gebhart/patrepeval huggingface dataset:
Numerous nuclear proteins bind the long control region of human papillomavirus type 16: a subset of 6 of 23 DNase I-protected segments coincides with the location of the cell-type-specific enhancer (1989)

The long control region of the human papillomavirus type 16 genome is 856 base pairs (bp) long. It contains a cell-type-specific enhancer, a glucocorticoid response element, and sequences mediating the response to the viral gene products of open reading frame E2; all three regulate the promoter P97. We mapped binding sites of trans-acting proteins relevant for the cell-type-specific enhancer and other cis-acting elements by DNase I footprint experiments with nuclear extracts from HeLa cells. Throughout the human papillomavirus type 16 long control region 23 footprints protect 557 of 900 bp. Nine footprints fall into a 400-bp segment that was previously identified to contain the cell-type-specific enhancer. Variations of the protein concentration in the footprint reaction do not affect six of these nine footprints. At high protein concentrations, three footprints fuse to a 106-bp protected region, suggesting that this segment specifically binds several proteins of lower affinity or abundance. Unexpectedly, extracts from human MCF7 and mouse 3T3 cells, in which the enhancer is inactive, give footprints identical to those obtained with HeLa extracts. Seven footprints contain the sequence 5'-TTGGC-3'. Footprint competition experiments suggest that factor NFI binds to these seven motifs. Competition with cloned oligonucleotides in transfections suggests that these elements contribute to the enhancer function. Subcloning identifies a 232-bp fragment between positions 7524 and 7755 as sufficient for full enhancer activity. Several of the six footprinted elements on this segment may cooperate functionally, since subclones of this region show decreased or no cell-type-specific enhancer function.
Development of immunohistochemistry services for cancer care in western Kenya: Implications for low- and middle-income countries (2016)

Development of low- and middle-income country models of services, such as the IHC laboratory presented in this paper, is critical for the infrastructure in resource-limited settings to address the growing cancer burden. We provide a low-cost model that effectively develops these necessary services in a challenging laboratory environment.
Two-color holography in reduced near-stoichiometric lithium niobate (1998)

We explored a number of factors affecting the properties relevant to holographic optical data storage by using a two-color recording scheme in reduced, near-stoichiometric lithium niobate. Two-color, or photon-gated, recording is achieved by use of 852-nm information-carrying beams and 488-nm gating light. Readout at 852 nm is nondestructive, with a gating ratio of ~10(4). Recording sensitivity, gating ratio, dynamic range, and dark decay were measured for crystals of differing stoichiometry, degree of reduction, wavelength of the gating light, temperature, and optical power density. The two-color sensitivity per incident photon is still somewhat less than that of the one-color process at 488 nm for ~1 W/cm(2) of gating light but is essentially the same in terms of absorbed photons. Two-color recording is an attractive way of achieving nondestructive readout in a read-write material, and it allows selective optical erasure.
Apple polysaccharides induce apoptosis in colorectal cancer cells (2012)

Certain components of apples have been shown to prevent cancer growth and impede cancer progression. We hypothesized that extracted apple polysaccharides (APs) might, therefore, have anticancer effects, through a mechanism involving the induction of apoptosis in cancer cells, partly via the NF-κB pathway. Two human colorectal cancer (CRC) cell lines, HT-29 and SW620, were exposed to different concentrations of APs (0.01, 0.1 or 1 mg/ml). Cell apoptosis was measured by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay by flow cytometry and incorporation of 5'-bromodeoxyuridine (BrdU) into DNA to identify the proliferating cell fraction, using fluorescence microscopy in vitro. The protein levels of NF-κB/p65, I-κBα, pI-κBα, Bax, Bcl-xl and Bcl-2 were evaluated by western blotting. The target sites of APs on CRC cells were assessed by flow cytometry. At concentrations of 0.1 and 1 mg/ml, APs showed apoptosis-inducing effects, increased expressions of Bax, nuclear p65 and cytoplasmic pI-κBα, and decreased expressions of Bcl-2, Bcl-xl and cytoplasmic I-κBα. APs induced apoptosis by slightly activating the NF-κB pathway; the AP target site could be the Toll-like receptor 4 on the cell membrane. These results demonstrate the potential of APs as agents for clinical prevention and treatment of CRC.
Window real objects (1993)

