gebhart/patrepeval huggingface dataset:
A live avirulent mutant Legionella pneumophila vaccine induces protective immunity against lethal aerosol challenge. (1989)

We have examined the capacity of a live avirulent mutant form of the intracellular bacterial pathogen Legionella pneumophila to induce immune responses and protective immunity in guinea pigs. The mutant L. pneumophila is nonlethal to guinea pigs and does not revert to virulence with passage through guinea pigs. In contrast, exposure of guinea pigs to aerosols containing wild-type L. pneumophila induces a pneumonic illness that clinically and pathologically resembles Legionnaires' disease in humans. Guinea pigs immunized by aerosol exposure to mutant L. pneumophila developed a strong humoral immune response to wild-type L. pneumophila antigens with reciprocal antibody titers of 32-512 (median 256) by the indirect fluorescent antibody assay, compared with titers of less than 2 for control (sham immunized) guinea pigs. Mutant immunized but not control guinea pigs also developed strong cell-mediated immune responses to wild-type L. pneumophila antigens, as demonstrated in assays of cutaneous delayed-type hypersensitivity and in vitro splenic lymphocyte proliferation. Mutant immunized guinea pigs developed strong protective immunity to lethal aerosol challenge with wild-type L. pneumophila. In four independent experiments 40-83% of mutant immunized guinea pigs survived compared with 0% of control guinea pigs. Overall, 13 of 21 (62%) mutant immunized guinea pigs survived compared with 0 of 21 (0%) control guinea pigs (P = 0.00002, Fisher's exact test, two-tailed). Mutant immunization induced protection comparable to wild-type immunization in these studies; 8 of 14 (57%) guinea pigs immunized by wild-type L. pneumophila survived. This study demonstrates that guinea pigs immunized with a live avirulent mutant L. pneumophila vaccine (a) develop a strong humoral immune response to wild-type L. pneumophila antigens; (b) develop a strong cell-mediated immune response to wild-type L. pneumophila antigens; and (c) develop protective immunity to lethal aerosol challenge with wild-type L. pneumophila. This study demonstrates the feasibility of a vaccine against Legionnaires' disease.
Submicron patterning of DNA oligonucleotides on silicon (2004)

The covalent attachment of DNA oligonucleotides onto crystalline silicon (100) surfaces, in patterns with submicron features, in a straightforward, two-step process is presented. UV light exposure of a hydrogen-terminated silicon (100) surface coated with alkenes functionalized with N-hydroxysuccinimide ester groups resulted in the covalent attachment of the alkene as a monolayer on the surface. Submicron-scale patterning of surfaces was achieved by illumination with an interference pattern obtained by the transmission of 248 nm excimer laser light through a phase mask. The N-hydroxysuccinimide ester surface acted as a template for the subsequent covalent attachment of aminohexyl-modified DNA oligonucleotides. Oligonucleotide patterns, with feature sizes of 500 nm, were reliably produced over large areas. The patterned surfaces were characterized with atomic force microscopy, scanning electron microscopy, epifluorescence microscopy and ellipsometry. Complementary oligonucleotides were hybridized to the surface-attached oligonucleotides with a density of 7 x 10(12) DNA oligonucleotides per square centimetre. The method will offer much potential for the creation of nano- and micro-scale DNA biosensor devices in silicon.
B Cells Limit Repair after Ischemic Acute Kidney Injury (2010)

There is no established modality to repair kidney damage resulting from ischemia-reperfusion injury (IRI). Early responses to IRI involve lymphocytes, but the role of B cells in tissue repair after IRI is unknown. Here, we examined B cell trafficking into postischemic mouse kidneys and compared the repair response between control (wild-type) and muMT (B cell-deficient) mice with and without adoptive transfer of B cells. B cells infiltrated postischemic kidneys and subsequently activated and differentiated to plasma cells during the repair phase. Plasma cells expressing CD126 increased and B-1 B cells trafficked into postischemic kidneys with distinct kinetics. An increase in B lymphocyte chemoattractant in the kidney preceded B cell trafficking. Postischemic kidneys of muMT mice expressed higher IL-10 and vascular endothelial growth factor and exhibited more tubular proliferation and less tubular atrophy. Adoptive transfer of B cells into muMT mice reduced tubular proliferation and increased tubular atrophy. Treatment with anti-CD126 antibody increased tubular proliferation and reduced tubular atrophy in the late repair phase. These results demonstrate that B cells may limit the repair process after kidney IRI. Targeting B cells could have therapeutic potential to improve repair after IRI.
ChemInform Abstract: Studies with 3‐Oxoalkanenitriles: Synthesis of New Pyrazolo[1,5‐a]pyrimidines and Pyrazolo[5,1‐c]‐1,2,4‐triazines and Reactivity of 4‐Phenyl‐3‐oxobutanenitrile Derivatives. (1997)

