Electron scattering cross sections from anthracene over a broad energy range (0.00001-10,000 eV).

We report a computational investigation of electron scattering by anthracene (C14H10) in the gas phase. Integral and differential cross sections have been calculated by employing two distinct ab-initio quantum scattering methods: the symmetry adapted-single centre expansion method (ePOLYSCAT) and a screening corrected form of the independent atom model (IAM-SCAR) at low and high energies, respectively. After a detailed evaluation of the current results, we present a complete set of integral scattering cross sections from 0.00001 to 10,000 eV.

Stopping power for electrons in pyrimidine in the energy range 20-3000 eV.

In this work, we present new experimental electron energy loss distribution functions for pyrimidine (C4H4N2) measured for the incident energy range 30-2000 eV. Theoretical total and elastic cross sections for electron scattering from pyrimidine were calculated using the screening-corrected additivity rule (IAM-SCAR) method. Based on the mean energy loss observed in the experiment and the theoretical integral inelastic cross section, the stopping power for electrons in pyrimidine is calculated in the energy range 20-3000 eV.

Electron scattering cross section calculations for polar molecules over a broad energy range.

We report computational integral and differential cross sections for electron scattering by two different polar molecules, HCN and pyrimidine, over a broad energy range. We employ, for low energies, either the single-centre expansion (ePOLYSCAT) or the R-matrix method, while for the higher energies we select a corrected form of the independent-atom representation (IAM-SCAR). We provide complete sets of integral electron scattering cross sections from low energies up to 10,000 eV. Our present calculated data agree well with prior experimental results.

Current prospects on Low Energy Particle Track Simulation for biomedical applications.

The Low Energy Particle Track Simulation code is a radiation interaction simulation tool specifically designed to describe electron and positron interactions below 10 keV at a molecular level. Relying on carefully selected, preferentially experimental input parameters that account for all expected scattering processes, it provides detailed results about all collisional events undergone by an incident radiation particle during its slowdown until thermalisation. Here, we give an up-to-date description of its input data sources and selection procedure and summarise the current contents of the resulting database.

An investigation into electron scattering from pyrazine at intermediate and high energies.

Total electron scattering cross sections for pyrazine in the energy range 10-500 eV have been measured with a new magnetically confined electron transmission-beam apparatus. Theoretical differential and integral elastic, as well as integral inelastic, cross sections have been calculated by means of a screening-corrected form of the independent-atom representation (IAM-SCAR) from 10 to 1000 eV incident electron energies. The present experimental and theoretical total cross sections show a good level of agreement, to within 10%, in the overlapping energy range. Consistency of these results with previous calculations (i.e., the R-matrix and Schwinger Multichannel methods) and elastic scattering measurements at lower energies, below 10 eV, is also discussed.

Electron scattering cross sections from HCN over a broad energy range (0.1-10,000 eV): Influence of the permanent dipole moment on the scattering process.

We report theoretical integral and differential cross sections for electron scattering from hydrogen cyanide derived from two ab initio scattering potential methods. For low energies (0.1-100 eV), we have used the symmetry adapted-single centre expansion method using a multichannel scattering formulation of the problem. For intermediate and high energies (10-10,000 eV), we have applied an optical potential method based on a screening corrected independent atom representation. Since HCN is a strong polar molecule, further dipole-induced excitations have been calculated in the framework of the first Born approximation and employing a transformation to a space-fixed reference frame of the calculated K-matrix elements. Results are compared with experimental data available in the literature and a complete set of recommended integral elastic, inelastic, and total scattering cross sections is provided from 0.1 to 10,000 eV.

Presynaptic effect of 7-OH-DPAT on evoked [3H]-acetylcholine release in rat striatal synaptosomes.

