gebhart/patrepeval huggingface dataset:
Physicochemical Properties of Montmorillonite Interlayered with Cationic Oxyaluminum Pillars (1983)

Abstract By ion exchanging expandable clay minerals with large, cationic oxyaluminum polymers, “pillars” were introduced that permanently prop open the clay layers. On the basis of thermal, infrared spectroscopic, adsorption, and X-ray powder diffraction (XRD) analysis, the interlayering of commercial sodium bentonite with aluminum chlorohydroxide, [Al 13 O 4 (OH) 24 (H 2 O) 12 ] +7 , polymers appears to have produced an expanded clay with a surface area of 200–300 m 2 /g. The pillared product contained both Brönsted and Lewis acid sites. XRD and differential scanning calorimetry measurements indicated that the micropore structure of this interlayered clay is stable to 540°C. Between 540° and 760°C, the pillared clay collapsed with a corresponding decrease in surface area (to 55 m 2 /g) and catalytic cracking activity for a Kuwait gas oil having a 260°-426°C boiling range.
Generating efficient protocol code from an abstract specification (1996)

A protocol compiler takes as input an abstract specification of a protocol and generates an implementation of that protocol. Protocol compilers usually produce inefficient code both in terms of code speed and code size. In this paper, we show that the combination of two techniques makes it possible to build protocol compilers that generate efficient code. These techniques are i) the use of a compiler that generates from the specification a unique tree-shaped automaton (rather than multiple independent automata), and ii) the use of optimization techniques applied at the automaton level, i.e. on the branches of the trees.We have developed a protocol compiler that uses both these techniques. The compiler takes as input a protocol specification written in the synchronous language Esterel. The specification is compiled into a unique automaton by the Esterel front end compiler. The automaton is then optimized and converted into C code by our protocol optimizer called HIPPCO. HIPPCO improves code performance and reduces code size by simultaneously optimizing the performance of the common path and optimizing the size of the uncommon path. We evaluate the gain expected with our approach on a real-life example, namely a working subset of the TCP protocol generated from an Esterel specification. We compare the protocol code generated with our approach to that derived from the standard BSD TCP implementation. The results are very encouraging. HIPPCO-generated code executes up to 25 % fewer instructions than the BSD code for input packet processing while maintaining comparable code size.
Enhanced Intracellular siRNA Delivery using Bioreducible Lipid‐Like Nanoparticles (2014)

A new library of lipid-like nanoparticles (lipidoids) comprising disulfide bond is developed for siRNA delivery. Bioreducible lipidoids deliver siRNA with greater efficiency than nonbioreducible lipidoids with similar chemical structures. A siRNA release investigation, as well as an intracellular siRNA trafficking study, reveals that the degradation of bioreducible lipidoid in a strongly reductive intracellular environment boosts siRNA release and enhances siRNA gene knockdown efficiency.
Linear algebraic methods applied to intensity modulated radiation therapy (2001)

Methods of linear algebra are applied to the choice of beam weights for intensity modulated radiation therapy (IMRT). It is shown that the physical interpretation of the beam weights, target homogeneity and ratios of deposited energy can be given in terms of matrix equations and quadratic forms. The methodology of fitting using linear algebra as applied to IMRT is examined. Results are compared with IMRT plans that had been prepared using a commercially available IMRT treatment planning system and previously delivered to cancer patients.
Selective Effects of PD-1 on Akt and Ras Pathways Regulate Molecular Components of the Cell Cycle and Inhibit T Cell Proliferation (2012)

