Structural Dependence of the Molecular Mobility in the Amorphous Fractions of Polylactide

Fragility index and cooperativity length characterizing the molecular mobility in the amorphous phase are for the first time calculated in drawn polylactide (PLA). The microstructure of the samples is investigated from wide-angle X-ray scattering (WAXS) whereas the amorphous phase dynamics are revealed from broadband dielectric spectroscopy (BDS) and temperature-modulated differential scanning calorimetry (TMDSC). The drawing processes induce the decrease of both cooperativity and fragility with the orientation of the macromolecules. Post-drawing annealing reveals an unusual absence of correlation between the evolutions of cooperativity length and fragility. The cooperativity length remains the same compared to the drawn sample while a huge increase of the fragility index is recorded. By splitting the fragility index in a volume contribution and an energetic contribution, it is revealed that the amorphous phase in annealed samples exhibits a high energetic parameter, even exceeding the amorphous matrix value. It is assumed that the relaxation process is driven in such a way that the volume hindrance caused by the thermomechanical constraint is compensated by the acceleration of segmental motions linked to the increase of degrees of freedom. This result should also contribute to the understanding of the constraint slackening in the amorphous phase during annealing of drawn PLA, which causes among others the decrease of its barrier properties

Low molecular mass dinitrosyl nonheme-iron complexes up-regulate noradrenaline release in the rat tail artery

BACKGROUND: Dinitrosyl nonheme-iron complexes can appear in cells and tissues overproducing nitric oxide. It is believed that due to their chemical nature these species may be implicated in certain pathophysiological events. We studied the possible role of low molecular mass dinitrosyl iron complexes in the control of noradrenaline release in electrically stimulated rat tail artery. RESULTS: A model complex, dinitrosyl-iron-thiosulfate (at 1–10 μM) produced a concentration-dependent enhancement of electrical field stimulated [(3)H]noradrenaline release (up to 2 fold). At the same time, dinitrosyl-iron-thiosulfate inhibited neurogenic vasoconstriction, consistent with its nitric oxide donor properties. A specific inhibitor of cyclic GMP dependent protein kinase, Rp-8pCPT-cGMPS, partially inhibited the effect of dinitrosyl-iron-thiosulfate on neurogenic vasoconstriction, but not on [(3)H]noradrenaline release. Another model complex, dinitrosyl-iron-cysteine (at 3 μM) elicited similar responses as dinitrosyl-iron-thiosulfate. Conventional NO and NO+ donors such as sodium nitroprusside, S-nitroso-L-cysteine or S-nitroso-glutathione (at 10 μM) had no effect on [(3)H]noradrenaline release, though they potently decreased electrically-induced vasoconstriction. The "false complex", iron(II)-thiosulfate showed no activity. CONCLUSIONS: Low molecular mass iron dinitrosyl complexes can up-regulate the stimulation-evoked release of vascular [(3)H]noradrenaline, apparently independently of their NO donor properties. This finding may have important implications in inflammatory tissues

Exogenous NG-hydroxy-l-arginine causes nitrite production in vascular smooth muscle cells in the absence of nitric oxide synthase activity

AbstractNitric oxide (NO) production from exogenous NG-hydroxy-l-arginine (OH-l-Arg) was investigated in rat aortic smooth muscle cells in culture by measuring nitrite accumulation in the culture medium. As well, the interaction between OH-l-Arg and l-arginine uptake via the y+ cationic amino acid transporter was studied. In cells without NO-synthase activity, OH-l-Arg (1–1000 μM) induced a dose-dependent nitrite production with a half-maximal effective concentration (EC50) of 18.0 ± 1.5 μM (n = 4–7). This nitrite accumulation was not inhibited by the NO-synthase inhibitor NG-nitro-l-arginine methyl ester, l-NAME (300 μM). In contrast, it was abolished by miconazole (100 μM), an inhibitor of cytochrome P450. Incubation of vascular smooth muscle cells with LPS (10 μgml) induced an l-name inhibited nitrite accumulation, but did not enhance the OH-l-Arg induced nitrite production. OH-l-Arg and other cationic amino acids, L-lysine and l-ornithine, competitively inhibited [3H]-l-arginine uptake m rat aortic smooth muscle cells, with inhibition constants of 195 ± 23 μM(n = 12), 260 ± 40 μM(n= 5) and 330 ± 10 μM(n = 5), respectively. These results show that OH-l-Arg is recognized by the cationic l-amino acid carrier present in vascular smooth muscle cells and can be oxidized to NO and nitrite in these cells in the absence of NO-synthase, probably by cytochrome P450 or by a reaction involving a cytochrome P450 byproduct

Y27632, a Rho-activated kinase inhibitor, normalizes dysregulation in alpha1-adrenergic receptor-induced contraction of Lyon hypertensive rat artery smooth muscle.

