Shape Changes in the Mirror Nuclei

We studied the proton-rich T_{z}=-1 nucleus ^{70}Kr through inelastic scattering at intermediate energies in order to extract the reduced transition probability, B(E2;0^{+}→2^{+}). Comparison with the other members of the A=70 isospin triplet, ^{70}Br and ^{70}Se, studied in the same experiment, shows a 3σ deviation from the expected linearity of the electromagnetic matrix elements as a function of T_{z}. At present, no established nuclear structure theory can describe this observed deviation quantitatively. This is the first violation of isospin symmetry at this level observed in the transition matrix elements. A heuristic approach may explain the anomaly by a shape change between the mirror nuclei ^{70}Kr and ^{70}Se contrary to the model predictions.

Angular momentum generation in nuclear fission.

When a heavy atomic nucleus splits (fission), the resulting fragments are observed to emerge spinning1; this phenomenon has been a mystery in nuclear physics for over 40 years2,3. The internal generation of typically six or seven units of angular momentum in each fragment is particularly puzzling for systems that start with zero, or almost zero, spin. There are currently no experimental observations that enable decisive discrimination between the many competing theories for the mechanism that generates the angular momentum4-12. Nevertheless, the consensus is that excitation of collective vibrational modes generates the intrinsic spin before the nucleus splits (pre-scission). Here we show that there is no significant correlation between the spins of the fragment partners, which leads us to conclude that angular momentum in fission is actually generated after the nucleus splits (post-scission). We present comprehensive data showing that the average spin is strongly mass-dependent, varying in saw-tooth distributions. We observe no notable dependence of fragment spin on the mass or charge of the partner nucleus, confirming the uncorrelated post-scission nature of the spin mechanism. To explain these observations, we propose that the collective motion of nucleons in the ruptured neck of the fissioning system generates two independent torques, analogous to the snapping of an elastic band. A parameterization based on occupation of angular momentum states according to statistical theory describes the full range of experimental data well. This insight into the role of spin in nuclear fission is not only important for the fundamental understanding and theoretical description of fission, but also has consequences for the γ-ray heating problem in nuclear reactors13,14, for the study of the structure of neutron-rich isotopes15,16, and for the synthesis and stability of super-heavy elements17,18.

Pseudospin Symmetry and Microscopic Origin of Shape Coexistence in the

Lifetime measurements of excited states of the light N=52 isotones ^{88}Kr, ^{86}Se, and ^{84}Ge have been performed, using the recoil distance Doppler shift method and VAMOS and AGATA spectrometers for particle identification and gamma spectroscopy, respectively. The reduced electric quadrupole transition probabilities B(E2;2^{+}→0^{+}) and B(E2;4^{+}→2^{+}) were obtained for the first time for the hard-to-reach ^{84}Ge. While the B(E2;2^{+}→0^{+}) values of ^{88}Kr, ^{86}Se saturate the maximum quadrupole collectivity offered by the natural valence (3s, 2d, 1g_{7/2}, 1h_{11/2}) space of an inert ^{78}Ni core, the value obtained for ^{84}Ge largely exceeds it, suggesting that shape coexistence phenomena, previously reported at N≲49, extend beyond N=50. The onset of collectivity at Z=32 is understood as due to a pseudo-SU(3) organization of the proton single-particle sequence reflecting a clear manifestation of pseudospin symmetry. It is realized that the latter provides actually reliable guidance for understanding the observed proton and neutron single particle structure in the whole medium-mass region, from Ni to Sn, pointing towards the important role of the isovector-vector ρ field in shell-structure evolution.

Neutron Skin Effects in Mirror Energy Differences: The Case of

Energy differences between analogue states in the T=1/2 ^{23}Mg-^{23}Na mirror nuclei have been measured along the rotational yrast bands. This allows us to search for effects arising from isospin-symmetry-breaking interactions (ISB) and/or shape changes. Data are interpreted in the shell model framework following the method successfully applied to nuclei in the f_{7/2} shell. It is shown that the introduction of a schematic ISB interaction of the same type of that used in the f_{7/2} shell is needed to reproduce the data. An alternative novel description, applied here for the first time, relies on the use of an effective interaction deduced from a realistic charge-dependent chiral nucleon-nucleon potential. This analysis provides two important results: (i) The mirror energy differences give direct insight into the nuclear skin; (ii) the skin changes along the rotational bands are strongly correlated with the difference between the neutron and proton occupations of the s_{1/2} "halo" orbit.

