gebhart/patrepeval huggingface dataset:
Radiometal-Labeled Agents (Non-Technetium) for Diagnostic Imaging (1999)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTRadiometal-Labeled Agents (Non-Technetium) for Diagnostic ImagingCarolyn J. Anderson and Michael J. WelchView Author Information Mallinckrodt Institute of Radiology, Washington University School of Medicine 510 S. Kingshighway, Campus Box 8225 St. Louis, Missouri 63110 Cite this: Chem. Rev. 1999, 99, 9, 2219–2234Publication Date (Web):August 11, 1999Publication History Received19 March 1999Revised5 July 1999Published online11 August 1999Published inissue 8 September 1999https://pubs.acs.org/doi/10.1021/cr980451qhttps://doi.org/10.1021/cr980451qresearch-articleACS PublicationsCopyright © 1999 American Chemical SocietyRequest reuse permissionsArticle Views2794Altmetric-Citations389LEARN 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 SUBJECTS:Anatomy,Nuclear medicine,Peptides and proteins,Pharmaceuticals,Receptors Get e-Alerts
Roles for Growth Factors in Cancer Progression (2010)

Under physiological conditions, cells receive fate-determining signals from their tissue surroundings, primarily in the form of polypeptide growth factors. Integration of these extracellular signals underlies tissue homeostasis. Although departure from homeostasis and tumor initiation are instigated by oncogenic mutations rather than by growth factors, the latter are the major regulators of all subsequent steps of tumor progression, namely clonal expansion, invasion across tissue barriers, angiogenesis, and colonization of distant niches. Here, we discuss the relevant growth factor families, their roles in tumor biology, as well as the respective downstream signaling pathways. Importantly, cancer-associated activating mutations that impinge on these pathways often relieve, in part, the reliance of tumors on growth factors. On the other hand, growth factors are frequently involved in evolvement of resistance to therapeutic regimens, which extends the roles for polypeptide factors to very late phases of tumor progression and offers opportunities for cancer therapy.
Design and evaluation of wafer scale clock distribution (2003)

The authors describe a computer program which is used for simulating the performance of large wafer scale integration clock distribution networks, made up of both passive transmission line elements and active buffers. The theoretical basis for the model is briefly reviewed. The authors present several example networks for 4-in wafers, comparing the AC performances as a function of power dissipation, layout area, and harvesting yield. The sensitivity of performance (as measured by propagation delays and clock skew) to random or systematic process-related fluctuations and defects is calculated using the model. A new measurement system is introduced for electrically characterizing the performance of clock distribution networks on fabricated wafers and within multichip modules.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
No association between microsomal triglyceride transfer protein ( MTP ) haplotype and longevity in humans (2005)

Human longevity is a multifactorial condition with a significant genetic contribution. A recent association study in two independent samples of long-lived U.S. Caucasians [long-lived individuals (LLI)] identified a SNP haplotype of the microsomal triglyceride transfer protein (MTP, 4q25) that was underrepresented among LLI when compared with younger controls. This suggested that variation in the MTP gene might modify human longevity. Because of its function in lipid metabolism, the MTP gene product could plausibly play a pivotal role in the physiology of aging. However, the association observed in the U.S. samples could not be replicated by the same authors in a larger French LLI sample. We have therefore investigated the MTP "risk" haplotype in our own collection of 1,589 German nonagenarians, centenarians, and appropriately matched controls. No statistically significant differences were observed between LLI and controls at the allele, genotype, or haplotype level. This indicates that a noteworthy influence of the respective MTP haplotype on human longevity in the German population is unlikely. Furthermore, in comparison with all other U.S. and European samples analyzed, the MTP "risk" haplotype was found to be overrepresented only in the U.S. controls. This implies that the putative association is more likely to reflect recent changes in the genetic structure of the U.S. Caucasian population as a whole, rather than genetic effects upon survival to old age. In our view, the original study therefore highlights potential problems that arise when the case-control design is used as a means to map longevity genes in humans.
Characterization of an Agrobacterium tumefaciens d -Psicose 3-Epimerase That Converts d -Fructose to d -Psicose (2006)

