The features of high-resolution and high-bandwidth are in an increasing demand considering to the wide range application fields based on high performance data converters. In this paper, a modeling of high-resolution hybrid analog-to-digital converter (ADC) is proposed to meet those requirements, and a 16-bit two-step pipelined successive approximation register (SAR) analog-to-digital converter (ADC) with first-order continuous-time incremental sigma-delta modulator (ISDM) assisted is presented to verify this modeling. The combination of high-bandwidth two-step pipelined-SAR ADC with low noise ISDM and background comparator offset calibration can achieve higher signal-to-noise ratio (SNR) without sacrificing the speed and plenty of hardware. The usage of a sub-ranging scheme consists of a coarse SAR ADC followed by an fine ISDM, can not only provide better suppression of the noise added in 2nd stage during conversion but also alleviate the demands of comparator’s resolution in both stages for a given power budget, compared with a conventional Pipelined-SAR ADC. At 1.2 V/1.8 V supply, 33.3 MS/s and 16 MHz input sinusoidal signal in the 40 nm complementary metal oxide semiconductor (CMOS) process, the post-layout simulation results show that the proposed hybrid ADC achieves a signal-to-noise distortion ratio (SNDR) and a spurious free dynamic range (SFDR) of 86.3 dB and 102.5 dBc respectively with a total power consumption of 19.2 mW.

No abstract

FTo investigate the molecular mutation leading to Hemophilia B in one patient. Methods FOne-stage method was used to detect APTT, PT, TT, Fibrinogen and FVIII:C, FIX:C. The genomic DNA was extracted from the peripheral blood of proband. All exons and their flanks of Factor IX gene were amplified by polymerase chain reaction (PCR). The PCR products were sequenced directly. Results FThe proband was a 20-month boy presenting with scalp hematoma after trauma. Regular coagulation tests showed that his APTT was 135.1s, PT 11.9s, TT 15.6s and Fibrinogen 2g/l. Normal mixed plasma could correct the prolonged APTT to 35s. His FIX:C was 6.4% and FVIII:C was normal. Direct sequencing of PCR products suggested that there was a 5085T>C mutation (NG_007994.1) in Exon1, and a 36060G>C mutation in Exon8 of F9 gene. The former mutation caused the substitution of Leu19 by Pro, which lies in -28th in signal peptide. The later mutation lead to the substituion of Gln370 by His. Conclusion FMutations of 5085T>C in Exon1 and 36060G>C in Exon8 might be the causes of coagulation factor IX defiency for the patient. These mutations are de novo ones according to the database presenting in http://www.factorix.org/. Disclosures: No relevant conflicts of interest to declare.