Features of the Carrier Concentration Determination during Irradiation of Wide-Gap Semiconductors: The Case Study of Silicon Carbide.

In this paper, the features of radiation compensation of wide-gap semiconductors are discussed, considering the case study of silicon carbide. Two classical methods of concentration determination are compared and analyzed: capacitance-voltage (-) and current-voltage () characteristics. The dependence of the base resistance in high-voltage 4H-SiC Schottky diodes on the dose of irradiation by electrons and protons is experimentally traced in the range of eight orders of magnitude.

Radiation Hardness of Silicon Carbide upon High-Temperature Electron and Proton Irradiation.

The radiation hardness of silicon carbide with respect to electron and proton irradiation and its dependence on the irradiation temperature are analyzed. It is shown that the main mechanism of SiC compensation is the formation of deep acceptor levels. With increasing the irradiation temperature, the probability of the formation of these centers decreases, and they are partly annealed out.

Microstructure of bismuth centers in silicon before and after irradiation with 15 MeV protons.

A decrease of two-gamma annihilation rate of a positron in a strong spin-orbit field of the annihilation site of bismuth impurity centerBi (= 9/2) in silicon with natural isotope composition was revealed (is the nuclear spin). This decrease was observed along with increasing occupancy of Bi donor states (binding energy{Bi} ≈ 69 meV). Atoms ofSi (= 1/2) isotope are involved in spin interactions of positron with Bi impurity centers.

Anti-thrombotic effects of nebivolol and carvedilol: Involvement of β2 receptors and COX-2/PGI2 pathways.

Background: Third generation β-adrenolytics, such as selective β1 adrenoceptor antagonist nebivolol and non-selective β1/β2 and α1 adrenoceptor antagonist carvedilol, display beneficial nitric oxide (NO)-dependent vasodilator activities that contribute to their therapeutic efficacy. In the present work, we analyzed whether nebivolol and carvedilol, as well as other β-adrenolytics with similar pharmacological profiles (selective β1 adrenoceptor antagonist - atenolol and non-selective α/β adrenoceptor antagonist - labetalol), possess the ability to induce PGI2-dependent anti-thrombotic activity in vivo in normotensive rats.

Methods: Anti-thrombotic effects of nebivolol and carvedilol were studied in vivo in anaesthetized rats with extracorporeal circulation superfusing collagen strips.

Positron annihilation on defects in silicon irradiated with 15 MeV protons.

Microstructure and thermal stability of the radiation defects in n-FZ-Si ([P] ≈ 7 × 10(15) cm(-3)) single crystals have been investigated. The radiation defects have been induced by irradiation with 15 MeV protons and studied by means of both the positron lifetime spectroscopy and low-temperature measurements of the Hall effect. At each step of the isochronal annealing over the temperature range ∼60-700 °C the positron lifetime has been measured for the temperature interval ∼30-300 K, and for samples-satellites the temperature dependences of the charge carriers and mobility have been determined over the range ∼4.

Large-conductance K+ channel opener CGS7184 as a regulator of endothelial cell function.

Large-conductance Ca(2+)-activated potassium (BK(Ca)) channels are present in endothelium, but their regulatory role remains uncharacterized. The aim of the present study was to investigate the pharmacological effects of the BK(Ca) channel opener ethyl-1-[[(4-chlorophenyl)amino]oxo]-2-hydroxy-6-trifluoromethyl-1H-indole-3-carboxylate (CGS7184) on endothelium in the aorta and coronary circulation, particularly with regard to nitric oxide (NO)-dependent regulation of vascular tone, as well as effects of CGS7184 on NO production, calcium homeostasis, and mitochondrial function in cultured endothelial cells. The vasorelaxant action of CGS7184 was studied in coronary circulation and in the aorta using isolated perfused guinea pig heart and rat aortic rings, respectively.

NO and PGI(2) in coronary endothelial dysfunction in transgenic mice with dilated cardiomyopathy.

Objective: The aim of the present work was to analyze coronary endothelial function in the transgenic mouse model of dilated cardiomyopathy (Tgalphaq*44 mice).

Methods: Coronary vasodilatation, both NO-dependent (induced by bradykinin) and PGI(2)-dependent (induced by acetylcholine), was assessed in the isolated hearts of Tgalphaq*44 and FVB mice. Cardiac function was analyzed in vivo (MRI).

Prostacyclin, but not nitric oxide, is the major mediator of acetylcholine-induced vasodilatation in the isolated mouse heart.

