Mask configurable readout circuit architecture for an ultra-high-resolution CMOS image sensor: publisher's note.

This publisher's note reports a correction in Appl. Opt.61, 2565 (2022)APOPAI0003-693510.1364/AO.453904.

Mask configurable readout circuit architecture for an ultra-high-resolution CMOS image sensor.

As the level of detail in today's images increases, so does the demand for resolution. Due to the necessity of mask stitching technology for full exposure of large array chips, we propose a mask configurable readout circuit architecture, which is suitable for large array structures. However, the stitchable readout circuit architecture has some non-ideal effects: row driver function failure and the column non-consistency problem. In our design, we solve the problem of column non-consistency after stitching. At the same time, we changed the signal transmission structure in order to avoid the row driver function failure caused by the mask stitching. In this paper, a prototype 2130×2130 CMOS image sensor is fabricated in 0.11 µm CMOS technology. The chip can capture images at 20 fps and reduce fixed pattern noise (FPN) from 3.5% to 1.5% through correction techniques. The architecture proposed in this paper is suitable for large array image sensors.

Upregulation of CENPF is linked to aggressive features of osteosarcoma.

Centromere protein F (CENPF) plays a key role in the regulation of the cell cycle. The present study revealed that CENPF was overexpressed in a variety of tumors and associated with the poor prognosis of osteosarcoma. The mRNA expression levels of CENPF were analyzed using the Gene Expression Profiling Interactive Analysis database and the protein levels of CENPF were detected in the specimens from patients with osteosarcoma using immunohistochemistry. Cell proliferation, cell cycle and flow cytometry assays were performed after the transfection of control or CENPF plasmids into osteosarcoma cells. A xenografts assay was used to determine the effects of CENPF on tumor growth in vivo. The results showed that CENPF was upregulated in osteosarcoma tissues and associated with high-grade tumor stage (P=0.023) and intraglandular dissemination (P=0.046). The transfection-induced depletion of CENPF in human osteosarcoma MG-63 and U-2 OS cell lines inhibited cell proliferation, stimulated apoptosis and induced cell cycle arrest. Induced CENPF depletion in MG-63 cells inhibited tumor growth of osteosarcoma cells in mice. These findings suggested that elevated CENPF levels contributed to increased cell proliferation by mediating apoptosis and cell cycle in osteosarcoma. Therefore, CENPF might be a potential biomarker for poor prognosis of osteosarcoma.