gebhart/patrepeval huggingface dataset:
Lattice-based access control models (1993)

Lattice-based access control models were developed in the early 1970s to deal with the confidentiality of military information. In the late 1970s and early 1980s, researchers applied these models to certain integrity concerns. Later, application of the models to the Chinese Wall policy, a confidentiality policy unique to the commercial sector, was demonstrated. A balanced perspective on lattice-based access control models is provided. Information flow policies, the military lattice, access control models, the Bell-LaPadula model, the Biba model and duality, and the Chinese Wall lattice are reviewed. The limitations of the models are identified.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Searching for pattern and mutation in the Drosophila genome with a P-lacZ vector. (1989)

A P-element vector has been constructed and used to generate lines of flies with single autosomal P-element insertions. The lines were analyzed in two ways: (1) the identification of cis-acting patterning information within the Drosophila genome, as revealed by a lacZ reporter gene within the P element, and (2) the isolation of lethal mutations. We examined 3768 independent lines for the expression of lacZ in embryos and looked among these lines for lethal mutations affecting embryonic neurogenesis. This type of screen appears to be an effective way to find new loci that may play a role in the development of the Drosophila nervous system.
tie-1 protein tyrosine kinase: a novel independent prognostic marker for gastric cancer. (1999)

Protein tyrosine kinases (PTKs) are a major class of proto-oncogenes that are involved in tumor progression. The purpose of this study was to establish a comprehensive PTK expression profile in gastric cancers, with the objective of identifying possible biomarkers for gastric cancer progression. We have designed degenerate primers according to the consensus catalytic motifs to amplify PTK molecules from gastric cancers by reverse transcriptase-PCR methods. The PTK expression profile was established by sequencing analysis of the cloned PCR products. We have identified 17 PTKs from a gastric adenocarcinoma. Two receptor PTKs, tie-1 and axl, were selected for in situ immunohistochemistry studies because of their higher expression level and their described roles in adhesion, invasion, and angiogenesis. Among the 97 gastric adenocarcinoma tissues examined, we observed positive immunohistochemical staining of tie-1 PTK in 69 and positive staining of axl kinase in 71 tissues. Statistical analysis with clinicopathological features indicates that tie-1 kinase expression is inversely correlated with patients' survival, whereas axl fails to show similar clinical significance. Our results illustrate the utility of tyrosine kinase gene family profiling in human gastric cancers and show that tie-1 tyrosine kinase may serve as a novel independent prognostic marker for gastric adenocarcinoma patients.
HIV gp120 inhibits the somatotropic axis: A possible GH-releasing hormone receptor mechanism for the pathogenesis of AIDS wasting (1998)

AIDS is often associated with growth retardation in children and wasting in adults. The dissociated envelope protein of the HIV (HIV-1), gp120, can be found in significant concentrations in the parenchyma and cerebrospinal fluid of brains in infected individuals, even in the earliest stages of HIV-1 disease. On the basis of this and the fact that we observed pentapeptide sequence homology between GH-releasing hormone (GHRH) and the V2 receptor-binding region of gp120, we initiated experiments to determine whether gp120 could affect GH secretion and growth in vivo and/or interact with anterior pituitary GHRH receptors in vitro. Although acute IV administration of gp120 in conscious rats had no effect on plasma GH levels, acute administration of gp120 (400 ng) into the brain significantly suppressed pulsatile GH release over a 6-h period compared with saline-injected controls. Furthermore, the putative gp120 antagonist, Peptide T (DAPTA), prevented the suppression of GH by gp120. In support of these in vivo findings, gp120 also significantly (P < 0.05) suppressed GHRH-stimulated GH release in static cultures of dispersed pituitary cells and from cells undergoing perifusion with the peptides. DAPTA prevented the GH suppression by gp120 in both of the pituitary cell paradigms. Furthermore, chronic administration of gp120 into the third ventricle significantly reduced body weight in juvenile rats, compared with saline-injected controls. Thus, gp120 appears to act both at the hypothalamus and pituitary to suppress GH release, and its action at these two locations is associated with a significant loss in body weight in chronically treated young animals. These findings may suggest a specific mechanism for the pathogenesis of wasting in HIV-1 patients that involves blockade of endogenous GHRH receptors by gp120.
Anti-ageing effect of a lactococcal strain: analysis using senescence-accelerated mice (2007)

