gebhart/patrepeval huggingface dataset:
A Web Service Architecture for Decentralised Identity- and Attribute-Based Access Control (2009)

The loosely coupled nature of service-oriented architectures raises the question how information for access control can be managed in an efficient way. Several specifications for Web services exist to describe security requirements and to facilitate a provision of identity information. However, the integration of different standards regarding the expression of identity information in policies, claims and assertions comes along with an increased complexity. In order to identify and address the problems occurring with the combined use of standards as XACML, SAML and WS-Trust, we designed and implemented an architecture for identity- and attribute-based access control in decentralized environments. Our implementation provides an automated generation of access control policies in a format called XACML, a way to communicate required user attributes as claims across different domains based on the standards WS-Trust and WS-Policy, and a consistent mapping of retrieved attribute assertions to the XACML attributes in the access control policy.
Empirical and theoretical investigation of the noise performance of indirect detection, active matrix flat‐panel imagers (AMFPIs) for diagnostic radiology (1997)

Noise properties of active matrix, flat‐panel imagers under conditions relevant to diagnostic radiology are investigated. These studies focus on imagers based upon arrays with pixels incorporating a discrete photodiode coupled to a thin‐film transistor, both fabricated from hydrogenated amorphous silicon. These optically sensitive arrays are operated with an overlying x‐ray converter to allow indirect detection of incident x rays. External electronics, including gate driver circuits and preamplification circuits, are also required to operate the arrays. A theoretical model describing the signal and noise transfer properties of the imagers under conditions relevant to diagnostic radiography, fluoroscopy, and mammography is developed. This frequency‐dependent model is based upon a cascaded systems analysis wherein the imager is conceptually divided into a series of stages having intrinsic gain and spreading properties. Predictions from the model are compared with x‐ray sensitivity and noise measurements obtained from individual pixels from an imager with a pixel format of 1536×1920 pixels at a pixel pitch of 127 μm. The model is shown to be in excellent agreement with measurements obtained with diagnostic x rays using various phosphor screens. The model is used to explore the potential performance of existing and hypothetical imagers for application in radiography, fluoroscopy, and mammography as a function of exposure, additive noise, and fill factor. These theoretical predictions suggest that imagers of this general design incorporating a CsI:Tl intensifying screen can be optimized to provide detective quantum efficiency (DQE) superior to existing screen‐film and storage phosphor systems for general radiography and mammography. For fluoroscopy, the model predicts that with further optimization of a ‐Si:H imagers, DQE performance approaching that of the best x‐ray image intensifier systems may be possible. The results of this analysis suggest strategies for future improvements of this imaging technology.
Human immune responses to major human cytomegalovirus glycoprotein complexes (1988)

Sera from both human cytomegalovirus (HCMV)-seropositive adults and infants with congenital HCMV infection recognized two major HCMV glycoprotein complexes. However, proliferative responses of peripheral blood mononuclear cells to these complexes varied among seropositive adults and were not detected in any of the infants. Thus, these glycoproteins alone may not be sufficient to develop a subviral HCMV vaccine.
Morphologic changes in the muscular pulmonary arteries: relationship to cigarette smoking, airway disease, and emphysema. (1980)

The muscular pulmonary arteries were studied by morphometric methods in 25 long-term cigarette smokers and were compared with those of 14 lifelong nonsmokers. Muscular pulmonary arteries < 500 microns in external diameter were identified and counted. The external diameter, medial thickness, and intimal thickness were measured in each of these arteries. Smokers had an increased number of transected muscular arteries < 200 microns in diameter (p < 0.03), increased medial smooth muscle (p < 0.02), and more intimal thickening (p < 0.04). Among smokers, these vascular changes correlated significantly with the severity of small airway disease and with the degree of emphysema, but not with bronchial mucous gland enlargement. We conclude that regular cigarette smoking is associated with morphologic changes in the muscular pulmonary arteries that evolve in parallel with small airway disease and emphysema. Although the functional significance of these findings is unknown, they may be important in the eventual development of pulmonary hypertension and cor pulmonale.
HAY QUE TENER CONCIENCIA PARA EL ACTO FINAL DE LA VIDA (2004)

