Neural Tissue Research Articles

Glucosylceramide synthase inhibitor ameliorates chronic inflammatory pain

Gangliosides play pivotal roles in neuronal tissue processes, such as axonal elongation, synaptic transmission, and neuronal degeneration. Several studies have shown that mice injected with gangliosides synthesized from glucosylceramide exhibit mechanical allodynia. Thus, we hypothesized that glucosylceramide synthase inhibitors affect nociceptive behavior. We investigated the analgesic effect of intrathecal glucosylceramide inhibition on bilateral allodynia caused by prolonged unilateral hind paw inflammation in mice. Repeated administration of a glucosylceramide inhibitor reduced mechanical allodynia in both inflamed and non-inflamed hind paws. These results suggested that ganglioside reduction is critical for analgesia during inflammatory pain.

Fabrication and characterization of bioresorbable, electroactive and highly regular nanomodulated cell interfaces

Biomaterial-based implantable scaffolds capable of promoting physical and functional reconnection of injured spinal cord and nerves represent the latest frontier in neural tissue engineering. Here, we report the fabrication and characterization of self-standing, biocompatible and bioresorbable substrates endowed with both controlled nanotopography and electroactivity, intended for the design of transient implantable scaffolds for neural tissue engineering. In particular, we obtain conductive and nano-modulated poly(D,L-lactic acid) (PLA) and poly(lactic-co-glycolic acid) free-standing films by simply iterating a replica moulding process and coating the polymer with a thin layer of poly(3,4-ethylendioxythiophene) polystyrene sulfonate. The capability of the substrates to retain both surface patterning and electrical properties when exposed to a liquid environment has been evaluated by atomic force microscopy, electrochemical impedance spectroscopy and thermal characterizations. In particular, we show that PLA-based films maintain their surface nano-modulation for up to three weeks of exposure to a liquid environment, a time sufficient for promoting axonal anisotropic sprouting and growth during neuronal cell differentiation. In conclusion, the developed substrates represent a novel and easily-tunable platform to design bioresorbable implantable devices featuring both topographic and electrical cues.

Comparisons of MR and EM inferred tissue microstructure properties using a human autopsy corpus callosum sample

Degeneration of white matter (WM) microstructure in the central nervous system is characteristic of many neurodegenerative conditions. Previous research indicates that axonal degeneration visible in ex vivo electron microscopy (EM) photomicrographs precede the onset of clinical symptoms. Measuring WM microstructural features, such as axon diameter and packing fraction, currently require these highly invasive methods of analysis and it is therefore of great importance to develop methods for in vivo measurements. Diffusion weighted Magnetic Resonance Imaging (MRI) is a non-invasive method which can be used in conjunction with temporal diffusion spectroscopy (TDS) and an oscillating gradient spin echo (OGSE) pulse sequence to probe micron-scale structures within neural tissue. The current experiment aims to compare axon diameter measurements, mean effective axon diameter (AxD¯), and packing fractions calculated from EM histopathological analysis and inferred values from MR images. Mathematical models of axon diameters used for analysis include the ActiveAx Frequency-Dependent Extra-Axonal Diffusion (AAD) model and the AxCaliber Frequency-Dependent Extra-Axonal Diffusion (ACD) model using ROI (Region of Interest) based analysis (RBA) and voxel-based analysis (VBA), respectively. Overall, it was observed that MRI inferred WM microstructural parameters overestimate those calculated from EM. This may be attributable to tissue shrinkage during EM dehydration, the sensitivity of MR pulse sequences to larger diameter axons, and/or inaccurate model assumptions. The results of the current study provide a means to characterize the precision and accuracy of RBA-ACD and VBA-AAD OGSE-TDS and highlight the need for further research investigating the relationship between ex vivo MRI and EM, with the goal of reaching in vivo MRI.