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.

Risk factors for immersion pulmonary edema: hyperoxia does not attenuate pulmonary hypertension associated with cold water-immersed prone exercise at 4.7 ATA.

Hyperoxia has been shown to attenuate the increase in pulmonary artery (PA) pressure associated with immersed exercise in thermoneutral water, which could serve as a possible preventive strategy for the development of immersion pulmonary edema (IPE). We tested the hypothesis that the same is true during exercise in cold water. Six healthy volunteers instrumented with arterial and PA catheters were studied during two 16-min exercise trials during prone immersion in cold water (19.9-20.9°C) in normoxia [0.21 atmospheres absolute (ATA)] and hyperoxia (1.75 ATA) at 4.7 ATA. Heart rate (HR), Fick cardiac output (CO), mean arterial pressure (MAP), pulmonary artery pressure (PAP), pulmonary artery wedge pressure (PAWP), central venous pressure (CVP), arterial and venous blood gases, and ventilatory parameters were measured both early (E, 5-6 min) and late (L, 15-16 min) in exercise. During exercise at an average oxygen consumption rate (Vo(2)) of 2.38 l/min, [corrected] CO, CVP, and pulmonary vascular resistance were not affected by inspired (Vo(2)) [corrected] or exercise duration. Minute ventilation (Ve), alveolar ventilation (Va), and ventilation frequency (f) were significantly lower in hyperoxia compared with normoxia (mean ± SD: Ve 58.8 ± 8.0 vs. 65.1 ± 9.2, P = 0.003; Va 40.2 ± 5.4 vs. 44.2 ± 9.0, P = 0.01; f 25.4 ± 5.4 vs. 27.2 ± 4.2, P = 0.04). Mixed venous pH was lower in hyperoxia compared with normoxia (7.17 ± 0.07 vs. 7.20 ± 0.07), and this result was significant early in exercise (P = 0.002). There was no difference in mean PAP (MPAP: 28.28 ± 8.1 and 29.09 ± 14.3 mmHg) or PAWP (18.0 ± 7.6 and 18.7 ± 8.7 mmHg) between normoxia and hyperoxia, respectively. PAWP decreased from early to late exercise in hyperoxia (P = 0.002). These results suggest that the increase in pulmonary vascular pressures associated with cold water immersion is not attenuated with hyperoxia.

Effects of head and body cooling on hemodynamics during immersed prone exercise at 1 ATA.

Immersion pulmonary edema (IPE) is a condition with sudden onset in divers and swimmers suspected to be due to pulmonary arterial or venous hypertension induced by exercise in cold water, although it does occur even with adequate thermal protection. We tested the hypothesis that cold head immersion could facilitate IPE via a reflex rise in pulmonary vascular pressure due solely to cooling of the head. Ten volunteers were instrumented with ECG and radial and pulmonary artery catheters and studied at 1 atm absolute (ATA) during dry and immersed rest and exercise in thermoneutral (29-31 degrees C) and cold (18-20 degrees C) water. A head tent varied the temperature of the water surrounding the head independently of the trunk and limbs. Heart rate, Fick cardiac output (CO), mean arterial pressure (MAP), mean pulmonary artery pressure (MPAP), pulmonary artery wedge pressure (PAWP), and central venous pressure (CVP) were measured. MPAP, PAWP, and CO were significantly higher in cold pool water (P < or = 0.004). Resting MPAP and PAWP values (means +/- SD) were 20 +/- 2.9/13 +/- 3.9 (cold body/cold head), 21 +/- 3.1/14 +/- 5.2 (cold/warm), 14 +/- 1.5/10 +/- 2.2 (warm/warm), and 15 +/- 1.6/10 +/- 2.6 mmHg (warm/cold). Exercise values were higher; cold body immersion augmented the rise in MPAP during exercise. MAP increased during immersion, especially in cold water (P < 0.0001). Except for a transient additive effect on MAP and MPAP during rapid head cooling, cold water on the head had no effect on vascular pressures. The results support a hemodynamic cause for IPE mediated in part by cooling of the trunk and extremities. This does not support the use of increased head insulation to prevent IPE.