This paper proposes a distributed shared memory, Window Real-Object (WROL which facilitates the construction of GUI applications with a set of cooperating parallel units running on multiple machines. To support unit cooperation, the WRO provides a shared data structure storing interaction objects displayed in a window among multiple machines. It also provides an event mechanism called absfrac[ everm to support control transfer among these units. Abstract events are generated when the shared data structure is updated, and invoke the units sharing the WRo.
Immunomodulatory and anticancer effects of intra-tumoral co-delivery of synthetic lipid A adjuvant and STAT3 inhibitor, JSI-124 (2008)

The efficiency of cancer immunotherapy strategies is hampered by the existence of an intra-tumoral immunosuppressive environment involving tolerogenic dendritic cells (DCs) and regulatory T (T(reg)) cells. Hyperactivation of STAT3 in tumor is implicated in the generation of this immunosuppressive environment. The purpose of this study was to test whether simultaneous inhibition of STAT3 in tumor and TLR4 ligand-induced activation of DCs can modulate tumor-induced immunosuppression. For this purpose, the effects of a TLR4 ligand, 7-acyl lipid A, delivered by poly(lactic-co-glycolic acid) nanoparticles (PLGA-NPs) to DCs on the activity of DCs and T(reg) cells was evaluated in vitro. In addition the immunomodulatory and anticancer effects of 7-acyl lipid A PLGA-NPs in combination with a STAT3 inhibitory agent, JSI-124, in a B16 mouse melanoma model was explored, in vivo. PLGA-NP delivery of 7-acyl lipid A to DCs reduced the suppressive effects of T(reg) cells on T cells in vitro. Besides, daily Intra-tumoral co-administration of 7-acyl lipid A PLGA-NPs and JSI-124 in C57BL/6 mice bearing B16-F10 tumor for 8 days resulted in a significant increase in the percentage of tumor infiltrated T cells as compared with control group that received PBS and monotherapy groups. The average tumor volume in the tumor-bearing mice that received JSI-124 plus 7-acyl lipid A PLGA-NPs combination therapy was found to be significantly lower than that in PBS and monotherapy groups. Our findings show a potential for the combination of STAT3 inhibition in tumor and TLR4 induced DC activation in increasing the efficacy of cancer immunotherapy.
Studies on the Antiviral Mechanisms of Protein Kinase Inhibitors K-252a and KT5926 against the Replication of Vesicular Stomatitis Virus. (1998)

We investigated the antiviral mechanisms of K-252a, a broad non-specific protein kinase inhibitor which was isolated from Nocardiopsis sp. and its derivative (KT5926), against vesicular stomatitis virus (VSV) replication in BHK-21 cells. Although K-252a (5 microM) and KT5926 (15 microM) similarly suppressed the viral primary and secondary transcriptions and genomic RNA synthesis in vivo, the inhibitory mechanisms did not seem to be the same; phosphorylation of the viral NS protein was suppressed by K-252a, which might account for the decreased viral RNA synthesis caused by K-252a. On the other hand, KT5926, being known to preferentially inhibit myosin light chain kinase (MLCK), had little effect on NS protein phosphorylation. Cellular casein kinase II, which is believed to be involved in the phosphorylation of the N-terminal side (domain I) of NS protein, was not inhibited at all by KT5926 even at 15 microM under in vitro assay conditions, and was only weakly inhibited by K-252a at 1 to 10 microM. Neither inhibitor seemed to directly affect viral protein synthesis, but affected it indirectly as a secondary effect of reduced viral RNA synthesis. These results suggest that both the KT5926-sensitive and the KT5926-resistant but K-252a-sensitive functions are involved in the essential processes of viral RNA synthesis. The KT5926-sensitive function(s) might not be involved in the NS protein phosphorylation, but may participate in some other way in the process of virus replication. On the other hand, the KT5926-resistant, K-252a-sensitive function(s) are probably involved in NS protein phosphorylation. The possible nature of those functions is discussed.
A general texture mapping framework for image-based 3D modeling (2010)

This paper presents a general texture mapping framework for image-based 3D modeling. It aims to generating seamless texture map for 3D model created by real-world photos under uncontrolled environment. Our proposed method addresses two challenging problems: 1) texture discontinuity due to system error in 3D modeling from self-calibration; 2) color/lighting difference among images due to real-world uncontrolled environments. The general framework contains two stages to resolve these problems. The first stage globally optimizes the registration of texture patches and triangle faces with Markov Random Field (MRF) to optimize texture mosaic. The second stage does local radiometric correction to adjust color difference between texture patches and then blend texture boundaries to improve color continuity. The proposed method is evaluated on several 3D models by image-based 3D modeling, and demonstrates promising results.
Lipid homeostasis and apolipoprotein E in the development and progression of Alzheimer's disease (2005)

