[Current application and limitations of augmented reality in the stomatology].

Computer-assisted technology are gradually integrated into dental education and clinical treatment. As a cutting-edge technology in computer-aided medicine, augmented reality can not only be used as an aid to dental education by presenting three-dimensional scenes for teaching demonstration and experimental skills training, but also can superimpose virtual image information of patients onto real lesion areas for real-time feedback and intraoperative navigation. This review explores the current applications and limitations of augmented reality in dentistry to provide a reference for future research.

Invasive pulmonary fungal infections in children with severe human adenovirus type 7 pneumonia: A retrospective study.

BACKGROUND: There has been a rapid increase in the number of human adenovirus type 7 (HAdV-7) and invasive pulmonary fungal infections (IPFIs) co-infection. METHODS: In this study, we included patients with confirmed HAdV-7 infection during the period from 2018 to 2019 to explore clinical characteristics of severe HAdV-7 pneumonia combined with IPFIs. RESULTS: Among the 143 patients, 35 cases were co-infected with IPFIs. Others were assigned to the control group (n Z 108). Patients wereprone to be complicated with respiratory failure, heart failure and hemophagocytic syndromein IPFIs group. Thirty-one species of fungi were detected in the IPFIs group, among whichAspergillus was the most common species. Compared to control group, patients had lowerlevels of WBC, CD3þ T lymphocyte counts and CD19þ B lymphocyte counts in IPFIs group. CONCLUSION: Aspergillus is the most common species in IPFIs combined with severe HAdV-7 pneumonia. For children with severe HAdV-7 pneumonia who are younger, have a long course of disease, and have been admitted to the ICU, we should predict the occurrence of IPFIs when there is multi-system dysfunction and the reduction of CD3+ T lymphocyte counts and CD19+ B lymphocyte counts in course of their disease.

LncRNA PCAT6 aggravates the progression of bladder cancer cells by targeting miR-513a-5p.

OBJECTIVE: Long non-coding RNAs (lncRNAs) have been demonstrated to play critical roles in tumorigenesis of bladder cancer (BC). Our research aimed to explore the underlying mechanisms of lncRNA prostate cancer-associated transcript 6 (PCAT6) in BC. PATIENTS AND METHODS: Real Time-quantitative Polymerase Chain reaction (RT-qPCR) was used to measure the levels of PCAT6 and miR-513a in BC tissues and cells. The Kaplan-Meier analysis was utilized to evaluate the overall survival time of BC patients. Besides, cell viability was detected by Cell Counting Kit-8 (CCK-8) assay. Cell migration and invasion were evaluated by wound healing and transwell assays. Furthermore, starBase and Dual-Luciferase reporter assay were used to determine the interaction between PCAT6 and miR-513a in BC cells. RESULTS: PCAT6 expression was upregulated, while miR-513a was downregulated in BC tissues and cell lines. BC patients with high expression of PCAT6 exhibited a shorter overall survival time compared with those patients with low expression of PCAT6. Moreover, PCAT6 knockdown notably suppressed cell progression. In addition, PCAT6 inhibited miR-513a expression through direct interaction, and the silencing of PCAT6 remarkably increased the expression of miR-513a. Finally, the knockdown of miR-513a partly abolished PCAT6 silencing-induced inhibitory effects on BC progression. CONCLUSIONS: Our study illustrated that PCAT6 knockdown inhibited cell progression of BC by regulating miR-513a, suggesting that PCAT6 might act as a prognostic biomarker and therapeutic target for BC patients.

Interleukin-10 does not modulate clopidogrel platelet response in mice.

UNLABELLED: ESSENTIALS: It is unclear whether interleukin-10 (IL-10) could affect clopidogrel metabolism and response. The bioactivation of and response to clopidogrel were determined between mice with or without IL-10. Maximum clopidogrel active metabolite levels were the major driver of platelet response to clopidogrel. IL-10 did not modulate maximum levels of clopidogrel active metabolite and its antiplatelet effects. BACKGROUND: Elevated plasma interleukin-10 (IL-10) levels were observed in patients who responded less to clopidogrel (a prodrug that is required for further metabolic bioactivation in the liver). However, no data are currently available suggesting whether there is such an association. OBJECTIVE: To systematically explore possible differences in the formation of and response to clopidogrel active metabolite (CAM) in mice with or without IL-10 gene expression. METHODS: A single oral dose of clopidogrel (10 mg kg(-1)) was given to IL-10 knockout (KO) mice and wild-type (WT) control mice, respectively, and pharmacokinetic parameters of clopidogrel and CAM were calculated. Moreover, adenosine diphosphate-induced whole-blood platelet aggregation was measured in mice receiving 0, 5, 10, or 20 mg kg(-1) of clopidogrel, respectively. RESULTS: Compared with IL-10 KO mice, WT mice had significantly lower area under the plasma concentration-time curve (AUC) of CAM as a result of a shorter mean elimination half-life but had significantly higher AUC of clopidogrel due to slower systemic clearance and smaller volume of distribution. Although AUC of CAM was significantly lower in WT mice than in KO mice, antiplatelet effects of clopidogrel did not differ significantly between the two mouse groups, as their maximum plasma concentrations (Cmax ) of CAM were not significantly different. CONCLUSIONS: IL-10 expression level affects AUC rather than Cmax of CAM, but the Cmax of CAM is the major driver of antiplatelet effects of clopidogrel in mice.

Cigarette smoke mediates epigenetic repression of miR-217 during esophageal adenocarcinogenesis.

Although microRNAs (miRs) have been implicated in the pathogenesis of various human malignancies, limited information is available regarding mechanisms by which these noncoding RNAs contribute to initiation and progression of tobacco-induced esophageal cancers. In this study, array and quantitative reverse transcriptase-PCR techniques were used to examine miR expression in immortalized esophageal epithelia (IEE) and esophageal adenocarcinoma (EAC) cells cultured in normal media with or without cigarette smoke condensate (CSC). Under relevant exposure conditions, CSC significantly decreased miR-217 expression in these cells. Endogenous levels of miR-217 expression in cultured EAC cells (EACC)/primary EACs were significantly lower than those observed in IEE/ paired normal esophageal tissues. RNA crosslink immunoprecipitation, quantitative reverse transcriptase-PCR (qRT-PCR) and immunoblot experiments demonstrated direct interaction of miR-217 with kallikrein 7 (KLK7), encoding a putative oncogene not previously implicated in EAC. Repression of miR-217 correlated with increased levels of KLK7 in primary EACs, particularly those from smokers. Chromatin and methylated DNA immunoprecipitation experiments demonstrated that CSC-mediated repression of miR-217 coincided with DNMT3b-dependent hypermethylation and decreased occupancy of nuclear factor 1 within the miR-217 genomic locus. Deoxyazacytidine induced miR-217 expression and downregulated KLK7 in EACC; deoxyazacytidine also attenuated CSC-mediated miR-217 repression and upregulation of KLK7 in IEE and EACC. Overexpression of miR-217 significantly decreased, whereas overexpression of KLK7 increased proliferation, invasion and tumorigenicity of EACC. Collectively, these data demonstrate that epigenetic repression of miR-217 contributes to the pathogenesis of EAC via upregulation of KLK7 and suggest that restoration of miR-217 expression may be a novel treatment strategy for these malignancies.