gebhart/patrepeval huggingface dataset:
Hydrolysis of diadenosine 5',5''-P',P''-triphosphate (Ap3A) by porcine aortic endothelial cells. (1986)

Diadenosine triphosphate is present in platelet-dense granules and released quantitatively on platelet aggregation. We have found that intact porcine aortic endothelial cells can efficiently hydrolyze extracellular diadenosine triphosphate. The products of diadenosine triphosphate hydrolysis are adenosine monophosphate and adenosine diphosphate. Adenosine diphosphate is a potent stimulus of platelet aggregation. Since platelet-dense granules contain high concentrations of adenosine triphosphate and adenosine diphosphate, we examined endothelial cell hydrolysis of a mixture of diadenosine triphosphate and adenosine triphosphate. We find that the presence of adenosine triphosphate severely inhibits the hydrolysis of diadenosine triphosphate. Thus, although endothelial cells can rapidly clear extracellular diadenosine triphosphate, during platelet aggregation the hydrolysis of diadenosine triphosphate may be slow due to the presence of high concentrations of other adenine nucleotides. This phenomenon may be important physiologically if, as current evidence implies, diadenosine triphosphate is involved in the maintenance of hemostasis.
Regulation of lnvasive Potential of Human Prostate Cancer Cell Lines by Hepatocyte Growth Factor (1998)

HGF plays an important role in the invasion and metastasis of the DU145 cell line through a paracrine mechanism mediated by the c-metreceptor. In the PC-3 cell line, the lack of downstream signal transduction after the c-met receptor is suggested.
Networks for the Separation of Sources that are Superimposed and Delayed (1991)

We have created new networks to unmix signals which have been mixed either with time delays or via filtering. We first show that a subset of the Herault-Jutten learning rules fulfills a principle of minimum output power. We then apply this principle to extensions of the Herault-Jutten network which have delays in the feedback path. Our networks perform well on real speech and music signals that have been mixed using time delays or filtering. 1
Review: Carteggio Verdi-Ricordi, 1880-1881, by Pierluigi Petrobelli, Marisa Di Gregorio Casati, and Carlo Matteo Mossa (1990)

Book Review| April 01 1990 Review: Carteggio Verdi-Ricordi, 1880-1881, by Pierluigi Petrobelli, Marisa Di Gregorio Casati, and Carlo Matteo Mossa Carteggio Verdi-Ricordi, 1880-1881Pierluigi PetrobelliMarisa Di Gregorio CasatiCarlo Matteo Mossa Piero Weiss Piero Weiss Search for other works by this author on: This Site PubMed Google Scholar 19th-Century Music (1990) 13 (3): 268–272. https://doi.org/10.2307/746453 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation Piero Weiss; Review: Carteggio Verdi-Ricordi, 1880-1881, by Pierluigi Petrobelli, Marisa Di Gregorio Casati, and Carlo Matteo Mossa. 19th-Century Music 1 April 1990; 13 (3): 268–272. doi: https://doi.org/10.2307/746453 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All Content19th-Century Music Search This content is only available via PDF. Copyright 1990 The Regents of the University of California Article PDF first page preview Close Modal You do not currently have access to this content.
Diagnosis and management of the antiphospholipid syndrome (2010)

#### Summary points

Antiphospholipid syndrome was first described 27 years ago in patients with systemic lupus erythematosus (SLE) and positive anticardiolipin antibodies, who presented with a clotting syndrome that affected arteries and veins.1 Female patients had a high risk of recurrent miscarriage and late fetal loss. The international classification criteria for this syndrome used today are based on those initial clinical observations.2

The syndrome is under-recognised and underdiagnosed and can have devastating consequences if untreated, mainly because of uncontrolled thrombosis. Difficulties in diagnosis are compounded by a lack of standardisation of diagnostic tests. Early recognition is crucial, because treatment can reduce mortality and morbidity in relatively young people who often present with diseases such as stroke, myocardial infarction, and deep vein thrombosis.

Because of its variable clinical presentation, patients with antiphospholipid syndrome present to a variety of medical practitioners. Here, we introduce this complicated and intriguing syndrome, and provide basic guiding principles for the recognition, diagnosis, and management of affected patients.