Mitochondrial Dysfunction as a Potential Mechanism Mediating Cardiac Comorbidities in Parkinson’s Disease

Individuals diagnosed with Parkinson’s disease (PD) often exhibit heightened susceptibility to cardiac dysfunction, reflecting a complex interaction between these conditions. The involvement of mitochondrial dysfunction in the development and progression of cardiac dysfunction and PD suggests a plausible commonality in some aspects of their molecular pathogenesis, potentially contributing to the prevalence of cardiac issues in PD. Mitochondria, crucial organelles responsible for energy production and cellular regulation, play important roles in tissues with high energetic demands, such as neurons and cardiac cells. Mitochondrial dysfunction can occur in different and non-mutually exclusive ways; however, some mechanisms include alterations in mitochondrial dynamics, compromised bioenergetics, biogenesis deficits, oxidative stress, impaired mitophagy, and disrupted calcium balance. It is plausible that these factors contribute to the increased prevalence of cardiac dysfunction in PD, suggesting mitochondrial health as a potential target for therapeutic intervention. This review provides an overview of the physiological mechanisms underlying mitochondrial quality control systems. It summarises the diverse roles of mitochondria in brain and heart function, highlighting shared pathways potentially exhibiting dysfunction and driving cardiac comorbidities in PD. By highlighting strategies to mitigate dysfunction associated with mitochondrial impairment in cardiac and neural tissues, our review aims to provide new perspectives on therapeutic approaches.

Dipeptide <i>L</i>-сarnosine (β-alanyl-<i>L</i>-histidine) — nervous tissue cryoprotector non-hybernate animals

In this work, the cryoprotective properties of dipeptide L-carnosine (β-alanyl-L-histidine) were studied on slices of the olfactory cortex of the brain of rats. Changes in the activity of N-methyl-D-aspartate receptors were analyzed as the most vulnerable to the effect of cryopreservation (CP), for this purpose, extracellular NMDA potentials were recorded. Slices were incubated with L-carnosine (20 mM) in the medium and frozen at a slow rate (0.1°C/min) down to –10°C and after CS (30 days) they were heated at the same rate (0.1°C/min) to +37°C. The effectiveness of cryoprotection of L-carnosine was determined by changes in the amplitudes of NMDA potentials after CP compared to before CP. The dipeptide restored the pH of the freezing medium 6.9 (without L-carnosine) to the optimum pH 7.3—7.4, promoted dehydration of free water from slices after CP, inhibited the development of glutamate excitotoxicity in slices. The data obtained prove that L-carnosine exhibits the properties of a non-toxic effective cryoprotector in the nervous tissue of warm-blooded non-hibernating animals.

An Algorithm for Creating a Synaptic Cleft Digital Phantom Suitable for Further Numerical Modeling

One of the most significant applications of mathematical numerical methods in biology is the theoretical description of the convectional reaction–diffusion of chemical compounds. Initial biological objects must be appropriately mimicked by digital domains that are suitable for further use in computational modeling. In the present study, an algorithm for the creation of a digital phantom describing a local part of nervous tissue—namely, a synaptic contact—is established. All essential elements of the synapse are determined using a set of consistent Boolean operations within the COMSOL Multiphysics software 6.1. The formalization of the algorithm involves a sequence of procedures and logical operations applied to a combination of 3D Voronoi diagrams, an experimentally defined inner synapse area, and a simple ellipsoid under different sets of biological parameters. The obtained digital phantom is universal and may be applied to different types of neuronal synapses. The clear separation of the designed domains reveals that the boundary’s conditions and internal flux dysconnectivity functions can be set up explicitly. Digital domains corresponding to the parts of a synapse are appropriate for further application of the derived numeric meshes, with various capacities of the included elements. Thus, the obtained digital phantom can be effectively used for further modeling of the convectional reaction–diffusion of chemical compounds in nervous tissue.

Optimizing Tubulin Yield from Porcine Brain Tissue.