EN CONFERENCIA LA VIDA BUENA Y BUENA JULIANA GONZ LEZ VALENZUELA, PROFESORA EMERITA DE FACULTAD DE FILOSOFIA Y LETRAS (FFL), AFIRMO QUE SE VIVE DE UNA MANERA HUMANIZADA MUERTE, LO CUAL SIGNIFICA HABER ASUMIDO VERDADERAMENTE QUE NOS VAMOS A SIGMUND FREUD DECIA QUE UNA DE LAS DIFERENCIAS ENTRE SER ADULTO Y INFANTILIDAD ES QUE EN ESTA NO SE TIENE CONCIENCIA DE MUERTE, EN UN SENTIDO ESTRICTO, CUAL REALMENTE SE DA CON CRECIMIENTO MORAL Y CONCIENCIA DEL SER HUMANO. AGREGO QUE FILOSOFO QUE M S TOCO, PENETRO, CALO, DANO Y NOS FASTIDIO A TODOS SOBRE TEMA FUE MARTIN HEIDEGGER. EN SU OBRA MAESTRA EL SER Y (1927) DIJO ALGO QUE SE HA EVADIDO A LO LARGO DE MUCHOS SIGLOS: IDEA DE QUE MUERTE NO ES UN HECHO QUE TE VA A ACONTECER UN DIA, SINO QUE TE OCURRE AHORA. LA VIDA ENTERA EST  YA MURIENDO. PENSADOR CONSIDERO, ADEM S, QUE MUERTE ES HECHO INTRINSECO DE VIDA Y REPRESENTA NADA. POR TANTO, MUERTE, EN SENTIDO ESTRICTO, NO ES OBJETO DE MIEDO SINO DE ANGUSTIA: DE ESTE NO SABER CU NDO, COMO NI QUE, DE LO CUAL ESTAMOS TAN PENETRADOS CADA INSTANTE DE VIDA Y QUE NO TENEMOS M S REMEDIO QUE ELUDIRLO. SENALO QUE ES TAN INTERNO Y DECISIVO HECHO DE QUE MAYORIA DE LOS SERES HUMANOS, SOBRE TODO DE ESTE TIEMPO, SE EVADEN. NADA IMPORTA EN SENTIDO ESTRICTO. ENTONCES ESPECIALISTA SE PREGUNTO: ¨DONDE EST N LAS CUESTIONES REALMENTE IMPORTANTES DE EXISTENCIA? LUCHA POR FELICIDAD HUMANA Y HUMANIDAD CONSTRUYENDO PAZ, POR EJEMPLO. EN REFERENCIA A EUTANASIA, EXPLICO, VAMOS A CUANDO QUERAMOS, NO CUANDO SE LE DE GANA A NADIE. POR ESO, NO SE ENTIENDE COMO ES POSIBLE QUE SE PROHIBA ESA PR CTICA. CUESTION, PRECISO JULIANA GONZ LEZ EN CASA DE LAS HUMANIDADES, ES QUE SE TIENE QUE VIVIR ACTO FINAL DE VIDA, QUE ES MUERTE, COMO SERES HUMANOS CONSCIENTES, LIBRES Y AMANTES DE NOSOTROS MISMOS Y LOS NUESTROS, PUES NO HAY VIDA HUMANA QUE NO SEA EN COMUNICACION CON OTRO. MORIR VIVO, DE ESO ES TODO LO QUE SE TRATA, RECALCO EN CICLO DE CONFERENCIAS TICA Y MUERTE. ES OBVIO QUE NO HAY QUE PERMITIR UNA EUTANASIA NO VIGILADA, CUIDADA HASTA FINAL. DEBE HABER CONSENSO SOBRE UN ENFERMO TIENE CONCIENCIA PARA DECIDIR Y PARA ELLO ES PRECISO SEGUIR LOS MECANISMOS QUE YA SE HAYAN ESTABLECIDO: PODRIA SER UN DOCUMENTO LEGAL EN QUE SE ESPECIFIQUE QUE SE DESEA EN DETERMINADOS CASOS. DE ESTA FORMA, CONSIDERO, CREO QUE TARDE O TEMPRANO SE ACEPTAR . VERDADERO OBST CULO ES: SI ESTO ME LO DIO DIOS COMO ME LO VOY A QUITAR. A FINAL ESPECIALISTA DESTACO QUE MOMENTO TERMINAL -QUE PUEDEN SER MINUTOS, DIAS O MESES- ES UNA CONDICION TEMPORAL QUE DEBE ASUMIRSE. NO SOLO HAY QUE COMPRENDER SIGNIFICADO DE SER FINITOS, QUE SE HA DE MORIR. EN CASO CONCRETO DE UN ENFERMO TERMINAL, ESE TIEMPO QUE QUEDA DEBE VIVIRSE CON PLENITUD, EN SUS TRES DIMENSIONES: PASADO (DEBE HACERSE MEMORIA), PRESENTE (NO ES VIDA ETERNA LO QUE BUSCO, SINO ETERNA VITALIDAD, ALGUNA VEZ DIJO FRIEDERICH NIETZCHE) Y FUTURO (PONIENDOSE EN PAZ CON LO QUE VIENE).
Proteomic Mapping of Mitochondria in Living Cells via Spatially Restricted Enzymatic Tagging (2012)