In many species, acetylcholine (Ach) induces coronary vasodilatation via endothelium-derived nitric oxide (NO). The aim of the present study was to examine if this rule pertains also to the coronary circulation of the mouse. We examined the involvement of NO and prostacyclin (PGI2) in the coronary flow response to Ach as compared to response to bradykinin (Bk) in hearts isolated from FVB or C57Bl/6 mice and perfused according to the Langendorff technique.

Inhibition of neutral endopeptidase by thiorphan does not modify coronary vascular responses to angiotensin I, angiotensin II and bradykinin in the isolated guinea pig heart.

Both angiotensin-converting enzyme (ACE) and neutral endopeptidase (NEP) are involved in the regulation of renin-angiotensin and kallikrein-kinin systems. The aim of the present study was to assess the role of NEPand ACE in the regulation of vascular responses to angiotensin I (Ang I), angiotensin II (Ang II) and bradykinin (Bk) in the coronary circulation. For this purpose we used typical inhibitors of ACE and NEP, perindoprilate (1 microM) and thiorphan (1 micromM and 10 microM), respectively, and analyzed their effects on the coronary vasoconstrictor responses to Ang I and Ang II and coronary vasodilator responses to Bk in the isolated guinea pig heart.

On the mechanism of coronary vasodilation induced by angiotensin-(1-7) in the isolated guinea pig heart.

Various mechanisms have been postulated to be involved in angiotensin-(1-7)-induced endothelium-dependent vasodilation. Here, we characterized the vasodilator action of angiotensin-(1-7) in the isolated guinea pig heart. Angiotensin-(1-7) (1-10 nmol, bolus) induced dose-dependent increase in the coronary flow.

Nebivovol and carvedilol induce NO-dependent coronary vasodilatation that is unlikely to be mediated by extracellular ATP in the isolated guinea pig heart.

In contrast to classical beta-adrenoreceptor antagonists, nebivolol and carvedilol possess endothelium-dependent vasorelaxant properties. It has been proposed that nebivolol and carvedilol activate microvascular endothelium into producing NO by the release of extracellular ATP and subsequent stimulation of endothelial P(2) receptors. Here we tested this hypothesis in the coronary circulation of the isolated guinea pig heart.

Radical scavenging and NO-releasing properties of selected beta-adrenoreceptor antagonists.

It is claimed that novel beta-adrenolytic drugs possess superior antioxidant properties as compared to classical selective or non-selective beta-adrenoceptor antagonists. Here we tested this notion by analyzing radical scavenging properties of selected beta-adrenolytic drugs and their ability to release nitric oxide in biological preparations. Selective beta1-adrenolytics such as nebivolol, atenolol, metoprolol and non-selective beta-adrenolytics with alpha1-receptor blocking properties such as carvedilol and labetalol were chosen for analysis.

Free radicals generated by xanthine/xanthine oxidase system augment nitric oxide synthase (NOS) and cyclooxygenase (COX)-independent component of bradykinin-induced vasodilatation in the isolated guinea pig heart.

Recently, we have reported that bradykinin (Bk)-induced vasodilation was selectively potentiated by a low concentration of reactive oxygen species (ROS) generated by xanthine/xanthine oxidase system (XOX) in the coronary circulation of the isolated guinea pig heart. In an attempt to identify a mechanism of Bk response that is amplified by XOX, we analyze here the involvement of B1/ B2 receptors and the participation of NOS/COX pathways in the Bk responses before and after intracoronary infusion of XOX in the isolated guinea pig heart. Bk (0.

Photoaddition of N-substituted piperazines to C60: an efficient approach to the synthesis of water-soluble fullerene derivatives.

An oxidative radical photoaddition of mono N-substituted piperazines to [60]fullerene was systematically investigated. Reactions of C60 with piperazines bearing bulky electron-withdrawing groups (2-pyridyl, 2-pyrimidinyl) were found to be the most selective and yielded C60(amine)4O as major products along with small amounts of C60(amine)2. In contrast, interactions of fullerene with N-methylpiperazine and N-(tert-butoxycarbonyl)piperazine were found to have low selectivity due to different side reactions.

Compensation of endothelium-dependent responses in coronary circulation of eNOS-deficient mice.

