Meson bunches formed by pulsed laser-induced processes in ultra-dense hydrogen H(0)

Ultra-dense hydrogen H(0) (reviewed in Holmlid and Zeiner-Gundersen, Physica Scripta 2019 ) consists of small strongly bound molecules with interatomic distance of 0.56 pm in spin state s = 1. It is a useful nuclear fuel for energy generation, giving heat above break-even (Holmlid, AIP Advances 2015) in laser-induced processes (Holmlid, Int. J. Hydr. Energy 2021). Nuclear processes in H(0) emit particles in typical meson decay chains with kinetic energy up to 100 MeV. These mesons decay and generate fast muons at up to 500 MeV energy at current densities of several mA cm-2 at 1–2 m distances, which corresponds to 1013 -1014 muons formed per laser pulse. It is shown that the mesons decay in chain processes with well-defined meson time constants in the range 10–60 ns. The time varying signals from H(0) agree well with mesons M in decay chains as A ◊ M ◊ N where N is a signal muon. M may be a charged kaon K± (decay time constant at rest 12.4 ns) or a charged pion π± (decay time constant at rest 26 ns) or a long-lived neutral kaon \({\text{K}}_{L}^{0}\) (decay time constant at rest 51 ns). Ultra-dense protium p(0) gives the same time constants as D(0) but slightly different decay-chains. The meson bunches observed are similar to the meson bunches from nucleon + antinucleon annihilation. The energy gain in the nuclear process is at least 8000, strongly indicating baryon annihilation for which process further evidence is given in other recent publications.

Stabilized Supralinear Network: Model of Layer 2/3 of the Primary Visual Cortex

Electrophysiological recording in the primary visual cortex (V1) of mammals have revealed a number of complex interactions between the center and surround. Understanding the underlying circuit mechanisms is crucial to understanding fundamental brain computations. In this paper we address the following phenomena that have been observed in V1 of animals with orientation maps: 1) surround suppression that is accompanied by a decrease in the excitatory and inhibitory currents that the cell receives as the stimulus size increases beyond the cell’s summation field; 2) surround tuning to the center orientation, in which the strongest suppression arises when the surround orientation matches that of the center stimulus; and 3) feature-specific suppression, in which a surround stimulus of a given orientation specifically suppresses that orientation’s component of the response to a center plaid stimulus. We show that a stabilized supralinear network that has biologically plausible connectivity and synaptic efficacies that depend on cortical distance and orientation difference between neurons can consistently reproduce all the above phenomena. We explain the mechanism behind each result, and argue that feature-specific suppression and surround tuning to the center orientation are independent phenomena. Specifically, if we remove some aspects of the connectivity from the model it will still produce feature-specific suppression but not surround tuning to the center orientation. We also show that in the model the activity decay time constant is similar to the cortical activity decay time constant reported in mouse V1. Our model indicates that if the surround activates neurons that fall within the reach of the horizontal projections in V1, the above mentioned phenomena can be generated by V1 alone without the need of cortico-cortical feedback. Finally, we show that these results hold both in networks with rate-based units and with conductance-based spiking units. This demonstrates that the stabilized supra-linear network mechanism can be achieved in the more biological context of spiking networks.

Multimodal Non-Contact Luminescence Thermometry with Cr-Doped Oxides

Luminescence methods for non-contact temperature monitoring have evolved through improvements of hardware and sensor materials. Future advances in this field rely on the development of multimodal sensing capabilities of temperature probes and extend the temperature range across which they operate. The family of Cr-doped oxides appears particularly promising and we review their luminescence characteristics in light of their application in non-contact measurements of temperature over the 5–300 K range. Multimodal sensing utilizes the intensity ratio of emission lines, their wavelength shift, and the scintillation decay time constant. We carried out systematic studies of the temperature-induced changes in the luminescence of the Cr3+-doped oxides Al2O3, Ga2O3, Y3Al5O12, and YAlO3. The mechanism responsible for the temperature-dependent luminescence characteristic is discussed in terms of relevant models. It is shown that the thermally-induced processes of particle exchange, governing the dynamics of Cr3+ ion excited state populations, require low activation energy. This then translates into tangible changes of a luminescence parameter with temperature. We compare different schemes of temperature sensing and demonstrate that Ga2O3-Cr is a promising material for non-contact measurements at cryogenic temperatures. A temperature resolution better than ±1 K can be achieved by monitoring the luminescence intensity ratio (40–140 K) and decay time constant (80–300 K range).

Paradoxical Anticonvulsant Effect of Cefepime in the Pentylenetetrazole Model of Seizures in Rats

Many β-lactam antibiotics, including cephalosporins, may cause neurotoxic and proconvulsant effects. The main molecular mechanism of such effects is considered to be γ-aminobutyric acid type a (GABAa) receptor blockade, leading to the suppression of GABAergic inhibition and subsequent overexcitation. We found that cefepime (CFP), a cephalosporin, has a pronounced antiepileptic effect in the pentylenetetrazole (PTZ)-induced seizure model by decreasing the duration and severity of the seizure and animal mortality. This effect was specific to the PTZ model. In line with findings of previous studies, CFP exhibited a proconvulsant effect in other models, including the maximal electroshock model and 4-aminopyridine model of epileptiform activity, in vitro. To determine the antiepileptic mechanism of CFP in the PTZ model, we used whole-cell patch-clamp recordings. We demonstrated that CFP or PTZ decreased the amplitude of GABAa receptor-mediated postsynaptic currents. PTZ also decreased the current decay time constant and temporal summation of synaptic responses. In contrast, CFP slightly increased the decay time constant and did not affect summation. When applied together, CFP prevented alterations to the summation of responses by PTZ, strongly reducing the effects of PTZ on repetitive inhibitory synaptic transmission. The latter may explain the antiepileptic effect of CFP in the PTZ model.

Contributing mechanisms underlying desensitization of cholecystokinin-induced activation of primary nodose ganglia neurons

Cholecystokinin (CCK) is a gut-derived peptide that potently promotes satiety and facilitates gastric function in part by activating G protein-coupled CCK1 receptors on primary vagal afferent neurons. CCK signaling is dynamic and rapidly desensitizes, due to decreases in either receptor function and the resulting signal cascade, ion channel effectors, or both. Here we report a decay-time analytical approach using fluorescent calcium imaging that relates peak and steady-state calcium responses in dissociated vagal afferent neurons, enabling discrimination between receptor and ion channel effector functions. We found desensitization of CCK-induced activation was predictable, consistent across cells, and strongly concentration dependent. The decay-time constant (tau) was inversely proportional to CCK concentration, apparently reflecting the extent of receptor activation. To test this possibility, we directly manipulated the ion channel effector(s) with either decreased bath calcium or the broad-spectrum pore blocker ruthenium red. Conductance inhibition diminished the magnitude of the CCK responses without altering decay kinetics, confirming changes in tau reflect changes in receptor function selectively. Next, we investigated the contributions of the PKC and PKA signaling cascades on the magnitude and decay-time constants of CCK calcium responses. While inhibition of either PKC or PKA increased CCK calcium response magnitude, only general PKC inhibition significantly decreased the decay-time constant. These findings suggest that PKC alters CCK receptor signaling dynamics, while PKA alters the ion channel effector of the CCK response. This analytical approach should prove useful in understanding receptor/effector changes underlying acute desensitization of G-protein coupled signaling and provide insight into CCK receptor dynamics.