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.

ß-Delayed One and Two Neutron Emission Probabilities Southeast of

The ß-delayed one- and two-neutron emission probabilities (P_{1n} and P_{2n}) of 20 neutron-rich nuclei with N≥82 have been measured at the RIBF facility of the RIKEN Nishina Center. P_{1n} of ^{130,131}Ag, ^{133,134}Cd, ^{135,136}In, and ^{138,139}Sn were determined for the first time, and stringent upper limits were placed on P_{2n} for nearly all cases. ß-delayed two-neutron emission (ß2n) was unambiguously identified in ^{133}Cd and ^{135,136}In, and their P_{2n} were measured. Weak ß2n was also detected from ^{137,138}Sn. Our results highlight the effect of the N=82 and Z=50 shell closures on ß-delayed neutron emission probability and provide stringent benchmarks for newly developed macroscopic-microscopic and self-consistent global models with the inclusion of a statistical treatment of neutron and γ emission. The impact of our measurements on r-process nucleosynthesis was studied in a neutron star merger scenario. Our P_{1n} and P_{2n} have a direct impact on the odd-even staggering of the final abundance, improving the agreement between calculated and observed Solar System abundances. The odd isotope fraction of Ba in r-process-enhanced (r-II) stars is also better reproduced using our new data.

Radiative Width of the Hoyle State from γ-Ray Spectroscopy.

The cascading 3.21 and 4.44 MeV electric quadrupole transitions have been observed from the Hoyle state at 7.65 MeV excitation energy in ^{12}C, excited by the ^{12}C(p,p^{'}) reaction at 10.7 MeV proton energy. From the proton-γ-γ triple coincidence data, a value of Γ_{rad}/Γ=6.2(6)×10^{-4} was obtained for the radiative branching ratio. Using our results, together with Γ_{π}^{E0}/Γ from Eriksen et al. [Phys. Rev. C 102, 024320 (2020)PRVCAN2469-998510.1103/PhysRevC.102.024320] and the currently adopted Γ_{π}(E0) values, the radiative width of the Hoyle state is determined as Γ_{rad}=5.1(6)×10^{-3} eV. This value is about 34% higher than the currently adopted value and will impact models of stellar evolution and nucleosynthesis.

Two-Proton Radioactivity of

In an experiment with the BigRIPS separator at the RIKEN Nishina Center, we observed two-proton (2p) emission from ^{67}Kr. At the same time, no evidence for 2p emission of ^{59}Ge and ^{63}Se, two other potential candidates for this exotic radioactivity, could be observed. This observation is in line with Q value predictions which pointed to ^{67}Kr as being the best new candidate among the three for two-proton radioactivity. ^{67}Kr is only the fourth 2p ground-state emitter to be observed with a half-life of the order of a few milliseconds. The decay energy was determined to be 1690(17) keV, the 2p emission branching ratio is 37(14)%, and the half-life of ^{67}Kr is 7.4(30) ms.

Isospin Mixing in

The isospin mixing was deduced in the compound nucleus ^{80}Zr at an excitation energy of E^{*}=54 MeV from the γ decay of the giant dipole resonance. The reaction ^{40}Ca+^{40}Ca at E_{beam}=136 MeV was used to form the compound nucleus in the isospin I=0 channel, while the reaction ^{37}Cl+^{44}Ca at E_{beam}=95 MeV was used as the reference reaction. The γ rays were detected with the AGATA demonstrator array coupled with LaBr_{3}:Ce detectors. The temperature dependence of the isospin mixing was obtained and the zero-temperature value deduced. The isospin-symmetry-breaking correction δ_{C} used for the Fermi superallowed transitions was extracted and found to be consistent with ß-decay data.

Hindered Gamow-Teller decay to the odd-odd N=Z (62)Ga: absence of proton-neutron T=0 condensate in A=62.

