[Initial establishment of digital reference standardized crown models of the primary teeth].

OBJECTIVE: To explore the construction process of the digital reference crown models, and to initially establish the digital reference crown models of the primary teeth to lay the foundation for the establishment of the standardized crown models and the future related applications of computer-aided design/computer-aided manufacture (CAD/CAM) technology to pediatric dentistry. METHODS: This study randomly selected children who were caries free, aged from 4 to 5 years in several kindergartens of Haidian District of Beijing.Plaster dental models were made for the children after taking complete impressions.The digital dental models were reconstructed by using the three-dimensional (3D) dental model scanner.And then, Geomagic Studio, a 3D reverse engineering software, was employed to extract the single dental crown data, the mesiodistal and buccolingual diameters and the height of the crowns were measured.The object was reduced or enlarged by a numerical factor, and then the size of each dental crown was standardized.A total of 3-5 points features on the crown were created, and all the objects were aligned through the functions of feature-based alignment.Finally, through average-based object creation and smoothing, the digital models of reference crowns of the primary teeth were established. RESULTS: A total of 40 plaster dental models from 16 boys and 26 girls were selected out for our further study.The digital dental models were reconstructed, and the mesiodistal and buccolingual diameters and the height of the crowns were measured by using reverse engineering technology.Comparing the results of using mesiodistal diameter, buccolingual diameter and height as the standards, we chose the mesiodistal diameters of crowns to do the standardization, and successfully established the digital reference models of 20 primary teeth crowns with detailed surface characteristics. CONCLUSION: In this study, the digital reference crown models of the primary teeth were established by reverse engineering technology, providing reference value for the standardized crown models and application for clinical practice, scientific research and teaching.Furthermore, this study also contributes to the extensive application of CAD/CAM technology in pediatric dentistry and the development of CAD/CAM dental systems with independent intellectual property rights.

A new method for detecting thermal characteristics of slow-wave structure of helix traveling-wave tube using external heat source.

This paper presents a method for detecting the heat-dissipation capability of the slow-wave structure (SWS) in a helix traveling wave tube (TWT) using an external heat source. This method utilizes transient temperature rise detection technology and structure function method to nondestructively detect the heat-dissipation capability of SWS. An analytical model is built, and the method is verified by using the simulation tool ANSYS. Furthermore, a dedicated test probe is designed based on this method, and a 2.5-mm diameter helix TWT is measured. The results reveal that the method can effectively detect parts with large thermal resistance in SWS, thereby providing the basis for eliminating the failure products and improving the production process of SWS.

Use of 0.4-Tesla static magnetic field to promote reparative dentine formation of dental pulp stem cells through activation of p38 MAPK signalling pathway.

AIM: To investigate whether static magnetic fields (SMFs) have a positive effect on the migration and dentinogenesis of dental pulp stem cells (DPSCs) to promote reparative dentine formation. METHODOLOGY: In vitro scratch assays and a traumatic pulp exposure model were performed to evaluate the effect of 0.4-Tesla (T) SMF on DPSC migration. The cytoskeletons of the DPSCs were identified by fluorescence immunostaining and compared with those of a sham-exposed group. Dentinogenic evaluation was performed by analysing the expressions of DMP-1 and DSPP marker genes using a quantitative real-time polymerase chain reaction (qRT-PCR) process. Furthermore, the formation of calcified deposits was examined by staining the dentinogenic DPSCs with Alizarin Red S dye. Finally, the role played by the p38 MAPK signalling pathway in the migration and dentinogenesis of DPSCs under 0.4-T SMF was investigated by incorporating p38 inhibitor (SB203580) into the in vitro DPSC experiments. The Student's t-test and the Kruskal-Wallis test followed by Dunn's post hoc test with a significance level of P < 0.05 were used for statistical analysis. RESULTS: The scratch assay results revealed that the application of 0.4-T SMF enhanced DPSCs migration towards the scratch wound (P < 0.05). The cytoskeletons of the SMF-treated DPSCs were found to be aligned perpendicular to the scratch wound. After 20 days of culture, the SMF-treated group had a greater number of out-grown cells than the sham-exposed group (nonmagnetized control). For the SMF-treated group, the DMP-1 (P < 0.05) and DSPP genes (P < 0.05), analysed by qRT-PCR, exhibited a higher expression. The distribution of calcified nodules was also found to be denser in the SMF-treated group when stained with Alizarin Red S dye (P < 0.05). Given the incorporation of p38 inhibitor SB203580 into the DPSCs, cell migration and dentinogenesis were suppressed. No difference was found between the SMF-treated and sham-exposed cells (P > 0.05). CONCLUSION: 0.4-T SMF enhanced DPSC migration and dentinogenesis through the activation of the p38 MAPK-related pathway.

