RESUMO
This paper describes the radio frequency (RF) measurement and tuning result of a 13 MeV Alvarez-type drift tube linac (DTL) for a compact pulsed hadron source (CPHS) at Tsinghua University. The design, machining, assembly, and alignment of the DTL are presented for integrity. The CPHS project consists of a high-current proton linac (13 MeV, 16 kW, peak current of 50 mA, 0.5 ms pulse width at 50 Hz), a neutron target station, a small-angle neutron scattering instrument, and a neutron imaging/radiology station. The linac contains an electron cyclotron resonance ion source, a low energy beam transport line, a four-vane radio frequency quadrupole (RFQ) accelerator, an Alvarez-type DTL, a high energy beam transport line, and a RF power supply and distributor. Construction on the CPHS started in June 2009, and the CPHS has provided 2000 h since 2013 to users with the neutrons produced by the 3 MeV proton beam from the radio frequency quadrupole bombarding on the beryllium target as an achievement of its mid-term objective. Presently, the tuning of the assembled DTL cavity has been completed successfully. The 4.3-m-long DTL consists of 40 accelerating cells, among which 39 full-length drift tubes (DTs) are suspended inside the cavity, and two half-length DTs are mounted inside the two end flanges of the cavity. Each DT contains a permanent magnet quadrupole. Thirteen post couplers and nine tuners are available for the tuning of the field. The relative error of the field after tuning is within ±1.6%, with a tilt sensitivity within ±33%/MHz in all cells. The beam energy will reach its designed value of 13 MeV after the DTL is installed in the beam line downstream the 3 MeV RFQ accelerator.
RESUMO
OBJECTIVE: To elucidate the chemosensitivity of human tongue squamous cell carcinoma Tca83 cell line to all-trans retinoid acid (RA) and to determine the potential genetic factors mediating this sensitivity. METHODS: RA in the amounts of 0.1, 1, and 10 microMol/L were used to treat human cell line Tca83 in vitro. Cell apoptosis as well as Fas/FasL expression were analyzed by TUNEL, RT-PCR, and immunohistochemistry approaches. RESULTS: RA in the amounts of 1 and 10 microMol/L RA began to inhibit cell proliferation at day 3 and had induced cell apoptosis on day 5. Both Fas and FasL could be detected in the treated and untreated cells. RA upregulated Fas mRNA and protein expression at day 5. RA had no obvious effect on FasL expression. CONCLUSION: The results suggest that apoptosis induced by RA may result from the enhancement of Fas gene transcription and translation.