Sandwich Integration Technique for the Pressure Sensor Detection of Occlusal Force In Vitro.

Bite force measurement is an important parameter when checking the function and integrity of the masticatory system, whereas it is currently very difficult to measure bite force during functional movement. Hence, the purpose of this study is to explore the potential technique and device for the measurement and intervention of the continuous bite forces on functional and dynamic occlusal condition. A portable biosensor by sandwich technique was designed, and the validity, reliability, and sensitivity were determined by mechanical pressure loading tests; meanwhile, the pressure signal is acquired by, and transmitted to, voltage changes by the electrical measurements of the sensors. The result is that, when the mechanical stress detection device is thicker than 3.5 mm, it shows relatively ideal mechanical properties; however, when the thickness is less than 3.0 mm, there is a risk of cracking. Mechanical stress changing and voltage variation had a regularity and positive relationship in this study. The mechanical stress-measuring device made by medical and industrial cross has a good application prospect for the measurement of bite force during function.

Nano nickel oxide promotes epithelial-mesenchymal transition through transforming growth factor ß1/smads signaling pathway in A549 cells.

Our previous study demonstrated that nano nickel oxide (NiO) induce pulmonary fibrosis in rats and collagen excessive formation in A549 cells, which mechanism was related with the increasing transforming growth factor ß1 (TGF-ß1) secretion. However, it remains unclear understanding the role of TGF-ß1 in collagen excessive formation. Here, we found nano NiO could directly promote epithelial-mesenchymal transition (EMT) via the TGF-ß1/Smads pathway in A549 cells. First, cytotoxicity induced by nano NiO has a dose- and time-dependent manner according to methylthiaozol tetrazolium assay. Second, nano NiO led to the increased contents of type I collagen (Col-I), TGF-ß1, p-Smad2, p-Smad3, alpha-smooth muscle actin (α-SMA), vimentin, and fibronectin, indicating Smads pathway activation and EMT occurence. Third, to verify whether TGF-ß1 activated Smads signaling pathway and EMT occurence, A549 cells were exposed to nano NiO and TGF-ß1 inhibitors (10 µM SB431542). The results showed that TGF-ß1 inhibitors alleviated the nano NiO-induced cytotoxicity and Col-I excessive formation. Meanwhile, TGF-ß1 inhibitors reversed the proteins expression trends of Col-I, p-Smad2, p-Smad3, α-SMA, vimentin, fibronectin, and E-cadherin. These observations suggested that EMT occurrence via TGF-ß1/Smads pathway might play an important role in the collagen excessive formation induced by nano NiO in A549 cells.

Does Probiotic Lactobacillus Have an Adjunctive Effect in the Nonsurgical Treatment of Peri-Implant Diseases? A Systematic Review and Meta-analysis.

OBJECTIVE: To evaluate the additional effect of probiotic Lactobacillus in the nonsurgical management of peri-implant diseases (peri-implant mucositis and peri-implantitis). METHODS: Six databases were searched up to May 2019 without time and language restrictions. Study selection and data extraction were conducted independently by 2 reviewers. The inclusion criteria for this systematic review were defined based on the participants, intervention, comparison, outcomes, and study design (PICOS) format. Randomized controlled trials comparing nonsurgical treatment combined with probiotic Lactobacillus or placebo agent in patients with peri-implant diseases were included. The methodological quality of retrieved studies was assessed according to the Cochrane Collaboration's Risk of Bias tool, and the quality of evidence was evaluated using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) tool. Odds ratio and 95% confidence interval (CI) were used to describe dichotomous data, while mean difference and standardized mean difference with 95% CI were used to describe continuous variables. RESULTS: Seven randomized controlled trials with 296 implants were included in this meta-analysis. The mean difference of probing pocket depth (PPD) was -0.05 (95% CI: -0.28 to 0.18; P = .67) immediately after treatment termination and -0.17 (95% CI: -1.01 to 0.67, P = .69) at least 2 months after treatment termination. There was a slight reduction of PPD after treatment termination. Compared with placebo, Lactobacillus provided limited benefits in peri-implant mucositis. There were no significant differences in the secondary outcomes of bleeding on probing or plaque index (P > .05). In a narrative synthesis of peri-implantitis, the effect of Lactobacillus on PPD and bleeding on probing remained controversial. CONCLUSIONS: This systematic review and meta-analysis showed that probiotic Lactobacillus provide limited benefits to the nonsurgical treatment of peri-implant mucositis or peri-implantitis.