Neural tissue from any source is an excellent material for tubulin isolation, as the dendrites and axons of neurons are rich in microtubules. Here, we present a procedure for extracting tubulin that can be employed, with minor modifications, for neural tissue from multiple sources. In the presented protocol, a new clarification step of the crude lysate has been introduced, which led to a significant reduction in the initial amount of insoluble debris before the first polymerization step occurred. This additional step allowed the processing of additional tissue while using the same instrumentation and, thus, increasing the relative volume of the processed homogenate. The newly introduced step has no significant effect on the quality of purified tubulin, as confirmed by in vitro activity assays and transmission electron microscopy. The described procedure contains all crucial steps, including tissue collection, transport, tissue homogenization, tubulin isolation cycles, and final polishing by ion exchange chromatography using FPLC and subsequent activity measurement assays. The homogeneity of purified tubulin was more than 97%, as confirmed by MS/MS analysis utilizing electrospray ionization and MALDI-TOF.

Drp1 acetylation mediated by CDK5-AMPK-GCN5L1 axis promotes cerebral ischemic injury via facilitating mitochondrial fission

The aberrant acetylation of mitochondrial proteins is involved in the pathogenesis of multiple diseases including neurodegenerative diseases and cerebral ischemic injury. Previous studies have shown that depletion of mitochondrial NAD+, which is necessary for mitochondrial deacetylase activity, leads to decreased activity of mitochondrial deacetylase and thus causes hyperacetylation of mitochondrial proteins in ischemic brain tissues, which results in altered mitochondrial dynamics. However, it remains largely unknown about how mitochondrial dynamics-related protein Drp1 is acetylated in ischemic neuronal cells and brain tissues. Here, we showed that Drp1 and GCN5L1 expression was up-regulated in OGD-treated neuronal cells and ischemic brain tissues induced by dMCAO, accompanied by the increased mitochondrial fission, mtROS accumulation, and cell apoptosis. Further, we confirmed that ischemia/hypoxia promoted Drp1 interaction with GCN5L1 in neuronal cells and brain tissues. GCN5L1 knockdown attenuated, while its overexpression enhanced Drp1 acetylation and mitochondrial fission, indicating that GCN5L1 plays a crucial role in ischemia/hypoxia-induced mitochondrial fission by acetylating Drp1. Mechanistically, ischemia/hypoxia induced Drp1 phosphorylation by CDK5 upregulation-mediated activation of AMPK in neuronal cells, which in turn facilitated the interaction of GCN5L1 with Drp1, thus enhancing Drp1 acetylation and mitochondrial fission. Accordingly, inhibition of AMPK alleviated ischemia/hypoxia- induced Drp1 acetylation and mitochondrial fission and protected brain tissues from ischemic damage. These findings provide a novel insight into the functional roles of GCN5L1 in regulating Drp1 acetylation and identify a previously unrecognized CDK5-AMPK-GCN5L1 pathway that mediates the acetylation of Drp1 in ischemic brain tissues.

Determination of Plasmalogen Molecular Species in Hen Eggs

(1) Background: Plasmalogens are vinyl ether-type glycerophospholipids that are characteristically distributed in neural tissues and are significantly reduced in the brains of individuals with dementia compared to those in healthy subjects, suggesting a link between plasmalogen deficiency and cognitive decline. Hen eggs are expected to be a potential source of dietary plasmalogens, but the details remain unclear. (2) Methods: We evaluated the fresh weight, dry weight, total lipid, neutral lipids, glycolipids, and phospholipids in the egg yolk and egg white of hen egg. Then, the molecular species of plasmalogens were quantified using HPLC-ESI-MS/MS. (3) Results: In egg yolk, the total plasmalogen content was 1292.1 µg/100 g fresh weight and predominantly ethanolamine plasmalogens (PE-Pls), specifically 18:0/22:6-PE-Pls, which made up 75.6 wt% of the total plasmalogen. In egg white, the plasmalogen content was 31.4 µg/100 g fresh weight and predominantly PE-Pls, specifically 18:0/20:4-PE-Pls, which made up 49.6 wt% of the total plasmalogen. (4) Conclusions: Plasmalogens were found to be more enriched in egg yolk than in egg white. It was found that humans are likely to ingest almost 0.3 mg of total plasmalogens from one hen egg. These findings highlight the importance of plasmalogens in the daily diet, and it is recommended to explore the impact of long-term dietary plasmalogen intake to assess its effect on human health. This provides a viewpoint for the development of new food products.

