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Auteur : Grafiati
Publié le 10 mars 2023

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1

Luchinat, Enrico, Erica Secci, Francesca Cencetti et Paola Bruni. « Sequential protein expression and selective labeling for in-cell NMR in human cells ». Biochimica et Biophysica Acta (BBA) - General Subjects 1860, no 3 (mars 2016) : 527–33. http://dx.doi.org/10.1016/j.bbagen.2015.12.023.

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Matos, Maria J., Libby Brown, Barbara Bernardim, Ana Guerreiro, Gonzalo Jiménez-Osés et Gonçalo J. L. Bernardes. « Sequential dual site-selective protein labelling enabled by lysine modification ». Bioorganic & ; Medicinal Chemistry 28, no 22 (novembre 2020) : 115783. http://dx.doi.org/10.1016/j.bmc.2020.115783.

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Morató, Anna, Carlos A. Elena-Real, Matija Popovic, Aurélie Fournet, Karen Zhang, Frédéric Allemand, Nathalie Sibille, Annika Urbanek et Pau Bernadó. « Robust Cell-Free Expression of Sub-Pathological and Pathological Huntingtin Exon-1 for NMR Studies. General Approaches for the Isotopic Labeling of Low-Complexity Proteins ». Biomolecules 10, no 10 (19 octobre 2020) : 1458. http://dx.doi.org/10.3390/biom10101458.

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The high-resolution structural study of huntingtin exon-1 (HttEx1) has long been hampered by its intrinsic properties. In addition to being prone to aggregate, HttEx1 contains low-complexity regions (LCRs) and is intrinsically disordered, ruling out several standard structural biology approaches. Here, we use a cell-free (CF) protein expression system to robustly and rapidly synthesize (sub-) pathological HttEx1. The open nature of the CF reaction allows the application of different isotopic labeling schemes, making HttEx1 amenable for nuclear magnetic resonance studies. While uniform and selective labeling facilitate the sequential assignment of HttEx1, combining CF expression with nonsense suppression allows the site-specific incorporation of a single labeled residue, making possible the detailed investigation of the LCRs. To optimize CF suppression yields, we analyze the expression and suppression kinetics, revealing that high concentrations of loaded suppressor tRNA have a negative impact on the final reaction yield. The optimized CF protein expression and suppression system is very versatile and well suited to produce challenging proteins with LCRs in order to enable the characterization of their structure and dynamics.
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Yoshida, Jun-ichi, Heejin Kim, Hyune-Jea Lee, Daiki Torii et Yongju Jeon. « Integrated Synthesis Using Isothiocyanate-Substituted Aryllithiums by Flow Chemistry ». Synlett 31, no 19 (21 août 2020) : 1899–902. http://dx.doi.org/10.1055/s-0040-1707251.

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The isothiocyanate (NCS) group is an attractive functional group in the field of organic and pharmaceutical chemistry. It can be transformed into other heteroatomic functional groups. It usually acts as the inductive group of biological activity and has also been traditionally used as the fluorescent-labeling reagent. However, it is not compatible with strong bases. When the NCS group is at para position in halobenzenes, it generally undergoes nucleophilic additions upon reaction with strong bases. To the best of our knowledge, there is currently no general methodology for the formation and reactions of NCS-functionalized aryllithiums for meta and para substituents. Herein, we report the continuous-flow generation of NCS-substituted aryllithiums from the corresponding haloarenes via a selective halogen–lithium exchange reaction and its reaction with various electrophiles to yield NCS-containing products. We also achieved an integrated synthesis through sequential reactions of the NCS-containing compounds with additional nucleophiles using the continuous-flow reactors.
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Gruba, Natalia, Ewa Bielecka, Magdalena Wysocka, Anna Wojtysiak, Magdalena Brzezińska-Bodal, Kamila Sychowska, Magdalena Kalińska et al. « Development of Chemical Tools to Monitor Human Kallikrein 13 (KLK13) Activity ». International Journal of Molecular Sciences 20, no 7 (28 mars 2019) : 1557. http://dx.doi.org/10.3390/ijms20071557.

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Kallikrein 13 (KLK13) was first identified as an enzyme that is downregulated in a subset of breast tumors. This serine protease has since been implicated in a number of pathological processes including ovarian, lung and gastric cancers. Here we report the design, synthesis and deconvolution of libraries of internally quenched fluorogenic peptide substrates to determine the specificity of substrate binding subsites of KLK13 in prime and non-prime regions (according to the Schechter and Berger convention). The substrate with the consensus sequential motive ABZ-Val-Arg-Phe-Arg-ANB-NH2 demonstrated selectivity towards KLK13 and was successfully converted into an activity-based probe by the incorporation of a chloromethylketone warhead and biotin bait. The compounds described may serve as suitable tools to detect KLK13 activity in diverse biological samples, as exemplified by overexpression experiments and targeted labeling of KLK13 in cell lysates and saliva. In addition, we describe the development of selective activity-based probes targeting KLK13, to our knowledge the first tool to analyze the presence of the active enzyme in biological samples.
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Di Liberto, Maurizio, Xiangao Huang, Jamieson Bretz, Scott A. Ely, Rediet Zewdu, David Jayabalan, Suzhen Chen et al. « Induction of Metabolic Impairment In Prolonged Early G1 Arrest Induced by CDK4/CDK6 Inhibition Sensitizes Myeloma Cells for Proteasome Inhibitor Killing During Subsequent S Phase Synchronization ». Blood 116, no 21 (19 novembre 2010) : 2989. http://dx.doi.org/10.1182/blood.v116.21.2989.2989.