#### Sources and selection criteria

We searched the following databases for evidence from systematic reviews, clinical trials, and prospective cohort studies: PubMed (1949 to January 2010), Embase (1980 to January 2010), Web of Science (1945 to January 2010), Cochrane Library (1990 to January 2010), CINAHL (1982 to January 2010), and Academic Search Premier (1865 to January 2010). All relevant keyword variations were used. In general, the …
Hormones and immunologic capacity. I. Effect of heterologous anti-growth hormone (ASTH) antiserum on thymus and peripheral lymphatic tissue in mice. Induction of a wasting syndrome. (1968)

Summary The relationship between somatotropic hormone (STH) and the development of lymphoid organs was investigated. Repeated injections of rabbit anti-Raben-type bovine somatotropic hormone (ASTH) globulins into 2- and 3-week-old Charles River mice produced body growth inhibition, thymic atrophy, involution of the lymphoid tissue in the spleen and a wasting syndrome. Similar treatment with normal rabbit serum (NRS) globulins produced a normal splenic cellular reaction and no wasting syndrome was observed. The same treatment in adult male mice produced similar effects on the lymphoid organs but no wasting syndrome. The simultaneous administration of STH to mice treated with ASTH globulins completely reversed the effects of ASTH globulins. Histologic examination revealed that the ASTH treatment resulted in disappearance of small lymphocytes in the cortex of the thymus, in the perifollicular mantles of the germinal centers and in thymus-dependent areas in the spleen. These results are discussed in relation to the hypothesis that wasting disease in neonatally thymectomized mice derives from disruption of a critical hypophysis-thymus axis in the perinatal age. A role for STH and other hormones for differentiation of antibody-producing cells is proposed.
Towards Cloud-based Asynchronous Elasticity for Iterative HPC Applications (2015)

Elasticity is one of the key features of cloud computing. It allows applications to dynamically scale computing and storage resources, avoiding over- and under-provisioning. In high performance computing (HPC), initiatives are normally modeled to handle bag-of-tasks or key-value applications through a load balancer and a loosely-coupled set of virtual machine (VM) instances. In the joint-field of Message Passing Interface (MPI) and tightly-coupled HPC applications, we observe the need of rewriting source codes, previous knowledge of the application and/or stop-reconfigure-and-go approaches to address cloud elasticity. Besides, there are problems related to how profit this new feature in the HPC scope, since in MPI 2.0 applications the programmers need to handle communicators by themselves, and a sudden consolidation of a VM, together with a process, can compromise the entire execution. To address these issues, we propose a PaaS-based elasticity model, named AutoElastic. It acts as a middleware that allows iterative HPC applications to take advantage of dynamic resource provisioning of cloud infrastructures without any major modification. AutoElastic provides a new concept denoted here as asynchronous elasticity, i.e., it provides a framework to allow applications to either increase or decrease their computing resources without blocking the current execution. The feasibility of AutoElastic is demonstrated through a prototype that runs a CPU-bound numerical integration application on top of the OpenNebula middleware. The results showed the saving of about 3 min at each scaling out operations, emphasizing the contribution of the new concept on contexts where seconds are precious.
Expression profiling of a hemopoietic cell survival transcriptome implicates osteopontin as a functional prognostic factor in AML (2009)

Deregulated cell survival programs are a classic hallmark of cancer. We have previously identified a serine residue (Ser585) in the betac subunit of the granulocyte-macrophage colony-stimulating factor receptor that selectively and independently promotes cell survival. We now show that Ser585 phosphorylation is constitutive in 20 (87%) of 23 acute myeloid leukemia (AML) patient samples, indicating that this survival-only pathway is frequently deregulated in leukemia. We performed a global expression screen to identify gene targets of this survival pathway and report a 138-gene betac Ser585-regulated transcriptome. Pathway analysis defines a gene network enriched for PI3-kinase target genes and a cluster of genes involved in cancer and cell survival. We show that one such gene, osteopontin (OPN), is a functionally relevant target of the Ser585-survival pathway as shown by siRNA-mediated knockdown of OPN expression that induces cell death in both AML blasts and CD34(+)CD38(-)CD123(+) leukemic progenitors. Increased expression of OPN at diagnosis is associated with poor prognosis with multivariate analysis indicating that it is an independent predictor of overall patient survival in normal karyotype AML (n = 60; HR = 2.2; P = .01). These results delineate a novel cytokine-regulated Ser585/PI3-kinase signaling network that is deregulated in AML and identify OPN as a potential prognostic and therapeutic target.
Operating system support for multimedia applications (1994)

