Many-body theory calculations of positronic-bonded molecular dianions.

The energetic stability of positron-dianion systems [A-; e+; A-] is studied via many-body theory, where A- includes H-, F-, Cl-, and the molecular anions (CN)- and (NCO)-. Specifically, the energy of the system as a function of ionic separation is determined by solving the Dyson equation for the positron in the field of the two anions using a positron-anion self-energy as constructed in Hofierka et al. [Nature 606, 688 (2022)] that accounts for correlations, including polarization, screening, and virtual-positronium formation. Calculations are performed for a positron interacting with H22-, F22-, and Cl22- and are found to be in good agreement with previous theory. In particular, we confirm the presence of two minima in the potential energy of the [H-; e+; H-] system with respect to ionic separation: a positronically bonded [H-; e+; H-] local minimum at ionic separations r ∼ 3.4 Å and a global minimum at smaller ionic separations r ≲ 1.6 Å that gives overall instability of the system with respect to dissociation into a H2 molecule and a positronium negative ion, Ps-. The first predictions are made for positronic bonding in dianions consisting of molecular anionic fragments, specifically for (CN)22- and (NCO)22-. In all cases, we find that the molecules formed by the creation of a positronic bond are stable relative to dissociation into A- and e+A- (positron bound to a single anion), with bond energies on the order of 1 eV and bond lengths on the order of several ångstroms.

Many-Body Theory Calculations of Positron Scattering and Annihilation in H_{2}, N_{2}, and CH_{4}.

The recently developed ab initio many-body theory of positron molecule binding [22J. Hofierka et al., Many-body theory of positron binding to polyatomic molecules, Nature (London) 606, 688 (2022)NATUAS0028-083610.1038/s41586-022-04703-3] is combined with the shifted pseudostates method [A. R. Swann and G. F. Gribakin, Model-potential calculations of positron binding, scattering, and annihilation for atoms and small molecules using a Gaussian basis, Phys. Rev. A 101, 022702 (2020)PLRAAN2469-992610.1103/PhysRevA.101.022702] to calculate positron scattering and annihilation rates on small molecules, namely H_{2}, N_{2}, and CH_{4}. The important effects of positron-molecule correlations are delineated. The method provides uniformly good results for annihilation rates on all the targets, from the simplest (H_{2}, for which only a sole previous calculation agrees with experiment), to larger targets, where high-quality calculations have not been available.

Maxwellianization of Positrons Cooling in CF_{4} and N_{2} Gases.

Positron cooling in CF_{4} and N_{2} gases via inelastic vibrational and rotational (de)excitations is simulated, importantly including elastic positron-positron collisions. For CF_{4}, it is shown that rotational (de)excitations play no role on the experimental timescale, and further, that in the absence of positron-positron collisions, cooling via excitation of the dipole-active ν_{3} and ν_{4} modes alone would lead to a non-Maxwellian positron momentum distribution, in contrast to the observations of experiment. It is shown that the observed Maxwellianization of the distribution may be effected by positron-positron collisions and/or cooling involving the combination of the dipole-inactive ν_{1} mode with the dipole-active modes. For N_{2}, rotational excitations alone are sufficient to Maxwellianize the distribution (vibrational effects are negligible).

Many-Body Theory for Positronium-Atom Interactions.

A many-body-theory approach has been developed to study positronium-atom interactions. As first applications, we calculate the elastic scattering and momentum-transfer cross sections and the pickoff annihilation rate ^{1}Z_{eff} for Ps collisions with He and Ne. For He the cross section is in agreement with previous coupled-state calculations, while comparison with experiment for both atoms highlights discrepancies between various sets of measured data. In contrast, the calculated ^{1}Z_{eff} (0.13 and 0.26 for He and Ne, respectively) are in excellent agreement with the measured values.

Probing Positron Cooling in Noble Gases via Annihilation γ Spectra.

γ spectra for positron annihilation in noble-gas atoms are calculated using many-body theory for positron momenta up to the positronium-formation threshold. These data are used, together with time-evolving positron-momentum distributions determined in the preceding Letter [Phys. Rev. Lett. 119, 203403 (2017)PRLTAO0031-9007], to calculate the time-varying γ spectra produced during positron cooling in noble gases. The γ spectra and their S[over ¯] and W[over ¯] shape parameters are shown to be sensitive probes of the time evolution of the positron momentum distribution and thus provide a means of studying positron cooling that is complementary to positron lifetime spectroscopy.

Positron Cooling and Annihilation in Noble Gases.

