gebhart/patrepeval huggingface dataset:
Long-term fate of bypass grafts: the Coronary Artery Surgery Study (CASS) and Montreal Heart Institute experiences. (1985)

Both the Veterans Administration Cooperative Study and the European Coronary Surgery Study have provided only brief accounts of graft patency rates in their surgically treated patients. In the Veterans Administration Cooperative Study, at an average of 1 year after operation, 69% of the grafts were patent among 208 patients; 88% of patients had at least one patent graft, and 58% had all grafts patent. In the European Coronary Surgery Study, angiographic examination of the grafts was performed within 9 months of operation in 84 patients, and showed a patency rate of 90%; in 223 patients, the examination was performed at between 9 and 18 months, and showed a 77% patency rate. In the Coronary Artery Surgery Study (CASS), graft patency rates were evaluated within 60 days of operation in 129 patients, a median of 18 months after operation in 121 patients, and a median of 5 years after operation in 197 patients. Cumulative vein graft patency (per distal anastomosis) was 90% early, 82% at 18 months, and 82% at 5 years. At least one graft anastomosis was patent early in 97% of patients, at 18 months in 96% of patients, and at 5 years in 97% of patients; all graft anastomoses were patent early in 81% of patients, at 18 months in 70% of patients, and at 5 years in 67% of patients. The incidence of vein graft stenosis of 50% or more was 10% at 18 months and 8% at 5 years after operation. The excellent results reported in CASS were associated with marked improvement in quality of life and excellent survival 5 years after operation in surgically treated patients, as previously reported.(ABSTRACT TRUNCATED AT 250 WORDS)
The CD40/CD40L costimulatory pathway in inflammatory bowel disease (2004)

The complexity of inflammatory bowel disease (IBD) is well recognised at both the clinical and therapeutic levels. Even more complex however appears to be the unravelling of its aetiology and pathogenesis where environmental, genetic, bacterial, and immune factors come together to generate the clinical entities we recognise as Crohn’s disease (CD) and ulcerative colitis (UC).1,2 When facing a complex problem, a wise approach is to select first its most obvious part, break it down into its various components, and then try to understand the contribution of each component to the problem. IBD is a chronic inflammatory process and therefore inflammation is the fundamental issue, the mechanism responsible for the tissue damage in CD and UC. If chronic inflammation is the central mechanism, what are its components? To keep the answers simple, one can envision a triggering event that initiates IBD, and a number of subsequent events that maintain inflammation and perpetuate IBD. The initial trigger is probably far more dependent on genetics and environmental factors than the events that perpetuate IBD.3,4 These are more likely to be tissue dependent events and there is little doubt that dysregulation of the local immune response is what underlies gut inflammation and allows it to persist unabated year after year.5 Thus until genetic and environmental factors are fully identified, it seems worthy to investigate the various biological systems that contribute to the chronicity of gut inflammation. The purpose of this review is to discuss one key contributor, the CD40/CD40 ligand (L) system, and present evidence that this system plays a major role in immunity and inflammation, can foster chronic inflammation, is directly relevant to IBD, and its modulation may offer therapeutic benefits to IBD patients. To achieve these aims, it is vital to first understand where the CD40/CD40L system …
Clustering based multi-label classification for image annotation and retrieval (2009)

This paper presents a novel multi-label classification framework for domains with large numbers of labels. Automatic image annotation is such a domain, as the available semantic concepts are typically hundreds. The proposed framework comprises an initial clustering phase that breaks the original training set into several disjoint clusters of data. It then trains a multi-label classifier from the data of each cluster. Given a new test instance, the framework first finds the nearest cluster and then applies the corresponding model. Empirical results using two clustering algorithms, four multi-label classification algorithms and three image annotation data sets suggest that the proposed approach can improve the performance and reduce the training time of standard multi-label classification algorithms, particularly in the case of large number of labels.
Regional cerebral function determined by FDG-PET in healthy volunteers: normal patterns and changes with age. (1995)

