Gotowe bibliografie tematyczne / PF4

Gotowa bibliografia na temat „PF4”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 11 marca 2023

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Artykuły w czasopismach na temat "PF4"

1

Esan, A. M., Z. Khan, R. Kiran, T. O. Omolekan, K. A. Aremu i H. R. Y. Adeyemi. "Ameliorative Effects of Pseudomonas fluorescence Strains on Growth and Antioxidant Potential of Okra (Abelmoschus esculentus) Plant under Nematode Infection". European Journal of Biology and Biotechnology 2, nr 3 (5.06.2021): 50–56. http://dx.doi.org/10.24018/ejbio.2021.2.3.168.

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Meloidogyne incognita is a plant pathogen causing root-knot nematodes disease in many crops worldwide. Due to the environmental threat on the use of chemical fumigants, there is a need for a biological control method using microbial antagonists on root-knot nematodes disease. Therefore, this study was conducted to screen and evaluate the biocontrol potential of P. fluorescens strains against root-knot nematodes. The effectiveness of six P. fluorescens strains viz., Pf1, Pf2, Pf3, Pf4, Pf5and Pf6 were tested in vitro and also in pots experiment for their inhibitory activities and biocontrol potential against root-knot nematodes disease caused by Meloidogyne incognita on okra plant. Treatments of the nematode with 1.0-6.0% concentrations of 108 CFU/mL of Pf4 and Pf5 strains caused 70.0-95.0% inhibition on nematode egg-hatch and 2nd stage juveniles activity. Pf3, Pf4 and Pf5showed a decrease in the number of roots galling with increased root and shoot dry weights of stressed okra plant. Moreover, there was 25.99-36.43%, 37.76-79.145% and 42.62-62.37%, 69.83-98.09% increase in shoot length and leaf areas after 15th and 30th day respectively of P. fluorescens inoculation. The inoculated okra plants exhibited higher photosynthetic pigments, higher antioxidant enzymes activity and mineral contents than the nematode treated groups. Higher mineral contents were observed in the roots than the leaves of the okra plant subjected to the nematode infection. The bacteria strains especially Pf4 and Pf3 have considerable potential to reduce the menace of the nematodes in the treated okra plant. Therefore, the strains can be used for crop management against root-knot nematodes disease.
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González-Serrano, Diego J., Milad Hadidi, Matin Varcheh, Aniseh Zarei Jelyani, Andres Moreno i Jose M. Lorenzo. "Bioactive Peptide Fractions from Collagen Hydrolysate of Common Carp Fish Byproduct: Antioxidant and Functional Properties". Antioxidants 11, nr 3 (6.03.2022): 509. http://dx.doi.org/10.3390/antiox11030509.

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Collagen isolated from byproducts of common carp was hydrolyzed with alcalase enzyme to obtain peptide fractions. The resulting >30 kDa (PF1), 10–30 kDa (PF2), 3–10 kDa (PF3) and <1 kDa (PF4) fractions were studied for their antioxidant and functional properties. All peptide fractions illustrated antioxidant activity at different concentrations (1, 5, and 10 mg/mL). Although PF4 indicated the highest DPPH radical-scavenging activity (87%) at a concentration of 1 mg/mL, the highest reducing power (0.34) and hydroxyl radical scavenging activity (95.4%) were also observed in PF4 at a concentration of 10 mg/mL. The solubility of the peptide fractions was influenced by pH. The lowest solubility of the peptide fractions was observed at pH 4. The highest emulsifying activity index (EAI) was observed for PF4 (121.1 m2/g), followed by PF3 (99.6 m2/g), PF2 (89.5 m2/g) and PF1 (78.2 m2/g). In contrast to what has been found in the case of EAI, the emulsion stability of the peptide fractions decreased at lower molecular weight, which ranged from 24.4 to 31.6 min. Furthermore, it was revealed that PF1 had the highest foam capacity (87.4%) and foam stability (28.4 min), followed by PF2 and PF3. Overall, the findings suggest that peptide fractions isolated from byproducts of common carp are a promising source of natural antioxidants for application in functional food and pharmaceutical products.
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Kakkar, Preeti Handa, R. M. Saxena i Mamta Joshi. "Histopathological analysis of liver in Puntius ticto exposed to water soluble fraction (WSF) of petrol". Journal of Applied and Natural Science 2, nr 2 (1.12.2010): 290–92. http://dx.doi.org/10.31018/jans.v2i2.136.

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The fresh water fish Puntius ticto were exposed to lethal concentration of water soluble fraction (WSF) of petrol (5%-PF1, 10%-PF2, 15%-PF3, 20%-PF4 and 25%-PF5) for 96 hours. The exposure of WSF produced some conspicuous histopathological changes in liver. The swelling of hepatocytes, degeneration, necrosis, hemolysis, dilation, congestion and fibrosis in blood sinusoids were the prominent changes observed. The histological analysis showed increasing damages dose-dependents and time-dependents.
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FELLOWES, R. A., A. G. MAULE, N. J. MARKS, T. G. GEARY, D. P. THOMPSON i D. W. HALTON. "Nematode neuropeptide modulation of the vagina vera of Ascaris suum: in vitro effects of PF1, PF2, PF4, AF3 and AF4". Parasitology 120, nr 1 (styczeń 2000): 79–89. http://dx.doi.org/10.1017/s0031182099005260.

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Ascaris suum possesses a large number of FMRFamide-related peptides (FaRPs) of which KNEFIRFamide (AF1), KHEYLRFamide (AF2) and KSAYMRFamide (AF8/PF3) have been shown to modulate the intrinsic, rhythmic activity of the vagina vera of A. suum in vitro. In the present study, the effects of the nematode FaRPs, SDPNFLRFamide (PF1), SADPNFLREamide (PF2) and KPNFIRFamide (PF4) (from Panagrellus redivivus) and AVPGVLRFamide (AF3) and GDVPGVLRFamide (AF4) (from A. suum) on the in vitro activity of the vagina vera were examined. The effects of each of the peptides were qualitatively and quantitatively distinct. All 3 FaRPs from P. redivivus were inhibitory, causing a cessation of contractions. PF2 was 3 times more potent than PF1, with a threshold of 1 nM. Although PF4 was the least potent (threshold, 10 nM), its effects at [ges ]10 nM were quantitatively the greatest. Both AF3 and AF4 (1 μM) induced complex, multiphasic responses consisting of an initial contraction and spastic paralysis followed by a return of contractile activity of increased amplitude. AF3 was 3 times more potent than AF4. The effects of these peptides had some similarities to those observed on A. suum somatic body wall muscle in vitro, with PF1, PF2 and PF4 being inhibitory and AF3 and AF4 being excitatory.
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5

Lecomte-Raclet, Laurence, Mònica Alemany, Anabelle Sequeira-Le Grand, Jean Amiral, Gérard Quentin, Anne Marie Vissac, Jacques P. Caen i Zhong Chao Han. "New Insights Into the Negative Regulation of Hematopoiesis by Chemokine Platelet Factor 4 and Related Peptides". Blood 91, nr 8 (15.04.1998): 2772–80. http://dx.doi.org/10.1182/blood.v91.8.2772.2772_2772_2780.

