gebhart/patrepeval huggingface dataset:
Design and Characterization of Lysine Cross-Linked Mercapto-Acid Biocompatible Quantum Dots (2006)

Semiconductor quantum dots (QDs) are a new generation of inorganic probes with advantageous properties over traditional organic-only probes for biological applications. A major hurdle in the use of QDs for biology is the inability of the hydrophobically synthesized QDs to interface with aqueous environments. There have been tremendous advances in the surface modification of hydrophobic QDs. However, none of the current techniques fits all of the criteria for an ideal QD coating for biological applications (e.g., maintain the small size and optical properties of QDs, have low nonspecific binding) while providing cost-effective, easy preparation on a large scale. We developed a highly stable biocompatible coating for the surface of ZnS-capped CdSe QDs that maintains all of the hydrophobic-coated QD optical properties. These QDs are prepared by first coating them with mercaptoundecanoic acid and are further cross-linked with the amino acid lysine in the presence of dicyclohexylcarbodiimide to form a stable hydrophilic shell. The surface contains carboxylic acid and amino functional groups for conjugation to biomolecules. Using a dynamic light scattering method, we found that the hydrodynamic diameter of these surface-modified QDs is approximately 20 nm. We demonstrated the feasibility of preparing >400 mg of the biocompatible QDs and the successful conjugation of proteins onto their surface. Finally, we characterized the QD stability and optical properties in various biologically relevant environments.
Magnetic Nanosensors for the Detection of Oligonucleotide Sequences (2001)

Superparamagnetic nanoparticles conjugated to oligonucleotides exert sensitive and reversible effects on the spin-spin relaxation rates of adjacent water protons when the conjugates hybridize to target oligonucleotides (see temperature cycle in the picture). The fluid-phase magnetic sensors provide the basis for detecting specific nucleic acid sequences in turbid media and potentially in tissues in vivo.
ENTEROGLUCAGON (1997)

The gene encoding proglucagon, the biosynthetic precursor of glucagon, is expressed not only in the pancreatic islets but also in endocrine cells of the gastrointestinal mucosa. The proglucagon (PG)-derived peptides from the gut include glicentin (corresponding to PG 1-69); smaller amounts of oxyntomodulin (PG 33-69) and glicentin-related pancreatic polypeptide (GRPP, PG 1-30); glucagon-like peptide-1 (GLP-1, PG 78-107 amide); intervening peptide-2 (IP-2, PG 111-122 amide); and glucagon-like peptide-2 (GLP-2, PG 126-158). All are secreted into the blood in response to ingestion of carbohydrates and lipids. Only oxyntomodulin and GLP-1 have proven biological activity; oxyntomodulin possibly because it interacts (but with lower potency) with GLP-1 and glucagon receptors. GLP-1 is the most potent insulinotropic hormone known and functions as an incretin hormone. It also inhibits glucagon secretion and, therefore, lowers blood glucose. This effect is preserved in patients with non-insulin-dependent diabetes mellitus, in whom infusions of GLP-1 may completely normalize blood glucose. However, GLP-1 also potently inhibits gastrointestinal secretion and motility, and its physiological functions include mediation of the "ileal-brake" effect, i.e. the inhibition of upper gastrointestinal functions elicited by the presence of unabsorbed nutrients in the ileum. As such it may serve to regulate food intake.
Human surfactant polypeptide SP‐B Disulfide bridges, C‐terminal end, and peptide analysis of the airway form (1992)

Human hydrophobic surfactant polypeptide, SP-B, purified from lung tissue by exclusion chromatography in organic solvents, has been characterized. The polypeptide is 79 residues long, has a C-terminal methionine, and contains seven Cys residues. Native human SP-B lacks free thiol groups. Three intrachain disulfide bridges were defined, linking Cys8 to Cys77, Cys11 to Cys71 and Cys35 to Cys46. The remaining Cys48 is concluded to link the protein chains into homodimers via an interchain disulfide to its counterpart in a second SP-B polypeptide. These SS bridges are identical to those in the porcine form and confirm a consestant and unique disulfide pattern for SP-B polypeptides in general.
Sendai Virus and Simian Virus 5 Block Activation of Interferon-Responsive Genes: Importance for Virus Pathogenesis (1999)

