Prolonged ethanol abuse has been associated with brain injury. In rodents, postnatal exposure to ethanol has been shown to be a major contributing factor to neurodegeneration in the hippocampus and cortex, leading to deficits in synaptic function and memory. Among the potential mechanisms involved in ethanol-induced brain damage, oxidative stress is considered a primary factor. However, the molecular mechanisms underlying ethanol-induced neurotoxicity remain incompletely understood. Evidence suggests that ethanol impairs the functions of both the cytoskeleton and cellular membranes, resulting in alterations to neuronal physiology. The plasma membrane of eukaryotic cells contains microdomains enriched in specific glycosphingolipids, gangliosides, and cholesterol, collectively forming membrane/lipid rafts (MLRs). As demonstrated in previous studies, MLRs function as scaffolds for a variety of molecular entities, including signaling receptors and ion channels. In addition, they mediate the organisation of the cytoskeleton. Indeed, numerous cytoskeletal components, their binding partners, and enzymes that regulate cytoskeletal dynamics localise to MLRs and contribute to the regulation of the lateral diffusion of membrane proteins and lipids in response to extracellular stimuli. The objective of the present research was to examine the effects of ethanol on the cytoskeleton, specifically actin and tubulin, in C6 glioma cells.

This study quantitatively evaluated the historical development and possible future trajectory of artificial intelligence (AI)-related biomedical research indexed in PubMed. AI-related publications were defined as publications explicitly identifying major AI concepts in their titles or abstracts, encompassing both biomedical applications of AI and studies of AI as a scientific subject. Annual publication output remained low for several decades before increasing sharply, with the most pronounced acceleration occurring in recent years. Two alternative growth descriptions closely represented the observed trend but produced contrasting interpretations of the field’s developmental stage. One placed the period of maximum growth near 2025 and projected approximately 184,000 publications in 2035, whereas the other placed maximum growth near 2033 and projected approximately 359,000 publications in 2035. The latter description received greater relative statistical support, although its predicted long-term publication level was associated with substantial uncertainty. These findings demonstrate rapid expansion of AI-related biomedical research and are particularly relevant to neuroscience, where artificial intelligence increasingly intersects with the investigation and computational modeling of learning, perception, reasoning, decision-making, and other neural and cognitive functions. Continued monitoring will determine whether this growth begins to approach saturation or remains accelerated into the next decade.

Whole-brain models of Drosophila melanogaster have progressed from connectome-constrained simulation to neuromorphic implementation and closed-loop embodiment. This progress creates an ethical question that is no longer purely hypothetical: could large numbers of such emulations instantiate negatively valenced states? We argue that the answer is presently indeterminate. The target is valence - whether a state is good or bad for the system - rather than consciousness, which remains a further unresolved question. Behaviour cannot decide the issue because the interpretation of pain-like behaviour in insects is itself contested. Connectivity cannot decide it because a connectome omits intrinsic dynamics, neuromodulation and internal state, all of which can reconfigure the functional meaning of the same anatomical pathways. A simulated body also supplies mechanics without necessarily supplying physiological variables whose preservation or violation could ground welfare. Instead of treating valence as a single hidden property, we propose an architectural audit of four component groups: aversive transduction, shared valence and motivational gating, persistence and valence-gated plasticity, and grounding in system-relevant variables. The audit should be paired with one-directional comparison against biological recordings and, where learning is present, a species-appropriate judgement-bias assay. Precaution should be triggered when any of three features appears: a persistent or plastic aversive state, a functional valence signal that globally biases action, or variables that are genuinely at stake for the system. Publicly documented implementations do not yet clearly meet these conditions, but the relevant components are technically accessible. The appropriate policy is therefore neither a declaration of suffering nor an assumption of harmlessness, but auditable uncertainty with explicit scaling safeguards.

Detecting moving objects is crucial in the animal kingdom and is fundamental to vision. In the vertebrate retina, starburst amacrine cells (SACs) are directionally selective in terms of their calcium responses to stimuli that move centrifugally from the soma. The mechanism by which starburst amacrine cells show calcium bias for centrifugal motion is still to be determined. Recent morphological studies using fluorescent microscopy and immunostaining have shown that the endoplasmic reticulum is omnipresent in the soma, extending to the distal processes of starburst amacrine cells. Electron microscopy for ChAT SAC in adult rat retina unequivocally proves the presence of local endoplasmic reticulum (ER) extending through the dendritic branches of SAC and the submicron diameter of the ER in SAC dendrites suggests that the ER is not luminally connected between the soma and the distal tips. We construct a computational model of a SAC dendrite with an ER to simulate the Ca2+-induced Ca2+ release (CICR)-based calcium waves in the presence of an unsaturated buffer to test the hypothesis a CICR mechanism can sustain constant calcium wave propagation in the centrifugal direction. Here, we focus on a working hypothesis, in which a CICR mechanism in the presence of local ER underlies the preference for directionality in the centrifugal direction and rather than the centripetal direction. Modeling the heterogeneity of calcium ER in simulated SACs sheds light on a possible explanation for the cause of speed tuning of direction-selective Ca2+ responses in dendrites of SACs. A simulation of the calcium-induced-calcium release-based Ca2+ waves in the presence of an unsaturated buffer is presented using an analytically derived solution of the two-pool model for cytosolic calcium. We find the conditions that support the calcium-induced calcium-release-based propagating Ca2+ wavefront in the centrifugal direction and its relation to where measurements are made. This suggests CICR from the ER can provide an initial seed underlying directionality in SAC.

​Epileptic seizures are often described as transitions into hypersynchrony, disorder or increased entropy. Prior neurotopological work argued that epileptic pathology may also be interpreted as breakdown of network geometry rather than entropy increase alone (Salazar Chon & Kadhim, 2025). Here, I report an expanded exploratory reconstruction of transition structure in a public HUP intracranial EEG cohort. The analysis used 85 derived ictal runs from 22 subjects and expanded the interictal control layer to 42 interictal pseudo-onset runs from 21 subjects. Markers were organized into algorithm-defined transition families, temporal first-crossing sequences, circular time-shift null controls and expanded ictal-versus-interictal screening. Across the expanded control, ictal runs showed stronger transition-risk escalation than interictal pseudo-onset segments at run level, subject level and matched-subject level. Early risk gain was higher in ictal runs at run level (median 0.4573 versus -0.0932, p