Extracellular amyloid plaques, intracellular neurofibrillary tangles, and loss of basal forebrain cholinergic neurons in the brains of Alzheimer's disease (AD) patients may be the end result of abnormalities in lipid metabolism and peroxidation that may be caused, or exacerbated, by beta-amyloid peptide (Abeta). Apolipoprotein E (apoE) is a major apolipoprotein in the brain, mediating the transport and clearance of lipids and Abeta. ApoE-dependent dendritic and synaptic regeneration may be less efficient with apoE4, and this may result in, or unmask, age-related neurodegenerative changes. The increased risk of AD associated with apoE4 may be modulated by diet, vascular risk factors, and genetic polymorphisms that affect the function of other transporter proteins and enzymes involved in brain lipid homeostasis. Diet and apoE lipoproteins influence membrane lipid raft composition and the properties of enzymes, transporter proteins, and receptors mediating Abeta production and degradation, tau phosphorylation, glutamate and glucose uptake, and neuronal signal transduction. The level and isoform of apoE may influence whether Abeta is likely to be metabolized or deposited. This review examines the current evidence for diet, lipid homeostasis, and apoE in the pathogenesis of AD. Effects on the cholinergic system and response to cholinesterase inhibitors by APOE allele carrier status are discussed briefly.
Soluble Flt-1 Regulates Flk-1 Activation to Control Hematopoietic and Endothelial Development in an Oxygen-Responsive Manner (2008)

Vascular endothelial growth factor (VEGF) and the vascular endothelial growth factor receptors (VEGFRs) regulate the development of hemogenic mesoderm. Oxygen concentration-mediated activation of hypoxia-inducible factor targets such as VEGF may serve as the molecular link between the microenvironment and mesoderm-derived blood and endothelial cell specification. We used controlled-oxygen microenvironments to manipulate the generation of hemogenic mesoderm and its derivatives from embryonic stem cells. Our studies revealed a novel role for soluble VEGFR1 (sFlt-1) in modulating hemogenic mesoderm fate between hematopoietic and endothelial cells. Parallel measurements of VEGF and VEGFRs demonstrated that sFlt-1 regulates VEGFR2 (Flk-1) activation in both a developmental-stage-dependent and oxygen-dependent manner. Early transient Flk-1 signaling occurred in hypoxia because of low levels of sFlt-1 and high levels of VEGF, yielding VEGF-dependent generation of hemogenic mesoderm. Sustained (or delayed) Flk-1 activation preferentially yielded hemogenic mesoderm-derived endothelial cells. In contrast, delayed (sFlt-1-mediated) inhibition of Flk-1 signaling resulted in hemogenic mesoderm-derived blood progenitor cells. Ex vivo analyses of primary mouse embryo-derived cells and analysis of transgenic mice secreting a Flt-1-Fc fusion protein (Fc, the region of an antibody which is constant and binds to receptors) support a hypothesis whereby microenvironmentally regulated blood and endothelial tissue specification is enabled by the temporally variant control of the levels of Flk-1 activation. Disclosure of potential conflicts of interest is found at the end of this article.
Anti-Spoofing Extended Kalman Filter for Satellite Navigation Receiver (2007)

There is a threat to the satellite navigation receiver from satellite signal spoofing because traditional algorithms for navigation solution may not fulfill the accuracy requirements of continuous navigation with spoofing signals. Therefore, an anti- spoofing filter has been proposed for accurate navigation with the spoofing signals. In this approach, the conventional extended Kalman filter is modified using the weight matrix of robust M- estimator, which is improved to decrease the computational complexity with enough navigation accuracy. Simulation of traditional extended Kalman filter, snapshot least squares estimation and the proposed anti-spoofing M-estimator based extended Kalman filter suggests that the proposed M-estimator based extended Kalman filter could effectively eliminate the influence of spoofing signal to the navigation solution accuracy with low complexity to realize.
Sweeping changes shape a new Pacific Asia (1995)