Destabilisation of Alzheimer's amyloid-β protofibrils by Baicalein: mechanistic insights from all-atom molecular dynamics simulations.

Alzheimer's disease (AD) is the most common form of dementia and the fifth leading cause of death globally. Aggregation and deposition of neurotoxic Aβ fibrils in the neural tissues of the brain is a key hallmark in AD pathogenesis. Destabilisation studies of the amyloid-peptide by various natural molecules are highly relevant due to their neuroprotective and therapeutic potential for AD. We performed molecular dynamics (MD) simulation to investigate the destabilisation mechanism of amyloidogenic protofilament intermediate by Baicalein (BCL), a naturally occurring flavonoid. We found that the BCL molecule formed strong hydrophobic contacts with non-polar residues, specifically F19, A21, V24, and I32 of Chain A and B of the pentameric protofibril. Upon binding, it competed with the native hydrophobic contacts of the Aβ protein. BCL loosened the tight packing of the hydrophobic core by disrupting the hydrogen bonds and the prominent D23-K28 inter-chain salt bridges of the protofibril. The decrease in the structural stability of Aβ protofibrils was confirmed by the increased RMSD, radius of gyration, solvent accessible surface area (SASA), and reduced β-sheet content. PCA indicated that the presence of the BCL molecule intensified protofibril motions, particularly affecting residues in Chain A and B regions. Our findings propose that BCL would be a potent destabiliser of Aβ protofilament, and may be considered as a therapeutic agent in treating AD.

Exploring protein-protein interactions for the development of new analgesics.

The development of new analgesics has been challenging. Candidate drugs often have limited clinical utility due to side effects that arise because many drug targets are involved in signaling pathways other than pain transduction. Here, we explored the potential of targeting protein-protein interactions (PPIs) that mediate pain signaling as an approach to developing drugs to treat chronic pain. We reviewed the approaches used to identify small molecules and peptide modulators of PPIs and their ability to decrease pain-like behaviors in rodent animal models. We analyzed data from rodent and human sensory nerve tissues to build associated signaling networks and assessed both validated and potential interactions and the structures of the interacting domains that could inform the design of synthetic peptides and small molecules. This resource identifies PPIs that could be explored for the development of new analgesics, particularly between scaffolding proteins and receptors for various growth factors and neurotransmitters, as well as ion channels and other enzymes. Targeting the adaptor function of CBL by blocking interactions between its proline-rich carboxyl-terminal domain and its SH3-domain-containing protein partners, such as GRB2, could disrupt endosomal signaling induced by pain-associated growth factors. This approach would leave intact its E3-ligase functions, which are mediated by other domains and are critical for other cellular functions. This potential of PPI modulators to be more selective may mitigate side effects and improve the clinical management of pain.

MICROBIOME: The trials and errors of developing an experimental model to study the impact of maternal gut microbiome disruption on perinatal asphyxia.

