gebhart/patrepeval huggingface dataset:
Human umbilical cord wharton's jelly stem cell (hWJSC) extracts inhibit cancer cell growth in vitro (2012)

Umbilical cord mesenchymal stem cells (MSCs) have been shown to inhibit breast cancer cell growth but it is not known whether this effect is specific to only breast cancer cells. We compared the effects of human Wharton's jelly stem cell (hWJSC) extracts [conditioned medium (hWJSC-CM) and cell lysate (hWJSC-CL)] on breast adenocarcinoma (MDA-MB-231), ovarian carcinoma (TOV-112D), and osteosarcoma (MG-63) cells. The cells were treated with either hWJSC-CM (50%) or hWJSC-CL (15 µg/ml) for 48-72 h and changes in cell morphology, proliferation, cycle, gene expression, migration, and cell death studied. All three cancer cell lines showed cell shrinkage, blebbing, and vacuolations with hWJSC-CL and hWJSC-CM compared to controls. MTT and BrdU assays showed inhibition of cell growth by 2-6% and 30-60%, while Transwell migration assay showed inhibition by 20-26% and 31-46% for hWJSC-CM and hWJSC-CL, respectively, for all three cancer cell lines. Cell cycle assays showed increases in sub-G1 and G2/M phases for all three cancer cell lines suggestive of apoptosis and metaphase arrest. AnnexinV-FITC and TUNEL positive cells seen in TOV-112D and MDA-MB-231 suggested that inhibition was via apoptosis while the presence of anti-BECLIN1 and anti-LC3B antibodies seen with MG-63 indicated autophagy. Upregulation of pro-apoptotic BAX and downregulation of anti-apoptotic BCL2 and SURVIVIN genes were observed in all three cancer cell lines and additionally the autophagy genes (ATG5, ATG7, and BECLIN1) were upregulated in MG-63 cells. hWJSCs possess tumor inhibitory properties that are not specific to breast cancer cells alone and these effects are mediated via agents in its extracts.
RAS transformation causes sustained activation of epidermal growth factor receptor and elevation of mitogen-activated protein kinase in human mammary epithelial cells (2000)

Activation of the ras oncogene is an important step in carcinogenesis. Human MCF-10A mammary epithelial cells were transformed with a point-mutated form of the Ha-ras oncogene. Epidermal growth factor receptor (EGFR) phosphorylation levels were chronically elevated after EGF induction and the EGFR ligand-driven internalization rate was slower in Ha-ras transformed MCF-10A cells. Additionally, basal levels of p42/44 mitogen-activated protein kinase (MAPK) expression and enzyme activity were significantly higher in Ha-ras transformed cells, localized predominantly in the nucleus. The anti-EGFR monoclonal antibody (MAb) 225 and the EGFR tyrosine kinase inhibitor PD153035 blocked anchorage-independent growth of Ha-ras transformed cells in soft agar and were more effective when used in combination. The MEK inhibitor PD98059 and anti-erbB-2 MAb L26 also suppressed colony formation of Ha-ras transformed cells in soft agar. Therefore, Ha-ras transformation leads to an augmentation in signaling through the EGFR as a result of an increase in ligand-dependent phosphorylation, a decrease in its internalization and an up-regulation in basal p44/42 MAPK levels. These effects may contribute to uncontrolled growth of Ha-ras-transformed human mammary epithelial cells.
Ellipsometric determination of optical constants for silicon and thermally grown silicon dioxide via a multi-sample, multi-wavelength, multi-angle investigation (1998)

Optical constant spectra for silicon and thermally grown silicon dioxide have been simultaneously determined using variable angle of incidence spectroscopic ellipsometry from 0.75 to 6.5 eV. Spectroscopic ellipsometric data sets acquired at multiple angles of incidence from seven samples with oxide thicknesses from 2 to 350 nm were analyzed using a self-contained multi-sample technique to obtain Kramers–Kronig consistent optical constant spectra. The investigation used a systematic approach utilizing optical models of increasing complexity in order to investigate the need for fitting the thermal SiO2 optical constants and including an interface layer between the silicon and SiO2 in modeling the data. A detailed study was made of parameter correlation effects involving the optical constants used for the interface layer. The resulting thermal silicon dioxide optical constants were shown to be independent of the precise substrate model used, and were found to be approximately 0.4% higher in index than published values for bulk glasseous SiO2. The resulting silicon optical constants are comparable to previous ellipsometric measurements in the regions of overlap, and are in agreement with long wavelength prism measurements and transmission measurements near the band gap.
A pilot study investigating a novel subcutaneously implanted pre-cellularised scaffold for tissue engineering of intestinal mucosa (2006)

