First Exploration of Monopole-Driven Shell Evolution above the N=126 Shell Closure: New Millisecond Isomers in

Isomer spectroscopy of heavy neutron-rich nuclei beyond the N=126 closed shell has been performed for the first time at the Radioactive Isotope Beam Factory of the RIKEN Nishina Center. New millisecond isomers have been identified at low excitation energies, 985.3(19) keV in ^{213}Tl and 874(5) keV in ^{215}Tl. The measured half-lives of 1.34(5) ms in ^{213}Tl and 3.0(3) ms in ^{215}Tl suggest spins and parities 11/2^{-} with the single proton-hole configuration πh_{11/2} as leading component. They are populated via E1 transitions by the decay of higher-lying isomeric states with proposed spin and parity 17/2^{+}, interpreted as arising from a single πs_{1/2} proton hole coupled to the 8^{+} seniority isomer in the ^{A+1}Pb cores. The lowering of the 11/2^{-} states is ascribed to an increase of the πh_{11/2} proton effective single-particle energy as the second νg_{9/2} orbital is filled by neutrons, owing to a significant reduction of the proton-neutron monopole interaction between the πh_{11/2} and νg_{9/2} orbitals. The new ms isomers provide the first experimental observation of shell evolution in the almost unexplored N>126 nuclear region below doubly magic ^{208}Pb.

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.

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)

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.

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.

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.

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.

La exposición crónica al uranio, un riesgo potencial de nefrotoxicidad / Uranium is a naturally occurring element widely distributed in the crust

El uranio es un elemento natural que se encuentra ampliamente distribuido en la corteza terrestre. Cierta cantidad de este metal se encuentra presente en los alimentos, en el aire, en el suelo y en el agua, por lo que el ser humano se encuentra expuesto al mismo de forma natural. Pero también puede ser objeto de una sobreexposición patológica como consecuencia de la deposición de uranio natural desde la atmósfera o debido a actividades industriales humanas que vierten productos de desecho directamente sobre el terreno. Actualmente la exposición debida a la actividad industrial se ha incrementado debido a que el uranio representa una de las pocas fuentes energéticas que cumplen con el “Protocolo de Kyoto”, sumándole la ventaja de que es muy económico. España, es uno de los países Europeos con más contenido de uranio en su suelo y por ello, susceptible de exposición natural, pero también industrial, ya que dada la demanda energética se están reabriendo algunas de sus minas. La nefrotoxicidad es el principal efecto observado tras exposición aguda a uranio. Este efecto se ha descrito en múltiples estudios realizados en animales de experimentación y en algunos casos de humanos expuestos a dosis elevadas de uranio de forma accidental. Sin embargo, la producción de daño renal por exposición crónica está poco documentada. Existen escasos estudios experimentales en los que se administren bajas dosis de uranio durante largos periodos de tiempo y los referidos en humanos son muy heterogéneos en cuanto a la vía de exposición, la dosis, el tipo de uranio etc, por lo que resulta muy difícil extraer conclusiones sobre los efectos renales por sobreexposición crónica. En esta revisión se pretende hacer una recopilación y discusión de gran parte de estudios epidemiológicos y de experimentación, a fin de obtener una idea de la nefrotoxicidad real que supone la exposición crónica a este metal para el ser humano (AU)

Certain amount of this metal is present in food, air, soil and water, for that humans are exposed to it naturally. But it can also be pathological overexposure as a result of natural uranium deposition from the atmosphere or due to human industrial activities that discharge waste products directly on the ground. Currently exposure due to industrial activity has increased because the uranium is one of the few sources of energy that meet the "Kyoto Protocol", adding the advantage that it is very economical. Spain is one of most European countries with uranium content in soil and thus susceptible to natural exposure, but also industrial, as given energy demand are reopening some of its mines. Nephrotoxicity is the main effect observed after acute exposure to uranium. This effect has been described in multiple studies in experimental animals and in some cases of humans accidentally exposed to high doses of uranium. However, the production of kidney damage from chronic exposure is poorly documented. There are few experimental studies in which low doses are administered uranium for long periods of time. Moreover, data in humans are very heterogeneous regarding the route of exposure, dose, type of uranium etc, so it is very difficult to draw findings on chronic renal effects of overexposure. In this review we tried to make a compilation and discussion of several epidemiological and experimental studies in order to get an idea of the real nephrotoxicity involving chronic exposure to this metal to humans (AU)

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.