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Platelet factor 4 (PF4) has been recognized as an inhibitor of myeloid progenitors. However, the mechanism of action of this chemokine remains poorly understood. The present study was designed to determine its structure/function relationship. A series of peptides overlapping the C-terminal and central regions of PF4 were analyzed in vitro for their action on murine hematopoietic progenitor growth to assess the minimal sequence length required for activity. The peptides p17-58 and p34-58 possessed an increased hematopoietic inhibitory activity when compared with PF4, whereas the shorter peptides p47-58 and p47-70 were equivalent to the native molecule and the peptide p58-70 was inactive. The PF4 functional motif DLQ located in 54-56 was required for the activity of these peptides. The peptide p34-58 impaired to a similar extent the growth of colony-forming unit-megakaryocyte (CFU-MK) as well as burst-forming unit-erythroid (BFU-E) and colony-forming unit–granulocyte-macrophage (CFU-GM), whereas PF4 was more active on CFU-MK. In the experiments using purified murine CD34+ marrow cells, statistically significant inhibition induced by p34-58 was shown at concentrations of 2.2 nmol/L or greater for progenitors of the three lineages, whereas that induced by PF4 was seen at 130 nmol/L for CFU-MK and 650 nmol/L for CFU-GM and BFU-E, indicating that the p34-58 acts directly on hematopoietic progenitors and its activity is approximately 60- to 300-fold higher than PF4. The p34-58, unlike PF4, lacked affinity for heparin and its inhibitory activity could not be abrogated by the addition of heparin. In addition, an antibody recognizing p34-58 neutralized the activity of p34-58 but not whole PF4 molecule. These results demonstrate that PF4 contains a functional domain in its central region, which is independent of the heparin binding properties, and provide evidence for a model of heparin-dependent and independent pathways of PF4 in inhibiting hematopoiesis.
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Karuppaija, Sinthuja, Kapilan Ranganathan i Vasantharuba Seevaratnam. "Characterization of best naringinase producing fungus strain isolated from palmyrah (Borrasus flabellifer) fruit pulp". International Journal of Biological Research 4, nr 2 (19.07.2016): 97. http://dx.doi.org/10.14419/ijbr.v4i2.6289.

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Background: The Palmyrah (Borrasus flabellifer L.) fruit pulp has the bitter compound flabelliferin (a tetraglycoside) which can be hydrolyzed by naringinase enzyme. The diverse groups of filamentous fungi and bacteria that live in different substrates have the capacity of producing extracellular naringinase enzyme which is of tremendous industrial value.Objective: The objective of the study was to isolate the naringinase producing fungal strains from Palmyrah and to identify the best naringinase producer under liquid and solid state fermentation systems.Methods: Fungal strains isolated from Palmyrah fruit pulp and the soil where pulp is allowed to decay, were grown on naringin agar selective medium at pH 6.0 at room temperature and the production of extracellular naringinase was measured in the liquid fermentation media and solid state fermentation system using paddy husk as support.Results: Five fungal strains isolated from the palmyrah pulp and the pulp decaying in sand designated as PF1,PF2,PF3,PF4 & PF5 had the ability to produce extracellular naringinase enzyme in liquid fermentation media. Fungal strain PF4 that showed highest naringinase enzyme activity (1.769U/ml) was selected among the isolated five fungal strains and identified as Rhizophus stolonifer based on the morphological and biochemical characteristics. When this strain was grown in the solid state fermentation system using paddy husk as media, narininase production was higher (269.84 U/gram of dry substrate) in seven days.Conclusion: Rhizophus stolonifer could be used to produce large scale naringinase enzyme under solid state fermentation system using very cheap, easily available, agricultural waste paddy husk as support without the need of expensive and well equipped laboratories.
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PURCELL, J., A. P. ROBERTSON, D. P. THOMPSON i R. J. MARTIN. "The time-course of the response to the FMRFamide-related peptide PF4 in Ascaris suum muscle cells indicates direct gating of a chloride ion-channel". Parasitology 124, nr 6 (czerwiec 2002): 649–56. http://dx.doi.org/10.1017/s0031182002001695.

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We investigated the effects of PF4 on Ascaris suum somatic muscle cells using a 2 electrode current-clamp technique. PF4 is a FaRP (FMRFamide-related peptide), originally isolated from the free-living nematode Panagrellus redivivus. PF4 caused hyperpolarization and an increase in chloride ion conductance when it was applied to the muscle cells of the Ascaris body wall. The delay between the application of the peptide and the appearance of the response was measured and compared with that of gamma-amino butyric acid (GABA), a compound that directly gates ion channels, and with PF1, a FaRP that acts via an intracellular signal transduction mechanism. The PF4 and GABA delay times were not significantly different; they were 1·51±0·11 sec and 1·22±0·10 sec respectively. The delay following application of PF1, 3·75±0·51 sec, was significantly longer. The rapid response to PF4 is consistent with direct gating of a chloride ion channel, which has not been described elsewhere in the literature.
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Bokka, Chandra Sekhar, Ganesh Kumar Veeramachaneni, V. B. S. C. Thunuguntla, Janakiram Bobbillapati i Jayakumar Singh Bondili. "Peptide Mapping, In Silico and In Vivo Analysis of Allergenic Sorghum Profilin Peptides". Medicina 55, nr 5 (21.05.2019): 178. http://dx.doi.org/10.3390/medicina55050178.

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Background and objectives: Nearly 20–30% of the world’s population suffers from allergic rhinitis, among them 15% are progressing to asthma conditions. Sorghum bicolor profilin (Sorb PF), one of the panallergens, was identified, but the allergen specificity is not yet characterized. Materials and Methods: To map the antigenic determinants responsible for IgE binding, the present study is focused on in silico modeling, simulation of Sorb PF and docking of the Sorb PF peptides (PF1-6) against IgG and IgE, followed by in vivo evaluation of the peptides for its allergenicity in mice. Results: Peptide PF3 and PF4 displayed high docking G-scores (−9.05) against IgE only. The mice sensitized with PF3 peptide showed increased levels of IL5, IL12, TNF-alpha, and GMCSF when compared to other peptides and controls, signifying a strong, Th2-based response. Concurrently, the Th1 pathway was inhibited by low levels of cytokine IL2, IFN-γ, and IL-10 justifying the role of PF3 in allergenic IgE response. Conclusions: Based on the results of overlapping peptides PF3 and PF4, the N-terminal part of the PF3 peptide (TGQALVI) plays a crucial role in allergenic response of Sorghum profilin.
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Ismail, Muhammad Hafiz, Katharine A. Michie, Yu Fen Goh, Parisa Noorian, Staffan Kjelleberg, Iain G. Duggin, Diane McDougald i Scott A. Rice. "The Repressor C Protein, Pf4r, Controls Superinfection of Pseudomonas aeruginosa PAO1 by the Pf4 Filamentous Phage and Regulates Host Gene Expression". Viruses 13, nr 8 (15.08.2021): 1614. http://dx.doi.org/10.3390/v13081614.

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It has been shown that the filamentous phage, Pf4, plays an important role in biofilm development, stress tolerance, genetic variant formation and virulence in Pseudomonas aeruginosa PAO1. These behaviours are linked to the appearance of superinfective phage variants. Here, we have investigated the molecular mechanism of superinfection as well as how the Pf4 phage can control host gene expression to modulate host behaviours. Pf4 exists as a prophage in PAO1 and encodes a homologue of the P2 phage repressor C and was recently named Pf4r. Through a combination of molecular techniques, ChIPseq and transcriptomic analyses, we show a critical site in repressor C (Pf4r) where a mutation in the site, 788799A>G (Ser4Pro), causes Pf4r to lose its function as the immunity factor against reinfection by Pf4. X-ray crystal structure analysis shows that Pf4r forms symmetric homo-dimers homologous to the E.coli bacteriophage P2 RepC protein. A mutation, Pf4r*, associated with the superinfective Pf4r variant, found at the dimer interface, suggests dimer formation may be disrupted, which derepresses phage replication. This is supported by multi-angle light scattering (MALS) analysis, where the Pf4r* protein only forms monomers. The loss of dimerisation also explains the loss of Pf4r’s immunity function. Phenotypic assays showed that Pf4r increased LasB activity and was also associated with a slight increase in the percentage of morphotypic variants. ChIPseq and transcriptomic analyses suggest that Pf4r also likely functions as a transcriptional regulator for other host genes. Collectively, these data suggest the mechanism by which filamentous phages play such an important role in P. aeruginosa biofilm development.
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Hara, Francisco Adilson dos Santos, i Luiz Antonio de Oliveira. "Características fisiológicas e ecológicas de isolados de rizóbios oriundos de solos ácidos e álicos de Presidente Figueiredo, Amazonas". Acta Amazonica 34, nr 3 (wrzesień 2004): 343–57. http://dx.doi.org/10.1590/s0044-59672004000300002.