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Abstract Abstract 2989 Sequential drug combination is a rational approach to maximize tumor killing and minimize side effects in cancer therapy. However, this is rarely achieved because the mechanism of drug action is often incompletely understood and the cell cycle specificity of individual drugs unknown. Dysregulation of cyclin-dependent kinase (CDK)4 and CDK6 is common in human cancer and precedes unrestrained proliferation of tumor cells in multiple myeloma (MM) patients, especially during refractory relapse. This highlights the critical importance of targeting CDK4/CDK6 in MM. We have now developed, for the first time, a novel therapeutic strategy to selectively inhibit CDK4/CDK6 in sequential combination with clinically relevant cytotoxic drugs for maximal tumor killing at reduced doses in MM. CDK4 and CDK6 promote reentry and progression of the cell cycle through G1. PD 0332991, the only known CDK4/CDK6-specific inhibitor, is potent, reversible and bioavailable. We showed that inhibition of CDK4/CDK6 with PD 0332991 induces early G1 arrest and upon release from the G1 block, synchronous progression to S phase and G2/M with exceptional precision and efficiency in MM cells in vitro and in animal models. This provides a unique means to determine the cell cycle targeting specificity of individual compounds for optimal combination. Simultaneous analysis of BrdU pulse-labeling (30 minutes) and DNA content per cell reveals that bortezomib, a reversible proteasome inhibitor; carfilzomib (PR-171), an irreversible selective inhibitor of the proteasom; and its oral analog ONX-0912 (PR-047) all preferentially target MM cells synchronized into S phase over those arrested in G1, but not cells in G2/M. On this basis, killing of myeloma cells by proteasome inhibitors is markedly enhanced in prolonged G1 arrest induced by PD 0332991 and further augmented during synchronous entry into and progression through S phase upon release from the G1 block, in vitro and in vivo in the native bone marrow niches. Induction of early G1 arrest by PD 0332991 requires Rb, the substrate of CDK4 and CDK6, but not p53. Importantly, the increase in carfilzomib, ONX-0912 or bortezomib mediated killing after S phase synchronization significantly surpasses the enrichment of S phase cells. It is in fact proportional to the time of prior G1 arrest. Kinetics analyses of global gene expression patterns, specific RNA and protein levels and functional shRNA interference show that prolonging early G1 arrest leads to time-dependent uncoupling of gene expression from the cell cycle. PD 0332991 withdraw rapidly restores the CDK4 and CDK6 catalytic activity and scheduled expression of cell cycle genes, hence synchronous progression to S phase and mitosis. This includes upregulation of cyclin A synthesis and Skp2 mediated ubiquitin-proteasome degradation of p27 for S phase entry, mini chromosome maintenance(MCM)s and thymidine kinase for DNA replication, and genes critical for G2/M checkpoint control and mitosis. However, it fails to fully reverse the metabolic impairment (altered glucose, nucleotide and ATP metabolism) induced in prolonged early G1 arrest. This culminates in the loss of IRF-4 required for myeloma survival and selective gain of pro-apoptotic Bim function in G1 arrest and Noxa in S phase in synergy with carfilzomib and bortezomib, which lowers the threshold for activation of the intrinsic apoptosis pathway. Selective inhibition of CDK4/CDK6 in sequential combination therapy thus not only halts tumor cell proliferation but also potently induces synergistic tumor killing. This sequential combination therapy has been implemented in a multi-center phase 1/2 clinical trial targeting CDK4/6 with PD 0332991 in combination with bortezomib and dexamethasone in relapsed refractory MM. Phase 1 data indicate that PD 0332991 is well tolerated, and directly and completely inhibits CDK4/CDK6 and the cell cycle in tumor cells in MM patients with promising clinical efficacy. Evidence from phase 2 trials of carfilzomib indicates that it is also well tolerated. The peripheral neuropathy commonly observed with bortezomib appears to be less severe and less frequent. Selective combination with carfilzomib or the oral agent ONX-0912 thus represents a promising alternative to refine targeting CDK4/6 in sequential combination therapy for multiple myeloma and potentially other cancers. Disclosures: Off Label Use: PD 0332991 is a cell cycle CDK4/CDK6 inhibitor Carfilzomib is a proteasome inhibitor. Kirk:Onyx: Employment, Equity Ownership. Randolph:Pfizer: Employment, Equity Ownership. Niesvizky:Celgene: Consultancy, Research Funding, Speakers Bureau; Onyx: Consultancy, Research Funding, Speakers Bureau; Millennium: Consultancy, Research Funding, Speakers Bureau.
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Falk Delgado, Alberto, Francesca De Luca, Danielle van Westen et Anna Falk Delgado. « Arterial spin labeling MR imaging for differentiation between high- and low-grade glioma—a meta-analysis ». Neuro-Oncology 20, no 11 (2 juin 2018) : 1450–61. http://dx.doi.org/10.1093/neuonc/noy095.

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Abstract Background Arterial spin labeling is an MR imaging technique that measures cerebral blood flow (CBF) non-invasively. The aim of the study is to assess the diagnostic performance of arterial spin labeling (ASL) MR imaging for differentiation between high-grade glioma and low-grade glioma. Methods Cochrane Library, Embase, Medline, and Web of Science Core Collection were searched. Study selection ended November 2017. This study was prospectively registered in PROSPERO (CRD42017080885). Two authors screened all titles and abstracts for possible inclusion. Data were extracted independently by 2 authors. Bivariate random effects meta-analysis was used to describe summary receiver operating characteristics. Trial sequential analysis (TSA) was performed. Results In total, 15 studies with 505 patients were included. The diagnostic performance of ASL CBF for glioma grading was 0.90 with summary sensitivity 0.89 (0.79–0.90) and specificity 0.80 (0.72–0.89). The diagnostic performance was similar between pulsed ASL (AUC 0.90) with a sensitivity 0.85 (0.71–0.91) and specificity 0.83 (0.69–0.92) and pseudocontinuous ASL (AUC 0.88) with a sensitivity 0.86 (0.79–0.91) and specificity 0.80 (0.65–0.87). In astrocytomas, the diagnostic performance was 0.89 with sensitivity 0.86 (0.79 to 0.91) and specificity 0.79 (0.63 to 0.89). Sensitivity analysis confirmed the robustness of the findings. TSA revealed that the meta-analysis was adequately powered. Conclusion Arterial spin labeling MR imaging had an excellent diagnostic accuracy for differentiation between high-grade and low-grade glioma. Given its low cost, non-invasiveness, and efficacy, ASL MR imaging should be considered for implementation in the routine workup of patients with glioma.
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Adnan, Ahmed, Abdullah Muhammed, Abdul Azim Abd Ghani, Azizol Abdullah et Fahrul Hakim. « Hyper-Heuristic Framework for Sequential Semi-Supervised Classification Based on Core Clustering ». Symmetry 12, no 8 (4 août 2020) : 1292. http://dx.doi.org/10.3390/sym12081292.

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Existing stream data learning models with limited labeling have many limitations, most importantly, algorithms that suffer from a limited capability to adapt to the evolving nature of data, which is called concept drift. Hence, the algorithm must overcome the problem of dynamic update in the internal parameters or countering the concept drift. However, using neural network-based semi-supervised stream data learning is not adequate due to the need for capturing quickly the changes in the distribution and characteristics of various classes of the data whilst avoiding the effect of the outdated stored knowledge in neural networks (NN). This article presents a prominent framework that integrates each of the NN, a meta-heuristic based on evolutionary genetic algorithm (GA) and a core online-offline clustering (Core). The framework trains the NN on previously labeled data and its knowledge is used to calculate the error of the core online-offline clustering block. The genetic optimization is responsible for selecting the best parameters of the core model to minimize the error. This integration aims to handle the concept drift. We designated this model as hyper-heuristic framework for semi-supervised classification or HH-F. Experimental results of the application of HH-F on real datasets prove the superiority of the proposed framework over the existing state-of-the art approaches used in the literature for sequential classification data with evolving nature.
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Martinez-Pena y Valenzuela, Isabel, et Mohammed Akaaboune. « Acetylcholinesterase Mobility and Stability at the Neuromuscular Junction of Living Mice ». Molecular Biology of the Cell 18, no 8 (août 2007) : 2904–11. http://dx.doi.org/10.1091/mbc.e07-02-0093.

