulation depth above 3 dB. This integrated device also has the potential of working at high speed.
Neutrophil-derived MMP-9 mediates synergistic mobilization of hematopoietic stem and progenitor cells by the combination of G-CSF and the chemokines GROβ/CXCL2 and GROβT /CXCL2Δ4 (2003)

Mobilized peripheral blood stem cells (PBSCs) are widely used for transplantation, but mechanisms mediating their release from marrow are poorly understood. We previously demonstrated that the chemokines GRObeta/CXCL2 and GRObetaT/CXCL2Delta4 rapidly mobilize PBSC equivalent to granulocyte colony-stimulating factor (G-CSF) and are synergistic with G-CSF. We now show that mobilization by GRObeta/GRObetaT and G-CSF, alone or in combination, requires polymorphonuclear neutrophil (PMN)-derived proteases. Mobilization induced by GRObeta/GRObetaT is associated with elevated levels of plasma and marrow matrix metalloproteinase 9 (MMP-9) and mobilization and MMP-9 are absent in neutrophil-depleted mice. G-CSF mobilization correlates with elevated neutrophil elastase (NE), cathepsin G (CG), and MMP-9 levels within marrow and is partially blocked by either anti-MMP-9 or the NE inhibitor MeOSuc-Ala-Ala-Pro-Val-CMK. Mobilization and protease accumulation are absent in neutrophil-depleted mice. Synergistic PBSC mobilization observed when G-CSF and GRObeta/GRObetaT are combined correlates with a synergistic rise in the level of plasma MMP-9, reduction in marrow NE, CG, and MMP-9 levels, and a coincident increase in peripheral blood PMNs but decrease in marrow PMNs compared to G-CSF. Synergistic mobilization is completely blocked by anti-MMP-9 but not MeOSuc-Ala-Ala-Pro-Val-CMK and absent in MMP-9-deficient or PMN-depleted mice. Our results indicate that PMNs are a common target for G-CSF and GRObeta/GRObetaT-mediated PBSC mobilization and, importantly, that synergistic mobilization by G-CSF plus GRObeta/GRObetaT is mediated by PMN-derived plasma MMP-9.
Modeling of Hot Carrier Effects for LDD MOSFETs (1985)

In the strive for faster and more complex integrated circuits, the device geometries and minimum feature size have been scaled down aggressively to achieve the desired circuit performance. The resulting high electric fields favor the generation and injection of hot carriers near the drain in MOS devices[1-3]. Both threshold voltage(Vt) shift and transconductance(gm) degradation have been reported by many researchers[4-8]. For LDD devices, only gm degradation was reported and was believed to be either caused by mobility degradation due to interface-state generation[6,7] or by localized charge [8]. One objective of our work is to show that for LDD devices in addition to gm degradation, Vt shift and variations for all short channel SPICE model parameters are observed. There are also good correlations between the variations of those short channel parameters. The other objective is to identify the degradation mechanisms by theoretical modeling, simulation, and experimental results. Our modeling results indicate that localized charge or mobility degradation alone can not explain the observed experimental results. A spatial charge distribution model was identified to predict the experimental results.
The Membrane-proximal Portion of CD3 ε Associates with the Serine/Threonine Kinase GRK2 (2007)

The activation of protein kinases is one of the primary mechanisms whereby T cell receptors (TCR) propagate intracellular signals. To date, the majority of kinases known to be involved in the early stages of TCR signaling are protein-tyrosine kinases such as Lck, Fyn, and ZAP-70. Here we report a constitutive association between the TCR and a serine/threonine kinase, which was mediated through the membrane-proximal portion of CD3 . Mass spectrometry analysis of CD3 -associated proteins identified G protein-coupled receptor kinase 2 (GRK2) as a candidate Ser/Thr kinase. Transient transfection assays and Western blot analysis verified the ability of GRK2 to interact with the cytoplasmic domain of CD3 within a cell. These findings are consistent with recent reports demonstrating the ability of certain G protein-coupled receptors (GPCR) and G proteins to physically associate with the / TCR. Because GRK2 is primarily involved in arresting GPCR signals, its interaction with CD3 may provide a novel means whereby the TCR can negatively regulate signals generated through GPCRs.