gebhart/patrepeval huggingface dataset:
CDMA: Access and Switching: For Terrestrial and Satellite Networks (2001)

From the Publisher:
Taking a close look at an integral part of next generation wireless communications, this book presents SS/CDMA system architecture (Satellite Switched Code Division Multiple Access) and its various communications services. TDMA-based satellite communications as well as related satellite systems and services are also examined in detail.
A sulfatide receptor distinct from L‐selectin is involved in lymphocyte activation (1997)

Sulfatide induces leukocyte activation, which is thought to be mediated via L-selectin. Here we demonstrate that lymphocytes express a receptor for sulfatide distinct from L-selectin and that this receptor is involved in sulfatide-induced cell activation. While cell surface L-selectin expression was abolished by phorbol 12-myristate 13-acetate (PMA), lymphocytes retained the ability to bind sulfatide in liquid phase as well as in immobilized solid phase. The novel sulfatide receptor obtained from PMA-treated lymphocytes showed a molecular size of 65 kDa. Stimulation through this receptor triggered cytosolic free Ca2+ elevation and intercellular aggregation.
IPSIM: SystemC 3.0 enhancements for communication refinement [SoC design] (2003)

Refinement is a key methodology for SoC design. The proposed IPSIM design environment, based on a C++ modeling library developed on top of SystemC 3.0, supports an object-oriented design methodology, separates IP modules into behavior and communication components, and further establishes two inter-module communication layers. The message box layer includes generic and system-specific communication, while the driver layer implements higher level user-defined communications as illustrated in a design example.
Antivascular endothelial growth factor receptor (fetal liver kinase 1) monoclonal antibody inhibits tumor angiogenesis and growth of several mouse and human tumors. (1999)

Tumor angiogenesis is mediated by tumor-secreted angiogenic growth factors that interact with their surface receptors expressed on endothelial cells. Vascular endothelial growth factor (VEGF) and its receptor [fetal liver kinase 1 (Flk-1)/kinase insert domain-containing receptor] play an important role in vascular permeability and tumor angiogenesis. Previously, we reported on the development of anti-Flk-1 and antikinase insert domain-containing receptor monoclonal antibodies (mAbs) that potently inhibit VEGF binding and receptor signaling. Here, we report the effect of anti-Flk-1 mAb (DC101) on angiogenesis and tumor growth. Angiogenesis in vivo was examined using a growth factor supplemented (basic fibroblast growth factor + VEGF) Matrigel plug and an alginate-encapsulated tumor cell (Lewis lung) assay in C57BL/6 mice. Systemic administration of DC101 every 3 days markedly reduced neovascularization of Matrigel plugs and tumor-containing alginate beads in a dose-dependent fashion. Histological analysis of Matrigel plugs showed reduced numbers of endothelial cells and vessel structures. Several mouse tumors and human tumor xenografts in athymic mice were used to examine the effect of anti-Flk-1 mAb treatment on tumor angiogenesis and growth. Anti-Flk-1 mAb treatment significantly suppressed the growth of primary murine Lewis lung, 4T1 mammary, and B16 melanoma tumors and growth of Lewis lung metastases. DC101 also completely inhibited the growth of established epidermoid, glioblastoma, pancreatic, and renal human tumor xenografts. Histological examination of anti-Flk-1 mAb-treated tumors showed evidence of decreased microvessel density, tumor cell apoptosis, decreased tumor cell proliferation, and extensive tumor necrosis. These findings support the conclusion that anti-Flk-1 mAb treatment inhibits tumor growth by suppression of tumor-induced neovascularization and demonstrate the potential for therapeutic application of anti-VEGF receptor antibody in the treatment of angiogenesis-dependent tumors.
Highly Efficient Enantioselective Synthesis of Optically Active Carboxylic Acids by Ru(OCOCH3)2[(S)-H8-BINAP] (1996)