Nox1 promotes colon cancer cell metastasis via activation of the ADAM17 pathway.

OBJECTIVE: Reactive oxygen species (ROS) generated by endogenous metabolic enzymes are involved in a variety of pathology processes, including cancer. In particular, superoxide-generating NADPH oxidase 1 (Nox1), a member of Nox enzyme family, is highly expressed in the colon tissue and has been implicated in physiological and pathophysiological states of colon cancer. However, the underlying molecular mechanism of Nox1 in the regulation of colon cancer progression remains largely unknown. MATERIALS AND METHODS: In vitro scratch wound healing and invasion assays were used to compare the migration and invasion abilities of HT29 cells in which Nox1 protein levels were manipulated. Western blot assay was performed to detect the expression of key proteins of the EGFR-PI3K-AKT signaling pathway. Immunoprecipitation assay was performed to detect the interaction between Nox1 and ADAM17. RESULTS: Nox1 overexpression promoted colon cancer cell growth, migration, and invasion through the EGFR-PI3K-AKT signaling pathway. At the molecular level, Nox1 regulated the expression of tumor necrosis factor-α (TNF-α) converting enzyme (TACE)/a disintegrin and metalloprotease domain 17 (ADAM17). Furthermore, Nox1 interacted with and stabilized ADAM17 from ubiquitin-mediated degradation, leading to the activation of the ADAM17 signaling pathway. CONCLUSIONS: This study suggests that Nox1 promotes colorectal cancer metastasis by modulating the stability of ADAM17.

The trend of chemotherapy-induced peripheral neurotoxicity in ovarian cancer survivors and its impacts on daily life during and one year after treatment.

PURPOSE: To explore the trend of progression and regression of peripheral neuropathy (PN) induced by combination of carboplatin and paclitaxel, and the impacts on daily activities. MATERIALS AND METHODS: PN was evaluated by nurse-based interview and patient-reported measures in their diary. The severity of PN scaled by National Cancer Institute Common Toxicity Criteria (NCI-CTC) before each cycle of chemotherapy and at three, six, and 12 months after drug withdrawal and coded as Grade I - V. RESULTS: The authors enrolled 106 eligible patients with ovarian cancer who underwent six cycles of combined chemotherapy of carboplatin plus paclitaxel. No patients showed Grade IV and V of PN and it was gradually aggravated following the dose accumulation. About 29.3% of the patients presented no PN, 64.2% Grade I, and 6.6% Grade II after the third course of chemotherapy, but increased to 36.8% of Grade I, 25.5% of Grade II, and 34.9% of Grade III after the sixth course of chemotherapy. At one-year follow-up, the rate of PN still existed with the rate of 88.5%, 57.3%, and 38.7% at three, six, and 12 months after drug withdrawal. Thirty-one patients encountered accidents, such as sharp injury (14.2%), fall (9.4%), burn (3.8%), and cold injury (1.9%). CONCLUSIONS: A significant proportion of patients with epithelial ovarian cancer treated with carboplatin plus paclitaxel suffer long term neuropathy and it affects patient's daily activities. Specialized care is necessary to provide not only during treatment, but also months to years after drugs withdrawal.

Remifentanil for labour analgesia: a double-blinded, randomised controlled trial of maternal and neonatal effects of patient-controlled analgesia versus continuous infusion.