Positron cooling and annihilation in room temperature noble gases is simulated using accurate scattering and annihilation cross sections calculated with many-body theory, enabling the first simultaneous probing of the energy dependence of the scattering and annihilation cross sections. A strikingly small fraction of positrons is shown to survive to thermalization: ∼0.1 in He, ∼0 in Ne, ∼0.15 in Ar, ∼0.05 in Kr, and ∼0.01 in Xe. For Xe, the time-varying annihilation rate Z[over ¯]_{eff}(τ) is shown to be highly sensitive to the depletion of the momentum distribution due to annihilation, conclusively explaining the long-standing discrepancy between gas-cell and trap-based measurements. Overall, the use of the accurate atomic data gives Z[over ¯]_{eff}(τ) in close agreement with experiment for all noble gases except Ne, the experiment for which is proffered to have suffered from incomplete knowledge of the fraction of positrons surviving to thermalization and/or the presence of impurities.

γ-Ray spectra and enhancement factors for positron annihilation with core electrons.

Many-body theory is developed to calculate the γ spectra for positron annihilation in noble-gas atoms. Inclusion of electron-positron correlation effects and core annihilation gives spectra in excellent agreement with experiment [K. Iwata et al., Phys. Rev. Lett. 79, 39 (1997)]. The calculated correlation enhancement factors γ_{nl} for individual electron orbitals nl are found to scale with the ionization energy I_{nl} (in eV), as γ_{nl}=1+sqrt[A/I_{nl}]+(B/I_{nl})^{ß}, where A≈40 eV, B≈24 eV, and ß≈2.3.

Transverse spreading of electrons in high-intensity laser fields.

We show that for collisions of electrons with a high-intensity laser, discrete photon emissions introduce a transverse beam spread that is distinct from that due to classical (or beam shape) effects. Via numerical simulations, we show that this quantum induced transverse momentum gain of the electron is manifest in collisions with a realistic laser pulse of intensity within reach of current technology, and we propose it as a measurable signature of strong-field quantum electrodynamics.

The role of routine spinal imaging and immobilisation in asymptomatic patients after gunshot wounds.

BACKGROUND: The role of routine dedicated spinal imaging and immobilisation following gunshot wounds (GSW) to the head, neck or torso has been debated. The purpose of this study was to determine the incidence of spinal column injury requiring stabilisation in evaluable patients following gunshot injury. METHODS: A retrospective study from of a Level I trauma centre from January 1995 to December 2004. All patients with GSW to the head, neck or torso and bony spinal column injury underwent medical record review to determine injury type, presentation, presence of concomitant spinal cord injury, treatment and outcome. RESULTS: A total of 4204 patients sustaining GSW to the head, neck or torso were identified. Complete medical records were available for the 327 (7.8%) patients with bony spinal column injury. Among these patients, 173 (52.9%) sustained spinal cord injury. Two patients (0.6%) with GSW to the torso and bony spinal column injury required operative spinal intervention. The indication for operative intervention in both cases was removal of a foreign body or bony fragment for decompression of the spinal canal. None of the 4204 patients sustaining GSW to the head, neck or torso demonstrated spinal instability requiring operative intervention, and only 2/327 (0.6%) required any form of operative intervention for decompression. CONCLUSION: Spinal instability following GSW with spine injury is very rare. Routine spinal imaging and immobilisation is unwarranted in examinable patients without symptoms consistent with spinal injury following GSW to the head, neck or torso.

Constitutive "light" adaptation in rods from G90D rhodopsin: a mechanism for human congenital nightblindness without rod cell loss.

A dominant form of human congenital nightblindness is caused by a gly90-->asp (G90D) mutation in rhodopsin. G90D has been shown to activate the phototransduction cascade in the absence of light in vitro. Such constitutive activity of G90D rhodopsin in vivo would desensitize rod photoreceptors and lead to nightblindness. In contrast, other rhodopsin mutations typically give rise to nightblindness by causing rod cell death. Thus, the proposed desensitization without rod degeneration would be a novel mechanism for this disorder. To explore this possibility, we induced mice to express G90D opsin in their rods and then examined rod function and morphology, after first crossing the transgenic animals with rhodopsin knock-out mice to obtain appropriate levels of opsin expression. The G90D mouse opsin bound the chromophore and formed a bleachable visual pigment with lambda(max) of 492 nm that supported rod photoresponses. (G+/-, R+/-) retinas, heterozygous for both G90D and wild-type (WT) rhodopsin, possessed normal numbers of photoreceptors and had a normal rhodopsin complement but exhibited considerable loss of rod sensitivity as measured electroretinographically. The rod photoresponses were desensitized, and the response time to peak was faster than in (R+/-) animals. An equivalent desensitization resulted by exposing WT retinas to a background light producing 82 photoisomerizations rod(-1) sec(-1), suggesting that G90D rods in darkness act as if they are partially "light-adapted." Adding a second G90D allele gave (G+/+, R+/-) animals that exhibited a further increase of equivalent background light level but had no rod cell loss by 24 weeks of age. (G+/+, R-/-) retinas that express only the mutant rhodopsin develop normal rod outer segments and show minimal rod cell loss even at 1 year of age. We conclude that G90D is constitutively active in mouse rods in vivo but that it does not cause significant rod degeneration. Instead, G90D desensitizes rods by a process equivalent to light adaptation.

