Triiodothyronine participates in odontoblast differentiation of apical papilla stem cells through regulation of ERK and p38MAPK signaling pathways

Purpose: To investigate the effect of triiodothyronine (T3) in odontoblast differentiation of apical papilla stem cells, and the mechanism of action involved. Methods: Apical unclosed permanent molars extracted from patients due to orthodontics and impaction were selected. The extracted teeth were cultured in the isolation stage of SCAP cells. The cells were exposed to different concentrations of T3. The effects of ERK and p38 MAPK signaling pathways on activity of alkaline phosphatase (ALP) were determined. Calcium deposition was measured using a calcium determination kit, while the expression of BMP - 2 protein by T3 was determined by Western blot assay. Fluorescence quantitative polymerase chain reaction (FqPCR) method was used to determine the mRNA expression of BMP. Results: The ALP activities were significantly higher in T3 groups than in control group. Relative to control, there were marked differences in ALP activity and calcium deposition in T3 group, T3 + PD group and T3 + SB group (p < 0.05). Relative to control, the mRNA and protein expressions of BMP-2 in T3 group were increased significantly (p < 0.05). Conclusion: Triiodothyronine regulates the differentiation of apical papilla stem cells into dentin through ERK and p38MAPK signaling pathways. This provides the mechanism underlying odontoblast differentiation of apical papilla stem cells

Performance of electronic dispersion compensator for 10Gb/s multimode fiber links

In high-speed optical links, electronic compensation circuits can be utilized to greatly improve the data transmission performance limited by fiber dispersion. In this paper, we develop a full link model, including multimode fibers, optical/electronics/optical components, clock-and-data recovery and electronic compensation circuits. The performance of various electronic compensation techniques, such as feed-forward equalizer and decision feedback equalizer for optical multimode fiber is investigated and numerically evaluated. Finally, a comparison of the performance of each compensation techniques and a proposal of optimal equalizer circuit implementation, achieving a 10-Gb/s transmission over 1-km standard multimode fiber are presented

Flame Boundary Measurement Using an Electrostatic Sensor Array

Flame boundary is an important geometrical characteristic for the evaluation of flame properties such as heat release rate and radiation. Reliable and accurate measurement of flame boundary is desirable for the prediction of flame structure and the optimization of combustion systems. Such measurement will inform the designers and operators of the combustion systems. This paper presents for the first time a study of using an electrostatic sensor array for flame boundary measurement. The electrostatic sensor is placed in the vicinity of the flame to sense its movement through charge transfer. The principle, design, implementation and assessment of a measurement system based on this methodology are introduced. Comparative experimental investigations with a digital camera conducted on a laboratory-scale combustion test rig show that the electrostatic sensor can respond to the variation of the distance between the electrode and the flame boundary. Reconstruction of the flame boundary is achieved using a set of distance measurements obtained from a sensor array. For diffusion flames over the range of fuel flow rate 0.60-0.80 L/min and premixed flames over the range of equivalence ratio 1.27-3.81, experimental results show that the measurement system is capable of providing reliable measurement of the flame boundary. The correlation coefficients under all test conditions are mostly larger than 0.96, the mean relative errors within 7.4% and the relative root mean square errors within 0.09. More accurate flame boundary measurements are achieved for diffusion flames. In addition, the overall polarity of charges in a flame can be determined from the polarity of the sensor signal

Isolation of a novel abscisic acid stress ripening (OsASR) gene from rice and analysis of the response of this gene to abiotic stresses

Abiotic stresses constitute a serious threat to agricultural production, which often develops into major crop production reducing factors around the world. Molecular biology technology has, however, emerged as a promising vehicle improving crop tolerance. A cold-, drought- and heat-inducible gene designated Oryza sativa L. abscisic acid stress-ripening (OsASR) gene, GenBank accession: AK318549.1 was identified in rice Pei’ai64s (O. sativa L. ssp. Indica cv.) using the GeneChip rice genome array (Affymetrix) representing 51, 279 transcripts from two rice subspecies japonica and indica. The expression profile of OsASR obtained by the microarray analysis was confirmed by quantitative real-time reverse transcription polymerase chain reaction (RT-PCR) analysis of the gene. The two sets of data matched very well, suggesting that OsASR is a multiple stresses responsive gene in rice. Based on the sequence, PCR primers were designed. The cDNA with the whole open reading frame (ORF) was amplified by PCR and cloned. Sequence analysis showed that the cDNA encodes a protein of 284 amino acid residues with M.W. ≈ 11.7 kD and pI ≈ 10.4. The gene encodes a protein with several conserved domains. Comparison of protein sequences indicates that OsASR encodes a putative abscisic acid stress-ripening protein. Analysis of the putative promoter region for candidate cis-regulatory elements using PlantCARE software identified seven kinds of cis-elements related to stress responses. Based on the aforementioned analyses and results obtained, we propose that OsASR is a novel candidate gene involved in stress tolerance in rice.Keywords: Rice, microarray, abiotic stress, reverse transcription polymerase chain reaction (RT-PCR), abscisic acid stress ripenin