The effects of oral administration of a lactococcal strain on physiological changes associated with ageing were investigated using senescence-accelerated mice (SAM). SAM develop normally, but then show an early onset and irreversible advancement of senescence. SAMP6 is a SAM strain that develops osteoporosis with ageing. Oral administration of heat-killed Lactococcus lactis subsp. cremoris H61 (strain H61) to aged SAMP6 mice was associated with reduced bone density loss, a suppression of incidence of skin ulcers and reduced hair loss, compared with controls. Spleen cells from mice fed strain H61 produced more interferon-γ and IL-12 than those from control mice, suggesting that administration of strain H61 altered immune responses. The numbers of viable cells of Bifidobacterium sp., Bacteroides sp. and Enterococcus sp. in faeces were similar for mice fed the strain H61 and control diets, but counts for Staphylococcus sp. were significantly lower ( P &lt; 0·05) in mice fed strain H61. Mice fed strain H61 had similar serum concentrations of thiobarbituric acid-reactive substances as in controls, indicating a lack of effect on lipid peroxidation status. Administration of living cells of strain H61 or fermented milk containing strain H61 was also associated with a suppression of incidence of skin ulcers and reduced hair loss. These results indicate that oral administration of strain H61 has the potential to suppress some of the manifestations associated with ageing.
RNA interference: A new mechanism by which FMRP acts in the normal brain? What can Drosophila teach us? (2004)

Fragile X syndrome is the most common heritable form of mental retardation caused by loss-of-function mutations in the FMR1 gene. The FMR1 gene encodes an RNA-binding protein that associates with translating ribosomes and acts as a negative translational regulator. Recent work in Drosophila melanogaster has shown that the fly homolog of FMR1 (dFMR1) plays an important role in regulating neuronal morphology, which may underlie the observed deficits in behaviors of dFMR1 mutant flies. Biochemical analysis has revealed that dFMR1 forms a complex that includes ribosomal proteins and, surprisingly, Argonaute2 (AGO2), an essential component of the RNA-induced silencing complex (RISC) that mediates RNA interference (RNAi) in Drosophila. dFMR1 also associates with Dicer, another essential processing enzyme of the RNAi pathway. Moreover, both a micro-RNA (miRNA) and short interfering RNAs (siRNAs) can coimmunoprecipitate with dFMR1. Together these findings suggest that dFMR1 functions in an RNAi-related apparatus to regulate the expression of its target genes at the level of translation. These findings raise the possibility that Fragile X syndrome may be the result of a protein synthesis abnormality caused by a defect in an RNAi-related apparatus. Because the core mechanisms of complex behaviors such as learning and memory and circadian rhythms appear to be conserved, studies of Fragile X syndrome using Drosophila as a model provide an economy-of-scale for identifying biological processes that likely underlie the abnormal morphology of dendritic spines and behavioral disturbances observed in Fragile X patients.
Recognition of the Carboxy-Terminal Peptide in Cyanogen Bromide Digests of Proteins (1995)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTRecognition of the Carboxy-Terminal Peptide in Cyanogen Bromide Digests of ProteinsConstance M. Murphy and Catherine. FenselauCite this: Anal. Chem. 1995, 67, 9, 1644–1645Publication Date (Print):May 1, 1995Publication History Published online1 May 2002Published inissue 1 May 1995https://pubs.acs.org/doi/10.1021/ac00105a027https://doi.org/10.1021/ac00105a027research-articleACS PublicationsRequest reuse permissionsArticle Views95Altmetric-Citations6LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
Information theory based T7-like promoter models: classification of bacteriophages and differential evolution of promoters and their polymerases (2005)