Predictors of increased PaCO2 during immersed prone exercise at 4.7 ATA.

During diving, arterial Pco(2) (Pa(CO(2))) levels can increase and contribute to psychomotor impairment and unconsciousness. This study was designed to investigate the effects of the hypercapnic ventilatory response (HCVR), exercise, inspired Po(2), and externally applied transrespiratory pressure (P(tr)) on Pa(CO(2)) during immersed prone exercise in subjects breathing oxygen-nitrogen mixes at 4.7 ATA. Twenty-five subjects were studied at rest and during 6 min of exercise while dry and submersed at 1 ATA and during exercise submersed at 4.7 ATA. At 4.7 ATA, subsets of the 25 subjects (9-10 for each condition) exercised as P(tr) was varied between +10, 0, and -10 cmH(2)O; breathing gas Po(2) was 0.7, 1.0, and 1.3 ATA; and inspiratory and expiratory breathing resistances were varied using 14.9-, 11.6-, and 10.2-mm-diameter-aperture disks. During exercise, Pa(CO(2)) (Torr) increased from 31.5 +/- 4.1 (mean +/- SD for all subjects) dry to 34.2 +/- 4.8 (P = 0.02) submersed, to 46.1 +/- 5.9 (P < 0.001) at 4.7 ATA during air breathing and to 49.9 +/- 5.4 (P < 0.001 vs. 1 ATA) during breathing with high external resistance. There was no significant effect of inspired Po(2) or P(tr) on Pa(CO(2)) or minute ventilation (Ve). Ve (l/min) decreased from 89.2 +/- 22.9 dry to 76.3 +/- 20.5 (P = 0.02) submersed, to 61.6 +/- 13.9 (P < 0.001) at 4.7 ATA during air breathing and to 49.2 +/- 7.3 (P < 0.001) during breathing with resistance. We conclude that the major contributors to increased Pa(CO(2)) during exercise at 4.7 ATA are increased depth and external respiratory resistance. HCVR and maximal O(2) consumption were also weakly predictive. The effects of P(tr), inspired Po(2), and O(2) consumption during short-term exercise were not significant.

Contributions of endothelial and neuronal nitric oxide synthases to cerebrovascular responses to hyperoxia.

Hyperoxia causes a transient decrease in CBF, followed by a later rise. The mediators of these effects are not known. We used mice lacking endothelial or neuronal nitric oxide synthase (NOS) isoforms (eNOS-/- and nNOS-/- mice) to study the roles of the NOS isoforms in mediating changes in cerebral vascular tone in response to hyperoxia. Resting regional cerebral blood flow (rCBF) did not differ between wild type (WT), eNOS-/- mice, and nNOS-/- mice. eNOS-/- mice showed decreased cerebrovascular reactivities to NG-nitro-L-arginine methyl ester (L-NAME), PAPA NONOate, acetylcholine (Ach), and SOD1. In response to hyperbaric oxygen (HBO2) at 5 ATA, WT and nNOS-/- mice showed decreases in rCBF over 30 minutes, but eNOS-/- mice did not. After 60 minutes HBO2, rCBF increased more in WT mice than in eNOS-/- or nNOS-/- mice. Brain NO-metabolites (NOx) decreased in WT and eNOS-/- mice within 30 minutes of HBO2, but after 45 minutes, NOx rose above control levels, whereas they did not change in nNOS-/- mice. Brain 3NT increased during HBO2 in WT and eNOS-/- but did not change in nNOS-/- mice. These results suggest that modulation of eNOS-derived NO by HBO2 is responsible for the early vasoconstriction responses, whereas late HBO2-induced vasodilation depends upon both eNOS and nNOS.

