gebhart/patrepeval huggingface dataset:
Transforming growth factor-beta activity in sheep lung lymph during the development of pulmonary hypertension. (1990)

Chronic pulmonary hypertension is associated with extensive structural remodeling of the pulmonary arterial bed. The structural changes in the arterial walls include increased production of extracellular matrix components and smooth muscle cell hypertrophy, changes that have been similarly induced by transforming growth factor-beta (TGF-beta) in culture. In the present study, experiments were performed to determine whether TGF-beta is present in sheep lung lymph, and whether TGF-beta levels were altered in an animal model of chronic pulmonary hypertension induced by continuous air embolization. Several standard biological assays for TGF-beta activity were used for these determinations including soft agar assays, inhibition of epithelial cell proliferation, and a TGF-beta-specific radioreceptor assay. In each case, control lung lymph contained high concentrations of TGF-beta (100 ng/ml) which required transient acidification for detection. Samples of lung lymph from hypertensive sheep showed a transient and early two- to threefold increase in concentrations of latent TGF-beta. This activity could be partially blocked by TGF-beta antibodies. These studies indicate that sheep lung lymph contains TGF-beta and that the level of TGF-beta increases early during the development of pulmonary hypertension. Thus, TGF-beta may contribute to the development of the structural changes in the pulmonary arteries that occur during the onset of chronic pulmonary hypertension.
Evidence for control of tumour necrosis factor-alpha (TNF-α) activity by TNF receptors in patients with proliferative diabetic retinopathy (1999)

TNF-alpha has been implicated in the pathogenesis of insulin- dependent diabetes mellitus (IDDM). At present there are no studies linking serum levels of soluble TNF receptors (sTNF-R) to the development of diabetic microvascular complications such as proliferative diabetic retinopathy (PDR), or to the production of TNF-alpha in these patients. We investigated serum levels of sTNF receptors (sTNF-RI and sTNF-RII) in IDDM patients with or without PDR, and related these to the in vitro production of TNF-alpha upon activation of whole blood and isolated mononuclear cells (MNC). We observed higher serum levels of sTNF-RI in IDDM patients with active (range 945-6630 pg/ml; P = 0.029) or quiescent PDR (range 1675-4970 pg/ml; P = 0.00092) than in individuals with IDDM without retinopathy (range 657-2617 pg/ml) or healthy controls (range 710-1819 pg/ml; P = 0.0092 and 0.0023, respectively). Increased serum levels of sTNF-RII were also seen in IDDM patients with active PDR (range 1749-5218 pg/ml; P = 0.034) or quiescent PDR (range 1494-5249 pg/ml; P = 0.0084) when compared with disease controls (range 1259-4210 pg/ml) or healthy subjects (range 1237-4283 pg/ml). Whole blood production of biologically active TNF-alpha was lower in PDR patients than in disease (P = 0.04) and healthy controls (P < 0.005), contrasting with a higher production of TNF-alpha by lipopolysaccharide (LPS)-activated MNC from PDR patients (P = 0.013). Inhibition of TNF-alpha by TNF-R in plasma supernatants of activated blood from PDR patients was demonstrated by increase of TNF-alpha activity in the presence of anti-TNF-RI and anti-TNF-RII antibodies. These observations suggest that abnormalities in TNF-alpha production and control may operate during the development of microvascular complications of diabetes mellitus.
Characterization of Multipotent Adult Progenitor Cells, a Subpopulation of Mesenchymal Stem Cells (2001)

Mesenchymal stem cells were isolated and a subpopulation of cells--multipotent adult progenitor cells--were identified that have the potential for multilineage differentiation. Their ability to engraft and differentiate in vivo is under investigation.
Scalable Coating and Properties of Transparent, Flexible, Silver Nanowire Electrodes (2010)