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Alguns isolados de rizóbio, além de fixarem o N2, são capazes de solubilizar fosfatos pouco solúveis, disponibilizando o P para as plantas e para si mesmos. No entanto, o Al e a acidez dos solos da Amazônia podem diminuir a população desses microrganismos. O presente trabalho avaliou a capacidade nodulífera, a tolerância à acidez e ao Al tóxico, bem como a capacidade de solubilizar fosfatos de Ca e de Al de 88 isolados de rizóbio de solos agrícolas, do município de Presidente Figueiredo, AM. Amostras de solo sob cultivos agrícolas foram coletadas e utilizadas como fontes de inóculo para plantas de feijão caupi. As amostras de solo continham isolados de rizóbio capazes de induzir a nodulação e incrementar a biomassa aérea do feijão caupi em condição ácida (pH 4,5) e álica (2cmol c Al. L-1). Os isolados de rizóbio presentes nas amostras de solo identificadas como INPA-PF2, INPA-PF3, INPA-PF4, INPA-PF5, INPA-PF13, INPA-PF15, INPA-PF22 e INPA-PF24 promoveram rendimentos de biomassa aérea superiores à testemunha. A tolerância à acidez foi apresentada por 25% dos isolados e apenas 23% apresentaram tolerância ao Al. O fosfato de Ca foi solubilizado por 39% dos isolados. No entanto, apenas um isolado apresentou alto índice de solubilização. A capacidade de solubilização de fosfato de Al foi identificada em 67% dos isolados. A maioria dos isolados de rizóbio que solubilizou fosfato de Ca (76,5% dos isolados) também solubilizou o fosfato de Al.
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Rozprawy doktorskie na temat "PF4"

1

Brousseau-Nault, Mathieu. "Chronic periodontitis is associated with platelet factor 4 (PF4) secretion". Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/59016.

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Aim: Platelets contribute to chronic inflammation but their role in periodontitis is not well understood. The aim of this study was to compare platelet recruitment and activation in healthy and inflamed periodontium. Materials and Methods: Gingival crevicular fluid (GCF) samples were obtained from sites of healthy periodontium, gingivitis and periodontitis. Platelets were quantified in the GCF by staining and microscopy. GCF concentrations of platelet factor 4 (PF4) [PF4]GCF and glycoprotein IIbIIIa ([GPIIbIIIa]GCF) were determined by ELISA. Blood samples were obtained from the 3 patient groups. Platelets were isolated from whole blood and stimulated with lipopolysaccharide (LPS) from P. gingivalis to evaluate and compare the LPS-induced PF4 release. Results: Compared to controls, platelet recruitment was increased at gingivitis and periodontitis sites, based on platelet counts and [GPIIbIIIa]GCF. [PF4]GCF was elevated in periodontal pockets but not at gingivitis or healthy sites. Circulating plasma levels of PF4 were higher in patients with generalized severe periodontitis (SP), compared to patients with gingivitis or healthy periodontium. Platelets isolated from SP patients contained and released more PF4 in response to P. gingivalis LPS than platelets from gingivitis or periodontally healthy patients. Conclusions: Periodontitis is associated with increased platelet activation and PF4 release, both locally and systemically.
Dentistry, Faculty of
Graduate
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XI, XIAODONG. "Role du pf4 et de l'il-13 dans la regulation de l'hematopoiese". Paris 7, 1995. http://www.theses.fr/1995PA077261.

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De nombreux regulateurs (positifs ou negatifs) sont impliques dans la regulation de l'hematopoiese. Deux de ces regulateurs, le pf4 et l'il-13, font l'objet de cette these. Le chapitre i presente les techniques utiles developpees pour la realisation du travail et les resultats obtenus a partir de ces techniques. Le chapitre ii porte sur les effets differenciateurs de l'il-13 sur la croissance des progeniteurs hematopoietiques: stimulation de la lignee megacaryocytaire et inhibition de la lignee granulomacrophagique. C'est un rapport original concernant l'effet de l'il-13 sur les megacaryocytes. Dans le chapitre iii, le mecanisme d'action du pf4 sur les progeniteurs megacaryocytaires a ete analyse en comparaison de l'action du tgf-beta 1. Une inhibition directe et reversible du pf4 sur la croissance des progeniteurs megacaryocytaires a ete montree. En outre, l'auteur a suggere qu'une conservation des cellules plus immatures, reactives au scf, resultant de l'inhibition reversible, peut etre responsable de la protection des progeniteurs vis-a-vis de la cytotoxicite du 5-fu
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Purcell, Jenny. "The effects of PF4 on Ascaris suum somatic muscle cells : an electrophysiological study". Thesis, University of Edinburgh, 2001. http://hdl.handle.net/1842/29954.

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PF4 is a FaRP which was isolated from the free-living nematode Panagrellus redivivus and which has been shown to have activity in other nematodes, including Ascaris suum. A. suum, the large parasitic nematode found in domestic pigs, is often used as an experimental model in studying nematodes due to its large size and easy availability. The nematodes used in this study were obtained from three different sources. The action of PF4 on the somatic muscle cells of A.suum was investigated using the two electrode current clamp technique. PF4 caused these cells to hyperpolarise by 2 to 12 mV. The FaRP also caused an increased in membrane conductance of up to 3mS. The response to PF4 was shown to be due to the opening of chloride ion channels in the somatic muscle cell membrane. In experiments to examine the delay between application of PF4 and the response, PF4 was found to act as the directly gating ligand g-amino butyric acid. This observation is consistent with the argument that PF4 directly gates ion channels. PF4 was investigated further with patch clamp experiments that were carried out on membrane vesicles produced by treating the muscle cells with collagenase. Using vesicle-attached and isolated inside-out patches, PF4 was shown to open small amplitude channels (1.5 to 6.2 pS) with a relatively high probability of opening (Popen) of 0.05 to 0.65 at [PF4] 0.003 mM. The channel conductance and the Popen recorded in each experiment varied with the origin of the worms, suggesting genetic diversity within A. suum. The mean open time of the channel was found to be voltage sensitive; it varied from 522±+120 mV. The behaviour of the channels did not alter after patch isolation, which is further evidence for them being directly gated by PF4. When the cytoplasmic side of the patches was exposed to a G-protein inhibitor (guanosine 5'-O-(2-thiodiphosphate), the conductance of the channels reduced and the Popen increased. This finding suggests that these ion channels can be modulated by one or more G-proteins. The results of this project suggest that that FaRP, PF4, directly activates low conductance chloride channels by combining with a receptor on the outside of the muscle membrane. The channels are different from those described previously in nematodes or vertebrates and therefore present a potential anthelmintic target site.
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Dubrac, Alexandre. "Analyse fonctionnelle et structurale du facteur antiangiogénique pf4v1". Thesis, Bordeaux 1, 2008. http://www.theses.fr/2008BOR13751/document.

