A new hybrid Dawson-type molybdenum arsenate derivative: (H2bpy)3[As2Mo18O62] (bpy = 4,4′-bipyridine)

The title compound, tris­(4,4′-bipyridinium) diarsenoocta­deca­molybdate(VI), (C10H10N2)3[As2Mo18O62], featuring protonated bipyridine mol­ecules and a classical Dawson-type polyoxo-anion, has been synthesized under hydro­thermal conditions. The polyoxoanions are linked together via the bipyridyl cations, acting as hydrogen-bond donors, generating a two-dimensional supra­molecular network. The asymmetric unit contains 1.5 4,4′-bipyridinium (H2bpy) units, with an inversion centre in the central bond of the second H2bpy unit. The site symmetry of the anion is

Poly[tetra­kis(2,2′-bipyridine)undeca-μ-oxido-hexa­oxidodicopper(II)hexa­vanadium(V)]

In the title organic–inorganic hybrid vanadate complex, [Cu2V6O17(C10H8N2)4]n, the CuII atom is six-coordinated by two chelating 2,2′-bipyridine (bipy) ligands and two vanadate O atoms in a distorted octa­hedral geometry. Two [Cu(bipy)2V3O8] units are linked by a bridging O atom, which lies on an inversion center, forming a dimeric unit. The dimeric units are further connected by bridging vanadate O atoms into a two-dimensional layer parallel to (100). The layers are connected by weak C—H⋯O hydrogen bonds

Coding Properties of Mouse Retinal Ganglion Cells with Dual-Peak Patterns with Respect to Stimulus Intervals

How visual information is encoded in spikes of retinal ganglion cells (RGCs) is essential in visual neuroscience. In the present study, we investigated the coding properties of mouse RGCs with dual-peak patterns with respect to visual stimulus intervals. We first analyzed the response properties, and observed that the latencies and spike counts of the two response peaks in the dual-peak pattern exhibited systematic changes with the preceding light-OFF interval. We then applied linear discriminant analysis (LDA) to assess the relative contributions of response characteristics of both peaks in information coding regarding the preceding stimulus interval. It was found that for each peak, the discrimination results were far better than chance level based on either latency or spike count, and were further improved by using the combination of the two parameters. Furthermore, the best discrimination results were obtained when latencies and spike counts of both peaks were considered in combination. In addition, the correct rate for stimulation discrimination was higher when RGC population activity was considered as compare to single neuron’s activity, and the correct rate was increased with the group size. These results suggest that rate coding, temporal coding, and population coding are all involved in encoding the different stimulus-interval patterns, and the two response peaks in the dual-peak pattern carry complementary information about stimulus interval

Hidden quantum mirage by negative refraction in semiconductor P-N junctions

We predict a novel quantum interference based on the negative refraction across a semiconductor P-N junction: with a local pump on one side of the junction, the response of a local probe on the other side behaves as if the disturbance emanates not from the pump but instead from its mirror image about the junction. This phenomenon is guaranteed by translational invariance of the system and matching of Fermi surfaces of the constituent materials, thus it is robust against other details of the junction (e.g., junction width, potential profile, and even disorder). The recently fabricated P-N junctions in 2D semiconductors provide ideal platforms to explore this phenomenon and its applications to dramatically enhance charge and spin transport as well as carrier-mediated long-range correlation

Salvianolic acid B prevents epithelial-to-mesenchymal transition through the TGF-β1 signal transduction pathway in vivo and in vitro

<p>Abstract</p> <p>Background</p> <p>Salvianolic Acid B (Sal B) is a water-soluble component from Danshen (a traditional Chinese herb widely used for chronic renal diseases) with anti-oxidative and cell protective properties. Sal B also has potential protective effects on renal diseases. Tubular epithelial cells can undergo epithelial-to-mesenchymal transition (EMT), which plays an important role in the pathogenesis of renal interstitial fibrosis (RIF) and is mainly regulated by TGF-β1/Smads pathway. The aims of the study are to investigate the effect of Sal B on tubular EMT <it>in vivo </it>and <it>in vitro</it>, and to elucidate its underlying mechanism against EMT related to TGF-β1/Smads pathway.</p> <p>Results</p> <p>For <it>in vivo </it>experiments, RIF was induced in rats by oral administration of HgCl₂and prophylaxised with Sal B and vitamin E. The protein expression of E-cadherin was down-regulated, while the expression of α-SMA, TGF-β1, TβR-I, p-Smad2/3 and the activity of matrix metalloproteinase-2 (MMP-2) were up-regulated in kidneys of model rats when compared with those of normal rats. In contrast, Sal B and vitamin E significantly attenuated the expression of α-SMA, TGF-β1, TβR-I, p-Smad2/3, and MMP-2 activity, but increased E-cadherin expression. For <it>in vitro </it>experiments, HK-2 cells were incubated with TGF-β1 to induce EMT, and the cells were co-cultured with 1 and 10 μM Sal B or SB-431542 (a specific inhibitor of TβR-I kinase). TGF-β1 induced a typical EMT in HK-2 cells, while it was blocked by Sal B and SB-431542, as evidenced by blocking morphologic transformation, restoring E-cadherin and CK-18 expression, inhibiting α-SMA expression and F-actin reorganization, and down-regulating MMP-2/9 activities in TGF-β1 mediated HK-2 cells. Furthermore, Sal B and SB-431542 profoundly down-regulated the expressions of TβR-I and p-Smad2/3 but prevented the decreased expression of Smad7 in TGF-β1 stimulated HK-2 cells.</p> <p>Conclusions</p> <p>Sal B can prevent tubular EMT in the fibrotic kidney induced by HgCl₂as well as HK-2 cells triggered by TGF-β1, the mechanism of Sal B is closely related to the regulation of TGF-β1/Smads pathway, manifested as the inhibition of TGF-β1 expression, suppression of TβR-I expression and function, down-regulation of Smad2/3 phosphorylation, and restoration of the down-regulation of Smad7, as well as inhibition of MMP-2 activity.</p