In the presence of a catalytic amount of Ru(OCOCH3)2[(S)-H8-BINAP] [H8-BINAP = 2,2‘-bis(diphenylphosphino)-5,5‘,6,6‘,7,7‘,8,8‘-octahydro-1,1‘-binaphthyl], the asymmetric hydrogenation of α,β- and β,γ-unsaturated carboxylic acids afforded the corresponding saturated carboxylic acids in higher enantiomeric excesses and at faster reaction rates than those using the Ru(OCOCH3)2[(R)-BINAP] catalyst [BINAP = 2,2‘-bis(diphenylphosphino)-1,1‘-binaphthyl]. The hydrogenation of (E)-2-alkyl-2-alkenoic acids by the H8-BINAP catalyst system produced saturated acids in 95−97% ee. 2-Methylcinnamic acid was treated with H8-BINAP−Ru(II) complex as a catalyst to yield a hydrogenated product in much higher ee than that produced by BINAP−Ru(II) (89 and 30% ee, respectively). This homogeneous catalysis using H8-BINAP−Ru(II) established a promising synthetic route to (S)-ibuprofen in up to 97% ee. Asymmetric hydrogenation of β-disubstituted acrylic acids also proceeded smoothly with good enantioselectivities (70−93% ee). In addition, the hydrogenation of trisubstituted acrylic acids (up to 88% ee) was investigated. Hydrogen pressure effect on the sense and level of enantioselection was shown to be substrate dependent. The difference between the H8-BINAP− and BINAP−Ru(II) complexes was also discussed.
Lung Cancer Cell Lines Harboring MET Gene Amplification Are Dependent on Met for Growth and Survival (2007)

Recent clinical successes of small-molecule epidermal growth factor receptor (EGFR) inhibitors in treating advanced non-small cell lung cancer (NSCLC) have raised hopes that the identification of other deregulated growth factor pathways in NSCLC will lead to new therapeutic options for NSCLC. Met, the receptor for hepatocyte growth factor, has been implicated in growth, invasion, and metastasis of many tumors including NSCLC. To assess the functional role for Met in NSCLC, we evaluated a panel of nine lung cancer cell lines for Met gene amplification, Met expression, Met pathway activation, and the sensitivity of the cell lines to short hairpin RNA (shRNA)-mediated Met knockdown. Two cell lines, EBC-1 and H1993, showed significant Met gene amplification and overexpressed Met receptors which were constitutively phosphorylated. The other seven lines did not exhibit Met amplification and expressed much lower levels of Met, which was phosphorylated only on addition of hepatocyte growth factor. We also found a strong up-regulation of tyrosine phosphorylation in beta-catenin and p120/delta-catenin in the Met-amplified EBC-1 and H1993 cell lines. ShRNA-mediated Met knockdown induced significant growth inhibition, G(1)-S arrest, and apoptosis in EBC-1 and H1993 cells, whereas it had little or no effect on the cell lines that do not have Met amplification. These results strongly suggest that Met amplification identifies a subset of NSCLC likely to respond to new molecular therapies targeting Met.
Molecular cloning and expression of Bacillus licheniformis beta-lactamase gene in Escherichia coli and Bacillus subtilis. (1981)

The chromosomal beta-lactamase (penicillinase, penP) gene from Bacillus licheniformis 749/C has been cloned in Escherichia coli. The locations of the target sites for various restriction enzymes on the 4.2-kilobase EcoRI fragment were determined. By matching the restriction mapping data with the potential nucleotide sequences of the penP gene deduced from known protein sequence, we established the exact position of the penP gene on the fragment. A bifunctional plasmid vector carrying the penP gene, plasmid pOG2165, was constructed which directs the synthesis of the heterologous beta-lactamase in both E. coli and Bacillus subtilis hosts. The protein synthesized in E. coli and B. subtilis is similar in size to the processed beta-lactamase made in B. licheniformis. Furthermore, the beta-lactamase made in B. subtilis is efficiently secreted by the host into the culture medium, indicating that B. subtilis is capable of carrying out the post-translational proteolytic cleavage(s) to convert the membrane-bound precursor enzyme into the soluble extracellular form.
Principal Neighborhood Dictionaries for Nonlocal Means Image Denoising (2009)

We present an in-depth analysis of a variation of the nonlocal means (NLM) image denoising algorithm that uses principal component analysis (PCA) to achieve a higher accuracy while reducing computational load. Image neighborhood vectors are first projected onto a lower dimensional subspace using PCA. The dimensionality of this subspace is chosen automatically using parallel analysis. Consequently, neighborhood similarity weights for denoising are computed using distances in this subspace rather than the full space. The resulting algorithm is referred to as principal neighborhood dictionary (PND) nonlocal means. We investigate PND's accuracy as a function of the dimensionality of the projection subspace and demonstrate that denoising accuracy peaks at a relatively low number of dimensions. The accuracy of NLM and PND are also examined with respect to the choice of image neighborhood and search window sizes. Finally, we present a quantitative and qualitative comparison of PND versus NLM and another image neighborhood PCA-based state-of-the-art image denoising algorithm.
In Vitro Production of Erythropoietin by Kidneys Perfused With a Serum-free Solution (1974)