Microscopy and mass spectrometry (MS) are complementary techniques: The former provides spatiotemporal information in living cells, but only for a handful of recombinant proteins at a time, whereas the latter can detect thousands of endogenous proteins simultaneously, but only in lysed samples. Here, we introduce technology that combines these strengths by offering spatially and temporally resolved proteomic maps of endogenous proteins within living cells. Our method relies on a genetically targetable peroxidase enzyme that biotinylates nearby proteins, which are subsequently purified and identified by MS. We used this approach to identify 495 proteins within the human mitochondrial matrix, including 31 not previously linked to mitochondria. The labeling was exceptionally specific and distinguished between inner membrane proteins facing the matrix versus the intermembrane space (IMS). Several proteins previously thought to reside in the IMS or outer membrane, including protoporphyrinogen oxidase, were reassigned to the matrix by our proteomic data and confirmed by electron microscopy. The specificity of peroxidase-mediated proteomic mapping in live cells, combined with its ease of use, offers biologists a powerful tool for understanding the molecular composition of living cells.
MicroRNA-429 inhibits the migration and invasion of colon cancer cells by targeting PAK6/cofilin signaling (2015)

MicroRNAs (miRs), a class of non-coding RNAs 18-25 nucleotides in length, can lead to mRNA degradation or inhibit protein translation by directly binding to the 3'-untranslational region (UTR) of their target mRNAs. The deregulation of miR-429 has been suggested to be involved in the development and progression of colon cancer. However, the detailed molecular mechanism involved remains to be determined. The aim of the present study was to investigate the role of miR-429 in the regulation of migration and invasion of colon cancer cells using RT-qPCR and western blotting. The results showed that the expression of miR-429 was reduced in colon cancer cell lines, when compared to a normal colon epithelial cell line. Treatment with DNA demethylation agent 5-aza-2'-deoxycytidine and histone deacetylase inhibitor phenylbutyrate (PBA), or transfection with the pre-miR-429 lentivirus plasmid led to the upregulation of miR-429 expression, as well as inhibition of migration and invasion in colon cancer cells. Investigation of the molecular mechanism showed that PAK6 was a novel target of miR-429, and the expression of PAK6 was upregulated in colon cancer tissues and cell lines, and was negatively regulated by miR-429 in colon cancer cells. Moreover, the cofilin signaling acted as a downstream effector of miR-429 in colon cancer cells. In conclusion, the results of the present study suggested that miR-429 inhibits the migration and invasion of colon cancer cells, partly at least, by mediating the expression of PAK6, as well as the activity of cofilin signaling. Therefore, miR-429 is as a potential molecular target for the treatment of colon cancer.
SPECIFIC HIGH AFFINITY BINDING SITES FOR SOMATOSTATIN-28 ON PANCREATIC 6-CELLS:DIFFERENCES WITH BRAIN SOMATOSTATIN RECEPTORS1 (1982)

