I-scan combined with laryngovideostroboscopy for predicting malignancy in vocal fold leukoplakia.

OBJECTIVE: This study evaluated vocal fold leukoplakia using i-scan combined with laryngovideostroboscopy for risk assessment prediction. METHODS: A total of 141 patients with 218 lesions were enrolled in this study. Morphological characteristics of leukoplakia, assessment of the vascular pattern using i-scan, and vocal fold vibratory function were analyzed. RESULTS: The number of patients with no, mild, moderate, severe dysplasia, and invasive carcinoma were 68, 40, 17, 46 and 47, respectively. The sensitivity of morphological characteristic, vascular pattern, vibratory function and predictive model were 77.4%, 72%, 69.9%, and 82.8%, respectively. Receiver operating characteristic curve analysis of morphological characteristic, vascular pattern, vibratory function and predictive model were 0.771, 0.824, 0.769, and 0.923, respectively. The results of logistic regression analysis showed that rough morphological types, perpendicular vascular pattern, severe decrease and absence of mucosal waves increased the risk of malignancy (OR = 5.531, 4.973, and 16.992, respectively; P < 0.001). CONCLUSIONS: I-scan combined with laryngovideostroboscopy can improve the differential diagnosis of low-risk and high-risk vocal fold leukoplakia.

Mitochondrial tRNA variants in Chinese subjects with coronary heart disease.

BACKGROUND: Coronary heart disease is the leading cause of death worldwide. Mitochondrial genetic determinants for the development of this disorder remain less explored. METHODS AND RESULTS: We performed a clinical and genetic evaluation and mutational screening of 22 mitochondrial tRNA genes in a cohort of 80 genetically unrelated Han Chinese subjects and 125 members of 4 families with coronary heart disease and 512 Chinese control subjects. This analysis identified 16 nucleotide changes among 9 tRNA genes. Of these, the T5592C mutation creates a highly conservative base pairing (5G-68C) on the acceptor stem of tRNA(Gln), whereas the G15927A mutation destabilizes a highly conserved base pairing (28C-42G) in the anticodon stem of tRNA(Thr). However, the other tRNA variants were polymorphisms. The pedigrees of BJH24 carrying the T5592C mutation, BJH15, and BJH45 harboring the G15927A mutation exhibited maternal transmission of coronary heart disease. Sequence analysis of their mitochondrial genomes revealed the presence of T5592C or G15927A mutation but the absence of other functionally significant mutations in all matrilineal relatives of these families. CONCLUSIONS: Our previous observations showed that altered structures of tRNAs by these mtDNA mutations caused mitochondrial dysfunction. These may be the first evidence that mtDNA mutations increase the risk of coronary heart disease. Our findings may provide new insights into the pathophysiology of this disorder.