The receptor programmed death 1 (PD-1) inhibits T cell proliferation and plays a critical role in suppressing self-reactive T cells, and it also compromises antiviral and antitumor responses. To determine how PD-1 signaling inhibits T cell proliferation, we used human CD4(+) T cells to examine the effects of PD-1 signaling on the molecular control of the cell cycle. The ubiquitin ligase SCF(Skp2) degrades p27(kip1), an inhibitor of cyclin-dependent kinases (Cdks), and PD-1 blocked cell cycle progression through the G(1) phase by suppressing transcription of SKP2, which encodes a component of this ubiquitin ligase. Thus, in T cells stimulated through PD-1, Cdks were not activated, and two critical Cdk substrates were not phosphorylated. Activation of PD-1 inhibited phosphorylation of the retinoblastoma gene product, which suppressed expression of E2F target genes. PD-1 also inhibited phosphorylation of the transcription factor Smad3, which increased its activity. These events induced additional inhibitory checkpoints in the cell cycle by increasing the abundance of the G(1) phase inhibitor p15(INK4) and repressing the Cdk-activating phosphatase Cdc25A. PD-1 suppressed SKP2 transcription by inhibiting phosphoinositide 3-kinase-Akt and Ras-mitogen-activated and extracellular signal-regulated kinase kinase (MEK)-extracellular signal-regulated kinase (ERK) signaling. Exposure of cells to the proliferation-promoting cytokine interleukin-2 restored activation of MEK-ERK signaling, but not Akt signaling, and only partially restored SKP2 expression. Thus, PD-1 blocks cell cycle progression and proliferation of T lymphocytes by affecting multiple regulators of the cell cycle.
Cooking up T cells (2005)

IFN- and that macrophages contained IL-6 and TNF- in situ. These findings are notable for 2 reasons. First, they confirm the idea that despite a variety of clinical and etiologic features, patients with hemophagocytic syndromes have similar disease pathophysiology. Second, this study directly demonstrates which cell type is producing each cytokine.
Evaluation of the feasibility of a far-infrared laser based on intersubband transitions in GaAs quantum wells (1989)

The threshold current and quantum efficiency are calculated for a far-infrared injection laser, based on intersubband transitions in GaAs single quantum wells. By considering the balance of gain against the free carrier and transverse optical (TO) phonon absorption, and the intersubband transition time in the intermediate to the far infrared, the wavelength dependence of the threshold current is calculated. We find that for the wavelength range 50–120 μm, the required threshold currents are the lowest and have reasonable values of 103–104 A/cm2. The threshold quantum efficiency in that range is expected to be ∼10−4.
Soluble PD-1 is Associated with Aberrant Regulation of T Cells Activation in Aplastic Anemia (2009)

Engagement of the membrane program death-1 (PD-1) receptor by its ligands suppresses T cell proliferation and cytokine production. Aberrant over-expression of costimulatory molecules, including PD-1, has been associated with persistent activation of self-reactive T cells in autoimmune diseases. However, the mechanism underlying the dysfunction of PD-1 in the regulation of T-cell activation in such diseases remains unclear. Here, we report the overexpression of CD4(+) and CD8(+) T cell PD-1 and elevated serum levels of soluble PD-1 in aplastic anemia (AA) patients. Detailed characterization of soluble PD-1 revealed that it corresponded to an alternative splice variant PD-1Deltaex3, which lacks the transmembrane domain but has a soluble extracellular domain of the PD-1 molecule. In a further study, PD-1 fusion protein displayed the ability of increasing the proliferation of T cells in vitro, which suggested that soluble PD-1 might serve as an autoimmune antibody to block the function of membrane-bound PD-1 on T cells and lead to aberrant T cell proliferation. Our study revealed a novel pathogenic pathway in which the function of overexpressed PD-1 to restrict over-self-reaction is counteracted by the excessive production of soluble PD-1.
New developments in bone marrow transplantation (1991)

A better understanding of the immunobiology after transplantation and of the available recombinant cytokines that enhance hematopoietic reconstitution following autologous and allogeneic bone marrow transplantation is likely to result in safer application of bone marrow transplantation. Residual tumor cells escaping chemotherapy or chemoradiotherapy given in the course of autologous and allogeneic bone marrow transplantation are still a barrier to complete eradication of malignancy. Recent experiments in animal models of human disease suggest that minimal residual disease can be controlled by an innovative therapy consisting of the administration of cytokines such as recombinant human interleukin-2 and interferon-alpha. Moreover, graft versus leukemia-like effects are induced in conjunction with autologous and allogeneic bone marrow transplantation by administration of allogeneic immunocompetent lymphocytes and recombinant interleukin-2 following bone marrow transplantation and especially by combined administration of allogeneic lymphocytes and recombinant interleukin-2. Similar approaches are currently being investigated in humans with encouraging preliminary results. Overall, our data suggest that eradication of the last tumor cell is neither feasible nor necessary for achieving operational cure. Control of minimal residual disease by activation of anticancer effector cells today seems closer than ever and we are optimistic that further advances in immunotherapy will be applicable to clinical practice in the near future.
Hepatocyte growth factor induction of macrophage chemoattractant protein‐1 and osteophyte‐inducing factors in osteoarthritis (2007)