Papel de la vía de Ras en un modelo de nefrotoxicidad inducida por cadmio. Efecto protector del antioxidante quercetina / Role of Ras signalling pathway in a model of cadmium-induced nephrotoxicity. Protective effect of the antioxidant quercetin

El cadmio (Cd) es un tóxico presente en el medio ambiente que afecta a los sistemas biológicos por varias rutas. Los mecanismos moleculares de su toxicidad no están bien definidos. Nosotros hemos demostrado recientemente en un modelo de administración crónica de Cd en ratas, que la quercetina, un potente “scavenger" de radicales libres de oxígeno, tiene un efecto protector sobre la nefrotoxicidad inducida por Cd. La potente actividad antioxidante de la quercetina pudiera ser la responsable de este efecto protector. Sin embargo, el Cd activa múltiples rutas de señalización relacionadas con respuestas celulares frente al estrés. Ras es un miembro de la familia de las pequeñas GTPasas, con una gran variedad de funciones que incluyen la regulación de genes de expresión y proliferación celular. Nuestro objetivo en este trabajo fue estudiar el efecto del cadmio y la quercetina en el proceso proliferativo relacionado con las vías de señalización mediadas por Ras. El estudio se realizó durante nueve semanas con ratas Wistar. Se dividieron en cuatro grupos: 1) Grupo control, 2) Grupo cadmio: 1,2 mg/Kg/día, s.c., 3) Grupo quercetina: 50 mg/Kg/día, i.p., 4) Grupo cadmio-quercetina: animales tratados con cadmio y quercetina a las dosis y vías de administración anteriormente descritas. Para valorar la toxicidad renal se determinó la excreción urinaria de proteínas y enzimas marcadoras de necrosis tubular, así como las concentraciones plasmáticas de creatinina y urea. La expresión y activación renal de Ras se evaluó mediante Western blot e inmunohistoquímica. La proliferación celular se determinó por detección del antígeno Ki-67. Los resultados mostraron que la co-administración de cadmio y quercetina mejoró la función renal alterada por la exposición a cadmio. Por otra parte, se observó una mayor activación de Ras y una mayor proliferación celular en los riñones de los animales tratados con cadmio. El tratamiento con quercetina redujo la activación renal de Ras y el número de células en proliferación. Nuestros resultados sugieren que el efecto protector de la quercetina sobre la nefrotoxicidad inducida por cadmio pudiera deberse a la inhibición de esta ruta de señalización (AU)

Cadmium (Cd) is an ubiquitous environmental toxicant that affects biological systems in various ways. The molecular mechanisms of its toxicity are not yet well defined. We have recently reported in an experimental model of chronic cadmium administration in rats, that quercetin, a potent oxygen free radical scavenger, has a protective effect on cadmium-induced nephrotoxicity. Quercetin´s strong antioxidant activity could be responsible for the protective effect. However, Cd activates multiple signal transduction pathways related to cellular responses to stress. Ras is a member of a family of small GTPases with a great variety of functions including regulation of gene expression and cell proliferation. Our aim in this work was to study the effect of Cd and quercetin on the proliferation related to Ras-mediated signal transduction pathways. Experiments were carried out in male Wistar rats during nine weeks. Rats were distributed in four experimental groups: 1) control rats; 2) cadmium group (1,2 mg Cd/Kg/day s.c.); 3) quercetin group (50 mg/Kg/day, i.p.) and 4) cadmium-quercetin group (Cd and quercetin at the same doses as in the groups 2 and 3 respectively). Renal toxicity was evaluated by measuring urinary excretion of proteins and enzyme markers of tubular necrosis, as well as plasma concentrations of creatinine and urea. Renal expression of Ras and Ras activation was assessed by Western blot and inmuhistochemistry. Assessment of cell proliferation was evaluated by detection of the Ki-67 antigen. Animals that received both Cd and quercetin showed a better renal function than those receiving Cd alone. On the other hand, Cd increased renal Ras activation and cell proliferation. Quercetin treatment reduced Ras activation and the number of cells in proliferation. Our results suggest that the protective effect of quercetin on cadmium-induced nephrotoxicity could be associated with the inhibition of Ras signal transduction pathway (AU)

Mecanismos implicados en la nefrotoxicidad producida por aminoglucósidos / Pathogenic factors in aminoglycoside-induced nephrotoxicity

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