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1       Here, we have identified a new type of rosetting.
2 parasitemia were not correlated with P vivax rosetting.
3 rum malaria through the mechanism of reduced rosetting.
4 rough the mechanism of reduced P. falciparum rosetting.
5 dilution of hyaluronic acid had no effect on rosetting.
6 line phosphatase binding assays, and in situ rosetting.
7                        Plasmodium falciparum rosetting, a parasite virulence phenotype associated wit
8  surmised that PfGARP may play a role in the rosetting and adhesion of malaria.
9                                         Both rosetting and cytoadherence are mediated by the parasite
10                                              Rosetting and cytoadherence have been widely studied as
11 e have mapped the region of CR1 required for rosetting and demonstrated that the CR1-dependent rosett
12 iates synchronicity of division and parasite rosetting and reveals that establishment and maintenance
13 peripheral blood cells obtained using immune rosetting and separation of progenitors was developed to
14 phorin A-specific antibody binding, CHO cell rosetting, and P falciparum invasion.
15  molecules involved in this so-called T-cell rosetting are important components of the immunological
16                            Sequestration and rosetting are key determinants of Plasmodium falciparum
17 ed predominantly toward nonmalignant T cells rosetting around Reed-Sternberg cells provided meaningfu
18 ernberg cells and by most polyclonal T cells rosetting around Reed-Sternberg cells.
19                    Using an antigen-specific rosetting assay and a mFc alpha R-expressing cell line,
20  A dilution of BSM but not PSM inhibited the rosetting assay by 17% (.2 mg/mL), 33% (1 mg/mL), and 53
21 d immunosorbent assay, flow cytometry, and a rosetting assay.
22 e all tested for inhibitory potential in the rosetting assay.
23 eF did not impair its ability to inhibit the rosetting assay.
24                                              Rosetting assays using CD236R knockdown normocytes deriv
25 with soybean lectin and by sheep-erythrocyte rosetting before transplantation.
26 ibility that C3b could be an intermediary in rosetting, bridging between the infected erythrocyte and
27 ivator knockout did not affect the extent of rosetting, but almost completely abrogated T-cell activa
28 rol on a subset of RIFINs expression and RBC rosetting by P. falciparum.
29 CD35; C3b/C4b receptor) have greatly reduced rosetting capacity, indicating an essential role for CR1
30 ther than reticulocytes, preferentially form rosetting complexes, indicating that this process is unl
31      Importantly, the IGFBP7-induced type II rosetting hampers phagocytosis of IRBC by host phagocyte
32                             In some studies, rosetting has been associated with malaria pathogenesis.
33  Here we report that the parasite ligand for rosetting in a P. falciparum clone is PfEMP1, encoded by
34                        In conclusion, T-cell rosetting in HL is established by formation of the IS, a
35                      They also show impaired rosetting interactions with non-parasitized erythrocytes
36                                  In malaria, rosetting is described as a phenomenon where an infected
37                                              Rosetting is more common in vivax than falciparum malari
38 osetting that involves direct interaction of rosetting ligands on IRBC and receptors on URBC, the IGF
39 ting and demonstrated that the CR1-dependent rosetting mechanism occurs commonly in P. falciparum iso
40 ed cell sorting (MACS) and sheep erythrocyte rosetting methods, and the quality of cell fractions was
41                       We established a novel rosetting model by coculturing HLA-II-matched peripheral
42                                     Although rosetting occurs in all causes of human malaria, most da
43 3 and anticapsular monoclonal antibodies and rosetting of fluorescent microspheres coated with anti-C
44                          The CD32A-dependent rosetting of fMLP-activated normal neutrophils also incr
45 nstrated centrilobular cholestasis and focal rosetting of hepatocytes, consistent with a cholestatic
46 ment receptor 1 (CR1) has been implicated in rosetting of uninfected red blood cells to Plasmodium fa
47 s separate entities; however, the ability of rosetting P. falciparum strains to cytoadhere has receiv
48                                              Rosetting phenomenon has been linked to malaria pathogen
49 d erythrocyte aggregation reminiscent of the rosetting phenomenon.
50  the preferential transcription of R29var in rosetting R29 parasites, a parasite line in which the A4
51 eptors on URBC, the IGFBP7-mediated, type II rosetting requires two additional serum factors, namely
52 ed by formation of the IS, and activation of rosetting T cells critically depends on the interaction
53  cells were CD25(-) provided that associated rosetting T cells expressed CD25.
54 s and showed IS formation with activation of rosetting T cells.
55                                Unlike type I rosetting that involves direct interaction of rosetting
56 mily and are essentially involved in the RBC rosetting, the hallmark of severe malaria.
57 ic peptide, increased the CD32A-dependent EA rosetting to 58%.
58                                              Rosetting to P vivax asexual and sexual stages was evide
59        In the same sample set, P. falciparum rosetting was reduced in parasite isolates from group O
60  cytoadherence of IT/R29 IE is distinct from rosetting, which is primarily mediated by NTS-DBL1alpha
61 on of individual cells based on differential rosetting with microspheres functionalized with monoclon
62  was induced by thrombin-activated platelets rosetting with neutrophils and was inhibited by anti-P-s
63                 Surface IgM+ (sIgM+) B cells rosetting with TT-coated beads produced anti-TT IgM, IgG