In osteoarthritis (OA), hepatocyte growth factor (HGF) is supposed to play a role in cartilage repair. Because the development of osteophytes is a major characteristic of OA and thought to be part of an attempted repair process, the purpose of this study was to determine whether HGF may be involved in osteophyte formation. HGF levels in synovial fluids from 41 patients assessed by enzyme immunosorbant assay were correlated with disease severity and osteophyte formation, evaluated by anteroposterior weight-bearing radiographs. Detection of HGF, c-Met, and CD68 in cartilage and synovial tissues was assessed by immunohistochemistry. Effects of HGF on the secretion of TGF-beta1 and BMP-2 by chondrocytes, fibroblast-like synovial cells (FLS), and macrophages as well as HGF-induced secretion of MCP-1 by FLS and chondrocytes were determined by ELISA. HGF was detected in all synovial fluids and concentrations correlated highly with disease severity and osteophyte formation (p < 0.001). Immunohistochemistry revealed weak synovial staining for HGF, whereas increasing numbers of HGF expressing chondrocytes were detected depending on disease severity. In addition, an increased number of macrophages in synovial specimens was observed, which was likewise severity dependent. In a series of subsequent in vitro studies, HGF remarkable induced MCP-1 secretion by FLS in a dose-dependent manner. No effect on TGF-beta1 and BMP-2 secretion by FLS and chondrocytes was evident upon HGF stimulation, whereas secretion of these growth factors by PMA-differentiated THP-1 cells was significantly increased by HGF. The results indicate that HGF may facilitate osteophyte development by promoting MCP-1-mediated entry of monocytes/macrophages into the OA-affected joint and/or by stimulating macrophage-derived growth factors.
Oxygen regulation in Salmonella typhimurium (1985)

Regulation by oxygen of the peptidase T (pepT) locus of Salmonella typhimurium was studied by measuring beta-galactosidase levels in strains containing a pepT::Mu d1(Apr lac) operon fusion. beta-Galactosidase was induced in anaerobic cultures and late-exponential and stationary-phase aerated cultures. Peptidase T activity also was induced under these growth conditions. pepT+ but not pepT strains will utilize as amino acid sources the tripeptides Leu-Leu-Leu and Leu-Gly-Gly only when grown anaerobically. Mutations at two loci, oxrA and oxrB (oxygen regulation) prevent induction of the pepT locus. The oxrA locus is homologous to the fnr locus of Escherichia coli. We have isolated 12 independent Mu d1 insertions (oxd::Mu d1, oxygen dependent) that show induction of beta-galactosidase in anaerobic cultures and stationary-phase aerated cultures. These insertions fall into nine classes based on map location. All of the oxd::Mu d1 insertions are regulated by oxrA and oxrB and therefore define a global regulon that responds to oxygen limitation.
Modulation of cytokine expression in mouse dendritic cell clones (1994)

Dendritic cells (DC) play an essential role in the induction of primary immune responses; however, very little information is available on cytokine production by DC. Here we determined the cytokine gene expression profile of two immortalized DC clones, CB1 and D2SC/1, both generated from mouse spleen but differing in their activation requirements. Among the cytokines tested, only transforming growth factor-beta 1 was transcribed constitutively, but its production was detected only in D2SC/1 cells after treatment with granulocyte/macrophage colony-stimulating factor (GM-CSF). GM-CSF also promoted transcription and synthesis of interleukin (IL)-1 beta in CB1 cells that need pretreatment with GM-CSF to present major histocompatibility complex class II-restricted antigens efficiently in vitro. Lipopolysaccharide (LPS) up-regulated gene expression and induced release of tumor necrosis factor-alpha in both DC clones. In addition, LPS induced transcription of IL-1 alpha and both gene expression and synthesis of IL-1 beta in D2SC/1 cells. Interferon-gamma was ineffective in inducing cytokine gene expression, although it augmented the antigen-presentation capacity of DC, IL-4, IL-10 and IL-12 mRNA were not induced by any of the tested stimuli. The results suggest that DC have a limited cytokine gene expression pattern compared to macrophages and are heterogenous in some functional properties.
Silicon-based phase shifters for high figure of merit in optical modulation (2016)

