Compound-Nucleus and Doorway-State Decays of ß-Delayed Neutron Emitters

We investigated decays of ^{51,52,53}K at the ISOLDE Decay Station at CERN in order to understand the mechanism of the ß-delayed neutron-emission (ßn) process. The experiment quantified neutron and γ-ray emission paths for each precursor. We used this information to test the hypothesis, first formulated by Bohr in 1939, that neutrons in the ßn process originate from the structureless "compound nucleus." The data are consistent with this postulate for most of the observed decay paths. The agreement, however, is surprising because the compound-nucleus stage should not be achieved in the studied ß decay due to insufficient excitation energy and level densities in the neutron emitter. In the ^{53}K ßn decay, we found a preferential population of the first excited state in ^{52}Ca that contradicted Bohr's hypothesis. The latter was interpreted as evidence for direct neutron emission sensitive to the structure of the neutron-unbound state. We propose that the observed nonstatistical neutron emission proceeds through the coupling with nearby doorway states that have large neutron-emission probabilities. The appearance of "compound-nucleus" decay is caused by the aggregated small contributions of multiple doorway states at higher excitation energy.

Towards the Limits of Existence of Nuclear Structure: Observation and First Spectroscopy of the Isotope

The most remote isotope from the proton dripline (by 4 atomic mass units) has been observed: ^{31}K. It is unbound with respect to three-proton (3p) emission, and its decays have been detected in flight by measuring the trajectories of all decay products using microstrip detectors. The 3p emission processes have been studied by the means of angular correlations of ^{28}S+3p and the respective decay vertices. The energies of the previously unknown ground and excited states of ^{31}K have been determined. This provides its 3p separation energy value S_{3p} of -4.6(2) MeV. Upper half-life limits of 10 ps of the observed ^{31}K states have been derived from distributions of the measured decay vertices.

Observation and Spectroscopy of New Proton-Unbound Isotopes ³°Ar and ²9Cl: An Interplay of Prompt Two-Proton and Sequential Decay.

Previously unknown isotopes (30)Ar and (29)Cl have been identified by measurement of the trajectories of their in-flight decay products (28)S+p+p and (28)S+p, respectively. The analysis of angular correlations of the fragments provided information on decay energies and the structure of the parent states. The ground states of (30)Ar and (29)Cl were found at 2.25(-0.10)(+0.15) and 1.8±0.1 MeV above the two- and one-proton thresholds, respectively. The lowest states in (30)Ar and (29)Cl point to a violation of isobaric symmetry in the structure of these unbound nuclei. The two-proton decay has been identified in a transition region between simultaneous two-proton and sequential proton emissions from the (30)Ar ground state, which is characterized by an interplay of three-body and two-body decay mechanisms. The first hint of a fine structure of the two-proton decay of (30)Ar*(2(+)) has been obtained by detecting two decay branches into the ground and first-excited states of the (28)S fragment.

First direct measurement of the 2H(α,γ)6Li cross section at big bang energies and the primordial lithium problem.

Recent observations of (6)Li in metal poor stars suggest a large production of this isotope during big bang nucleosynthesis (BBN). In standard BBN calculations, the (2)H(α,γ)(6)Li reaction dominates (6)Li production. This reaction has never been measured inside the BBN energy region because its cross section drops exponentially at low energy and because the electric dipole transition is strongly suppressed for the isoscalar particles (2)H and α at energies below the Coulomb barrier. Indirect measurements using the Coulomb dissociation of (6)Li only give upper limits owing to the dominance of nuclear breakup processes. Here, we report on the results of the first measurement of the (2)H(α,γ)(6)Li cross section at big bang energies. The experiment was performed deep underground at the LUNA 400 kV accelerator in Gran Sasso, Italy. The primordial (6)Li/(7)Li isotopic abundance ratio has been determined to be (1.5 ± 0.3) × 10(-5), from our experimental data and standard BBN theory. The much higher (6)Li/(7)Li values reported for halo stars will likely require a nonstandard physics explanation, as discussed in the literature.

Large ß-delayed one and two neutron emission rates in the decay of 86Ga.

