A new linear phenyloxazole-benzothiadiazole luminophore: crystal growth, structure and fluorescence properties.

A new linear luminophore consisting of five conjugated units of oxazole, phenylene and a central benzothiadiazole fragment, 4,7-bis[4-(1,3-oxazol-5-yl)phenyl]-2,1,3-benzothiadiazole, has been synthesized and characterized. Needle-like single-crystal samples up to 10 mm in length were obtained by physical vapor transport. The crystal structure was determined at 95 K and 293 K using single-crystal X-ray diffraction. With decreasing temperature, the space group P21/n does not change, but the unit-cell volume of the crystal decreases. The presence of intra- and intermolecular hydrogen bonds was established. Melting parameters (Tm = 305.5°C, ΔHm = 52.2 kJ mol-1) and the presence of a liquid-crystalline mesophase (TLC = 336.3°C, ΔHLC = 1.4 kJ mol-1) were determined by differential scanning calorimetry and in situ thermal polarization optical microscopy studies. The presence of linear chains of hydrogen bonds ensures high stability of the crystal structure in a wide temperature range. The luminophore is characterized by a large Stokes shift (5120-5670 cm-1) and a high quantum yield of fluorescence, reaching 96% in solutions (λmax = 517 nm) and 27% in thin crystalline films (λmax = 529 nm). The calculated absorption and emission spectra are in good agreement with the experimental data. Because of the excellent optical properties and high thermal stability, the new linear luminophore has great potential for application in organic photonics and optoelectronic devices.

A monoclinic semiorganic molecular crystal GUHP for terahertz photonics and optoelectronics.

In this paper we describe the properties of the crystal of guanylurea hydrogen phosphate (NH[Formula: see text])[Formula: see text]CNHCO(NH[Formula: see text])H[Formula: see text]PO[Formula: see text] (GUHP) and propose its application in terahertz photonics and optoelectronics. GUHP crystal has a wide window of transparency and a high optical threshold in the visible and NIR spectral regions and narrow absorption bands in the terahertz frequency range. The spectral characteristics of absorption and refraction in the THz range were found to be strongly dependent on crystal temperature and orientation. Computer simulations made it possible to link the nature of the resonant response of the medium at THz frequencies with the molecular structure of the crystal, in particular, with intermolecular hydrogen bonds and the layered structure of the lattice. The possibility of application of the crystal under study for the conversion of femtosecond laser radiation from visible an NIR to terahertz range was demonstrated. It was shown that dispersion properties of the crystal allow the generation of narrow band terahertz radiation, whose spectral properties are determined by conditions close to phase matching. The properties of the generated terahertz radiation under various temperatures suggest the possibility of phonon mechanism of enhancement for nonlinear susceptibility of the second order.

Structure of fluorite-like compound based on Nd5Mo3O16 with lead partly substituting for neodymium.

A single crystal of Nd5Mo3O16 with lead partly substituting for neodymium, which has a fluorite-like structure, was studied by precision X-ray diffraction, high-resolution transmission microscopy and EDX microanalysis. The crystal structure is determined in the space group Pn3¯n. It was found that the Pb atoms substitute in part for Nd atoms in the structure and are located in the vicinity of Nd2 positions. Partial substitutions of Mo cations for Nd positions and of Nd for Mo positions in crystals of the Ln5Mo3O16 oxide family are corroborated by X-ray diffraction for the first time. The first experimental verification of the location of an additional oxygen ion in the voids abutting MoO4 tetrahedra was obtained.

X-ray diffraction study of oxygen-conducting compounds Ln2Mo2O9 (Ln = La, Pr).

The La2Mo2O9 (LM) and Pr2Mo2O9 (PM) single crystals are studied using precision X-ray diffraction and high-resolution transmission microscopy at room temperature. The crystal structures are determined in the space group P2(1)3. La and Pr atoms, as well as Mo1 and O1 atoms, are located in the vicinity of the threefold axes rather than on the axes as in the high-temperature cubic phase. In both structures studied, the O2 and O3 positions are partially occupied. The coexistence of different configurations of the Mo coordination environment facilitates the oxygen-ion migration in the structure. Based on the X-ray data, the activation energies of O atoms are calculated and the migration paths of oxygen ions in the structures are analysed. The conductivity of PM crystals is close to that of LM crystals. The O2 and O3 atoms are the main contributors to the ion conductivity of LM and PM.