The noncharacterized gene previously proposed as the D-tagatose 3-epimerase gene from Agrobacterium tumefaciens was cloned and expressed in Escherichia coli. The expressed enzyme was purified by three-step chromatography with a final specific activity of 8.89 U/mg. The molecular mass of the purified protein was estimated to be 132 kDa of four identical subunits. Mn2+ significantly increased the epimerization rate from D-fructose to D-psicose. The enzyme exhibited maximal activity at 50 degrees C and pH 8.0 with Mn2+. The turnover number (k(cat)) and catalytic efficiency (k(cat)/Km) of the enzyme for D-psicose were markedly higher than those for d-tagatose, suggesting that the enzyme is not D-tagatose 3-epimerase but D-psicose 3-epimerase. The equilibrium ratio between D-psicose and D-fructose was 32:68 at 30 degrees C. D-Psicose was produced at 230 g/liter from 700-g/liter D-fructose at 50 degrees C after 100 min, corresponding to a conversion yield of 32.9%.
Metabolomics and Biomarker Discovery in Traumatic Brain Injury (2018)

Traumatic brain injury (TBI) is one of the leading causes of disability and mortality worldwide. The TBI pathogenesis can induce broad pathophysiological consequences and clinical outcomes attributed to the complexity of the brain. Thus, the diagnosis and prognosis are important issues for the management of mild, moderate, and severe forms of TBI. Metabolomics of readily accessible biofluids is a promising tool for establishing more useful and reliable biomarkers of TBI than using clinical findings alone. Metabolites are an integral part of all biochemical and pathophysiological pathways. Metabolomic processes respond to the internal and external stimuli resulting in an alteration of metabolite concentrations. Current high-throughput and highly sensitive analytical tools are capable of detecting and quantifying small concentrations of metabolites, allowing one to measure metabolite alterations after a pathological event when compared to a normal state or a different pathological process. Further, these metabolic biomarkers could be used for the assessment of injury severity, discovery of mechanisms of injury, and defining structural damage in the brain in TBI. Metabolic biomarkers can also be used for the prediction of outcome, monitoring treatment response, in the assessment of or prognosis of post-injury recovery, and potentially in the use of neuroplasticity procedures. Metabolomics can also enhance our understanding of the pathophysiological mechanisms of TBI, both in primary and secondary injury. Thus, this review presents the promising application of metabolomics for the assessment of TBI as a stand-alone platform or in association with proteomics in the clinical setting.
Squamous Cell Carcinoma Antigen, Tumor-Associated Trypsin Inhibitor, and Carcinoembryonic Antigen for Monitoring Cervical Cancer (1994)

A total of 120 patients with squamous cell carcinoma of the cervix were prospectively monitored with simultaneous serum level estimations of SCC, CEA, and TATI in different stages and phases of their disease. Positive values were observed for SCC in 72 patients (60%), for CEA in 47 (39%), and for TATI in 12 (10%). There was no increase in the SCC serum levels in the early stages of disease (IA, IB, IIA), whereas they increased significantly with advancing stage. Serum marker levels quickly dropped to normal in patients with advanced stages (IIB or higher) or recurrent disease who responded to treatment, as well as in patients with early-stage disease following local therapy. In addition, 28 patients, who had a renewed progression after a complete remission with normal marker levels, showed an increase in SCC in 26 cases (92%) and CEA in 7 (25%). TATI did not vary in these patients. In patients whose disease did not respond to treatment, a change in serum marker levels cannot be evidenced with the available numbers. This study indicates that the routine measurement of all three markers is not justified in squamous cell carcinoma of the cervix, and that SCC estimation is a potential tool for monitoring the efficacy of treatment in advanced stages or relapse.
Cellular growth inhibition by IGFBP‐3 and TGF‐β 1 requires LRP‐1 (2003)