Enhanced expression of circ_0000267 in hepatocellular carcinoma indicates poor prognosis and facilitates cell progression by sponging miR-646.

Hepatocellular carcinoma (HCC) is a highly aggressive carcinoma worldwide. Circular RNAs (circRNAs) have been proved to be involved in the pathogenesis of several carcinomas. circ_0000267 was reported to be elevated in HCC tissue samples by circRNA microarray. In this study, quantitative reverse-transcription polymerase chain reaction was induced to further detect the expression of circ_0000267 in HCC tissues and cells. The clinical significance was also explored by Fisher's exact test, Kaplan-Meier curves and Cox regression analysis. Cell counting kit-8, colony formation, flow cytometry and transwell experiments were conducted on HCC cells to elucidate the functions of circ_0000267. Dual-luciferase reporter assay was induced to explore the mechanism of circ_0000267. Moreover, rescue experiments were also performed on HCC cells. As a result, circ_0000267 was enhanced in HCC tissues and cell lines. This upregulation is associated with patients' clinical severity and poor prognosis. Functionally, circ_0000267 could facilitate cell growth, migration and invasion and attenuate cell apoptosis in HCC cells. Mechanistically, circ_0000267 could directly sponge miR-646 to exert its oncogenic properties. In summary, we identified a novel HCC-associated circRNA in the progression of this fatal disease.

Intelligent Occlusion Stabilization Splint with Stress-Sensor System for Bruxism Diagnosis and Treatment.

Bruxism is a masticatory muscle activity characterized by high prevalence, widespread complications, and serious consequences but without specific guidelines for its diagnosis and treatment. Although occlusal force-based biofeedback therapy is proven to be safe, effective, and with few side effects in improving bruxism, its mechanism and key technologies remain unclear. The purpose of this study was to research a real-time, quantitative, intelligent, and precise force-based biofeedback detection device based on artificial intelligence (AI) algorithms for the diagnosis and treatment of bruxism. Stress sensors were integrated and embedded into a resin-based occlusion stabilization splint by using a layering technique (sandwich method). The sensor system mainly consisted of a pressure signal acquisition module, a main control module, and a server terminal. A machine learning algorithm was leveraged for occlusal force data processing and parameter configuration. This study implemented a sensor prototype system from scratch to fully evaluate each component of the intelligent splint. Experiment results showed reasonable parameter metrics for the sensors system and demonstrated the feasibility of the proposed scheme for bruxism treatment. The intelligent occlusion stabilization splint with a stress sensor system is a promising approach to bruxism diagnosis and treatment.

[Impact of subchronic exposure to low-dose nano-nickel oxide on the reproductive function and offspring of male rats].