The objective of the present experiments was to study the presynaptic effect of 7-hydroxy-N,N-di-n-propyl-2-aminotetraline (7-OH-DPAT, a D(2)-like dopamine receptor agonist) on [3H]-acetylcholine ([3H]-ACh) release induced by potassium (15 mM, 25 mM and 60 mM), potassium channel-blockers (4-aminopyridine, 4-AP; tetraethylammonium, TEA and quinine) and veratridine to gain insight into the mechanisms involved in the activation of the D(2) dopamine-receptor subtype located at striatal cholinergic nerve terminals. 7-OH-DPAT (1 microM) inhibited the evoked [3H]-ACh release induced by K(+) 15 mM in a similar percentage than that obtained during basal conditions (30% and 27%, respectively). Nevertheless, in the presence of 25 mM and 60 mM of K(+) the inhibitory effect of 7-OH-DPAT was completely abolished. 4-AP (1-100 microM) and TEA (1 and 5 mM) significantly enhanced [3H]-ACh release, showing 69.32%+/-7.60% (P<0.001) and 52.27%+/-5.64% (P<0.001), respectively, at the highest concentrations tested. In these conditions, 7-OH-DPAT (1 microM) inhibited the release induced by potassium channel-blockers approximately 25-27%. Quinine (0.1-1 microM) did not alter [3H]-ACh release either in the presence or absence of 7-OH-DPAT. Veratridine 10 microM evoked [3H]-ACh release in the presence of a low-calcium medium, but in such conditions 7-OH-DPAT (1 microM) did not modify the neurotransmitter release in the absence or presence of veratridine. Present data indicate that activation of the presynaptic D(2) dopamine receptor inhibits the [3H]-ACh release by increasing K(+) conductance, as high K(+) concentrations abolished the inhibitory control of 7-OH-DPAT on [3H]-ACh release. This effect could be mediated by potassium channels different from those sensitive to 4-AP, TEA and quinine. In addition, the presynaptic D(2) dopamine-receptor activation seems to not involve changes in intracellular Ca(2+).

Role of calcium on the modulation of spontaneous acetylcholine efflux by the D2 dopamine receptor subtype in rat striatal synaptosomes.

The role of calcium in the modulation of spontaneous [3H]acetylcholine ([3H]ACh) efflux through presynaptic D2 dopamine hetero-receptors was investigated in rat striatal synaptosomes. The kinetic studies of [3H]ACh efflux in the presence or absence of Ca2+ were carried out in nonstimulating conditions. When Ca2+ was omitted from the superfusion medium, a notable and significant (P<0.001) decrease of tritium efflux (39%) was obtained. While [3H]ACh efflux was insensitive to tetrodotoxin (TTX) 1 microM, cadmium (10 microM), a nonselective antagonist of calcium channels, significantly reduced the tritium efflux by 24% (P<0.001), while the L-type calcium antagonist, nifedipine, (30 microM) inhibited the tritium efflux by only 10% (P<0.02). 2-(4-Fenylpiperidine)cyclohexanol (vesamicol), an inhibitor of the vesicular [3H]ACh carrier, significantly depressed the spontaneous tritium efflux in the presence of Ca2+ (60%; P<0.001) and in a low-calcium medium (20%; P<0.001). Although 1 microM of 7-hydroxy-N,N-di-n-propyl-2-aminotetraline (7-OH-DPAT) inhibited spontaneous [3H]ACh efflux in the presence of calcium, this dopaminergic agonist did not modify the neurotransmitter release in either the low-Ca2+ medium or in the presence of vesamicol. These results suggest that the spontaneous [3H]ACh efflux is a process involving a Ca2+-dependent component (39%), sensitive to calcium channel-blockers and vesamicol, in rat striatal synaptosomes. In addition, activation of the D2 dopamine hetero-receptor only modulates the calcium-dependent component of spontaneous [3H]ACh efflux.

Purine metabolism in patients with gout: the role of lead.

Primary gout is characterized by increased plasma and decreased urinary concentrations of hypoxanthine, xanthine and uric acid. To examine whether lead could explain the disturbance of purine metabolism in gout, we determined hypoxanthine, xanthine and uric acid metabolism and 5-day cumulative urinary lead excretion rates after an EDTA (calcium disodium edetate) test in 27 patients with primary gout and reduced creatinine clearance (C(cr)) and in 50 patients with gout and normal C(cr). The results were compared to those obtained in 26 normal subjects matched for age. All gout patients evidenced a marked renal underexcretion of hypoxanthine, xanthine and uric acid relative to their increased plasma levels. Purine metabolism was remarkably similar in both gout groups except for a significantly lower uric acid excretion in patients with reduced C(cr). Blood lead levels and cumulative lead excretion rates were significantly higher in gout patients with renal failure as compared to patients with normal C(cr). Fourteen patients (52%) with renal insufficiency and 6 (12%) with normal C(cr) showed increased lead excretion rates (95% Cl for the difference, 29-51%, p < 0.001). Mobilizable lead was not significantly correlated with serum or urinary purine concentrations. Hypoxanthine, xanthine and uric acid underexcretion was similar in gout patients with increased or normal cumulative lead excretion rates. The prevalence of atheromatosis and arterial hypertension together was significantly higher in gout patients with renal failure than in patients with normal C(cr) (81 vs. 60%, 95% Cl for the difference, 11-31%, p < 0.005). These results indicate that lead is not a significant contributor to the renal underexcretion of purines in gout. An increased mobilizable lead is not by itself evidence that lead is the cause of the renal insufficiency in patients with primary gout. Atheromatous nephropathy and/or nephroangiosclerosis may explain impaired renal function in patients with primary gout.