RhoA-activated kinase (ROK) is involved in the disorders of smooth muscle contraction found in hypertension model animals and patients. We examined whether the alpha1-adrenergic receptor agonist-induced ROK signal is perturbed in resistance small mesentery artery (SMA) of Lyon genetically hypertensive (LH) rats, using a ROK antagonist, Y27632. Smooth muscle strips of SMA and aorta were isolated from LH and Lyon normotensive (LN) rats. After Ca(2+)-depletion and pre-treatment with phenylephrine (PE), smooth muscle contraction was induced by serial additions of CaCl(2). In LH SMA Ca(2+) permeated cells to a lesser extent as compared with LN SMA, while CaCl(2)-induced contraction of LH SMA was greater than that of LN SMA, indicating a higher ratio of force to Ca(2+) in LH SMA contraction (Ca(2+) sensitization). No hyper-contraction was observed in LH aorta tissues. Treatment of LH SMA with Y27632 restored both Ca(2+) permeability and Ca(2+)-force relationship to levels seen for LN SMA. In response to PE stimulation, phosphorylation of CPI-17, a phosphorylation-dependent myosin phosphatase inhibitor protein, and MYPT1 at Thr853, the inhibitory phosphorylation site of the myosin phosphatase regulatory subunit, was increased in LN SMA, but remained unchanged in LH SMA. These results suggest that the disorder in ROK-dependent Ca(2+) permeability and Ca(2+)-force relationship is responsible for LH SMA hyper-contraction. Unlike other hypertensive models, the ROK-induced hyper-contractility of LH SMA is independent of MYPT1 and CPI-17 phosphorylation, which suggests that ROK-mediated inhibition of myosin phosphatase does not affect SMA hyper-contractility in LH SMA cells

Semiaromatic polyamides with enhanced charge carrier mobility

The control of local order in polymer semiconductors using non-covalent interactions may be used to engineer materials with interesting combinations of mechanical and optoelectronic properties. To investigate the possibility of preparing n-type polymer semiconductors in which hydrogen bonding plays an important role in structural order and stability, we have used solution-phase polycondensation to incorporate dicyanoperylene bisimide repeat units into an aliphatic polyamide chain backbone. The morphology and thermomechanical characteristics of the resulting polyamides, in which the aliphatic spacer length was varied systematically, were comparable with those of existing semiaromatic engineering polyamides. At the same time, the charge carrier mobility as determined by pulse-radiolysis time-resolved microwave conductivity measurements was found to be about 10-2 cm2 V-1 s-1, which is similar to that reported for low molecular weight perylene bisimides. Our results hence demonstrate that it is possible to use hydrogen bonding interactions as a means to introduce promising optoelectronic properties into high-performance engineering polymers.Peer ReviewedPostprint (author's final draft

Role of Endothelium on the Effects of Neuropeptide Y in Mesenteric Resistance Arteries of Spontaneously Hypertensive and Wistar-Kyoto Normotensive Rats1

ABSTRAC

A pertussis toxin-insensitive calcium influx mediated by neuropeptide Y2 receptors in a human neuroblastoma cell line

Stimulation of neuropeptide Y (NPY) Y-2 receptors induced an intracellular free Ca2+ ([Ca2+](i)) increase in a human neuroblastoma cell line, CHP-234. When NPY in a Ca2+-free solution was applied, this increase was abolished. Depolarization with high KC1 evoked no response, suggesting that the responses were not mediated by voltage-gated Ca2+ channels. There was no evidence that the NPY response consisted of a capacitative Ca2+ entry sensitive to internal Ca2+ store levels. The [Ca2+](i) elevation was diminished by Ni2+, a blocker of Ca2+ entry. Mn2+ induced a quench of the fura-2 fluorescence, which ceased promptly upon the removal of NPY, indicating that Ca2+ entry was linked tightly to receptor activation. Although thapsigargin- and ryanodine-sensitive Ca2+ stores were present, NPY induced responses were not impaired by pretreatment with either drug. Further-more, NPY had no effect on the thapsigargin sensitive store. Pertussis toxin did not affect the NPY-stimulated [Ca2+](i) increase, although it abolished the NPY-dependent inhibition of cAMP production. It is concluded that the Y-2 receptors couple directly to receptor-operated Ca2+ channels without the involvement of intracellular Ca2+ stores. The results also indicate that Y-2 receptors can activate both pertussis toxin-sensitive and -insensitive mechanisms in the same cell

Influence of polymerization pressure and post-cure treatment on conversion degree and viscoelastic properties of polymer infiltrated ceramic network

This study aimed at determining an optimum polymerization pressure for Polymer Infiltrated Ceramic Network (PICN) blocks by characterizing the conversion degree (DC) and the viscoelastic properties of experimental PICN blocks polymerized at 90 °C under various high pressures followed or not by post-cure treatment (PC). Near infrared analysis and dynamic mechanical analysis were used to characterize DC and viscoelastic properties of sixteen PICN: one control (thermo-cured) and fifteen experimental groups (one thermo-cured followed by PC and fourteen high pressure polymerized PICN, in the range of 50–350 MPa without and with PC). Conversion degree of high pressure polymerized PICN blocks without post curing displays an optimum between 100 and 150 MPa resulting in an improved E′ and Tg. Post curing induces a higher DC with a controversial effect on thermomechanical properties. The results suggested that 100–150 MPa without PC is an optimum polymerization parameter, resulting in PICN blocks with significantly better DC, Tg, E’.Dr Michael Sadoun (Majeb, Liege) is gratefully acknowledged for his help in PICN synthesis