OBJECTIVE: To investigate the influence of subchronic exposure to low-dose subchronic nano-nickel oxide (NNO) on the reproductive function of male rats and embryonic development of the pregnant rats. METHODS: Fifty normal healthy male SD rats weighing 180－220 g were randomly divided into five groups of equal number, negative control, 4 mg/ml micro-nickel oxide (MNO), and 0.16, 0.8 and 4 mg/ml NNO, those of the latter four groups exposed to MNO or NNO by non-contact intratracheal instillation once every 3 days for 60 days, and then all mated with normal adult female rats in the ratio of 1∶2. After the female animals were confirmed to be pregnant, the males were sacrificed and the weights of the body, testis and epididymis obtained, followed by calculation of the visceral coefficients, determination of epididymal sperm concentration and viability and the nickel contents in the blood and semen by atomic fluorescence spectrometry. The female rats were killed on the 20th day of gestation for counting of the implanted fertilized eggs and live, dead and resorbed fetuses. RESULTS: After 60 days of exposure, the rats of the NNO groups showed no statistically significant differences from those of the negative control and MNO groups in the weights of the body, testis and epididymis or visceral coefficients. Compared with the negative control group, the animals of the 0.8 and 4 mg/ml NNO groups exhibited markedly decreased sperm concentration (ï¼»9.36 ± 0.98ï¼½ vs ï¼»7.49 ± 1.46ï¼½ and ï¼»6.30 ± 1.36ï¼½ ×106/ml, P < 0.05) and viable sperm (ï¼»85.35 ± 9.16ï¼½% vs ï¼»68.26 ± 16.63ï¼½% and ï¼»65.88 ± 14.68ï¼½ %, P < 0.05), increased morphologically abnormal sperm (ï¼»8.30 ± 2.47ï¼½% vs ï¼»13.99 ± 4.87ï¼½% and ï¼»15.38 ± 8.86ï¼½ %, P < 0.05), and elevated rate of dead and resorbed fetuses (1.18% vs 6.89% and 7.37%, P < 0.05), blood nickel content (ï¼»0.13 ± 0.16ï¼½ vs ï¼»0.52 ± 0.34ï¼½ and ï¼»0.82 ± 0.44ï¼½ mg/L, P < 0.05) and semen nickel content (ï¼»0.08 ± 0.13ï¼½ vs ï¼»0.35 ± 0.23ï¼½ and ï¼»0.63 ± 0.61ï¼½ mg/L, P < 0.05). The nickel level in the semen was correlated significantly with that in the blood (r = 0.912, P <0.01), negatively with the rate of viable sperm (r = －0.879, P <0.01) and positively with the percentage of morphologically abnormal sperm (r = －0.898, P <0.01). CONCLUSIONS: Sixty-day exposure to nano-nickel oxide at 0.8 and 4 mg/ml can produce reproductive toxicity in male rats and result in fetal abnormality in the females, while that at 0.16 mg/ml has no significant toxic effect on the reproductive function of the males.

Long non-coding RNA AC023115.3 suppresses chemoresistance of glioblastoma by reducing autophagy.

Malignant glioma is an aggressive brain cancer that responds poorly to chemotherapy. However, the molecular mechanism underlying the development of chemoresistance in glioma is not well-understood. In this study, we show that long non-coding RNA AC023115.3 is induced by cisplatin in human glioblastoma cells and that elevated AC023115.3 promotes cisplatin-induced apoptosis by inhibiting autophagy. Further mechanistic studies revealed that AC023115.3 acts as a competing endogenous RNA for miR-26a and attenuates the inhibitory effect of miR-26a on GSK3ß, a proline-directed serine-threonine kinase that promotes the degradation of Mcl1, leading to an increase in GSK3ß and a decrease in autophagy. Additionally, we discovered that AC023115.3 improves chemosensitivity of glioma cells to cisplatin by regulating the miR-26a-GSK3ß-Mcl1 pathway. Thus, these data indicate that the AC023115.3-miR-26a-GSK3ß signalling axis plays an important role in reducing the chemoresistance of glioma.

Circular RNA circPVT1 Promotes Proliferation and Invasion Through Sponging miR-125b and Activating E2F2 Signaling in Non-Small Cell Lung Cancer.

