Home About us Contact | |||
Efficient Activation (efficient + activation)
Selected AbstractsEfficient Activation of 2-Iminomethylpyridine/Cobalt-Based Alkyne [2+2+2],Cycloaddition Catalyst by Addition of a Silver SaltADVANCED SYNTHESIS & CATALYSIS (PREVIOUSLY: JOURNAL FUER PRAKTISCHE CHEMIE), Issue 14-15 2007Avijit Goswami Abstract The addition of silver triflate (AgOTf) or silver hexafluoroantimonate (AgSbF6) significantly increased the activity of the 2-(arylimino)methylpyridine/cobalt(II) chloride hexahydrate (CoCl2,6,H2O)/zinc catalyst in alkyne cyclotrimerizations thereby accelerating the reaction and enabling the use of unactivated, simple internal alkynes as the monoyne substrate: The rate of reaction was found to be highly dependent on the nature of the counter anion (X,) and the ligand (L) in the postulated cationic cobalt(I) complex [LCo(I)]+X,. [source] HLA-DRB1*16-restricted recognition of myeloid cells, including CD34+ CML progenitor cellsBRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2003Saskia B. Ebeling Summary. The therapeutic effect of a human leucocyte antigen (HLA)-identical allogeneic stem cell transplantation (allo-SCT) for the treatment of haematological malignancies is mediated partly by the allogeneic T cells that are administered together with the stem cell graft. Chronic myeloid leukaemia (CML) is particularly sensitive to this graft-versus-leukaemia (GVL) effect. Several studies have shown that in allogeneic responses both CD4 and CD8 cells are capable of strong antigen-specific growth inhibition of leukaemic progenitor cells, but that CD4 cells mainly exert the GVL effect against CML. Efficient activation of allogeneic CD4 cells, as well as CD8 cells, may explain the sensitivity of CML cells to elimination by allogeneic T cells. Identification of the antigens recognized by CD4 cells is crucial in understanding the mechanism through which CML cells are so successful in activating allogeneic T cells. In the present report, we describe the characterization of an allogeneic CD4 T-cell clone, DDII.4.4. This clone was found to react against an antigen that is specifically expressed in myeloid cells, including CD34+ CML cells. The antigen recognition is restricted by HLA-DRB1*16. To our knowledge, this is only the second report on an allogeneic CD4 T-cell clone that reacts with early CD34+ myeloid progenitor cells. [source] Ankle eversion torque response to sudden ankle inversion Torque response in unbraced, braced, and pre-activated situationsJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 2 2005Lars Konradsen Abstract In 13 young ankle stable subjects, ankle eversion torque and peroneal EMG were simultaneously recorded in response to sudden ankle inversion. The eversion torque response was bi-phasic. The initial development of torque, which was responsible for 30% of the maximal eversion torque response, was observed 135ms after the start of platform rotation and correlated well with the onset of the automatic postural peroneal EMG response. The remaining eversion torque response commenced after 305 ms, strongly correlating with the onset of the peroneal long latency voluntary EMG activity. With the ankle unbraced, 66% of the maximal torque level was reached in 326ms. While braced, the same torque magnitude was reached using 230ms (p < 0.02), and pre-activation of the peroneal muscles allowed the subjects to reach the same level of torque in 89ms (p < 0.0005). Prior to the study, a common reaction pattern to sudden inversion was expected in an ankle stable population, but review of the eversion torque and EMG data from the 13 subjects revealed three different voluntary reaction patterns: 10 subjects showed an efficient activation of evertor muscles; two subjects stiffened their ankles with activation of both in- and evertor muscles; and one subject showed a marginal voluntary activation of the ankle evertors. The results of the study indicate that the reaction to sudden ankle inversion is not solely automatic. The main part of the torque response is voluntarily mediated and inter-individual differences in strategy seem to exist in healthy subjects. © 2004 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved. [source] From pathogen to medicine: HIV-1-derived lentiviral vectors as vehicles for dendritic cell based cancer immunotherapyTHE JOURNAL OF GENE MEDICINE, Issue 1 2006Melissa Dullaers Abstract Over the years, the unique capacity of dendritic cells (DC) for efficient activation of naive T cells has led to their extensive use in cancer immunotherapy protocols. In order to be able to fulfil their role as antigen-presenting cells, the antigen of interest needs to be efficiently introduced and subsequently correctly processed and presented by the DC. For this purpose, a variety of both viral and non-viral antigen-delivery systems have been evaluated. Amongst those, HIV-1-derived lentiviral vectors have been used successfully to transduce DC. This review considers the use of HIV-1-derived lentiviral vectors to transduce human and murine DC for cancer immunotherapy. Lentivirally transduced DC have been shown to present antigenic peptides, prime transgene-specific T cells in vitro and elicit a protective cytotoxic T-lymphocyte (CTL) response in animal models. Different parameters determining the efficacy of transduction are considered. The influence of lentiviral transduction on the DC phenotype and function is described and the induction of immune responses by lentivirally transduced DC in vitro and in vivo is discussed in detail. In addition, direct in vivo administration of lentiviral vectors aiming at the induction of antigen-specific immunity is reviewed. This strategy might overcome the need for ex vivo generation and antigen loading of DC. Finally, future perspectives towards the use of lentiviral vectors in cancer immunotherapy are presented. Copyright © 2005 John Wiley & Sons, Ltd. [source] |