Triadic interaction in the background of a pairwise spin-glass.

Developing an equilibrium solution for a pairwise spin-glass with a quenched random infinite range shows a continuous phase transition. Models with p-spin interactions have been studied and the exact solution was provided that shows a continuous phase transition for p=2 and a first-order one for p>2. Although the p-spin interactions were studied individually without considering lower-order interactions, is it always feasible to ignore the lower ones? Here, we are interested in finding an analytical solution for considering a triadic interaction as a perturbation in the background of a pairwise interaction in the Sherrington-Kirkpatrick spin-glass model. Our results indicate a sudden phase transition as a consequence of considering triadic interactions that signal a switch from a continuous to an explosive phase transition.

Optomechanically induced gain using a trapped interacting Bose-Einstein condensate.

We investigate the realization of the phenomenon of optomechanically induced gain in a hybrid optomechanical system consisting of an interacting Bose-Einstein condensate trapped inside the optical lattice of a cavity which is generated by an external coupling laser tuned to the red sideband of the cavity. It is shown that the system behaves as an optical transistor while the cavity is exposed to a weak input optical signal which can be amplified considerably in the cavity output if the system is in the unresolved sideband regime. Interestingly, the system has the capability to switch from the resolved to unresolved sideband regime by controlling the s-wave scattering frequency of atomic collisions. We show that the system gain can be enhanced considerably by controlling the s-wave scattering frequency as well as the coupling laser intensity while the system remains in the stable regime. Based on our obtained results, the input signal can be amplified more than 100 million percent in the system output which is much larger than those already reported in the previously proposed similar schemes.

Ultraslow light realization using an interacting Bose-Einstein condensate trapped in a shallow optical lattice.

In this article, we propose an experimentally feasible scheme for the ultraslow light realization based on the optomechanically induced transparency (OMIT) phenomenon using a hybrid optomechanical system consisting of a one-dimensional Bose-Einstein condensate trapped in a shallow optical lattice considering the nonlinear effect of atom-atom interaction. It is shown how the system can switch from the normal mode splitting to the OMIT regime by manipulation of the s-wave scattering frequency of atomic collisions when the cavity is pumped at a fixed rate. Then, it is shown that an ultraslow light with a time delay more than 150 ms corresponding to a group velocity about 1 mm/s is achievable by controlling the optical lattice depth as well as the strength of atom-atom interaction and the number of atoms. Importantly, such an ultraslow light is detectable in the output of the cavity since it occurs in the frequency region of coupling-probe detuning where the reflection coefficient of the cavity is maximum.

Persistent homology of fractional Gaussian noise.

In this paper, we employ the persistent homology (PH) technique to examine the topological properties of fractional Gaussian noise (fGn). We develop the weighted natural visibility graph algorithm, and the associated simplicial complexes through the filtration process are quantified by PH. The evolution of the homology group dimension represented by Betti numbers demonstrates a strong dependency on the Hurst exponent (H). The coefficients of the birth and death curves of the k-dimensional topological holes (k-holes) at a given threshold depend on H which is almost not affected by finite sample size. We show that the distribution function of a lifetime for k-holes decays exponentially and the corresponding slope is an increasing function versus H and, more interestingly, the sample size effect completely disappears in this quantity. The persistence entropy logarithmically grows with the size of the visibility graph of a system with almost H-dependent prefactors. On the contrary, the local statistical features are not able to determine the corresponding Hurst exponent of fGn data, while the moments of eigenvalue distribution (M_{n}) for n≥1 reveal a dependency on H, containing the sample size effect. Finally, the PH shows the correlated behavior of electroencephalography for both healthy and schizophrenic samples.

Armillaria mellea as a cause of oak decline in Hatam-baigh forest of Iran.