BACKGROUND/AIMS: Circular RNAs (circRNAs) are key regulators in the development and progression of human cancers, however its role in non-small cell lung cancer (NSCLC) tumorigenesis is not well understood. The aim of this study is to identify the expression level of circPVT1 in NSCLC and further investigated its functional relevance with NSCLC progression both in vitro and in vivo. METHODS: Quantative real-time PCR was used for the measurement of circPVT1 in NSCLC specimens and cell lines. Fluorescence in situ hybridization analysis (FISH) assay was used for the identification of sublocation of circPVT1 in NSCLC cells. Bioinformatics analysis, luciferase reporter assay and RNA immunoprecipitation (RIP) were performed to verify the binding of c-Fos at circPVT1 promoter region, and the direct interaction between circPVT1 and miR-125b. Gain- or loss-function assays were performed to evaluate the effects of circPVT1 on cell proliferation and invasion. Western blot and immunohistochemistry assays were performed to detect the protein levels involved in E2F2 pathway. RESULTS: We found that circPVT1 was upregulated in NSCLC specimens and cells. The transcription factor c-Fos binded to the promoter region of circPVT1, resulting in the overexpression of circPVT1 in NSCLC. Knockdown of circPVT1 suppressed NSCLC cell proliferation, migration and invasion, and increased apoptosis. In addition, circPVT1 mediated NSCLC progression via the regulation of E2F2 signaling pathway. More importantly, circPVT1 was predominantly abundant in the cytoplasm of NSCLC cells, and circPVT1 could serve as a competing endogenous RNA to regulate E2F2 expression and tumorigenesis in a miR-125b-dependent manner, which is further verified by using an in vivo xenograft model. CONCLUSION: circPVT1 promotes NSCLC cell growth and invasion, and may serve as a promising therapeutic target for NSCLC patients. Therefore, silence of circPVT1 could be a future direction to develop a novel treatment strategy.

mir-233 modulates the unfolded protein response in C. elegans during Pseudomonas aeruginosa infection.

The unfolded protein response (UPR), which is activated by perturbations of the endoplasmic reticulum homeostasis, has been shown to play an important role in innate immunity and inflammation. However, little is known about the molecular mechanisms underlying activation of the UPR during immune responses. Using small RNA deep sequencing and reverse genetic analysis, we show that the microRNA mir-233 is required for activation of the UPR in Caenorhabditis elegans exposed to Pseudomonas aeruginosa PA14. P. aeruginosa infection up-regulates the expression of mir-233 in a p38 MAPK-dependent manner. Quantitative proteomic analysis identifies SCA-1, a C. elegans homologue of the sarco/endoplasmic reticulum Ca2+-ATPase, as a target of mir-233. During P. aeruginosa PA14 infection, mir-233 represses the protein levels of SCA-1, which in turn leads to activation of the UPR. Whereas mir-233 mutants are more sensitive to P. aeruginosa infection, knockdown of sca-1 leads to enhanced resistance to the killing by P. aeruginosa. Our study indicates that microRNA-dependent pathways may have an impact on innate immunity by activating the UPR.

[Physiologically based toxicokinetic model for nickel].

OBJECTIVE: To estimate the metabolic parameters in different tissues and organs, build the physiologically based pharmacokinetic( PBPK) model of rat and occupational population, and predict the toxic dynamic characteristics exposure to nickel. METHODS: The partition coefficients in different tissues and organs were estimated using vector datas of nickel by the optimization and statistics files of acslx software. The PBTK model of occupational population exposure to nickel was built according to the metabolic parameters by acslx software. RESULTS: The evaluated partition coefficient of nickel were kidney blood( 0. 668), lung blood( 0. 102), spleen blood( 0. 037), liver blood( 0. 028), heart blood( 0. 022), and brain blood( 0. 006). The constructed successful PBPK model of occupational population exposed to 0. 1 mg/m~3 nickel for 8 hours showed that the nickel concentration is higher in kidney reached at 3. 328 µg/kg, followed by the spleen( 0. 185 µg/kg), liver( 0. 140 µg/kg) and heart( 0. 110 µg/kg). The content of nickel is lower in the brain( 0. 030 µg/kg). The kidneys is the major metabolic organs for nickel. CONCLUSION: The PBPK model can be used to convert the nickel levels from external exposure to internal exposure for each organ and to evaluate the time-dose relationship exposure to nickel in both rat and occupational population studies.