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.
On the nature of peptides involved in T cell alloreactivity. (1991)

The strong reaction of T cells against foreign major histocompatibility complex (MHC) antigens, commonly termed "alloreactivity", is not only a nuisance for clinical organ transplantation; it also remains a puzzling question for immunologists. By making use of recent technical developments, alloreactive T cells nominally directed against a mutation in a single MHC class I molecule were found to fall into several major categories. One is recognizing peptides whose occurrence is dependent on one particular MHC allele, another is recognizing peptides supported by several MHC alleles, and a third is recognizing peptides occurring independently of MHC alleles. In a fourth category, the binding to MHC of any of a broad range of peptides appears sufficient. In addition, there are T cells for which no peptide involvement could be detected at all. Even within these categories, the heterogeneity of T cells is considerable: among 16 Kb-reactive T cells analyzed, 15 different modes of reactions were found.
Photonic Analog-to-Digital Converters A Tutorial (2009)

Each new bit of ADC resolution requires an increase in signal-to-noise-and-distortion ratio (SNDR) of 6 dB ENOB without noise bandwidth is meaningless Decreasing the noise bandwidth by a factor of 4 increases ADC resolution by 1 ENOB – e.g. the Tektronix 50 GS/s digital oscilloscope has 5 ENOB over 16 GHz 7 ENOB over 1 GHz Every time you sneeze, you lose a few 1/10’s of an ENOB Optical photons are very energetic compared to RF photons – Shot noise is irrelevant for electronic ADCs – Shot noise is a fundamental limit in photonic ADCs Photonic ADCs usually contain a microwave photonic link – Standard analysis gives the SNR/CNR – Max ENOB over a given noise bandwidth readily estimated If commercialized, photonic ADCs will resemble data conversion modules and digital oscilloscopes rather than single chip ADCs
Yersinia enterocolitica infections in non-human primates. (1977)

Yersinia enterocolitica was isolated from ten non-human primates in the Netherlands. The following species were represented: Potto, Senegalgalago, wooly monkey, black spider monkey, common marmoset, cottonhead tamarin, pigtailed macaque and lesser whitenosed guenon.
Rehabilitation in the Community for Patients with Stroke: A Review (2000)

Sixteen studies that evaluated the effectiveness of community rehabilitation for patients with stroke are reviewed, reference is made to 14 papers pertinent to the issue, and data from 36 papers relevant to stroke are mentioned. Admission to the hospital during the acute phase is the best option for the majority of patients with stroke; however, inpatient stay may be shortened and effective rehabilitation provided in community settings in all phases of stroke. Development of effective community rehabilitation may be the alternative to the addition of hospital beds in anticipation of an increased incidence of stroke and consequent rise in its expenditure.
Induction of colony stimulating factor in vivo by recombinant interleukin 1 alpha and recombinant tumor necrosis factor alpha 1. (1987)

In response to a potent inflammatory challenge, such as Gram-negative endotoxin, a number of cytokines are induced that, in turn, mediate many of the pathophysiologic alterations associated with endotoxicity. In this study, we have observed two endotoxin-associated monokines, recombinant interleukin-1 alpha (rIL 1 alpha) and recombinant tumor necrosis factor alpha (rTNF alpha), to induce colony stimulating factor (CSF) in vivo. The CSF activities produced in response to rIL 1 alpha or rTNF alpha gave rise to a mixture of granulocyte-macrophage colonies and were induced in a dose- and time-dependent fashion, peaking within 3 hr of cytokine injection (preceding peak CSF induction by endotoxin by several hours). Combined injection of suboptimal concentrations of rIL 1 alpha and rTNF alpha were additive, and simultaneous injection of optimal concentrations of each failed to increase CSF levels over that observed with either cytokine alone. Unlike endotoxin, neither cytokine induced interferon in vivo. These findings extend our understanding of the cytokine cascade that is operative in an inflammatory response and may account for many of the observed hematopoietic alterations that accompany inflammation.
Inhibition by salbutamol of the proliferation of human airway smooth muscle cells grown in culture (1994)