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Acetylcholinesterase (AChE) is an enzyme that terminates acetylcholine neurotransmitter function at the synaptic cleft of cholinergic synapses. However, the mechanism by which AChE number and density are maintained at the synaptic cleft is poorly understood. In this work, we used fluorescence recovery after photobleaching, photo-unbinding, and quantitative fluorescence imaging to investigate the surface mobility and stability of AChE at the adult innervated neuromuscular junction of living mice. In wild-type synapses, we found that nonsynaptic (perisynaptic and extrasynaptic) AChEs are mobile and gradually recruited into synaptic sites and that most of the trapped AChEs come from the perijunctional pool. Selective labeling of a subset of synaptic AChEs within the synapse by using sequential unbinding and relabeling with different colors of streptavidin followed by time-lapse imaging showed that synaptic AChEs are nearly immobile. At neuromuscular junctions of mice deficient in α-dystrobrevin, a component of the dystrophin glycoprotein complex, we found that the density and distribution of synaptic AChEs are profoundly altered and that the loss rate of AChE significantly increased. These results demonstrate that nonsynaptic AChEs are mobile, whereas synaptic AChEs are more stable, and that α-dystrobrevin is important for controlling the density and stability of AChEs at neuromuscular synapses.
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Todd, Melvi, Timothy Guetterman, Jako Volschenk, Martin Kidd et Elizabeth Joubert. « Healthy or Not Healthy ? A Mixed-Methods Approach to Evaluate Front-of-Pack Nutrition Labels as a Tool to Guide Consumers ». Nutrients 14, no 14 (8 juillet 2022) : 2801. http://dx.doi.org/10.3390/nu14142801.

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This study explored how South African food labels could be improved, with a focus on comparison of front-of-pack (FOP) nutrition labels as a quick assessment tool to enhance customer evaluation of the overall healthiness of packaged food. The exploratory sequential mixed-methods design used qualitative interviews (n = 49) to gain insight into labeling challenges and select FOP nutrition labels for consumer testing. Consumers (n = 1261) randomly assessed two of six possible FOP nutrition labels relative to a ‘no-label’ control applied to a fictitious cereal product in 12 online surveys. A mixed-model analysis of variance was used to compare the differences in health ratings for the different FOP nutrition labels. The interviews revealed three themes for label improvement, that are presented over three time horizons. In terms of helping consumers identify less healthy products, the effect sizes were most prominent for health warnings (p < 0.01) and low health star ratings (p < 0.01). The findings of this research not only clarify whether FOP nutrition labeling formats used in other regions such as Europe, South America and Australia could be useful in the South African context, but they can assist policymakers and decision-makers in selecting an effective FOP label.
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Kupiec-Weglinski, J. W., B. Wasowska, I. Papp, G. Schmidbauer, M. H. Sayegh, W. M. Baldwin, K. J. Wieder et W. W. Hancock. « CD4 mAb therapy modulates alloantibody production and intracardiac graft deposition in association with selective inhibition of Th1 lymphokines. » Journal of Immunology 151, no 9 (1 novembre 1993) : 5053–61. http://dx.doi.org/10.4049/jimmunol.151.9.5053.

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Abstract The accelerated (24 h) rejection of (LEWxBN)F1 cardiac allografts (Tx) in LEW rats sensitized with BN skin grafts, is abrogated with CD4 mAb (BWH-4) administration between skin (day -7) and heart (day 0) transplantation (Tx survival ca. 11 days, p &lt; 0.0001). This study analyzed the effects of CD4-targeted therapy upon host IgG and IgM alloantibody (allo-Ab) within the serum by two-color flow cytometry, and within the Tx, by immunohistology. These data were correlated with mRNA and protein production profiles of Th1 (IL-2, IFN-gamma) vs Th2 (IL-4) specific cytokines (polymerase chain reaction and/or immunohistology). Skin grafts elicited a strong systemic IgM allo-Ab response, which peaked at the time of cardiac Tx rejection at 24 h. It was associated with extensive deposits of IgM on Tx endothelium. Treatment with BWH-4 mAb diminished circulating IgM allo-Ab levels, and only low levels of IgM could be detected at the Tx site. Conversely, the low circulating IgG allo-Ab levels during rejection at 24 h in untreated recipients were accompanied by a strong labeling for intra-Tx IgG. BWH-4 mAb therapy did not prevent totally the switch of the IgM to IgG, but the IgG allo-Ab response was earlier, less intense and more transient than in untreated recipients. Accelerated rejection triggered sequential lymphokine mRNA expression in cardiac Tx, with the peak of transcription for IL-2 (6-12 h) preceding that for IL-4 (24 h). Interestingly, although CD4 targeted therapy virtually ablated the induction of IL-2 mRNA, it preserved transcription of the IL-4 gene. BWH-4 mAb therapy decreased otherwise abundant intra-Tx IL-2 and IFN-gamma, but allowed a vigorous elaboration of IL-4, confirming the translation of mRNA to the protein in vivo. Thus, CD4 mAb-mediated abrogation of accelerated cardiac Tx injury correlates with suppression of Th1 responses (depressed IL-2 and IFN-gamma production), but sparing of the Th2 function (enhanced IL-4 elaboration). Indeed, CD4 mAb-induced allo-Ab depression and immunosuppressive effects may reflect selective targeting of proinflammatory Th1-like cells and the multifaceted effects of IL-4 produced by unopposed Th2-like cells.
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Ma, Yuchao, et Hassan Ghasemzadeh. « LabelForest : Non-Parametric Semi-Supervised Learning for Activity Recognition ». Proceedings of the AAAI Conference on Artificial Intelligence 33 (17 juillet 2019) : 4520–27. http://dx.doi.org/10.1609/aaai.v33i01.33014520.

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Activity recognition is central to many motion analysis applications ranging from health assessment to gaming. However, the need for obtaining sufficiently large amounts of labeled data has limited the development of personalized activity recognition models. Semi-supervised learning has traditionally been a promising approach in many application domains to alleviate reliance on large amounts of labeled data by learning the label information from a small set of seed labels. Nonetheless, existing approaches perform poorly in highly dynamic settings, such as wearable systems, because some algorithms rely on predefined hyper-parameters or distribution models that needs to be tuned for each user or context. To address these challenges, we introduce LabelForest 1, a novel non-parametric semi-supervised learning framework for activity recognition. LabelForest has two algorithms at its core: (1) a spanning forest algorithm for sample selection and label inference; and (2) a silhouette-based filtering method to finalize label augmentation for machine learning model training. Our thorough analysis on three human activity datasets demonstrate that LabelForest achieves a labeling accuracy of 90.1% in presence of a skewed label distribution in the seed data. Compared to self-training and other sequential learning algorithms, LabelForest achieves up to 56.9% and 175.3% improvement in the accuracy on balanced and unbalanced seed data, respectively.
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Cariappa, Annaiah, Catharine Chase, Haoyuan Liu, Paul Russell et Shiv Pillai. « Naive recirculating B cells mature simultaneously in the spleen and bone marrow ». Blood 109, no 6 (21 novembre 2006) : 2339–45. http://dx.doi.org/10.1182/blood-2006-05-021089.

