Dose calculation models for re-entering nuclear rocket debris

Mathematical models of biological hazards from nuclear rocket engine flight failure

Comparison of Nuclear and Explosive Destruct Concepts for Nuclear Rocket Engines

Nuclear and explosive destruct concepts for nuclear rocket engine

VEGF and semaphorins modulate the migration of GnRH-secreting neurons: link with the blood vessels?

Aim: Gonadotropin-releasing hormone (GnRH) neurons originate in the olfactory placode and during development (E11-E18 in mouse) migrate along olfactory nerves to reach the hypothalamus. We have recently described that neuropilins NRP1 and NRP2, co-receptors for two distinct classes of molecules (the class 3 semaphorins, SEMAs, and the vascular endothelial growth factor A, VEGFA), are expressed by GnRH neurons. In this study, a possible correlation between blood vessels formation and GnRH-system has been investigated. Methods: E12-12.5 mice were processed for immunocytochemistry and RT-PCR analysis. GN11 neurons were cultured in DMEM/10%FBS and used for RT-PCR and microchemotaxis assay in Boyden\u2019s chamber. Results: Using a specific marker for neoforming blood vessels (isolectin B4), we found that at E12.5, concomitantly with the start of migration of GnRH neurons, the mouse olfactory placode is densely surrounded by small blood vessels. Accordingly, we demonstrated by RT-PCR the expression of SEMA3A, SEMA3F and VEGF in E12 mouse nasal tissue. We also found that immortalised GnRH neurons (GN11 cells) express NRP1 and NRP2, as well as FLT1 and that recombinant SEMA3A and 3F inhibited the their chemomigration in vitro. However, VEGFA exerted an opposite effect, suggesting that the migration of GnRH neurons may be the results of a balance between negative (SEMAs) and positive (VEGFA) cues. Conclusions: Taken together, these preliminary data raise the possibility that GnRH neuron migration is influenced by SEMAs and VEGF signalling, suggesting that a \u2018cross-talk\u2019 between the vascular and GnRH-neuron systems can occur to control their development. (granted by PRIN 2005051740

Usefulness of high-sensitive troponin elevation after effort stress to unveil vulnerable myocardium in patients with hart failure

Elevation of resting high-sensitivity troponin (hs-Tn) holds prognostic value in heart failure (HF), but its pathophysiological meaning is unclear. We aimed to investigate hs-Tn elevation after maximal exercise in patients with systolic HF and its neurohormonal and hemodynamic correlates: 30 patients diagnosed with systolic HF (left ventricular ejection fraction 32 ± 8%, mean ± SD), on guideline-directed medical therapy and not recognized inducible ischemia, underwent maximal cardiopulmonary stress test, with assay of plasma N-terminal proB-type natriuretic peptide (NT-proBNP), norepinephrine (NE), and hs-TnT (hs-TnT) at baseline, peak, and 1 and 4 hours after exercise. Cardiac output (CO) was measured during effort, with a rebreathing technique. The natural logarithm of the ratio between percentage (%) increase in CO and NT-proBNP (ln[CO%/NT-proBNP% increase]) was evaluated, as a noninvasive estimate of Frank-Starling adaptation to effort, with NT-proBNP variation considered as a surrogate of end-diastolic left ventricular pressure variation. Hs-TnT increased during exercise with a 4-hour peak (p = 0.001); 10 patients had hs-TnT increase >20%. Patients with Hs-TnT increase >20% were more symptomatic at rest (p = 0.039) and showed greater NE at peak exercise (p = 0.003) and less ln[CO%/NT-proBNP% increase] (p = 0.034). A lower ln[CO%/NT-proBNP% increase] correlated with greater NE at peak exercise (r = -0.430, p = 0.018). In conclusion, acute troponin elevation after maximal exercise was detected in 1/3 of this series. The association of troponin release with NE, CO, and NT-proBNP changes after effort suggests a pathophysiological link among transient hemodynamic overload, adrenergic activation, and myocardial cell damage, likely identifying a clinical subset at greater risk for HF progression

Evidence for a rapid action of levetiracetam compared to topiramate in refractory partial epilepsy

The objective of this observational study was to compare the efficacy of levetiracetam and topiramate during the first 15 days of add-on treatment in adults with refractory partial epilepsy. Two cohorts of patients with > or =3 simple or complex partial seizures with or without secondary generalisation per month over an 8-week baseline period received levetiracetam or topiramate in two distinct phases, in addition to standard antiepileptic treatment. During the first 15 days of the therapy, levetiracetam was added at the dosage of 250 mg b.i.d. or topiramate at 25mg o.i.d. Efficacy parameters included number of seizure-free days (SFDs), mean and percent reduction in seizure frequency (in general and by type), and number of seizure-free patients in the first 15 days of treatment compared to last 15 days of the baseline period. Sixty-one patients received levetiracetam and 61 topiramate. The general characteristics of the two treatment groups were similar. The total number of SFDs during 15 days before treatment was 637 with levetiracetam and 621 with topiramate; in the 15-day evaluation period the SFDs increased to 748 (17.4%) and 668 (7.6%), respectively (ANOVA, p<0.05). Twenty-six patients (42.6%) taking levetiracetam were seizure free compared to 10 (16.4%) receiving topiramate (chi-square, p=0.003). This open-label non-controlled study suggests an early efficacy of levetiracetam as add-on therapy in patients with refractory partial epilepsy: these results appear to confirm previous indications of a rapid onset of action and seem to suggest first evaluation of the patient at the dose of 500 mg/day before increasing to the considered minimum standard dose of 1000 mg/day, as some patients could respond to the starting dose

Evidence for a rapid action of levetiracetam compared to topiramate in refractory partial epilepsy.

The objective of this observational study was to compare the efficacy of levetiracetam and topiramate during the first 15 days of add-on treatment in adults with refractory partial epilepsy. Two cohorts of patients with > or =3 simple or complex partial seizures with or without secondary generalisation per month over an 8-week baseline period received levetiracetam or topiramate in two distinct phases, in addition to standard antiepileptic treatment. During the first 15 days of the therapy, levetiracetam was added at the dosage of 250 mg b.i.d. or topiramate at 25mg o.i.d. Efficacy parameters included number of seizure-free days (SFDs), mean and percent reduction in seizure frequency (in general and by type), and number of seizure-free patients in the first 15 days of treatment compared to last 15 days of the baseline period. Sixty-one patients received levetiracetam and 61 topiramate. The general characteristics of the two treatment groups were similar. The total number of SFDs during 15 days before treatment was 637 with levetiracetam and 621 with topiramate; in the 15-day evaluation period the SFDs increased to 748 (17.4%) and 668 (7.6%), respectively (ANOVA, p<0.05). Twenty-six patients (42.6%) taking levetiracetam were seizure free compared to 10 (16.4%) receiving topiramate (chi-square, p=0.003). This open-label non-controlled study suggests an early efficacy of levetiracetam as add-on therapy in patients with refractory partial epilepsy: these results appear to confirm previous indications of a rapid onset of action and seem to suggest first evaluation of the patient at the dose of 500 mg/day before increasing to the considered minimum standard dose of 1000 mg/day, as some patients could respond to the starting dose