For more about the East-West Center, see <a href="http://www.eastwestcenter.org/">http://www.eastwestcenter.org/</a>
Lowering of Microalbuminuria in Diabetic Patients by a Sympathicoplegic Agent (2001)

There is convincing evidence for a specific BP-independent effect of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers on albuminuria in glomerular disease. Because progression of glomerular disease is not consistently halted by these agents, there is a need to explore potential renoprotective effects of other drugs. Recent animal work documented that nonhypotensive doses of moxonidine, a sympathicoplegic agent, reduce albuminuria and development of glomerulosclerosis in a BP-independent manner. A randomized, crossover design was used to assess the human relevance of the experimental data in 15 normotensive, nonsmoking type 1 diabetic mellitus patients with good glycemic control (age, 37.3 +/- 6.6 yr; 9 men/6 women; duration of diabetes, 23.6 +/- 5.1 yr) with baseline urinary albumin excretion rates (AER) >20 microg/min in the run-in phase. AER was assessed in overnight timed urine collections. The patients were assigned to a 3-wk placebo and a 3-wk moxonidine (0.2 mg twice a day) period, respectively, in random order. This dose causes modest BP lowering in hypertensive individuals but does not affect BP in normotensive individuals. There was no significant effect on ambulatory BP (mean arterial pressure, 91.8 +/- 7.1 mmHg in the third week of placebo and 91.1 +/- 8.7 mm Hg on moxonidine). There was a significant (P< 0.006) difference of the treatment effects between placebo and moxonidine, respectively, on AER; median AER at the end of the placebo period was 39.8 microg/min (range, 15.9 to 117 microg/min) versus 29.0 (range, 9.03 to 85.8 microg/min) at the end of the moxonidine period. The data document an antialbuminuric effect of nonhypotensive doses of moxonidine. Diminished sympathetic traffic to the kidney is the most plausible explanation for the finding.
The role of Tec family kinases in T cell development and function (2003)

Three members of the Tec family kinases, Itk, Rlk and Tec, have been implicated in signaling downstream of the T cell receptor (TCR). The activity of these kinases in T cells has been shown to be important for the full activation of phospholipase C-gamma1 (PLC-gamma1). Disruption of Tec family signaling in Itk-/- and Rlk-/-Itk-/- mice has multiple effects on T cell development, cytokine production and T-helper cell differentiation. Furthermore, mice possessing mutations in signaling molecules upstream of PLC-gamma1, such as Src homology 2 (SH2) domain-containing phosphoprotein of 76 kDa (SLP-76), linker for activation of T cells (LAT) and Vav1, or in members of the nuclear factor for activated T cells (NFAT) family of transcription factors, which are downstream of PLC-gamma1, have been found to have similar phenotypes to Tec family-deficient mice, emphasizing the importance of this pathway in regulating T cell activation, differentiation and homeostasis.
A Comparison of Software Refactoring Tools (2002)

The principal aim of this paper is to apply the Taxonomy of Software Evolution, developed by Mens et. al [1], to position various software tools that support the activity of software refactoring as part of the evolutionary process. This taxonomy is based on the mechanisms of change and the factors that impact upon these mechanisms. The goal of this taxonomy is to position concrete tools and techniques within the domain of software evolution, so that it becomes easier to compare and combine them. In this paper, we apply the taxonomy to four tools that provide explicit support for refactoring. The tools that were considered for this detailed study are the following: Smalltalk VisualWorks 7.0 [2], Eclipse 2.0 [3], Guru (for SELF 4.0) [4] and the Together ControlCenter 6.0 [5]. After a detailed discussion and comparison of these tools, we analyse the strengths, weaknesses and limitations of the evolution taxonomy that was used.
Antigens of Human T-Lymphotropic Virus Type III/Lymphadenopathy-Associated Virus (1986)