These data indicate that qualitative interpretation of FDG-PET images allows accurate assessment of regional metabolic activity of the brain in normal subjects similar to those described with quantitative techniques. Adequate knowledge of normal variations and changes related to normal aging is necessary for optimal assessment of pathologic states.
Oligomerisation of ethene by new palladium iminophosphine catalysts (1998)

Oligomerisation of ethene in polar solvents at higher temperatures is achieved using new palladium iminophosphine catalysts and the oligomer selectivity can be controlled by the nature of the ligand substituents.
Adoptive T-cell therapy for the treatment of solid tumours (2002)

Solid tumours can be eradicated by infusion of large amounts of tumour-specific T-cells in animal models. The successes seen in preclinical models, however, have not been adequately translated to human disease due, in part, to the inability to expand tumour antigen-specific T-cells ex vivo. Polyclonality and retention of antigen-specificity are two important properties of infused T-cells that are necessary for successful eradication of tumours. Investigators are beginning to evaluate the impact of attempting to reconstitute full T-cell immunity representing both major T-cell subsets, cytolytic T-cells and T-helper (Th) cells. One of the more important and often overlooked steps of successful adoptive T-cell therapy is the ex vivo expansion conditions, which can dramatically alter the phenotype of the T-cell. A number of cytokines and other soluble activation factors that have been characterised over the last decade are now available to supplement in vitro antigen presentation and IL-2. Newer molecular techniques have been developed and are aimed at genetically altering the characteristics of T-cells including their antigen-specificity and growth in vivo. In addition, advanced imaging techniques, such as positron emission tomography (PET), are being implemented in order to better define the in vivo function of ex vivo expanded tumour-specific T-cells.
A high-performance CMOS 70-MHz palette/DAC (1987)

A VLSI circuit has been developed that combines dual-ported RAMs and three high-speed 8-b digital-to-analog converters (DACs). It is known as a palette/DAC. A 6-2 segmented DAC architecture improves differential linearity and monotonicity. The current-source cell uses a cascode device to improve the DAC's linearity. A reference current, set by an on-chip bandgap reference voltage generator, and its associated distribution scheme eliminate the negative effects of threshold mismatches between current source cells, supply line resistance, and noise. The maximum conversion rate is 70 MHz with typical DC differential nonlinearity of 0.48 LSB (least significant bit). The 253-mil/SUP 2/ is designed on a double-metal CMOS process and consumes 1.2 W of power.
Point defect formation in optical materials expos ed to the space environment (1995)

Point defect formation associated with early stages of optical damage was observed unexpectedly in two, and possibly three, different optical materials subjected to short-duration space exposure. Three calcium fluoride, two lithium fluoride, and three magnesium fluoride samples were flown on Space Shuttle flight STS-46 as part of the Evaluation of Oxygen Interactions with Materials - Third Phase experiment. One each of the calcium and magnesium fluoride samples was held at a fixed temperature of 60 C during the space exposure, while the temperatures of the other samples were allowed to vary with the ambient temperature of the shuttle cargo bay. Pre-flight and post-flight optical absorption measurements were performed on all of the samples. With the possible exception of the magnesium fluoride samples, every sample clearly showed the formation of F-centers in that section of the sample that was exposed to the low earth orbit environment. Solar vacuum ultraviolet radiation is the most probable primary cause of the defect formation; however, the resulting surface metallization may be synergistically altered by the atomic oxygen environment.
Role of Angiotensin and Oxidative Stress in Essential Hypertension (1999)