This paper briefly describes a resource reservation operating system abstraction that supports real-time multimedia applications alongside non-real-time applications. This approach facilitates predictable behavior in applications while still maintaining the flexibility required by multimedia applications in a dynamic system. The accompanying video tape shows how to reserve processor capacity for multimedia applications and how to control processor usage even when real-time and non-real-time applications compete for access to system servers.
Tyrphostin AG 1478 preferentially inhibits human glioma cells expressing truncated rather than wild-type epidermal growth factor receptors. (1996)

The effects of a new epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, tyrphostin AG 1478, were tested on three related human glioma cell lines: U87MG, which expressed endogenous wild-type (wt) EGFR, and two retrovirally infected U87MG cell populations which over-expressed either wt (U87MG.wtEGFR) or truncated EGFR (U87MG. delta EGFR). Although AG 1478 inhibited cell growth, DNA synthesis, EGFR tyrosine kinase activity, and receptor autophosphorylation of each cell line in a dose-dependent manner, it was significantly more potent in U87MG. delta EGFR cells than in the other two cell lines. The increased inhibitory response of U87MG. delta EGFR cells was due to a greater sensitivity of the constitutively autophosphorylated Mr 140,000 and 155,000 delta EGFR species to AG 1478. These results suggest that AG 1478 is a relatively specific inhibitor of the delta EGFR, and this finding may have important therapeutic implications since the delta EGFR occurs frequently in glioblastomas and in breast, lung, and ovarian cancers.
Release of C-type natriuretic peptide accounts for the biological activity of endothelium-derived hyperpolarizing factor (2003)

Endothelial cells in most vascular beds release a factor that hyperpolarizes the underlying smooth muscle, produces vasodilatation, and plays a fundamental role in the regulation of local blood flow and systemic blood pressure. The identity of this endothelium-derived hyperpolarizing factor (EDHF), which is neither NO nor prostacyclin, remains obscure. Herein, we demonstrate that in mesenteric resistance arteries, release of C-type natriuretic peptide (CNP) accounts for the biological activity of EDHF. Both produce identical smooth muscle hyperpolarizations that are attenuated in the presence of high [K(+)], the G(i) G protein (G(i)) inhibitor pertussis toxin, the G protein-gated inwardly rectifying K(+) channel inhibitor tertiapin, and a combination of Ba(2+) (inwardly rectifying K(+) channel blocker) plus ouabain (Na(+)K(+)-ATPase inhibitor). Responses to EDHF and CNP are unaffected by the natriuretic peptide receptor (NPR)-AB antagonist HS-142-1, but mimicked by the selective NPR-C agonist, cANF(4-23). EDHF-dependent relaxation is concomitant with liberation of endothelial CNP; in the presence of the myoendothelial gap-junction inhibitor 18alpha-glycyrrhetinic acid or after endothelial denudation, CNP release and EDHF responses are profoundly suppressed. These data demonstrate that acetylcholine-evoked release of endothelial CNP activates NPR-C on vascular smooth muscle that via a G(i) coupling promotes Ba(2+)ouabain-sensitive hyperpolarization. Thus, we have revealed the identity of EDHF and established a pivotal role for endothelial-derived CNP in the regulation of vascular tone and blood flow.
A cell‐surface antigen which is present in the ganglioside fraction and shared by human melanomas (1982)

We have raised a hybridoma, 4.2, which forms an IgM antibody to an antigen expressed on cultivated cells from most human melanomas, more infrequently on cells from other human tumors, and very weakly on cultivated fibroblasts, T cells and B cells. The antigen can be detected in biopsy material of human melanoma and, in smaller amounts, in fresh samples of normal human lung and kidney. Preliminary biochemical characterization indicates that it is associated with the ganglioside fraction. We feel that the antigen (referred to as 4.2) has a sufficient degree of tumor specificity to be rated as a human melanoma-associated antigen.
Active synovial matrix metalloproteinase-2 is associated with radiographic erosions in patients with early synovitis (2000)