Giant photoinduced lattice distortion in oxygen-vacancy ordered SrCoO2.5 thin films

Despite of the tremendous efforts spent on the oxygen vacancy migration in determining the property optimization of oxygen-vacancy enrichment transition metal oxides, few has focused on their dynamic behaviors non-equilibrium states. In this work, we performed multi-timescale ultrafast X-ray diffraction measurements by using picosecond synchrotron X-ray pulses and femtosecond table-top X-ray pulses to monitor the structural dynamics in the oxygen-vacancy ordered SrCoO2.5 thin films. A giant photoinduced strain ({\Delta}c/c > 1%) was observed, whose distinct correlation with the pump photon energy indicates a non-thermal origin of the photoinduced strain. The sub-picosecond resolution X-ray diffraction reveals the formation and propagation of the coherent acoustic phonons inside the film. We also simulate the effect of photoexcited electron-hole pairs and the resulting lattice changes using the Density Function Theory method to obtain further insight on the microscopic mechanism of the measured photostriction effect. Comparable photostrictive responses and the strong dependence on excitation wavelength are predicted, revealing a bonding to anti-bonding charge transfer or high spin to intermediate spin crossover induced lattice expansion in the oxygen-vacancy films.Comment: 12 pages, 4 figures, support materia

Src kinase up-regulates the ERK cascade through inactivation of protein phosphatase 2A following cerebral ischemia

<p>Abstract</p> <p>Background</p> <p>The regulation of protein phosphorylation requires a balance in the activity of protein kinases and protein phosphatases. Our previous data indicates that Src can increase ERK activity through Raf kinase in response to ischemic stimuli. This study examined the molecular mechanisms by which Src activates ERK cascade through protein phosphatases following cerebral ischemia.</p> <p>Results</p> <p>Ischemia-induced Src activation is followed by phosphorylation of PP2A at Tyr307 leading to its inhibition in the rat hippocampus. SU6656, a Src inhibitor, up-regulates PP2A activity, resulting in a significant decreased activity in ERK and its targets, CREB and ERα. In addition, the PP2A inhibitor, cantharidin, led to an up-regulation of ERK activity and was able to counteract Src inhibition during ischemia.</p> <p>Conclusion</p> <p>Src induces up-regulation of ERK activity and its target transcription factors, CREB and ERα, through attenuation of PP2A activity. Therefore, activation of ERK is the result of a crosstalk between two pathways, Raf-dependent positive regulators and PP2A-dependent negative regulators.</p

NMI inhibits cancer stem cell traits by downregulating hTERT in breast cancer.

N-myc and STAT interactor (NMI) has been proved to bind to different transcription factors to regulate a variety of signaling mechanisms including DNA damage, cell cycle and epithelial-mesenchymal transition. However, the role of NMI in the regulation of cancer stem cells (CSCs) remains poorly understood. In this study, we investigated the regulation of NMI on CSCs traits in breast cancer and uncovered the underlying molecular mechanisms. We found that NMI was lowly expressed in breast cancer stem cells (BCSCs)-enriched populations. Knockdown of NMI promoted CSCs traits while its overexpression inhibited CSCs traits, including the expression of CSC-related markers, the number of CD44+CD24- cell populations and the ability of mammospheres formation. We also found that NMI-mediated regulation of BCSCs traits was at least partially realized through the modulation of hTERT signaling. NMI knockdown upregulated hTERT expression while its overexpression downregulated hTERT in breast cancer cells, and the changes in CSCs traits and cell invasion ability mediated by NMI were rescued by hTERT. The in vivo study also validated that NMI knockdown promoted breast cancer growth by upregulating hTERT signaling in a mouse model. Moreover, further analyses for the clinical samples demonstrated that NMI expression was negatively correlated with hTERT expression and the low NMI/high hTERT expression was associated with the worse status of clinical TNM stages in breast cancer patients. Furthermore, we demonstrated that the interaction of YY1 protein with NMI and its involvement in NMI-mediated transcriptional regulation of hTERT in breast cancer cells. Collectively, our results provide new insights into understanding the regulatory mechanism of CSCs and suggest that the NMI-YY1-hTERT signaling axis may be a potential therapeutic target for breast cancers