Effects of age and exercise on physiological dead space during simulated dives at 2.8 ATA.

Physiological dead space (Vds), end-tidal CO(2) (Pet(CO(2))), and arterial CO(2) (Pa(CO(2))) were measured at 1 and 2.8 ATA in a dry hyperbaric chamber in 10 older (58-74 yr) and 10 younger (19-39 yr) air-breathing subjects during rest and two levels of upright exercise on a cycle ergometer. At pressure, Vd (liters btps) increased from 0.34 +/- 0.09 (mean +/- SD of all subjects for normally distributed data, median +/- interquartile range otherwise) to 0.40 +/- 0.09 (P = 0.0060) at rest, 0.35 +/- 0.13 to 0.45 +/- 0.11 (P = 0.0003) during light exercise, and 0.38 +/- 0.17 to 0.45 +/- 0.13 (P = 0.0497) during heavier exercise. During these conditions, Pa(CO(2)) (Torr) increased from 33.8 +/- 4.2 to 35.7 +/- 4.4 (P = 0.0059), 35.3 +/- 3.2 to 39.4 +/- 3.1 (P < 0.0001), and 29.6 +/- 5.6 to 37.4 +/- 6.5 (P < 0.0001), respectively. During exercise, Pet(CO(2)) overestimated Pa(CO(2)), although the absolute difference was less at pressure. Capnography poorly estimated Pa(CO(2)) during exercise at 1 and 2.8 ATA because of wide variability. Older subjects had higher Vd at 1 ATA but similar changes in Vd, Pa(CO(2)), and Pet(CO(2)) at pressure. These results are consistent with an effect of increased gas density.

Nitric oxide production is enhanced in rat brain before oxygen-induced convulsions.

Central nervous system oxygen toxicity (CNS O2 toxicity) is preceded by release of hyperoxic vasoconstriction, which increases regional cerebral blood flow (rCBF). These increases in rCBF precede the onset of O2-induced convulsions. We have tested the hypothesis that hyperbaric oxygen (HBO2) stimulates NO* production in the brain that leads to hyperemia and anticipates electrical signs of neurotoxicity. We measured rCBF and EEG responses in rats exposed at 4 to 6 atmospheres (ATA) of HBO2 and correlated them with brain interstitial NO* metabolites (NO(x)) as an index of NO* production. During exposures to hyperbaric oxygen rCBF decreased at 4 ATA, decreased for the initial 30 min at 5 ATA then gradually increased, and increased within 30 min at 6 ATA. Changes in rCBF correlated positively with NO(x) production; increases in rCBF during HBO2 exposure were associated with large increases in NO(x) at 5 and 6 ATA and always preceded EEG discharges as a sign of CNS O2 toxicity. In rats pretreated with L-NAME, rCBF remained maximally decreased throughout 75 min of HBO2 at 4, 5 and 6 ATA. These data provide the first direct evidence that increased NO* production during prolonged HBO2 exposure is responsible for escape from hyperoxic vasoconstriction. The finding suggests that NO* overproduction initiates CNS O2 toxicity by increasing rCBF, which allows excessive O2 to be delivered to the brain.

Nitric oxide and cerebral blood flow responses to hyperbaric oxygen.

We have tested the hypothesis that cerebral nitric oxide (NO) production is involved in hyperbaric O(2) (HBO(2)) neurotoxicity. Regional cerebral blood flow (rCBF) and electroencephalogram (EEG) were measured in anesthetized rats during O(2) exposure to 1, 3, 4, and 5 ATA with or without administration of the NO synthase inhibitor (N(omega)-nitro-L-arginine methyl ester), L-arginine, NO donors, or the N-methyl-D-aspartate receptor inhibitor MK-801. After 30 min of O(2) exposure at 3 and 4 ATA, rCBF decreased by 26-39% and by 37-43%, respectively, and was sustained for 75 min. At 5 ATA, rCBF decreased over 30 min in the substantia nigra by one-third but, thereafter, gradually returned to preexposure levels, preceding the onset of EEG spiking activity. Rats pretreated with N(omega)-nitro-L-arginine methyl ester and exposed to HBO(2) at 5 ATA maintained a low rCBF. MK-801 did not alter the cerebrovascular responses to HBO(2) at 5 ATA but prevented the EEG spikes. NO donors increased rCBF in control rats but were ineffective during HBO(2) exposures. The data provide evidence that relative lack of NO activity contributes to decreased rCBF under HBO(2), but, as exposure time is prolonged, NO production increases and augments rCBF in anticipation of neuronal excitation.