Tris(piperazinediium) phosphatododeca­molybo(V,VI)phosphate

The title compound, (C4H12N2)3[PMo12O40] or (H2pip)3[PMo12O40] (pip is piperazine), was prepared under hydro­thermal conditions. The asymmetric unit contains one-sixth of a mixed-valent Mo(V,VI) pseudo-Keggin-type [PMo12O40]6− anion and half a piperazinediium cation, (H2pip)2+. The discrete Keggin-type [PMo12O40]6- anion has site symmetry and the three (H2pip)2+ cations each have site symmetry at the centres of the mol­ecules. The central P atom is on special position , which is a roto-inversion position and generates the disorder of the PO4 tetra­hedron. Furthermore, six doubly bridging oxide groups are also disordered with an occupancy factor of 0.5 for each O atom. The anions and cations are linked by an extensive network of inter­molecular N—H⋯O and C—H⋯O hydrogen bonds

Method for Thermo-optic Analysis in a Star Sensor

An autonomous star sensor is a highly accurate attitude-measuring instrument used in spacecraft, and its performance is restricted by ambient temperature of the outer space. This paper puts forward an effective scheme to the thermooptic analysis using finite element analysis (FEA) and ray tracing in star sensor. Specific difficulties: (a) how to evaluate thermo-optic effect in star sensor, and (b) how to make FEA results useful in optical design mode have been resolved using the scheme. Based on this scheme, the errors of star sensor, which are caused by thermo-optic effects, can be investigated in any complicated temperature condition, and the required temperature scope for the thermal design can be achieved. For example, the errors of the star sensor were 0.0863" and 2.2933", when the temperature differences of the experimental optical system were 10 °C and 5 °C in axial and lateral, respectively.Defence Science Journal, 2010, 60(3), pp.276-281, DOI:http://dx.doi.org/10.14429/dsj.60.35

Heat Shock Protein 70 Protects the Heart from Ischemia/Reperfusion Injury through Inhibition of p38 MAPK Signaling.

BackgroundHeat shock protein 70 (Hsp70) has been shown to exert cardioprotection. Intracellular calcium ([Ca2+]i) overload induced by p38 mitogen-activated protein kinase (p38 MAPK) activation contributes to cardiac ischemia/reperfusion (I/R) injury. However, whether Hsp70 interacts with p38 MAPK signaling is unclear. Therefore, this study investigated the regulation of p38 MAPK by Hsp70 in I/R-induced cardiac injury.MethodsNeonatal rat cardiomyocytes were subjected to oxygen-glucose deprivation for 6 h followed by 2 h reoxygenation (OGD/R), and rats underwent left anterior artery ligation for 30 min followed by 30 min of reperfusion. The p38 MAPK inhibitor (SB203580), Hsp70 inhibitor (Quercetin), and Hsp70 short hairpin RNA (shRNA) were used prior to OGD/R or I/R. Cell viability, lactate dehydrogenase (LDH) release, serum cardiac troponin I (cTnI), [Ca2+]i levels, cell apoptosis, myocardial infarct size, mRNA level of IL-1β and IL-6, and protein expression of Hsp70, phosphorylated p38 MAPK (p-p38 MAPK), sarcoplasmic/endoplasmic reticulum Ca2+-ATPase2 (SERCA2), phosphorylated signal transducer and activator of transcription3 (p-STAT3), and cleaved caspase3 were assessed.ResultsPretreatment with a p38 MAPK inhibitor, SB203580, significantly attenuated OGD/R-induced cell injury or I/R-induced myocardial injury, as evidenced by improved cell viability and lower LDH release, resulted in lower serum cTnI and myocardial infarct size, alleviation of [Ca2+]i overload and cell apoptosis, inhibition of IL-1β and IL-6, and modulation of protein expressions of p-p38 MAPK, SERCA2, p-STAT3, and cleaved-caspase3. Knockdown of Hsp70 by shRNA exacerbated OGD/R-induced cell injury, which was effectively abolished by SB203580. Moreover, inhibition of Hsp70 by quercetin enhanced I/R-induced myocardial injury, while SB203580 pretreatment reversed the harmful effects caused by quercetin.ConclusionsInhibition of Hsp70 aggravates [Ca2+]i overload, inflammation, and apoptosis through regulating p38 MAPK signaling during cardiac I/R injury, which may help provide novel insight into cardioprotective strategies