We report a comprehensive study of transparent and conductive silver nanowire (Ag NW) electrodes, including a scalable fabrication process, morphologies, and optical, mechanical adhesion, and flexibility properties, and various routes to improve the performance. We utilized a synthesis specifically designed for long and thin wires for improved performance in terms of sheet resistance and optical transmittance. Twenty Omega/sq and approximately 80% specular transmittance, and 8 ohms/sq and 80% diffusive transmittance in the visible range are achieved, which fall in the same range as the best indium tin oxide (ITO) samples on plastic substrates for flexible electronics and solar cells. The Ag NW electrodes show optical transparencies superior to ITO for near-infrared wavelengths (2-fold higher transmission). Owing to light scattering effects, the Ag NW network has the largest difference between diffusive transmittance and specular transmittance when compared with ITO and carbon nanotube electrodes, a property which could greatly enhance solar cell performance. A mechanical study shows that Ag NW electrodes on flexible substrates show excellent robustness when subjected to bending. We also study the electrical conductance of Ag nanowires and their junctions and report a facile electrochemical method for a Au coating to reduce the wire-to-wire junction resistance for better overall film conductance. Simple mechanical pressing was also found to increase the NW film conductance due to the reduction of junction resistance. The overall properties of transparent Ag NW electrodes meet the requirements of transparent electrodes for many applications and could be an immediate ITO replacement for flexible electronics and solar cells.
Evaluation of the Recombigen HIV-1 Latex Agglutination Test (1990)

The Recombigen HIV-1 Latex Agglutination (LA) Test was recently licensed by the U.S. Food and Drug Administration for use as a rapid screening assay for human immunodeficiency virus type 1 (HIV-1) antibodies. However, its performance in various settings and in different populations has not been firmly established. Consequently, we evaluated the test in the Cleveland Clinic Retrovirus Laboratory, a regional reference laboratory for HIV diagnostic testing and a testing laboratory for the Ohio Department of Health Anonymous HIV Testing and Counseling Program. Serum samples from 93 individuals presumed to be at high risk for HIV infection were evaluated. The sera were initially tested for HIV antibodies by enzyme-linked immunosorbent assay (ELISA). All repeatedly reactive sera were subjected to confirmatory Western blot (WB; immunoblot) testing. Of 97 serum specimens tested (5 were from one seroconverter), 44 were repeatedly reactive by ELISA and 53 were nonreactive. Of the reactive serum specimens, 31 were confirmed positive and 12 were indeterminate by WB. All of the sera were coded and then retested by the LA test. Of 53 serum specimens nonreactive by ELISA, 51 were also nonreactive in the LA test. Of the 44 serum specimens reactive by ELISA, 16 were nonreactive by LA; however, 3 of the latter were WB positive. No serum specimen with an ELISA ratio (specimen optical density/cutoff optical density) of less than 2.1 scored reactive in the LA test. The LA test was positive for only two of five consecutive serum specimens from a seroconverter despite the fact that all but the earliest of these were ELISA reactive and WB positive. Although the LA test appears to be an adequate first-line screening test when appropriately used according to the directions of the manufacturer, our data suggest that occasional sera with low levels of reactivity by ELISA may not be readily detected as reactive by the LA test.
Regulation and Specificity of MHC2TA Promoter Usage in Human Primary T Lymphocytes and Cell Line (2002)

Abstract Although activated human T cells express MHC class II antigens, the regulation of these antigens in T cells is poorly understood. This study focuses on the control of the MHC2TA gene in these cells. MHC2TA encodes the transcriptional master regulator of MHC class II, the class II trans-activator (CIITA). It has at least three distinct promoters (PI, PIII, and PIV), each active in an overlapping subset of cell types and directing a slightly different product. This report used highly purified blood T cells prepared by negative immunoselection to analyze CIITA. Real-time PCR analysis indicates that resting T cells do not express detectable CIITA transcript, while activated T cells express the PIII CIITA form. Transient transfection of activated blood T cells using wild-type and mutant PIII promoter-reporter constructs shows that two promoter elements, activation response element-1 (ARE-1) and ARE-2, are important for PIII function. cAMP response element binding protein, a known activator of gene expression in activated T cells, activates PIII in primary T cells. However, an intact ARE-2 site is not required for this activation, indicating that cAMP response element binding protein does not activate via this site. EMSAs indicate that an activating transcription factor/cAMP response element binding protein/cAMP response element modulator family member, but not phosphorylated cAMP response element binding protein-1, binds to ARE-2. ARE-2 also forms a complex with an unidentified protein. The ARE-2 binding protein is constitutively expressed in a DR+ T cell line, reflecting differences between the DR+ cell line and primary blood lymphocytes. These results show that MHC2TA PIII is induced in activated T lymphocytes, and that the induced binding of ARE-2 is a crucial step in this process.
The Osteoblast and osteocyte (1990)