Search for a new kind of superfluidity built on collective proton-neutron pairs with aligned spin is performed studying the Gamow-Teller decay of the T=1, J(π)=0+ ground state of (62)Ge into excited states of the odd-odd N=Z nucleus (62)Ga. The experiment is performed at GSI Helmholtzzentrum für Shwerionenforshung with the (62)Ge ions selected by the fragment separator and implanted in a stack of Si-strip detectors, surrounded by the RISING Ge array. A half-life of T1/2=82.9(14) ms is measured for the (62)Ge ground state. Six excited states of (62)Ga, populated below 2.5 MeV through Gamow-Teller transitions, are identified. Individual Gamow-Teller transition strengths agree well with theoretical predictions of the interacting shell model and the quasiparticle random phase approximation. The absence of any sizable low-lying Gamow-Teller strength in the reported beta-decay experiment supports the hypothesis of a negligible role of coherent T=0 proton-neutron correlations in (62)Ga.

Half-life systematics across the N=126 shell closure: role of first-forbidden transitions in the ß decay of heavy neutron-rich nuclei.

This Letter reports on a systematic study of ß-decay half-lives of neutron-rich nuclei around doubly magic (208)Pb. The lifetimes of the 126-neutron shell isotone (204)Pt and the neighboring (200-202)Ir, (203)Pt, (204)Au are presented together with other 19 half-lives measured during the "stopped beam" campaign of the rare isotope investigations at GSI collaboration. The results constrain the main nuclear theories used in calculations of r-process nucleosynthesis. Predictions based on a statistical macroscopic description of the first-forbidden ß strength reveal significant deviations for most of the nuclei with N<126. In contrast, theories including a fully microscopic treatment of allowed and first-forbidden transitions reproduce more satisfactorily the trend in the measured half-lives for the nuclei in this region, where the r-process pathway passes through during ß decay back to stability.

Isospin character of low-lying pygmy dipole states in 208Pb via inelastic scattering of 17O ions.

The properties of pygmy dipole states in 208Pb were investigated using the 208Pb(17O, 17O'γ) reaction at 340 MeV and measuring the γ decay with high resolution with the AGATA demonstrator array. Cross sections and angular distributions of the emitted γ rays and of the scattered particles were measured. The results are compared with (γ, γ') and (p, p') data. The data analysis with the distorted wave Born approximation approach gives a good description of the elastic scattering and of the inelastic excitation of the 2+ and 3- states. For the dipole transitions a form factor obtained by folding a microscopically calculated transition density was used for the first time. This has allowed us to extract the isoscalar component of the 1- excited states from 4 to 8 MeV.

Biotransformation of three pharmaceutical active compounds by the fungus Phanerochaete chrysosporium in a fed batch stirred reactor under air and oxygen supply.

White-rot fungi are a group of microorganisms capable of degrading xenobiotic compounds, such as polycyclic aromatic hydrocarbons or synthetic dyes, by means of the action of extracellular oxidative enzymes secreted during secondary metabolism. In this study, the transformation of three anti-inflammatory drugs: diclofenac, ibuprofen and naproxen were carried out by pellets of Phanerochaete chrysosporium in fed-batch bioreactors operating under continuous air supply or periodic pulsation of oxygen. The performance of the fungal reactors was steady over a 30-day treatment and the effect of oxygen pulses on the pellet morphology was evidenced. Complete elimination of diclofenac was achieved in the aerated and the oxygenated reactors, even with a fast oxidation rate in the presence of oxygen (77% after 2 h), reaching a total removal after 23 h. In the case of ibuprofen, this compound was completely oxidized under air and oxygen supply. Finally, naproxen was oxidized in the range of 77 up to 99% under both aeration conditions. These findings demonstrate that the oxidative capability of this microorganism for the anti-inflammatory drugs is not restricted to an oxygen environment, as generally accepted, since the fungal reactor was able to remove these compounds under aerated and oxygenated conditions. This result is very interesting in terms of developing viable reactors for the oxidation of target compounds as the cost of aeration can be significantly reduced.

Effect of the flavonoid quercetin on cadmium-induced hepatotoxicity.

