gebhart/patrepeval huggingface dataset:
Non‐Uniqueness in Seismic Refraction Analysis (2011)

Any seismic refraction analysis is essentially non‐unique. In most cases, it is difficult to obtain a true velocity model from traveltimes observed only at the ground surface. Even with a one‐dimensional two‐layer model, it is impossible to obtain true thickness and velocity without a priori knowledge that the model is two layers. Non‐uniqueness is a problem not only for the seismic refraction method but also for most geophysical methods in which underground physical property models are estimated from geophysical data observed at the ground surface. All seismic practitioners and algorithm developers must admit this fundamental problem and try to develop alternative approaches. There are many approaches to reduce the non‐uniqueness. Using priory information is the one of the most promising approach. It is well known that the result of a non‐linear least squares inversion depends highly on the initial model. For instance, in the one‐dimensional case, if we have a priori knowledge (perhaps from a downhole survey) that there are two layers, we can easily estimate a 1D true velocity function from a traveltime curve that indicates two layers. On the contrary, it is very difficult to estimate a true velocity function from the same traveltime curve if we know from other sources that they are actually three layers. Constraints during an inversion are also very important. Most of the geophysical inversions need spatial regularization in order to obtain stable results. During the inversion of the surface seismic refraction method, a constraint that velocity is increasing with depth is generally very effective. In this paper, we discuss the non‐uniqueness of the seismic refraction method and demonstrate the importance of using appropriate initial model, constraints and model parameterization.
Designed Semisynthetic Protein Inhibitors of Ub/Ubl E1 Activating Enzymes (2010)

Semisynthetic, mechanism-based protein inhibitors of ubiquitin (Ub) and ubiquitin-like modifier (Ubl) activating enzymes (E1s) have been developed to target E1-catalyzed adenylation and thioesterification of the Ub/Ubl C-terminus during the processes of protein SUMOylation and ubiquitination. The inhibitors were generated by intein-mediated expressed protein ligation using a truncated Ub/Ubl protein (SUMO residues 1-94; Ub residues 1-71) with a C-terminal thioester and synthetic tripeptides having a C-terminal adenosine analogue and an N-terminal cysteine residue. SUMO-AMSN (4a) and Ub-AMSN (4b) contain a sulfamide group as a nonhydrolyzable mimic of the phosphate group in the cognate Ub/Ubl-AMP adenylate intermediate in the first half-reaction, and these constructs selectively inhibit SUMO E1 and Ub E1, respectively, in a dose-dependent manner. SUMO-AVSN (5a) and Ub-AVSN (5b) contain an electrophilic vinyl sulfonamide designed to trap the incoming E1 cysteine nucleophile (Uba2 Cys173 in SUMO E1; Uba1 Cys593 in Ub E1) in the second half-reaction, and these constructs selectively, covalently, and stably cross-link to SUMO E1 and Ub E1, respectively, in a cysteine nucleophile-dependent manner. These inhibitors are powerful tools to probe outstanding mechanistic questions in E1 function and can also be used to study the biological functions of E1 enzymes.
Two Distinct Pathways Exist for Down-Regulation of the TCR (1998)

TCR down-regulation plays an important role in modulating T cell responses both during T cell development and in mature T cells. Down-regulation of the TCR is induced by engagement of the TCR by specific ligands and/or by activation of protein kinase C (PKC). We report here that ligand- and PKC-induced TCR down-regulation is mediated by two distinct, independent mechanisms. Ligand-induced TCR down-regulation is dependent on the protein tyrosine kinases p56(lck) and p59(fyn) but independent of PKC and the CD3gamma leucine-based (L-based) internalization motif. In contrast, PKC-induced TCR down-regulation is dependent on the CD3gamma L-based internalization motif but independent of p56(lck) and p59(fyn). Finally, our data indicate that in the absence of TCR ligation, TCR expression levels can be finely regulated via the CD3gamma L-based motif by the balance between PKC and serine/threonine protein phosphatase activities. Such a TCR ligation-independent regulation of TCR expression levels could probably be important in determining the activation threshold of T cells in their encounter with APC.
Cognitive Orthogonal Precoder for Two-Tiered Networks Deployment (2013)