Microangiopathy and disseminated platelet aggregation have been reported in thrombotic thrombocytopenic purpura (TTP) and pregnancy-induced hypertension (PIH). Since unusually large von Willebrand factor (vWF) multimers have been implicated in the evolvement of TTP, we analyzed factor VIII/vWF parameters in patients with PIH. Mean vWF: Ag level was significantly higher in 27 patients with PIH as compared to 20 matched healthy pregnant women (358 +/- 160 u/dl vs. 274 +/- 125 u/dl. p less than 0.05). Moreover, plasma vWF: Ag levels and the ratio of vWF: Ag to factor VIII were found to be linearly correlated to the severity of PIH. In contrast, no significant differences in mean levels of factor VIII and ristocetin cofactor were observed between these groups. Crossed immunoelectrophoresis of vWF revealed a higher incidence of a pre-peak and an increased migration index in the PIH group as compared to the control group (60% vs. 44% and 1.27 +/- 0.26 vs. 1.19 +/- 0.18, p less than 0.01 respectively). Analysis of plasma vWF multimer patterns by 1.4% agarose electrophoresis in 0.1% SDS revealed excessive amounts of large, medium and small size multimers in the PIH patients. Conceivably, the quantitative changes in vWF multimers reflect endothelial injury and may play a role in the microangiopathy observed in PIH.
Nanotransfer printing of organic and carbon nanotube thin-film transistors on plastic substrates (2005)

A printing process for high-resolution transfer of all components for organic electronic devices on plastic substrates has been developed and demonstrated for pentacene (Pn), poly (3-hexylthiophene) and carbon nanotube (CNT) thin-film transistors (TFTs). The nanotransfer printing process allows fabrication of an entire device without exposing any component to incompatible processes and with reduced need for special chemical preparation of transfer or device substrates. Devices on plastic substrates include a Pn TFT with a saturation, field-effect mobility of 0.09cm2(Vs)−1 and on/off ratio approximately 104 and a CNT TFT which exhibits ambipolar behavior and no hysteresis.
TCR Activation of Human T Cells Induces the Production of Exosomes Bearing the TCR/CD3/ζ Complex (2002)

We show in this study that human T cells purified from peripheral blood, T cell clones, and Jurkat T cells release microvesicles in the culture medium. These microvesicles have a diameter of 50-100 nm, are delimited by a lipidic bilayer membrane, and bear TCR beta, CD3epsilon, and zeta. This microvesicle production is regulated because it is highly increased upon TCR activation, whereas another mitogenic signal, such as PMA and ionomycin, does not induce any release. T cell-derived microvesicles also contain the tetraspan protein CD63, suggesting that they originate from endocytic compartments. They contain adhesion molecules such as CD2 and LFA-1, MHC class I and class II, and the chemokine receptor CXCR4. These transmembrane proteins are selectively sorted in microvesicles because CD28 and CD45, which are highly expressed at the plasma membrane, are not found. The presence of phosphorylated zeta in these microvesicles suggests that the CD3/TCR found in the microvesicles come from the pool of complexes that have been activated. Proteins of the transduction machinery, tyrosine kinases of the Src family, and c-Cbl are also observed in the T cell-derived microvesicles. Our data demonstrate that T lymphocytes produce, upon TCR triggering, vesicles whose morphology and phenotype are reminiscent of vesicles of endocytic origin produced by many cell types and called exosomes. Although the exact content of T cell-derived exosomes remains to be determined, we suggest that the presence of TCR/CD3 at their surface makes them powerful vehicles to specifically deliver signals to cells bearing the right combination of peptide/MHC complexes.
Extracellular truncated tau causes early presynaptic dysfunction associated with Alzheimer’s disease and other tauopathies (2017)