This trial aimed to compare the maternal and neonatal effects of remifentanil given by patient-controlled analgesia (PCA) or continuous infusion for labour analgesia. Patient controlled analgesia was administered using increasing stepwise boluses from 0.1 to 0.4 µg.kg(-1) (0.1 µg.kg(-1) increment, 2 min lockout, n = 30). Continuous infusion used rates from 0.05 to 0.2 µg.kg(-1) .min(-1) (0.05 µg.kg(-1) .min(-1) increment, n = 30). Dose increments were given on request. Women reported lowest pain scores (median (IQR [range]) of 3 (2-4 [2-5]) for PCA and 4 (3-5.25 [3-7]) for continuous infusion (p = 0.004) at 60 min after the beginning of analgesia. The mean (SD) remifentanil umbilical vein/maternal artery ratio in the PCA and infusion groups were 0.74 (0.45) vs 0.70 (0.52), respectively (p = 0.776). The mean (SD) umbilical artery/umbilical vein ratios were 0.31 (0.12) vs 0.26 (0.07), respectively (p = 0.088). Maternal and neonatal adverse reactions of remifentanil were similar between the two groups. The total remifentanil consumption (median (IQR [range]) during PCA administration was lower than continuous infusion, 1.34 (1.22-1.48 [0.89-1.69]) mg vs 1.49 (1.35-1.61 [1.12-1.70] mg; p = 0.011). The results suggest that remifentanil PCA provides better pain relief and similar placental transfer compared with continuous infusion.

Addition of adrenaline to chloroprocaine provides a moderate duration time for epidural anaesthesia in elective caesarean section.

OBJECTIVE: Epidural anaesthesia using chloroprocaine with or without adrenaline and lidocaine with adrenaline were compared. METHODS: Sixty parturients undergoing elective caesarean section under epidural anaesthesia were randomized to receive 3% chloroprocaine (group C), 3% chloroprocaine with adrenaline (group CA) or 2% lidocaine with adrenaline (group LA). Onset time, duration time and various maternal, fetal and neonatal parameters were monitored. Pain was assessed using a visual analogue scale. RESULTS: The onset time of analgesia in group CA was similar to that in group C but was shorter than that in group LA. Duration of analgesia, loss of cold sensation and motor blockade in group CA were prolonged compared with group C, but were shorter than those in group LA. No differences in maternal, fetal or neonatal effects were seen. A higher pain score was reported in group C than in groups CA or LA at the end of surgery. CONCLUSIONS: Epidural anaesthesia using chloroprocaine with adrenaline has a quick onset and moderate duration and is an attractive alternative to lidocaine and adrenaline or chloroprocaine alone for caesarean section.

Dynamic distribution of bone marrow-derived mesenchymal stromal cells and change of pathology after infusing into mdx mice.

BACKGROUND: Mesenchymal stromal cells (MSC) are attractive candidates for the treatment of Duchenne muscular dystrophy (DMD) but how the donor MSC distribute in multiple organs and whether the increased dystrophin leads to a change in the pathology of mdx mice is still uncertain. In this research we detected the distribution of MSC and the pathology of mdx mice after MSC infusion. METHODS: MSC were isolated from rat bone marrow (BM) and expanded in proliferation medium. MSC of the fifth passage were delivered intravenously into irradiated mdx mice. The distribution of MSC labeled by [3H]TdR into a recipient's organs was calculated by radioactivity. The expression of dystrophin was detected at weeks 4, 8, 12 and 16 after MSC transplantation by immunofluorescence staining, RT-PCR and Western blot. Serum creatine kinase (CK) and centrally nucleated fiber (CNF) were also detected to assess the change in pathology. RESULTS: 24-48 h after transplantation, MSC were mainly found in the BM, liver and lung. The radioactivity in these organs decreased, whereas skeletal and myocardial muscle radioactivity increased gradually over time. In accordance with the increased radioactivity in skeletal muscle, the amount of dystrophin-positive myofibers increased. Furthermore, serum CK and CNF decreased slightly, suggesting specific pathophysiologic features of the dystrophic muscle were partially restored. DISCUSSION: Upon certification of the distribution of transplanted MSC in irradiated mdx mice, we found evidence of myogenic differentiation of MSC in skeletal muscle. This research may help us understand the mechanism of therapy of MSC transplantation.

Activated beta-catenin induces myogenesis and inhibits adipogenesis in BM-derived mesenchymal stromal cells.

