Anti-SCTR (full length) polyclonal antibody

A 35-39 GHz linearized differential in-phase and quadrature components (I/Q) receiver (Rx) fabricated in 65-nm CMOS for 5G massive front-ends phased-array systems is introduced. The two linearization techniques, multi-gate transistor (MGTR) and splitting cascode transistors (SCTR) linearizers, are adopted at RF amplifier and down-conversion mixers respectively which greatly cancel the 3rd-order intermodulation (IM3) power with P-1dB, IP3, and 3rd-harmonic rejection ratio (RR3) enhancements. According to measurements at RF 38 GHz in normal/linearized modes, the IP1dB/OP1dB showed 6 dB/2.4 dB enhancement (IP1dB improved from -19 to -13 dBm, and OP1dB improved from -1.6 to 0.8 dBm.) with 3.6 dB conversion gain (CG) degeneration (18.4 dB decreased to 14.8 dB). The power consumption is 62.5 mW. According to two-tone measurements, the IM3 power decreased 20-28 dB with IIP3/OIP3 enhancement of 13 dB/9.4 dB (IIP3 improved from -11 to 2 dBm, and OIP3 improved from 7.4 to 16.8 dBm.). The maximum IF power with RR3 value < -40 dBc improved 7 dB (-12 dBm improved to -5 dBm). Furthermore, the quadrature amplitude modulation (QAM) carrier demodulation test is demonstrated. In larger RF/IF power region, the measurement exhibits that the 256 QAM constellation diagram in normal mode is dispersed but recovered in linearized mode due to the improved RR3. Compared with republications, the proposed Rx has good IP1dB, OIP3 values, significant IP1dB, IP3, RR3 improvement with IM3 suppression. This linearized Rx is satisfactory for 5G massive front-ends phased-array systems.

Wang X, Ye H, Ward CJ, Chu JY, Masyuk TV, LaRusso NF, Harris PC, Chow BK, Torres VE. Insignificant effect of secretin in rodent models of polycystic kidney and liver disease. Am J Physiol Renal Physiol 303: F1089-F1098, 2012. First published July 18, 2012; doi:10.1152/ajprenal.00242.2012.-Polycystic kidney (PKD) and liver (PLD) diseases cause significant morbidity and mortality. A large body of evidence indicates that cyclic AMP plays an important role in their pathogenesis. Clinical trials of drugs that reduce cyclic AMP levels in target tissues are now in progress. Secretin may contribute to adenylyl cyclase-dependent urinary concentration and is a major agonist of adenylyl cyclase in cholangiocytes. To investigate the role of secretin in PKD and PLD, we have studied the expression of secretin and the secretin receptor in rodent models orthologous to autosomal recessive (PCK rat) and dominant (Pkd2(-/WS25) mouse) PKD; the effects of exogenous secretin administration to PCK rats, PCK rats lacking circulating vasopressin (PCKdi/di), and Pkd2(-/WS25) mice; and the impact of a nonfunctional secretin receptor on disease development in Pkd2(-/WS25):SCTR-/- double mutants. Renal and hepatic secretin and secretin receptor mRNA and plasma secretin were increased in both models, and secretin receptor protein was increased in the kidneys and liver of Pkd2(-/WS25) mice. However, exogenous secretin administered subcutaneously via osmotic pumps had minimal or negligible effects and the absence of a functional secretin receptor had no influence on the severity of PKD or PLD. Therefore, it is unlikely that by itself secretin plays a significant role in the pathogenesis of PKD and/or PLD.