Molecular information theory was used to create sequence logos and promoter models for eight phages of the T7 group: T7, phiA1122, T3, phiYeO3-12, SP6, K1-5, gh-1 and K11. When these models were used to scan the corresponding genomes, a significant gap in the individual information distribution was observed between functional promoter sites and other sequences, suggesting that the models can be used to identify new T7-like promoters. When a combined 76-site model was used to scan the eight phages, 108 of the total 109 promoters were found, while none were found for other T7-like phages, phiKMV, P60, VpV262, SIO1, PaP3, Xp10, P-SSP7 and Ppu40, indicating that these phages do not belong to the T7 group. We propose that the T7-like transcription system, which consists of a phage-specific RNA polymerase and a set of conserved T7-like promoters, is a hallmark feature of the T7 group and can be used to classify T7-like phages. Phylogenetic trees of the T7-like promoter models and their corresponding RNA polymerases are similar, suggesting that the eight phages of the T7 group can be classified into five subgroups. However the SP6-like polymerases have apparently diverged from other polymerases more than their promoters have diverged from other promoters.
Recurrent radial artery aneurysm in a five-month-old infant. (2000)

Distal radial artery aneurysms are an infrequent occurrence in adults and rare in children. The rate of aneurysm formation in adults has been reported as 0.048% following catheterization. A case report of a 5-month-old girl with a recurrent left radial artery aneurysm is presented. The etiology of the aneurysm was radial artery catheterization in the neonatal intensive care unit. Recurrence occurred after resection for an end-to-end repair. Ligation of the artery was required for ultimate treatment. No deleterious sequelae were found after the final operation.
Cromolyn inhibits assembly of the NADPH oxidase and superoxide anion generation by human neutrophils. (1995)

Early and late phase reactions have been observed in asthma; the late phase reaction is characterized by accumulation of inflammatory cells such as neutrophils. Activated neutrophils degranulate and assemble an active NADPH oxidase, which generates superoxide anion (O2-), reactions that have been implicated in lung tissue damage. Preincubation of neutrophils with the asthma drug cromolyn sodium selectively inhibited FMLP (10(-7) M) and PMA (0.1 microgram/ml) elicited O2- generation but not degranulation. To further characterize the mechanism of this inhibition we examined the effect of cromolyn on the NADPH oxidase complex and the signaling pathways for its assembly. Ca2+ mobilization and activation of protein kinase C have been implicated as signals for activation of the NADPH oxidase. Ca2+ mobilization triggered by FMLP was significantly decreased by 21.2% in cromolyn-treated cells. In contrast, cromolyn did not interfere with translocation or activity of protein kinase C. Membranes prepared from neutrophils stimulated with 0.5 microgram/ml PMA generated O2-, indicating assembly of an active NADPH oxidase; cromolyn did not inhibit this membrane-associated, preassembled oxidase. In contrast, preincubation of neutrophils with 100 microM cromolyn before addition of PMA decreased the capacity of the membranes to generate O2- by 57.3%. These results indicate that cromolyn inhibited the assembly of an active NADPH oxidase. The efficacy of cromolyn may be associated with inhibition of assembly of an active NADPH oxidase in the neutrophil and prevention of oxygen radical-induced tissue damage.
Maternal Rescue of Transforming Growth Factor-β 1 Null Mice (1994)

Maternal sources of transforming growth factor-beta 1 (TGF-beta 1) are shown here to contribute to the normal appearance and perinatal survival of TGF-beta 1 null newborn mice. Labeled TGF-beta 1 crossed the placenta and was recovered intact from various tissues after oral administration to mouse pups. TGF beta-1 protein was also detected in cells recovered from breast milk. In immunohistochemical analyses, TGF-beta 1 null embryos and null newborn pups born to TGF-beta 1 heterozygotes stained positive for TGF-beta 1, whereas those born to a null female were negative and had severe cardiac abnormalities. These results suggest an important role for maternal sources of TGF-beta 1 during development and, more generally, provide evidence for maternal rescue of targeted gene disruption in the fetus.
Epigenetic Inactivation of RASSF1A in Lung and Breast Cancers and Malignant Phenotype Suppression (2001)

RASSF1A is a potential tumor suppressor gene that undergoes epigenetic inactivation in lung and breast cancers through hypermethylation of its promoter region.
Granulocyte-Macrophage Colony Stimulating Factor Up-Regulates CCR1 in Human Neutrophils (2001)