Partial rescue of the ocular retardation phenotype by genetic modifiers.

The or(J) allele of the murine ocular retardation mutation is caused by a premature stop codon in the homeodomain of the Chx10 gene. When expressed on an inbred 129/Sv strain, the or(J) phenotype is characterized by microphthalmia and a thin, poorly differentiated retina in which the peripheral portion is affected to a greater extent than the central portion. Such mutant retinae lack differentiated bipolar cells and the optic nerve typically fails to form, leading to blindness. Here, we show that progeny from an outcrossed backcross between 129/Sv-or(J) /or(J) and Mus musculus castaneus produce animals that are homozygous for the or(J) mutation and exhibit a much ameliorated eye phenotype. Although not of normal size, such modified or(J) eyes are significantly larger than those in 129/Sv-or(J) /or(J) mice, and contain a better organized retina which includes bipolar cells. Furthermore, optic nerves are frequently present, and the eyes show a degree of function as reflected by electroretinogram and pupillary response. As in 129/Sv-or(J) /or(J) mice, however, modified or(J) eyes show incomplete growth and a lack of cell differentiation in the periphery of the retina. The selective, and apparently nonmodifiable, effect of the ocular retardation phenotype on the periphery of the retina indicates that Chx10 plays an important role in the central-to-peripheral gradient of retinal development. These findings demonstrate that the ocular retardation phenotype can be greatly modified by the genetic background, and help to define a role for Chx10 in ocular development.

Open problems in artificial life.

This article lists fourteen open problems in artificial life, each of which is a grand challenge requiring a major advance on a fundamental issue for its solution. Each problem is briefly explained, and, where deemed helpful, some promising paths to its solution are indicated.

A dissection of the electroretinogram from the isolated rat retina with microelectrodes and drugs.

The origins of the a- and b-wave of the ERG were studied using simultaneous recordings made across the receptor layer and the full thickness of a piece of isolated albino rat retina. An inwardly directed current flowing across the rod outer segments was eliminated from the recording when postsynaptic activity was blocked with cobalt or when current source density measurements were made along the length of the outer segments. Rod photovoltages were inferred by removing extraneous field potentials from the recordings made across the photoreceptor layer. The spatial properties of the photovoltage indicates the responses came from an area about 100 microm in diameter. The glutamate analog. APB, which blocks depolarizing bipolar cells, eliminated the b-wave but left the a-wave unaffected. The ERG component due to depolarizing bipolar cells was inferred by subtracting recordings obtained before and after APB. After treatment with APB a slow component remained. This component was completely blocked by barium (200 microM), which blocks potassium channels on Müller cells. Barium had virtually no effect on low-intensity photovoltages but did affect the amplitude and shape of the saturated responses. Barium increased the amplitude of the component of the ERG which underlies the b-wave. It was concluded that the depolarizing bipolar cells directly generate the b-wave of the ERG.

Effects of inhibiting glutamine synthetase and blocking glutamate uptake on b-wave generation in the isolated rat retina.

The purpose of the present experiments was to evaluate the contribution of the glutamate-glutamine cycle in retinal glial (Müller) cells to photoreceptor cell synaptic transmission. Dark-adapted isolated rat retinas were superfused with oxygenated bicarbonate-buffered media. Recordings were made of the b-wave of the electroretinogram as a measure of light-induced photoreceptor to ON-bipolar neuron transmission. L-methionine sulfoximine (1-10 mM) was added to superfusion media to inhibit glutamine synthetase, a Müller cell specific enzyme, by more than 99% within 5-10 min, thereby disrupting the conversion of glutamate to glutamine in the Müller cells. Threo-hydroxyaspartic acid and D-aspartate were used to block glutamate transporters. The amplitude of the b-wave was well maintained for 1-2 h provided 0.25 mM glutamate or 0.25 mM glutamine was included in the media. Without exogenous glutamate or glutamine the amplitude of the b-wave declined by about 70% within 1 h. Inhibition of glutamate transporters led to a rapid (2-5 min) reversible loss of the b-wave in the presence and absence of the amino acids. In contrast, inhibition of glutamine synthetase did not alter significantly either the amplitude of the b-wave in the presence of glutamate or glutamine or the rate of decline of the b-wave found in the absence of these amino acids. Excellent recovery of the b-wave was found when 0.25 mM glutamate was resupplied to L-methionine sulfoximine-treated retinas. The results suggest that in the isolated rat retina uptake of released glutamate into photoreceptors plays a more important role in transmitter recycling than does uptake of glutamate into Müller cells and its subsequent conversion to glutamine.