No AccessJournal of Urology1 Aug 1986Antigens of Human T-Lymphotropic Virus Type III/Lymphadenopathy-Associated Virus M. Essex, J. Allan, P. Kanki, M.F. McLane, G. Malone, L. Kitchen, and T.H. Lee M. EssexM. Essex More articles by this author , J. AllanJ. Allan More articles by this author , P. KankiP. Kanki More articles by this author , M.F. McLaneM.F. McLane More articles by this author , G. MaloneG. Malone More articles by this author , L. KitchenL. Kitchen More articles by this author , and T.H. LeeT.H. Lee More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(17)44960-3AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "Antigens of Human T-Lymphotropic Virus Type III/Lymphadenopathy-Associated Virus." The Journal of Urology, 136(2), p. 547 © 1986 by The American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetails Volume 136Issue 2August 1986Page: 547 Advertisement Copyright & Permissions© 1986 by The American Urological Association Education and Research, Inc.MetricsAuthor Information M. Essex More articles by this author J. Allan More articles by this author P. Kanki More articles by this author M.F. McLane More articles by this author G. Malone More articles by this author L. Kitchen More articles by this author T.H. Lee More articles by this author Expand All Advertisement PDF downloadLoading ...
Olfactory deposition of inhaled nanoparticles in humans (2015)

Our results suggest that the percentage of inhaled particles that deposit in the olfactory region is lower in humans than in rats. However, olfactory dose per unit surface area is estimated to be higher in humans in the 1--7 nm size range due to the larger inhalation rate in humans. These dose estimates are important for risk assessment and dose-response studies investigating the neurotoxicity of inhaled nanoparticles.
Transcriptional silencing of Cyclooxygenase-2 by hyper-methylation of the 5' CpG island in human gastric carcinoma cells. (2001)

It has been well established that overexpression of Cyclooxygenase-2 (Cox-2) in epithelial cells inhibits apoptosis and increases the invasiveness of malignant cells, favoring tumorigenesis and metastasis. However, the molecular mechanism that regulates Cox-2 expression has not been well defined in gastric carcinoma. In this study, we examined whether the Cox-2 expression could be regulated by hyper-methylation of the Cox-2 CpG island (spanning from -590 to +186 with respect to the transcription initiation site) in human gastric carcinoma cell lines. By Southern analysis, we found that three gastric cells (SNU-601, -620, and -719) without Cox-2 expression demonstrated hyper-methylation at the Cox-2 CpG island. A detailed methylation pattern using bisulfite sequencing analysis revealed that all of the CpG sites were completely methylated in SNU-601. Treatment with demethylating agents effectively reactivated the expression of Cox-2 and restored IL-1beta sensitivity in the previously resistant SNU-601. By transient transfection experiments, we demonstrate that constitutively active Cox-2 promoter activities were exhibited even without an exogenous stimulation in SNU-601. Furthermore, when the motif of the nuclear factor for interleukin-6 expression site, the cyclic AMP response element, or both was subjected to point mutation, the constitutive luciferase activity was markedly reduced. In addition, Cox-2 promoter activity was completely blocked by in vitro methylation of all of the CpG sites in the Cox-2 promoter region with SssI (CpG) methylase in SNU-601. Taken together, these results indicate that transcriptional repression of Cox-2 is caused by hyper-methylation of the Cox-2 CpG island in gastric carcinoma cell lines.
Major Anticodon-binding Region Missing from an Archaebacterial tRNA Synthetase (1999)

The small size of the archaebacterial Methanococcus jannaschii tyrosyl-tRNA synthetase may give insights into the historical development of tRNAs and tRNA synthetases. The L-shaped tRNA has two major arms-the acceptor.TpsiC minihelix with the amino acid attachment site and the anticodon-containing arm. The structural organization of the tRNA synthetases parallels that of tRNAs. The more ancient synthetase domain contains the active site and insertions that interact with the minihelix portion of the tRNA. A second, presumably more recent, domain interacts with the anticodon-containing section of tRNA. The small size of the M. jannaschii enzyme is due to the absence of most of the second domain, including a segment thought to bind to the anticodon. Consistent with the absence of an anticodon-binding motif, a mutation of the central base of the anticodon had a relatively small effect on the aminoacylation efficiency of the M. jannaschii enzyme. In contrast, others showed earlier that the same mutation severely reduced charging by a normal-sized bacterial enzyme that has the aforementioned anticodon-binding motif. However, the M. jannaschii enzyme has a peptide insertion into its catalytic domain. This insertion is shared with all other tyrosyl-tRNA synthetases and is needed for a critical minihelix interaction. We show that the M. jannaschii enzyme is active on minihelix substrates over a wide temperature range and has preserved the same peptide-dependent minihelix specificity seen in other tyrosine enzymes. These findings are consistent with the concept that anticodon interactions of tRNA synthetases were later adaptations to the emerging synthetase-tRNA complex that was originally framed around the minihelix.