Abstract Normal rabbits exposed to 0.4 atmospheric pressure for 3 hr will generate about 40-60 U of erythropoietin during a subsequent 3-hr period. If the kidneys were removed from 3-hr hypoxic animals, washed carefully, and perfused for 3 hr by recirculation with a serum-tissue culture mixture, each kidney generated about 14 U of erythropoietin in vitro. Perfusion of normal kidneys did not result in the production of erythropoietin, and only small amounts were generated if the perfusate contained Puromycin. Three-hour hypoxic kidneys perfused for 3 hr with a serum-free tissue culture medium were found to generate about 8 U of erythropoietin per kidney and similar kidneys perfused with saline about 1 U. These results indicate that erythropoietin is synthesized by kidney tissue and not produced by enzymatic activation of a plasma substrate.
The Cardiac β-Adrenoceptor–Mediated Signaling Pathway and Its Alterations in Hypertensive Heart Disease (1997)

Hypertension-induced cardiac hypertrophy is a predictor of the development of cardiac failure. It is unknown which cellular markers contribute to the progression from compensated hypertrophy to failure. In heart failure, several signal transduction defects leading to adenylate cyclase desensitization have been demonstrated, such as beta-adrenoceptor downregulation, increase of inhibitory G protein expression, and uncoupling of beta-adrenergic receptors, presumably by an increase of receptor kinase activity. In hypertensive heart disease, most studies have been performed in rat models of hypertension. As in heart failure, heterologous adenylyl cyclase desensitization occurs. The mechanisms are often different between the heterogeneous models for acquired and genetic hypertension, but Gi protein alterations and beta-adrenoceptor downregulation have been observed frequently. The underlying mechanism for desensitization is most likely a sympathetic activation in established hypertension rather than genetic alterations of signal transduction proteins. The data available suggest that beta-adrenergic desensitization could represent a mechanism that contributes to the progression from hypertrophy to failure. The key question remains whether those hypertensive patients who develop heart failure are more prone to beta-adrenergic desensitization or whether early intervention to reduce sympathetic activity is more effective in preventing or delaying the transition from compensated hypertrophy to overt failure.
Activated ketone based inhibitors of human renin (1993)

Application of the concept of activated ketones to the design of novel and potent transition-state analog inhibitors of the aspartyl protease renin is described. Three different classes of peptidic activated ketones were synthesized: 1,1,1-trifluoromethyl ketones, alpha-keto esters, and alpha-diketones. The corresponding alcohols were also evaluated as renin inhibitors in each series. While the trifluoromethyl alcohol 12 (I50 = 4000 nM) was equipotent to the simple methyl alcohol 7 (I50 = 3200 nM), the structurally similar alpha-hydroxy esters (32 and 30, I50's = 5.3 and 4.7 nM, respectively) and alpha-hydroxy ketones (41 and 42, I50 = 23 and 15 nM, respectively) were 150-300-fold more active. The hydrating capability of the activated ketone functionality was important for intrinsic potency in the case of trifluoromethyl ketones, as illustrated by the significantly better activity of trifluoromethyl ketone 13 (I50 = 250 nM) compared to its alcohol analog 12 (I50 = 4000 nM). It was however unimportant for the alpha-keto ester (20 and 31, I50 = 15 and 4.1 nM, respectively) and alpha-diketone (43 and 44, I50 = 52 and 28 nM, respectively) based inhibitors, since their activity was essentially similar to that of the corresponding alcohols. These results collectively suggest that, whereas the trifluoromethyl ketones derive their renin inhibitory potency primarily from their ability to become hydrated, this is not a critical feature for the activity of alpha-dicarbonyl-based inhibitors. The alpha-keto ester and alpha-diketone based renin inhibitors benefit predominantly from the hydrophobic and/or H-bonding type binding interactions of the neighboring ester or acyl group itself, rather than the ability of this group to deactivate the adjacent ketone group and thereby make it susceptible to hydration.
Detection of clonal B cells in microdissected reactive lymphoproliferations: possible diagnostic pitfalls in PCR analysis of immunoglobulin heavy chain gene rearrangement. (1999)