Beta decay of 86Ga was studied by means of ß-neutron-γ spectroscopy. An isotopically pure ^{86}Ga beam was produced at the Holifield Radioactive Ion Beam Facility using a resonance ionization laser ion source and high-resolution electromagnetic separation. The decay of 86Ga revealed a half-life of 43(-15)(+21) ms and large ß-delayed one-neutron and two-neutron branching ratios of P1n=60(10)% and P2n=20(10)%. The ßγ decay of 86Ga populated a 527 keV transition that is interpreted as the deexcitation of the first 2+ state in the N=54 isotone 86Ge and suggests a quick onset of deformation in Ge isotopes beyond N=50.

New half-lives of r-process Zn and Ga isotopes measured with electromagnetic separation.

The ß decays of neutron-rich nuclei near the doubly magic (78)Ni were studied at the Holifield Radioactive Ion Beam Facility using an electromagnetic isobar separator. The half-lives of (82)Zn (228±10 ms), (83)Zn (117±20 ms), and (85)Ga (93±7 ms) were determined for the first time. These half-lives were found to be very different from the predictions of the global model used in astrophysical simulations. A new calculation was developed using the density functional model, which properly reproduced the new experimental values. The robustness of the new model in the (78)Ni region allowed us to extrapolate data for more neutron-rich isotopes. The revised analysis of the rapid neutron capture process in low entropy environments with our new set of measured and calculated half-lives shows a significant redistribution of predicted isobaric abundances strengthening the yield of A>140 nuclei.

In vitro and in vivo DNA damage of male and female rat liver nuclei by oncogenic and nononcogenic beta blockers.

The beta blocker DL-1-(2-nitro-3-methyl-phenoxy)-3-tert-butylamino-propan-2-ol (ZAMI 1305), hepatocarcinogenic to the female rat, and the nononcogenic beta blockers DL-1-(2-nitro-5-methyl-phenoxy)-3-tert-butylamino-propan-2-ol (ZAMI 1327), DL-propranolol, and DL-atenolol were tested for their capacity to damage liver DNA in vitro and in vivo. As revealed by alkaline sucrose gradient analysis, all the beta blockers tested, with the exception of DL-atenolol, caused a dose-dependent DNA fragmentation when they were added in vitro to nuclei isolated from livers of both male and female Wistar rats. Analysis of the DNA sedimentation patterns in neutral sucrose gradients demonstrated the absence of DNA fragmentation, thus indicating that the drugs did not induce double-strand DNA breaks. When the beta blockers were administered in vivo, liver DNA damage was observed only in female Wistar rats treated with ZAMI 1305. A single injection of ZAMI 1305 caused the onset of two distinct episodes of DNA damage. The first episode occurred within 5 minutes, and the damage was repaired within 1 hour after the injection; the second, apparently spontaneous, episode occurred 14 hours after the injection, and the damage was more pronounced than that seen in the first episode and took a much longer time to subside. However, a second injection of ZAMI 1305 into female Wistar rats 8 hours after the first injection did not induce the immediate short-lived episode of DNA damage but, like the first injection, it caused late DNA damage that peaked about 16 hours after drug administration.

Early activation of vascular endothelium in nonobese, nondiabetic essential hypertensive patients with multiple metabolic abnormalities.