Tissue engineering of the small intestine offers an alternative to long-term intravenous nutrition and transplantation in patients with intestinal failure. Initial work, although encouraging, is limited by the volume of neonatal tissue required to produce a small neomucosal cyst. Our novel approach is to implant tubular poly-lactide-co-glycolide (PGLA) foam scaffolds subcutaneously. The aim of this study was to investigate whether these scaffolds would support growth of intestinal neomucosa. PGLA scaffolds were implanted subcutaneously into 8 Lewis rats; after 5 weeks, 'organoid units' were injected into the lumens. Tissue was assessed histologically after harvesting and quantitative immunohistochemistry was performed using antibodies against vascular endothelial growth factor (VEGF), vascular endothelial growth factor receptor 2 (VEGF-R2), fibroblast growth factor basic (bFGF) and fibroblast growth factor receptor 2 (FGF-R2). At 4 weeks post organoid unit implantation, clearly recognisable mucosa and submucosa was present on the luminal surface of the scaffold. Densities of VEGF and VEGF-R2 positive cells increased with time post organoid unit implantation. This pilot study demonstrates that it is possible to tissue engineer small intestinal neomucosa using subcutaneously implanted PLGA scaffolds. The yield of the process compares favourably to the published literature. Further work is required to optimise the technique.
Dendritic cells with TGF-β1 differentiate naïve CD4+CD25−T cells into islet-protective Foxp3+regulatory T cells (2007)

CD4(+)CD25(+)Foxp3(+) regulatory T cells (T regs) are important for preventing autoimmune diabetes and are either thymic-derived (natural) or differentiated in the periphery outside the thymus (induced). Here we show that beta-cell peptide-pulsed dendritic cells (DCs) from nonobese diabetic (NOD) mice can effectively induce CD4(+)CD25(+)Foxp3(+) T cells from naïve islet-specific CD4(+)CD25(-) T cells in the presence of TGF-beta1. These induced, antigen-specific T regs maintain high levels of clonotype-specific T cell receptor expression and exert islet-specific suppression in vitro. When cotransferred with diabetogenic cells into NOD scid recipients, T regs induced with DCs and TGF-beta1 prevent the development of diabetes. Furthermore, in overtly NOD mice, these cells are able to significantly protect syngeneic islet grafts from established destructive autoimmunity. These results indicate a role for DCs in the induction of antigen-specific CD4(+)CD25(+)Foxp3(+) T cells that can inhibit fully developed autoimmunity in a nonlymphopoenic host, providing an important potential strategy for immunotherapy in patients with autoimmune diabetes.
Audio-visual tracking for natural interactivity (1999)

The goal in user interfaces is natural interactivity unencumbered by sensor and display technology. In this paper, we propose that a multi-modal approach using inverse modeling techniques from computer vision, speech recognition, and acoustics can result in such interfaces. In particular, we demonstrate a system for audio-visual tracking, showing that such a system is more robust, more accurate, more compact, and yields more information than using a single modality for tracking. We also demonstrate how such a system can be used to find the talker among a group of individuals, and render 3D scenes to the user.
A novel impulse radio network for tactical military wireless communications (2002)

Two of the major concerns in tactical military wireless communication networks are covertness and throughput. Impulse radio is an ultra-wideband code division multiple access (UWB-CDMA) technique being considered as the physical layer for future networks. Impulse radio exhibits low power spectral density and relatively high immunity to fading but suffers from relatively long acquisition times. In traditional packet radio networks (PRNs), the physical layer link is terminated while scheduling half-duplex transmissions or in the absence of data packets. To re-establish physical layer links in an impulse radio system, signaling packets containing exceptionally long acquisition headers transmitted at higher powers are required. Hence, to improve covertness in an impulse radio based network, we propose a MAC layer scheme we call sustained link networks (SLN) where the physical layer links are maintained continuously. We develop a full-duplexing scheme which takes advantage of the low duty cycle nature of impulse radio to maintain physical layer links capable of supporting bi-directional data transfer. During the periods between data bursts, the physical layer links are maintained by transmitting supplementary data at low bit rates and low power levels. We quantify the performance of an impulse radio receiver implementing the full-duplex scheme developed. We also present performance comparisons of an SLN based on impulse radio with traditional PRN variations implemented using impulse radio.
Falling into TRAPS – receptor misfolding in the TNF receptor 1-associated periodic fever syndrome (2007)