Sendai virus (SeV) is highly pathogenic for mice. In contrast, mice (including SCID mice) infected with simian virus 5 (SV5) showed no overt signs of disease. Evidence is presented that a major factor which prevented SV5 from productively infecting mice was its inability to circumvent the interferon (IFN) response in mice. Thus, in murine cells that produce and respond to IFN, SV5 protein synthesis was rapidly switched off. In marked contrast, once SeV protein synthesis began, it continued, even if the culture medium was supplemented with alpha/beta IFN (IFN-alpha/beta). However, in human cells, IFN-alpha/beta did not inhibit the replication of either SV5 or SeV once virus protein synthesis was established. To begin to address the molecular basis for these observations, the effects of SeV and SV5 infections on the activation of an IFN-alpha/beta-responsive promoter and on that of the IFN-beta promoter were examined in transient transfection experiments. The results demonstrated that (i) SeV, but not SV5, inhibited an IFN-alpha/beta-responsive promoter in murine cells; (ii) both SV5 and SeV inhibited the activation of an IFN-alpha/beta-responsive promoter in human cells; and (iii) in both human and murine cells, SeV was a strong inducer of the IFN-beta promoter, whereas SV5 was a poor inducer. The ability of SeV and SV5 to inhibit the activation of IFN-responsive genes in human cells was confirmed by RNase protection experiments. The importance of these results in terms of paramyxovirus pathogenesis is discussed.
Cloning and Characterization of a RNase L Inhibitor. (1995)

The 2-5A/RNase L system is considered as a central pathway of interferon (IFN) action and could possibly play a more general physiological role as for instance in the regulation of RNA stability in mammalian cells. We describe here the expression cloning and initial characterization of RLI (for RNase L inhibitor), a new type of endoribonuclease inhibitor. RLI cDNA codes for a 68-kDa polypeptide whose expression is not regulated by IFN. Its expression in reticulocyte extracts antagonizes the 2-5A binding ability and the nuclease activity of endogenous RNase L or the cloned 2DR polypeptide. The inhibition requires the association of RLI with the nuclease and is dependent on the ratio between the two proteins. Likewise RLI is coimmunoprecipitated with the RNase L complex by a nuclease-specific antibody. RLI does not lead to 2-5A degradation or to irreversible modification of RNase L. The overexpression of RLI in stably transfected HeLa cells inhibits the antiviral activity of IFN on encephalomyocarditis virus but not on vesicular stomatitis virus. RLI therefore appears as the first described and potentially important mediator of the 2-5A/RNase L pathway.
Optically induced changes in the couplings between vergence and accommodation. (1987)

Vergence-induced accommodation (V-A) and accommodation-induced vergence (A-V) were measured in human subjects before and after they had worn various optical devices for 30 min. Laterally displacing periscopic spectacles, which increase the required change in vergence per unit change in accommodation, caused decreases and increases in the gain of V-A and A-V responses, respectively. These observations are consistent with the view that the gain of the neural cross-linkages between vergence and accommodation are subject to adaptive regulation. However, there were strong asymmetries: Medially displacing periscopes (cyclopean spectacles), which reduce the required change in vergence per unit change in accommodation to zero, were almost totally without effect. Base-out prisms, which increase the required convergence by an amount that is constant for all viewing distances, caused downward and upward shifts in the V-A and A-V response curves, respectively. Base-in prisms, which reduce the required convergence by a constant amount for all viewing distances, caused downward shifts of A-V curves but had no significant effect on V-A curves. These effects of prisms are in essential agreement with the work of others and confirm the existence of adaptive elements that regulate the bias in the vergence and/or accommodation control systems. Secondary effects of wearing periscopes and prisms indicated a certain lack of specificity in the sensing of gain and bias errors: vertical shifts of V-A and A-V curves (resembling those seen with base-out prisms) often occurred with the laterally displacing periscopes, and gain changes (generally resembling those seen with laterally displacing periscopes) often occurred with the base-out prisms.
Matrix Metalloproteinase-2 Dysregulation in Type 1 Diabetes (2007)

Urine and plasma MMP-2 concentrations are dysregulated in type 1 diabetes; urinary excretion of MMP-2, in particular, might provide a unique biomarker of diabetes-induced intrarenal pathologic processes.
Diversity in Mitochondrial Function Explains Differences in Vascular Oxygen Sensing (2002)