This paper focuses on latest progress in experimental and theoretical studies on silicon-based carrier-depletion PNjunction phase shifters in terms of high modulation efficiency for energy-efficient photonic networks of high transmission capacity. Modulation efficiency of rib-waveguide phase shifters having various PN-junction configuration are characterized with respect to DC figure of merit defined for phase shifters using carrier-plasma dispersion as the physical principle of refractive-index modulation. In addition, RF drive voltage required for 10-Gb/s on-off keying is characterized for rib-waveguide phase shifters including lateral and vertical PN-junction configurations.
Phase I Trial of Recombinant Immunotoxin Anti-Tac(Fv)-PE38 (LMB-2) in Patients With Hematologic Malignancies (2000)

LMB-2 has clinical activity in CD25(+) hematologic malignancies and is relatively nonimmunogenic. It is the first recombinant immunotoxin to induce major responses in cancer. LMB-2 and similar agents that target other cancer antigens merit further clinical development.
Cadmium-Induced Toxicity in Rat Primary Mid-brain Neuroglia Cultures: Role of Oxidative Stress from Microglia (2007)

This study examined the role of oxidative stress in neurotoxic effects of cadmium chloride (Cd) in rat primary mid-brain neuron-glia cultures. Cd accumulated in neuron-glia cultures and produced cytotoxicity in a dose-dependent manner, with IC(50) of 2.5microM 24 h after exposure. (3)H-dopamine uptake into neuron-glia cultures was decreased 7 days after Cd exposure, with IC(50) of 0.9microM, indicative of the sensitivity of dopaminergic neurons to Cd toxicity. To investigate the role of microglia in Cd-induced toxicity to neurons, microglia-enriched cultures were prepared. Cd significantly increased intracellular reactive oxygen species production in microglia-enriched cultures, as evidenced by threefold increases in 2',7'-dichlorofluorescein signals. Using 5,5-dimethyl-1-pyrroline N-oxide as a spin-trapping agent, Cd increased electron spin resonance signals by 3.5-fold in microglia-enriched cultures. Cd-induced oxidative stress to microglia-enriched cultures was further evidenced by activation of redox-sensitive transcription factor nuclear factor kappa B and activator protein-1 (AP-1), and the increased expression of oxidative stress-related genes, such as metallothionein, heme oxygenase-1, glutathione S-transferase pi, and metal transport protein-1, as determined by gel-shift assays and real-time reverse transcription-PCR, respectively, in microglia-enriched cultures. In conclusion, Cd is toxic to neuron-glia cultures, and the oxidative stress from microglia may play important roles in Cd-induced damage to dopaminergic neurons.
Effect Of Interleukin-1 Receptor Antagonist And Soluble Tumor Necrosis Factor Receptor In Animal Models Of Infection (1995)

Intracisternal or intraarticular inoculation of rabbit recombinant interleukin (IL)-1 beta and rabbit tumor necrosis factor-alpha combined with IL-1 receptor antagonist (IL-1RA) and soluble tumor necrosis factor receptor (sTNFR), respectively, produced significantly less inflammation in rabbits than after inoculation of these cytokines alone. In contrast, when Haemophilus influenzae type b (Hib) or Hib lipooligosaccharide (LOS) was given intraarticularly with IL-1RA, sTNFR, or the combination, there was no significant or consistent modulation of synovial inflammation and cartilage proteoglycan degradation. In the experimental meningitis model, IL-1RA and sTNFR did not significantly reduce the meningeal inflammatory response associated with intracisternal inoculation of Hib LOS. These data indicate that specific cytokine inhibitors (sTNFR and IL-1RA) may not be effective in modulating inflammation induced by a broad inflammatory stimulus such as gram-negative bacteria or their products and suggest caution in using them to treat these infectious conditions in humans.
Anti-tumor effect of α-pinene on human hepatoma cell lines through inducing G2/M cell cycle arrest (2015)