Substrate-enzyme competition attenuates upregulated anaplerotic flux through malic enzyme in hypertrophied rat heart and restores triacylglyceride content: attenuating upregulated anaplerosis in hypertrophy.

Recent work identifies the recruitment of alternate routes for carbohydrate oxidation, other than pyruvate dehydrogenase (PDH), in hypertrophied heart. Increased carboxylation of pyruvate via cytosolic malic enzyme (ME), producing malate, enables "anaplerotic" influx of carbon into the citric acid cycle. In addition to inefficient NADH production from pyruvate fueling this anaplerosis, ME also consumes NADPH necessary for lipogenesis. Thus, we tested the balance between PDH and ME fluxes in hypertrophied hearts and examined whether low triacylglyceride (TAG) was linked to ME-catalyzed anaplerosis. Sham-operated (SHAM) and aortic banded rat hearts (HYP) were perfused with buffer containing either 13C-palmitate plus glucose or (13)C glucose plus palmitate for 30 minutes. Hearts remained untreated or received dichloroacetate (DCA) to activate PDH and increase substrate competition with ME. HYP showed a 13% to 26% reduction in rate pressure product (RPP) and impaired dP/dt versus SHAM (P<0.05). DCA did not affect RPP but normalized dP/dt in HYP. HYP had elevated ME expression with a 90% elevation in anaplerosis over SHAM. Increasing competition from PDH reduced anaplerosis in HYP+DCA by 18%. Correspondingly, malate was 2.2-fold greater in HYP than SHAM but was lowered with PDH activation: HYP=1419+/-220 nmol/g dry weight; HYP+DCA=343+/-56 nmol/g dry weight. TAG content in HYP (9.7+/-0.7 micromol/g dry weight) was lower than SHAM (13.5+/-1.0 micromol/g dry weight). Interestingly, reduced anaplerosis in HYP+DCA corresponded with normalized TAG (14.9+/-0.6 micromol/g dry weight) and improved contractility. Thus, we have determined partial reversibility of increased anaplerosis in HYP. The findings suggest anaplerosis through NADPH-dependent, cytosolic ME limits TAG formation in hypertrophied hearts.

The absence of endogenous lipid oxidation in early stage heart failure exposes limits in lipid storage and turnover.

Intramyocardial lipid handling in pressure-overload-induced heart failure remains poorly understood, and the balance between endogenous and exogenous lipid utilization for mitochondrial ATP production is essentially unknown. In this study, we determined the contribution of endogenous triacylglycerols (TAG) to mitochondrial oxidation relative to that of exogenous palmitate, glucose, and endogenous glycogen in the failing, pressure-overloaded rat heart. TAG content and turnover were also assessed to determine if lipid availability and mobility were altered. Dynamic-mode (13)C NMR was performed in intact hearts from aortic banded and sham operated Spraque-Dawley rats perfused with (13)C-labeled palmitate or glucose to assess TAG turnover rate and palmitate oxidation rate. The fractional contributions from palmitate, glucose, glycogen, and TAG to mitochondrial ATP production were determined from NMR analysis of heart extracts. TAG oxidation was not evident in HF, whereas the contribution of TAG to oxidative ATP production was significant in shams. TAG content was 39% lower in HF compared to sham, and TAG turnover rate was 60% lower in HF. During adrenergic challenge, TAG sources were again not oxidized in the HF group. In early cardiac failure, endogenous TAG oxidation was reduced in parallel to increased carbohydrate oxidation, with no change in exogenous palmitate oxidation. This finding was consistent with reduced TAG storage and mobilization. These data further elucidate the role of intermediary and lipid metabolism in the progression of LVH to failure, and contribute to emerging evidence linking the disruption of myocardial substrate use to cardiomyopathies.