Renal arteries (RAs) dilate in response to hypoxia, whereas the pulmonary arteries (PAs) constrict. In the PA, O2 tension is detected by an unidentified redox sensor, which controls K+ channel function and thus smooth muscle cell (SMC) membrane potential and cytosolic calcium. Mitochondria are important regulators of cellular redox status and are candidate vascular O2 sensors. Mitochondria-derived activated oxygen species (AOS), like H2O2, can diffuse to the cytoplasm and cause vasodilatation by activating sarcolemmal K+ channels. We hypothesize that mitochondrial diversity between vascular beds explains the opposing responses to hypoxia in PAs versus RAs. The effects of hypoxia and proximal electron transport chain (pETC) inhibitors (rotenone and antimycin A) were compared in rat isolated arteries, vascular SMCs, and perfused organs. Hypoxia and pETC inhibitors decrease production of AOS and outward K+ current and constrict PAs while increasing AOS production and outward K+ current and dilating RAs. At baseline, lung mitochondria have lower respiratory rates and higher rates of AOS and H2O2 production. Similarly, production of AOS and H2O2 is greater in PA versus RA rings. SMC mitochondrial membrane potential is more depolarized in PAs versus RAs. These differences relate in part to the lower expression of proximal ETC components and greater expression of mitochondrial manganese superoxide dismutase in PAs versus RAs. Differential regulation of a tonically produced, mitochondria-derived, vasodilating factor, possibly H2O2, can explain the opposing effects of hypoxia on the PAs versus RAs. We conclude that the PA and RA have different mitochondria.
Lipid-DNA Complexes Induce Potent Activation of Innate Immune Responses and Antitumor Activity When Administered Intravenously (1999)

Cationic lipid-DNA complexes (CLDC) are reported to be safe and effective for systemic gene delivery, particularly to the lungs. However, we observed that i.v. injection of CLDC induced immunologic effects not previously reported. We found that even very low doses of CLDC administered i.v. induced marked systemic immune activation. This response included strong up-regulation of CD69 expression on multiple cell types and systemic release of high levels of Th1 cytokines, from both lung and spleen mononuclear cells. CLDC were much more potent immune activators on a per weight basis than either LPS or poly(I:C). The remarkable potency of CLDC appeared to result from enhancement of the immune stimulatory properties of DNA, since cationic lipids alone were without immune stimulatory activity. Systemic treatment with CLDC controlled tumor growth and significantly prolonged survival times in mice with metastatic pulmonary tumors. NK cells accumulated to high levels in the lungs of CLDC-treated mice, were functionally activated, and released high levels of IFN-gamma. The antitumor activity induced by CLDC injection was dependent on both NK cells and IFN-gamma. Thus, DNA complexed to cationic liposomes becomes highly immunostimulatory and capable of inducing strong antitumor activity when administered systemically.
N‐Chloroacyl Derivatives of Valine Esters (2002)

Abstract For Abstract see ChemInform Abstract in Full Text.
A Banach space of test functions for Gabor analysis (1998)

We introduce the Banach space S 0 ⊑ L 2 which has a variety of properties making it a useful tool in Gabor analysis. S 0 can be characterized as the smallest time-frequency homogeneous Banach space of (continuous) functions. We also present other characterizations of S 0 turning it into a very flexible tool for Gabor analysis and allowing for simplifications of various proofs. A careful analysis of both the coefficient and the synthesis mapping in Gabor theory shows that an arbitrary window in S 0 not only is a Bessel atom with respect to arbitrary time-frequency lattices, but also yields boundedness between S 0 and e 1. On the other hand, we can study properties of general L 2-atoms since they induce mappings from S 0 to S′0. This enables us to introduce a new, very natural concept of weak duality of Gabor atoms, applying also to the classical pair of the Gauss-function and its dual function determined by Bastiaans. Using the established results, we show a variety of properties that are desirable in applications, like the continuous dependence of the canonical dual window on the given Gabor window and on the lattice; continuity of thresholding and masking operators from signal processing; and an algorithm for the reconstruction of bandlimited functions from samples of the Gabor transform in a corresponding horizontal strip in the time-frequency plane. We also present an approximate Balian-Low Theorem stating that for close-to-critical lattices, the dual Gabor atoms progressively lose their time-frequency localization.
Ectopic Expression of SUPERMAN Suppresses Development of Petals and Stamens (2002)

