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The technique ofquot;simulative habitat cultivationquot; is to preserve the quality of traditional Chinese medicine by simulating the original habitat and site environment of wild Chinese medicine resources. Dendrobium nobile is the most representative variety of traditional Chinese medicine which reflects the coordinated development of medicinal material production and ecological environment. In this paper, the main technical points of the simulated cultivation model of D. nobile were summarized as follows: rapid propagation of seedling tissue technology to ensure the genetic stability of provenance; line card+fermented cow manure+live moss method to improve the survival rate; epiphytic stone cultivation to improve the quality of medicinal materials; and the integration of mycorrhizal fungi to improve the quality stability of medicinal materials. On the basis of summarizing the ecological benefits, economical and social benefits generated by the application of the technology, the paper systematically analyzes the principle of the technology for the cultivation of D. nobile to promote the excellent quality, the light, gas, heat and fertilizer resources of the undergrowth niche are in line with the wild site environment of D. nobile. The rich and complex soil microbial community in the forest laid the foundation for the species diversity needed for the growth of D. nobile.The stress effect on the growth of D. nobile resulted in the accumulation of secondary metabolites. The symbiotic relationship between the symbiotic fungi such as bryophytes and D. nobile promotes the synthesis of plant secondary metabolites. The high quality D. nobile was produced efficiently by improving and optimizing the cultivation techniques.

Mo-Cu alloy with high density can be fabricated at lower sintering temperature by high-energy ball-milling mechanical-alloying method and adding activation element. The rule of change of microstructure and its effect on the thermal expansion coefficient are studied. It is found that the holes in the Mo-Cu alloy sintered at lower temperature disappear, and Mo and Cu distribute uniformly. The Mo particles are fine-grained, and distribute uniformly in the Cu particles using the mechanical-alloying method. The change of thermal expansion coefficient with temperature is in accordance with the effect of adding activation element. There is a minor inflexion in the thermal expansion coefficient curve at 500°C. The change of thermal expansion coefficient with temperature is the same as 95% Al2O3 sealing material. Thus, the thermal property between Mo-Cu alloy and 95% Al2O3 match well.

International audience; Since the early Cretaceous, the Bay of Bengal was formed during rifting between India and Antarctica and then by subsequent seafloor spreading. The nature of the crust underlying the Bay of Bengal is oceanic south of 15°N, but remains unknown (thinned continental crust, serpentinized mantle or oceanic crust) north of this limit. In order to better define the nature of the crust in the northern Bay of Bengal, three wide-angle reflection seismic and refraction profiles were acquired during the multichannel seismic reflection Bengal cruise. Nine ocean-bottom seismometers were deployed alternatively on three profiles. A seismic source consisting of 64 air guns with a volume of 6180 in3 was used simultaneously with a 10.05-km long streamer to acquire both seismic reflection and refraction data. Tomographic and forward modelings of the three refraction profiles reveal a 20-km thick crust north of the Bengal delta front beneath a minimum of 13 km thick sedimentary cover. The crust thins to about 10 km immediately south of the EW trending delta front and the thickness of sediments reaches a minimum of 7 km. Crustal velocities and velocity gradients are consistent with a continental origin of the crust in this area. At the base of the crust, high seismic velocities (>7.2 km/s) are interpreted as magmatic underplating. Wide-angle seismic reflection and refraction data cannot resolve the nature of the upper 4–5 km of crust (oceanic crust, exhumed mantle or thinned continental crust). But coincident seismic reflection profiles show the emplacement of a volcanic intrusion, sills and some seaward dipping reflectors (SDRs) located close to the northern prolongation of the Ninety East ridge before 70 Ma (Maastrichtian). However, most of the fan-shaped reflectors identified in the northern Bay of Bengal are synrift features. We conclude that the crust in the northern Bay of Bengal is thinned continental crust intruded by volcanic products with the presence of a minor amount of underplating material at its base. Such a crustal structure probably extends from the northern Bay of Bengal (19°N) to the Shillong Plateau (25°N). These new findings are critical for the oil and gas exploration presently very active in the northern Bay of Bengal area

Death-associated protein kinase (DAPK) is a calmodulin-regulated serine/threonine kinase and elicits tumor suppression function through inhibiting cell adhesion/migration and promoting apoptosis. Despite these biological functions, the signaling mechanisms through which DAPK is regulated remain largely elusive. Here, we show that the leukocyte common antigen-related (LAR) tyrosine phosphatase dephosphorylates DAPK at pY491/492 to stimulate the catalytic, proapoptotic, and antiadhesion/antimigration activities of DAPK. Conversely, Src phosphorylates DAPK at Y491/492, which induces DAPK intra-/intermolecular interaction and inactivation. Upon EGF stimulation, a rapid Src activation leads to subsequent LAR downregulation, and these two events act in synergism to inactivate DAPK, thereby facilitating tumor cell migration and invasion toward EGF. Finally, DAPK Y491/492 hyperphosphorylation is found in human cancers in which Src activity is aberrantly elevated. These results identify LAR and Src as a DAPK regulator through their reciprocal modification of DAPK Y491/492 residues and establish a functional link of this DAPK-regulatory circuit to tumor progression.