These results confirm that PCR based IgH gene rearrangement analysis is a sensitive and specific method for demonstrating B cell clonality in whole paraffin wax embedded sections. However, oligoclonal and monoclonal rearrangement patterns are regularly encountered in small tissue fragments from otherwise unremarkable reactive lymphoproliferations, possibly because of preferential priming or detection of local B cell clones. Data from clonal analysis of small, microdissected or lymphocyte poor samples must be evaluated critically. It is recommended that analyses should be run in parallel on at least two tissue specimens. Only reproducible bands present in more than one sample should be considered to be suggestive of neoplasia.
Mometasone furoate is a less specific glucocorticoid than fluticasone propionate (2002)

Fluticasone propionate (FP) and mometasone furoate (MF) are potent synthetic corticosteroids that are widely used as anti-inflammatory agents to treat respiratory diseases. As part of the assessment of the potential for side-effects associated with their use, their activities, not only at the glucocorticoid receptor (GR) but also at the other members of the steroid nuclear receptor family, have been compared. Cell-based functional systems were established to measure different aspects of GR function, as well as the activity at all the other steroid nuclear receptors. The effects of MF and FP on the GR were potent and indistinguishable. Neither corticosteroid showed any activity at the oestrogen receptor, while both were weak antagonists of the androgen receptor. FP was a relatively weak agonist of the progesterone receptor but MF was a very potent agonist of the progesterone receptor, giving activity at similar concentrations to those that stimulate the GR (concentration generating 50% maximal effect (EC50)=50 pM). Moreover, while FP was a weak antagonist of the mineralocorticoid receptor (concentration generating 50% maximal inhibitory effect=80 nM), MF displayed potent partial agonist activity (EC50=3 nM, 30%). Mometasone furoate is considerably less specific for the glucocorticoid receptor than fluticasone propionate, showing significant activity at other nuclear steroid receptors.
High expression of B‐cell receptor inducible gene BIC in all subtypes of Hodgkin lymphoma (2003)

In a search for genes specifically expressed in Reed-Sternberg (RS) cells of Hodgkin lymphoma (HL), we applied the serial analysis of gene expression (SAGE) technique on the HL-derived cell line DEV. Genes highly expressed in DEV were subjected to an RT-PCR analysis to confirm the SAGE results. For one of the genes, a high expression was observed in DEV and other HL-derived cell lines but not in non-Hodgkin lymphoma (NHL)-derived cell lines and normal controls, suggesting an HL-specific expression. This gene corresponds to the human BIC gene, a member of the noncoding mRNA-like molecules. RNA in situ hybridization (ISH) indicated an exclusive nucleolar localization of BIC transcripts in all RS cells in 91% of HL cases, including nodular lymphocyte predominance (NLP) HL and classical HL. Analyses of normal human tissues revealed BIC transcripts in only a small number of CD20-positive B-cells in lymph node and tonsil tissue, albeit at a much lower level compared to that of RS cells. BIC RT-PCR in the Burkitt lymphoma-derived cell line Ramos demonstrated a significant up-regulation upon cross-linking of the B-cell receptor (BcR). IkappaBalpha-mediated blocking of NF-kappaB translocation in Ramos did not effect the up-regulation of BIC expression upon BcR triggering, suggesting that activation of NF-kappaB is not involved in regulation of BIC expression. In summary, our data show that expression of BIC is specific for RS cells of HL. In normal tissue, BIC is expressed weakly in a minority of germinal center B cells. Expression of BIC can be modified/influenced by BcR triggering, indicating that BIC might play a role in the selection of B cells.
Use of RNA Fluorescence In Situ Hybridization in the Prenatal Molecular Diagnosis of Myotonic Dystrophy Type I (2006)

Nuclear foci, and therefore the DM1 mutation they are caused by, can be detected efficiently on interphase nuclei of trophoblast cells with RNA-FISH when the CTG expansion is >200 copies.
Retinol Dehydrogenase (RDH12) Protects Photoreceptors from Light-induced Degeneration in Mice (2006)

RDH12 has been suggested to be one of the retinol dehydrogenases (RDH) involved in the vitamin A recycling system (visual cycle) in the eye. Loss of function mutations in the RDH12 gene were recently reported to be associated with autosomal recessive childhood-onset severe retinal dystrophy. Here we show that RDH12 localizes to the photoreceptor inner segments and that deletion of this gene in mice slows the kinetics of all-trans-retinal reduction, delaying dark adaptation. However, accelerated 11-cis-retinal production and increased susceptibility to light-induced photoreceptor apoptosis were also observed in Rdh12(-/-) mice, suggesting that RDH12 plays a unique, nonredundant role in the photoreceptor inner segments to regulate the flow of retinoids in the eye. Thus, severe visual impairments of individuals with null mutations in RDH12 may likely be caused by light damage(1).
Recurrent Continuous Translation Models (2013)

