A YBCO RF-SQUID magnetometer and its applications

An applicable RF-superconducting quantum interference detector (SQUID) magnetometer was made using a bulk sintered yttrium barium copper oxide (YBCO). The temperature range of the magnetometer is 77 to 300 K and the field range 0 to 0.1T. At 77 K, the equivalent flux noise of the SQUID is 5 x 10 to minus 4 power theta sub o/square root of Hz at the frequency range of 20 to 200 Hz. The experiments show that the SQUID noise at low-frequency end is mainly from 1/f noise. A coil test shows that the magnetic moment sensitivity delta m is 10 to the minus 6th power emu. The RF-SQUID is shielded in a YBCO cylinder with a shielding ability B sub in/B sub ex of about 10 to the minus 6th power when external dc magnetic field is about a few Oe. The magnetometer is successfully used in characterizing superconducting thin films

A YBCO RF-squid variable temperature susceptometer and its applications

The Superconducting QUantum Interference Device (SQUID) susceptibility using a high-temperature radio-frequency (rf) SQUID and a normal metal pick-up coil is employed in testing weak magnetization of the sample. The magnetic moment resolution of the device is 1 x 10(exp -6) emu, and that of the susceptibility is 5 x 10(exp -6) emu/cu cm

Iron Metabolism Regulates p53 Signaling through Direct Heme-p53 Interaction and Modulation of p53 Localization, Stability, and Function

Iron excess is closely associated with tumorigenesis in multiple types of human cancers, with underlying mechanisms yet unclear. Recently, iron deprivation has emerged as a major strategy for chemotherapy, but it exerts tumor suppression only on select human malignancies. Here, we report that the tumor suppressor protein p53 is downregulated during iron excess. Strikingly, the iron polyporphyrin heme binds to p53 protein, interferes with p53-DNA interactions, and triggers both nuclear export and cytosolic degradation of p53. Moreover, in a tumorigenicity assay, iron deprivation suppressed wild-type p53-dependent tumor growth, suggesting that upregulation of wild-type p53 signaling underlies the selective efficacy of iron deprivation. Our findings thus identify a direct link between iron/heme homeostasis and the regulation of p53 signaling, which not only provides mechanistic insights into iron-excess-associated tumorigenesis but may also help predict and improve outcomes in iron-deprivation-based chemotherapy