In this review, we examine the possibility that small increments in angiotensin II are responsible for an increase in blood pressure and maintenance of hypertension through the stimulation of oxidative stress. A low dose of angiotensin II (2 to 10 ng x kg(-1) x min(-1), which does not elicit an immediate pressor response), when given for 7 to 30 days by continuous intravenous infusion, can increase mean arterial pressure by 30 to 40 mm Hg. This slow pressor response to angiotensin is accompanied by the stimulation of oxidative stress, as measured by a significant increase in levels of 8-iso-prostaglandin F(2alpha) (F(2)-isoprostane). Superoxide radicals and nitric oxide can combine chemically to form peroxynitrite, which can then oxidize arachidonic acid to form F(2)-isoprostanes. F(2)-isoprostanes exert potent vasoconstrictor and antinatriuretic effects. Furthermore, angiotensin II can stimulate endothelin production, which also has been shown to stimulate oxidative stress. In this way, a reduction in the concentration of nitric oxide (which is quenched by superoxide) along with the formation of F(2)-isoprostanes and endothelin could potentiate the vasoconstrictor effects of angiotensin II. We hypothesize that these mechanisms, which underlie the development of the slow pressor response to angiotensin II, also participate in the production of hypertension when circulating angiotensin II levels appear normal, as occurs in many cases of essential and renovascular hypertension.
Peritoneal dialysis in refractory end-stage congestive heart failure: a challenge facing a no-win situation (2005)

Peritoneal dialysis appears to be a promising therapeutic tool for patients affected by refractory CHF. Clinical improvement of cardiac function may be related to clearing blood from middle molecular weight myocardial depressant substances, including atrial natriuretic peptide. Prospective multicentre trials are needed to confirm these encouraging results.
The mechanism of spinal cord cavitation following spinal cord transection (1977)

Cavitation adjacent to transection of spinal cords can be successfully eliminated by a second operation 1 week after the initial spinal cord transection. The second operation consists of removal of the necrotic spinal cord tissue, thus producing a gap. Segments of autogenous sciatic nerve are inserted into the gap between the spinal cord stumps. If the spinal cord is injured by retransection at the second operation, cavitation again occurs in the spinal cord stumps resulting in separation of the nerve grafts from the spinal cord. The results of the present experiments support the concept that lysosomal spinal cord autotomy, which causes spinal cord cavitation, is a self-limiting process and that once the spinal cord has completed the autotomy, the process will not occur again unless the spinal cord is agiain traumatized.
Force-enhanced atomic refinement: Structural modeling with interatomic forces in a reverse Monte Carlo approach applied to amorphous Si andSiO2 (2015)

We introduce a structural modeling technique, called force-enhanced atomic refinement (FEAR). The technique incorporates interatomic forces in reverse Monte Carlo (RMC) simulations for structural refinement by fitting experimental diffraction data using the conventional RMC algorithm, and minimizes the total energy and forces from an interatomic potential. We illustrate the usefulness of the approach by studying $a\text{\ensuremath{-}}{\text{SiO}}_{2}$ and $a\text{\ensuremath{-}}\text{Si}$. The structural and electronic properties of the FEAR models agree well with experimental neutron and x-ray diffraction data and the results obtained from previous molecular dynamics simulations of $a\text{\ensuremath{-}}{\text{SiO}}_{2}$ and $a\text{\ensuremath{-}}\text{Si}$. We have shown that the method is more efficient than the conventional molecular dynamics simulations via ``melt quench.'' The computational time in FEAR has been observed to scale quadratically with the number of atoms.
Lymphocytes from SJL/J mice immunized with spinal cord respond selectively to a peptide of proteolipid protein and transfer relapsing demyelinating experimental autoimmune encephalomyelitis (1991)