Hyperbaric oxygen reduces cerebral blood flow by inactivating nitric oxide.

Based on recent evidence that nitric oxide (NO(.)) is involved in hyperoxic vasoconstriction, we tested the hypothesis that decreases in NO(.) availability in brain tissue during hyperbaric oxygen (HBO(2)) exposure contribute to decreases in regional cerebral blood flow (rCBF). rCBF was measured in rats exposed to HBO(2) at 5 atmospheres (ATA) and correlated with interstitial brain levels of NO(.) metabolites (NO(X)) and production of hydroxyl radical ((.)OH). Changes in rCBF were also correlated with the effects of NO(.) synthase inhibitor (l-NAME), NO(.) donor PAPANONOate, and intravascular superoxide dismutase (MnSOD) during HBO(2). After 30 min of O(2) exposure at 5 ATA, rCBF had decreased in the substantia nigra, caudate putamen, hippocampus, and parietal cortex by 23 to 37%. These reductions in rCBF were not augmented by exposure to HBO(2) in animals pre-treated with l-NAME. After 30 min at 5 ATA, brain NO(X) levels had decreased by 31 +/- 9% and correlated with the decrease in rCBF, while estimated (.)OH production increased by 56 +/- 8%. The decrease in rCBF at 5 ATA was completely abolished by MnSOD administration into the circulation before HBO(2) exposure. Doses of NO(.) donor that significantly increased rCBF in animals breathing air had no effect at 5 ATA of HBO(2). These results indicate that decreases in rCBF with HBO(2) are associated with a decrease in effective NO(.) concentration and an increase in ROS production in the brain. The data support the hypothesis that inactivation of NO(.) antagonizes basal relaxation of cerebral vessels during HBO(2) exposure, although an effect of HBO(2) on NO(.) synthesis has not been excluded.

Measurement of cerebral blood flow in rats and mice by hydrogen clearance during hyperbaric oxygen exposure.

The hydrogen (H2) clearance method was adapted for the measurement of regional cerebral blood flow (rCBF) in anesthetized rats and mice during hyperbaric oxygen (HBO2) exposure. Polarographic platinum electrodes 0.1 mm in diameter were used to record H2 clearance curves from the parietal cortex (PC), substantia nigra (SN), and caudate putamen nucleus (CPN) after inhalation of 2.5% H2 in air. The system for H2 breathing under hyperbaric conditions was designed for remote operation from outside the chamber. The rCBF values (measured every 10 min) were calculated from the H2 clearance curves using the initial slope method. During air breathing control, rCBF values were similar to values reported using other methods. Considering all control rats together, blood flow (ml.100 g-1.min-1) was 89 +/- 3.6 in the SN, 78 +/- 4.7 in the CPN, and 76 +/- 6.7 in the PC. Blood flow (ml.100 g-1.min-1) for air-breathing mice was 108 +/- 11.4 in the SN and 74 +/- 8.8 in the CPN. During HBO2 exposure to 3 atm abs, rCBF in rats fell within 30 min by 26-39% (P < 0.05) and by 27-29% in mice (P < 0.05). HBO2 exposure to 4 atm abs induced maximal rCBF decreases in rats within 60 min by 37% (P < 0.01) in the SN and by 47% (P < 0.01) in the CPN. Breathing CO2 during HBO2 exposure to 4 atm abs reversed the vasoconstriction and led to a rCBF increase of 80-96% in rats. The H2 clearance method seems to be an accurate and sensitive technique for the repeated measurement of local CBF under hyperbaric conditions.