In the resistive-shell tokamak, JIPP T-II , a control of the current density profile has been attempted by programming both gas puffing and plasma current waveform. A stable high-density plasma has been obtained with the following parameters: the maximum line-average electron density is n̄e = 8.5 × 1013cm−3, the minimum q(a)-value is 2.2, and the relative amplitude of the m/n = 2/l mode is suppressed to an extent less than 10−3. A derivation of the current density profile by solving the magnetic-diffusion equation on the basis of the experimental data shows that the current density profile favourable to the stability of low-m kink and tearing modes is realized by combining the effects of cooling through an increase in density and of heating by a current rise in the outer plasma region. The results of kink and tearing modes analysis agree well with the experimental observations. The criterion that the current density profile is successfully controlled by this method is derived as a function of the ratio of plasma current to electron density in the current-rise phase, i.e. 20 × 10−13 ⪅ Ip/n̄e ⪅ 30 × 10−13 kA·cm3. The major disruption due to the density increase is completely suppressed by the method proposed in this paper. The major disruption due to a reduction of q(a) to less than 2.2 has, however, not yet been suppressed. In future, the current density profile should be maintained more precisely at its optimum shape by using a feedback-control technique and a control of the plasma boundary with titanium gettering, etc.
We have demonstrated that a 72-kDa non-receptor-type protein-tyrosine kinase (~7 2 "~" ) was coimmunoprecipitated with membrane IgM in digitonin lysates of porcine tonsillar cells and was rapidly activated following the engagement of membrane IgM. This activation was occurred within 5 s, even in the presence of EGTA and 5,5'-dimethyl-bis-(O-aminophenoxy)-ethane-N,N,~,~-te~a-acetic acid as extracellular and intracellular Ca2+-chelating agents, respectively, as well as in the presence of the protein-kinase-C inhibitor, H-7. Additionally, genistein, a potent protein-tyrosine kinase inhibitor, was capable of reducing both IgM-stimulated Ca'+ mobilization and p7Tyk activation in a dose-dependent manner. These results indicate that p72'Yk is physically associated with the B-cell-antigen receptor, participating in antigen-mediated signal transduction in both a Ca2+-independent and protein-kinase-C-independent manners.
Graft-versus-host disease (GVHD) is the most common and well-known cause of morbidity and mortality following allogeneic bone marrow transplantation. Sporadic cases have been reported after cadaveric donor liver transplantation with usually fatal outcomes, however, the actual incidence and the characteristics of GVHD after living donor liver transplantation (LDLT) remain unknown. We herein report a person who developed fatal GVHD following LDLT and discuss the applicability of an HLA-homozygous donor to an HLA-haploidentical recipient. A 48-year-old male underwent LDLT for unresectable hepatocellular carcinoma with alcoholic liver cirrhosis. The donor was his 20-year-old son whose pretransplant HLA typing was homozygous at all loci. GVHD occurred 35 days after LDLT and was characterized by fever, diarrhea, maculopapular rash, and leukopenia, which led to the development of fatal pneumonia. We
DAV-IFN-β therapy brought no significant improvement in either disease-free survival rates or melanoma-specific survival rates of patients with stage II or III cutaneous melanoma. A randomized controlled trial would be required to further evaluate the efficacy of DAV-IFN-β therapy as an adjuvant chemotherapy.
The efficacy of this gene therapy was generally insufficient; however, some immunological responses were recognized in one patient. No adverse events were observed. HuIFNbeta gene therapy could be an attractive strategy for treatment of a variety of malignancies, including melanoma, though some modifications should be required.
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