A200 ha forest of "Hatam-baig" is located in Ardebil Province on the Northwest of Iran. Oak trees (Quercus macranthera Fisch & Mey) in this forest have been faced with declining and extinction since 1991, that has destructed about one third of the forest trees until now. This disorder was expressed in various symptoms including wilting, defoliation and decline. In order to identify factors causing decline, a study was managed from 1998 to 2001. Samples were taken from roots, trunks, crowns and soil beneath the canopy and were cultured on different culture media subsequently. Armillaria mellea (Vahl) P. Kumm., Phytophthora cryptogea Pethybr. & Laff., Dematophora sp., Pythium aphanidermatum (Edson) Fitzp. and Fusarium spp. were the most common isolated fungi. A. mellea appeared to be the essential causal agent of the decline according to the studies made on oak tress decline around the world and based on brown rot observed beneath mycelial fans in the cross section prepared from the trunk and characteristics of the isolated fungi. The fungus activity had been favored by physiological weakness and stresses in oak rootstocks caused by brown- tail moth (Euproctis chrysorhoea L.) and drought stress in infected trees. The biological species of this fungus was identified as Armillaria mellea, using hybridization tests and application of haploid test strains. The fungi such as Phytophthora sp., Pythium sp., and Dematophora sp. can not be infective in this forest due to being hydrophylous. In the southern part of the forest with remarked steepness, the severity of the decline appears to be more than that in the smoothly northern part. The decline of Q. macranthera is reported as matrix nova. The report of the isolated fungi from this oak species is also universally new.

Oleate, not ligands of the receptor for advanced glycation end-products, promotes proliferation of human arterial smooth muscle cells.

AIMS/HYPOTHESIS: Diabetes accelerates cardiovascular disease caused by atherosclerosis. Accordingly, diabetes accelerates atherosclerotic lesion progression and increases arterial smooth muscle cell proliferation. We hypothesized that diabetes can exert growth-promoting effects on smooth muscle cells via increased advanced glycation end-products or by dyslipidaemia. METHODS: Primary human arterial smooth muscle cells were stimulated with advanced glycation end-products, other ligands of the receptor for advanced glycation end-products or fatty acids common in triglycerides. Cell proliferation was measured as DNA synthesis, cell cycle distribution and cell number. Effects of oleate on cellular phospholipids, diacylglycerol, triglycerides and cholesterol esters were analyzed by thin-layer chromatography, and oleate accumulation into diacylglycerol was confirmed by gas chromatography. RESULTS: Human arterial smooth muscle cells express the receptor for advanced glycation end-products, but its ligands N(epsilon)-(carboxymethyl)lysine-modified proteins, methylglyoxal-modified proteins, S100B polypeptide and amyloid-beta (1-40) peptide, exert no mitogenic action. Instead, oleate, one of the most common fatty acids in triglycerides, enhances platelet-derived growth factor-BB-mediated proliferation and oleate-containing 1,2-diacylglycerol formation in smooth muscle cells. This mitogenic effect of oleate depends on phospholipase D activity and is associated with an increased formation of oleate-enriched 1,2-diacylglycerol. CONCLUSION/INTERPRETATION: Oleate, not ligands of the receptor for advanced glycation end-products, acts as an enhancer of human smooth muscle cell proliferation. Thus, lipid abnormalities, rather than hyperglycaemia, could be a major factor promoting proliferation of smooth muscle cells in atherosclerotic lesions.

Regulation of smooth muscle cell accumulation in diabetes-accelerated atherosclerosis.

Diabetes leads to accelerated formation/progression of lesions of atherosclerosis. Cardiovascular disease thus develops earlier in people with type 1 or type 2 diabetes compared to people without diabetes, and cardiovascular (macrovascular) disease is the major cause of death in adults with diabetes. The molecular and cellular mechanisms leading to diabetes-accelerated atherosclerosis are not well understood. The arterial smooth muscle cell (SMC), one of the three or four principal cell types in atherosclerosis, has been extensively studied over the years. Proliferation and accumulation of SMCs are believed to play important roles in the progression of macrophage-rich lesions to fibroatheromas. Further progression of these atheromas into complicated vulnerable lesions that are likely to cause the acute clinical symptoms of atherosclerosis (myocardial infarction and stroke) may involve cell death and loss of SMCs from the fibrous cap of the lesion. Recent animal studies have shown that diabetes causes a marked increase in SMC accumulation and proliferation in atheromas. Hyperglycemia, advanced glycation end-products, insulin and lipid abnormalities associated with the diabetic environment have been suggested to increase SMC accumulation. Indeed, it is becoming increasingly clear that macrovascular disease associated with diabetes is a multifactorial disease. We review the factors and mechanisms that may regulate SMC proliferation and accumulation in different stages of lesion progression in diabetes. We propose that lipid abnormalities associated with diabetes can act in combination with growth factors present in the diabetic environment to increase SMC accumulation and accelerate lesion progression.