Nitric oxide plays a fundamental role in the regulation of blood flow. Here we analyzed compensatory mechanisms for the genetic eNOS deficiency in aorta and in coronary circulation. Vasodilation induced by acetylcholine, bradykinin, adenosine, and ADP as well as by S-nitroso-penicillamine (SNAP) was assessed in isolated aorta and in isolated mouse hearts from eNOS-/- and age-matched eNOS+/+ mice.

Antiarrhythmic profile and endothelial action of novel decahydroquinoline derivatives.

We tested antiarrhythmic and endothelial action of novel decahydroquinoline derivatives. Antiarrhythmic activity was analyzed using models of aconitine-, calcium chloride-, and adrenaline-induced arrhythmias in rats. Potency to induce nitric oxide (NO)-dependent coronary vasodilation was assessed in isolated guinea pig heart perfused according to Langendorff technique.

The methylester of gamma-butyrobetaine, but not gamma-butyrobetaine itself, induces muscarinic receptor-dependent vasodilatation.

Gamma-butyrobetaine (GBB) is known mostly as a bio-precursor of carnitine, a key molecule in the regulation of myocardial energy metabolism. The metabolites of carnitine and GBB were investigated for acetylcholine-like activity decades ago. The present study shows that the methylester of GBB (GBB-ME) exerts its biological activity by binding to muscarinic acetylcholine receptors.

Novel experimental arrangement developed for direct fullerene analysis by electrospray time-of-flight mass spectrometry.

A novel electrospray setup was found effective for direct analysis of fullerene solutions by electrospray (ES) mass spectrometry. The electrospray capillary needle used for the analysis is equipped with a thin metal (copper, platinum or stainless steel) wire installed inside the capillary. The wire tip protrudes slightly from the capillary end.

Clonidine-induced coronary vasodilatation in isolated guinea pig heart is not mediated by endothelial alpha2 adrenoceptors.

Functional role of endothelial alpha(2)-adrenoceptor in coronary circulation remains unclear. Clonidine, an agonist of alpha(2)-adrenoceptors, was reported to induce coronary vasodilatation via stimulation of endothelial alpha(2)-adrenoceptors or coronary vasoconstriction involving vascular smooth muscle alpha(2)-adrenoceptors. Moreover, H(2) receptor-dependent responses to clonidine were described.

Effects of two beta3-agonists, CGP 12177A and BRL 37344, on coronary flow and contractility in isolated guinea pig heart.

The functional role of beta(3)-adrenergic receptors in the heart is still not clear. The actions of two widely used beta(3)-adrenoceptor agonists, such as BRL 37344 and CGP 12177, were studied in the isolated guinea pig heart, perfused at constant pressure according to the Langendorff technique. Heart contractility (dP/dt, first derivative of pressure measured over time) and coronary flow (CF) were assessed simultaneously.

Paradoxical augmentation of bradykinin-induced vasodilatation by xanthine/xanthine oxidase-derived free radicals in isolated guinea pig heart.

Increased generation of reactive oxygen species contribute to endothelial dysfunction in atherosclerosis, hypertension and heart failure. Recently, it was suggested that bursts of superoxide anions may inactivate endothelial surface-bound enzymes such as angiotensin converting enzyme (ACE). Here, we tested effects of xanthine/xanthine oxidase-derived superoxide anions on vascular responses and ACE activity in the isolated guinea pig heart.

No-dependent vasodilation induced by nebivolol in coronary circulation is not mediated by beta-adrenoceptors or by 5 HT1A-receptors.

Nebivolol is a unique beta1-adrenoceptor antagonist which possesses peripheral vasodilator properties dependent on endothelial NO. Nebivolol-induced release of NO was attributed to its L stereoisomer and to its ability to stimulate endothelial beta2, beta3 adrenoceptors or 5-HT1A receptors. Here, in the isolated guinea pig heart we analysed coronary vasodilator potency of L- and D-nebivolol and a possible role of beta2, beta3 adrenoceptors and 5-HT1A receptors in nebivolol-induced vasodilation.

Flavonoids and nitric oxide synthase.

Induction of NOS-2 in macrophages and smooth muscles within vascular wall with concomittant suppression of endothelial NOS-3 activity is considered to be a hallmark of vascular inflammation that triggers atherogenesis. Accordingly, drugs designed to reverse these changes should not only support vaning function of NOS-3 but also suppress proinflammatory NO production by NOS-2. It means that using selective inhibitors of induction of NOS-2 (they spare ex definitione constitutive activity of NOS-3) is a more rational approach than using "selective" inhibitors of activity of previously induced NOS-2.