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Abstract We have recently demonstrated that IgDhi B cells can occupy an extravascular perisinusoidal niche in the bone marrow in addition to the well-established follicular niche in conventional secondary lymphoid organs. The spleen has long been considered to be the site at which newly formed B lymphocytes mature into IgDhi naive recirculating B cells, but the existence of mutant mice that have selectively lost mature B cells in the bone marrow prompted an examination of B-cell maturation at this latter site. Following a single pulse of BrdU in intact mice, sequential labeling of more mature B-cell populations in the bone marrow suggested ongoing maturation at this site. Further evidence for B-cell maturation in the bone marrow was obtained from analyses of transitional B cells in splenectomized lymphotoxin α-deficient mice that lack all secondary lymphoid organs. In these mice, antibody-secreting cells recognizing multivalent antigens were also observed in the bone marrow following an intravenous microbial challenge. These data suggest that newly formed B cells mature into IgDhi B cells simultaneously in the spleen and the bone marrow and establish in a stringent manner that humoral immune responses can be initiated in situ in the bone marrow.
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Huang, Xiangao, Maurizio Di Liberto, David Jayabalan, Mohamad Hussein, Sophia Randolph, Ruben Niesvizky et Selina Chen-Kiang. « Lenalidomide Targets Myeloma Cells Preferentially During Prolonged Early G1 Arrest but Not Synchronization Into S Phase by Selective and Reversible Inhibition of CDK4/CDK6 through Loss of IRF-4 ». Blood 116, no 21 (19 novembre 2010) : 449. http://dx.doi.org/10.1182/blood.v116.21.449.449.

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Abstract Abstract 449 Dysregulation of cyclin-dependent kinase (CDK)4 and CDK6 is common in human cancer and precedes unrestrained proliferation of tumor cells in multiple myeloma (MM) patients, especially during refractory relapse. MM remains incurable due to the eventual development of drug resistance despite initial response to two main lines of therapy with proteasome inhibitors and immunomodulatory drugs. Therapeutic strategies that both control the cell cycle and enhance cytotoxic killing are thus urgently needed in MM. Although targeting the cell cycle in cancer therapy has only been modestly successful because broad-spectrum CDK inhibitors lack specificity and are highly toxic, we have recently developed such a therapy by selective inhibition of CDK4/CDK6 in sequential combination with proteasome inhibitors. Using PD 0332991, the only known selective inhibitor of CDK4/CDK6 that is also potent, reversible and bioavailable, we have demonstrated that 1) induction of prolonged early G1 arrest by inhibition of CDK4/CDK6 markedly enhances the killing of primary BM myeloma cells by proteasome inhibitors despite stromal protection, and 2) release from the G1 block upon PD 0332991 withdraw leads to synchronous progression to S phase, which further augments cytotoxic killing of MM cells. To optimize targeting CDK4/CDK6 in MM, we have investigated lenalidomide as an alternative cytotoxic partner by first determining its cell cycle targeting specificity, taking advantage of the exceptional precision and efficiency with which PD 0332991 induces early G1 arrest and cell cycle synchronization. We show by simultaneous analyses of BrdU pulse labeling and DNA content per cell that lenalidomide preferentially targets MM cells following prolonged early G1 arrest by PD 0332991 pretreatment for 24 hours (twice the time needed to induce G1 arrest in MM cells), but not those synchronized into S phase after release from the G1 block. This is distinct from proteasome inhibitors (bortezomib, carfilzomib and ONX-0921), which preferentially target MM cells synchronized into S phase over those arrested in G1. MM cells in G2/M appear to be less sensitive to both proteasome inhibitors and lenalidomide. However, these cells are rendered sensitive to these compounds upon cell cycle reentry through inhibition of CDK4/CDK6 and induction of early G1 arrest. Time course studies of DNA replication further reveal that lenalidomide alone (3 uM, daily) induces G1 arrest by 48 hours, which precedes evidence of apoptosis and reduction of viable cells at 72 hours. While the magnitude of G1 arrest induced by lenalidomide is dose-dependent (1-50 uM), the timing of cytotoxic killing does not vary. Prior induction of prolonged early G1 arrest by PD 0332991 (24 hours) enhances (> 5-fold) and also accelerates lenalidomide killing by at least 24 hours, leading to eradication of some MM cell lines. This acceleration and enhancement of lenalidomide killing appears to be mediated by synergistic reduction of IRF-4, as we have found in cell cycle enhancement of proteasome inhibitor killing. Most importantly, acceleration of early G1 arrest by inhibition of CDK4/CDK6 in primary bone marrow myeloma cells enhances lenalidomide killing in the presence of bone marrow stromal cells. Thus, the immunomodulatory compound lenalidomide induces G1 arrest and is cytotoxic for myeloma cells directly and preferentially in G1, in contrast to proteasome inhibitors, which preferentially target MM cells in S phase. Induction of prolonged early G1 arrest accelerates and enhances subsequent lenalidomide killing, which appears to be mediated by loss of IRF-4 in common with cell cycle enhancement of proteasome inhibitor killing. To implement targeting CDK4/CDK6 in combination therapy, a multi-center phase 1/2 clinical trial targeting CDK4/6 with PD 0332991 in sequential combination with bortezomib and dexamethasone in relapsed refractory MM is in progress. Data from the phase 1 portion indicate that PD 0332991 is well tolerated, and directly and completely inhibits CDK4/CDK6 and the cell cycle in tumor cells in MM patients with promising clinical efficacy. Given the known clinical efficacy of lenalidomide in MM, our findings suggest lenalidomide as an attractive cytotoxic partner for targeting CDK4/CDK6 in sequential combination therapy to both control tumor expansion and enhance tumor killing in the treatment of MM. Disclosures: Off Label Use: PD 0332991 is a cell cycle CDK4/CDK6 inhibitor. Hussein:Celgene: Employment. Randolph:pfizer: Employment, Equity Ownership. Niesvizky: Celgene: Consultancy, Research Funding, Speakers Bureau; Millennium: Consultancy, Research Funding, Speakers Bureau; Onyx: Consultancy, Research Funding, Speakers Bureau.
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Vargas-Sanchez, Karina, Antonios Vekris et Klaus G. Petry. « DNA Subtraction of In Vivo Selected Phage Repertoires for Efficient Peptide Pathology Biomarker Identification in Neuroinflammation Multiple Sclerosis Model ». Biomarker Insights 11 (janvier 2016) : BMI.S32188. http://dx.doi.org/10.4137/bmi.s32188.