The present study was designed to evaluate whether treatment with quercetin exerts any beneficial effect on cadmium (Cd)-induced hepatotoxicity in order to establish the possible protective mechanisms of quercetin. Wistar rats were distributed in four experimental groups: control, Cd, quercetin, and Cd+quercetin. Hepatic toxicity was evaluated by measuring plasma concentrations of markers of hepatic injury. The activity of antioxidant enzymes in liver was also measured. Hepatic expression of metallothioneins (MT), and endothelial nitric oxide synthase (eNOS) was assayed by Western and Northern blot. Our results demonstrated that Cd administration induced an increased marker enzyme activity in plasma. This effect was not inhibited by quercetin. However, the administration of quercetin softened Cd-induced oxidative damage. MT levels in liver were substantially increased when the animals received Cd and quercetin. Hepatic eNOS expression was significantly increased after treatment with Cd and quercetin, being this increase higher than in animals receiving Cd alone. In conclusion, in this experimental model, quercetin was not able to prevent the Cd-induced liver damage although the animals that received both, Cd and quercetin showed a marked improvement in oxidative stress and an increase in the MT and eNOS expression. These results suggest that other mechanisms different to oxidative stress could be involved in hepatic damage.

Protective effect of quercetin on experimental chronic cadmium nephrotoxicity in rats is based on its antioxidant properties.

Oxidative stress can play a key role in Cd-induced dysfunctions. Quercetin is a potent oxygen free radicals scavenger and a metal chelator. Our aim was to study the effect of quercetin on Cd-induced kidney damage and oxidative stress as well as its mechanism of action. Wistar rats were distributed in four experimental groups: control rats; Cd; quercetin and Cd+quercetin. Renal toxicity was evaluated by measuring urinary excretion of proteins, albumin, glucose and enzymes markers of tubular necrosis, as well as plasma concentration of creatinine. Plasma TBARS concentration and activity of antioxidant enzymes in kidney were also measured. Renal cell damage was assessed by electron microscopy. Animals that received both Cd and quercetin showed a better renal function than those receiving Cd alone. Cd-induced tubular lesions were markedly reduced in rats that also received quercetin. Cd-induced increase in plasma TBARS was prevented by the administration of quercetin. Total plasma antioxidants and renal superoxide dismutase and glutathione-reductase activities were higher in the group that received Cd and quercetin than in rats that received Cd alone. Quercetin administration does not modify the renal content or the urinary excretion of Cd. In conclusion, quercetin treatment prevents renal tubular damage and increased oxidative stress induced by chronic Cd administration, most probably throughout its antioxidant properties.

Neurotoxicidad por exposición a metales pesados: evidencias y cuestiones por resolver / Neurotoxicity due to exposure to heavy metals: evidence and unresolved issues

Los metales pesados son un grupo de agentes químicos que están presentes en la corteza terrestre en concentraciones variables. Muchos de estos compuestos tienen una gran importancia en el mundo actual, ya que se emplean en numerosos procesos industriales. Debido a su abundancia en la naturaleza y considerando que las investigaciones realizadas durante los últimos años han demostrado la implicación de los metales pesados en el desarrollo de numerosos procesos patológicos, se ha realizado una revisión bibliográfica con el objetivo de evaluar la relación entre la exposición a determinados metales pesados y el desarrollo de neurotoxicidad. Este análisis se ha llevado a cabo empleando la base de datos Medline y, tras un primer screening de las referencias encontradas, se ha centrado en la evaluación de siete agentes: aluminio, plomo, arsénico, mercurio, cadmio, manganeso y talio. La neurotoxicidad desarrollada tras la exposición aguda o crónica se debe a su capacidad para atravesar la barrera hematoencefálica. Algunos de los mecanismos de toxicidad no se han podido definir completamente aún, pero en casi todas las investigaciones se han relacionado con la capacidad de interferir con los procesos biológicos y de inducir estrés oxidativo y apoptosis neuronal. Existen determinadas patologías para las que se ha encontrado una relación directa con la exposición. Sin embargo, en el campo de las enfermedades neurodegenerativas la evidencia encontrada es menos concluyente. (AU)