The floral regulatory gene SUPERMAN (SUP) encodes a C2H2 type zinc finger protein that is required for maintaining boundaries between floral organs in Arabidopsis. It has been proposed that the main function of SUP is to balance cell proliferation in the third and fourth whorl of developing flowers, thereby maintaining the boundaries between the two whorls. To gain further insight into the function of SUP, we have ectopically expressed SUP using the promoter of APETALA1 (AP1), a gene that is initially expressed throughout floral meristems and later becomes restricted to the first and second whorls. Flowers of AP1::SUP plants have fewer floral organs, consistent with an effect of SUP on cell proliferation. In addition, the AP1::SUP transgene caused the conversion of petals to sepals and suppressed the development of stamens. The expression of the B function homeotic gene APETALA3 (AP3) and its regulator UNUSUAL FLORAL ORGANS (UFO) were delayed and reduced in AP1::SUP flowers. However, SUP does not act merely through UFO, as constitutive expression of UFO did not rescue the defects in petal and stamen development in AP1::SUP flowers. Together, these results suggest that SUP has both indirect and direct effects on the expression of B function homeotic genes.
Heregulin-HER3-HER2 signaling promotes matrix metalloproteinase-dependent blood-brain-barrier transendothelial migration of human breast cancer cell lines (2015)

HER2-positive breast tumors are associated with a high risk of brain relapse. HER3 is thought to be an indispensible signaling substrate for HER2 (encoded by ERBB2) and is induced in breast cancer-brain metastases, though the molecular mechanisms by which this oncogenic dimer promotes the development of brain metastases are still elusive. We studied the effects of the HER3-HER2 ligand, heregulin (neuregulin-1, broadly expressed in the brain), on luminal breast cancer cell lines in vitro. Treatment of SKBr3 (ERBB2-amplified), MDA-MB-361 (ERBB2-amplified, metastatic brain tumor-derived) and MCF7 (HER2-positive, not ERBB2-amplified) cells with exogenous heregulin increased proliferation and adhesive potential, concomitant with induction of cyclin D1 and ICAM-1, and suppression of p27. All three cell lines invaded through matrigel toward a heregulin chemotactic signal in transwell experiments, associated with activation of extracellular cathepsin B and matrix metalloproteinase-9 (MMP-9). Moreover, heregulin induced breast cancer cell transmigration across a tight barrier of primary human brain microvascular endothelia. This was dependent on the activity of HER2, HER3 and MMPs, and was completely abrogated by combination HER2-HER3 blockade using Herceptin® and the humanized HER3 monoclonal antibody, EV20. Collectively these data suggest mechanisms by which the HER3-HER2 dimer promotes development of metastatic tumors in the heregulin-rich brain microenvironment.
Requirements for the destruction of human Aurora-A (2004)

The mitotic kinase Aurora A (Aur-A) is overexpressed in a high proportion of human tumors, often in the absence of gene amplification. In somatic cells, Aur-A protein levels fall following mitosis or upon overexpression of Cdh1, an activator of the ubiquitin ligase APC/C. Thus, mutations that reduce or block the rate of Aur-A destruction might also be expected to contribute to its oncogenic potential. Previous work had defined two short sequences of Xenopus Aur-A that are required for its Cdh1-inducible destruction in extracts of Xenopus eggs, an N-terminal A box and a C-terminal D box, and a serine residue within the A box whose phosphorylation might inhibit destruction. Here, we show that these same sequences are required for the destruction of human Aur-A during mitotic exit and G1 in the somatic cell cycle. Expression of a dominant negative Cdh1 protein leads to accumulation of Aur-A, further indicating that the Cdh1-activated form of the APC/C is responsible for destruction of Aur-A during the somatic cell cycle in vivo. During the course of this work, we found some previously unsuspected problems in commonly used in vitro destruction assays, which can result in misleading results. Potentially confounding factors include: (i) the presence of D-box- and A-box-dependent destruction-promoting activities in the reticulocyte in vitro translation mix that is used to produce radiolabeled substrates for destruction assays; and (ii) the ability of green-fluorescent-protein tags to reduce the destruction rate of Aur-A substantially. These findings have direct relevance for studies of Aur-A destruction itself, and for broader approaches that use in vitro translation products in screens for additional APC/C targets.
Characterization of the High Affinity Cell-binding Domain in the Cell Surface Proteoglycan Syndecan-4 (1998)