In this work, the problem of cross-tier interference in a two-tiered (macro-cell and cognitive small-cells) network, under the complete spectrum sharing paradigm, is studied. A new orthogonal precoder transmit scheme for the small base stations, called multi-user Vandermonde-subspace frequency division multiplexing (MU-VFDM), is proposed. MU-VFDM allows several cognitive small base stations to coexist with legacy macro-cell receivers, by nulling the small- to macro-cell cross-tier interference, without any cooperation between the two tiers. This cleverly designed cascaded precoder structure, not only cancels the cross-tier interference, but avoids the co-tier interference for the small-cell network. The achievable sum-rate of the small-cell network, satisfying the interference cancelation requirements, is evaluated for perfect and imperfect channel state information at the transmitter. Simulation results for the cascaded MU-VFDM precoder show a comparable performance to that of state-of-the-art dirty paper coding technique, for the case of a dense cellular layout. Finally, a comparison between MU-VFDM and a standard complete spectrum separation strategy is proposed. Promising gains in terms of achievable sum-rate are shown for the two-tiered network w.r.t. the traditional bandwidth management approach.
N-phenethyl-2-phenylacetamide isolated from Xenorhabdus nematophilus induces apoptosis through caspase activation and calpain-mediated Bax cleavage in U937 cells (2003)

The present study was designed to assess the mechanism of N-phenethyl-2-phenylacetamide (NPPA), one of three new compounds isolated from Xenorhabdus nematophilus, on the induction of apoptosis in U937 cells. NPPA displayed strong inhibitory effects on cell proliferation and viability of U937 cells and induced apoptosis. Investigation of the mechanism of NPPA-induced apoptosis revealed that treatment with NPPA produced morphological features of apoptosis and DNA fragmentation. This was associated with caspase-3 activation and cleavage of poly(ADP-ribose) polymerase. U937 cells treated with NPPA demonstrated cytochrome c accumulation in the cytosol during apoptosis induction. Pretreatment of cells with the pan-caspase inhibitor (z-VAD-fmk) prevented NPPA-induced apoptosis. These results suggested that NPPA induces apoptosis through cytochrome c-dependent caspase-3 activation in U937 cells. In late stage of apoptosis, 18 kDa fragment of Bax was generated with the down-regulation of the expressions of XIAP following NPPA treatment, suggesting that the modulation of Bax and XIAP proteins plays some roles in NPPA-mediated apoptosis. Pretreatments of z-VAD-fmk and the calpain inhibitor, calpeptin, inhibited Bax cleavage. Pretreatment of z-VAD-fmk restored the expression level of XIAP, but pretreatment of calpeptin did not. These results suggest that the elevated caspase activities cleave XIAP in this experiment. And Bcl-2 over-expression attenuates NPPA-induced apoptosis by inhibiting caspase-3 activation, and subsequently inhibits calpain autolysis and Bax cleavage. These results suggested that Bax cleavage is mediated by calpain, and calpain activation may be caspase-dependent. Taken together, the apoptotic effects of NPPA may be related, in part to the caspase-3 activation, the down-regulation of XIAP, and Bax cleavage mediated by caspase-dependent calpain activation.
<i>N</i>-Methylamino acids in peptide synthesis. V. The synthesis of <i>N</i>-<i>tert</i>-butyloxycarbonyl, <i>N</i>-methylamino acids by <i>N</i>-methylation (1977)

The preparation of enantiomerically pure N-tert-butyloxycarbonyl,N-methylamino acids by N-methylation of the parent amino acid derivatives using sodium hydride and methyl iodide in tetrahydrofuran at room temperature is described for neutral amino acids including O-benzyl-protected threonine and tyrosine. Methylation of the O-benzylserine derivative under these conditions gives the N-methyldehydroalanine derivative. The β-elimination is completely suppressed, giving the corresponding N-methylserine derivative when the reaction is carried out at 5 °C. Other related data on N-methylation and N-methylamino acid derivatives are presented.
Hepatocyte Growth Factor Protects against Hypoxia/Reoxygenation-induced Apoptosis in Endothelial Cells (2004)