The largest part of tau secreted from AD nerve terminals and released in cerebral spinal fluid (CSF) is C-terminally truncated, soluble and unaggregated supporting potential extracellular role(s) of NH<sub>2</sub> -derived fragments of protein on synaptic dysfunction underlying neurodegenerative tauopathies, including Alzheimer's disease (AD). Here we show that sub-toxic doses of extracellular-applied human NH<sub>2</sub> tau 26-44 (aka NH <sub>2</sub> htau) -which is the minimal active moiety of neurotoxic 20-22kDa peptide accumulating <i>in vivo</i> at AD synapses and secreted into parenchyma- acutely provokes presynaptic deficit in K<sup>+</sup> -evoked glutamate release on hippocampal synaptosomes along with alteration in local Ca<sup>2+</sup> dynamics. Neuritic dystrophy, microtubules breakdown, deregulation in presynaptic proteins and loss of mitochondria located at nerve endings are detected in hippocampal cultures only after prolonged exposure to NH <sub>2</sub> htau. The specificity of these biological effects is supported by the lack of any significant change, either on neuronal activity or on cellular integrity, shown by administration of its reverse sequence counterpart which behaves as an inactive control, likely due to a poor conformational flexibility which makes it unable to dynamically perturb biomembrane-like environments. Our results demonstrate that one of the AD-relevant, soluble and secreted N-terminally truncated tau forms can early contribute to pathology outside of neurons causing alterations in synaptic activity at presynaptic level, independently of overt neurodegeneration.
Influence of the apoA-II gene locus on HDL levels and fatty streak development in mice. (1993)

Previous studies have shown that distal mouse chromosome 1 contains the apolipoprotein AII (apoAII) gene, encoding the second most abundant apolipoprotein in high density lipoproteins (HDLs), as well as a gene termed Ath-1 that controls aortic fatty streak development and HDL cholesterol levels in response to a high-fat, high-cholesterol diet. We report genetic studies confirming that the genes are distinct. Using molecular markers for mouse chromosome 1, we have further mapped the two genes, and our results indicate that they are separated by a minimum of 2 cM. We also report evidence that in mice on a low-fat chow diet, the apoAII gene locus influences HDL cholesterol levels. Thus, statistical analysis of two sets of recombinant inbred strains revealed concordant segregation patterns of HDL cholesterol levels and the apoAII gene locus. The effect of apoAII expression on HDL cholesterol levels was further tested by using a congenic strain that exhibits increased apoAII synthesis in comparison to the background strain. The results support the concept that increased synthesis of apoAII results in increased HDL cholesterol levels. Unexpectedly, increased expression of apoAII appeared to promote rather than retard aortic fatty streak development.
Nucleotide sequence of the envelope gene of Friend murine leukemia virus (1983)

The envelope gene of the helper-independent, highly leukemogenic virus Friend murine leukemia virus was sequenced by using a molecular clone of a Friend murine leukemia provirus. The deduced amino acid sequences of the envelope proteins gp70 and p15env were homologous to the sequences of Moloney murine leukemia virus (86%) and Akv (76%). However, a stretch of about 40 amino acid residues near the middle of gp70 was dissimilar in Friend and Moloney murine leukemia viruses and Akv. In this type-specific region the gp70s of all three viruses contained more than 30% proline residues, giving this sequence a very rigid conformation. We suggest that this rigid and highly variable region of gp70 participates in infection by recognition of cell surface receptors and, in addition, might contribute to the different oncogenic spectra of murine leukemia viruses.
Detection in alpha-stable noise environments based on prediction (1997)

In this paper we consider detection of baseband signals in partial response signalling (PRS) systems in the presence of additive, coloured noise. The additive noise in the system is a mixture of Gaussian noise and impulsive noise modelled as an alpha-stable process. The dependence in observation samples results from the excess bandwidth in the matched filters of the receivers. The detectors proposed are based on a noise estimation–cancellation technique. In particular, by exploiting past decisions as well as past received samples, we estimate the noise and subsequently cancel it. We adopt two approaches for designing predictors: in the first we use a minimum mean square error (MMSE) criterion and we employ Volterra filters as predictors; in the second we use the minimum dispersion (MD) criterion and we limit our attention to linear predictors. The effects of the predictor order, the number of exploited samples and the filtering allocation on the system performance are examined through Monte Carlo simulations. It is demonstrated that the proposed detectors, while having simple structures, offer substantial performance improvements over conventional detectors. © 1997 John Wiley & Sons, Ltd.
Identification of ACAT1- and ACAT2-specific inhibitors using a novel, cell-based fluorescence assay (2004)