Saturable and high affinity binding sites have been obtained for an iodinated somatostatin-28 (SS-28) analog, [Leu8,D-Trp22,125I-Tyr25] SS-28, in a membrane preparation from hamster insulinoma, mainly composed of pancreatic beta-cells. Specific binding is maximal after 1 hour incubation at 22C and represents 65% of the total binding. KD for [Leu8,D-Trp22,Tyr25] SS-28 is 0.25 nM with the number of sites corresponding to 68 fmol/mg protein. The KD for SS-28 (1nM) is more than 5 times lower than that for SS-14. SS-28 analogs, such as [D-Trp22] SS-28 and analogs which selectively inhibit insulin release in vivo (Des-Asn5[D-Trp8,D-Ser13] SS-14 and Des-Asn19[D-Trp22,D-Ser27] SS-28), are the most potent compounds in this assay. C-terminal replacement of L-cysteine by D-cysteine reduces the apparent affinity of SS analogs. Unrelated peptides and the inactive analog Des-Trp8-SS-14 have no affinity for insulinoma binding sites. There are differences between the insulinoma SS binding sites and those monitored under similar conditions from rat cerebral cortex. In cerebral cortex, SS-14 and SS-28 have similar affinity for the binding sites, and the insulin selective analogs are less potent than SS-14. It is concluded that pancreatic beta-cells, as well as brain, possess high affinity binding sites for SS, but that they differ in some of their pharmacological properties.
Aberrantly activated claudin 6 and 18.2 as potential therapy targets in non‐small‐cell lung cancer (2014)

Claudins (CLDNs) are central components of tight junctions that regulate epithelial-cell barrier function and polarity. Altered CLDN expression patterns have been demonstrated in numerous cancer types and lineage-specific CLDNs have been proposed as therapy targets. The objective of this study was to assess which fraction of patients with non-small-cell lung cancer (NSCLC) express CLDN6 and CLDN18 isoform 2 (CLDN18.2). Protein expression of CLDN6 and CLDN18.2 was examined by immunohistochemistry on a tissue microarray (n = 355) and transcript levels were supportively determined based on gene expression microarray data from fresh-frozen NSCLC tissues (n = 196). Both were analyzed with regard to frequency, distribution and association with clinical parameters. Immunohistochemical analysis of tissue sections revealed distinct membranous positivity of CLDN6 (6.5%) and CLDN18.2 (3.7%) proteins in virtually non-overlapping subgroups of adenocarcinomas and large-cell carcinomas. Pneumocytes and bronchial epithelial cells were consistently negative. Corresponding to the protein expression, in subsets of non-squamous lung carcinoma high mRNA levels of CLDN6 (7-16%) and total CLDN18 (5-12%) were observed. Protein expression correlated well with total mRNA expression of the corresponding gene (rho = 0.4-0.8). CLDN18.2 positive tumors were enriched among slowly proliferating, thyroid transcription factor 1 (TTF-1)-negative adenocarcinomas, suggesting that isoform-specific CLDN expression may delineate a specific subtype. Noteworthy, high CLDN6 protein expression was associated with worse prognosis in lung adenocarcinoma in the univariate [hazard ratio (HR): 1.8; p = 0.03] and multivariate COX regression model (HR: 1.9; p = 0.02). These findings encourage further clinical exploration of targeting ectopically activated CLDN expression as a valuable treatment concept in NSCLC.
Glucagon-like peptide-2 enhances intestinal epithelial barrier function of both transcellular and paracellular pathways in the mouse (2000)

GLP-2 enhances intestinal epithelial barrier function by affecting both paracellular and transcellular pathways and thus may be of therapeutic value in a number of gastrointestinal conditions.
c-Jun NH2-Terminal Kinase-Mediated Up-regulation of Death Receptor 5 Contributes to Induction of Apoptosis by the Novel Synthetic Triterpenoid Methyl-2-Cyano-3,12-Dioxooleana-1, 9-Dien-28-Oate in Human Lung Cancer Cells (2004)