Relapsing experimental autoimmune encephalomyelitis (R-EAE) can be induced in SJL/J mice by immunization with spinal cord homogenate and adjuvant. The specific Ag(s) responsible for acute disease and subsequent relapses in this model is unknown. Myelin basic protein (BP), an encephalitogenic peptide of BP (BP 87-99), and proteolipid protein (PLP) can each induce R-EAE in SJL/J mice, and a peptide of PLP (PLP 139-151) has been reported to induce acute EAE. To determine the encephalitogens in cord-immunized mice with R-EAE, the in vitro proliferative responses of lymph node cells (LNC) and central nervous system mononuclear cells to BP, BP peptides, and PLP peptides were examined during acute EAE and during relapses. LNC responded only to PLP peptides 139-151 and 141-151 and did not respond to BP or its peptides during acute or chronic disease. Central nervous system mononuclear cells also preferentially responded to PLP 139-151 and 141-151 during acute and relapsing disease. A PLP 139-151 peptide-specific Th cell line was selected from LNC of cord-immunized donors. Five million peptide-specific line cells transferred severe relapsing demyelinating EAE to naive recipients. We conclude that PLP peptide 139-151 is the major encephalitogen for R-EAE in cord-immunized SJL/J mice. We demonstrate for the first time that Th cells specific for this peptide are sufficient to transfer relapsing demyelinating EAE. The predominance of a PLP immune response rather than a BP response in SJL/J mice suggests that genetic background may determine the predominant myelin Ag response in human demyelinating diseases such as multiple sclerosis.
Modulating the Fibrinolytic System of Peripheral Blood Mononuclear Cells with Adenovirus (2001)

Gene therapy utilizing leukocytes is an unexplored therapeutic strategy for targeting tissue-type plasminogen activator (t-PA) to fibrin and sites of inflammation. In this study, five cationic lipids were observed to enhance the adenovirus (Ad)-mediated expression of t-PA in human peripheral blood mononuclear cells (PBMCs) in a dose-dependent manner between 1000 and 15,000 lipid molecules per Ad particle (efficiency:LipofectAMINE > GenePORTER > Effectene > SuperFect > DMRIE-C). PBMCs treated with Ad/t-PA * LipofectAMINE complexes displayed elevated t-PA expression over a 4-day period and the t-PA-expressing cells facilitated the lysis of plasma clots in vitro. Functional and immunologic assays revealed that the Ad * LipofectAMINE infection protocol did not affect monocyte adhesion in vitro or elevate the expression of procoagulant activity, interleukin 8, or tumor necrosis factor alpha. The potential of this system was documented with an in vivo rat model system that involved the injection of lipopolysaccharide into the peritoneal cavity to induce an inflammatory response. Infusion of Ad/t-PA-infected rat PBMCs into the vasculature of lipopolysaccharide-treated animals was found to increase local fibrinolytic activity by 4-fold. These data provide a framework for utilizing adenovirus to transfer genes into PBMCs.
Transforming growth factor-beta-stimulated connective tissue growth factor expression during corneal myofibroblast differentiation. (2001)

This is the first study to present evidence for the induction of CTGF by TGF-beta treatment of corneal fibroblasts. It is doubtful that CTGF is the TGF-beta mediator of the corneal fibroblast to myofibroblast transition because CTGF does not induce alpha-SM actin in subconfluent fibroblast cultures. CTGF may play a supporting role in myofibroblast differentiation.
Neuropilin 1 binds PDGF-D and is a co-receptor in PDGF-D–PDGFRβ signaling (2017)

ABSTRACT Platelet-derived growth factor (PDGF)-D is a PDGF receptor β (PDGFRβ)-specific ligand implicated in a number of pathological conditions, such as cardiovascular disease and cancer, but its biological function remains incompletely understood. In this study, we demonstrate that PDGF-D binds directly to neuropilin 1 (NRP1), in a manner that requires the PDGF-D C-terminal Arg residue. Stimulation with PDGF-D, but not PDGF-B, induced PDGFRβ–NRP1 complex formation in fibroblasts. Additionally, PDGF-D induced translocation of NRP1 to cell–cell junctions in endothelial cells, independently of PDGFRβ, altering the availability of NRP1 for VEGF-A–VEGFR2 signaling. PDGF-D showed differential effects on pericyte behavior in ex vivo sprouting assays compared to PDGF-B. Furthermore, PDGF-D-induced PDGFRβ–NRP1 interaction can occur in trans between molecules located in different cells (endothelial cells and pericytes). In summary, we show that NRP1 can act as a co-receptor for PDGF-D–PDGFRβ signaling and is possibly implicated in intercellular communication in the vascular wall.
Cardiac size and function in acromegaly. (1977)