Acyl CoA:cholesterol acyltransferase 1 (ACAT1) and ACAT2 are enzymes responsible for the formation of cholesteryl esters in tissues. While both ACAT1 and ACAT2 are present in the liver and intestine, the cells containing either enzyme within these tissues are distinct, suggesting that ACAT1 and ACAT2 have separate functions. In this study, NBD-cholesterol was used to screen for specific inhibitors of ACAT1 and ACAT2. Incubation of AC29 cells, which do not contain ACAT activity, with NBD-cholesterol showed weak fluorescence when the compound was localized in the membrane. When AC29 cells stably transfected with either ACAT1 or ACAT2 were incubated with NBD-cholesterol, the fluorescent signal localized to the nonpolar core of cytoplasmic lipid droplets was strongly fluorescent and was correlated with two independent measures of ACAT activity. Several compounds were found to have greater inhibitory activity toward ACAT1 than ACAT2, and one compound was identified that specifically inhibits ACAT2. The demonstration of selective inhibition of ACAT1 and ACAT2 provides evidence for uniqueness in structure and function of these two enzymes. To the extent that ACAT2 is confined to hepatocytes and enterocytes, the only two cell types that secrete lipoproteins, selective inhibition of ACAT2 may prove to be most beneficial in the reduction of plasma lipoprotein cholesterol concentrations.
Flk-1 + Adipose-Derived Mesenchymal Stem Cells Differentiate into Skeletal Muscle Satellite Cells and Ameliorate Muscular Dystrophy in MDX Mice (2007)

Duchenne muscular dystrophy (DMD) is a severe hereditary disease characterized by the absence of dystrophin on the sarcolemma of muscle fiber. This absence results in widespread muscle damage and satellite cell activation. After depletion of the satellite cell pool, skeletal muscle is then invariably replaced by connective tissue, leading to progressive muscle weakness. Herein, we isolated Flk-1(+) mesenchymal stem cells (MSCs) from adult adipose tissue and induced them to differentiate into skeletal muscle cells in culture. Within mdx mice, an animal model of DMD, adipose tissue-derived Flk-1(+) MSCs (AD-MSCs) homed to and differentiated into cells that repaired injured muscle tissue. This repair correlated with reconstitution of dystrophin expression on the damaged fibers. Flk-1(+) AD-MSCs also differentiated into muscle satellite cells. This differentiation may have accounted for long-term reconstitution. These cells also differentiated into endothelial cells, thereby possibly improving fiber regeneration as a result of the induced angiogenesis. Therefore, Flk-1(+) AD-MSC transplants may repair muscular dystrophy.
[24-hour esophago-gastric pH-metry: clinical indications]. (1991)

Esophago-gastric 24 h pH-metry recording is a diagnostic technique that allows ambulatory monitoring of acid esophageal reflux during 24 h while the patient pursues his everyday activities. Prolonged pH recording allows evaluation of the correlation of esophageal or extraesophageal symptoms (i.e. arrhythmias, chest pain, asthma) with intraesophageal pH. It permits us to evaluate the effectiveness of antireflux therapy, to modify therapy, or change daily dosages.
Fluorescent sensor of imidazole and histidine (1997)

The dizinc(II) complex of an octamine containing the anthracene subunit binds both the imidazolate anion and the imidazolate moiety of L-histidine, and signals the binding through the fluorescence quenching of the fluorophore.
H-2 class I knockout, HLA-A2.1-transgenic mice: a versatile animal model for preclinical evaluation of antitumor immunotherapeutic strategies (1999)

H-2 class I-negative, HLA-A2.1-transgenic HHD mice were used for a comparative evaluation of the immunogenicity of HLA-A2.1-restricted human tumor-associated cytotoxic T lymphocyte (CTL) epitopes. A hierarchy was established among these peptides injected into mice in incomplete Freund's adjuvant which correlates globally with their capacity to bind and stabilize HLA-A2.1 molecules. Co-injection of a helper peptide enhanced most CTL responses. In contrast, classical HLA class I-transgenic mice which still express their own class I molecules did not, in most cases, develop HLA-A2.1-restricted CTL responses under the same experimental conditions. Different monoepitope immunization strategies of acceptable clinical usage were compared in HHD mice. Recombinant Ty-virus-like particles, or DNA encoding epitopes fused to the hepatitis B virus middle envelope protein gave the best results. Using this latter approach and a melanoma-based polyepitope construct, CTL responses against five distinct epitopes could be elicited simultaneously in a single animal. Thus, HHD mice provide a versatile animal model for preclinical evaluation of peptide-based cancer immunotherapy.