TNF receptor-associated periodic syndrome (TRAPS) is a dominantly inherited disease caused by missense mutations in the TNF receptor 1 (TNFR1) gene. Patients suffer from periodic bouts of severe abdominal pain, localised inflammation, migratory rashes, and fever. More than 40 individual mutations have been identified, all of which occur in the extracellular domain of TNFR1. In the present review we discuss new findings describing aberrant trafficking and function of TNFR1 harbouring TRAPS mutations, challenging the hypothesis that TRAPS pathology is driven by defective receptor shedding, and we suggest that TNFR1 might acquire novel functions in the endoplasmic reticulum, distinct from its role as a cell surface receptor. We also describe the clinical manifestations of TRAPS, current treatment regimens, and the widening array of patient mutations.
Expression of a bacterial mtlD gene in transgenic tobacco leads to production and accumulation of mannitol. (1992)

A bacterial gene encoding mannitol-1-phosphate dehydrogenase, mtlD, was engineered for expression in higher plants. Gene constructions were stably incorporated into tobacco plants. The mtlD gene was expressed and translated into a functional enzyme in tobacco, resulting in the synthesis and accumulation of mannitol, which was identified by NMR and mass spectroscopy. Mannitol concentrations exceeded 6 mumol/g (fresh weight) in the leaves and in the roots of some transformants, whereas this sugar alcohol was not detected in these organs of wild-type tobacco plants or of untransformed tobacco plants that underwent the same regeneration scheme. These experiments demonstrate that branch-points in plant carbohydrate metabolism can be generated by which novel gene products can utilize endogenous substrates to divert metabolic energy into novel compounds. Additionally, the system described here allows for physiological studies in which the responses of wild-type and transgenic tobacco to various environmental stimuli can be compared directly. Such studies will facilitate our understanding of the roles of sugar alcohols (e.g., in stress tolerance) in higher plants.
Obesity Is an Independent Risk Factor for GERD Symptoms and Erosive Esophagitis (2005)

Overweight and obesity are strong independent risk factor of GERD symptoms and esophageal erosions. The amount or composition of dietary intake does not appear to be a likely explanation for these findings.
Rational and Modular Design of Potent Ligands Targeting the RNA That Causes Myotonic Dystrophy 2 (2009)

Most ligands targeting RNA are identified through screening a therapeutic target for binding members of a ligand library. A potential alternative way to construct RNA binders is through rational design using information about the RNA motifs ligands prefer to bind. Herein, we describe such an approach to design modularly assembled ligands targeting the RNA that causes myotonic dystrophy type 2 (DM2), a currently untreatable disease. A previous study identified that 6'-N-5-hexynoate kanamycin A (1) prefers to bind 2x2 nucleotide, pyrimidine-rich RNA internal loops. Multiple copies of such loops are found in the RNA hairpin that causes DM2. The 1 ligand was then modularly displayed on a peptoid scaffold with varied number and spacing to target several internal loops simultaneously. Modularly assembled ligands were tested for binding to a series of RNAs and for inhibiting the formation of the toxic DM2 RNA-muscleblind protein (MBNL-1) interaction. The most potent ligand displays three 1 modules, each separated by four spacing submonomers, and inhibits the formation of the RNA-protein complex with an IC(50) of 25 nM. This ligand has higher affinity and is more specific for binding the DM2 RNA than MBNL-1. It binds the DM2 RNA at least 30 times more tightly than related RNAs and 15-fold more tightly than MBNL-1. A related control peptoid displaying 6'-N-5-hexynoate neamine (2) is >100-fold less potent at inhibiting the RNA-protein interaction and binds to DM2 RNA >125-fold more weakly. Uptake studies into a mouse myoblast cell line also show that the most potent ligand is cell permeable.
Akkermansia muciniphila link gut barrier function with inflammation and metabolic disorders associated with obesity. (2012)