Neutrophils (polymorphonuclear leukocytes; PMN) are phagocytic cells instrumental in the clearance of infectious pathogens. Human PMN are commonly thought to respond primarily to chemokines from the CXC family. However, recent findings suggest that under specific cytokine activation conditions, PMN can also respond to some CC chemokines. In this study, the effect of GM-CSF, a well-characterized PMN priming and maturation factor, on CC-chemokine receptor (CCR) expression in PMN was investigated. Constitutive expression of CCR1 and CCR3 mRNA in PMN was detected by ribonuclease protection assay. Following incubation of PMN with GM-CSF (0.01-10 ng/ml; 6 h) CCR1 mRNA expression was rapidly (approximately 1 h) up-regulated. In contrast, no significant induction of CCR2, CCR3, CCR4, or CCR5 mRNA was observed. CCR1 protein was also up-regulated by GM-CSF stimulation. GM-CSF-induced up-regulation of CCR1 showed functional consequences because GM-CSF-treated PMN, but not control cells, responded to the CC chemokines macrophage inflammatory protein-1alpha, monocyte chemoattractant protein-3, and RANTES in assays of chemotactic migration and intracellular calcium mobilization. These results suggest that PMN activated by the proinflammatory cytokine GM-CSF can change their receptor expression pattern and become responsive to CC chemokines.
Chronic lymphocytic leukaemia (CLL) and CLL‐type monoclonal B‐cell lymphocytosis (MBL) show differential expression of molecules involved in lymphoid tissue homing (2010)

CLL-type MBL is phenotypically identical to CLL for a very broad range of markers. Differential expression is predominantly related to known prognostic markers and proteins involved in homing to lymphoid tissue.
Insights into the Mechanism of the Antibiotic‐Synthesizing Enzyme MoeO5 from Crystal Structures of Different Complexes (2012)

Barrel-shaped: The enzyme MoeO5 catalyzes the transfer of the C15 moiety of farnesyl pyrophosphate to the 2-hydroxy group of 3-phosphoglycerate to give 2-(Z,E)-farnesyl-3-phosphoglycerate (FPG; ligand in the center of the shown structure). X-ray crystallographic structures showed that MoeO5 forms a triose-phosphate-isomerase barrel structure and binds FPG in a curved pocket, mainly as a result of its long λ3 loop (magenta in picture).
Liver involvement in systemic infection. (1997)

The liver is heavily involved in the vast majority of systemic infections. Pathophysiological mechanisms involved in hepatic involvement in generalized sepsis require further study, as does the importance of bacterial infection in the presence of cirrhosis. Although parasitic involvement is theoretically dominated by Plasmodium spp., in clinical practice Entamoeba histolytica, Schistosoma spp. and Echinococcus spp. infections are far more important. Hepatobiliary involvement is also a feature of Ascaris lumbricoides, Fasciola hepatica and 'oriental' cholangiohepatitis. Various bacteria (including Mycobacterium tuberculosis, Treponema pallidum and Salmonella spp.) and viruses (e.g., cytomegalovirus, Herpes simplex and dengue) also cause significant hepatic involvement. A high index of suspicion for infection is required in paediatric hepatology.
The lethal effects of cytokine-induced nitric oxide on cardiac myocytes are blocked by nitric oxide synthase antagonism or transforming growth factor beta. (1995)