Hypoxia/reoxygenation causes cellular injury and death associated with a number of pathophysiological conditions, including myocardial ischemia/reperfusion injury and stroke. The cell death pathways induced by hypoxia/reoxygenation and their underlying regulatory mechanisms remain poorly understood. Recent studies have shown that hypoxia/reoxygenation can induce Bax translocation and cytochrome c release. Using murine lung endothelial cells as a model, we found that the induction of apoptosis by hypoxia/reoxygenation involved the activation of both Bax-dependent and death receptor-mediated pathways. We demonstrated the activation of the death-inducing signal complex and Bid pathway after hypoxia/reoxygenation. Hepatocyte growth factor markedly inhibited hypoxia/reoxygenation-induced endothelial cell apoptosis. The cytoprotection afforded by hepatocyte growth factor was mediated in part by the stimulation of FLICE-like inhibiting protein expression, the attenuation of death-inducing signal complex formation, and the inhibition of Bid and Bax activation. Hepatocyte growth factor also prevented cell injury and death by increasing the expression of the antiapoptotic Bcl-XL protein. The inhibition of Bid/Bax-induced cell death by hepatocyte growth factor primarily involved p38 MAPK and in part Akt-dependent pathways but not ERK1/ERK2.
A novel bifunctional metabolizable linker for the conjugation of antibodies with radionuclides (1991)

A novel heterogeneous bifunctional reagent containing an ester bond, N-[[4-(2-maleimidoethoxy)-succinyl]oxy]succinimide (MESS), was designed and synthesized for the conjugation of antibodies with the gallium-67 (67Ga) chelate of succinyldeferoxamine (SDF) via the ester bond. MESS was synthesized by the acylation of N-(2-hydroxyethyl)maleimide with succinic anhydride, followed by the activation of the resulting carboxylic acid to a succinimido ester. MESS possesses a maleimide group for protein conjugation and an active ester group for deferoxamine (DFO) coupling, and the two functional groups are linked via ester bonding. Conjugation of 67Ga-SDF with nonspecific human IgG was performed by reacting freshly thiolated IgG with the reaction product of MESS and DFO, followed by 67Ga labeling of the resulting conjugate using GaCl3 (67Ga-DFO-MESS-IgG). For comparison, 67Ga-DFO conjugated nonspecific human IgG with a nonmetabolizable linkage was synthesized under the same conjugation conditions as those for 67Ga-DFO-MESS-IgG, using a nonmetabolizable heterogenous bifunctional reagent [N-[(6-maleimidocaproyl)oxy]succinimide, EMCS] instead of MESS (67Ga-DFO-EMCS-IgG). HPLC size-exclusion chromatography of both preparations showed a single radioactivity and UV peak corresponding to the intact IgG. Generation of 67Ga-SDF from the 67Ga-DFO-MESS-IgG was demonstrated by reverse-phase HPLC analysis and cellulose acetate electrophoresis after the incubation of 67Ga-DFO-MESS-IgG in a buffered solution containing carboxyesterase. After injection of 67Ga-DFO-MESS-IgG into mice, faster radioactivity clearance from the blood and less radioactivity accumulation in the liver, kidney, and spleen was noted than when 67Ga-DFO-EMCS-IgG was injected.(ABSTRACT TRUNCATED AT 250 WORDS)
Hierarchical virtual partitioning-algorithms for virtual private networking (2002)

This paper discusses the hierarchical virtual partitioning (HVP) concept, which facilitates the sharing of a resource, such as a link, by multiple customers, each having various service classes. Calls of each service class have distinctive bandwidth requirements, arrival rates, and mean holding times, and quality of service (QoS) is in terms of call blocking probabilities. The algorithms devised provide for the desired mix of fairness, robustness, and multiplexing efficiency at each of two levels — namely, at the customer level and at the level of the various services of each customer. The HVP scheme relies on nominal allocations of capacities to each customer and service, as well as priorities in the call admission process implemented by dynamic trunk reservations. The paper gives an approximate method of analysis based on fixed-point equations. In addition, a reward/penalty paradigm is devised to reflect the issues in virtual private networking, and the performance of our algorithms is compared to the optimal solution. The results show that the HVP scheme is fair, efficient, and robust.
Elevated Interleukin-6 and G-CSF in Human Pancreatic Cancer Cell Conditioned Medium Suppress Dendritic Cell Differentiation and Activation (2007)