The type V TGF-beta receptor (TbetaR-V)/IGFBP-3 receptor mediates the IGF-independent growth inhibition induced by IGFBP-3. It also mediates the growth inhibitory response to TGF-beta1 in concert with other TGF-beta receptor types, and its loss may contribute to the malignant phenotype of human carcinoma cells. Here we demonstrate that TbetaR-V is identical to LRP-1/alpha2M receptor as shown by MALDI-TOF analysis of tryptic peptides of TbetaR-V purified from bovine liver. In addition, 125I-IGFBP-3 affinity-labeled TbetaR-V in Mv1Lu cells is immunoprecipitated by antibodies to LRP-1 and TbetaR-V. RAP, an LRP-1 antagonist, inhibits binding of 125I-TGF-beta1 and 125I-IGFBP-3 to TbetaR-V and diminishes IGFBP-3-induced growth inhibition in Mv1Lu cells. Absent or low levels of LRP-1, as with TbetaR-V, have been linked to the malignant phenotype of carcinoma cells. Mutagenized Mv1Lu cells selected for reduced expression of LRP-1 have an attenuated growth inhibitory response to TGF-beta1 and IGFBP-3. LRP-1-deficient mouse embryonic fibroblasts lack a growth inhibitory response to TGF-beta1 and IGFBP-3. On the other hand, stable transfection of H1299 human lung carcinoma cells with LRP-1 cDNA restores the growth inhibitory response. These results suggest that the LRP-1/TbetaR-V/IGFBP-3 receptor is required for the growth inhibitory response to IGFBP-3 and TGF-beta1.
Cooperative space-time coding for wireless networks (2004)

We consider a cooperative system in which the partnering mobiles are equipped with multiple antennas. We present space-time codes that have the capability of providing full cooperation diversity, while achieving maximum possible diversity and best performance in the inter-user channel. Our codes also perform well when cooperation does not take place. We illustrate that cooperative space-time coding offers significant performance improvement over direct transmission even when the inter-user channel is noisy. We also consider code design for users with different numbers of antennas.
A PILOT TRIAL OF RECOMBINANT HUMAN INTERLEUKIN-10 IN KIDNEY TRANSPLANT RECIPIENTS RECEIVING OKT3 INDUCTION THERAPY1,2 (1997)

Pretreatment with doses of up to 1 microg/kg rhIL-10 is safe and reduces the release of TNF-alpha induced by OKT3. However, higher doses might promote early sensitization to OKT3.
The helicase XPD unwinds bubble structures and is not stalled by DNA lesions removed by the nucleotide excision repair pathway (2009)

Xeroderma pigmentosum factor D (XPD) is a 5'-3' superfamily 2 helicase and the founding member of a family of DNA helicases with iron-sulphur cluster domains. As a component of transcription factor II H (TFIIH), XPD is involved in DNA unwinding during nucleotide excision repair (NER). Archaeal XPD is closely related in sequence to the eukaryal enzyme and the crystal structure of the archaeal enzyme has provided a molecular understanding of mutations causing xeroderma pigmentosum and trichothiodystrophy in humans. Consistent with a role in NER, we show that archaeal XPD can initiate unwinding from a DNA bubble structure, differentiating it from the related helicases FancJ and DinG. XPD was not stalled by substrates containing extrahelical fluorescein adducts, abasic sites nor a cyclobutane pyrimidine dimer, regardless of whether these modifications were placed on either the displaced or translocated strands. This suggests that DNA lesions repaired by NER may not present a barrier to XPD translocation in vivo, in contrast to some predictions. Preferential binding of a fluorescein-adducted oligonucleotide was observed, and XPD helicase activity was readily inhibited by both single- and double-stranded DNA binding proteins. These observations have several implications for the current understanding of the NER pathway.
The role of Ito cells in the biosynthesis of HGF-SF in the liver. (1993)