Recruitment of compensatory pathways to sustain oxidative flux with reduced carnitine palmitoyltransferase I activity characterizes inefficiency in energy metabolism in hypertrophied hearts.

BACKGROUND: Transport rates of long-chain free fatty acids into mitochondria via carnitine palmitoyltransferase I relative to overall oxidative rates in hypertrophied hearts remain poorly understood. Furthermore, the extent of glucose oxidation, despite increased glycolysis in hypertrophy, remains controversial. The present study explores potential compensatory mechanisms to sustain tricarboxylic acid cycle flux that resolve the apparent discrepancy of reduced fatty acid oxidation without increased glucose oxidation through pyruvate dehydrogenase complex in the energy-poor, hypertrophied heart. METHODS AND RESULTS: We studied flux through the oxidative metabolism of intact adult rat hearts subjected to 10 weeks of pressure overload (hypertrophied; n=9) or sham operation (sham; n=8) using dynamic 13C-nuclear magnetic resonance. Isolated hearts were perfused with [2,4,6,8,10,12,14,16-(13)C8] palmitate (0.4 mmol/L) plus glucose (5 mmol/L) in a 14.1-T nuclear magnetic resonance magnet. At similar tricarboxylic acid cycle rates, flux through carnitine palmitoyltransferase I was 23% lower in hypertrophied (P<0.04) compared with sham hearts and corresponded to a shift toward increased expression of the L-carnitine palmitoyltransferase I isoform. Glucose oxidation via pyruvate dehydrogenase complex did not compensate for reduced palmitate oxidation rates. However, hypertrophied rats displayed an 83% increase in anaplerotic flux into the tricarboxylic acid cycle (P<0.03) that was supported by glycolytic pyruvate, coincident with increased mRNA transcript levels for malic enzyme. CONCLUSIONS: In cardiac hypertrophy, fatty acid oxidation rates are reduced, whereas compensatory increases in anaplerosis maintain tricarboxylic acid cycle flux and account for a greater portion of glucose oxidation than previously recognized. The shift away from acetyl coenzyme A production toward carbon influx via anaplerosis bypasses energy, yielding reactions contributing to a less energy-efficient heart.

Recruitment of NADH shuttling in pressure-overloaded and hypertrophic rat hearts.

Glucose metabolism in the heart requires oxidation of cytosolic NADH from glycolysis. This study examines shuttling reducing equivalents from the cytosol to the mitochondria via the activity and expression of the oxoglutarate-malate carrier (OMC) in rat hearts subjected to 2 wk (Hyp2, n = 6) and 10 wk (Hyp10, n = 8) of pressure overload hypertrophy vs. that of sham-operated rats (Sham2, n = 6; and Sham10, n = 7). Moderate aortic banding produced increased atrial natriuretic factor (ANF) mRNA expression at 2 and 10 wk, but only at 10 wk did hearts develop compensatory hypertrophy (33% increase, P < 0.05). Isolated hearts were perfused with the short-chain fatty acid [2,4-(13)C(2)]butyrate (2 mM) and glucose (5 mM) to enable dynamic-mode (13)C NMR of intermediate exchange across OMC. OMC flux increased before the development of hypertrophy: Hyp2 = 9.6 +/- 2.1 vs. Sham2 = 3.7 +/- 1.2 muM.min(-1).g dry wt(-1), providing an increased contribution of cytosolic NADH to energy synthesis in the mitochondria. With compensatory hypertrophy, OMC flux returned to normal: Hyp10 = 3.9 +/- 1.7 vs. Sham10 = 3.8 +/- 1.2 muM.g(-1).min(-1). Despite changes in activity, no differences in OMC expression occurred between Hyp and Sham groups. Elevated OMC flux represented augmented cytosolic NADH shuttling, coupled to increased nonoxidative glycolysis, in response to hypertrophic stimulus. However, development of compensatory hypertrophy moderated the pressure-induced elevation in OMC flux, which returned to control levels. The findings indicate that the challenge of pressure overload increases cytosolic redox state and its contribution to mitochondrial oxidation but that hypertrophy, before decompensation, alleviates this stress response.