Death receptor (DR) 4 or 5, on binding to its ligand, tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), triggers apoptosis via activating the caspase-8-mediated caspase cascade. Certain anticancer drugs up-regulate the expression of these receptors and thereby induce apoptosis or enhance TRAIL-induced apoptosis. In this study, we explored the ability of methyl-2-cyano-3,12-dioxooleana-1,9-dien-28-oate (CDDO-Me) to activate the extrinsic DR-mediated apoptotic pathway in human lung cancer cells. We found that CDDO-Me not only activated caspase-8 but also induced expression of DRs, particularly DR5, in a p53-independent mechanism. Correspondingly, CDDO-Me augmented TRAIL-induced apoptosis in these cells regardless of p53 status as evidenced by enhanced DNA fragmentation and activation of caspase cascades, suggesting that CDDO-Me-induced DRs are functionally active. Moreover, silencing of DR5 expression using small interfering RNA suppressed apoptosis induced by CDDO-Me alone or by combination of CDDO-Me and TRAIL, indicating that DR5 up-regulation is required for induction of apoptosis by CDDO-Me and for enhancement of TRAIL-induced apoptosis by CDDO-Me. CDDO-Me rapidly activated c-Jun NH(2)-terminal kinase (JNK) before DR up-regulation and caspase-8 activation. Moreover, application of the JNK-specific inhibitor SP600125 blocked CDDO-Me-induced increases in JNK activation, DR up-regulation, caspase-8 activation, and DNA fragmentation. These results show that activation of JNK pathway results in CDDO-Me-induced DR up-regulation, caspase-8 activation, and apoptosis. Collectively, we conclude that CDDO-Me induces apoptosis via the JNK-mediated DR up-regulation in human lung cancer cells.
Skeletal Repair by in Situ Formation of the Mineral Phase of Bone (1995)

A process has been developed for the in situ formation of the mineral phase of bone. Inorganic calcium and phosphate sources are combined to form a paste that is surgically implanted by injection. Under physiological conditions, the material hardens in minutes concurrent with the formation of dahllite. After 12 hours, dahllite formation was nearly complete, and an ultimate compressive strength of 55 megapascals was achieved. The composition and crystal morphology of the dahllite formed are similar to those of bone. Animal studies provide evidence that the material is remodeled in vivo. A novel approach to skeletal repair is being tested in human trials for various applications; in one of the trials the new biomaterial is being percutaneously placed into acute fractures. After hardening, it serves as internal fixation to maintain proper alignment while healing occurs.
Melanoma Cell Expression of Fas(Apo-1/CD95) Ligand: Implications for Tumor Immune Escape (1996)

Malignant melanoma accounts for most of the increasing mortality from skin cancer. Melanoma cells were found to express Fas (also called Apo-1 or CD95) ligand (FasL). In metastatic lesions, Fas-expressing T cell infiltrates were proximal to FasL+ tumor cells. In vitro, apoptosis of Fas-sensitive target cells occurred upon incubation with melanoma tumor cells; and in vivo, injection of FasL+ mouse melanoma cells in mice led to rapid tumor formation. In contrast, tumorigenesis was delayed in Fas-deficient lpr mutant mice in which immune effector cells cannot be killed by FasL. Thus, FasL may contribute to the immune privilege of tumors.
Characterization of a thiamin diphosphate‐dependent phenylpyruvate decarboxylase from Saccharomyces cerevisiae (2011)