Hepatocyte Growth Factor-Scatter Factor (HGF-SF) is produced by sinusoidal cells in normal rat liver. Analysis of isolated cells has proven that Ito cells (fat-storing cells, hepatic lipocytes) are the source of hepatic HGF. In diseased liver the HGF-expression pattern is more complex. In acute liver injury HGF is expressed by an increased number of resident liver cells, which may be due to recruitment of other nonparenchymal liver cells as well as an increased number of Ito cells due to cell division. In cirrhotic rat liver tissue, the number of HGF-expressing cells is decreased. This may be explained by the complete loss of HGF-expression in myofibroblast-like cells derived from Ito cells. Quiescent Ito cells seem to be in a strategic position to control parenchymal cell proliferation. Activation of Ito cells, which occurs in chronic fibrotic liver disease, may lead to the loss of this control function.
A2B Adenosine and P2Y2 Receptors Stimulate Mitogen-activated Protein Kinase in Human Embryonic Kidney-293 Cells (1999)

Mitogen-activated protein kinase (MAPK) cascades underlie long-term mitogenic, morphogenic, and secretory activities of purinergic receptors. In HEK-293 cells, N-ethylcarboxamidoadenosine (NECA) activates endogenous A2BARs that signal through Gs and Gq/11. UTP activates P2Y2 receptors and signals only through Gq/11. The MAPK isoforms, extracellular-signal regulated kinase 1/2 (ERK), are activated by NECA and UTP. H-89 blocks ERK activation by forskolin, but weakly affects the response to NECA or UTP. ERK activation by NECA or UTP is unaffected by a tyrosine kinase inhibitor (genistein), attenuated by a phospholipase C inhibitor (U73122), and is abolished by a MEK inhibitor (PD098059) or dominant negative Ras. Inhibition of protein kinase C (PKC) by GF 109203X failed to block ERK activation by NECA or UTP, however, another PKC inhibitor, Ro 31-8220, which unlike GF 109203X, can block the zeta-isoform, and prevents UTP- but not NECA-induced ERK activation. In the presence of forskolin, Ro 31-8220 loses its ability to block UTP-stimulated ERK activation. PKA has opposing effects on B-Raf and c-Raf-1, both of which are found in HEK-293 cells. The data are explained by a model in which ERK activity is modulated by differential effects of PKC zeta and PKA on Raf isoforms.
Prognostic angiogenic markers (endoglin, VEGF, CD31) and tumor cell proliferation (Ki67) for gastrointestinal stromal tumors (2015)

The IMVD cutoff values for the angiogenic markers CD105 and CD31, may be prognostic factors for GIST, in addition to VEGF and Ki67.
Quantitative photothermal characterization of ion-implanted layers in Si (2002)

Quantitative analysis of ion-implanted layers in Si using the damage-based theoretical modeling and experimental results obtained with the photomodulated reflectance (PMR) technique are described. Our theoretical approach combines the conventional quantum mechanics based calculations of the ion-induced damage depth profiles in semiconductors with the corresponding scaling of the thermal and carrier plasma parameters followed by the calculation of the photothermal response from a multilayered sample. The theoretical limit of the photothermal signal sensitivity to the implantation dose in the absence of optical and carrier plasma-wave interference effects is estimated. Simulations of the photothermal amplitude and phase dose dependencies allow us to follow the dynamics of the thermal- and carrier plasma waves in an ion-implanted semiconductor. The validity of the proposed damage-based modeling approach to the problem of quantitative analysis of surface-modified semiconductors is analyzed. It is shown that the results of the photothermal damage-based modeling are in a very good agreement with experimentally observed PMR signal implantation dose behavior for B+-implanted Si across the entire range of practically important implantation doses: 109–1015 cm−2.
BANYULS, a novel negative regulator of flavonoid biosynthesis in the Arabidopsis seed coat (1997)

