The Neutrons for Science Facility at SPIRAL-2.

The neutrons for science (NFS) facility is a component of SPIRAL-2, the new superconducting linear accelerator built at GANIL in Caen (France). The proton and deuteron beams delivered by the accelerator will allow producing intense neutron fields in the 100 keV-40 MeV energy range. Continuous and quasi-mono-kinetic energy spectra, respectively, will be available at NFS, produced by the interaction of a deuteron beam on a thick Be converter and by the 7Li(p,n) reaction on thin converter. The pulsed neutron beam, with a flux up to two orders of magnitude higher than those of other existing time-of-flight facilities, will open new opportunities of experiments in fundamental research as well as in nuclear data measurements. In addition to the neutron beam, irradiation stations for neutron-, proton- and deuteron-induced reactions will be available for cross-sections measurements and for the irradiation of electronic devices or biological cells. NFS, whose first experiment is foreseen in 2018, will be a very powerful tool for physics, fundamental research as well as applications like the transmutation of nuclear waste, design of future fission and fusion reactors, nuclear medicine or test and development of new detectors.

The role of increased Ca++ influx as a possible additional adaptive mechanism in experimental left ventricular hypertrophy (exp LVH).

Membrane potentials, isometric contraction and autohistoradiography with 45Ca in papillary muscle of rats with experimental LVH without cardiac failure as compared with sham-operated animals proved an increased Ca influx per beat and a Ca accumulation at or near the sarcolemma. This phenomenon is regarded as an additional mechanism for the improvement of the cardiac performance in the compensatory stage of the experimental LVH without cardiac failure.

Absence of increased cardiac voltage and the importance of Q vectors for the diagnosis of left ventricular hypertrophy in early stages of hypertension in patients over 40 years of age.

The quantitative VCG criteria (VCGer) for left ventricular hypertrophy (LVH) and their diagnostic power were determined in 165 hypertensive men and 86 women over 40 years of age without congestive cardiac failure in comparison with 91 normal men and 108 normal women. The patients were grouped according to the presence or absence of LVH determined by X-ray (men: 96 without and 69 with LVH, women: 41 without and 45 with LVH). The proper statistical methods were used taking into account whether their distributions were symmetrical or asymmetrical. We found some sex differences of VCG criteria. The most striking results were the lack of increased voltage, and the great sensitivity of the orientation of Q vectors to the left (Q left). Q left may be induced by: 1. a septal hypertrophy, alone or accompanied by a hypertrophy of the anterior and posterior paraseptal regions of LV wall, 2. by a subendocardial ischemia at these levels induced by the increase of intraventricular pressure, 3. by possible spatial change of the septum, 4. by all these factors acting synchronously, 5. by other, unknown factors. These VCGcr for LVH found by us are different from those in the literature, but they are valid in Romania.

Studies concerning the role of myocardial hypertrophy and of intramural tension as determinants of the increased voltage in concentric left ventricular hypertrophy.

In order to study the role of myocardial hypertrophy and of the intramural tension as determinants of the increased voltage in concentric left ventricular hypertrophy, the amplitude of intracellular action potentials in frog and rat myocardium and of monophasic action potentials recorded in dogs by suction electrodes were studied. Increased amplitudes of intracellular action potentials were seen neither in experimental LVH in rats nor during stretch in frog and rat myocardium. The increased intramural tension in dog heart during norepinephrine perfusion or in heart-lung preparation during increased peripheral resistance does not increase the amplitude of monophasic action potentials. The abrupt hypertension induced by norepinephrine is an inadequate model for the study of the effect of increased intramural tension. The increase of the voltage in LVH cannot be accounted for by the increase of action potentials of each hypertrophied fibre. Many factors cooperate in producing increased voltage of LV in LVH.