Robust entropy requires strong and balanced excitatory and inhibitory synapses.

It is widely appreciated that balanced excitation and inhibition are necessary for proper function in neural networks. However, in principle, balance could be achieved by many possible configurations of excitatory and inhibitory synaptic strengths and relative numbers of excitatory and inhibitory neurons. For instance, a given level of excitation could be balanced by either numerous inhibitory neurons with weak synapses or a few inhibitory neurons with strong synapses. Among the continuum of different but balanced configurations, why should any particular configuration be favored? Here, we address this question in the context of the entropy of network dynamics by studying an analytically tractable network of binary neurons. We find that entropy is highest at the boundary between excitation-dominant and inhibition-dominant regimes. Entropy also varies along this boundary with a trade-off between high and robust entropy: weak synapse strengths yield high network entropy which is fragile to parameter variations, while strong synapse strengths yield a lower, but more robust, network entropy. In the case where inhibitory and excitatory synapses are constrained to have similar strength, we find that a small, but non-zero fraction of inhibitory neurons, like that seen in mammalian cortex, results in robust and relatively high entropy.

Hospital-Acquired Sacral Pressure Ulcer Complicated by a Spinal Epidural Abscess.

A spinal epidural abscess is a rare condition characterized by the accumulation of pus between the dura mater and vertebral column, often caused by hematogenous spread from a distant site or local spread from infection in nearby structures. The abscess leads to compression of the spinal cord and can result in neurological damage, including dysfunction or permanent neurological deficits. Treatment of spinal epidural abscesses should not be delayed and requires a combination of decompression by surgical drainage and antibiotic therapy. The authors present a rare case in which a spinal epidural abscess developed from a hospital-acquired pressure ulcer, further complicated by bacteremia.

Complex Cardiovascular Morbidities in Prader-Willi Syndrome: A Multidisciplinary Approach.

This case emphasizes the complexity of Prader-Willi syndrome (PWS), the need for a collaborative approach from specialists, and a closer look at the various cardiovascular complexities associated with this syndrome. While current treatments focus on managing symptoms, ongoing genetic research offers hope for more favorable outcomes. Further studies are crucial to gauge the effectiveness of these treatments for PWS patients. We detail a patient with a complex medical history of PWS, further complicated by congenital heart disease with Eisenmenger's syndrome, diabetes mellitus, pulmonary hypertension, venous insufficiency, hypothyroidism, and hyperlipidemia. Reported in this study is a compilation of clinical data as well as suggestions from several medical specialists in applying a multifaceted approach to treatment, significantly emphasizing the need for interdisciplinary care and management of patients experiencing a combination of various medical issues with an emphasis on cardiovascular complications.

An Effective Electric Dipole Model for Voltage-induced Gating Mechanism of Lysenin.

Lysenin is a pore-forming toxin, which self-inserts open channels into sphingomyelin containing membranes and is known to be voltage regulated. The mechanistic details of its voltage gating mechanism, however, remains elusive despite much recent efforts. Here, we have employed a novel combination of experimental and computational techniques to examine a model for voltage gating, that is based on the existence of an "effective electric dipole" inspired by recent reported structures of lysenin. We support this mechanism by the observations that (i) the charge-reversal and neutralization substitutions in lysenin result in changing its electrical gating properties by modifying the strength of the dipole, and (ii) an increase in the viscosity of the solvent increases the drag force and slows down the gating. In addition, our molecular dynamics (MD) simulations of membrane-embedded lysenin provide a mechanistic picture for lysenin conformational changes, which reveals, for the first time, the existence of a lipid-dependent bulge region in the pore-forming module of lysenin, which may explain the gating mechanism of lysenin at a molecular level.