Obesity and related metabolic disorders such as insulin resistance and type 2 diabetes are associated with a low-grade inflammatory state. These disorders may be related to the gut microbiota possibly through the development of metabolic endotoxemia (i.e., increased plasma lipopolysaccharide levels (LPS)). This higher plasma LPS is associated with gut permeability. We have also previously shown that gut microbiota modulations (i.e., prebiotics) improve gut barrier functions, inflammation and metabolic disorders. However, no specific bacteria have been causally linked with these beneficial effects. More recently, by using metagenomic approaches, we found that prebiotic treatment dramatically increases Akkermansia muciniphila in genetic obese mice. The aim of this study was 1Â° to investigate the effect of high-fat diet-induced obesity and type 2 diabetes on this bacteria, 2Â° to evaluate the impact of prebiotic on the abundance of Akkermansia muciniphila in this model, 3Â° to unravel its implication on gut barrier functions, inflammation and metabolism. In this study we show for the first time that Akkermansia muciniphila is dramatically decreased upon high-fat diet (83-fold decrease), whereas its abundance was dramatically increased after prebiotic treatment (294-fold increase). Moreover this bacteria was inversely correlated with several markers of inflammation in the gut (TLR4 and IL-1 beta mRNA), the liver (Myd88 and IL-1 beta mRNA) and the adipose tissue (CD11c mRNA). We also found that Akkermansia muciniphila correlates positively with muscle mass and negatively with adiposity and body weight gain. Importantly, we are currently investigating the impact of Akkermansia muciniphila administration in several obese and type 2 diabetes models. In conclusion, we propose Akkermansia muciniphila as a novel bacteria causally linked with gut barrier, whole body inflammation and metabolism in obesity.
Safety of Withdrawing Inhaled Nitric Oxide Therapy in Persistent Pulmonary Hypertension of the Newborn (1999)

For infants classified as treatment successes, a dose response between the I-NO dose and decrease in PaO(2) after discontinuing I-NO was found. A reduction in I-NO to 1 ppm before discontinuation of the drug seems to minimize the decrease in PaO(2) seen. For infants failing treatment, discontinuation of I-NO could pose a life-threatening reduction in oxygenation should extracorporeal membrane oxygenation not be readily available or I-NO cannot be continued on transport.
Connected components of sets of finite perimeter and applications to image processing (2001)

This paper contains a systematic analysis of a natural measure theoretic notion of connectedness for sets of finite perimeter in \mathbb R^N , introduced by H. Federer in the more general framework of the theory of currents. We provide a new and simpler proof of the existence and uniqueness of the decomposition into the so-called M -connected components. Moreover, we study carefully the structure of the essential boundary of these components and give in particular a reconstruction formula of a set of finite perimeter from the family of the boundaries of its components. In the two dimensional case we show that this notion of connectedness is comparable with the topological one, modulo the choice of a suitable representative in the equivalence class. Our strong motivation for this study is a mathematical justification of all those operations in image processing that involve connectedness and boundaries. As an application, we use this weak notion of connectedness to provide a rigorous mathematical basis to a large class of denoising filters acting on connected components of level sets. We introduce a natural domain for these filters, the space \mathrm{WBV}(\Omega) of functions of weakly bounded variation in \Omega , and show that these filters are also well behaved in the classical Sobolev and BV spaces.
[Synthesis and preliminary pharmacological screening of 2,4-disubstituted N,N-dialkyl-1,8-naphthyridine-3-carboxamides]. (1989)

By treating at 100 degrees C 2-aminonicotinic acid with ethyl N,N-dialkylmalonamate (I) and phosphorus oxychloride N,N-dialkyl-4-chloro-1,2-dihydro-2-oxo-1,8-naphthyridine- 3-carboxamides (II) were obtained. The reaction of compounds (II) with an excess of refluxing phosphorus oxychloride afforded N,N-dialkyl-2,4-dichloro-1,8-naphthyridine-3-carboxamides (III), which in turn were treated at room temperature with excess primary amines to give a mixture of isomeric N,N-dialkyl-2-(alkylamino or cycloalkylamino)-4-chloro-1,8-naphthyridine-3-carboxamides (IV) and N,N-dialkyl-4-(alkylamino or cycloalkylamino)-2-chloro-1,8-naphthyridine-3-carboxamides (V). When this last reaction was performed at 160 degrees C, only N,N-dialkyl-2,4-bis(alkylamino or cycloalkylamino)-1,8-naphthyridine-3-carboxamides (VI) were obtained; under the same conditions (IV c) or (V c) reacted with methylamine to give isomeric 2,4-bis(alkylamino)derivatives (VII) or (VIII), respectively. Compounds (II b), (III b), (IV a,c,d), (V a,c,d) were submitted to a wide preliminary pharmacological screening. Some of them, depending on the structure, showed antihypertensive [(IV c)], anti-inflammatory [(IV c) greater than (III b)], or, in the behavioral test, anti-aggressive [(IV d) greater than (III b)] activity. Furthermore compound (III b) caused moderate inhibition of the 5-HT induced contraction of the guinea-pig ileum.
CCD polarization imaging sensor with aluminum nanowire optical filters (2010)

