Acupuncture and Transcutaneous Electrical Acupoint Stimulation Do Not Suppress Gag Reflex.

Objective: Gagging is a problem for many dental patients, as well as patients undergoing medical procedures, such as intubation. Research to date on the gag reflex has been limited by a lack of objective measures for measuring this reflex. Materials and Methods: A validated quantitative method was used to measure if acupuncture or transcutaneous electrical acupoint stimulation (TEAS) at Pericardium 6 (PC 6) and Stomach 36 (ST 36) suppressed the gag reflex, compared with a sham placebo. The subjects were 60 healthy adults randomly chosen to receive acupuncture, TEAS, or sham-TEAS on PC 6, located on the forearm, and ST 36, located on the lower leg. The gag reflex was measured by inserting a saliva ejector slowly down each participant's throat to determine the maximum tolerance of the gag reflex; the insertion length was used as an index of this reflex. Results: There was a significant difference in pre- and postintervention insertion lengths in all groups (paired t-test; all groups; P < 0.001). The differences in the insertion length among the groups (P = 0.76) and the interaction effect (group × time) were not significant (P = 0.79; 2-way analysis of variance). Conclusions: This study suggested that PC 6 and ST 36 stimulation was no different than placebo for alleviating the gag reflex.

Potential protein biomarkers for burning mouth syndrome discovered by quantitative proteomics.

Burning mouth syndrome (BMS) is a chronic pain disorder characterized by severe burning sensation in normal looking oral mucosa. Diagnosis of BMS remains to be a challenge to oral healthcare professionals because the method for definite diagnosis is still uncertain. In this study, a quantitative saliva proteomic analysis was performed in order to identify target proteins in BMS patients' saliva that may be used as biomarkers for simple, non-invasive detection of the disease. By using isobaric tags for relative and absolute quantitation labeling and liquid chromatography-tandem mass spectrometry to quantify 1130 saliva proteins between BMS patients and healthy control subjects, we found that 50 proteins were significantly changed in the BMS patients when compared to the healthy control subjects ( p ≤ 0.05, 39 up-regulated and 11 down-regulated). Four candidates, alpha-enolase, interleukin-18 (IL-18), kallikrein-13 (KLK13), and cathepsin G, were selected for further validation. Based on enzyme-linked immunosorbent assay measurements, three potential biomarkers, alpha-enolase, IL-18, and KLK13, were successfully validated. The fold changes for alpha-enolase, IL-18, and KLK13 were determined as 3.6, 2.9, and 2.2 (burning mouth syndrome vs. control), and corresponding receiver operating characteristic values were determined as 0.78, 0.83, and 0.68, respectively. Our findings indicate that testing of the identified protein biomarkers in saliva might be a valuable clinical tool for BMS detection. Further validation studies of the identified biomarkers or additional candidate biomarkers are needed to achieve a multi-marker prediction model for improved detection of BMS with high sensitivity and specificity.

MicroRNA-92b promotes tumor growth and activation of NF-κB signaling via regulation of NLK in oral squamous cell carcinoma.

miR-92b has been reported to be dysregulated in many types of human cancers. However, the role of miR-92b in oral squamous cell carcinoma (OSCC) is unknown. The aim of the present study was to investigate the function and mechanism of miR-92b in human OSCC. Using quantitative reverse­transcription PCR (qRT-PCR), we found that the miR-92b level in primary tumors (n=85) was significantly elevated compared with that in the adjacent normal tissues (p<0.001). A high level of miR-92b was significantly associated with a large tumor size (p=0.005), advanced tumor stage (p<0.001) and poorer prognosis (p=0.04). Functionally, miR-92b was shown to not only promote the proliferation of OSCC cells in MTT and colony formation and xenograft assays, but also to inhibit cell apoptosis in a flow cytometric assay. In western blotting and luciferase assay, NLK was identified as a direct and functional target of miR-92b. We also found that NLK was involved in miR-92b-induced cell proliferation, and its protein level was obviously downregulated in the miR-92b-overexpressing xenograft tumors. Finally, luciferase reporter assay and fluorescent immunostaining revealed that miR-92b activated the NF-κB signaling pathway, which may be responsible for the effects of miR-92b on cell proliferation. Taken together, our results indicate that miR-92b upregulation accelerates tumor growth and present a novel mechanism of miRNA­mediated NF-κB activation in OSCC.