Continuous-time linear equalizer with automatic boosting gain adaptation and input offset cancellation

A continuous-time linear equalizer (CTLE) for high-speed serial link is presented whose adaptive boosting gain is obtained with the data and edge values sampled by clock and data recovery circuit. The input offset of the serial link receiver is estimated by the data and edge values as well and cancelled by the CTLE. The adaptation of the CTLE boosting gain is immune to the phase error of the clock and data recovery sampling clock, and the cancellation of the input offset is independent of the boosting gain adaptation. The performance of the proposed adaptive CTLE has been evaluated by applying it to a 5-Gb/s serial link receiver implemented in a 65-nm CMOS technology.This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (NRF-2016R1D1A1 B03930310) and the Ministry of Trade, Industry, and Energy (MOTIE), Korea under the Industrial Technology Innovation Program (10080285, IP development and standard definition for 8 K/4 K display). The CAD tools were provided by IC Design Education Centre (IDEC)

Graves병의 외과적 치료에 대한 전후향적 연구

학위논문(석사)--서울대학교 대학원 :의학과 외과학전공,1995.Maste

The expression of matrix metalloproteinases (MMPs), tissue inhibitor of metalloproteinases (TIMPs) and angiogenesis in relation to the depth of tumor invasion and lymph node metastasis in submucosally invasive colorectal carcinoma

BACKGROUND/AIMS: Lymph node (LN) metastasis occurs in approximately 10% of patients with submucosally invasive colorectal carcinoma. This study was performed to determine the role of matrix metalloproteinases (MMPs), tissue inhibitors of metalloproteinases (TIMPs) production and microvessel formation on the LN metastasis in submucosally invasive colorectal carcinoma. METHODS: A total of forty-one subjects with surgically resected submucosally invasive colorectal carcinoma were included in this study. Immunohistochemical staining of MMP-2, MMP-9, TIMP-1, TIMP-2, and urokinase-type plasminogen activator were performed. Angiogenesis was evaluated by counting the number of microvessels in each pathologic specimen as identified by CD34 immunohistochemical staining. RESULTS: The depth of submucosal invasion was not significantly correlated with the expression of MMP-2, MMP-9, TIMP-1, TIMP-2, or urokinase-type plasminogen activator, but the microvessel count was significantly correlated with the absolute depth of invasion (r=0.312, p<0.05). Upregulation of TIMP-2 was positively correlated with adjacent lymphatic invasion (p<0.05) and increased TIMP-2 expression was correlated with LN metastasis in submucosally invasive colorectal carcinoma (p=0.088). CONCLUSIONS: These results suggest that the expression of TIMP-2 and the microvessel count may be useful parameters for considering additional surgery after endoscopic treatment of submucosally invasive colorectal carcinoma.