Enabling technologies for manipulating multiple genes on complex pathways.

Many complex biochemical pathways in plants have now been manipulated genetically, usually by suppression or over-expression of single genes. Further exploitation of the potential for plant genetic manipulation, both as a research tool and as a vehicle for plant biotechnology, will require the co-ordinate manipulation of multiple genes on a pathway. This goal is currently very difficult to achieve. A number of approaches have been taken to combine or 'pyramid' transgenes in one plant and have met with varying degrees of success. These approaches include sexual crossing, re-transformation, co-transformation and the use of linked transgenes. Novel, alternative 'enabling' technologies are also being developed that aim to use single transgenes to manipulate the expression of multiple genes. A chimeric transgene with linked partial gene sequences placed under the control of a single promoter can be used to co-ordinately suppress numerous plant endogenous genes. Constructs modelled on viral polyproteins can be used to simultaneously introduce multiple protein-coding genes into plant cells. In the course of our work on the lignin biosynthetic pathway, we have tested both conventional and novel methods for achieving co-ordinate suppression or over-expression of up to three plant lignin genes. In this article we review the literature concerning the manipulation of multiple genes in plants. We also report on our own experiences and results using different methods to perform directed manipulation of lignin biosynthesis in tobacco.

Regulation of prostacyclin synthesis by angiotensin II and TNF-alpha in vascular smooth muscle.

We had previously established that in a model of Ang II-induced hypertension, administration of an anti-TNF-alpha antibody caused additional increases in mean arterial pressure. Production of vasodilator prostanoids (i.e. PGI2 and PGE2) is increased by Ang II in vascular smooth muscle and is part of a counter-regulatory mechanism that opposes increases in vascular tone. We, therefore, examined the effects of TNF-alpha on Ang II-induced increases in PGI2 production in vascular smooth muscle cells (VSMC). Addition of Ang II caused an increase in the production of PGI2, while addition of TNF-alpha had no effect. However, pretreatment with TNF-alpha potentiated the stimulatory effects of Ang II. The potentiating effect of TNF-alpha was neither at the level of prostacyclin synthetase nor at the level of acyl hydrolase activity. This potentiation was dependent on tyrosine kinase activity, as preincubation with genistein completely abolished the effect of TNF-alpha. TNF-alpha upregulated AA-induced PGI2 synthesis, indicating that the effect of TNF-alpha is at the level of cyclooxygenase (COX). These data suggest that TNF-alpha potentiates Ang II-induced synthesis of PGI2 and PGE2 in a tyrosine kinase-dependent manner, an effect that may contribute to the counter-regulatory influence of prostaglandins on the pressor effects of Ang II in the vasculature.

Analysis of eicosanoid mediation of the renal functional effects of hyperchloremia.

Depression of GFR and antinatriuresis in response to high chloride has been linked to a cyclooxygenase (COX)-dependent mechanism involving thromboxane A2 (TxA2) and prostaglandin endoperoxide (PGH2), because inhibition of COX prevented the fall in GFR and antinatriuresis produced by hyperchloremia. However, hyperchloremia did not increase, but unexpectedly decreased, renal prostaglandin and TxA2 efflux (Yin et al., 1995). To resolve questions regarding the role of eicosanoids in mediating the renal functional effects of high chloride (117 mM), by stimulating either TxA2 synthesis or TxA2/PGH2 receptors, we compared the ability of indomethacin to block high-chloride effects in the rat isolated kidney with that of BMS 180291 and SQ 29548, antagonists of the TxA2/PGH2 receptor. These antagonists differ in terms of their selectivity and their capacity to inhibit isoforms of the TxA2/PGH2 receptor. Indomethacin and SQ 29548 had identical actions, preventing the decrease of GFR and antinatriuresis evoked by hyperchloremia, e.g., sodium excretion rate in the SQ 29548 and indomethacin groups increased to 7.2 +/- 1.3 and 7.1 +/- 1.2 microEq/min, respectively, compared with 2.6 +/- 0.7 microEq/min in the control group. In contrast, neither BMS 180291 nor the TxA2 synthase inhibitors, OKY 046 and CGS 13080, modified the negative effects of high chloride on GFR or sodium excretion. These results argue against either TxA2 or PGH2 acting as mediator of the effects of high chloride on renal function and suggest a product of COX activity such as a 20-HETE analog of prostaglandin endoperoxide. Evidence to support this proposal was obtained: 1) Hyperchloremia increased 20-HETE release from the rat kidney by 2-fold when compared with low-chloride conditions of renal perfusion. 2) The renal vasoconstrictor action of 20-HETE was shown to be dependent on COX activity and to be antagonized by blockade of the TxA2/PGH2 receptor.