Design and Implement Strategy of Wireless Bite Force Device.

Abnormal bite force is an important risk factor for oral and maxillofacial disorders, which is a critical dilemma that dentists face every day without effective solutions. Therefore, it is of great clinical significance to develop a wireless bite force measurement device and explore quantitative measurement methods to help find effective strategies for improving occlusal diseases. This study designed the open window carrier of a bite force detection device through 3D printing technology, and then the stress sensors were integrated and embedded into a hollow structure. The sensor system mainly consisted of a pressure signal acquisition module, a main control module, and a server terminal. A machine learning algorithm will be leveraged for bite force data processing and parameter configuration in the future. This study implemented a sensor prototype system from scratch to fully evaluate each component of the intelligent device. The experimental results showed reasonable parameter metrics for the device carrier and demonstrated the feasibility of the proposed scheme for bite force measurement. An intelligent and wireless bite force device with a stress sensor system is a promising approach to occlusal disease diagnosis and treatment.

The Status of Occupational Stress and Its Influence on the Health of Medical Staff in Lanzhou, China.

This study aimed to understand the status quo of occupational stress and its impact on the health of medical staff and provide a theoretical basis for relieving occupational stress and improving the health status of medical staff. The occupational stress and health status of medical staff in 14 hospitals in Lanzhou were studied using a general questionnaire, Effort-Reward Imbalance questionnaire, and Self-Rated Health Measurement Scale. A total of 2169 participants were included in the analysis, and 59.4% of the medical staff experienced occupational stress. The results of the occupational stress survey showed that the prevalence of occupational stress among medical staff aged 40-50, with a master's degree or above, senior professional title, working for 10-20 years, and working more than 48 h per week was higher than in the other groups. The health survey results showed that, compared with other groups, the scores of physical, mental, and social health were lower in medical staff with working years of 10-20 years and working hours of more than 48 h per week. The results show that working years and working hours per week affect not only the level of occupational stress but also physiological, psychological, and social health.

Mitochondrial PKM2 deacetylation by procyanidin B2-induced SIRT3 upregulation alleviates lung ischemia/reperfusion injury.

Apoptosis is a critical event in the pathogenesis of lung ischemia/reperfusion (I/R) injury. Sirtuin 3 (SIRT3), an important deacetylase predominantly localized in mitochondria, regulates diverse physiological processes, including apoptosis. However, the detailed mechanisms by which SIRT3 regulates lung I/R injury remain unclear. Many polyphenols strongly regulate the sirtuin family. In this study, we found that a polyphenol compound, procyanidin B2 (PCB2), activated SIRT3 in mouse lungs. Due to this effect, PCB2 administration attenuated histological lesions, relieved pulmonary dysfunction, and improved the survival rate of the murine model of lung I/R injury. Additionally, this treatment inhibited hypoxia/reoxygenation (H/R)-induced A549 cell apoptosis and rescued Bcl-2 expression. Using Sirt3-knockout mice and specific SIRT3 knockdown in vitro, we further found that SIRT3 strongly protects against lung I/R injury. Sirt3 deficiency or enzymatic inactivation substantially aggravated lung I/R-induced pulmonary lesions, promoted apoptosis, and abolished PCB2-mediated protection. Mitochondrial pyruvate kinase M2 (PKM2) inhibits apoptosis by stabilizing Bcl-2. Here, we found that PKM2 accumulates and is hyperacetylated in mitochondria upon lung I/R injury. By screening the potential sites of PKM2 acetylation, we found that SIRT3 deacetylates the K433 residue of PKM2 in A549 cells. Transfection with a deacetylated mimic plasmid of PKM2 noticeably reduced apoptosis, while acetylated mimic transfection abolished the protective effect of PKM2. Furthermore, PKM2 knockdown or inhibition in vivo significantly abrogated the antiapoptotic effects of SIRT3 upregulation. Collectively, this study provides the first evidence that the SIRT3/PKM2 pathway is a protective target for the suppression of apoptosis in lung I/R injury. Moreover, this study identifies K433 deacetylation of PKM2 as a novel modification that regulates its anti-apoptotic activity. In addition, PCB2-mediated modulation of the SIRT3/PKM2 pathway may significantly protect against lung I/R injury, suggesting a novel prophylactic strategy for lung I/R injury.