1 beta 2-Adrenoceptor agonists may exacerbate asthma by reducing the release of the anti-proliferative and anti-inflammatory molecule, heparin from mast cells in the airway. In this study, the direct effects of the clinically used bronchodilator, salbutamol, on the proliferation of airway smooth muscle cells grown in culture and stimulated with a range of mitogens have been examined. 2 In mitogen-stimulated cells, salbutamol (0.1-100 nM) inhibited [3H]-thymidine incorporation in a concentration-dependent manner. Salbutamol (100 nM) pretreatment reduced the mitogenic responses to thrombin (0.3 u ml-1), epidermal growth factor (EGF) (300 pM) and U46619 (100 nM) by 61.7 +/- 6.1%, 46.9 +/- 13.9% and 57.6 +/- 12.7%, respectively. However, salbutamol pretreatment did not appear to reduce the small mitogenic response to endothelin-1. 3 Increases in [3H]-leucine incorporation in thrombin (0.3 u ml-1)-stimulated cells were reduced by salbutamol (100 nM) by 27.7 +/- 2.8%. Similarly, thrombin (0.3 u ml-1)-stimulated increases in cell number were also inhibited by salbutamol (100 nM) pretreatment. Thus, the effect of salbutamol in decreasing thrombin-induced [3H]-leucine incorporation may, at least in part, be explained by inhibition of cell proliferation. 4 The inhibition of cell proliferation by salbutamol was prevented by pretreatment with either the non-selective beta-adrenoceptor antagonist, propranolol (0.3 microM) or the selective beta 2-adrenoceptor antagonist, ICI 118551 (50 nM). 5. These results indicate that salbutamol, through activation of a beta 2-adrenoceptor, has a direct inhibitory effect on proliferation elicited by the mitogens thrombin, EGF, and U46619. Thus, it seems likely that this direct inhibitory action of Beta2-adrenoceptor agonists would override any indirect action to accelerate airway smooth muscle proliferation. These observations lead us to suggest that Beta2-adrenoceptor agonists exacerbate asthma by mechanisms unrelated to airway smooth muscle proliferation.
Characterization of the Murine Immunological Signaling Network with Phosphospecific Flow Cytometry (2005)

The immune system is a multitiered network that at the first level uses changes to intracellular signaling proteins to commit cells to determined fates. At the second tier, cells interact with one another via specifically expressed surface receptors and their cognate signaling molecules. At the third level, the local environments of immune cells change the outcomes of intracellular signaling pathways and thereby the role of cells during immune challenge. The interplay among these three tiers allows the distinct cell types of the immune system to respond cohesively to eliminate foreign Ags. In this study, using phosphospecific flow cytometry, we analyze elements of these network tiers by generating profiles of single-cell phosphoprotein responses in B cells, T cells, and myeloid cells to a number of mechanistically and clinically relevant cytokines (IFN-gamma, GM-CSF, IL-2, and IL-10) as well as LPS at key regulatory interfaces (Jak-Stat and MAPK pathways). The stimuli typically induced phosphorylation of specific signaling pathways and exerted their effects on distinct subsets of immune cells. However, upon comparison of stimulation in vitro and in vivo, we noted that signaling pathway specificity and cell type specificity were influenced strongly by the external environment. When taken from the in vivo environment, certain cell subsets became hypo- or hyper-responsive, showed profound differences in sensitivity to cytokine levels, or displayed altered phosphorylation kinetics. Thus, simultaneous analysis of the three tiers of the immune system network illustrates the principles by which immune regulation is context dependent and how in vitro culture systems compare with the in vivo environment.
Improvement of Stability of Oil‐in‐Water Emulsions Containing Caseinate‐Coated Droplets by Addition of Sodium Alginate (2007)