Circulating soluble E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1) concentrations were evaluated in 93 nonobese essential hypertensive patients, of whom 16 had impaired glucose tolerance and hyperlipidemia (group I); 25 had impaired glucose tolerance (group II); 28 had hyperlipidemia (group III); and 24 had no metabolic abnormalities (group IV). A group of 22 healthy volunteers served as a control group. All groups were without clinical or ultrasound evidence of vascular lesion and were matched for age, sex, and BMI. Endothelial soluble adhesion molecules were measured at baseline, during an oral glucose tolerance test, and after 12 weeks of either enalapril or placebo treatments. Plasma soluble E-selectin, ICAM-1, and VCAM-1 were higher (P < 0.05) in group I and II than in the other groups (group I: E-selectin, 96.1+/-27.1; ICAM-1, 304.0+/-102.1; VCAM-1, 626.1+/-156.2 microg/l. Group II: E-selectin, 88.0+/-18.0; ICAM-1, 268.0+/-84.1; VCAM-1, 594.1+/-140.9 microg/I. Group III: E-selectin, 70.1+/-18.1; ICAM-1, 195.1+/-68.0; VCAM-1, 495.9+/-110.1 microg/l. Group IV: E-selectin, 65.1+/-16.1; ICAM-1, 168.1+/-64.0; VCAM-1, 472.1+/-108.2 microg/l). Soluble adhesins levels were not higher than normal in groups III and IV. Plasma soluble ICAM-1 concentrations increased in group I after glucose administration and were directly correlated with 2-h insulin levels (r=0.648, P=0.007). Compared with placebo, 12 weeks of enalapril treatment significantly (P < 0.0001) reduced soluble E-selectin, ICAM-1, and VCAM-1. Decrements of soluble adhesins were not dependent on enalapril-related blood pressure changes. Therefore, an early endothelial activation was present in essential hypertensive patients with impaired glucose tolerance, regardless of the presence of hyperlipidemia. ACE inhibition counteracted such endothelial activation.

Rat bite fever caused by Streptobacillus moniliformis in a child: human infection and rat carriage diagnosed by PCR.

A child owning pet rats developed an eruptive fever with blisters, polyarthritis, and spectacular desquamation of the hands. Streptobacillus moniliformis was identified after culture of the child's blister fluid and was detected in rat samples by molecular methods. Such detection in the pet of a human victim of rat bite fever has not been reported previously.

Age-dependent, seasonal and daily variations of the DNA damaging capacity of the hepatocarcinogen ZAMI 1305 in female rat liver.

A single injection of the sex-dependent hepatocarcinogen DL-1-(2-nitro-3-methyl-phenoxy)-3-tert-butylamino-propan-2-ol (ZAMI 1305) caused age-related DNA damage, as evaluated by alkaline sucrose gradient analysis, in the liver of female Wistar rats. DNA damage reached a maximum at 4-6 weeks of age, about the onset of sexual maturity, and decreased thereafter. In young rats (5-8 weeks of age), the amount of ZAMI 1305-induced DNA damage showed seasonal and daily differences, being higher when the molecule was administered in winter in respect to summer and in the evening in respect to the morning. In older rats (15-22 weeks of age), no seasonal and daily variations were observed.

Tumor-initiating activity of the beta-blocker ZAMI 1305 in the liver of the female Wistar rat.

A 1-week treatment with the hepatocarcinogen beta-blocker DL-1-(2-nitro-3-methyl-phenoxy)-3-tert-butylamino-propan-2-ol (ZAMI 1305) induces the appearance of preneoplastic liver lesions--oval cell hyperplasia, basophilic and gamma-glutamyltranspeptidase positive (GGT+) foci--in female Wistar rats, as evidenced by the Solt and Farber short-term test of carcinogenesis. ZAMI 1305-treatment also induces liver DNA damage, as evaluated by alkaline sucrose gradient analysis. The data suggest that the oncogenic B-blocker ZAMI 1305 has initiating activity in the liver of the female Wistar rat.

Early liver alterations induced by the sex-dependent hepatocarcinogen beta-blocker ZAMI 1305.

Liver alterations occurring after 1, 6 or 10 days of treatment with the hepatocarcinogen beta-blocker DL-1-(2-nitro-3-methyl-phenoxy)-3-tert-butyl-amino-propan-2-ol (ZAMI 1305) were studied in male and female Wistar rats. In agreement with its sex-dependent oncogenicity, ZAMI 1305 administration causes DNA damage in the liver of the female but not of the male rat, with the only exception of 2 out of 4 males treated for 6 days. In female rat, the amount of DNA damage increases from 1 to 6 days of treatment, being unchanged at 10 days; a small portion of DNA is however damaged. ZAMI 1305 administration to female rat induces also: (i) an increase of the relative liver weight, of the DNA and RNA synthesizing activity; (ii) a decrease of the number of hepatocytes in mitosis; (iii) a minimal oval cell hyperplasia. When the same parameters were studied in ZAMI 1305-treated male rats, they were unaffected or changed to a less extent in respect to female rats.

Optical isomers of the hepatocarcinogenic beta-blocker ZAMI 1305: influence on nucleic acids synthesis and DNA integrity.

