Myo3a is expressed in cochlear hair cells and retinal cells and is responsible for human recessive hereditary nonsyndromic deafness (DFNB30). To investigate the mechanism of DFNB30-type deafness, we established a mouse model of Myo3a kinase domain Y137C mutation by using CRISPR/Cas9 system. No difference in hearing between 2-month-old Myo3a mutant mice and wild-type mice was observed. The hearing threshold of the ≥6-month-old mutant mice was significantly elevated compared with that of the wild-type mice. We observed degeneration in the inner ear hair cells of 6-month-old Myo3a mutant mice, and the degeneration became more severe at the age of 12 months. We also found structural abnormality in the cochlear hair cell stereocilia. Our results showed that Myo3a is essential for normal hearing by maintaining the intact structure of hair cell stereocilia, and the kinase domain plays a critical role in the normal functions of Myo3a. This mouse line is an excellent model for studying DFNB30-type deafness in humans.

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Objective. This study aimed to determine if variations in the expression profiles of CA 19-9 and carcinoembryonic antigen (CEA) within the reference range could serve as possible biomarkers for postoperative CRC recurrence. Method. This retrospective cohort investigation enrolled 2,596 cases of CRC that received curative surgery. Serum CEA/CA 19-9 were measured through chemiluminescence immunoassay (CLIA). Results. During follow-up (median follow-up = 5.2 years), in total, 837 patients experienced recurrence. The fully adjusted hazard ratios (HRs) were significantly higher, ≥1 standard deviation (±SD), in patients with upregulated CEA/CA 19-9 levels ( HRCEA = 7.06 ; HRCA   19 − 9 = 3.98 ) than in those with downregulated CEA/CA 19-9 levels. The likelihood of recurrence remained consistently greater in cases of elevated CEA/CA 19-9 levels during sensitivity analyses. Conclusions. The findings of this analysis showed that variations in CEA/CA 19-9 expression profiles within the reference range impact CRC recurrence.

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