The syndecan family of cell surface proteoglycans regulates cell adhesion via their glycosaminoglycan chains and discrete domains of their core proteins. Core protein domains that are variable between syndecan family members may regulate syndecan-specific associations, thereby endowing individual syndecans with unique functions. A syndecan-4-specific domain has been identified in the extracellular syndecan-4 protein. This region mediates cell adhesion when provided as an artificial substratum and is localized within amino acids 56-109 of the recombinant extracellular protein domain of mouse syndecan-4 (mS4ED) (McFall, A. J., and Rapraeger, A. C. (1997) J. Biol. Chem. 272, 12901-12904). To characterize its interaction with the cell surface, radiolabeled ligand binding studies were performed. A single high affinity interaction, with a dissociation constant of 2 x 10(-9) M, was observed between mS4ED and both human and mouse cells. Both chicken S4ED and mS4ED compete for this interaction, although they are only 34% identical within the cell-binding domain sequence. The extracellular protein domains of syndecan-1, -2, and -3, however, fail to compete. The interaction is also observed with native syndecan-4 shed from cell surfaces. Interestingly, the extracellular protein domain of syndecan-1 also mediates cell adhesion, suggesting a similar but discrete interaction for this family member.
Evaluation of the Polymorphisms Associated with Tandem Repeats for Pseudomonas aeruginosa Strain Typing (2003)

We report on the development of a scheme for the typing of Pseudomonas aeruginosa, multiple-locus variable number of tandem repeat (VNTR) analysis (MLVA). We first evaluated the polymorphisms of 201 tandem repeat loci selected from more than 3,000 such sequences present in strain PAO1 with a test collection of 12 genotypically distinct clinical strains. Seven VNTR loci which can be easily scored with the technology used here were identified and used to genotype a collection of 89 clinical isolates that had previously been classified into 46 ribotypes, including 2 widespread ribotypes. Seventy-one different MLVA genotypes could be distinguished. With only two exceptions, strains with identical ribotypes were grouped together upon cluster analysis of the MLVA data. The 27 isolates with the most frequent ribotype were divided into 14 MLVA types, and the 18 isolates with the second most frequent ribotype were divided into 15 MLVA types. Analysis of a subset of 17 strains belonging to the major ribotype by pulsed-field gel electrophoresis with the enzyme SpeI distinguished seven types, identical to the number of MLVA types in this subset. Our data show that MLVA typing of P. aeruginosa based on the first set of loci has a high discriminatory power. Because MLVA is highly reproducible and easily portable among laboratories, it represents a very promising tool for the molecular surveillance of P. aeruginosa. A free, online strain identification service based on the genotyping data produced herein has been developed.
Photochemical Reaction in Monolayer MoS2 via Correlated Photoluminescence, Raman Spectroscopy, and Atomic Force Microscopy (2016)

Photoluminescence (PL) from monolayer MoS2 has been modulated using plasma treatment or thermal annealing. However, a systematic way of understanding the underlying PL modulation mechanism has not yet been achieved. By introducing PL and Raman spectroscopy, we analyze that the PL modulation by laser irradiation is associated with structural damage and associated oxygen adsorption on the sample in ambient conditions. Three distinct behaviors were observed according to the laser irradiation time: (i) slow photo-oxidation at the initial stage, where the physisorption of ambient gases gradually increases the PL intensity; (ii) fast photo-oxidation at a later stage, where chemisorption increases the PL intensity abruptly; and (iii) photoquenching, with complete reduction of PL intensity. The correlated confocal Raman spectroscopy confirms that no structural deformation is involved in slow photo-oxidation stage; however, the structural disorder is invoked during the fast photo-oxidation stage, and severe structural degradation is generated during the photoquenching stage. The effect of oxidation is further verified by repeating experiments in vacuum, where the PL intensity is simply degraded with laser irradiation in a vacuum due to a simple structural degradation without involving oxygen functional groups. The charge scattering by oxidation is further explained by the emergence/disappearance of neutral excitons and multiexcitons during each stage.