Tris{2-[4-(2-pyrid­yl)pyrimidin-2-ylsulfan­yl]eth­yl}amine

The tripodal character of the title compound, C33H30N10S3, arises from the three thio­ether arms surrounding a central amine N atom. The three arms have approximately the same conformation but distinct geometries in a trans–trans–cis conformation, resulting in a short pyridine–sulfanyl N⋯S distance of 4.320 (7) Å. The distances of the central N atom to the N atoms of three pyridine rings in the arms are 8.305 (7), 8.032 (7) and 5.076 (9)Å. In the crystal, mol­ecules are joined into a three-dimensional supra­molecular network via effective π–π stacking between adjacent heterocycles [centroid–centroid distances of 3.700 (3)–4.118 (4) Å between adjacent inter­layer pyrimidine rings and 3.676 (4) Å between the pyridine rings]

Bridging the gap between the gas and solution phase : solvent specific photochemistry in 4-tert-butylcatechol

Eumelanin is a naturally synthesized ultraviolet light absorbing biomolecule, possessing both photoprotective and phototoxic properties. We infer insight into these properties of eumelanin using a bottom-up approach, by investigating a subunit analogue, 4-tert-butylcatechol. Utilizing a combination of femtosecond transient electronic absorption spectroscopy and time-re-solved velocity map ion imaging, our results suggest an environmental-dependent relaxation pathway, following irradiation at 267 nm to populate the S1 (1ππ*) state. Gas-phase and non-polar solution-phase measurements reveal that the S1 state decays through coupling onto the S2 (1πσ*) state that is dissociative along the non-intramolecular hydrogen bonded ‘free’ O–H bond. This process is mediated by tunneling beneath an S1/S2 conical intersection and occurs in 4.9 ± 0.6 ps in the gas-phase and 27 ± 7 ps in the non-polar cyclohexane solution. Comparative studies on the deuterated isotopologue of 4-tert-butylcatechol in both the gas- and solution-phase (cyclohexane) reveals an average kinetic isotope effect of ~19 and ~7, respectively, supportive of O–H dissociation mediated by a quantum tunneling mechanism. In contrast, in the polar acetonitrile, the S1 state decays on a much longer timescale of 1.7 ± 0.1 ns. We propose that the S1 decay is now multicomponent, likely driven by internal conversion, intersystem crossing and fluorescence, as well as O–H dissociation. The attribution of conformer driven excited state dynamics to explain how the S1 state decays in the gas- and non-polar solution-phase versus the polar solution-phase, elegantly demonstrates the influence the environment has on the ensuing excited state dynamics

An Improved Volume of Fluid Method for Two-Phase Flow Computations on Collocated Grid System

An improved volume of fluid method called the accurate density and viscosity volume of fluid (ADV- VO

Retaining individualities: the photodynamics of self-ordering porphyrin assemblies

The retention of photochemical properties of individual chromophores is a key feature of biological light harvesting complexes. This is achieved despite extensive aggregation of the chromophores, which in synthetic chromophore assemblies often yields a change in spectral characteristics. As an alternative approach towards mimicking biological light harvesting complexes, we report the synthesis of porphyrin assemblies which retained the photochemical properties of the individual chromophore units despite their substantial aggregation. These new materials highlight a new bottom-up approach towards the design and understanding of more complex biomimetic and naturally occurring biological systems

Beta-estradiol attenuates hypoxic pulmonary hypertension by stabilizing the expression of p27kip1 in rats

<p>Abstract</p> <p>Background</p> <p>Pulmonary vascular structure remodeling (PVSR) is a hallmark of pulmonary hypertension. P27^kip1, one of critical cyclin-dependent kinase inhibitors, has been shown to mediate anti-proliferation effects on various vascular cells. Beta-estradiol (β-E2) has numerous biological protective effects including attenuation of hypoxic pulmonary hypertension (HPH). In the present study, we employed β-E2 to investigate the roles of p27^kip1and its closely-related kinase (Skp-2) in the progression of PVSR and HPH.</p> <p>Methods</p> <p>Sprague-Dawley rats treated with or without β-E2 were challenged by intermittent chronic hypoxia exposure for 4 weeks to establish hypoxic pulmonary hypertension models, which resemble moderate severity of hypoxia-induced PH in humans. Subsequently, hemodynamic and pulmonary pathomorphology data were gathered. Additionally, pulmonary artery smooth muscle cells (PASMCs) were cultured to determine the anti-proliferation effect of β-E2 under hypoxia exposure. Western blotting or reverse transcriptional polymerase chain reaction (RT-PCR) were adopted to test p27^kip1, Skp-2 and Akt-P changes in rat lung tissue and cultured PASMCs.</p> <p>Results</p> <p>Chronic hypoxia significantly increased right ventricular systolic pressures (RVSP), weight of right ventricle/left ventricle plus septum (RV/LV+S) ratio, medial width of pulmonary arterioles, accompanied with decreased expression of p27^kip1in rats. Whereas, β-E2 treatment repressed the elevation of RVSP, RV/LV+S, attenuated the PVSR of pulmonary arterioles induced by chronic hypoxia, and stabilized the expression of p27^kip1. Study also showed that β-E2 application suppressed the proliferation of PASMCs and elevated the expression of p27^kip1under hypoxia exposure. In addition, experiments both <it>in vivo </it>and <it>in vitro </it>consistently indicated an escalation of Skp-2 and phosphorylated Akt under hypoxia condition. Besides, all these changes were alleviated in the presence of β-E2.</p> <p>Conclusions</p> <p>Our results suggest that β-E2 can effectively attenuate PVSR and HPH. The underlying mechanism may partially be through the increased p27^kip1by inhibiting Skp-2 through Akt signal pathway. Therefore, targeting up-regulation of p27^kip1or down-regulation of Skp-2 might provide new strategies for treatment of HPH.</p