Investigation on the Current Status of Middle and Primary School Teachers’ Career Development Impetus in the Context of Urban and Rural Planning: Based on Districts B and Y of Chongqing City, and County R

Professional development of teachers is an issue under heated discussion in reform and development of education, while impetus for a teacher’s professional development is the key to teacher’s development. In the context of planned urban and rural development, the career impetus for the development of teachers in primary and middle school has received more and more attention. This study, adopting methods of questionnaire and interviews, conducts an investigation and analysis over the current status of career development impetus among teachers of middle and primary schools in County R, and Districts B and Y, Chongqing City. The result shows that, for the surveyed teachers, career development motivations totally are in good conditions but individually vary a lot, the impetus mainly derives from the teachers’ own need, the generation of career development impetus is restricted by paradox factors and need cooperation of the society, schools, and teachers themselves. It also indicates that, for different groups of teachers in middle schools and primary schools, there exists certain level of difference in career development impetus

Time-delay signature suppression in a chaotic semiconductor laser by fiber random grating induced distributed feedback

We demonstrate that a semiconductor laser perturbed by the distributed feedback from a fiber random grating can emit light chaotically without the time delay signature. A theoretical model is developed based on the Lang-Kobayashi model in order to numerically explore the chaotic dynamics of the laser diode subjected to the random distributed feedback. It is predicted that the random distributed feedback is superior to the single reflection feedback in suppressing the time-delay signature. In experiments, a massive number of feedbacks with randomly varied time delays induced by a fiber random grating introduce large numbers of external cavity modes into the semiconductor laser, leading to the high dimension of chaotic dynamics and thus the concealment of the time delay signature. The obtained time delay signature with the maximum suppression is 0.0088, which is the smallest to date

Hydrodynamics and heat transfer of suspended surface in a supercritical cfb furnace

With the scaling-up of CFB boilers, more heating surfaces like suspended surfaces and/or mid-partition walls, are arranged in the furnace to ensure adequate heat absorption. The length of suspended surface reaches almost half height of the furnace in the Baima 600MW supercritical CFB boiler. Since the gas-solids hydrodynamics and heat transfer on those surfaces are different from that on waterwall, further researches are needed to investigate the characteristics of hydrodynamics and heat transfer on the suspended surfaces. Beside the experimental measurements on the suspended surfaces in a scale down test rig, the hydrodynamic characteristics on the suspended surfaces were computed by a CFD simulation combined with EMMS model in a supercritical CFB of annular furnace. The results present an uneven axial solid concentration profile on the suspended surface, and descending particles are found on some locations especially where those surfaces far away from the furnace exits. Based on the gas-solids hydrodynamic results, the modified cluster renewal model was applied in the heat transfer coefficient calculation of the suspended surfaces. The result shows the heat transfer coefficient varies with the height and it has difference between two sides of a surface. In addition, the average heat transfer coefficients of suspended surface at different locations are compared. References Basu P, Nag P K. Heat transfer to walls of a circulating fluidized-bed furnace[J]. Chemical Engineering Science, 1996, 51(1): 1-26. Cen K F, Ni M J, Luo Z Y, et al. Theoretical design and operation of circulating fluidized bed boiler[J]. China Electric Power Press, Beijing, 1998: 647-663. Cheng L M, Wang Q H, Shi Z L, et al. Heat transfer in a large circulating fluidized bed boiler[J]. Journal of Power Engineering, 2006, 26(3): 305-310. Huang C, Cheng L M, Zhou X L, et al. Suspended surface heat transfer in a large circulating fluidized bed boiler furnace[J]. Journal of Zhejiang University. Engineering Science, 2012, 46(11): 2128-2132. Sundaresan R, Kolar A K. Axial heat transfer correlations in a circulating fluidized bed riser[J]. Applied Thermal Engineering, 2012. * “Strategic Priority Research Program” of the Chinese Academy of Sciences, Grant No. XDA0703010

Jiedu Tongluo granules ameliorates post-stroke depression rat model via regulating NMDAR/BDNF signaling pathway