Grape seed proanthocyanidin extract ameliorates cisplatin-induced testicular apoptosis via PI3K/Akt/mTOR and endoplasmic reticulum stress pathways in rats.

Testicular toxicity is an adverse reaction of the effective chemotherapy drug cisplatin (CIS). Our previous study found that grape seed proanthocyanidin extract (GSPE) had a protective effect on CIS-induced testicular toxicity. However, the protective mechanism of GSPE against CIS-induced testicular toxicity remains unknown. In this study, we aimed to investigate whether GSPE can reduce CIS-induced testicular toxicity and its potential mechanism in rats. The results showed that GSPE ameliorated CIS-induced the apoptosis of testicular cells and inhibited the protein levels of Bad, Cyt c, caspase-9, caspase-3, caspase-12, GRP78, CHOP, IRE1α, p-IRE1α, XBP-1S, PERK, p-PERK, eIF2α, and p-eIF2α. Besides, GSPE reversed the downregulation of PI3K, p-PI3K, Akt, p-Akt, mTOR, and p-mTOR protein expression induced by CIS. These results indicated that GSPE can improve CIS-induced testicular cells apoptosis via activating PI3K/Akt/mTOR and inhibiting Bad/Cyt c/caspase-9/caspase-3 pathways. And GSPE relieved endoplasmic reticulum stress-mediated apoptosis via inhibiting PREK/eIF2α and IRE1α/XBP-1S/caspase-12 pathways. In conclusion, the evidence suggested that GSPE can act as a protective agent against testicular toxicity induced by CIS. PRACTICAL APPLICATIONS: Testicular toxicity was a well-known adverse effect of cisplatin (CIS) in cancer treatment. Grape seed proanthocyanidin extract (GSPE) has been reported to serve as one of the most therapeutic potentials agents. In present study, we explored the regulatory effects of GSPE on the apoptosis induced by CIS, which involved testicular apoptosis mechanisms in rats. Our results indicated that CIS caused testicular toxicity via PI3K/AKT/mTOR and ERS mediated apoptosis pathway in rats. This toxicity was attenuated by GSPE treatment via activated PI3K/Akt/mTOR pathway, and inhibiting Bad/CytC/caspase-9/caspase-3 as well as PREK/eIF2α, IRE1α/XBP-1S/caspase-12 pathways. Our findings suggest that GSPE may be a novel protective agent against testicular toxicity induced by CIS.

Comparison of the effects of sevoflurane and propofol anesthesia on pulmonary function, MMP-9 and postoperative cognition in patients receiving lung cancer resection.

Effects of sevoflurane and propofol anesthesia on pulmonary function, matrix metalloproteinase-9 (MMP-9) and postoperative cognition were compared in patients undergoing simple resection of lower lobe of left lung. Retrospective method was used to analyze 58 cases of lung cancer patients treated by simple resection of lower lobe of left lung in the Second Hospital of Dalian Medical University from October 2016 to October 2017, and they were divided into two groups: Sevoflurane group (n=32) with sevoflurane anesthesia and propofol group (n=26) with propofol anesthesia. In the present study, the moment before induction of anesthesia (T1), before the start of one-lung ventilation (T2), before the end of one-lung ventilation (T3), after closed chest surgery (T4), 24 h after surgery (T5), calculate alveolar-arterial oxygen difference (A-aDO2), respiratory index (RI) and intrapulmonary shunt ratio (Qs/Qt), were compared between the two groups. The serum MMP-9 concentration at T1, T4 and T5 were detected by enzyme linked immunosorbent assay. The cognitive function of two groups was assessed by Mini-Mental State Examination (MMSE) 1 day before surgery and 1 and 10 days after surgery. The A-aDO2 level at T4 in sevoflurane group was significantly higher than that in propofol group (P<0.05). The RI level at T3, T4, the Qs/Qt and the MMP-9 level at T4 in the sevoflurane group was significantly higher than that in the propofol group (P<0.05). The MMSE score in sevoflurane group was significantly lower than that in propofol group 1 and 10 days after surgery (P<0.05). Propofol has little effect on pulmonary function and can decrease inflammatory factor MMP-9. Both sevoflurane and propofol have an effect on cognitive function after lung cancer resection, but propofol can reduce cognitive impairment in patients with lung cancer.

