Showing papers by "Yuan Gao published in 2009"

Paired box 6 (PAX6) regulates glucose metabolism via proinsulin processing mediated by prohormone convertase 1/3 (PC1/3).

Abstract: Human patients with aniridia caused by heterozygous PAX6 mutations display abnormal glucose metabolism, but the underlying molecular mechanism is largely unknown. Disturbed islet architecture has been proposed as the reason why mice with complete inactivation of paired box 6 (PAX6) in the pancreas develop diabetes. This is not, however, the case in human aniridia patients with heterozygous PAX6 deficiency and no apparent defects in pancreatic development. We investigated the molecular mechanism underlying the development of abnormal glucose metabolism in these patients. A human aniridia pedigree with a PAX6 R240Stop mutation was examined for abnormal glucose metabolism using an OGTT. The underlying mechanism was further investigated using Pax6 R266Stop mutant small-eye mice, which also have abnormal glucose metabolism similar to that in PAX6 R240Stop mutation human aniridia patients. Paired box 6 (PAX6) deficiency, both in aniridia patients with a heterozygous PAX6 R240Stop mutation and in mice with a heterozygous Pax6 R266Stop mutation, causes defective proinsulin processing and abnormal glucose metabolism. PAX6 can bind to the promoter and directly upregulate production of prohormone convertase (PC)1/3, an enzyme essential for conversion of proinsulin to insulin. Pax6 mutations lead to PC1/3 deficiency, resulting in defective proinsulin processing and abnormal glucose metabolism. This study indicates a novel function for PAX6 in the regulation of proinsulin processing and glucose metabolism via modulation of PC1/3 production. It also provides an insight into the abnormal glucose metabolism caused by heterozygous PAX6 mutations in humans and mice.

3–5GHz IR-UWB timed array transmitter in 0.18μm CMOS

Abstract: This paper presents a dual-channel timed array transmitter for impulse radio ultra wide band wireless communication system. The transmitter can generate UWB pulses in two separate transmitter paths with tunable path delay difference of 0~250ps to achieve beamforming capability. Through injection locking with 800MHz input reference, the generated UWB pulse centers at 4GHz and covers 3~5GHz band with 10-dB side-lobe rejection. Fabricated in 0.18μm CMOS technology, the transmitter consumes 37mA at 10Mbps under 1.8V supply.

A 0.18-µm CMOS 3.2-10 GHz quadrature VCO for IEEE 802.15.4a UWB transceivers

Abstract: A fully integrated 3.2 to 10 GHz multi-band QVCO for UWB low data rate (LDR) communication is presented in this paper. The QVCO design supports all channel frequencies of the IEEE 802.15.4a standard which consists of 8 high band channels between 6-10 GHz and 3 low band channels between 3-5 GHz. The QVCO generates 6.4-10.3 GHz covering all high band carrier frequencies while the low band carrier frequencies are generated using the divider-by-2 circuit. The start-up time of the QVCO is 100 ns which enables the turning on/off powers supply in sync with the burst transmission to reduce power consumption. At 1 Mb/s data rate, the average current consumption of the QVCO core is 3.6 - 4.9 mA from 1.8V supply.