Experimental demonstration of the time reversal Aharonov-Casher effect

We demonstrate the time reversal Aharonov-Casher (AC) effect in small arrays of mesoscopic semiconductor rings. By using an electrostatic gate we can control the spin precession rate and follow the AC phase over several interference periods. We show that we control the precession rate in two different gate voltage ranges; in the lower range the gate voltage dependence is strong and linear and in the higher range the dependence in almost an order of magnitude weaker. We also see the second harmonic of the AC interference, oscillating with half the period. We finally map the AC phase to the spin-orbit interaction parameter alpha and find it is consistent with Shubnikov-de Haas analysis.Comment: 4 pages, 6 figure

Therapeutic Efficacy of Adoptive Cell Transfer on Survival of Patients with Glioblastoma Multiforme: Case Reports

Glioblastoma multiforme (GBM), which occurs mostly in individuals over the age of 40, accounts for 12–15% of all primary brain tumors. Patients with GBM have a poor prognosis, even after aggressive upfront therapies. The present study documents that in 5 of these patients, the use of a novel immunotherapeutic approach combined with standard initial therapies resulted in a prolonged survival of over 3 years, which is significantly longer than the expected survival time with conventional therapies. During the course of intravenous cell-transfer immunotherapy, axial magnetic resonance images of the tumor region were monitored for over 5 years. The discontinuation of adoptive transfer regimens resulted in the rapid deterioration of patients with development of Gd-enhancing regions, indicating the initiation of tumor recurrence. Among patients with recurrence, the reinstatement of adoptive cell regimens with more frequent cell-transfers resulted in an apparent re-regression of tumors. Significantly longer survival times were seen in patients receiving transferred autologous lymphoid cells which were expanded in vitro, and which had a considerable proportion of γδT cells. We conclude that immunotherapy, combined with standard treatment, plays a significant role in the management of GBM patients and provides patients with a better prognosis

Generation of mouse models for type 1 diabetes by selective depletion of pancreatic beta cells using toxin receptor-mediated cell knockout

AbstractBy using the toxin receptor-mediated cell knockout (TRECK) method, we have generated two transgenic (Tg) murine lines that model type 1 (insulin-dependent) diabetes. The first strain, C.B-17/Icr-Prkdcscid/Prkdcscid-INS-TRECK-Tg, carries the diphtheria toxin receptor (hDTR) driven by the human insulin gene promoter, while the other strain, C57BL/6-ins2(BAC)-TRECK-Tg, expresses hDTR cDNA under the control of the mouse insulin II gene promoter. With regard to the C.B-17/Icr-Prkdcscid/Prkdcscid-INS-TRECK-Tg strain, only one of three Tg strains exhibited proper expression of hDTR in pancreatic β cells. By contrast, hDTR was expressed in the pancreatic β cells of all four of the generated C57BL/6-ins2(BAC)-TRECK-Tg strains. Hyperglycemia, severe ablation of pancreatic β cells and depletion of serum insulin were observed within 3days after the administration of diphtheria toxin (DT) in these Tg mice. Subcutaneous injection of a suitable dosage of insulin was sufficient for recovery from hyperglycemia in all of the examined strains. Using the C.B-17/Icr-Prkdcscid/Prkdcscid-INS-TRECK-Tg model, we tried to perform regenerative therapeutic approaches: allogeneic transplantation of pancreatic islet cells from C57BL/6 and xenogeneic transplantation of CD34+ human umbilical cord blood cells. Both approaches successfully rescued C.B-17/Icr-Prkdcscid/Prkdcscid-INS-TRECK-Tg mice from hyperglycemia caused by DT administration. The high specificity with which DT causes depletion in pancreatic β cells of these Tg mice is highly useful for diabetogenic research