Although dendritic cell (DC) function is impaired in pancreatic cancer patients, the underlying mechanisms are unknown. This study analyzed the soluble factors released by pancreatic cancer cells responsible for inhibiting DC differentiation and activation. Medium conditioned by a highly metastatic human pancreatic cancer cell line BxPC-3 [BxPC-3 conditioned medium (BxCM)] was mainly used for the study. Both CD34+ hematopoietic progenitor cell-derived and CD14+ monocyte-derived immature DCs and mature DCs (mDCs) were inhibited by BxCM. Allostimulation of CD4+ and CD8+ T cells by BxCM-treated mDCs was inefficient and resulted in production of lower levels of Th1 and Th2 cytokines. Antigen-specific T-cell activation capability was also reduced in BxCM-treated mDCs. Addition of exogenous interleukin-6 (IL-6) and granulocyte colony-stimulating factor (G-CSF), which were present in high amounts in BxCM, mimicked the inhibitory effect of BxCM on DC differentiation and maturation. IL-6 was able to suppress DC differentiation and G-CSF mainly acted on the suppressing allostimulatory capacity of DCs. In addition, pancreatic cancer patient sera were able to inhibit DC differentiation of CD14+ monocytes obtained from healthy donors. Depleting IL-6 or G-CSF from BxCM could reverse the DC-inhibitory properties of BxCM. Furthermore, BxCM, IL-6, or G-CSF led to the activation of signal transducer and activator of transcription 3 (STAT3) in CD14+ monocytes to different degrees. Blocking BxCM-induced STAT3 activation also reversed the inhibitory effect of BxCM on DC differentiation. Therefore, IL-6 and G-CSF in BxCM represent two main factors responsible for suppression of DC differentiation, maturation, and antigen presentation, and this suppression of DC functions may be due to the aberrant activation of STAT3 by BxCM.
First-line medicines in the treatment of hypertension (2005)

The goal of therapy in uncomplicated hypertension is to reduce cardiovascular risk by lowering the patient's blood pressure. If non-drug treatment is ineffective, the choice of drug treatment is determined by its safety and efficacy. When safety and efficacy are equal the lowest cost drug should be prescribed. For most patients the first choice drug is a low-dose thiazide diuretic.
Design Tradeoffs and Hardware Architecture for Real-Time Iterative MIMO Detection using Sphere Decoding and LDPC Coding (2008)

We explore the performance and hardware complexity tradeoffs associated with performing iterative multiple- input multiple-output (MIMO) detection using a sphere decoder and a low-density parity-check (LDPC) decoder. Iterations are performed both within the LDPC decoder as well as via an outer iteration loop through which refined soft information is fed back from the LDPC decoder to a MIMO detector. A hardware architecture and associated implementation results on Xilinx Virtex-5 field programmable gate array for a 4 x 4 QPSK MIMO system are presented. The system offers a performance improvement of approximately 1 dB over systems without the outer iteration loop, and provides an information bit throughput that ranges from 60 to 300 megabits per second when a length 1944 rate 1/2 LDPC code is used.
Trimerization of the Amino Propeptide of Type IIA Procollagen Using a 14-Amino Acid Sequence Derived from the Coiled-Coil Neck Domain of Surfactant Protein D (2002)

The folding of a collagen triple helix usually requires the presence of additional sequences that contribute to the association and correct alignment of the collagen chains. We recently reported that the C-terminal neck and lectin domains of a collagenous C-type lectin, rat pulmonary surfactant protein D (SP-D), are sufficient to drive the trimerization of a heterologous type IIA procollagen amino propeptide sequence. However, the conformation of the resulting trimeric IIA propeptide and the specific contributions of the SP-D sequence to trimerization were not elucidated. In the present study, we show that trimerization of the fusion protein is associated with correct folding of the collagen helix within the IIA propeptide domain (as assessed by circular dichroism) and that the constituent chains are hydroxylated. Chemical cross-linking and analytical ultracentrifugation showed that the IIA amino-propeptide retains its trimeric configuration even after proteolytic removal of the SP-D domains. By contrast, IIA amino-propeptides synthesized without fusion to the neck or lectin domains are assembled exclusively as monomers. To localize the trimerization sequence, mutant chimeric cDNA constructs were designed containing premature termination codons within the coiled-coil neck domain. A short, 14-amino acid sequence corresponding to the first two heptad repeats of the neck domain was sufficient to drive the trimeric association of the IIA amino-propeptide alpha-chains. However, deletion of the collagen domain resulted in the secretion of monomers. These studies demonstrate that two heptad repeats are sufficient for trimeric association of the propeptide but indicate that cooperative interactions between the coiled-coil and collagen domains are required for the formation of a stable helix.
ChemInform Abstract: REARRANGEMENTS OF HETEROCYCLES. VIII. MESOIONIC SIX‐MEMBERED‐RING HETEROCYCLES. XII. KETENOID REARRANGEMENTS OF MESOIONIC PYRIMIDINES (1979)

