Transcutaneous Sonography for Detection of the Cervical Vagus Nerve.

Cervical vagus nerve is not identified by computed tomography or magnetic resonance imaging. Transcutaneous sonography may be the best imaging study to evaluate the cervical vagus nerve. A 7 to 18 MHz linear array transducer was placed transversely on the lateral neck focusing on the carotid sheath from the clavicle level upward to the digastric muscle level bilaterally. The gray-scale technique was used, with the scan setting for the thyroid gland. Between January 2015 and March 2016, 314 patients with 628 cervical vagus nerves were enrolled, including 104 men and 210 women. Their ages ranged from 14 to 84 years. Transcutaneous sonography identified the entire trunk of bilateral cervical vagus nerves in 254 (80.9%) patients and did not identify 1 or both cervical vagus nerves in the other 60 (19.1%) patients. Among 628 cervical vagus nerves, transcutaneous sonography identified 626 (99.6%) lower cervical vagus nerves and 551 (87.7%) upper cervical vagus nerves. Among 551 visible upper cervical vagus nerves, 495 (89.8%) nerves were located laterally, 17 (3%) nerves were located medially, 9 (1.6%) nerves were located anteriorly, and 30 (5.4%) nerves were located posterior to the internal carotid artery. Man and left-side nerve were the factors associated with the anatomical variation in the upper cervical vagus nerve. Transcutaneous sonography can be the best imaging study to show the cervical vagus nerve and may be helpful to evaluate the nerve before neck operation.

Whole-Exome Sequencing of Nasopharyngeal Carcinoma Families Reveals Novel Variants Potentially Involved in Nasopharyngeal Carcinoma.

Genetic susceptibility is likely involved in nasopharyngeal carcinoma (NPC), a cancer caused by Epstein-Barr virus (EBV) infection. Understanding of genetic factors involved in NPC and how they contribute to EBV-induced carcinogenesis is limited. We conducted whole-exome capture/sequencing among 251 individuals from 97 multiplex families from Taiwan (205 affected, 21 obligate carriers, and 25 unaffected) using SeqCap EZ Human Exome Library v3.0 and Illumina HiSeq. Aligned sequences were filtered to identify likely-to-be-functional deleterious variants that co-segregated with disease. Ingenuity Pathway analysis was performed. Circulating magnesium levels were measured in 13 individuals in 2 families with NIPAL1 mutations and in 197 sporadic NPC cases and 237 controls. We identified variants in 12 genes likely involved in cancer pathogenesis, viral infection or immune responses to infection. These included genes postulated to be involved in magnesium transport (NIPAL1), EBV cell entry (ITGB6), modulation of EBV infection (BCL2L12, NEDD4L), telomere biology (CLPTM1L, BRD2, HNRNPU), modulation of cAMP signaling (RAPGEF3), DNA repair (PRKDC, MLH1), and Notch signaling (NOTCH1, DLL3). Pathway based analysis demonstrated enrichment for Notch signaling genes (p-value = 0.0006). Evaluation of individuals within NIPAL1 families suggested lower serum magnesium in NPC compared to unaffected members. A significant reduction in serum magnesium levels was observed among sporadic NPC cases compared to controls (7.1% NPC/1.7% controls below normal range; OR = 4.5; 95% CI = 1.4,14) and is consistent with findings demonstrating a role for magnesium channeling in T-cell responses to EBV. We identified novel genes associated with NPC that point to new areas of inquiry to better understand genetic factors that determine the fate of viral infections and/or otherwise predisposes to NPC.

Prevalence of current oral HPV infection among 100 betel nut chewers or cigarette smokers in Northern Taiwan.

BACKGROUND: The incidence of HPV positive oropharyngeal cancer is increasing in Taiwan. Given this, it is critical to understand the prevalence of oral HPV infection since this cancer is potentially preventable. A community-based study was conducted to evaluate the prevalence of oral HPV infection and sexual behavior changes. METHODS: Between January and December 2016, 100 subjects between 20 and 70 years-old with current/ever betel nut chewing or current cigarette smoking visited the Department of Health, New Taipei City. Subjects with cancer history or known HIV/AIDS were excluded. Sexual behavior information was collected through a questionnaire. Oral rinse samples and oropharyngeal swabs were obtained for HPV genotyping using the EasyChip HPV genotyping array (King-Car, Taiwan). RESULTS: 92 men and 8 women were recruited. The prevalence of oral HPV infection was 3%, present between 60 and 70 (11%) and between 30 and 40 years old (4%). The prevalence of the first sexual contact at younger than 20 years old were 71.4%, 53.6%, 15.4% and 44% in <40, 40-49, 50-59 and 60+ years old, respectively (p for trend = 0.0036). The prevalence of 3 or more lifetime sexual partners were 60.7%, 57.1%, 23.1% and 16.7%, respectively for <40, 40-49, 50-59 and 60+ years old (p for trend = 0.0005). CONCLUSION: The prevalence of oral HPV infection is 3%, in current/ever betel nut chewers or current cigarette smokers in Northern Taiwan. Younger generation have more lifetime sexual partners and younger first sexual contact. This could explain the rising incidence of HPV positive oropharyngeal cancer in Taiwan.

The PTEN-AKT-mTOR/RICTOR Pathway in Nasal Natural Killer Cell Lymphoma Is Activated by miR-494-3p via PTEN But Inhibited by miR-142-3p via RICTOR.

Nasal natural killer (NK) cell lymphoma (NNL) is an Epstein-Barr virus-associated lymphoma of cytotoxic NK cell origin. The Epstein-Barr virus-encoded miR-BART20-5p inhibits T-bet (TBX21), the master transcription factor of cytotoxic NK cells. To further explore the roles of miRNAs in NNLs, we measured the miRNA expression profiles of 36 NNLs. miR-21, miR-142-3p, miR-126, miR-451, and miR-494-3p were the top five miRNAs with the highest expression levels. By using pathway analysis, we identified associations between all of the five miRNAs with the PTEN-AKT-mTOR pathway, in which PTEN suppresses the oncogenic AKT, and mTOR mediates the oncogenic effects of AKT. YT and NK92 cells derived from NK cell lymphomas were used. miR-494-3p inhibited PTEN with secondary activation of AKT in NK92 cells, and miR-142-3p inhibited RICTOR, a key component of the mTOR complex, with secondary suppression of AKT in YT cells. Significantly, T-bet inhibited the PTEN-AKT-mTOR/RICTOR pathway through induction of PTEN and suppression of RICTOR. Therefore, a molecular circuit of T-bet, PTEN, AKT, and RICTOR is regulated by miR-BART20-5p, miR-494-3p, and miR-142-3p. This circuit is involved in the pathogenesis of NNL. Hence, antagomirs to miR-BART20-5p or miR-494-3p, miR-142-3p mimics, or AKT inhibitors may be useful in NNL therapy.