Topological and geometrical disorder correlate robustly in two-dimensional foams

A 2D foam can be characterised by its distribution of bubble areas, and of number of sides. Both distributions have an average and a width (standard deviation). There are therefore at least two very different ways to characterise the disorder. The former is a geometrical measurement, while the latter is purely topological. We discuss the common points and differences between both quantities. We measure them in a foam which is sheared, so that bubbles move past each other and the foam is "shuffled" (a notion we discuss). Both quantities are strongly correlated; in this case (only) it thus becomes sufficient to use either one or the other to characterize the foam disorder. We suggest applications to the analysis of other systems, including biological tissues

Electronic and optical properties of doped TiO2 by many-body perturbation theory

Doping is one of the most common strategies for improving the photocatalytic and solar energy conversion properties of TiO2, hence an accurate theoretical description of the electronic and optical properties of doped TiO2 is of both scientific and practical interest. In this work we use many-body perturbation theory techniques to investigate two typical n-type dopants, niobium and hydrogen, in TiO2 rutile. Using the GW approximation to determine band edges and defect energy levels, and the Bethe-Salpeter equation for the calculation of the absorption spectra, we find that the defect energy levels form nondispersive bands lying 3c2.2 eV above the top of the corresponding valence bands ( 3c0.9 eV below the conduction bands of the pristine material). The defect states are also responsible for the appearance of low-energy absorption peaks that enhance the solar spectrum absorption of rutile. The spatial distributions of the excitonic wave functions associated with these low-energy excitations are very different for the two dopants, suggesting a larger mobility of photoexcited electrons in Nb-TiO2

Nitric Oxide-cGMP Signaling in Hypertension:Current and Future Options for Pharmacotherapy

For the treatment of systemic hypertension, pharmacological intervention in nitric oxide-cyclic guanosine monophosphate signaling is a well-explored but unexploited option. In this review, we present the identified drug targets, including oxidases, mitochondria, soluble guanylyl cyclase, phosphodiesterase 1 and 5, and protein kinase G, important compounds that modulate them, and the current status of (pre)clinical development. The mode of action of these compounds is discussed, and based upon this, the clinical opportunities. We conclude that drugs that directly target the enzymes of the nitric oxide-cyclic guanosine monophosphate cascade are currently the most promising compounds, but that none of these compounds is under investigation as a treatment option for systemic hypertension

Environmental Impact Assessment of artificial feeding plans: the Hammami plain in Iran

The research was conducted with the aim of assessing the environmental impacts of artificial feeding plans of Hammami Plain in Fars Province in Iran. In this paper, EIA was undertaken using the ICOLD matrix. In this method, the effect of each project activity on the environmental components in the region was assessed in two stages; project construction and operation based on physical, ecological, socio-economic, and cultural environments. Findings indicate that positive effects will be generally exerted on the environment of the region by establishing and operating artificial feeding plans in Hammami Plain. In other words, the existence of negative impacts on the environment, will mean substantial positive impacts will be seen in the region consequently; the rise in the average level of aquifer, enhancement of agricultural wells, and development of agriculture in the region, to name a few

Pseudogap phase of cuprate superconductors confined by Fermi surface topology

The properties of cuprate high-temperature superconductors are largely shaped by competing phases whose nature is often a mystery. Chiefly among them is the pseudogap phase, which sets in at a doping $p^*$ that is material-dependent. What determines $p^*$ is currently an open question. Here we show that the pseudogap cannot open on an electron-like Fermi surface, and can only exist below the doping $p_{FS}$ at which the large Fermi surface goes from hole-like to electron-like, so that $p^*$ $\leq$ $p_{FS}$. We derive this result from high-magnetic-field transport measurements in La$_{1.6-x}$Nd$_{0.4}$Sr$_x$CuO$_4$ under pressure, which reveal a large and unexpected shift of $p^*$ with pressure, driven by a corresponding shift in $p_{FS}$. This necessary condition for pseudogap formation, imposed by details of the Fermi surface, is a strong constraint for theories of the pseudogap phase. Our finding that $p^*$ can be tuned with a modest pressure opens a new route for experimental studies of the pseudogap.Comment: 15 pages, 5 figures, 7 supplemental figure

Adiponectin secretion by perivascular adipose tissue supports impaired vasodilation in a mouse model of accelerated vascular smooth muscle cell and adipose tissue aging