BACKGROUND: Mesenchymal stromal cells (MSC) have been thought to be attractive candidates for the treatment of degenerative muscle diseases. However, little is known about the molecular mechanisms governing the myogenic differentiation in MSC. As the Wnt signaling pathway has been associated with myogenesis in embryogenesis and post-natal muscle regeneration, we hypothesized that the Wnt signaling pathway may be involved in governing the myogenic differentiation in MSC. METHODS: Primary MSC were isolated from Sprague-Dawley rats and expanded in proliferation medium. The rMSC were transfected with a constitutively active hbeta-catenin (S37A) plasmid or control vector by Lipofectamine followed by G418 selection. The transfected rMSC were grown to 80% confluence and then cultured in myogenic or adipogenic differentiation medium. Cells were characterized by light microscopy, immunofluorescence and RT-PCR at different time points after myogenic or adipogenic introduction. RESULTS: Ectopic expression of activated beta-catenin located primarily in the nucleus and activated transcription in rMSC. Overexpression of stabilized beta-catenin induced 27.1 +/- 3.91% rMSC forming long multinucleated cells expressing MyoD, myogenin, desmin and myosin heavy chain (MHC) via evoking the expression of skeletal muscle-specific transcription factors. In addition, overexpression of activated beta-catenin inhibited the adipogenic differentiation in rMSC through down-regulated expressions of C/EBPalpha and PPARgamma. DISCUSSION: To our knowledge, this is the first evidence that activated beta-catenin can induce myogenic differentiation in rMSC. The ability of stabilized beta-catenin to induce myogenic differentiation in rMSC may allow for its therapeutic application.

Human mesenchymal stromal cells ameliorate the phenotype of SOD1-G93A ALS mice.

BACKGROUND: Amyotrophic lateral sclerosis (ALS) is a progressive, lethal, neurodegenerative disease, currently without any effective therapy. Multiple advantages make mesenchymal stromal cells (MSC) a good candidate for cellular therapy in many intractable diseases such as stroke and brain injury. Until now, no irrefutable evidence exists regarding the outcome of MSC transplantation in the mouse model of ALS. The present study was designed to investigate the therapeutic potential of human MSC (hMSC) in the mouse model of ALS (SOD1-G93A mice). METHODS: hMSC were isolated from iliac crest aspirates from healthy donors and kept in cell cultures. hMSC of the fifth passage were delivered intravenously into irradiated pre-symptomatic SOD1-G93A mice. Therapeutic effects were analyzed by survival analysis, rotarod test, motor neuron count in spinal cord and electrophysiology. The engraftment and in vivo differentiation of hMSC were examined in the brain and spinal cord of hMSC-transplanted mice. RESULTS: After intravenous injection into irradiated pre-symptomatic SOD1-G93A mice, hMSC survived more than 20 weeks in recipient mice, migrated into the parenchyma of brain and spinal cord and showed neuroglia differentiation. Moreover, hMSC-transplanted mice showed significantly delayed disease onset (14 days), increased lifespan (18 days) and delayed disease progression compared with untreated mice. DISCUSSION: Our data document the positive effects of hMSC transplantation in the mouse model of ALS. It may signify the potential use of hMSC in treatment of ALS.

Ketamine inhibits polymorphonuclear leucocyte CD11b expression and respiratory burst activity in endotoxemic rats.

OBJECTIVE AND DESIGN: To observe the effect of ketamine on polymorphonuclear leucocytes (PMN) adhesion and respiratory burst activity in endotoxemia rats. MATERIALS: 30 rats were randomly allocated to five groups: rats challenged with intraperitoneal injection of saline (saline group); challenged with intraperitoneal injection of LPS 10 mg/kg (LPS group); challenged with intraperitoneal injection of LPS 10 mg/kg and treated by intraperitoneal injection of ketamine 5, 25, 50 mg/kg at 0, 1, 2, 3, 4, 5 h after the injection of LPS, respectively (three ketamine treatment groups). METHODS: PMN respiratory burst and CD11b expression were measured with flow cytometry at the end of 1 h, 4 h, and 6 h. RESULTS: LPS challenge significantly increased PMN respiratory burst activity and CD11b expression when compared with the saline group (p < 0.01). There was a significant decrease in LPS-induced PMN respiratory burst activity and CD11b expression in three ketamine treatment groups when compared with LPS group (p < 0.01). CONCLUSIONS: Ketamine significantly inhibits PMN CD11b expression and respiratory burst activity in endotoxemic rats.