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To streamline in vivo biomarker discovery, we developed a suppression subtractive DNA hybridization technique adapted for phage-displayed combinatorial libraries of 12 amino acid peptides (PhiSSH). Physical DNA subtraction is performed in a one-tube-all-reactions format by sequential addition of reagents, producing the enrichment of specific clones of one repertoire. High-complexity phage repertoires produced by in vivo selections in the multiple sclerosis rat model (experimental autoimmune encephalomyelitis, EAE) and matched healthy control rats were used to evaluate the technique. The healthy repertoire served as a physical DNA subtractor from the EAE repertoire to produce the subtraction repertoire. Full next-generation sequencing (NGS) of the three repertoires was performed to evaluate the efficiency of the subtraction technique. More than 96% of the clones common to the EAE and healthy repertoires were absent from the subtraction repertoire, increasing the probability of randomly selecting various specific peptides for EAE pathology to about 70%. Histopathology experiments were performed to confirm the quality of the subtraction repertoire clones, producing distinct labeling of the blood–brain barrier (BBB) affected by inflammation among healthy nervous tissue or the preferential binding to IL1-challenged vs. resting human BBB model. Combining PhiSSH with NGS will be useful for controlled in vivo screening of small peptide combinatorial libraries to discover biomarkers of specific molecular alterations interspersed within healthy tissues.
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Huang, Xiangao, Maurizio Di Liberto, Scott Ely, David S. Jayabalan, Isan Chen, Keith D. Wilner, Malcolm Moore, Ruben Niesvizky et Selina Chen-Kiang. « Induction of sequential G1 arrest and synchronous S phase entry by reversible CDK4/CDK6 inhibition sensitizes myeloma cells for cytotoxic killing through loss of IRF-4. » Blood 114, no 22 (20 novembre 2009) : 299. http://dx.doi.org/10.1182/blood.v114.22.299.299.

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Abstract Abstract 299 Dysregulation of the cell cycle is a hallmark of cancer. However, targeting the cell cycle in cancer therapy has only been modestly successful since broad-spectrum cyclindependent kinase (CDK) inhibitors lack specificity and are highly toxic. The critical importance of controlling CDK4/CDK6 in cancer treatment is further exemplified by recent evidence of prominent CDK4/CDK6 dysregulation in human cancers, including breast cancer, metastatic lung adenocarcinoma, glioblastoma, mantle cell lymphoma and multiple myeloma (MM). To advance mechanism-based targeting of the cell cycle in cancer, we have developed a novel strategy that both inhibits cell cycle progression and enhances cytotoxic killing in tumor cells using PD 0332991(PD), the only known CDK4/CDK6-specific inhibitor that is also reversible, potent and orally bioavailable. We demonstrated by BrdU pulse-labeling that inhibition of CDK4/CDK6 with PD in primary bone marrow (BM) myeloma cells and human myeloma cell lines (HMCL) (IC50 60nM) leads to a complete early G1 arrest in the absence of apoptosis and upon release of the G1 block, synchronous cell cycle progression to S phase. Furthermore, prolonged early G1 arrest enhances cytotoxic killing of MM cells by diverse clinically relevant drugs at low dose, including bortezomib, carfilzomib (PR-171) and dexamethasone, and this is dramatically augmented during synchronous S phase entry. The enhancement of cytotoxic killing in either G1 arrest or synchronous S phase entry is sustained in the presence of BM stromal cells. This killing is caspase-dependent and triggered by the loss of mitochondrial outer membrane potential and activation of the intrinsic apoptosis pathway. Time course studies of cell cycle-specific gene expression by expression profiling, quantitative real time RT-PCR and immunoblotting further revealed that the expression of IRF-4, essential for normal plasma cell differentiation and myeloma cell survival, is strictly cell cycle-dependent: elevated in G1 and markedly declined in S phase. The IRF-4 protein is also markedly reduced (50%) by bortezomib treatment, resulting in a combined 5-fold reduction in S phase. This suggests that differential enhancement of cytotoxic killing in G1 arrest and S phase is mediated by cell cycle-dependent IRF-4 expression. Indeed, shRNA interference confirms that by antagonizing mitochondrial depolarization, IRF-4 is required to protect myeloma cells from cell cycle-dependent enhancement of bortezomib killing. By timely administration and discontinuation of PD treatment, we have further demonstrated in a human MM 1.S. xenograft myeloma model that it is feasible to induce sequential G1 arrest and synchronous S phase in vivo. This leads to synergistic tumor suppression through amplification of bortezomib killing of myeloma cells, but not normal BM cells. As PD is orally bio-available, specific and low in toxicity, our novel strategy has been implemented in the first phase I/II multi-center clinical trial targeting CDK4/CDK6 with PD in combination with bortezomib and dexamethasone in MM. Preliminary bone marrow immunohistochemistry demonstrates PD preferentially and completely inhibits CDK4/CDK6-specific phosphorylaton of Rb and DNA replication in tumor cells, but not other bone marrow cells in all patients. One patient achieved VGPR (12.5%) while 1 patient each achieved MR and SD respectively for an ORR 25% (Niesvizky et al, submitted). Collectively, our preclinical and clinical data indicate, for the fist time, that selective targeting of CDK4/CDK6 in combination therapy is a promising mechanism-based therapy for MM and potentially other cancers. Disclosures: Off Label Use: PD 0332991 is going to be used as a CDK4/6-specific inhibitor.. Chen:Pfizer, Inc.: Employment, Equity Ownership. Wilner:Pfizer, Inc.: Employment, Equity Ownership. Niesvizky:Millenium: Research Funding, Speakers Bureau; Celgene: Research Funding, Speakers Bureau; Seattle Genetics, Inc: Research Funding; Proteolix: Research Funding, data monitoring committee. Chen-Kiang:Pfizer Inc.: Research Funding.
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Bokkers, Reinoud P. H., Laurens J. De Cocker, M. J. P. van Osch, Nolan S. Hartkamp et J. Hendrikse. « Selective Arterial Spin Labeling ». Topics in Magnetic Resonance Imaging 25, no 2 (avril 2016) : 73–80. http://dx.doi.org/10.1097/rmr.0000000000000078.

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Kang, Qiyu, et Wee Peng Tay. « Sequential Multi-Class Labeling in Crowdsourcing ». IEEE Transactions on Knowledge and Data Engineering 31, no 11 (1 novembre 2019) : 2190–99. http://dx.doi.org/10.1109/tkde.2018.2874003.

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Cserép, Gergely B., András Herner, Otto S. Wolfbeis et Péter Kele. « Tyrosine specific sequential labeling of proteins ». Bioorganic & ; Medicinal Chemistry Letters 23, no 21 (novembre 2013) : 5776–78. http://dx.doi.org/10.1016/j.bmcl.2013.09.002.

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Bella, Angelo, et Camillo Costantini. « Sequential separability vs selective sequential separability ». Filomat 29, no 1 (2015) : 121–24. http://dx.doi.org/10.2298/fil1501121b.

