Primary benign paroxysmal positional vertigo vestibular detection of evoked myogenic potential significance / 临床耳鼻咽喉头颈外科杂志

OBJECTIVE@#To analyze the clinical significance of ocular vestibular evoked myogenic potentials (oVEMP) and cervical vestibular evoked myogenic potentials (cVEMP) in primary unilateral benign paroxysmal positional vertigo (BPPV).@*METHOD@#Fifty-two patients with unilateral primary BPPV (BPPV group) and 38 normal subjects (control group) received ocular vestibular evoked myogenic potential (oVEMP) and cervical vestibular evoked myogenic potential (cVEMP) test using tone burst stimuli. The response rate, latency and amplitude were analyzed.@*RESULT@#In BPPV group, the response rate of oVEMP was 46.15% in lesioned side and 48.08% in healthy side, respectively. The response rate of cVEMP was 67.31% in lesioned side and 65.38% in healthy side, respectively. In control group, the response rate on the left ear was 84.21% for oVEMP and 92.11% for cVEMP. On the right ear, was 81.58% for oVEMP and 94.74% for cVEMP in control group, there was no significant difference in cVEMP and oVEMP P1, N1 N1-P1 latency and amplitude between left and right ear. The interaural amplitude ratio and asymmetry of cVEMP and oVEMP was significantly different between BPPV group and control group (P<0.05).@*CONCLUSION@#Unilateral primary BPPV with bilateral impaired vestibular otolith pathways function can be objectively evaluated by oVEMP and cVEMP detection. Abnormal oVEMP responses were more frequently detected than cVEMP.

Clinicopathological significance of PTPN12 expression in human breast cancer

Protein tyrosine phosphatase non-receptor type 12 (PTPN12) is a recently identified tumor suppressor gene (TSG) that is frequently compromised in human triple-negative breast cancer. In the present study, we investigated the expression of PTPN12 protein by patients with breast cancer in a Chinese population and the relationship between PTPN12 expression levels and patient clinicopathological features and prognosis. Additionally, we explored the underlying down-regulation mechanism from the perspective of an epigenetic alteration. We examined PTPN12 mRNA expression in five breast cancer cell lines using semi-quantitative reverse-transcription PCR, and detected PTPN12 protein expression using immunohistochemistry in 150 primary invasive breast cancer cases and paired adjacent non-tumor tissues. Methylation-specific PCR was performed to analyze the promoter CpG island methylation status of PTPN12. PTPN12 was significantly down-regulated in breast cancer cases (48/150) compared to adjacent noncancerous tissues (17/150; P < 0.05). Furthermore, low expression of PTPN12 showed a significant positive correlation with tumor size (P = 0.047), lymph node metastasis (P = 0.001), distant metastasis (P = 0.009), histological grade (P = 0.012), and survival time (P = 0.019). Additionally, promoter CpG island hypermethylation occurs more frequently in breast cancer cases and breast cancer cell lines with low PTPN12 expression. Our findings suggest that PTPN12 is potentially a methylation-silenced TSG for breast cancer that may play an important role in breast carcinogenesis and could potentially serve as an independent prognostic factor for invasive breast cancer patients.