Inducible nitric oxide (NO) produced by macrophages is cytotoxic to invading organisms and has an important role in host defense. Recent studies have demonstrated inducible NO production within the heart, and that cytokine-induced NO mediates alterations in cardiac contractility, but the cytotoxic potential of nitric oxide with respect to the heart has not been defined. To evaluate the role of inducible nitric oxide synthase (iNOS) on cardiac myocyte cytotoxicity, we exposed adult rat cardiac myocytes to either cytokines alone or to activated J774 macrophages in coculture. Increased expression of both iNOS message and protein was seen in J774 macrophages treated with IFN gamma and LPS and cardiac myocytes treated with TNF-alpha, IL-1 beta, and IFN gamma. Increased NO synthesis was confirmed in both the coculture and isolated myocyte preparations by increased nitrite production. Increased NO synthesis was associated with a parallel increase in myocyte death as measured by CPK release into the culture medium as well as by loss of membrane integrity, visualized by trypan blue staining. Addition of the competitive NO synthase inhibitor L-NMMA to the culture medium prevented both the increased nitrite production and the cytotoxicity observed after cytokine treatment in both the isolated myocyte and the coculture experiments. Because transforming growth-factor beta modulates iNOS expression in other cell types, we evaluated its effects on cardiac myocyte iNOS expression and NO-mediated myocyte cytotoxicity. TGF-beta reduced expression of cardiac myocyte iNOS message and protein, reduced nitrite production, and reduced NO-mediated cytotoxicity in parallel. Taken together, these experiments show the cytotoxic potential of endogenous NO production within the heart, and suggest a role for TGF-beta or NO synthase antagonists to mute these lethal effects. These findings may help explain the cardiac response to sepsis or allograft rejection, as well as the progression of dilated cardiomyopathies of diverse etiologies.
Virtual Screening of 4‐Anilinoquinazoline Analogues as EGFR Kinase Inhibitors: Importance of Hydrogen Bonds in the Evaluation of Poses and Scoring Functions. (2005)

Virtual Screening (VS) is a computational technique that allows selection and ranking of possible hits from\na library of compounds. We have carried out VS on 128 selected EGFR kinase inhibitors with GOLD and\nLigandFit. From the experimental crystal structure of the erlotinib−EGFR complex, three key hydrogen\nbonds were identified as responsible for anchoring the ligand in the active site. These are of the N−H···N,\nO&lt;sub&gt;w&lt;/sub&gt;−H···N, and C−H···O types. Failure to include the hydrogen-bonded water molecule that forms the\nO&lt;sub&gt;w&lt;/sub&gt;−H···N bond leads to incorrect results. Of the three interactions, the C−H···O formed by an activated\nC−H group is the best conserved. On the basis of the efficacy of these hydrogen bonds, the poses were\nclassified into one of three categories: close, shifted, and misoriented. In the VS context, all three interactions\nneed to be modeled correctly so that correct poses and affinities are obtained, and this happens in ligands\nof the close variety. Cross scoring wherein the poses from one software are input into another for scoring\nand consensus scoring wherein the scores from various software packages are weighted are also helpful in\nobtaining better agreements.
SM22alpha is required for agonist-induced regulation of contractility: evidence from SM22alpha knockout mice. (2007)

The present study was undertaken to determine whether SM22alpha participates in the regulation of vascular smooth muscle contractility using SM22alpha knockout mice and, if so, to investigate the mechanisms involved. Aortic ring preparations were mounted and equilibrated in organ baths for 60 min before observing contractile responses to 50 mM KCl, and then exposed to contractile agents such as phenylephrine and phorbol ester. Measurement of isometric contractions using a computerized data acquisition system was combined with molecular or cellular experiments. Interestingly, the aortas from SM22alpha-deficient mice (SM22(-/-LacZ)) displayed an almost three-fold increase in the level of SM22beta protein compared to wild-type mice, but no change in the levels of caldesmon, actin, desmin or calponin. Ca2+-independent contraction in response to phenylephrine or phorbol ester was significantly decreased in the SM22alpha-deficient mice, whereas in the presence of Ca2+ neither contraction nor subcellular translocation of myosin light chain kinase (MLCK) in response to phenylephrine or 50 mM KCl was significantly affected. A decrease in phosphorylation of extracellular signal regulated kinase (ERK) 1/2 was observed in the SM22alpha-deficient mice and this may be related to the decreased vascular contractility. Taken together, this study provides evidence for a pivotal role of SM22alpha in the regulation of Ca2+-independent vascular contractility.
Generation of Potent Antitumor CTL from Patients with Multiple Myeloma Directed against HM1.24 (2005)

Our results indicate that HM1.24 is a promising target for immunotherapy of multiple myeloma.
The intestinal microbiota in health and disease (2011)

Understanding how the gut microbiome contributes to intestinal health should lead to novel preventive strategies and therapies for a variety of gastrointestinal conditions.
A Longitudinal Evaluation of the Relationship Between Reproductive Status and Mood in Perimenopausal Women (2004)

These preliminary data suggest that events related to the late perimenopause may be associated with an increased susceptibility to develop depression in some women.