Pine needle oil from crude extract of pine needles has been used as an anti-cancer agent in Traditional Chinese Medicine. The α-pinene is a natural compound isolated from pine needle oil which has been shown anti-cancer activity. In previous study, we found that pine needle oil exhibited significant inhibitory effect on hepatoma carcinoma BEL-7402 cells. In this study, we investigate the inhibition of α-pinene on hepatoma carcinoma BEL-7402 cells in vitro and in vivo and further explore the mechanism. The results show that liver cancer cell growth was inhibited obviously with inhibitory rate of 79.3% in vitro and 69.1% in vivo, Chk1 and Chk2 levels were upregulated, CyclinB, CDC25 and CDK1 levels were downregulated.
New 4 + 1 radical annulations. A formal total synthesis of (.+-.)-camptothecin (1992)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTNew 4 + 1 radical annulations. A formal total synthesis of (.+-.)-camptothecinDennis P. Curran and Hui LiuCite this: J. Am. Chem. Soc. 1992, 114, 14, 5863–5864Publication Date (Print):July 1, 1992Publication History Published online1 May 2002Published inissue 1 July 1992https://pubs.acs.org/doi/10.1021/ja00040a060https://doi.org/10.1021/ja00040a060research-articleACS PublicationsRequest reuse permissionsArticle Views1713Altmetric-Citations158LEARN 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
Global Die Ultra-Thin Silicon for Backside Diagnostics and Circuit Edit (2009)

Abstract For more than 10 years, silicon thinning techniques have been relegated to an art form of mere necessity to enable complex optical probing and circuit edit analysis. Silicon thinning is a fundamental aspect of diagnostic analysis and while it is well-understood that limitations in the area of silicon thinning can severely limit high-quality diagnostic results, poor thinning results have generally been accepted as standard environmental operating conditions with which optical probe and circuit edit engineers must cope. Presented here is a scientific approach to thinning silicon to enable predictable high-precision, high-quality results. Remaining silicon thickness (RST) has been debated throughout the years because it was uncertain how much thinning was excessive. Primary perceived limitations included mechanical constraints (package / die warping) and post-thinning thermal control. Adding to the complexity of the discussion has been the fact that RST has been largely uncertain because analysis usually involved determining how much silicon was removed rather than how much silicon remains. All of these challenges have been overcome. A novel process has been developed to ultra-thin bulk Si to as low as 10um remaining Si thickness, eliminating the need for the Laser Chemical Etcher for circuit edit and improving optical emission probing considerably. This sample preparation process has been used on Intel Core2 Duo products with a success rate of 98%. Post FIB unit testing is a critical step in this debug process. A technique was developed to calibrate the change in thermal resistivity of the ultra-thin unit such that it will remain within 100ps of its original FMax performance in 90% of tests.
Low Levels of Extrahepatic Nonmacrophage ApoE Inhibit Atherosclerosis Without Correcting Hypercholesterolemia in ApoE-Deficient Mice (2000)

The prevention of atherosclerosis by apolipoprotein E (apoE) is generally attributed to the removal of plasma lipoprotein remnant particles. We developed transgenic apoE-knockout mice expressing apoE specifically in the adrenal gland and found that only 3% of the wild-type plasma level of apoE was sufficient to normalize plasma cholesterol levels in the apoE-deficient mouse. As expected, mice expressing apoE at levels that correct hypercholesterolemia had almost no cholesteryl ester deposition in their aortas. In contrast, their nontransgenic siblings had significant atherosclerosis. Unexpectedly, we found that atherosclerosis was also reduced in 2 transgenic lines expressing too little apoE (<1% to 2% of wild type) to correct their hypercholesterolemia. Gel exclusion chromatographic profiles of plasma lipoproteins and the size distributions of lipoproteins with density <1.063 (low density and very low density lipoproteins), as determined by dynamic laser light scattering, were the same in mice expressing <2 microg/mL plasma apoE and their nontransgenic littermates. We conclude that the antiatherogenic action of low levels of plasma apoE is not due to the clearance of remnant lipoproteins. Thus, low levels of apoE provided systemically, but not made in the liver or in macrophages, can block atherogenesis in the vascular wall independently of normalizing the plasma concentration of atherogenic remnant lipoprotein particles.