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De nombreuses équipes se sont intéressées aux fonctions antiangiogéniquesde PF4 (Platelet Factor 4 ou Facteur Plaquettaire 4). Ses capacités inhibitrices vis-àvisde la prolifération et de la migration des cellules endothéliales in vitro et son effetinhibiteur sur lʼangiogenèse in vivo ne sont plus à démontrer. En revanche, il existeencore de nombreuses interrogations sur les mécanismes dʼaction responsables deson activité antiangiogénique. La chimiokine PF4v1 (Platelet Factor 4 variant 1)mature ne diverge de PF4 que par trois acides aminés mais son potentielangiostatique est beaucoup plus élevé que celui de PF4. Lʼétude comparative de PF4et PF4v1 est donc susceptible de fournir des éclairages intéressants sur lesmécanismes dʼaction de lʼactivité antiangiogénique de PF4. La question se pose desavoir si la différence dʼactivité antiangiogénique entre ces deux chimiokines pourraitsʼexpliquer par des différences dʼaffinité aux GAGs (Glycoaminoglycans), à unrécepteur ou bien aux voies de transduction utilisées pour médier leurs effets ?Comme les mécanismes dʼaction de PF4v1 demeurent très largement incompris(bien que son utilisation comme agent thérapeutique antiangiogénique soit trèsprometteuse), nous avons adopté plusieurs axes de travail pour élucider lescaractéristiques spécifiques de cette chimiokine.Dans un premier temps, nous avons étudié les caractéristiques de diffusibilité etde biodisponibilité des facteurs PF4 et PF4v1. Nous avons déterminé que cesparamètres étaient liés aux affinités de PF4 et PF4v1 pour lʼhéparine et les GAGs, etnous avons identifié lʼacide aminé principalement responsable des différencesobservées.Sur le plan de lʼactivité antiangiogénique de ces deux chimiokines, nousmontrons une absence de corrélation avec lʼaffinité respective aux GAGs. Par contre,nous identifions que la liaison avec un récepteur spécifique pourrait être à lʼorigine dela différence dʼactivité antiangiogénique. Nous avons mené une étude permettant decomprendre le rôle de chaque acide aminé variant entre ces deux chimiokines dansla liaison spécifique au récepteur.Enfin, nous avons développé le premier anticorps monoclonal spécifique de laprotéine PF4v1 qui, de plus, neutralise son activité antiangiogénique. Ce nouvel outilapporte des informations sur la structure et sur lʼactivité biologique de PF4v1. Il nousa aussi permis de démontrer que la protéine PF4v1 est un nouveau biomarqueur ducancer du pancréas. Grâce à ce nouvel outil, nous avons aussi développé un dosageELISA anti-PF4v1. Dans le cadre de la recherche de nouveaux biomarqueurs pour ladétection précoce des cancers, nous pouvons envisager une utilisation de cet ELISAen collaboration avec des services cliniques
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5

El, Golli Nargès. "Etude du trafic intracellulaire de la protéine alpha-granulaire plaquettaire : le facteur plaquettaire (PF4)". Paris 7, 2005. http://www.theses.fr/2005PA077136.

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6

Lazar, Noureddine. "Structure secondaire et activité biologique : relations structure-fonction dans le PF4 Humain et la Prosomatostatine". Paris 6, 2003. http://www.theses.fr/2003PA066181.

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7

Pertuy, Fabien. "Etude des mécanismes de formation des plaquettes sanguines : rôle de l'environnement médullaire". Thesis, Strasbourg, 2014. http://www.theses.fr/2014STRAJ092/document.

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Les mécanismes de formation des plaquettes sanguines à partir des mégacaryocytes ne sont pas totalement compris, mais l’environnement médullaire semble y avoir une influence cruciale. Dans ce travail nous montrons que i) les intégrines β3, récepteurs de protéines de matrice extracellulaire, semblent impliquées dans la mégacaryopoïèse et la formation des plaquettes, ii) la différenciation des cellules hématopoïétiques dans un environnement 3D de rigidité comparable à la moelle osseuse améliore la maturation des mégacaryocytes différenciés in vitro et iii) la myosine IIA est impliquée dans la distribution des organelles dans les mégacaryocytes. Parallèlement, Nous avons caractérisé la spécificité d’expression du transgène Pf4-cre pour valider son utilisation dans nos approches expérimentales. Ce travail apporte un éclairage nouveau sur le rôle de la myosine IIA et des intégrines dans les mégacaryocytes et souligne l’influence de la rigidité de l’environnement dans la mégacaryopoïèse
Megakaryocytes differentiation (megakaryopoiesis) and platelet formation mechanisms are not entirely understood, but the bone marrow environment seems to be crucial in these processes. In this thesis, we show i) that integrin β3, the extracellular matrix protein receptors, are involved in megakaryopoiesis and platelet formation, ii) that recreating a 3D environment of stiffness in the range of that of bone marrow improves the maturation of in vitro differentiated megakaryocytes and iii) a new role for myosin IIA in the cytoplasmic distribution of organelles within the megakaryocyte. As a side-project, we characterized the specificity of expression of the Pf4-cre transgene to validate its use in our experimental approaches. This work enlightens new roles for myosin IIA and integrins in megakaryocytes and indicates that stiffness of the environment influences megakaryopoiesis
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Schulze, Annika [Verfasser]. "Charakterisierung der anti-PF4/Heparin-Antikörper-sezernierenden B-Zellen im Mausmodell nach systemischer Immunisierung / Annika Schulze". Greifswald : Universitätsbibliothek Greifswald, 2015. http://d-nb.info/1068082143/34.

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AIDOUDI, SALLOUHA. "Effet protecteur du facteur plaquettaire 4 (pf4) en comparaison avec un myeloprotecteur, le tetrapeptide acsdkp, sur l'hematopoiese de souris traitees par la chimiotherapie". Paris 7, 1997. http://www.theses.fr/1997PA077354.

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Le pf4 est une proteine synthetisee par la lignee megacaryocytes/plaquettes dont l'activite inhibitrice a ete recemment montree sur la lignee megacaryocytaire humaine et murine. Il a ete montre que l'effet du pf4 est predominant sur la lignee megacaryocytaire, mais a plus forte doses, il inhibe aussi la proliferation des autres lignees hematopoietiques. Le but de ce travail a consiste a etudier l'effet du pf4, en comparaison avec un inhibiteur et myeloprotecteur connu de l'hematopoiese l'acsdkp, sur l'hematopoiese des souris traitees avec deux chimiotherapies : le 5-fu ou ara-c. Les resultats obtenus dans cette etude ont montre que le pretraitement des souris avec le pf4 ou l'acsdkp chez les souris traitees par la chimiotherapie entraine une augmentation significative du nombre des cellules souches hpp-cfc des progeniteurs medullaires (cfu-gm, cfu-mk) et des mk matures. Ces resultats indiquent que le pf4 et l'acsdkp agissent aussi bien sur les cellules souches hpp-cfc que sur les progeniteurs hematopoietiques augmentant leur nombre, ce qui traduit une meilleure recuperation et donc une protection. La suite de ce travail a consiste a essayer de caracteriser le domaine responsable de l'activite inhibitrice/protectrice du pf4. Les resultats obtenus in vitro et in vivo chez la souris normale ont montre que les peptides correspondant aux regions 1-24 et 13-24 c-terminale du pf4 native (c1-24, c13-24, c13-24de) mais pas c1-13 ont une activite inhibitrice similaire au pf4 natif sur la formation des colonies cfu-mk et le nombre des mk isoles. De facon interessante, le pretraitement des souris avec le c13-24 de chez les souris traitees avec le 5-fu provoque, comme le pf4 natif, une augmentation significative des cellules souches hpp-cfc, des progeniteurs (cfu-gm et cfu-mk) ainsi que des mk matures. Ces resultats suggerent fortement que la region 13-24 c-terminale du pf4 est impliquee dans son activite inhibitrice/protectrice.
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Libraire, Julie. "Le facteur 4 plaquettaire (PF4/CXCL4) prévient la formation du complexe initial de l’inhibiteur de l’activateur du plasminogène (PAI-1) avec sa cible d’origine tissulaire (t-PA)". Thesis, Paris 5, 2012. http://www.theses.fr/2012PA05P654.

