Non-isothermal decomposition kinetics of the interaction of poly(ethylene terephthalate) with alkyd varnish

The recycling of soft drink bottles poly(ethylene terephthalate) (PET) has been used as an additive in varnish containing alkyd resin. The PET, called to recycled PET (PET-R), was added to the varnish in increasing amounts. Samples of varnish containing PET-R (VPET-R) were used as a film onto slides and its thermal properties were evaluated using thermogravimetry (TG). Throughout the visual analysis and thermal behavior of VPET-R it is possible to identify that the maximum amount of PET-R added to the varnish without changing in the film properties was 2%.The kinetic parameters, such as activation energy (E) and the pre-exponential factor (A) were calculated by the isoconversional Flynn-Wall-Ozawa method for the samples containing 0.5 to 2.0% PET-R. A decrease in the values of E was verified for lower amounts of PET-R for the thermal decomposition reaction. A kinetic compensation effect (KCE) represented by the lnA=-13.42+0.23E equation was observed for all samples. The most suitable kinetic model to describe this decomposition process is the autocatalytic Sestak-Berggren, being the model applied to heterogeneous systems.

Nanocoating of Al2O3 additive on ZrO2 powder and its effect on the sintering behaviour in ZrO2 ceramic

ZrO2 powder was coated with Al2O3 precursor generated by a polymeric precursor method in aqueous solution. The system of nanocoated particles formed a core shell-like structure in which the particle is the core and the nanocoating (additive) is the shell. A new approach is reported in order to control the superficial mass transport and the exaggerated grain growth during the sintering of zirconia powder. Transmission electron microscopy (TEM) observations clearly showed the formation of an alumina layer on the surface of the zirconia particles. This layer modifies the sintering process and retards the maximum shrinkage temperature of the pure zirconia.

Effect of a non-peptide angiotensin receptor antagonist on water intake caused by centrally administered carbachol in the rat

Angiotensin II (ANG II) administered centrally produces drinking by acting on subtype 1 ANG II (AT1) receptors, Carbachol, a cholinergic receptor agonist, also induces drinking behavior by a central action. In the present study we determined whether the response to carbachol also involves AT1 receptors. Male Holtzman rats (250-300 g) with stainless steel cannula implanted into the lateral ventricle (LV) were used. Water intake after injection of 0.15 M NaCl (1.0 mu l) into the LV was 0.2 +/- 0.01 ml/h (N = 8). The AT1 receptor antagonist DUP-753 (50 nmol/mu l) injected into the LV reduced water intake induced by ANG II (10 nmol/mu l) from 9.2 +/- 1.4 to 0.4 +/- 0.1 ml/h (N = 8), and water intake induced by carbachol (2 nmol/mu l) from 9.8 +/- 1.4 ml/h to 3.7 +/- 0.8 ml/h (N = 8), These results suggest that AT1 receptors play a role in the drinking behavior observed after central cholinergic stimulation in rats.

Study of the annealing temperature effect on the structural and luminescent properties of SrWO4:Eu phosphors prepared by a non-hydrolytic sol-gel process

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Effect of non-steroidal anti-inflammatory drugs (NSAID) on the histamine release induced by compound 48/80 and cardiac anaphylaxis in guinea-pig isolated heart

Histamine release from guinea pig heart treated with compound 48/80 was potentiated by the cyclooxygenase inhibitors indomethacin and piroxicam but not by aspirin or phenylbutazone. This differential effect suggests that the potentiation is not merely due to an inhibition of prostaglandin synthesis. Piroxicam potentiated the histamine release induced by cardiac anaphylaxis whereas indomethacin reduced this effect. The SRS-A antagonist FPL 55712 inhibited histamine release induced by cardiac anaphylaxis, but not that evoked by compound 48/80, and also prevented the potentiation due to indomethacin and piroxicam. In total, these data suggest that the potentiation of histamine release by piroxicam and indomethacin is probably due to a diversion of arachidonic acid metabolism from the cyclooxygenase to the lipoxygenase pathways. The resulting lipoxygenase products may then regulate histamine release, with the secretion due to antigen being more sensitive to such modulation than that evoked by compound 48/80.

The effect of non-antihypertensive doses of angiotensin converting enzyme inhibitor on myocardial necrosis and hypertrophy in young rats with renovascular hypertension

In renovascular hypertensive rats, low doses of angiotensin converting enzyme (ACE) inhibitors have been found to prevent myocardial hypertrophy independent of blood pressure level. This finding would suggest humoral rather than mechanical control of myocyte growth. The aim of this study was to examine the effect of nonantihypertensive doses of ACE inhibitor on myocardial hypertrophy and necrosis in hypertensive rats. Renovascular hypertension (RHT) was induced in four-week-old Wistar rats. Twenty-eight animals were treated for four weeks with three doses of ramipril (0.01, 0.1 or 1.0 mg/kg/day, which are unable to lower blood pressure. Fourteen animals were not treated (RHT group). A sham operated, age/sex-matched group was used as control (n=10). Myocardial histology was analysed in 3 μm thick sections of the ventricle stained with either haematoxylin-eosin, reticulin silver stain or Masson's trichrome. There was a significant correlation between systolic blood pressure and left ventricular to body weight ratio in both sets of animals: untreated plus controls and ramipril-treated rats. ACE inhibition prevented myocyte and perivascular necrosis and fibrosis in a dose-dependent manner. We conclude that myocardial hypertrophy in rats with renovascular hypertension is directly related to arterial pressure, and that this relationship is not affected by nonantihypertensive doses of ACE inhibitor. Myocardial necrosis/fibrosis and coronary artery damage induced by angiotensin II are prevented by ACE inhibitor in a dose-dependent manner, despite the presence of arterial hypertension.

The effect of non-antihypertensive doses of angiotensin converting enzyme inhibitor on myocardial necrosis and hypertrophy in young rats with renovascular hypertension

In renovascular hypertensive rats, low doses of angiotensin converting enzyme (ACE) inhibitors have been found to prevent myocardial hypertrophy independent of blood pressure level. This finding would suggest humoral rather than mechanical control of myocyte growth. The aim of this study was to examine the effect of nonantihypertensive doses of ACE inhibitor on myocardial hypertrophy and necrosis in hypertensive rats. Renovascular hypertension (RHT) was induced in four-week-old Wistar rats. Twenty-eight animals were treated for four weeks with three doses of ramipril (0.01, 0.1 or 1. 0 mg/kg/day, which are unable to lower blood pressure. Fourteen animals were not treated (RHT group). A sham operated, age/sex-matched group was used as control (n = 10). Myocardial histology was analysed in 3 microm thick sections of the ventricle stained with either haematoxylin-eosin, reticulin silver stain or Masson's trichrome. There was a significant correlation between systolic blood pressure and left ventricular to body weight ratio in both sets of animals: untreated plus controls and ramipril-treated rats. ACE inhibition prevented myocyte and perivascular necrosis and fibrosis in a dose-dependent manner. We conclude that myocardial hypertrophy in rats with renovascular hypertension is directly related to arterial pressure, and that this relationship is not affected by nonantihypertensive doses of ACE inhibitor. Myocardial necrosis/fibrosis and coronary artery damage induced by angiotensin II are prevented by ACE inhibitor in a dose-dependent manner, despite the presence of arterial hypertension.