Abstract Die Pyridopyrimidin‐Mesoionen (I) lagern sich bei 260‐300°C über die resonanzstabilisierten Ketene (II)/(III) in die Chinolone (IV) um.
Combined cystic teratoma and hepatoblastoma of the liver: Probable divergent differentiation of an uncommitted hepatic precursor cell (1993)

The tumor was considered most likely to originate from divergent differentiation of a single uncommitted liver precursor cell.
Engines of Creation (1986)

Part 1 The foundations of foresight: engines of construction the principles of change predicting and projecting. Part 2 Profiles of the possible: engines of abundance thinking machines the world beyond Earth engines of healing long life in an open world a door to the future the limits to growth. Part 3 Dangers and hopes: engines of destruction strategies and survival finding the facts the network of knowledge world enough and time.
Expression of A2B adenosine receptors in human lymphocytes: Their role in T cell activation (1999)

Extracellular adenosine has a key role in the development and function of the cells of the immune system. Many of the adenosine actions seem to be mediated by specific surface receptors positively coupled to adenylate cyclase: A2A and A2B. Despite the fact that A2A receptors (A2ARs) can be easily studied due to the availability of the specific agonist CGS21680, a pharmacological and physiological characterization of adenosine A2B receptors (A2BRs) in lymphocytes has not been possible due to the lack of suitable reagents. Here we report the generation and characterization of a polyclonal antipeptide antibody raised against the third extracellular loop of the A2BR human clone which is useful for immunocytochemical studies. This antibody has permitted the detection of A2BR+ cells in lymphocyte samples isolated from human peripheral blood. The pharmacology of cAMP-producing compounds is consistent with the presence of functional A2BRs but not of A2A receptors in these human cells. The percentage of A2BR-expressing cells was similar in the CD4(+) or CD8(+) T cell subpopulations. Interestingly activation signals delivered by either phytohemagglutinin or anti-T cell receptor/CD3 complex antibodies led to a significant increase in both the percentage of cells expressing the receptor and the intensity of the labeling. These receptors are functional since interleukin-2 production in these cells is reduced by NECA but not by R-PIA or CGS21680. These results show that A2BR expression is regulated in T cell activation and suggest that the role of adenosine in lymphocyte deactivation is mediated by A2BRs.
Characterization of genes in the <i>ASYMMETRIC LEAVES2/LATERAL ORGAN BOUNDARIES</i> (<i>AS2/LOB</i>) family in <i>Arabidopsis thaliana</i>, and functional and molecular comparisons between <i>AS2</i> and other family members (2009)

The ASYMMETRIC LEAVES2 (AS2) gene is required for the generation of the flat and symmetrical shape of the leaf lamina in Arabidopsis. AS2 encodes a plant-specific protein with an AS2/LATERAL ORGAN BOUNDARIES (AS2/LOB) domain that includes a cysteine repeat, a conserved single glycine residue and a leucine-zipper-like sequence in its amino-terminal half. The Arabidopsis genome contains 42 genes, including AS2, that encode proteins with an AS2/LOB domain in their amino-terminal halves, and these genes constitute the AS2/LOB gene family. In the present study, we cloned and characterized cDNAs that covered the putative coding regions of all members of this family, and investigated patterns of transcription systematically in Arabidopsis plants. Comparisons among amino acid sequences that had been deduced from the cloned cDNAs revealed eight groups of genes, with two or three members each, and high degrees of identity among entire amino acid sequences, suggesting that some members of the AS2/LOB family might have redundant function(s). Moreover, no member of the family exhibited significant similarity, in terms of the deduced amino acid sequence of the carboxy-terminal half, to AS2. Results of domain swapping between AS2 and other members of the family showed that the AS2/LOB domain of AS2 cannot be functionally replaced by those of other members of the family, and that only a few dissimilarities among respective amino acid residues of the AS2/LOB domain of AS2 and those of other members are important for the specific functions of AS2.