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Le facteur 4 plaquettaire (PF4/CXCL4) est un tétramère constitué de quatre sous-unités identiques de 7,8 kDa qui est libéré en grande quantité par les plaquettes lors de l’hémostase primaire (ensemble des phénomènes permettant un colmatage initial d’une lésion vasculaire). L’étude de la formation d’un caillot de fibrine en présence de PF4 montre une augmentation de la turbidité finale du caillot : le PF4 modifie le réseau formé. Etant donné que la plupart des acteurs de la fibrinolyse se lie au caillot de fibrine et que le PF4 modifie sa structure, nous avons pensé qu’il serait intéressant de rechercher si le PF4 influençait aussi la fibrinolyse. La lyse d'un caillot est effectuée par la plasmine issue de l'activation du plasminogène par son activateur d’origine tissulaire (t-PA) en présence d’un cofacteur qui n'est autre que la fibrine. Nous avons étudié la lyse de caillots de plasma, obtenus par activation de la cascade de la coagulation, en condition statique et à l'aide d'un modèle de thrombose artérielle (système Chandler loop). Dans les deux cas, une diminution du temps de demi-lyse a été observée en présence de PF4. Cependant, la lyse de caillots préparés par simple ajout de thrombine sur du fibrinogène ne permet pas de retrouver cet effet du PF4. Ceci suggère que l’influence du PF4 sur la structure du caillot n’est pas à l’origine de l’effet sur sa lyse et que le PF4 n’influence pas (ou très peu) l'activation du plasminogène, ainsi que l'activité de la plasmine résultante. Cette hypothèse a été confirmée par l’étude de l’activité amydolytique du t-PA et de la plasmine (quelle soit ajoutée ou générée). En système purifié, les inhibiteurs plasmatiques de la fibrinolyse sont absents. Les deux principaux sont l'inhibiteur de l'activateur du plasminogène de type 1 (PAI-1) et l’α2-antiplasmine (α2-AP). La lyse de caillots préparés à partir de plasma déficient en α2-AP montre une diminution du temps de demi-lyse en présence de PF4 (comme pour le plasma normal), alors qu’avec le plasma dépourvu de PAI-1 le temps de demi-lyse n'est plus influencé. De plus, l’ajout de PAI-1 dans le système purifié entraine une diminution du temps de demi-lyse en présence de PF4. Ceci suggère que le PF4 prévient directement ou indirectement l'inhibition du t-PA par PAI-1. L’étude de la cinétique d'inhibition de l’activité amidolytique du t-PA par le PAI-1, la détermination de la stœchiométrie de cette inhibition, et l’analyse de ces cinétiques par immuno-empreinte montrent que le PF4 est un modulateur de la fibrinolyse qui agit en retardant la formation d'un complexe initial entre le t-PA et le PAI-1. Cette nouvelle fonction du PF4 est cohérente, et vient en complément de celle décrite récemment d’inhibiteur de l'activation du TAFI
Platelet factor 4 (PF4/CXCL4) is a tetramer constituted of four identical 7,8 kDa subunits released in large quantities by platelets during primary heamostasis (allowing initial clogging of a vascular injury). Study of fibrin clot formation in the presence of PF4 shows an increase of the final clot turbidity: PF4 modifies the formed network. Given that most fibrinolysis actors are bound to the fibrin clot and that PF4 modifies its structure we thought it would be interesting to investigate if PF4 also influences fibrinolysis. Clot lysis is performed by plasmin originating from activation of its precursor by tissue plasminogen activator (t-PA) with fibrin itself as cofactor of the reaction. We have studied lysis of plasma clots formed by activation of the coagulation cascade in static condition and in a Chandler loop model mimicking arterial thrombosis. Half-times of lysis decreased in the presence of PF4 in both systems. However, PF4 had no longer detectable influence on the half-time of lysis with clots formed by direct addition of thrombin on purified fibrinogen. Observation suggested that the observed decrease of the half-time of lysis induced by PF4 did not originate from its influence on fibrin clot formation and that PF4 had little effect if any on plasminogen activation or plasmin activity. We confirmed this hypothesis by comparing amydolytic activities of t-PA and plasmin (added or generated through plasminogen activation). In purified system, fibrinolysis inhibitors are absent. The two main inhibitors are plasminogen activator inhibitor-1 (PAI-1) and α2-antiplasmin (α2-AP). Lysis of clots obtained from α2-AP deficient plasma showed a decrease of the half-time of lysis in the presence of PF4 (as in normal plasma), whereas in PAI-1 deficient plasma half-time of lysis was unchanged. Moreover if PAI-1 was added to the purified system, half-time of lysis decreased in the presence of PF4. Observations therefore suggested that PF4 prevented directly or indirectly t-PA inhibition by PAI-1. Kinetics of the amidolytic activity of t-PA inhibition by PAI-1 in the presence or not of PF4, determination of its stoichiometry and Western blot analysis of these inhibition kinetics revealed that PF4 is a fibrinolysis modulator which delays formation of the initial (Michaelis) complex between t-PA and PAI-1. This new feature of PF4 is consistent and complementary with its recently described role as a modulator of TAFI activation
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Książki na temat "PF4"

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Borčić, Barbara. P74 20 years: P74 20 let. Ljubljana: Zavod P.A.R.A.S.I.T.E., 2020.

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Fieled, Adam. Gauntlet: (PFS). Redaktor Adam Fieled. Conshohocken, Pa: Internet Archive, 2013.

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O PFL. São Paulo, SP: Publifolha, 2001.

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Fieled, Adam. Gauntlet: (PFS). Redaktor Adam Fieled. Conshohocken, Pa: Internet Archive, 2013.

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Fieled, Adam. Gauntlet: (PFS). Redaktor Adam Fieled. Conshohocken, Pa: Internet Archive, 2013.

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Fieled, Adam. Gauntlet: (PFS). Redaktor Adam Fieled. Conshohocken, Pa: Internet Archive, 2013.

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Fieled, Adam. Gauntlet: (PFS). Conshohocken, Pa: Internet Archive, 2013.

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Crowley, W. Robert. Using the IBM PC: PFS,file/PFS,report. New York: Holt, Rinehart and Winston, 1985.

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Terry, Neville, Association of Chartered Certified Accountants. i Certified Accountants Educational Trust, red. PFI: Practical perspectives. London: Association of Chartered Certified Accountants for the Certified Accountants Educational Trust, 2002.

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Labour Research Department. Profiting from PFI. London: UNISON, 2003.

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Części książek na temat "PF4"

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Stöcker, W., i C. Krüger. "Antikörper gegen Heparin/PF4". W Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_234-1.

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Stöcker, W., i C. Krüger. "Antikörper gegen Heparin/PF4". W Springer Reference Medizin, 157–58. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_234.

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Abbadessa, V., P. Citarrella, R. Perricone i P. Di Marco. "β-TG and PF4 in the Diagnosis of Thrombosis". W Advances in Hemostasis and Thrombosis, 315–21. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4615-9424-6_30.

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Gass, Saul I., i Carl M. Harris. "PFI". W Encyclopedia of Operations Research and Management Science, 614. New York, NY: Springer US, 2001. http://dx.doi.org/10.1007/1-4020-0611-x_751.

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Gooch, Jan W. "PFA". W Encyclopedic Dictionary of Polymers, 528. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_8615.

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Donato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou i in. "PFT". W Encyclopedia of Signaling Molecules, 1364. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101022.

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Braun-Falco, Markus, Henry J. Mankin, Sharon L. Wenger, Markus Braun-Falco, Stephan DiSean Kendall, Gerard C. Blobe, Christoph K. Weber i in. "PFO". W Encyclopedia of Molecular Mechanisms of Disease, 1607. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_5128.

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Braun-Falco, Markus, Henry J. Mankin, Sharon L. Wenger, Markus Braun-Falco, Stephan DiSean Kendall, Gerard C. Blobe, Christoph K. Weber i in. "PFO". W Encyclopedia of Molecular Mechanisms of Disease, 1633. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8674.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, V. Kuprysyuk i I. Savysyuk. "In2Ti6(PO4)6[Si2O(PO4)6]". W Structure Types. Part 9: Space Groups (148) R-3 - (141) I41/amd, 71. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-02702-4_33.

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Villars, P., K. Cenzual, J. Daams, R. Gladyshevskii, O. Shcherban, V. Dubenskyy, N. Melnichenko-Koblyuk i in. "Tl3[PO4]". W Structure Types. Part 5: Space Groups (173) P63 - (166) R-3m, 55. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/978-3-540-46933-9_10.

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Streszczenia konferencji na temat "PF4"

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Rucinski, B., G. J. Stewart, G. Boden i S. Niewiarowski. "INTERACTION OF PLATELET FACTOR 4 WITH HEPATOCYTES AND ITS POSSIBLE SIGNIFICANCE IN HEMOSTASIS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643500.