The low-cycle fatigue performance and fracture of the P/M Ti-Fe-Mo-Al-Nd Alloys after sintering and forging have been studied, and the linear regression equation of low-cycle fatigue lifetime was obtained. The fatigue performances were investigated [Comment: Not quite sure what is mean by ‘objected’ here.] under two different conditions. The fatigue fracture surface was analyzed by SEM. The low-cycle fatigue behavior of the P/M titanium alloy are discussed.

Summary Neural patterning relies on transcriptional cross-repressive interactions that ensure unequivocal assignment of neural progenitor identity to proliferating cells. Progenitors of spinal motor neurons (pMN) and V2 interneurons (p2) are specified by a pair of cross-repressive transcription factors, Olig2 and Irx3. Lineage tracing revealed that many p2 progenitors transiently express the pMN marker Olig2 during spinal cord development. Here we demonstrate that the repression of Olig2 in p2 domain is controlled by mir-17-3p microRNA-mediated silencing of Olig2 mRNA. Mice lacking all microRNAs or just the mir-17∼92 cluster manifest a dorsal shift in pMN/p2 boundary and impairment in the production of V2 interneurons. Our findings suggest that microRNA-mediated repression of Olig2 mRNA plays a critical role during the patterning of ventral spinal progenitor domains by shifting the balance of cross-repressive interactions between Olig2 and Irx3 transcription factors.

Retinal ischemia is a common cause of visual impairment for humans and animals. Herein, the neuroprotective effects of phenylbutyrate (PBA) upon retinal ischemic injury were investigated using a rat model. Retinal ganglion cells (RGCs) were retrograde labeled with the fluorescent tracer fluorogold (FG) applied to the superior collicoli of test Sprague-Dawley rats. High intraocular pressure and retinal ischemia were induced seven days subsequent to such FG labeling. A dose of either 100 or 400 mg/kg PBA was administered intraperitoneally to test rats at two time points, namely 30 min prior to the induction of retinal ischemia and 1 h subsequent to the cessation of the procedure inducing retinal ischemia. The test-rat retinas were collected seven days subsequent to the induction of retinal ischemia, and densities of surviving RGCs were estimated by counting FG-labeled RGCs within the retina. Histological analysis revealed that ischemic injury caused the loss of retinal RGCs and a net decrease in retinal thickness. For PBA-treated groups, almost 100% of the RGCs were preserved by a pre-ischemia treatment with PBA (at a dose of either 100 or 400 mg/kg), while post-ischemia treatment of RGCs with PBA did not lead to the preservation of RGCs from ischemic injury by PBA as determined by the counting of whole-mount retinas. Pre-ischemia treatment of RGCs with PBA (at a dose of either 100 or 400 mg/kg) significantly reduced the level of ischemia-associated loss of thickness of the total retina, especially the inner retina, and the inner plexiform layer of retina. Besides, PBA treatment significantly reduced the ischemia-induced loss of cells in the ganglion-cell layer of the retina. Taken together, these results suggest that PBA demonstrates a marked neuroprotective effect upon high intraocular pressure-induced retinal ischemia when the PBA is administered prior to ischemia induction.

Brk (for breast tumor kinase) is a nonreceptor tyrosine kinase containing SH3, SH2, and tyrosine kinase catalytic domains. Brk was originally identified from a human metastatic breast tumor, and its overexpression is frequently observed in breast cancer and several other cancer types. However, the molecular mechanism by which this kinase participates in tumorigenesis remains poorly characterized. In the present study, we not only identified paxillin as the binding partner and substrate of Brk but also discovered a novel signaling pathway by which Brk mediates epidermal growth factor (EGF)-induced paxillin phosphorylation. We show that EGF stimulation activates the catalytic activity of Brk, which in turn phosphorylates paxillin at Y31 and Y118. These phosphorylation events promote the activation of small GTPase Rac1 via the function of CrkII. Through this pathway, Brk is capable of promoting cell motility and invasion and functions as a mediator of EGF-induced migration and invasion. In accordance with these functional roles, Brk translocates to membrane ruffles, where it colocalizes with paxillin during cell migration. Together, our findings identify novel signaling and biological roles of Brk and indicate the first potential link between Brk and metastatic malignancy.

To enhance our understanding of the seismic characteristics of the Tatun volcanic area, a small aperture seismic array consisting of 5 seismic stations has been deployed in the area since May 2003. Each of the seismic stations was installed with both short-period and broadband sensors to record micro-earthquakes as well as long-period volcanic tremors. The preliminary results of the seismic monitoring of the Tatun volcanic area show a large number of shallow micro-earthquakes clustered beneath the Chihsingshan volcano and Tayoikeng areas. Among these, some swarms were also detected. Intensifying the issue further, some complex seismograms with harmonic codas and seismic tremors have been identified. Considlerable crustal heterogeneity in the Tatun volcanic area is indicated by the presence of strong coda waves. Combining our findings with other geological and geochemical observations, we postulate that volcanic activities might not be totally extinct in the Tatun volcanic area. Thus, further investigations of Tatun volcanic area ought be conducted to examine the possibility of such potential volcanic activity.