Electrophysiological properties of a new isolated rat retina preparation.

A piece of rat retina was mounted in an open chamber and perfused with a Ringer solution at 37 degrees C. The electroretinogram (ERG) was recorded between an extracellular microelectrode in contact with the rod outer segments and a reference electrode under the retina. The addition of 250-500 microM of glutamate to the media prevented the b-wave from decaying in amplitude with time. Minor components of the ERG, the scotopic threshold response (STR) and oscillatory potentials (OPs), were well maintained with glutamate in the media. Experiments on the spatial properties of the recordings indicated that a small area immediately around the microelectrode contributes most strongly to the response. The similarity of ERGs recorded in vivo from the cornea to the transretinal ERGs from the isolated retina of the same animal indicated that the functional integrity of the isolated retina was well preserved in the media with glutamate.

Effects of dystrophin isoforms on signal transduction through neural retina: genotype-phenotype analysis of duchenne muscular dystrophy mouse mutants.

Duchenne and Becker muscular dystrophy patients have mutations in the dystrophin gene. Most show reduced b-wave amplitudes in the dark-adapted electroretinogram (ERG). We studied normal C57BL/6J mice and five X-linked muscular dystrophy strains with different dystrophin mutations to determine whether the location of the mutation within the gene affects the mouse ERG and to correlate such effects with dystrophin isoform expression. Amplitudes and implicit times were measured for a-waves, b-waves, and digitally filtered oscillatory potentials. mdx and mdxCv5 mice, with mutations near the amino terminus and lacking expression of Dp427, had ERGs similar to those of C57BL/6J mice. mdxCv2 and mdxCv4 mice, with mutations in the center of dystrophin and who do not express isoforms Dp427, Dp260, or Dp140 (mdxCv4), had increased b-wave and oscillatory potential implicit times. mdxCv3 mice, with a mutation near the carboxy terminus resulting in deficiency of all dystrophin isoforms, had increased b-wave and oscillatory potential implicit times and reduced scotopic b-wave amplitudes. Fitting the a-wave data to a transduction activation phase mathematical model showed normal responses for all phenotypes, suggesting that the b-wave delays are due to defects beyond the rod outer segment, most likely at the rod to on-bipolar cell synapse. The variation in the ERG phenotype with the position of the dystrophin gene mutation suggests that there are different contributions by each isoform to retinal electrophysiology. Although Dp427 and Dp140 isoforms do not appear to be important contributors to the ERG, lack of Dp260 and possibly Dp71 isoforms is associated with an abnormal ERG.

Retinal image quality in the rodent eye.

Many rodents do not see well. For a target to be resolved by a rat or a mouse, it must subtend a visual angle of a degree or more. It is commonly assumed that this poor spatial resolving capacity is due to neural rather than optical limitations, but the quality of the retinal image has not been well characterized in these animals. We have modified a double-pass apparatus, initially designed for the human eye, so it could be used with rodents to measure the modulation transfer function (MTF) of the eye's optics. That is, the double-pass retinal image of a monochromatic (lambda = 632.8 nm) point source was digitized with a CCD camera. From these double-pass measurements, the single-pass MTF was computed under a variety of conditions of focus and with different pupil sizes. Even with the eye in best focus, the image quality in both rats and mice is exceedingly poor. With a 1-mm pupil, for example, the MTF in the rat had an upper limit of about 2.5 cycles/deg, rather than the 28 cycles/deg one would obtain if the eye were a diffraction-limited system. These images are about 10 times worse than the comparable retinal images in the human eye. Using our measurements of the optics and the published behavioral and electrophysiological contrast sensitivity functions (CSFs) of rats, we have calculated the CSF that the rat would have if it had perfect rather than poor optics. We find, interestingly, that diffraction-limited optics would produce only slight improvement overall. That is, in spite of retinal images which are of very low quality, the upper limit of visual resolution in rodents is neurally determined. Rats and mice seem to have eyes in which the optics and retina/brain are well matched.