MMP-2 and MMP-9 are thought to play an important role in the evolution of joint erosions in patients with an inflammatory arthritis. Most studies have concentrated on the contribution of MMP-9 to the synovitis, because synovial fluid and serum MMP-9 levels are markedly increased in inflammatory arthropathies. Previously reported serum levels of MMP-9 have varied widely. In the present sample of patients with synovitis of recent onset, serum MMP-9 levels were elevated in only 21%. Moreover, these elevations were not specific for RA, the tissue expression of MMP-9 was focal, and the levels of MMP-9 activity were not well correlated with early erosions. Although serum MMP-2 levels were not of prognostic value, high synovial tissue levels of MMP-2 activity were significantly correlated with the presence of early erosions. This may reflect augmented activation of MMP-2 by the relatively high levels of MMP-14 and low levels of TIMP-2 seen in these tissues. We were able to localize the components of this trimolecular complex to the synovial lining layer in consecutive tissue sections, a finding that is consistent with their colocalization. In conclusion, we have provided evidence that active MMP-2 complexes are detectable in the inflamed RA synovium and may be involved in the development of early bony erosions. These results suggest that strategies to inhibit the activation of MMP-2 may have the potential for retarding or preventing early erosions in patients with inflammatory arthritis.
Electrostatics of nanosystems: Application to microtubules and the ribosome (2001)

Evaluation of the electrostatic properties of biomolecules has become a standard practice in molecular biophysics. Foremost among the models used to elucidate the electrostatic potential is the Poisson-Boltzmann equation; however, existing methods for solving this equation have limited the scope of accurate electrostatic calculations to relatively small biomolecular systems. Here we present the application of numerical methods to enable the trivially parallel solution of the Poisson-Boltzmann equation for supramolecular structures that are orders of magnitude larger in size. As a demonstration of this methodology, electrostatic potentials have been calculated for large microtubule and ribosome structures. The results point to the likely role of electrostatics in a variety of activities of these structures.
Production of matrix metalloproteinases and tissue inhibitor of metalloproteinases-1 by human brain tumors (1994)

The role of matrix metalloproteinases (MMP's) and their inhibitor, tissue inhibitor of metalloproteinases-1 (TIMP-1), in human brain tumor invasion was investigated. Gelatinolytic activity was assayed via gelatin zymography, and four MMP's (MMP-1, MMP-2, MMP-3, and MMP-9) and TIMP-1 were immunolocalized in human brain tumors and in normal brain tissues using monoclonal antibodies. The tissue was surgically removed from 44 patients: glioblastoma (five cases), anaplastic astrocytoma (six cases), astrocytoma (four cases), metastatic tumor (six cases), neurinoma (10 cases), meningioma (10 cases), and normal brain tissue (three cases). Glioblastomas, anaplastic astrocytomas, and metastatic tumors showed high gelatinolytic activity and positive immunostaining for MMP's; TIMP-1 was also expressed in these tumors, but some tumor cells were negative for the antibody. Astrocytomas had low gelatinolytic activity and the tumor cells showed no immunoreactivity for MMP's and TIMP-1. Although neurinomas and meningiomas had only moderate proteinase activity and exhibited positive immunoreactivity for MMP-9, intense expression of TIMP-1 was simultaneously observed in these tumor cells. These findings suggest that MMP's play an important role in human brain tumor invasion, probably due to an imbalance between the production of MMP's and TIMP-1 by the tumor cells.
A model of muscle-tendon function in human walking (2009)

In this paper, we study the mechanical behavior of leg muscles and tendons during human walking in order to motivate the design of economical robotic legs. We hypothesize that quasi-passive, series-elastic clutch units spanning the knee joint in a musculoskeletal arrangement can capture the dominant mechanical behaviors of the human knee in level-ground walking. Since the mechanical work done by the knee joint throughout a level-ground self-selected-speed walking cycle is negative, and since there is no element capable of dissipating mechanical energy in the musculoskeletal model, biarticular elements would necessarily need to transfer energy from the knee joint to hip and/or ankle joints. This mechanism would reduce the necessary actuator work and improve the mechanical economy of a human-like walking robot. As a preliminary evaluation of these hypotheses, we vary model parameters, or spring constants and clutch engagement times, using an optimization scheme that minimizes ankle and hip actuator positive work while still maintaining human-like knee mechanics. For model evaluation, kinetic and kinematic gait data were employed from one study participant walking across a level-ground surface at a self-selected gait speed. With this under-actuated leg model, we find good agreement between the model's quasi-passive knee torque and experimental knee values, suggesting that a knee actuator is not necessary for level-ground robotic ambulation at self-selected gait speeds.
Contact-induced neutrophil activation by platelets in human cell suspensions and whole blood (1992)