Overexpression of microRNA-183 promotes apoptosis of substantia nigra neurons via the inhibition of OSMR in a mouse model of Parkinson's disease.

The present study aimed to investigate the effect of microRNA­183 (miR­183) on substantia nigra neurons by targeting oncostatin M receptor (OSMR) in a mouse model of Parkinson's disease (PD). The positive expression rates of OSMR and the apoptosis of substantia nigra neurons were detected by immunohistochemistry and terminal deoxynucleotidyl transferase­mediated dUTP­biotin nick end­labeling, respectively. Substantia nigra neurons in normal and PD mice were cultured in vitro. The association between miR­183 and OSMR was verified using a dual luciferase reporter gene assay. The expression of miR­183 and the phosphoinositide 3­kinase­Akt signaling pathway­associated genes were detected by reverse transcription­quantitative polymerase chain reaction and western blot analysis, respectively. Cell apoptosis was detected by flow cytometry. OSMR is the target gene of miR­183. The number of OSMR­positive cells and the apoptotic rate of substantia nigra neurons were increased in the PD group. Neurons transfected with miR­183 mimic exhibited elevated expression levels of miR­183, B­cell lymphoma 2 (Bcl­2)­associated X protein (Bax) and caspase­9 and increased apoptotic rate, and reduced expression levels of OSMR, Akt, phosphorylated (p­)Akt, glycogen synthase kinase­3 (GSK­3ß), p­GSK­3ß, Bcl­2, insulin­like growth factor 1 (IGF­1), mammalian target of rapamycin (mTOR) and p­mTOR. The miR­183 inhibitor decreased the expression levels of miR­183, Bax and caspase­9 and the apoptotic rate; however, increased the expression of OSMR, Akt, p­Akt, GSK­3ß, p­GSK­3ß, Bcl­2, IGF­1, mTOR and p­mTOR. The results of the present study provide evidence that the overexpression of miR­183 promotes the apoptosis of substantia nigra neurons by inhibiting the expression of OSMR.

Silencing NUDT21 Attenuates the Mesenchymal Identity of Glioblastoma Cells via the NF-κB Pathway.

The proneural (PN) and mesenchymal (MES) subtypes of glioblastoma multiforme (GBM) are robust and generally consistent with classification schemes. GBMs in the MES subclass are predominantly primary tumors that, compared to PN tumors, exhibit a worse prognosis; thus, understanding the mechanism of MES differentiation may be of great benefit for the treatment of GBM. Nuclear factor kappa B (NF-κB) signaling is critically important in GBM, and activation of NF-κB could induce MES transdifferentiation in GBM, which warrants additional research. NUDT21 is a newly discovered tumor-associated gene according to our current research. The exact roles of NUDT21 in cancer incidence have not been elucidated. Here, we report that NUDT21 expression was upregulated in human glioma tissues and that NUDT21 promoted glioma cell proliferation, likely through the NF-κB signaling pathway. Gene set enrichment analysis, western blotting, and quantitative real-time reverse transcription polymerase chain reaction confirmed that NF-κB inhibitor zeta (NFKBIZ) was a downstream target affected by NUDT21 and that the MES identity genes in glioblastoma cells, CHI3L1 and FN1, were also differentially regulated. Our results suggest that NUDT21 is an upstream regulator of the NF-κB pathway and a potential molecular target for the MES subtype of GBM.