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Previous experiments have demonstrated the rapid clearance of himan platelet factor 4 (PF4) from rabbit and rat blood, its accumulation in the liver and its elimination of PF4 degradation products with urine. Injection of heparin resulted in a rapid loss of 125 i-pF4-radioactivity from the liver (Rucinski et al Amer. J. Physiol. 251, H800, 1986). Current experiments demonstrate the uptake of human 125i-pf4 by hepatocytes reaching maximum at 180 min. This uptake is 2-3 times greater at 37°C than at 4°C. At 37°C degradation of 125I-PF4 by hepatocytes was also observed as indicated by the increase of 125j_pf4 radioactivity soluble in 6% trichloracetic acid. By contrast, no uptake of 125I-β was observed. Autoradiography demonstrated association of l25I-PF4 with hepatocytes membranes while after longer incubation (20-60 min) radioactivity was also localized in endosanes. The heparin inhibited binding and uptake of PF4 by hepatocytes; accordingly the injection of heparin to or into rabbits within 10 min resulted in a rapid urinary clearance of 125I-PF4 and the injection of PF4 resulted in a rapid urinary clearance of 3H-heparin. We propose that 1) PF4 released to the circulating blood by activated platelets is bound to the surface of hepatocytes and that it is further processed by these cells over time; 2) the presence of PF4 in the liver may contribute to the regulation of hemostasis by neutralizing anticoagulant activity of endogenous heparin-like molecules; 3) in clinical situations PF4 may enhance clearance of injected heparin by accelerating its urinary excretion.
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Morrison, J. EJ, A. B. Latif, C. Mason, P. Bramley i T. R. Criag. "THE PROFILE OF IN VIVO PLATELET ACTIVATION IN NOCTURNAL ASTHMA". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643495.

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The precise pathophysiology of nocturnal asthma still remains to be elucidated. Activated platelets have the ability to release potent broncho- and vaso-constrictors and therefore, have been implicated in asthma. However, there is no information on the status of in vivo platelet activation in patients with nocturnal asthmaIn a randomised controlled study five healthy volunteers and five asthmatics were investigated during a period of 24h after acclimatisation for one day. Both peak flow rate (PFR) and blood samples were obtained at 4 hourly intervals. Plasma levels of platelet factor 4 (PF4) and beta- thromboglobulin(BTG) were measured by radioimmunoassay and adrenaline (A), noradrenaline (NA) and dopamine (DOP) by radioenzymatic analysis.PFR (1/min) for the 24h period was significantly lower in asthmatics (401±15SEM, P<0.001) than in controls (598+4SEM) with an apparent circadian rhythm peak (442±73, P<0.05 Wilcoxon's test) at 4.00pm only in asthmatics. Although there was no significant differences in either PF4 and BTG (ng/ml) or A, NA and DOP (nmol/1) between asthmatics and controls an apparent circadian rhythm in all of these parameters was demonstrated in both groups. Peak values (mean+SEM) for PF4 (8.9±1.5) and BTG (44.4±3.8) occurred at 8.00am whereas the highest values for the catecholamines (A: 0.36±0.08, NA: 1.75±0.23, DOP: 0.78±0.16) were observed at 4.00pm indicating a lag of 8h between the peaks for catecholamines and the platelet specific proteinsThese initial data demonstrate a clear difference in PFR between asthmatics and controls which is apparently not associated with changes in either PF4 or BTG but which may concur with circadian changes in plasma levels of catecholamines at least in asthmatic patients. Thus, in vivo platelet activation is probably not a contributing factor in nocturnal asthma. Finally, the phase lag between peak plasma levels of platelet proteins and catecholamines requires further investigation
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Gewirtz, A., W. Y. Xu, B. Rucinski i S. Niewiarowski. "SELECTIVE INHIBITION OF HUMAN MEGAKARYOCYTOPOIESIS IN VITRO BY HIGHLY PURIFIED PLATELET FACTOR 4". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644621.

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Platelet (plt) factor 4 (PF4) is an alpha granule protein which can modulate T lymphocyte function. T cells may help regulate megakaryocytopoiesis. Therefore, we hypothesized that T cell-PF4 interactions might play a role in autoregulating marrow megakaryocyte (MEG) production. To test this idea, we studied MEG colony formation in plasma clot cultures containing human serum derived solely from pit poor normal AB plasma, enriched hematopoietic progenitor cells (HPC), autologous T cells, and exogenous PF4. Highly purified PF4 (single band on SDS gel) was prepared from outdated human pits by a combination of heparin-agarose, Sephacryl G-200, and Sephadex G-50 column chromatography. HPC were prepared by depleting normal light density marrow mononuclear cells of adherent monocytes, and T cells. T cells were further fractionated into helper (Leu 3+) and suppressor (Leu 2+) subtypes by solid phase immunoabsorption ("panning"). MEG colonies were enumerated by indirect immunofluorescence with an anti-human platelet glycoprotein antiserum. HPC(5×105/ml) were co-cultured with Leu 3+, or Leu 2+ T cells at target;T cell ratios of 2:1 (n=3; n=4 respectively) and l:l(n=4; n=4 respectively) in the presence of 2.5 μg/ml PF4. Under these growth conditions, MEG colony formation was unchanged (p>0.5) when compared to colonies formed by HPC in the absence of PF4. When the above experiments were repeated (n=2-3/condition) at a higher PF4 concentration [25 μg/ml], MEG colony formation was markedly (>60%) inhibited. To determine if PF4 directly inhibited MEG or erythroid progenitor cell growth (CFU-Meg; CFU-E) in vitro, HPC were cloned in PF4 (25μg/ml) without added T cells. Mean ± SEM of MEG and CFU-E derived colonies formed without vs. with PF4 was as follows:These results suggest that: 1) PF4 may be a non-T cell dependent, lineage specific inhibitor of CFU-MEG, and 2) PF4 may play a role in autoregulating human megakaryocytopoiesis.
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Celia, G., M. Prosdocimi i A. A. Sasahara. "IN VIVO INTERACTION BETWEEN HUMAN PLATELET FACTOR 4 (PF4) AND PROTAMINE SULPHATE (PS) IN THE PRESENCE OF DIFFERENT GLYCOSAMI-NOGLYCANS (GAGs)". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643501.

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Anti-heparin substances, like PF4 or PS, have been studied largely in reference to their ability to neutralize the anticoagulant activity of heparin. On the other hand, few data are available concerning the relationship between GAGs and anti-heparin proteins clearance. We studied the action of PS on human PF4 kinetics in anesthetized rabbits pre-treated with heparin (H, 1000 I.U.), heparan sulphate (HS, 30 mg) and derma tan sulphate (DS, 30 mg). PF4 (given at a dose of 45 μgAg) disappearance reflected its different affinity for the GAGs, with the following half lives (min): control 2.09±0.28, H 14.80±1.47, HS 10.90±1.91, DS 6.87±0.68. Moreover, circulating PF4 (ng/ml) at 1 min was as follows: control 109±8, H 873±134, HS 751±34 and DS 473±15. In another group of H pre-treated rabbits, a bolus injection of PS (10 or 20 mg) caused an immediate disappearance in th.e circulating plasma PF4, from 900±23 ng/ml (1 min after PF4) to 75±11 ng/ml (1 min after 10 mg PS). However, a subsequent H injection 10 min after PS induced a peak release of PF4 (520±21 ng/ml). In a further group of animals pre-treated with HS, the interaction between PS and PF4 was similar to that observed after H treatment. In the last group, pre-treated with DS, the interaction between PF4 and PS was also similar, however, unexpectedly, when 20 mg of PS were given a subsequent bolus of H did not produce any increase of circulating PF4We suggest that PS displaces PF4 from its binding sites on H or HS, thus allowing its uptake by the storage sites in the body, from where it can be harvested again after the subsequent H administration. In the presence of DS again PS is able to displace PF4, however the remaining excess of PS could neutralize the subsequent H injection, thus rendering it unable to induce PF4 release.
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Boschetti, C., A. Vicari, E. Cofrancesco, A. Della Volpe, G. Moreo, E. Po-gliani, G. Pozza i E. Polli. "HEPARIN-RELEASED PLATELET FACTOR 4 (HR-PF4) IN DIABETIC MICR0VAS-CULAR DISEASE". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643498.

