Objective To study the expression of c-kit and Ki-67 in the basal cell adenoma(BCA)and adenoid cystic carcinoma (ACC) of salivary gland. Methods The expression of c-kit and Ki-67 was determined by immunohistochemistry method in BCA and ACC of salivary gland. Results The positive immuostaining of c-kit in BCA and ACC were 72.2 ％(13/18) and 83.3 ％(35/42),respectively, There was no significant difference in the expression of c-kit between the two tissues (x2=0.11,P＞0.05).The expression of Ki-67 was significantly different between BCA[(3.72±1.41) ％]and ACC[(23.81±10.19)％](t=14.145,P＜0.01).Conclusion Detection of Ki-67 might be helpful to distinguish between BCA and ACC,but c-kit has no effect in differentiating BCA from ACC.

Hearing impairment (HI) affects 1/1000 children and over 2% of the aged population. We have previously reported that mutations in the gene encoding gap junction protein connexin-31 (C×31) are associated with HI. The pathological mechanism of the disease mutations remains unknown. Here, we show that expression of C×31 in the mouse inner ear is developmentally regulated with a high level in adult inner hair cells and spiral ganglion neurons that are critical for the hearing process. In transfected cells, wild type C×31 protein (C×31wt) forms functional gap junction at cell-cell-contacts. In contrast, two HI-associated C×31 mutants, C×31R180X and C×31E183K resided primarily in the ER and Golgi-like intracellular punctate structures, respectively, and failed to mediate lucifer yellow transfer. Expression of C×31 mutants but not C×31wt leads to upregulation of and increased association with the ER chaperone BiP indicating ER stress induction. Together, the HI-associated C×31 mutants are impaired in trafficking, promote ER stress, and hence lose the ability to assemble functional gap junctions. The study reveals a potential pathological mechanism of HI-associated C×31 mutations.
Animals ; Connexins ; genetics ; Ear, Inner ; metabolism ; Endoplasmic Reticulum ; physiology ; Gap Junctions ; genetics ; metabolism ; physiology ; Golgi Apparatus ; genetics ; metabolism ; Hearing Loss ; genetics ; metabolism ; pathology ; Mice ; Mutation ; Neurons ; metabolism ; Protein Transport ; genetics ; Stress, Physiological