The influence on nucleic acids synthesis and DNA integrity of the D-isomer and of the DL-racemic form of the oncogenic beta-blocker 1-(2-nitro-3-methyl-phenoxy)-3-tert-butylamino-propan-2-ol (ZAMI 1305) and of the non-oncogenic beta-blocker propranolol was tested in vitro and in vivo. Both D- and DL-ZAMI 1305, when added in vitro to nuclei isolated from rat liver, cause inhibition of DNA and RNA synthesis and DNA fragmentation, as evaluated by alkaline sucrose gradient analysis, in a similar dose-dependent fashion. D- and DL-ZAMI 1305 also inhibit to a similar extent the activity of DNA polymerase alpha and beta from regenerating rat liver. When administered in vivo to female rats both D and DL-ZAMI 1305 cause a dose-dependent fragmentation of liver DNA. The D-isomer and DL-racemic form of the non-oncogenic beta-blocker propranolol inhibit DNA and RNA synthesis and cause DNA fragmentation when added in vitro to isolated liver nuclei, being instead without effect when administered in vivo.

[Zinc deficiency in mucoviscidosis]. / Carence en zinc au cours de la mucoviscidose.

UNLABELLED: Zinc deficiencies can induce dermatitis in subjects presenting cystic fibrosis. CASE REPORT: A patient, Clement, presented with a digestive form of cystic fibrosis. At four months of age, he presented a dermatitis similar to acrodermatitis enteropathica. Early clinical diagnosis and treatment led to a rapid response to zinc sulfate therapy. DISCUSSION: Less intestinal absorption, malnutrition, and diet are just some of the numerous reasons for the zinc deficiency in this case. Biological support is not necessary to begin the treatment.

Large beta-delayed neutron emission probabilities in the 78Ni region.

The beta-delayed neutron branching ratios (P{betan}) for nuclei near doubly magic 78Ni have been directly measured using a new method combining high-resolution mass separation, reacceleration, and digital beta-gamma spectroscopy of 238U fission products. The P{betan} values for the very neutron-rich isotopes ;{76-78}Cu and 83Ga were found to be much higher than previously reported and predicted. Revised calculations of the betan process, accounting for new mass measurements and an inversion of the pi2p{3/2} and pi1f{5/2} orbitals, are in better agreement with these new experimental results.

Alpha decay of 109I and its implications for the proton decay of 105Sb and the astrophysical rapid proton-capture process.

An alpha-decay branch of (1.4+/-0.4) x 10(-4) has been discovered in the decay of 109I, which predominantly decays via proton emission. The measured Q(alpha) value of 3918+/-21 keV allows the indirect determination of the Q value for proton emission from 105Sb of 356+/-22 keV, which is approximately of 130 keV more bound than previously reported. This result is relevant for the astrophysical rapid proton-capture process, which would terminate in the 105Sn(p,gamma)106Sb(p,gamma)107Te(alpha decay)103Sn cycle at the densities expected in explosive hydrogen burning scenarios, unless unusually strong pairing effects result in a 103Sn(p,gamma)104Sb(p,gamma)105Te(alpha decay)101Sn) cycle.

Streptococcus pneumoniae thoracic empyema in children: rapid diagnosis by using the Binax NOW immunochromatographic membrane test in pleural fluids.

AIM: To evaluate an immunochromatographic membrane test for Streptococcus pneumoniae antigen (Binax NOW, Inverness medical France) applied to pleural fluid samples. METHODS: Binax NOW was applied to the pleural fluids of 69 children with thoracic empyema, in comparison with conventional culture and molecular techniques. RESULTS: Binax NOW was positive on all 15 pleural fluid samples that yielded S. pneumoniae in culture, on two samples that yielded S. oralis and S. salivarius in culture and on 34 culture-negative samples. Fifteen of these 34 culture-negative samples were retrospectively tested by PCR methods, and 14 were shown to contain S. pneumoniae DNA. Thus, S. pneumoniae was identified by culture in 22% of samples and by Binax NOW in 69% of samples. CONCLUSION: Binax NOW may thus be useful for rapid diagnosis of S. pneumoniae thoracic empyema.