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A low-power, high-gain, and low-noise analog front-end (AFE) for wearable photoplethysmography (PPG) acquisition systems is designed and fabricated in a 0.35 μm CMOS process. A high transimpedance gain of 142 dBΩ and a low input-referred noise of only 64.2 pArms was achieved. A Sub-Hz filter was integrated using a pseudo resistor, resulting in a small silicon area. To mitigate the saturation problem caused by background light (BGL), a BGL cancellation loop and a new simple automatic gain control block are used to enhance the dynamic range and improve the linearity of the AFE. The measurement results show that a DC photocurrent component up-to-10 μA can be rejected and the PPG output swing can reach 1.42 Vpp at THD < 1%. The chip consumes a total power of 14.85 μW using a single 3.3-V power supply. In this work, the small area and efficiently integrated blocks were used to implement the PPG AFE and the silicon area is minimized to 0.8 mm × 0.8 mm.

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Kinase non-catalytic C-lobe domain containing 1 (KNDC1) exists in dendrites, guanine nucleotide exchange factor complexes and neuronal cell bodies as a putative protein-protein interaction module that regulates a number of signaling pathways. Previous studies have demonstrated that the knockdown of KNDC1 delays human umbilical vein endothelial cell (HUVEC) senescence. However, the effect of KNDC1 overexpression on HUVEC function remains unclear. In the present study, an adenovirus vector carrying KNDC1 was constructed and then transfected into endothelial cells to observe cell senescence. Furthermore, the effect of KNDC1 overexpression on HUVEC senescence was investigated in vitro and the underlying molecular mechanism was investigated. Senescence-associated β-galactosidase staining was used to determine cellular senescence and reactive oxygen species (ROS) were monitored to detect the level of cell oxidative stress. The mRNA transcription level and protein expression were analyzed by reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. The results demonstrated that KNDC1 overexpression possibly inhibited HUVEC activity and function and promoted HUVEC senescence. Mechanistic studies demonstrated that KNDC1 triggered a p53-ROS positive feedback loop, which serves a crucial role in regulating senescence. In conclusion, to the best of the authors' knowledge, this is the first time that KNDC1-adenovirus vector inhibition of HUVEC proliferation by activating the p53 signaling pathway has been reported. Theoretically, the results of the present study also support KNDC1 as a therapeutic target for future anti-senescence.