Post-stroke depression (PSD) is one of the most common stroke complications, which seriously affects stroke’s therapeutic effect and brings great pain for patients. The pathological mechanism of PSD has not been revealed. Jiedu Tongluo granules (JDTLG) is an effective traditional Chinese medicine for PSD treatment which is widely used in clinical treatment. JDTLG has a significant therapeutic effect against PSD, but the mechanism is still unclear. The PSD rat model was established by carotid artery embolization combined with chronic sleep deprivation followed by treating with JDTLG. Neurobehavioral and neurofunctional experiments were engaged in studying the neural function of rats. Histomorphology, proteomics, and western blotting researches were performed to investigate the potential molecular mechanisms related to JDTLG therapy. Oral treatment of JDTLG could significantly improve the symptoms of neurological deficit and depression symptoms of PSD rats. Proteomic analysis identified several processes that may involve the regulation of JDTLG on the PSD animal model, including energy metabolism, nervous system, and N-methyl-D-aspartate receptor (NMDAR)/brain-derived neurotrophic factor (BDNF) signal pathway. Our results showed that JDTLG could reduce glutamate (Glu) level and increase gamma-aminobutyric acid (GABA) level via regulating the NMDAR/BDNF pathway, which may play a vital role in the occurrence and development of PSD

Cardiac Sca-1+ cells are not intrinsic stem cells for myocardial development, renewal and repair

Background: For over a decade, Sca-1+ cells within the mouse heart have been widely recognized as a stem cell population with multipotency that can give rise to cardiomyocytes, endothelial cells and smooth muscle cells in vitro and after cardiac grafting. However, the developmental origin and authentic nature of these cells remain elusive. Methods: Here, we used a series of high-fidelity genetic mouse models to characterize the identity and regenerative potential of cardiac resident Sca-1+ cells. Results: With these novel genetic mouse models, we found that Sca-1 does not label cardiac precursor cells during early embryonic heart formation. Postnatal cardiac resident Sca-1+ cells are in fact a pure endothelial cell population. They retain endothelial properties and exhibit minimal cardiomyogenic potential during development, normal aging and upon ischemic injury. Conclusions: Our study provides definitive insights into the nature of cardiac resident Sca-1+ cells. The observations challenge the current dogma that cardiac resident Sca-1+ cells are intrinsic stem cells for myocardial development, renewal and repair and suggest that the mechanisms of transplanted Sca-1+ cells in heart repair need to be reassessed

MicroRNA-223 ameliorates alcoholic liver injury by inhibiting the IL-6–p47phox–oxidative stress pathway in neutrophils

Objectives Chronic-plus-binge ethanol feeding activates neutrophils and exacerbates liver injury in mice. This study investigates how recent excessive drinking affects peripheral neutrophils and liver injury in alcoholics, and how miR-223, one of the most abundant microRNAs (miRNAs) in neutrophils, modulates neutrophil function and liver injury in ethanol-fed mice. Designs Three hundred alcoholics with (n=140) or without (n=160) recent excessive drinking and 45 healthy controls were enrolled. Mice were fed an ethanol diet for 10 days followed by a single binge of ethanol. Results Compared with healthy controls or alcoholics without recent drinking, alcoholics with recent excessive drinking had higher levels of circulating neutrophils, which correlated with serum levels of alanine transaminase (ALT) and aspartate transaminase (AST). miRNA array analysis revealed that alcoholics had elevated serum miR-223 levels compared with healthy controls. In chronic-plus-binge ethanol feeding mouse model, the levels of miR-223 were increased in both serum and neutrophils. Genetic deletion of the miR-223 gene exacerbated ethanol-induced hepatic injury, neutrophil infiltration, reactive oxygen species (ROS) and upregulated hepatic expression of interleukin (IL)-6 and phagocytic oxidase (phox) p47phox. Mechanistic studies revealed that miR-223 directly inhibited IL-6 expression and subsequently inhibited p47phox expression in neutrophils. Deletion of the p47phox gene ameliorated ethanol-induced liver injury and ROS production by neutrophils. Finally, miR-223 expression was downregulated, while IL-6 and p47phox expression were upregulated in peripheral blood neutrophils from alcoholics compared with healthy controls. Conclusions miR-223 is an important regulator to block neutrophil infiltration in alcoholic liver disease and could be a novel therapeutic target for the treatment of this malady

Hyperactive Ras/MAPK signaling is critical for tibial nonunion fracture in neurofibromin-deficient mice