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When heparin is injected i.v. as a bolus, PF4 but not (β-throm boglobulin ((βTG) is released immediately. HR-PF4 is not liberated from platelets but from the endothelial cells of vessels which serve as storage sites. The role of platelet activation in diabetic microvascular disease is still controversial, however there is experimental evidence of vascular injury and hemostatic activation preceding the appearance of microvascular disease. The contradictory results so far obtained in man may be partly attributed to the heterogeneity of the diabetic patients studied. We studied 20 insulin-dependent diabetics (age 21-40) in stable metabolic equilibrium (mean HbAlc=7.6%). 10 without fluoroangiographic evidence of retinopathy (Group l) and 10 with retinopathy (Group 2). None had signs or symptoms of macrovascular disease. The control group consisted of 10 healthy volunteers (age 22-39). No medication except insulin was taken for at least 10 days preceding the study. 12 h before the study all subjects received aspirin 500 mg p.o. Plasma (βTG and PF4 were determined before (basal) and 5,30,90 min after a heparin bolus i.v. (5000 U). Protein C, factor VIIIR:Ag and tissue plasminogen activator were also measured in plasma.
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Liu, Chenglian, Kun Lu, Chen Liu, Qingqing Du, Yujun Dong, Jun Wang, Kaizhong Ding, Xiaoshi Tang, Xiongyi Huang i Yuntao Song. "ITER PF4 CFT 80 K Cold Test at ASIPP". W 2018 IEEE International Conference on Applied Superconductivity and Electromagnetic Devices (ASEMD). IEEE, 2018. http://dx.doi.org/10.1109/asemd.2018.8558989.

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Kotze, H. F., P. N. Badenhorst, A. du, P. Heyns, P. Heyns i V. van Wyk. "THE EFFECT OF ARTERIAL DE-ENDOTHELIALIZATION ON IN VIVO AND EX VIVO PLATELET FUNCTION TESTS IN THE BABOON". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643950.

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The effect of endothelial cell injury on platelet function was evaluated in eight baboons with a normal vasculature. Endothelium was removed with a balloon catheter. On each baboon, the left carotid artery was de-endothelialized on day 0 and the right carotid artery and abdominal aorta on day 7. Mean platelet density (MPD; gm/ml), circulating platelet aggregate ratio (CPA), the number of electron-dense bodies per platelet (DBP) , and the plasma concentration (ng/ml) of platelet factor 4 x(PF4) and beta thromboglobulin (bTG) were determined on day -7 (baseline). These ex vivo measurements were repeated on days 1, 9 and 16. The mean lifespan (MPLS) and sites of sequestration of In-111-labelled platelets were determined from day 7 onwards. The results of the ex vivo platelet function tests were:De-endothelialization of only the left carotid artery did not affect ex vivo platelet function. More extensive denudation decreased MPD, and increased CPA, PF4 and bTG. CPA were still abnormal 7 days after the insult. MPLS, 120±21 hours, was shorter (p<0.05) than normal, 145±15 hours. The sequestration pattern of senescent platelets was normal. We conclude that a decrease in the MPD, an increase in CPA, bTG and PF4, and a shortened MPLS are the most sensitive tests for in vivo platelet activation.
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Teruya, J., N. Shimizu, J. Matsuda, M. Kazama i T. Abe. "PROFILE DIAGNOSIS OF HEMOSTATIC DISORDERS BY SIMULTANEOUS ASSAY OF HEMOSTATIC MOLECULAR MARKERS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643052.

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Simultaneous measurements of molecular markers of platelet, coagulation, fibrinolysis, and vascular system give us precise-and comprehensive information about hemostatic profile of various diseases. We adopted 6-thromboglobulin(B-TG) and platelet factor 4(PF4) for platelet function, fibrinopeptide A(FPA) and soluble fibrin monomer complex(SFMC) for coagulation, fibrinopeptide BB15-42(BB) and fibrin degradation product(FDP), for fibrinolysis, and tissue plasminogen activator(TPA) antigen for vascular system.(l).The results of normal values were as follow(n=20); 6-TG 40.6ng/ml, PF4 9.9ng/ml, FPA 3-lng/ml, BB 8.2ng/ml, and TPA 4.4ng/ml. (2).The mean values of 6-TG and PF4 were 72.1ng/ml and 30.9ng/ml, respectively in all patients with SLE(n=53)-FPA and BB were 7-lng/ml and 32.2ng/ml, respectively. All the markers mentioned above were significantly increased compared with normal. It means that hemostatic profile of SLE was hyperfunction of platelet, coagulation, and fibriolysis systems. (3)-In patients with ischemic heart diseases(IHD) including angina pectoris and acute myocardial infarction(n=17) B-TG and PF4 increased to 60.1ng/ml and 21.7ng/ml, respectively. But FPA did not change significantly. And BB increased to 4l.8ng/ml. It means that occurrence of IHD is closely related to hyperfunction of platelets rather than coagulation. (4). Patients with occlusive cerebrovascular accident(CVA) were divided into two groups; cases with high FPA and those with normal FPA. The average value of FPA of the former group was 10.2ng/ml and they had higher levels of BB of 23.1ng/ml than normal. TPA was measured before and after venous occlusion (VO) of lOOmmHg for 7 minutes. TPA increased 2 or 3 folds after VO test in normal subjects, but in 5 of 17 cases of CVA it did not change before and after VO test.It was postulated that the profile diagnosis of hemostatic disorders is possible by simultaneous measurement of molecular markers, because this method informs us what aspect of hemostatic function is hyperactive. It will also provide us the appropriate indication of treatment for various types of thrombotic disease.
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Gralnick, H. R., L. M. Magurder, K. Hansmann, M. Vail, G. Marti, R. McEver i S. Williams. "THE SURFACE EXPRESSION OF ALPHA GRANULE PROTEINS FOLLOWING THROMBIN STIMULATION". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643859.

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We have studied the platelet glycoproteins (GP) GPIb and the GPIIb/IIIa and the expression of alpha granule proteins (AGP) on the platelet (P) surface following thrombin (T) stimulation. The platelets were separated from plasma proteins on a arabinogalactan gradient. The P were stimulated with purified alpha T 0.1u/108p. Either monospecific polyclonal or murine monoclonal antibodies were used to detect the P glycoprotein and AGP. The platelets were analyzed on an EPICS V Flow Cytometer. Resting P had small amounts of AGP (2-8%) present on their surface. Within 1-3 min. after T stimulation significantly increased amounts of PF4 (26%) vWf (8%) Ig (10%) and the 140 kD alpha granule membrane (70%) were present on the P surface. The peak expression of all the AGP occurred within 5 mins. The 140 kD activation protein remained stable over 3-60 mins, in contrast the PF4 and the vWf expression peaked at 5 mins. and then decreased to near baseline levels. The GPIb and GPIIb/IIIa showed different patterns after activation. The GPIb intensity and number of positive cells decreased over time, while the GPIIb/ IIIa increased in flourescent intensity and the number of positive cells. These studies indicate that T stimulation of AGP on the P surface. vWf and P4 have a transient appearance on the P surface while Ig and the 140 kD activation protein both appear to become stable components of the P plasma membrane. This technique of detecting platelet activation is a specific, sensitive, and rapid method.
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Fujii, S., i T. Kariya. "PLATELET FUNCTION AND LIPOPROTEINS IN PATIENTS WITH HYPOTHYROIDISM". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643474.