We introduce a class of probabilistic continuous translation models called Recurrent Continuous Translation Models that are purely based on continuous representations for words, phrases and sentences and do not rely on alignments or phrasal translation units.The models have a generation and a conditioning aspect.The generation of the translation is modelled with a target Recurrent Language Model, whereas the conditioning on the source sentence is modelled with a Convolutional Sentence Model.Through various experiments, we show first that our models obtain a perplexity with respect to gold translations that is > 43% lower than that of stateof-the-art alignment-based translation models.Secondly, we show that they are remarkably sensitive to the word order, syntax, and meaning of the source sentence despite lacking alignments.Finally we show that they match a state-of-the-art system when rescoring n-best lists of translations.
Luminescent Quantum Dot-Adaptor Protein-Antibody Conjugates for Use in Fluoroimmunoassays (2002)

A method for the preparation and characterization of bioinorganic conjugates made with highly luminescent semiconductor CdSe–ZnS core-shell quantum dots (QDs) and antibodies for use in fluoroimmunoassays is presented. The conjugation strategy employs two routes: 1. Use of an engineered molecular adaptor protein, attached to the QDs via electrostatic/hydrophobic self-assembly, to link the inorganic fluorophore with antibodies, and 2. use of avidin, also electrostatically self-assembled onto the nanocrystal surface, which allows QD conjugation to biotinylated antibodies via avidin–biotin binding scheme. With this approach, the average number of antibodies conjugated to a single QD can be varied. In addition, we have developed a simple purification strategy based on mixed composition conjugates of the molecular adaptor and a second “inert” two-domain fusion protein that allows the use of affinity chromatography. QD/adaptor-antibody conjugates were successfully employed in fluoroimmunoassays for the detection of small molecule analytes, 2,4,6-trinitrobenzene (TNB) and hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX). We also demonstrate the use of QD/avidin-antibody conjugates for fluoroimmunoassays using a model protein system.
EARLY AND LATE MECHANISMS OF INCREASED VASCULAR PERMEABILITY FOLLOWING EXPERIMENTAL CEREBRAL INFARCTION (1979)

Cerebral infarction was produced in rats by a combination of transient unilateral common carotid artery occlusion and systemic hypoxia. Horseradish peroxidase (HRP) and Evans blue were given 5 minutes prior to sacrifice to assess the integrity of the blood-brain barrier (BBB) at 1 minute, 30 minutes, and 2 hours following the ischemic insult. There was immediate permeability to HRP in the early (1 minute and 30 minutes) post-ischemic period, whereas, Evans blue was not seen until the late (1.5 to 2 hours) post-ischemic period. Ultrastructural examination showed two routes of barrier permeability to HRP. In the early post-ischemic period, HRP was transported by pinocytosis through endothelial cells in areas of brain containing ischemic neurons. In the late post-ischemic period, HRP diffusely leaked into the brain through the necrotic walls of vessels in areas of infarction. In contrast to previous reports, these results show that the BBB becomes permeable immediately following hypoxia-ischemia. In addition, this study shows that BBB permeability to HRP during cerebral ischemia occurs through two mechanisms: an active, energy-requiring permeability through enhanced pinocytosis within endothelial cells and a passive leakage of protein tracers through necrotic vessel walls.
Amantadine reduces levodopa‐induced dyskinesias in parkinsonian monkeys (1998)

The antidyskinetic potential of the glutamate NMDA receptor channel blocker amantadine was evaluated in four levodopa-primed parkinsonian monkeys using two different regimens (1.25 or 2.5 mg/kg administered subcutaneously twice daily for 3-6 days). When administered with a relatively low dose of levodopa, amantadine produced a near-total suppression of choreiform dyskinesias and a substantial reduction in dystonic dyskinesias at the expense of a significant reduction in antiparkinsonian response. With a high dose of levodopa, amantadine had a smaller but still significant effect on dyskinesias without altering the antiparkinsonian response. These results lend support to the view that glutamate receptor-mediated mechanisms contribute to levodopa-induced dyskinesias. They also suggest that amantadine could alleviate such complications in parkinsonian patients, especially with careful dose optimization.