A mutant of Arabidopsis that accumulates a high level of red pigments within the seed coat has been isolated from a population of T-DNA-transformed plants. Genetic analysis revealed that the mutation is recessive and affects maternal seed tissues only. Due to the color of the immature seeds, this mutation was named banyuls (ban). Pigments accumulated continuously from early seed development to the desiccation stage in the seed coat of the mutant. The phenotype of the double mutant banyuls/ transparent testa confirmed the flavonoid nature of the pigments and enabled assignment of the regulatory TT (Transparent Testa) genes to two groups according to their epistatic relationship to ban. The flavonoid content of germinated ban and wild-type seedlings was similar. Plants harbouring the ban mutation had a normal formation of trichomes and root hairs and were not affected in their responses to light. The seeds of ban plants exhibited reduced germination compared to wild-type which may be a direct consequence of the high level of pigments. These results suggest that BANYULS functions as a negative regulator of flavonoid biosynthesis that prevents accumulation of pigments in the seed coat during early embryogenesis in Arabidopsis.
Interactions between Eph kinases and ephrins provide a mechanism to support platelet aggregation once cell-to-cell contact has occurred (2002)

Eph kinases are receptor tyrosine kinases whose ligands, the ephrins, are also expressed on the surface of cells. Interactions between Eph kinases and ephrins on adjacent cells play a central role in neuronal patterning and vasculogenesis. Here we examine the expression of ephrins and Eph kinases on human blood platelets and explore their role in the formation of the hemostatic plug. The results show that human platelets express EphA4 and EphB1, and the ligand, ephrinB1. Forced clustering of EphA4 or ephrinB1 led to cytoskeletal reorganization, adhesion to fibrinogen, and alpha-granule secretion. Clustering of ephrinB1 also caused activation of the Ras family member, Rap1B. In platelets that had been activated by ADP and allowed to aggregate, EphA4 formed complexes with two tyrosine kinases, Fyn and Lyn, and the cell adhesion molecule, L1. Blockade of Eph/ephrin interactions prevented the formation of these complexes and caused platelet aggregation at low ADP concentrations to become more readily reversible. We propose that when sustained contacts between platelets have occurred in response to agonists such as collagen, ADP, and thrombin, the binding of ephrins to Eph kinases on adjacent platelets provides a mechanism to perpetuate signaling and promote stable platelet aggregation.
The Major Form of ADP-Glucose Pyrophosphorylase in Maize Endosperm Is Extra-Plastidial (1996)

Preparations enriched in plastids were used to investigate the location of ADP-glucose pyrophosphorylase (AGPase) in the developing endosperm of maize (Zea mays L.). These preparations contained more than 25% of the total activity of the plastid marker enzymes alkaline pyrophosphatase and soluble starch synthase, less than 2% of the cytosolic marker enzymes alcohol dehydrogenase and pyrophosphate, fructose 6-phosphate 1-phosphotransferase, and approximately 3% of the AGPase activity. Comparison with the marker enzyme distribution suggests that more than 95% of the activity of AGPase in maize endosperm is extra-plastidial. Two proteins were recognized by antibodies to the small subunit of AGPase from maize endosperm Brittle-2 (Bt2). The larger of the two proteins was the major small subunit in homogenates of maize endosperm, and the smaller, less abundant of the two proteins was enriched in preparations containing plastids. These results suggest that there are distinct plastidial and cytosolic forms of AGPase, which are composed of different subunits. Consistent with this was the finding that the bt2 mutation specifically eliminated the extraplastidial AGPase activity and the larger of the two proteins recognized by the antibody to the Bt2 subunit.
A Multibiomarker-Based Outcome Risk Stratification Model for Adult Septic Shock* (2013)

We have derived, tested, calibrated, and validated a risk stratification tool and found that it reliably estimates the probability of mortality in adults with septic shock.
Laser management of subfoveal choroidal neovascularization in age-related macular degeneratior (1993)

Subfoveal choroidal neovascularization in eyes with age-related macular degeneration is associated with a poor natural prognosis. The Macular Photocoagulation Study Group recently has demonstrated that subfoveal photocoagulation in select cases of subfoveal choroidal neovascularization for patients with age-related macular degeneration effectively prevents severe visual acuity loss and reduces the average loss of contrast sensitivity and reading speed associated with this condition. Eligibility criteria and treatment recommendations from the Macular Photocoagulation Study will be reviewed. Results of alternative strategies for laser photocoagulation of such lesions are also discussed; however, the Macular Photocoagulation Study results stand alone in documenting a long-term treatment benefit of photocoagulation for subfoveal choroidal neovascularization.