Heavy metals are a group of chemical agents that are present in the Earth crust in varying concentrations. Many of these compounds are of great importance in today’s world, as they are used in many industrial processes. Due to their abundance in nature and considering that research carried out in recent years has shown the involvement of heavy metals in the development of numerous pathological processes, a bibliographic review has been carried out with the aim of evaluating the relationship between exposure to certain heavy metals and the development of neurotoxicity. This analysis has been carried out using the Medline database and, after a first screening of the references, it has focused on the evaluation of seven agents: aluminum, lead, arsenic, mercury, cadmium, manganese and thallium. Neurotoxicity developed after acute or chronic exposure has been shown to be due to its ability to cross the blood-brain barrier. Some of the toxicity mechanisms have not yet been fully defined, but in almost all investigations they have been related to the ability to interfere with biological processes and to induce oxidative stress and neuronal apoptosis. There are certain pathologies for which a direct relationship with exposure has been found. However, in the field of neurodegenerative diseases, the evidence found is less conclusive. (AU)

Serological monitoring of vesicular stomatitis New Jersey virus in enzootic regions of Costa Rica.

The activity of vesicular stomatitis viruses was monitored on 3 dairy farms in Costa Rica. Antibody levels were measured and clinical disease monitored in 165 cattle during a 20 month period (1986-1988). Vesicular stomatitis New Jersey (VS NJ) virus was shown to be enzootic on these farms by a 94.2% prevalence of neutralizing antibody; this did not vary significantly between herds. The mean prevalence of antibody to vesicular stomatitis Indiana (VS IN) virus was 15.2%, but was significantly higher in 1 herd. A total of 25 cases (annual incidence rate of 9%) of clinical vesicular stomatitis (VS) was reported. VS NJ virus was identified as the causal agent by detection of VS NJ virus antigens by the complement fixation test. VS NJ virus was isolated in 11 cases. All episodes of disease occurred between November and January, the beginning of the dry season. Most animals maintained stable neutralizing antibody titers throughout the study, and all diseased animals were previously seropositive to VS NJ virus. A total of 31 animals with neutralizing antibodies to VS NJ virus had a VS NJ virus-specific IgM response, and 6 animals had IgM responses that persisted for as long as 6 months. There was no relation between IgM responses and clinical disease occurrence. VS NJ virus persisted predominantly as a subclinical infection in cattle throughout the year in enzootic areas of Costa Rica. The humoral response did not prevent reinfection with VS NJ virus.

Effect of cicletanine on renal cGMP production.

The aim of the present study was to assess the effect of cicletanine on renal cGMP production. To do so we measured mean arterial pressure (MAP), creatinine clearance (CC), and urinary excretion of electrolytes and cGMP under basal conditions and after 6 h of cicletanine administration (10 and 15 mg/kg body weight by oral gavage) in conscious Wistar rats. Also, the in vitro effect of cicletanine was assessed by incubating renal slices and isolated rat glomeruli with two concentrations of cicletanine (0.1 and 1 mM) for different times (1, 2, 5, and 30 min) in the presence of 3-isobutyl-1-methylxanthine. Oral administration of cicletanine induced an increase in urinary flow (V) and the urinary excretion of electrolytes and cGMP, with no changes in CC. In addition, a significant decrease in MAP was observed, but only with the lower dose. Incubation with cicletanine did not induce significant changes in cGMP production in glomeruli or renal slices. These results show that cicletanine, administered in vivo at diuretic and antihypertensive doses, induces an increase in urinary cGMP excretion.

Effect of maternal cholestasis on biliary lipid and bile acid secretion in the infant rat.