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Platelet function and serum lipoprotein levels were studied in ten patients (two males and eight females) with hypothyroidism. Platelet aggregation and ATP release were determined by Lumi-aggregometer using ADP , collagen and epinephrine as stimulants. Platelet factor 4 (PF4) and thromboxane B2 (TXB2) were determined by radioimmunoassay. High density lipoproteincholesterol (HDL-C) was determined by heparin-manga-nese method. HDL subfractions were separated by gradient gel electrophoresis (PAA 4/30). Apolipopro-teins were measured by single radial immunodiffusion. Platelet aggregation increased in those patients at stimulating by epinephrine. ATP release also increased at stimulating by epinephrine. PF4 increased at stimulating by epinephrine. TXB2 increased at stimu-lating--by ADP or epinephrine significantly (p<0.05), respectively. Platelet aggregation was not correlated with thyroid hormones or total cholesterol levels.But it had a positive correlation tendency with HDL-C or HDL2-C and a negative one with HDL3-C levels.These results suggested some relationships between platelet function and HDL metabolism in patients with hypothyroidism.
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Raporty organizacyjne na temat "PF4"

1

Drypolcher, Katherine Carr. Pu Workers in PF4. Office of Scientific and Technical Information (OSTI), kwiecień 2019. http://dx.doi.org/10.2172/1511208.

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Schanken, Mary D., i John W. Taylor. Evaluation Report of Sytek PFX A2000 and PFX A2100. Fort Belvoir, VA: Defense Technical Information Center, listopad 1986. http://dx.doi.org/10.21236/ada208048.

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Aftanas, B. L. PFP solution stabilization. Office of Scientific and Technical Information (OSTI), kwiecień 1996. http://dx.doi.org/10.2172/362484.

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Chen, Cheng-Che, i Hao-En Lin. Survival Benefits and Bleeding Risk of Anti-VEGF Agents for Renal Cell Carcinoma (RCC): A Updated Systematic Review and Meta-Analysis of Phase 2 and 3 Randomized Clinical Trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, marzec 2023. http://dx.doi.org/10.37766/inplasy2023.3.0007.

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Review question / Objective: To investigate the survival benefits (PFS, DFS, OS) and bleeding risk of the anti-VEGF agents compared with placebo or interferon alpha (IFNa) in patients with RCC. Condition being studied: Part 1. The hazard ratio (HR) of the progression-free survival (PFS) and overall survival (OS) of anti-VEGF agents vs. non/placebo for patients with unresectable, advanced, metastatic, renal cell carcinoma (RCC). Part 2. The HR of the disease-free survival (PFS) and OS of anti-VEGF agents vs. non/placebo for patients with post-nephrectomy RCC (adjuvant use). Part 3. The HR of the PFS and OS of anti-VEGF agents vs. IFN-alpha for patients with RCC. Part 4. The relative risk (RR) of bleeding events of anti-VEGF agents vs. placebo or IFN-alpha for patients with RCC.
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Price, Roz. Climate Adaptation: Lessons and Insights for Governance, Budgeting, and Accountability. Institute of Development Studies (IDS), grudzień 2020. http://dx.doi.org/10.19088/k4d.2022.008.

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This rapid review draws on literature from academic, policy and non-governmental organisation sources. There is a huge literature on climate governance issues in general, but less is known about effective support and the political-economy of adaptation. A large literature base and case studies on climate finance accountability and budgeting in governments is nascent and growing. Section 2 of this report briefly discusses governance of climate change issues, with a focus on the complexity and cross-cutting nature of climate change compared to the often static organisational landscape of government structured along sectoral lines. Section 3 explores green public financial management (PFM). Section 4 then brings together several principles and lessons learned on green PFM highlighted in the guidance notes. Transparency and accountability lessons are then highlighted in Section 5. The Key findings are: 1) Engaging with the governance context and the political economy of climate governance and financing is crucial to climate objectives being realised. 2) More attention is needed on whether and how governments are prioritising adaptation and resilience in their own operations. 3) Countries in Africa further along in the green PFM agenda give accounts of reform approaches that are gradual, iterative and context-specific, building on existing PFM systems and their functionality. 4) A well-functioning “accountability ecosystem” is needed in which state and non-state accountability actors engage with one another. 5) Climate change finance accountability systems and ecosystems in countries are at best emerging. 6) Although case studies from Nepal, the Philippines and Bangladesh are commonly cited in the literature and are seen as some of the most advanced developing country examples of green PFM, none of the countries have had significant examples of collaboration and engagement between actors. 7) Lessons and guiding principles for green PFM reform include: use the existing budget cycle and legal frameworks; ensure that the basic elements of a functional PFM system are in place; strong leadership of the Ministry of Finance (MoF) and clear linkages with the overall PFM reform agenda are needed; smart sequencing of reforms; real political ownership and clearly defined roles and responsibilities; and good communication to stakeholders).
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Khan, Mahreen. Public Financial Management and Transitioning out of Aid. Institute of Development Studies, wrzesień 2022. http://dx.doi.org/10.19088/k4d.2022.145.

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This rapid review found an absence of literature focused specifically on measuring the impact of PFM and governance systems in countries that have transitioned from aid, by moving up the income ladder. However, there are a few academic publications and a limited number of studies by multilateral, such as the World Bank, that examine the role of PFM and governance systems in countries that are transitioning or have moved away from aid. However, the importance of public financial management (PFM) and governance systems in development is well established and seen as a pre-requisite for economic growth. To effectively transition from aid, most low-income countries (LICs) need to upgrade their PFM and governance systems to meet the different scale, resources, accountability mechanisms, and capacity-building requirements of a middle-income country (MIC). The absence of the above empirical evidence may be due to the complexity of measuring the impact of PFM reforms as the results are non-linear, difficult to isolate from other policies to establish causality, and manifest in a longer time frame. However, through comparative country studies, the consequences of deficient PFM and governance have been well documented. So impaired budgetary planning, implementation, and reporting, limited fiscal transparency, weak accountability mechanisms, resource leakage, and inefficient service delivery are well recognised as detrimental to economic growth and development. The literature on transitioning countries focuses predominantly on the impact of aid withdrawal on the social sector, where comparative qualitative data is easier to obtain and the effects are usually more immediate, visible, and may even extend to global health outcomes, such as in AIDS prevention programmes. Thus, tracking the progress of donor-assisted social sector programmes is relatively easier than for PFM and governance reforms. The literature is more abundant on the overall lessons of transitions from aid both for country governments and donors. The key lessons underscore the importance of PFM and governance systems and mechanisms to a successful transition up the income ladder: Planning for transition should be strategic, detailed and specifically geared to mitigate against risks, explicitly assessing the best mix of finance options to mitigate the impact of aid reduction/withdrawal on national budgets. The plan must be led by a working group or ministry and have timelines and milestones; Where PFM and governance is weak transition preparation should include strengthening PFM especially economic and fiscal legislation, administration, and implementation; Stakeholders such as donor partners (DPs) and NGOs should participate in the planning process with clear, open, and ongoing communication channels; Political and economic assessments in the planning and mid-term phases as well as long-term monitoring and evaluation should be instituted; Build financial, technical, and management capacity throughout the plan implementation This helpdesk report draws on academic, policy, and grey sources from the previous seven years rather than the usual K4D five-year window, to account for the two-year disruption of COVID-19. As cross-country studies on PFM and governance are scarce, a few older studies are also referenced to ensure a comprehensive response to the query. The report focuses on low-income countries transitioning from aid due to a change in status to lower-middle-income countries.
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Silvan, G. R. PFP MICON maintenance manual. Office of Scientific and Technical Information (OSTI), listopad 1994. http://dx.doi.org/10.2172/10106293.

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Hirzel, D. R. PFP Wastewater Sampling Facility. Office of Scientific and Technical Information (OSTI), maj 1995. http://dx.doi.org/10.2172/80949.

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BUSCH, M. S. PFP Emergency Lighting Study. Office of Scientific and Technical Information (OSTI), luty 2000. http://dx.doi.org/10.2172/801369.

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Morley, J. M. PFP Harrington lever hoists. Office of Scientific and Technical Information (OSTI), sierpień 1994. http://dx.doi.org/10.2172/10185637.

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