Neurofibromatosis type 1 (NF1) is a common genetic disorder affecting 1 in 3500 individuals. Patients with NF1 are predisposed to debilitating skeletal manifestations, including osteopenia/osteoporosis and long bone pseudarthrosis (nonunion fracture). Hyperactivation of the Ras/mitogen-activated protein kinase (MAPK) pathway in NF1 is known to underlie aberrant proliferation and differentiation in cell lineages, including osteoclast progenitors and mesenchymal stem cells (MSCs) also known as osteoblast progenitors (pro-OBLs). Our current study demonstrates the hyper Ras/MAPK as a critical pathway underlying the pathogenesis of NF1-associated fracture repair deficits. Nf1-deficient pro-OBLs exhibit Ras/MAPK hyperactivation. Introduction of the NF1 GTPase activating-related domain (NF1 GAP-related domain) in vitro is sufficient to rescue hyper Ras activity and enhance osteoblast (OBL) differentiation in Nf1−/− pro-OBLs and NF1 human (h) MSCs cultured from NF1 patients with skeletal abnormalities, including pseudarthrosis or scoliosis. Pharmacologic inhibition of mitogen-activated protein kinase kinase (MEK) signaling with PD98059 partially rescues aberrant Erk activation while enhancing OBL differentiation and expression of OBL markers, osterix and osteocalcin, in Nf1-deficient murine pro-OBLs. Similarly, MEK inhibition enhances OBL differentiation of hMSCs. In addition, PD98059 rescues aberrant osteoclast maturation in Nf1 haploinsufficient bone marrow mononuclear cells (BMMNCs). Importantly, MEK inhibitor significantly improves fracture healing in an NF1 murine model, Col2.3CreNf1flox/−. Collectively, these data indicate the Ras/MAPK cascade as a critical pathway in the pathogenesis of bone loss and pseudarthrosis related to NF1 mutations. These studies provide evidence for targeting the MAPK pathway to improve bone mass and treat pseudarthrosis in NF1

Loss of Asxl1 leads to myelodysplastic syndrome-like disease in mice

ASXL1 is mutated/deleted with high frequencies in multiple forms of myeloid malignancies, and its alterations are associated with poor prognosis. De novo ASXL1 mutations cause Bohring-Opitz syndrome characterized by multiple congenital malformations. We show that Asxl1 deletion in mice led to developmental abnormalities including dwarfism, anophthalmia, and 80% embryonic lethality. Surviving Asxl1(-/-) mice lived for up to 42 days and developed features of myelodysplastic syndrome (MDS), including dysplastic neutrophils and multiple lineage cytopenia. Asxl1(-/-) mice had a reduced hematopoietic stem cell (HSC) pool, and Asxl1(-/-) HSCs exhibited decreased hematopoietic repopulating capacity, with skewed cell differentiation favoring granulocytic lineage. Asxl1(+/-) mice also developed mild MDS-like disease, which could progress to MDS/myeloproliferative neoplasm, demonstrating a haploinsufficient effect of Asxl1 in the pathogenesis of myeloid malignancies. Asxl1 loss led to an increased apoptosis and mitosis in Lineage(-)c-Kit(+) (Lin(-)c-Kit(+)) cells, consistent with human MDS. Furthermore, Asxl1(-/-) Lin(-)c-Kit(+) cells exhibited decreased global levels of H3K27me3 and H3K4me3 and altered expression of genes regulating apoptosis (Bcl2, Bcl2l12, Bcl2l13). Collectively, we report a novel ASXL1 murine model that recapitulates human myeloid malignancies, implying that Asxl1 functions as a tumor suppressor to maintain hematopoietic cell homeostasis. Future work is necessary to clarify the contribution of microenvironment to the hematopoietic phenotypes observed in the constitutional Asxl1(-/-) mice

Consecutive epigenetically-active agent combinations act in ID1-RUNX3-TET2 and HOXA pathways for Flt3ITD+ve AML

Co-occurrence of Flt3ITD and TET2 mutations provoke an animal model of AML by epigenetic repression of Wnt pathway antagonists, including RUNX3, and by hyperexpression of ID1, encoding Wnt agonist. These affect HOXA over-expression and treatment resistance. A comparable epigenetic phenotype was identified among adult AML patients needing novel intervention. We chose combinations of targeted agents acting on distinct effectors, at the levels of both signal transduction and chromatin remodeling, in relapsed/refractory AML's, including Flt3ITD+ve, described with a signature of repressed tumor suppressor genes, involving Wnt antagonist RUNX3, occurring along with ID1 and HOXA over-expressions. We tracked patient response to combination of Flt3/Raf inhibitor, Sorafenib, and Vorinostat, pan-histone deacetylase inhibitor, without or with added Bortezomib, in consecutive phase I trials. A striking association of rapid objective remissions (near-complete, complete responses) was noted to accompany induced early pharmacodynamic changes within patient blasts in situ, involving these effectors, significantly linking RUNX3/Wnt antagonist de-repression (80%) and ID1 downregulation (85%), to a response, also preceded by profound HOXA9 repression. Response occurred in context of concurrent TET2 mutation/hypomorphy and Flt3ITD+ve mutation (83% of complete responses). Addition of Bortezomib to the combination was vital to attainment of complete response in Flt3ITD+ve cases exhibiting such Wnt pathway dysregulation