Lymphotoxin-beta and TNF regulation in T cell subsets: differential effects of PGE2.

The effects of prostaglandin E2 (PGE2) on lymphotoxin beta (LT-beta) and tumour necrosis factor alpha (TNF) were assessed in murine CD4+ Th1 and Th2 T cell clones. LT-beta mRNA was constitutively expressed by both T cell subsets. However, PGE2 inhibited its accumulation only in Th1, but not Th2 clones. PGE2 inhibited TNF mRNA accumulation and production and release of bioactive material by both Th1 and Th2 T cells. The effects of PGE2 were also evaluated on production of IL-3, another cytokine produced by both T cell subsets, and interleukin 4 (IL-4), which is produced only by Th2 cells. Though IL-3 was produced by both T cell subsets it was only inhibited in Th1 cells, a pattern similar to that observed for LT-beta. Accumulation of IL-4 mRNA in Th2 cells was not inhibited by PGE2. These results demonstrate that PGE2 does not affect LT-beta, IL-4, or IL-3 in Th2 cells, but inhibits TNF mRNA accumulation and production in this T cell subset. Thus, TNF appears to be the only cytokine susceptible to inhibition by PGE2 in Th2 cells. The fact that PGE2 inhibits LT-beta and IL-3 in Th1 but not Th2 cells points to a different mechanism of regulation of the same cytokine in different subsets. The mechanisms that contribute to TNF mRNA accumulation also may differ in the two CD4+ T cell subsets, because cycloheximide superinduced TNF mRNA in Th2 cells, but not in Th1 cells. The inhibitory effects of PGE2 on TNF mRNA accumulation by either T cell subset did not require de novo protein synthesis since preincubation with the protein synthesis inhibitor, cycloheximide, did not alter the PGE2-mediated effects. Cross-regulation of cytokine production and function has been demonstrated for both T cell subsets, and PGE2 may modulate the outcome of an immune response via differential regulation of cytokine production.

A heme oxygenase product, presumably carbon monoxide, mediates a vasodepressor function in rats.

Heme oxygenase is a mammalian enzyme that converts heme to biliverdin and carbon monoxide. Carbon monoxide activates soluble guanylate cyclase and relaxes vascular smooth muscle, and it has been implicated as a potential neuromessenger. The regulatory functions of endogenous carbon monoxide on hemodynamics are not known. Zinc deuteroporphyrin 2,4-bis glycol (ZnDPBG) inhibits heme oxygenase in rats and thus permits assessment of the hemodynamic response to inhibition of endogenous carbon monoxide synthesis. In chronically instrumented, awake male Sprague-Dawley rats, ZnDPBG (45 mumol/kg IP) increased mean arterial pressure (19 +/- 2%, P < .05) and total peripheral resistance (47 +/- 4%, P < .05), decreased cardiac output (-16 +/- 2%, P < .05), but did not affect heart rate. Another heme oxygenase inhibitor, zinc protoporphyrin IX (45 mumol/kg IP), also increased arterial pressure (17 +/- 5%, P < .05), with no effect on heart rate. In contrast, neither the nonmetallic deuteroporphyrin 2,4-bis glycol (45 mumol/kg IP) nor bilverdin (45 mumol/kg IP) had any effect on blood pressure or heart rate. These findings suggest that ZnDPBG and zinc protoporphyrin IX increase arterial pressure by inhibiting heme oxygenase activity. After pretreatment with chlorisondamine (5 mg/kg IP) or prazosin (5 mg/kg IP) to inhibit autonomic ganglionic or alpha 1-adrenoceptor functions, respectively, ZnDPBG did not affect arterial pressure or heart rate. This suggests that ZnDPBG-induced increases in blood pressure rely on autonomic nervous function. We conclude that the pressor response to heme oxygenase inhibitors results from withdrawal of the inhibitory influence of endogenous carbon monoxide on a pressor mechanism mediated by the autonomic nervous system.