dupA + H. pylori reduces diversity of gastric microbiome and increases risk of erosive gastritis.

Helicobacter pylori is believed to induce gastropathy; however, the exact pathogenic molecules involved in this process have not been elucidated. Duodenal ulcer promoting gene A (DupA) is a virulence factor with a controversial role in gastric inflammation and carcinogenesis. To explore and confirm the function of DupA in gastropathy from the perspective of the microbiome, we investigated the microbial characteristics of 48 gastritis patients through 16S rRNA amplicon sequencing. In addition, we isolated 21 H. pylori strains from these patients and confirmed the expression of dupA using PCR and qRT-PCR. Bioinformatics analysis identified diversity loss and compositional changes as the key features of precancerous lesions in the stomach, and H. pylori was a characteristic microbe present in the stomach of the gastritis patients. Co-occurrence analysis revealed that H. pylori infection inhibits growth of other gastric inhabiting microbes, which weakened the degradation of xenobiotics. Further analysis showed that dupA+ H. pylori were absent in precancerous lesions and were more likely to appear in erosive gastritis, whereas dupA- H. pylori was highly abundant in precancerous lesions. The presence of dupA in H. pylori caused less disturbance to the gastric microbiome, maintaining the relatively richness of gastric microbiome. Overall, our findings suggest that high dupA expression in H. pylori is correlated with a high risk of erosive gastritis and a lower level of disturbance to the gastric microbiome, indicating that DupA should be considered a risk factor of erosive gastritis rather than gastric cancer.

Three-Dimensional Evaluation of the Upper Airway Morphological Changes in Growing Patients with Skeletal Class III Malocclusion Treated by Protraction Headgear and Rapid Palatal Expansion: A Comparative Research.

OBJECTIVE: The aim of this study was to evaluate the morphological changes of upper airway after protraction headgear and rapid maxillary expansion (PE) treatment in growing patients with Class III malocclusion and maxillary skeletal deficiency compared with untreated Class III patients by cone-beam computed tomography (CBCT). METHODS: Thirty growing patients who have completed PE therapy were included in PE group. The control group (n = 30) was selected from the growing untreated patients with the same diagnosis. The CBCT scans of the pre-treatment (T1) and post-treatment (T2) of PE group and the control group were collected. Reconstruction and registration of the 3D models of T1 and T2 were completed. By comparing the data obtained from T1, T2 and control group, the morphological changes of the upper airway during the PE treatment were evaluated. RESULTS: Comparing with the data from T1 group, the subspinale (A) of maxilla and the upper incisor (UI) of the T2 group were moved in the anterior direction. The gnathion (Gn) of mandible was moved in the posterior-inferior direction. The displacement of the hyoid bone as well as the length and width of dental arch showed significant difference. The volume and mean cross-sectional area of nasopharynx, velopharynx and glossopharynx region showed significant difference. The largest anteroposterior/the largest lateral (AP/LR) ratios of the velopharynx and glossopharynx were increased, but the AP/LR ratio of the hypopharynx was decreased. In addition, the length and width of the maxillary dental arch, the displacement of the hyoid bone, the volume of nasopharynx and velopharynx, and the AP/LR ratio of the hypopharynx and velopharynx showed significant difference between the data from control and T2 group. CONCLUSION: The PE treatment of Class III malocclusion with maxillary skeletal hypoplasia leads to a significant increase in the volume of nasopharynx and velopharynx.

Cantharidin inhibits cell proliferation and promotes apoptosis in tongue squamous cell carcinoma through suppression of miR-214 and regulation of p53 and Bcl-2/Bax.

Cantharidin, a type of terpenoid, is a chemical compount secreted by the blister beetle or Mylabris phelarata pallas of the Meloidae family. Cantharidin is known to have good antitumor activity. The present study aimed to investigate the anticancer effect of cantharidin and its possible underlying mechanism using tongue squamous cell carcinoma (TSCC) TCA8113 cells. TCA8113 cells were treated with various concentrations of cantharidin, and the cell viability and cytotoxicity were assessed using MTT and LDH assays, respectively. Flow cytometry was conducted to examine cell apoptosis and colorimetric protease assay was performed to analyze caspase-9/3 activities in TCA8113 cells. qPCR and western blot analysis were used to investigate microRNA-214 (miR-214) expression, as well as the expression of p53, Bcl-2 and Bax proteins in TCA8113 cells. miR-214 and anti-miR-214 were transfected with mimics to examine whether miR-214 expression regulated the anticancer effect of cantharidin on TCA8113 cells and p53, Bcl-2 and Bax protein expression. The anticancer effect of cantharidin significantly inhibited cell proliferation and increased cytotoxicity of TSCC Tca8113 cells in a dose- and time-dependent manner. In addition, cantharidin induced cell apoptosis and activated caspase-9/3 activities of TSCC Tca8113 cells. Cantharidin markedly weakened miR-214 expression level, activated p53 protein expression, and suppressed the Bcl-2/Bax signaling pathway in Tca8113 cells. Downregulation of miR-214 increased p53 protein expression and decreased the Bcl-2/Bax signaling pathway of TSCC Tca8113 cells. However, the overexpression of miR-214 reduced the anticancer effect of cantharidin on the proliferation and apoptosis of TSCC Tca8113 cells, inhibited p53 protein expression, and increased the Bcl-2/Bax signaling pathway. The results suggested that cantharidin is a potential anticancer drug that can be used to regulate the proliferation and apoptosis of human TSCC Tca8113 cells. Additionally, its mechanism may partially be associated with the downregulation of miR-214, upregulation of p53 protein expression and suppression of the Bcl-2/Bax signaling pathway.

[Patients' experiences with the Forsus appliance].

PURPOSE: To investigate patients' experiences with the Forsus appliance. METHODS: This questionnaire survey was focused on patients' comprehensive experiences with Forsus, both initially and after several months of wearing, including the patients' overall impressions of the appliance. The survey was conducted in 64 patients wearing Forsus. RESULTS: A high percentage of patients(83.7%) reported neutral to favorable experience with Forsus. 85.4% of patients reported gradual adaption to the appliance within 4 weeks. Cheek irritation was the most serious side effect (about 52%). Cheek irritation and other side effect disappeared over time. CONCLUSIONS: The Forsus appliance is relatively well accepted by patients. Most patients experience some discomfort and functional limitations at first. However, the side effect gradually diminishes with time, and the patients adapt to the appliance finally. Practitioners should be especially vigilant about problems of cheek irritation.

Novel mutations in the IRF6 gene for Van der Woude syndrome.

Van der Woude syndrome (VWS, OMIM 119300) is an autosomal dominant craniofacial disorder characterized by pits of the lower lip, hypodontia, and cleft lip and/or cleft palate. It is the most common form of syndromic orofacial clefting and has very high penetrance with varied expressivity. The disease locus for VWS has been mapped to a 1.6-cM region on 1q32-41 between D1S205 and D1S491. Recently, mutations have been found in the interferon regulatory factor 6 ( IRF6) gene in patients with VWS and popliteal pterygium syndrome. To identify novel mutations of IRF6 in VWS patients, we screened four Chinese VWS families in all nine exons and their flanking splice junctions by direct sequencing. We identified three missense mutations and one nonsense mutation in IRF6. Our study further confirmed that IRF6 is essential for craniofacial development.