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A space X is sequentially separable if there is a countable D ? X such that every point of X is the limit of a sequence of points from D. We present two examples of a sequentially separable space which is not selectively sequentially separable. One of them is in addition countable and sequential.
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Dorantes-Aldama, Alejandro, et Dmitri Shakhmatov. « Selective sequential pseudocompactness ». Topology and its Applications 222 (mai 2017) : 53–69. http://dx.doi.org/10.1016/j.topol.2017.02.016.

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Qin, Jie, Li Liu, Zhaoxiang Zhang, Yunhong Wang et Ling Shao. « Compressive Sequential Learning for Action Similarity Labeling ». IEEE Transactions on Image Processing 25, no 2 (février 2016) : 756–69. http://dx.doi.org/10.1109/tip.2015.2508600.

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Maoying Qiao, Wei Bian, Richard Yi Da Xu et Dacheng Tao. « Diversified Hidden Markov Models for Sequential Labeling ». IEEE Transactions on Knowledge and Data Engineering 27, no 11 (1 novembre 2015) : 2947–60. http://dx.doi.org/10.1109/tkde.2015.2433262.

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Elloumi, Samir. « An adaptive model for sequential labeling systems ». Multimedia Tools and Applications 78, no 16 (12 avril 2019) : 22183–97. http://dx.doi.org/10.1007/s11042-019-7558-8.

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Chen, Xi, et Yao-Wen Wu. « Selective chemical labeling of proteins ». Organic & ; Biomolecular Chemistry 14, no 24 (2016) : 5417–39. http://dx.doi.org/10.1039/c6ob00126b.

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Liu, Chaoxing, Xiaomeng Luo, Yuqi Chen, Fan Wu, Wei Yang, Yafen Wang, Xiong Zhang, Guangrong Zou et Xiang Zhou. « Selective Labeling Aldehydes in DNA ». Analytical Chemistry 90, no 24 (16 novembre 2018) : 14616–21. http://dx.doi.org/10.1021/acs.analchem.8b04822.

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Wong, Eric C., Matthew Cronin, Wen-Chau Wu, Ben Inglis, Lawrence R. Frank et Thomas T. Liu. « Velocity-selective arterial spin labeling ». Magnetic Resonance in Medicine 55, no 6 (2006) : 1334–41. http://dx.doi.org/10.1002/mrm.20906.

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Schmid, Sophie, Eidrees Ghariq, Wouter M. Teeuwisse, Andrew Webb et Matthias J. P. van Osch. « Acceleration-selective arterial spin labeling ». Magnetic Resonance in Medicine 71, no 1 (8 mars 2013) : 191–99. http://dx.doi.org/10.1002/mrm.24650.

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Pacini, L., C. Limatola, L. Frati, P. Luly et A. Spinedi. « Muscarinic stimulation of SK-N-BE(2) human neuroblastoma cells elicits phosphoinositide and phosphatidylcholine hydrolysis : relationship to diacylglycerol and phosphatidic acid accumulation ». Biochemical Journal 289, no 1 (1 janvier 1993) : 269–75. http://dx.doi.org/10.1042/bj2890269.

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Muscarinic stimulation of the human neuroblastoma cell line SK-N-BE(2) elicits hydrolysis of phosphoinositides and phosphatidylcholine (PtdCho) and produces a rapid and sustained elevation of diacylglycerol (DG) mass. PtdIns(4,5)P2 cleavage by phospholipase C (PLC) occurred immediately after carbachol (CCh) addition, and phosphoinositide hydrolysis was then sustained for at least 5 min. Cell stimulation, after extensive PtdCho labelling by long-term [3H]choline administration, resulted in an enhanced release of [3H]phosphocholine (PCho) into the external medium; enhanced [3H]PCho release, which occurred with a 15 s delay with respect to CCh addition, was particularly pronounced within the first minute of stimulation and proved to be caused by PtdCho-specific PLC activation. In fact, when cells were exposed to [3H]choline for a short period, to extensively label the intracellular PCho pool but not PtdCho, stimulation did not result in an enhanced release of [3H]PCho into the medium. PtdCho-specific phospholipase D (PLD) activation was documented by the accumulation of [3H]phosphatidylethanol in cells prelabelled with [3H]myristic acid and stimulated in the presence of 1% (v/v) ethanol; this metabolic pathway, however, proved to be a minor one leading to generation of phosphatidic acid (PtdOH) during cell stimulation, whereas DG production by the sequential action of PtdCho-specific PLD and PtdOH phosphohydrolase was not observed. Studies on cells which were double-labelled with [3H]myristic acid and [14C]arachidonic acid indicated that within 15 s of stimulation DG is uniquely derived from PtdIns(4,5)P2, whereas PtdCho is the major source at later times. Evidence is provided that rapid and selective conversion of phosphoinositide-derived DG into PtdOH may play an important role in determining the temporal accumulation profile of DG from the above-mentioned sources.
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Seoud, M. A., M. El-Zekey et E. F. El-Gazar. « Mean, Odd Sequential and Triangular Sum Graphs ». Circulation in Computer Science 2, no 4 (20 mai 2017) : 40–52. http://dx.doi.org/10.22632/ccs-2017-252-08.

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In this paper, we prove that all odd sequential graphs are mean graphs, but not all mean graphs are an odd sequential graph. We show that some new families generated by some graph operations on some standard graphs are admitting mean labeling and odd sequential labeling. Finally, we conclude some new results in triangular sum graphs.
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Kiessling, Marika, Eberhard Herchenhan et Hans R. Eggert. « Cerebrovascular and metabolic effects on the rat brain of focal Nd:YAG laser irradiation ». Journal of Neurosurgery 73, no 6 (décembre 1990) : 909–17. http://dx.doi.org/10.3171/jns.1990.73.6.0909.

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✓ To investigate the effects of focal neodymium:yttrium-aluminum-garnet (Nd:YAG) laser irradiation (λ = 1060 nm) on regional cerebral blood flow, cerebral protein synthesis, and blood-brain barrier permeability, the parietal brain surface of 44 rats was irradiated with a focused laser beam at a constant output energy of 30 J. Survival times ranged from 5 minutes to 48 hours. Laser irradiation immediately caused well-defined cortical coagulation necrosis. Within 5 minutes after unilateral irradiation, 14C-iodoantipyrine autoradiographs demonstrated severely reduced blood flow to the irradiation site and perilesional neocortex, but a distinct reactive hyperemia in all other areas of the forebrain. Apart from a persistent ischemic focus in the vicinity of the cortical coagulation necrosis, blood flow alterations in remote areas of the brain subsided within 3 hours after irradiation. Autoradiographic assessment of 3H-tyrosine incorporation into brain proteins revealed rapid onset and prolonged duration of protein synthesis inhibition in perifocal morphologically intact cortical and subcortical structures. Impairment of amino acid incorporation proved to be completely reversible within 48 hours. Immunoautoradiographic visualization of extravasated plasma proteins using 3H-labeled rabbit anti-rat immunoglobulins showed that, up to 1 hour after irradiation, immunoreactive proteins were confined to the neocortex at the irradiation site. At 4 hours, vasogenic edema was present in the vicinity of the irradiation site and the subcortical white matter, and, at later stages (16 to 36 hours), also extended into the contralateral hemisphere. Although this was followed by a gradual decrease in labeling intensity, resolution of edema was still not complete after 48 hours. Analysis of sequential functional changes in conjunction with morphological alterations indicates that the evolution of morphological damage after laser irradiation does not correlate with the time course and spatial distribution of protein synthesis inhibition or vasogenic edema. Although the central coagulation necrosis represents a direct effect of radiation, the final size of the laser-induced lesion is determined by a delayed colliquation necrosis due to persistent perifocal ischemia. Extent and severity of ischemia in a zone with initial preservation of neuroglial cells can be explained by the optical properties of the Nd:YAG laser; extensive scattering of light within brain parenchyma associated with a high blood-to-brain absorption ratio selectively affects blood vessels outside the irradiation focus.
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Brushart, Thomas M. E. « Preferential motor reinnervation : a sequential double-labeling study ». Restorative Neurology and Neuroscience 1, no 3,4 (1990) : 281–87. http://dx.doi.org/10.3233/rnn-1990-13416.