We report an imaging sensor capable of recording the optical properties of partially polarized light by monolithically integrating aluminum nanowire optical filters with a CCD imaging array. The imaging sensor, composed of 1000 by 1000 imaging elements with 7.4 μm pixel pitch, is covered with an array of pixel-pitch matched nanowire optical filters with four different orientations offset by 45°. The polarization imaging sensor has a signal-to-noise ratio of 45 dB and captures intensity, angle and degree of linear polarization in the visible spectrum at 40 frames per second with 300 mW of power consumption.
The Expanding World of Trinucleotide Repeats (1996)

A paper in this week's issue of Science (Campuzano et al. , p. 1423 ) reports that Friedreich's ataxia has now joined the list of diseases caused by expanding trinucleotide repeats. In his Perspective, S. Warren discusses how some unusual features of the repeats in this disease challenge some generalizations that have been made about the mechanisms by which these unusual mutations cause disease.
Epstein-Barr Virus Immediate-Early Proteins BZLF1 and BRLF1 Activate the ATF2 Transcription Factor by Increasing the Levels of Phosphorylated p38 and c-Jun N-Terminal Kinases (2000)

Expression of either Epstein-Barr virus (EBV) immediate-early protein BZLF1 (Z) or BRLF1 (R) is sufficient to convert EBV infection from the latent to lytic form. Disruption of viral latency requires transcriptional activation of the Z and R promoters. The Z and R proteins are transcriptional activators, and each immediate-early protein activates expression of the other immediate-early protein. Z activates the R promoter through a direct binding mechanism. However, R does not bind directly to the Z promoter. In this study, we demonstrate that the ZII element (a cyclic AMP response element site) in the Z promoter is required for efficient activation by R. The ZII element has been shown to be important for induction of lytic EBV infection by tetradecanoyl phorbol acetate and surface immunoglobulin cross-linking and is activated by Z through an indirect mechanism. We demonstrate that both R and Z activate the cellular stress mitogen-activated protein (MAP) kinases, p38 and JNK, resulting in phosphorylation (and activation) of the cellular transcription factor ATF2. Furthermore, we show that the ability of R to induce lytic EBV infection in latently infected cells is significantly reduced by inhibition of either the p38 kinase or JNK pathways. In contrast, inhibition of stress MAP kinase pathways does not impair the ability of Z expression vectors to disrupt viral latency, presumably because expression of Z under the control of a strong heterologous promoter bypasses the need to activate Z transcription. Thus, both R and Z can activate the Z promoter indirectly by inducing ATF2 phosphorylation, and this activity appears to be important for R-induced disruption of viral latency.
Analysis of Fine-Line Screen and Stencil-Printed Metal Contacts for Silicon Wafer Solar Cells (2015)

Primary challenges to fine-line silver printing for solar cells are achieving high aspect ratios and uniform lines with a low level of striations. This paper compares two high-throughput printing technologies, namely, printing by screens versus stencils. A statistical method is introduced to evaluate the quality of the printed front grid based on the distributions of printed metal line profiles, line segment conductance, overall electroluminescence (EL) pattern, and solar cell light current-voltage (I-V) characteristics. The model distribution, combined with finite-element modeling to predict realistic cell-level voltage variations, adequately describes all four kinds of characteristics. It predicts well the diverging performance of screen- and stencil-printed solar cells as the line width becomes less than 50 μm. Experimentally, the highest batch average efficiency of 18.8% was achieved on 156 mm × 156 mm p-type monocrystalline silicon solar cells printed with stencils having 30-μm line openings, using only 78 mg of silver paste per cell.
ChemInform Abstract: Ultrasonic Accelerated Hydrogenation of α,β‐Unsaturated Ketones with Raney Nickel Catalyst. (1999)

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.