Objective: Perivascular adipose tissue (PVAT) function during aging has not been investigated in detail so far and its effect on vasodilation remains to be fully elucidated. The aim of this study was to investigate endothelium-dependent vasodilation of thoracic aorta in a mouse model of accelerated, selective vascular smooth muscle and PVAT aging, induced by SM22α-Cre-driven genetic deletion of the endonuclease ERCC1 (SMC-KO mice) versus healthy littermates (LM). We hypothesized that PVAT enhances vasodilation in LM, possibly through adiponectin secretion, which might be compromised in SMC-KO animals. Methods: Thoracic aorta was isolated from SMC-KO animals and LM and segments with and without PVAT were mounted in wire myography setups. The endothelium-dependent vasodilation was assessed via acetylcholine dose-response curves and pathway contribution was studied. Moreover, adiponectin secretion was measured after stimulating the aortic segments with PVAT with acetylcholine. Results: Adiponectin, secreted by PVAT, led to increased NO-contribution to endothelium-dependent vasodilation in healthy LM, although this did not increase maximum relaxation due to loss of EDH. Endothelium-dependent vasodilation was decreased in SMC-KO animals due to reduced NO-contribution and complete EDH loss. Despite strong lipodystrophy the PVAT partially compensated for lost vasodilation in SMC-KO. LM PVAT contained acetylcholinesterase that attenuated acetylcholine responses. This was lost in SMC-KO. Conclusions: PVAT-derived adiponectin is able to partially compensate for age-related decline in NO-mediated vasodilation, even during strong lipodystrophy, in conditions of absence of compensating EDH. In aorta with healthy PVAT acetylcholinesterase modulates vascular tone, but this is lost during aging, further compensating for decreased acetylcholine responsiveness. Thus, preservation of adiponectin levels, through relatively increased production in lipodystrophic PVAT, and reduction of cholinesterase might be regulatory mechanisms of the PVAT to preserve cholinergic vasodilation during aging.</p

Adiponectin secretion by perivascular adipose tissue supports impaired vasodilation in a mouse model of accelerated vascular smooth muscle cell and adipose tissue aging

Objective: Perivascular adipose tissue (PVAT) function during aging has not been investigated in detail so far and its effect on vasodilation remains to be fully elucidated. The aim of this study was to investigate endothelium-dependent vasodilation of thoracic aorta in a mouse model of accelerated, selective vascular smooth muscle and PVAT aging, induced by SM22α-Cre-driven genetic deletion of the endonuclease ERCC1 (SMC-KO mice) versus healthy littermates (LM). We hypothesized that PVAT enhances vasodilation in LM, possibly through adiponectin secretion, which might be compromised in SMC-KO animals. Methods: Thoracic aorta was isolated from SMC-KO animals and LM and segments with and without PVAT were mounted in wire myography setups. The endothelium-dependent vasodilation was assessed via acetylcholine dose-response curves and pathway contribution was studied. Moreover, adiponectin secretion was measured after stimulating the aortic segments with PVAT with acetylcholine. Results: Adiponectin, secreted by PVAT, led to increased NO-contribution to endothelium-dependent vasodilation in healthy LM, although this did not increase maximum relaxation due to loss of EDH. Endothelium-dependent vasodilation was decreased in SMC-KO animals due to reduced NO-contribution and complete EDH loss. Despite strong lipodystrophy the PVAT partially compensated for lost vasodilation in SMC-KO. LM PVAT contained acetylcholinesterase that attenuated acetylcholine responses. This was lost in SMC-KO. Conclusions: PVAT-derived adiponectin is able to partially compensate for age-related decline in NO-mediated vasodilation, even during strong lipodystrophy, in conditions of absence of compensating EDH. In aorta with healthy PVAT acetylcholinesterase modulates vascular tone, but this is lost during aging, further compensating for decreased acetylcholine responsiveness. Thus, preservation of adiponectin levels, through relatively increased production in lipodystrophic PVAT, and reduction of cholinesterase might be regulatory mechanisms of the PVAT to preserve cholinergic vasodilation during aging.</p

Wiedemann-Franz law and abrupt change in conductivity across the pseudogap critical point of a cuprate superconductor

The thermal conductivity $\kappa$ of the cuprate superconductor La$_{1.6-x}$Nd$_{0.4}$Sr$_x$CuO$_4$ was measured down to 50 mK in seven crystals with doping from $p=0.12$ to $p=0.24$, both in the superconducting state and in the magnetic field-induced normal state. We obtain the electronic residual linear term $\kappa_0/T$ as $T \to 0$ across the pseudogap critical point $p^{\star}= 0.23$. In the normal state, we observe an abrupt drop in $\kappa_0/T$ upon crossing below $p^{\star}$, consistent with a drop in carrier density $n$ from $1 + p$ to $p$, the signature of the pseudogap phase inferred from the Hall coefficient. A similar drop in $\kappa_0/T$ is observed at $H=0$, showing that the pseudogap critical point and its signatures are unaffected by the magnetic field. In the normal state, the Wiedemann-Franz law, $\kappa_0/T=L_0/\rho(0)$, is obeyed at all dopings, including at the critical point where the electrical resistivity $\rho(T)$ is $T$-linear down to $T \to 0$. We conclude that the non-superconducting ground state of the pseudogap phase at $T=0$ is a metal whose fermionic excitations carry heat and charge as conventional electrons do.Comment: 10 pages, including Supplementary Materia