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Wu, Xian, Wei Fan et Yong Yu. « Sembler : Ensembling Crowd Sequential Labeling for Improved Quality ». Proceedings of the AAAI Conference on Artificial Intelligence 26, no 1 (20 septembre 2021) : 1713–19. http://dx.doi.org/10.1609/aaai.v26i1.8351.

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Many natural language processing tasks, such as named entity recognition (NER), part of speech (POS) tagging, word segmentation, and etc., can be formulated as sequential data labeling problems. Building a sound labeler requires very large number of correctly labeled training examples, which may not always be possible. On the other hand, crowdsourcing provides an inexpensive yet efficient alternative to collect manual sequential labeling from non-experts. However the quality of crowd labeling cannot be guaranteed, and three kinds of errors are typical: (1) incorrect annotations due to lack of expertise (e.g., labeling gene names from plain text requires corresponding domain knowledge); (2) ignored or omitted annotations due to carelessness or low confidence; (3) noisy annotations due to cheating or vandalism. To correct these mistakes, we present Sembler, a statistical model for ensembling crowd sequential labelings. Sembler considers three types of statistical information: (1) the majority agreement that proves the correctness of an annotation; (2) correct annotation that improves the credibility of the corresponding annotator; (3) correct annotation that enhances the correctness of other annotations which share similar linguistic or contextual features. We evaluate the proposed model on a real Twitter and a synthetical biological data set, and find that Sembler is particularly accurate when more than half of annotators make mistakes.
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Glass, George, Jason A. Papin et James W. Mandell. « Simple : A Sequential Immunoperoxidase Labeling and Erasing Method ». Journal of Histochemistry & ; Cytochemistry 57, no 10 (13 avril 2009) : 899–905. http://dx.doi.org/10.1369/jhc.2009.953612.

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Row, R. David, Hui-Wen Shih, Austin T. Alexander, Ryan A. Mehl et Jennifer A. Prescher. « Cyclopropenones for Metabolic Targeting and Sequential Bioorthogonal Labeling ». Journal of the American Chemical Society 139, no 21 (17 mai 2017) : 7370–75. http://dx.doi.org/10.1021/jacs.7b03010.

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Yu, Dong, Shizhen Wang et Li Deng. « Sequential Labeling Using Deep-Structured Conditional Random Fields ». IEEE Journal of Selected Topics in Signal Processing 4, no 6 (décembre 2010) : 965–73. http://dx.doi.org/10.1109/jstsp.2010.2075990.

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Zhang, Guopeng, Massimo Piccardi et Ehsan Zare Borzeshi. « Sequential Labeling With Structural SVM Under Nondecomposable Losses ». IEEE Transactions on Neural Networks and Learning Systems 29, no 9 (septembre 2018) : 4177–88. http://dx.doi.org/10.1109/tnnls.2017.2757504.

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Sumathi, P., et G. Geetha Ramani. « Arithmetic Sequential Graceful Labeling on Star Related Graphs ». Indian Journal Of Science And Technology 15, no 44 (28 novembre 2022) : 2356–62. http://dx.doi.org/10.17485/ijst/v15i44.1863.

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Ngo, John T., Julie A. Champion, Alborz Mahdavi, I. Caglar Tanrikulu, Kimberly E. Beatty, Rebecca E. Connor, Tae Hyeon Yoo, Daniela C. Dieterich, Erin M. Schuman et David A. Tirrell. « Cell-selective metabolic labeling of proteins ». Nature Chemical Biology 5, no 10 (9 août 2009) : 715–17. http://dx.doi.org/10.1038/nchembio.200.

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Werner, Richard, David G. Norris, Karsten Alfke, H. Maximilian Mehdorn et Olav Jansen. « Continuous artery-selective spin labeling (CASSL) ». Magnetic Resonance in Medicine 53, no 5 (2005) : 1006–12. http://dx.doi.org/10.1002/mrm.20475.

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Le, Phu H., et W. David Nes. « Sterols : Tritium-labeling and selective oxidations ». Chemistry and Physics of Lipids 40, no 1 (mai 1986) : 57–69. http://dx.doi.org/10.1016/0009-3084(86)90062-9.

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Panes, Olga, Valeria Matus, César González, Claudia G. Sáez, Jaime Pereira et Diego Mezzano. « Circulating Human Platelets Express LRP-1 and uPAR mRNAs and Synthesize the Proteins : The Complex LRP-1, uPAR, PAI-1 and uPA Play a Role in Modulating Fibrinolysis in Platelet-Rich Thrombi ». Blood 120, no 21 (16 novembre 2012) : 1116. http://dx.doi.org/10.1182/blood.v120.21.1116.1116.