Platelet-dependent activation of polymorphonuclear neutrophils (PMNL) was investigated with a lumi-aggregometer in heparinized whole blood and platelet-PMNL suspensions. The lumi-aggregometer allowed us to simultaneously monitor increases in impedance or light transmission as consequences of platelet aggregation and luminol-enhanced chemiluminescence (CL) as a measure of the oxidative burst in PMNL. Aggregation and platelet-PMNL contacts were also checked by light and electron microscopy. In whole blood, adenosine diphosphate (ADP) and the thromboxane A2 mimetic U 46619 induced the aggregation (increase in impedance) and the CL, which were both suppressed by EDTA, arginyl-glycyl-aspartyl-serine (RGDS) peptide, and the absence of stirring. In contrast, FMLP caused only CL that was unaffected by EDTA, RGDS peptide, and nonstirring. Similar observations were obtained with mixed suspensions containing washed platelets and PMNL at their physiologic concentrations. ADP, U 46619, and thrombin induced both aggregation (increase in light transmission) and CL, whereas FMLP caused CL but only very weak aggregation. Exogenous fibrinogen strongly enhanced the effects of ADP and U 46619. Iloprost, EDTA, RGDS peptide, red blood cell (RBC) ghosts, and nonstirring inhibited the effects induced by the platelet agonists, but were ineffective on the CL induced by FMLP. Treatment of platelets with aspirin did not affect the CL of PMNL induced by platelets. Microscopic examination, the requirements of stirring, Ca2+, and fibrinogen, and the inhibitory effects of RGDS peptide and RBC ghosts show that stimulated platelets activate PMNL in a contact-dependent manner that depends on fibrinogen binding. This was confirmed by the immunochemical demonstration of fibrinogen (but not of fibronectin) in the contact spaces between activated platelets and PMNL. Because supernatants and lysates of resting or thrombin-stimulated platelets did not induce the CL of PMNL, soluble agonists did not appear to be involved. Nonstimulated washed platelets also caused CL of PMNL that required stirring and Ca2+ and was inhibited by RBC ghosts. No CL occurred in unstimulated stirred whole blood, suggesting that a preactivation of platelets during the preparation may be responsible for the effects of unstimulated washed platelets. The results show that platelets provide a strong stimulus for PMNL that requires intercellular contact. Fibrinogen exposure on the platelet surface seems to be necessary for the activation of PMNL by stimulated platelets.
Analysis of pp60c-src protein kinase activity in human tumor cell lines and tissues. (1986)

We have evaluated the level of pp60c-src protein kinase activity in a variety of human tumor tissues and human tumor cell lines, and have estimated the abundance of the c-src protein in several of these tissues and cell lines. All cell lines derived from tumors of neuroectodermal origin that express a neural phenotype were found to possess c-src molecules with high levels of tyrosine-specific protein kinase activity. In contrast, cell lines derived from tumors of neuroectodermal origin that do not express neural characteristics, such as glioblastomas and melanomas, were found to have pp60c-src molecules with low levels of protein kinase activity. A similar pattern was observed when we analyzed the activity of c-src molecules extracted directly from corresponding tumor tissues. Analysis of human tumor cell lines derived from tissues other than those of neuroectodermal origin revealed that pp60c-src protein kinase activity was low in most cases. Exceptions to this observation were all rhabdomyosarcoma, osteogenic sarcoma, Ewing's sarcoma, and colon carcinoma lines tested. Comparison of pp60c-src kinase activity in normal skeletal muscle and rhabdomyosarcoma tissue and in normal breast tissue and breast adenocarcinoma tissue revealed that pp60c-src kinase activity was specifically elevated in the tumor tissues in both cases. However, the amount of pp60c-src protein in both normal and tumor tissues was found to be similar. These observations suggest that increases in the specific activity of the pp60c-src phosphotransferase in some rhabdomyosarcomas and breast carcinomas may be a characteristic acquired during the malignant transformation of the cells that is retained in cell lines established from these tumors.