Sixteen acromegalic patients underwent echocardiography, phonocardiography, stress electrocardiography with Thallium perfusion scanning and gated radioisotope left ventricular angiocardiograms. Abnormalities consisting of increased echo left ventricular mass index, low velocity of circumferential fiber shortening or elevated pre-ejection period to left ventricular ejection time ratio were found in six patients with coexistent hypertension or coronary disease. Concentric left ventricular hypertrophy was also found in three patients with no known etiology other than acromegaly of greater than thirteen years' duration or with fasting growth hormone concentrations greater than 100 ng/ml. One of these three also had left ventricular dysfunction. Neither hypertrophy nor ventricular dysfunction was found in other acromegalics with shorter duration of disease or lower growth hormone concentrations or with normal growth hormone concentrations after therapy. A high prevalence of coronary artery and hypertensive heart disease is associated with acromegaly. A few patients with acromegaly have a specific, potentially reversible cardiomyopathy probably related to prolonged acromegaly or very high growth hormone concentrations.
Identification of cell‐binding site of angiomodulin (AGM/TAF/Mac25) that interacts with heparan sulfates on cell surface (1999)

Angiomodulin (AGM/TAF/mac25) is a 30-kDa glycoprotein that was identified as an integrin-independent cell adhesion protein secreted by human bladder carcinoma cells. AGM is highly accumulated in small blood vessels of tumor tissues. In the present study, we attempted to identify the cell surface receptor and the cell-binding site of AGM using ECV-304 human vascular endothelial cells and BALB/c3T3 mouse fibroblasts. Heparin, heparan sulfate, and dextran sulfate, but not chondroitin sulfate, inhibited both adhesion of the two cell lines to AGM-coated plates and binding of AGM to these cells. Treatment of cells with heparinase, but not chondroitinase, inhibited both cell adhesion to AGM and AGM binding to cells. These results strongly suggested that heparan sulfates are the major receptor for AGM. Furthermore, we determined a 20-amino acid sequence within AGM molecule as its major cell-binding site. The synthetic peptide for the cell-binding sequence showed cell adhesion activity comparable to that of AGM, and the activity was inhibited by heparin and heparan sulfate. The peptide competitively inhibited cell adhesion to AGM and the binding of AGM to cells. These results indicated that AGM binds to cells through interaction of the identified cell-binding sequence with heparan sulfates on cell surface. It was also found that the heparan sulfate-binding peptide inhibited the formation of capillary tube-like structures of vascular endothelial cells in culture. J. Cell. Biochem. 75:187–195, 1999. © 1999 Wiley-Liss, Inc.
Comparison of Experimental Binding Data and Theoretical Models in Proteins Containing Subunits* (1966)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTComparison of Experimental Binding Data and Theoretical Models in Proteins Containing Subunits*D. E. Koshland, Jr., G. Némethy, and D. FilmerCite this: Biochemistry 1966, 5, 1, 365–385Publication Date (Print):January 1, 1966Publication History Published online1 May 2002Published inissue 1 January 1966https://pubs.acs.org/doi/10.1021/bi00865a047https://doi.org/10.1021/bi00865a047research-articleACS PublicationsRequest reuse permissionsArticle Views4576Altmetric-Citations2398LEARN 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
A high-speed ray tracing engine built on a field-programmable system (2004)

Ray tracing is a method of rendering high-quality images and video by calculating what happens to virtual light rays in a 3-dimensional scene. It is capable of creating for more realism than traditional Z-buffering methods. This paper describes the design of a hardware ray tracing system implemented on a multi-FPGA Xilinx Virtex-E prototyping system. The result is a hardware ray tracer that is capable of out-performing a 2.4GHz Pentium 4, running a well-known high performance software ray tracing algorithm, by up to a factor of thirty. When these results are projected forward into a next generation FPGA system, consisting of a single large Virtex 2 Pro FPGA, it is found that the system should be able to out perform the same Pentium 4 by up to two orders of magnitude, and the fastest known hardware implementation, the AR350, by up to a factor of three.