The potential of sodium alginate for improving the stability of emulsions containing caseinate-coated droplets was investigated. One wt% corn oil-in-water emulsions containing anionic caseinate-coated droplets (0.15 wt% sodium caseinate) and anionic sodium alginate (0 to 1 wt%) were prepared at pH 7. The pH of these emulsions was then adjusted to 3.5, so that the anionic alginate molecules adsorbed to the cationic caseinate-coated droplets. Extensive droplet aggregation occurred when there was insufficient alginate to completely saturate the droplet surfaces due to bridging flocculation, and when the nonadsorbed alginate concentration was high enough to induce depletion flocculation. Emulsions with relatively small particle sizes could be formed over a range of alginate concentrations (0.1 to 0.4 wt%). The influence of pHs (3 to 7) and sodium chloride (0 to 500 mM) on the properties of primary (0 wt% alginate) and secondary (0.15 wt% alginate) emulsions was studied. Alginate adsorbed to the droplet surfaces at pHs 3, 4, and 5, but not at pHs 6 and 7, due to electrostatic attraction between anionic groups on the alginate and cationic groups on the adsorbed caseinate. Secondary emulsions had better stability than primary emulsions at pH values near caseinate's isoelectric point (pHs 4 and 5). In addition, secondary emulsions were stable up to higher ionic strengths (< 300 mM) than primary emulsions (<50 mM). The controlled electrostatic deposition method utilized in this study could be used to extend the range of application of dairy protein emulsifiers in the food industry.
Antigen-specific therapy of experimental allergic encephalomyelitis by soluble class II major histocompatibility complex-peptide complexes. (1991)

Experimental allergic encephalomyelitis is a T-cell-mediated, major histocompatibility complex (MHC) class II gene-linked autoimmune demyelinating disease of the central nervous system. To develop therapies that will specifically inactivate only the autoantigen-reactive T cells, mice were treated with soluble MHC class II molecules that had been complexed with encephalitogenic peptides. Intravenous injections of 300 micrograms of complexes consisting of encephalitogenic peptide 91-103 of myelin basic protein plus I-As protein on day 0, 4, and 7 were effective in preventing experimental allergic encephalomyelitis. Similarly, administration of 45 micrograms of I-As protein complexed to peptide 139-151 from proteolipoprotein on day 1, 4, and 7 prevented mortality and significantly reduced paralysis induced by immunization with the encephalitogenic proteolipoprotein peptide. Histological examination of sections of animal brains revealed that treatment with I-As protein plus myelin basic protein 91-103 peptide prevents the development of inflammatory lesions characteristic of experimental allergic encephalomyelitis. Thus, treatment with MHC-self-peptide complexes could serve as a highly specific therapeutic modality in treating autoimmune disease when the putative autoantigen and the MHC restricting elements are known.
The S1, S2 and SGA1 ancestral genes for the STA glucoamylase genes all map to chromosome IX in Saccharomyces cerevisiae (1995)

The polymorphic extracellular glucoamylase-encoding genes STA1 (chr. IV), STA2 (chr. II) and STA3 (chr. XIV), from Saccharomyces cerevisiae var. diastaticus probably evolved by genomic rearrangement of DNA regions (S1, S2 and SGA1) present in S. cerevisiae, and subsequent translocation to unlinked regions of chromosomal regions. S1, encoding a homologue to the threonine/serine-rich domain of STA glucoamylases (GAI-III), mapped to the right arm of chromosome IX. S2, encoding the hydrophobic leader peptide of GAI-III), was also mapped on the right arm of chromosome IX, next to S1, close to DAL81. The SGA1 sporulation-specific, intracellular glucoamylase-encoding gene is located on the left arm of chromosome IX, 32 kb proximal of HIS5.
The Cysteine-rich Domain of the Secreted Proprotein Convertases PC5A and PACE4 Functions as a Cell Surface Anchor and Interacts with Tissue Inhibitors of Metalloproteinases (2005)