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Abstract Abstract 1116 Platelets are intrinsic components of hemostatic and pathological clots, and are essential for clot retraction. However, their role and sequential involvement in clot stabilization and lysis are still poorly understood. Human platelets contain several components of the fibrinolytic system, including functional PAI-1, TAFI, uPA and α 2-antiplasmin. Moreover, platelets possess a rich transcriptome and synthesize several proteins, among them, PAI-1. Using a global, modified clot lysis time assay in platelet-rich plasma (CLT-PRP; Panes et al., Platelets 2012) we found that the CLT-PRP was significantly longer than that of CLT in platelet-free plasma (PFP), reflecting a down-regulation of the fibrinolytic process. However, the prolonged CLT in subjects receiving tranexamic acid was normalized earlier in PRP than in PPP, denoting some pro-fibrinolytic activity in clots formed in a platelet milieu. Aim: to study the presence, origin, association and functional role of components of the fibrinolytic system in human platelets. Also, we aim to getting insight into the dynamic balance and modulation of the fibrinolytic process by the interplay of pro- and anti-fibrinolytic platelet factors. Methods and Results: in washed, leukocyte-free human platelets we detected expression of LRP-1, uPAR, PAI-1 mRNAs, and synthesis of these proteins (metabolic radiolabeling). Neither uPA mRNA nor synthesis of uPA was evidenced. All of these proteins, including uPA were detected in membrane or cytosol fractions by western blotting (WB). LRP-1 and uPAR were present in the outer leaflet of platelet membranes, with increased uPAR labeling after platelet activation (confocal microscopy-immunofluorescence). Non-stimulated whole platelets exhibit a low basal uPA activity (specific chromogenic substrate) selectively inhibited by amiloride. uPA activity falls slightly immediately after VWF-Ristocetin (VWF-R) and TRAP stimulation, but recovers to basal levels after 15min. Biotinylated washed platelets were immunoprecipitated (IP) with α -uPAR MoAb at different times before and after activation with either TRAP or VWF-Ristocetin. Co-precipitations with LRP-1, PAI-1 and uPA were detected in WB only after platelet activation with TRAP for 5 min, denoting the formation of a tetrameric complex, likely involved in endocytosis and receptor recycling. Interestingly, 5min after TRAP stimulation, uPA was sharply reduced, disappearing at 15 min, either in membrane or cytosol fractions, suggesting degradation of the protein. Similar pattern of co-precipitations were observed when IP was done with α -LRP-1 MoAb. Co-precipitations were more prominent in purified platelet membrane than in cytosolic fractions. Conclusions: human platelets express LRP-1, uPAR and PAI-1 mRNAs, and synthesize these proteins. uPA activity is present in whole, purified, washed platelets, and the protein is likely bound to the external platelet membrane. Co-precipitation of all these fibrinolytic components presumably denotes the formation of a tetrameric complex with endocytic and recycling capacities, as demonstrated in other cell lineages. Sequential IP′s after platelet activation disclose the disappearance of uPA, but not of PAI-1, from the complex, probably explained by a degradation process. Taken together, these results suggest that platelets play a predominantly antifibrinolytic role during early stages of formation of platelet-rich clots. Disclosures: No relevant conflicts of interest to declare.
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Schmid, Sophie, Esben T. Petersen et Matthias J. P. Van Osch. « Insight into the labeling mechanism of acceleration selective arterial spin labeling ». Magnetic Resonance Materials in Physics, Biology and Medicine 30, no 2 (27 octobre 2016) : 165–74. http://dx.doi.org/10.1007/s10334-016-0596-6.

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Kantabutra, Sanpawat. « Fast Sequential and Parallel Vertex Relabelings of Km,m ». International Journal of Foundations of Computer Science 26, no 01 (janvier 2015) : 33–50. http://dx.doi.org/10.1142/s0129054115500021.

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Given an undirected, connected, simple graph G = (V,E), two vertex labelings LV and L'V of the vertices of G, and a label flip operation that interchanges a pair of labels on adjacent vertices, the Vertex Relabeling Problem is to transform G from LV into L'V using the flip operation. Agnarsson et al. showed solving the Vertex Relabeling Problem on arbitrary graphs can be done in θ(n2), where n is the number of vertices in G. In this article we study the Vertex Relabeling Problem on graphs Km,m and introduce the concept of parity and precise labelings. We show that, when we consider the parity labeling, the problem on graphs Km,m can be solved quickly in O(log m) time using m processors on an EREW PRAM. Additionally, we also show that the number of processors can be further reduced to [Formula: see text] in this case while the time complexity does not change. When the labeling is precise, the parallel time complexity increases by a factor of log m while the processor complexities remain m and [Formula: see text]. We also show that, when graphs are restricted to Km,m, this problem can be solved optimally in O(m) time when the labeling is parity, and can be solved in O(m log m) time when the labeling is precise, thereby improving the result in Agnarsson et al. for this specific case. Moreover, we generalize the result in the case of precise labeling to the cases when LV and L'V can be any configuration. In the end we give a conclusion and a list of some interesting open problems.
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Payet, Nadia, et Sinisa Todorovic. « SLEDGE : Sequential Labeling of Image Edges for Boundary Detection ». International Journal of Computer Vision 104, no 1 (2 février 2013) : 15–37. http://dx.doi.org/10.1007/s11263-013-0612-5.

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Tangaro, Sabina, Nicola Amoroso, Massimo Brescia, Stefano Cavuoti, Andrea Chincarini, Rosangela Errico, Paolo Inglese et al. « Feature Selection Based on Machine Learning in MRIs for Hippocampal Segmentation ». Computational and Mathematical Methods in Medicine 2015 (2015) : 1–10. http://dx.doi.org/10.1155/2015/814104.

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Neurodegenerative diseases are frequently associated with structural changes in the brain. Magnetic resonance imaging (MRI) scans can show these variations and therefore can be used as a supportive feature for a number of neurodegenerative diseases. The hippocampus has been known to be a biomarker for Alzheimer disease and other neurological and psychiatric diseases. However, it requires accurate, robust, and reproducible delineation of hippocampal structures. Fully automatic methods are usually the voxel based approach; for each voxel a number of local features were calculated. In this paper, we compared four different techniques for feature selection from a set of 315 features extracted for each voxel: (i) filter method based on the Kolmogorov-Smirnov test; two wrapper methods, respectively, (ii) sequential forward selection and (iii) sequential backward elimination; and (iv) embedded method based on the Random Forest Classifier on a set of 10 T1-weighted brain MRIs and tested on an independent set of 25 subjects. The resulting segmentations were compared with manual reference labelling. By using only 23 feature for each voxel (sequential backward elimination) we obtained comparable state-of-the-art performances with respect to the standard tool FreeSurfer.
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Nguyen, Kim, Michael Fazio, Miles Kubota, Sarah Nainar, Chao Feng, Xiang Li, Scott X. Atwood, Timothy W. Bredy et Robert C. Spitale. « Cell-Selective Bioorthogonal Metabolic Labeling of RNA ». Journal of the American Chemical Society 139, no 6 (7 février 2017) : 2148–51. http://dx.doi.org/10.1021/jacs.6b11401.

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Ngo, John T., Brett M. Babin, Julie A. Champion, Erin M. Schuman et David A. Tirrell. « State-Selective Metabolic Labeling of Cellular Proteins ». ACS Chemical Biology 7, no 8 (12 juin 2012) : 1326–30. http://dx.doi.org/10.1021/cb300238w.

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Qin, Qin, et Peter C. M. van Zijl. « Velocity-selective-inversion prepared arterial spin labeling ». Magnetic Resonance in Medicine 76, no 4 (28 octobre 2015) : 1136–48. http://dx.doi.org/10.1002/mrm.26010.

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Rawale, Dattatraya G., Kalyani Thakur, Srinivasa Rao Adusumalli et Vishal Rai. « Chemical Methods for Selective Labeling of Proteins ». European Journal of Organic Chemistry 2019, no 40 (26 septembre 2019) : 6749–63. http://dx.doi.org/10.1002/ejoc.201900801.

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