Does Bruxism Contribute to Dental Implant Failure? A Systematic Review and Meta-Analysis.

BACKGROUND: Bruxism was usually considered as a contraindication for oral implanting. The causal relationship between bruxism and dental implant failure was remained controversial in existing literatures. PURPOSE: This meta-analysis was performed to investigate the relationship between them. MATERIALS AND METHODS: This review conducted an electronic systematic literature search in MEDLINE (PubMed) and EmBase in November 2013 without time and language restrictions. Meanwhile, a hand searching for all the relevant references of included studies was also conducted. Study information extraction and methodological quality assessments were accomplished by two reviewers independently. A discussion ensued if any disagreement occurred, and unresolved issues were solved by consulting a third reviewer. Methodological quality was assessed by using the Newcastle-Ottawa Scale tool. Odds ratio (OR) with 95% confidence interval (CI) was pooled to estimate the relative effect of bruxism on dental implant failures. Fixed effects model was used initially; if the heterogeneity was high, random effects model was chosen for meta-analysis. Statistical analyses were carried out by using Review Manager 5.1. RESULTS: In this meta-analysis review, extracted data were classified into two groups based on different units. Units were based on the number of prostheses (group A) and the number of patients (group B). In group A, the total pooled OR of bruxers versus nonbruxers for all subgroups was 4.72 (95% CI: 2.66-8.36, p = .07). In group B, the total pooled OR of bruxers versus nonbruxers for all subgroups was 3.83 (95% CI: 2.12-6.94, p = .22). CONCLUSIONS: This meta-analysis was performed to evaluate the relationship between bruxism and dental implant failure. In contrast to nonbruxers, prostheses in bruxers had a higher failure rate. It suggests that bruxism is a contributing factor of causing the occurrence of dental implant technical/biological complications and plays a role in dental implant failure.

Evaluation of the efficacy of potassium nitrate and sodium fluoride as desensitizing agents during tooth bleaching treatment­A systematic review and meta-analysis.

OBJECTIVES: This meta-analysis was performed to evaluate the efficacy of potassium nitrate and sodium fluoride as desensitizing agents during tooth bleaching treatment. DATA, SOURCES AND STUDY SELECTION: An electronic systematic literature search was conducted in Cochrane Center Register of Controlled Trials, MEDLINE (PubMed) and EmBase in April, 2014 in English and without time restrictions. Study information extraction and methodological quality assessments were accomplished by two reviewers independently. Methodological quality was assessed by using the "Criteria for judging risk of bias in the 'Risk of bias' assessment tool". Dichotomous data was summarized by odds ratio (OR) with 95% confidence interval (CI) and continuous data was summarized by mean difference (MD) or standardised mean difference (SMD) with 95% confidence interval (CI). Statistical analyses were carried out by using Review Manager 5.2. For evaluation of percent of patients experiencing tooth sensitivity (POTS), the pooled OR of desensitizers vs. placebo was 0.45 (95% CI: 0.28-0.73, P=0.29). The pooled SMD of desensitizers vs. placebo was -0.47 (95% CI: -0.77 to -0.18, P=0.13) in evaluation of level of tooth sensitivity (LOTS). The results of shade evaluation remained inconsistent by evaluating subjective shade guide unit difference (ΔSGU or SGU) and objective colour difference (ΔE). CONCLUSIONS: This meta-analysis was performed to evaluate the efficacy of desensitizing agents, potassium nitrate and sodium fluoride, for tooth bleaching treatments. Potassium nitrate and sodium fluoride reduce tooth sensitivity while no consistent conclusion of tooth colour change was found. CLINICAL SIGNIFICANCE: Tooth sensitivity is a typical side effect associated with tooth bleaching procedures. Potassium nitrate and sodium fluoride are used widely to treat tooth sensitivity. This meta-analysis was performed to evaluate the efficacy of potassium nitrate and sodium fluoride as desensitizing agents during tooth bleaching treatment.