The proprotein convertases PC5, PACE4 and furin contain a C-terminal cysteine-rich domain (CRD) of unknown function. We demonstrate that the CRD confers to PC5A and PACE4 properties to bind tissue inhibitors of metalloproteinases (TIMPs) and the cell surface. Confocal microscopy and biochemical analyses revealed that the CRD is essential for cell surface tethering of PC5A and PACE4 and that it colocalizes and coimmunoprecipitates with the full-length and C-terminal domain of TIMP-2. Surface-bound PC5A in TIMP-2 null fibroblasts was only observed upon coexpression with TIMP-2. In COS-1 cells, plasma membrane-associated PC5A can be displaced by heparin, suramin, or heparinases I and III and by competition with excess exogenous TIMP-2. Furthermore, PC5A and TIMP-2 are shown to be colocalized over the surface of enterocytes in the mouse duodenum and jejunum, as well as in liver sinusoids. In conclusion, the CRD of PC5A and PACE4 functions as a cell surface anchor favoring the processing of their cognate surface-anchored substrates, including endothelial lipase.
Murine monoclonal anti-DNA antibodies penetrate cells, bind to nuclei, and induce glomerular proliferation and proteinuria in vivo. (1992)

The production of relatively high quantities of autoantibodies (autoAb) that react with DNA and other intranuclear antigens is characteristic of individuals with systemic lupus erythematosus and other autoimmune diseases. However, the capacity of these Ab to penetrate cells and induce functional perturbations in vivo is not well appreciated. To address this issue, monoclonal (m) anti-DNA Ab (mAb), derived from MRL-lpr/lpr and (NZB x SWR)F1 mice, were administered to normal mice, and the animals were examined for morphologic and functional abnormalities. A subset of five mAb produced intranuclear immunoglobulin deposits in multiple organs. Intranuclear immunoglobulin deposits were also observed after cross-linking the tissue before direct immunofluorescence and after i.v. injection of F(ab')2 fragments of one anti-DNA Ab. This phenomenon was reproducible and was only associated with this subset of autoAb. Furthermore, intranuclear deposits of anti-DNA Ab within glomeruli were associated with morphologic and functional abnormalities including: hypercellularity, epithelial foot process fusion, new fiber bundle formation within the mesangium suggestive of new collagen synthesis, and proteinuria. These results indicate that a subset of autoAb may penetrate cells in vivo to influence normal cellular and nuclear function and to contribute to functional and pathologic abnormalities in individuals with systemic lupus.
Vascular Origin of a Soluble Truncated Form of the Hepatocyte Growth Factor Receptor (c-met) (2002)

Hepatocyte growth factor (scatter factor) is an angiogenic growth factor that binds to its cellular transmembrane receptor, c-met. Both HGF and c-met are expressed by vascular smooth muscle and endothelial cells, where HGF may exert autocrine and paracrine effects. We have found that human aortic smooth muscle cells (HASMCs) and human umbilical vein endothelial cells (HUVECs) release a soluble, truncated form of c-met. Receptor shedding was induced by treatment of the cells with phorbol 12-myristate 13-acetate (PMA) and by the ligand, HGF. Shedding was inhibited by cycloheximide, a metalloproteinase inhibitor, and protein kinase C inhibitors. The soluble form of c-met was able to bind HGF, although with reduced affinity (K d ≈10 nmol/L) compared with the membrane bound receptor. Conditioned medium containing soluble c-met inhibited the induction of Akt phosphorylation by HGF in HUVECs. The soluble truncated form of c-met was detectable in the plasma of 5 healthy volunteers. The shedding of c-met may represent a novel mechanism for regulating the mitogenic, motogenic, and morphogenic effects of hepatocyte growth factor.
A Polystyrene−Oligothiophene−Polystyrene Triblock Copolymer (1998)

A well-defined triblock copolymer is synthesized by using a strategy in which the α-coupling of 11 thiophene rings of the middle block and the monodispersity (DP = 30 and M̄w/M̄n = 1.1) of the two polystyrene outer blocks is ensured. Monofunctional polystyrene 1 is first modified with an α-terthiophene unit 2 to form 3, and two of these units are coupled in a double Stetter reaction of 4 with a difunctional α-terthiophene 5 to yield a tetraketone 6 as the precursor of the triblock copolymer, which was formed with excess Lawesson's reagent. The polymer 7 is fully characterized with IR and NMR spectroscopy and MALDI-TOF mass spectrometry. Size exclusion chromatography, transmission electron microscopy, and scanning force microscopy show that 7 is self-assembled into spherical, micellar structures with average diameters of 12 nm, which corresponds to about 60 block copolymer molecules per aggregate. The optical properties of 7 are in full agreement with an associated unsubstituted oligothiophene. Electrochemical doping is hampered by the polystyrene shell; however, chemical doping afforded small nanoscopic charged aggregates that are soluble in organic solvents.