The product of the ARO10 gene from Saccharomyces cerevisiae was initially identified as a thiamine diphosphate-dependent phenylpyruvate decarboxylase with a broad substrate specificity. It was suggested that the enzyme could be responsible for the catabolism of aromatic and branched-chain amino acids, as well as methionine. In the present study, we report the overexpression of the ARO10 gene product in Escherichia coli and the first detailed in vitro characterization of this enzyme. The enzyme is shown to be an efficient aromatic 2-keto acid decarboxylase, consistent with it playing a major in vivo role in phenylalanine, tryptophan and possibly also tyrosine catabolism. However, its substrate spectrum suggests that it is unlikely to play any significant role in the catabolism of the branched-chain amino acids or of methionine. A homology model was used to identify residues likely to be involved in substrate specificity. Site-directed mutagenesis on those residues confirmed previous studies indicating that mutation of single residues is unlikely to produce the immediate conversion of an aromatic into an aliphatic 2-keto acid decarboxylase. In addition, the enzyme was compared with the phenylpyruvate decarboxylase from Azospirillum brasilense and the indolepyruvate decarboxylase from Enterobacter cloacae. We show that the properties of the two phenylpyruvate decarboxylases are similar in some respects yet quite different in others, and that the properties of both are distinct from those of the indolepyruvate decarboxylase. Finally, we demonstrate that it is unlikely that replacement of a glutamic acid by leucine leads to discrimination between phenylpyruvate and indolepyruvate, although, in this case, it did lead to unexpected allosteric activation.
Survivin expression predicts early recurrence in early-stage breast cancer. (2007)

Survivin is an indicator of the recurrence of early-stage breast cancer. Survivin might be used as a new marker to stratify early-stage breast cancer patients for more optimal treatment modalities, or it could be a promising target for therapy.
Prenatal detection of unbalanced chromosomal rearrangements by array CGH (2005)

Analysis of 30 uncultured prenatal samples showed that array CGH is capable of detecting aneuploidy in DNA isolated from as little as 1 ml of uncultured amniotic fluid; 29/30 samples were correctly diagnosed, the exception being another case of triploidy. These studies demonstrate the potential for array CGH to replace conventional cytogenetics in the great majority of prenatal diagnosis cases.
Graphene Field Effect Transistors for Biomedical Applications: Current Status and Future Prospects (2017)

Since the discovery of the two-dimensional (2D) carbon material, graphene, just over a decade ago, the development of graphene-based field effect transistors (G-FETs) has become a widely researched area, particularly for use in point-of-care biomedical applications. G-FETs are particularly attractive as next generation bioelectronics due to their mass-scalability and low cost of the technology's manufacture. Furthermore, G-FETs offer the potential to complete label-free, rapid, and highly sensitive analysis coupled with a high sample throughput. These properties, coupled with the potential for integration into portable instrumentation, contribute to G-FETs' suitability for point-of-care diagnostics. This review focuses on elucidating the recent developments in the field of G-FET sensors that act on a bioaffinity basis, whereby a binding event between a bioreceptor and the target analyte is transduced into an electrical signal at the G-FET surface. Recognizing and quantifying these target analytes accurately and reliably is essential in diagnosing many diseases, therefore it is vital to design the G-FET with care. Taking into account some limitations of the sensor platform, such as Debye-Hükel screening and device surface area, is fundamental in developing improved bioelectronics for applications in the clinical setting. This review highlights some efforts undertaken in facing these limitations in order to bring G-FET development for biomedical applications forward.
Precursor Balancing for Metabolic Engineering of Lycopene Production in Escherichia coli (2001)

One issue that must be addressed in the rational design of metabolic pathways is the elimination of potential bottlenecks in the upstream pathways. We have reconstructed the isoprenoid pathway to overproduce the carotenoid lycopene in Escherichia coli. Here we show that the distribution between pyruvate and glyceraldehyde 3-phosphate (G3P), the originating precursors of the isoprenoid pathway, is a major factor that can limit isoprenoid production yields in E. coli. In particular, alterations in the central metabolism that redirect flux from pyruvate back to G3P enhance lycopene production, while alterations that channel carbon flux away from the G3P pool have the opposite effect. These results suggest that G3P may be limiting in the biosynthesis of lycopene, and modifications that achieve a more equitable distribution between the two precursors are able to increase the lycopene yield in metabolically engineered E. coli.
Phase I Clinical and Pharmacokinetic Study of Bcl-2 Antisense Oligonucleotide Therapy in Patients With Non-Hodgkin’s Lymphoma (2000)

Bcl-2 antisense therapy is feasible and shows potential for antitumor activity in NHL. Downregulation of Bcl-2 protein suggests a specific antisense mechanism.