Partial and reversible impairment of bile formation has been reported to occur in the offspring of rats undergoing common bile duct ligation during the last third of pregnancy. This situation was defined as latent cholestasis of the neonate and was suggested to be related to the multilamellar bodies partially occupying the canalicular lumen. The current study was undertaken to investigate the presence of alterations in the secretion of biliary lipids in these infant rats. Using both high-performance liquid chromatography (HPLC) and gas chromatography-mass spectrometry (GC-MS) analyses, no changes caused by maternal cholestasis were found in either the conjugation pattern, or in the ratio of primary to secondary major bile acids in bile samples collected from 4-week-old and 8-week-old rats. However, a decrease in the proportion of cholate together with an increase in the amount of alpha- and omega-muricholate were found at 4 weeks of age. These changes were different from those observed in the pattern of maternal plasma bile acids, in which beta-, but not alpha-muricholate, concentrations were increased. Moreover, studies performed by labeling the bile acid pool of the cholestatic mother-fetus tandem with [14C]glycocholic acid (GC) at day 16 of pregnancy indicated that only a minor proportion (approximately 10%) of bile acids found in 4-week-old pups was of maternal origin. Changes in the bile acid pool composition were fully reversed by 8 weeks of age. Bile lecithin and cholesterol output were determined by enzymatic techniques, both under basal conditions and during stepwise taurocholate (TC) infusion. At the time when multilamellar bodies were found, i.e., 4 weeks after birth, no change in either nonstimulated or TC-induced cholesterol output was observed. By contrast, both spontaneous and TC-induced lecithin secretion were markedly higher (+200%) in pups of cholestatic mothers as compared with control rats. These differences were abolished at 8 weeks of age. At this time, cholesterol output was significantly lower than that found in younger animals. This reduction was more pronounced in the control than in the cholestatic group. Histological examination of liver samples collected from the cholestatic group at 4 weeks of age revealed the presence of multilamellar bodies not only in the canalicular lumen but also within vesicular structures located in the pericanalicular area or near the Golgi apparatus. Both intracellular and intracanalicular bodies were present before and after TC infusion for 2 hours. These results indicate that maternal cholestasis in rats induces profound alterations in biliary lipids and bile acid secretion in their pups. Because bile acids are important activators of different steps responsible for biliary lipid secretion (intracellular trafficking, releasing into bile, and solubilization), alterations in maternal bile acid pool size and composition may affect the fetal development of biliary lipid secretion mechanisms, which may result in the appearance of multilamellar bodies within bile canaliculi, which in turn may be involved in the reversible latent cholestasis observed in these infants rats.

Reversible impairment of neonatal hepatobiliary function by maternal cholestasis.

The effect of total blockage of maternal biliary excretion during the last third of the pregnancy on the maturation of hepatobiliary function was investigated in neonatal rats. Extrahepatic obstruction of the common bile duct on day 14 of pregnancy induced a marked enhancement in serum bilirubin--mainly conjugated bilirubin--and bile acid concentrations as compared with sham-operated pregnant rats. Excretion of bile acids by the kidney was significantly increased, whereas fecal elimination of these compounds was almost abolished. Most of the cholestatic mothers (CMs) (77%) were able to carry pregnancy to term and lactation until weaning (21 days after birth). The body and liver weights of their offspring were lower than for offspring of control healthy mothers in all postnatal periods considered. Serum bile acid concentrations were higher in the fetuses and neonates of CMs. This difference was evident up to 1 week after weaning and disappeared in young adult animals (8 weeks old). When the bile secretion rate was investigated in these animals at 4 or 8 weeks of age, no significant difference was found as far as nonstimulated bile flow and bile acid output was concerned. However, the biliary response to stepwise sodium taurocholate (TC) intravenous infusion showed that 4-week-old neonates of CMs had impaired bile acid secretion. Moreover, the maximal secretion rate (SRmax) for TC was significantly reduced (-30%), whereas the choleretic ability of taurocholate was not modified. This alteration was not selective for bile acids. The SRmax for bromosulfophthalein (BSP) was also significantly lowered (-40%). These dysfunctions were overcome during subsequent development. No impaired biliary response to either TC or BSP infusion was observed at 8 weeks of age. Morphological abnormalities in the canaliculi were found in animals with impaired biliary function. In summary, these results indicate that maternal cholestasis may profoundly but transiently impair the normal liver maturation. The importance of the implications derived from these findings both in the nutrition and management of human neonates demands further evaluation of the hepatobiliary function of babies born after alterations of fetal-maternal bile acid homeostasis, such as in maternal obstetric cholestasis.