Maternal gut microbiome impairment has garnered attention for its potential role in influencing neurodevelopmental outcomes in offspring, especially in situations that increase brain vulnerability such as perinatal asphyxia (PA). Maternal microbiome and fetal brain interplay emerge as a critical link between maternal health and offspring neurodevelopment. This study aims to generate a model to assess the impact of maternal dysbiosis triggered by gestational antibiotic administration and PA on offspring neurodevelopment. Wistar rats were subjected to antibiotics in drinking water from the 11th gestational day until birth. On the 6th postnatal day, pups were subjected to PA/normoxia, resulting in four experimental groups: control-normoxia, antibiotics-normoxia, control-asphyxia, and antibiotics-asphyxia. Early-life behavioral tests were conducted between postnatal days 7 and 9. The initial antimicrobial cocktail (ampicillin, vancomycin, neomycin, clindamycin, amphotericin-B) led to an increased number of miscarriages, poor weight gain during pregnancy, reduced offspring weight, and changes in the maternal gut microbiome compared to control. Offspring presented impaired neurodevelopmental reflexes in both PA and antibiotic groups and increased hippocampal neuroinflammation. Due to these detrimental effects, a more pregnancy-safe antibiotic cocktail was used for a second experiment (ampicillin, vancomycin, neomycin, meropenem). This resulted in no miscarriages or pregnancy-weight loss but was still linked to gut microbiome disruption. PA impaired neurodevelopmental reflexes and increased neuroinflammation, effects amplified by antibiotic administration. These preliminary findings reveal the cumulative potential of maternal dysbiosis and PA on neurodevelopment impairment, emphasizing caution in gestational antimicrobial use. Further investigations should include offspring long-term follow-up and maternal behavior and integrate probiotics to counteract antibiotic effects. This study investigates the impact of maternal gut microbiome disruptions caused by gestational antibiotic treatment and low oxygen exposure shortly after birth on the development of the rats' babies. We found that both antibiotic exposure and reduced oxygen levels led to changes in early behavior and increased inflammation of the nervous tissue in the baby rats. Although using a different, potentially safer antibiotic combination reduced pregnancy complications, it still changed the bacteria in the mother's gut and worsened early behavior. These findings show that antibiotics during pregnancy can affect the developing brain of baby rats and careful consideration should be used before prescribing them. Future research will explore longer-term effects and potential medicines.

Folic acid ameliorates high glucose–induced neurotoxicity in human forebrain organoids: Insights from proteomics

AbstractPregestational diabetes (PGDM) has been associated with an elevated risk of congenital abnormalities, particularly those affecting the nervous system. The efficacy of folic acid (FA) supplementation in reducing the incidence of neurodevelopmental damage caused by PGDM has been well documented. However, the exact mechanism is unclear. Here, a human forebrain organoid model, which replicates the three‐dimensional structure of the early fetal neural tissue, was employed to study the neuroprotective effects of FA in PGDM. In this study, the forebrain organoids were cultured at high glucose (HG) concentrations from Days 20 to 40 with or without FA. Immunostaining revealed that the supplementation of FA significantly decreased HG‐induced neuron apoptosis. The proteomics examination suggested HG caused an increase in glial fibrillary acidic protein expression, a marker of astrocytes, leading to the upregulation of metallothionein expression and perturbation of mineral absorption, whereas FA reversed this effect. Proteomics analysis further showed that FA reduced HG‐induced cell migration. Moreover, Western blot analysis verified that FA mitigated HG‐induced apoptosis and cell migration via AMPK/FOXO pathway. Overall, current findings indicate that FA, as a functional food ingredient, has a protective effect on HG‐induced abnormal fetal neurodevelopment.

A Method for Electrical Stimulus Artifact Removal Exploiting Neural Refractoriness: Validation by Contrasting Cathodic and Anodic Stimulation.

To present a novel method for removing stimulus transient that exploits the absolute refractory period of electrically excitable neural tissues. Electrical stimulation often generates significant signal artifacts that can obscure important physiological signals. Removal of the artifact and understanding latent information from these signals could provide objective measures of circuit engagement, potentially driving advancements in neuromodulation research and therapies. We conducted intracranial physiology studies on five consecutive patients with Parkinson's disease who underwent deep brain stimulation (DBS) surgery as part of their routine care. Monopolar stimuli (either cathodic or anodic) were delivered in pairs through the DBS electrode across a range of inter-stimulus intervals. Recordings from adjacent unused electrode contacts used broadband sampling and precise synchronization to generate a robust template for the stimulus transient during the absolute refractory period. These templates of stimulus transient were then subtracted from recordings at different intervals to extract and analyze the residual neural potentials. After artifact removal, the residual signals exhibited absolute and relative refractory periods with timing indicative of neural activity. Cathodic and anodic DBS pulses generated distinct patterns of local tissue activation, showing phase independence from the prior stimulus. The earliest detectable neural responses occurred at short peak latencies (ranging from 0.19 to 0.38 ms post-stimulus) and were completely or partially obscured by the stimulus artifact prior to removal. Cathodic stimuli produced stronger local tissue responses than anodic stimuli, aligning with clinical observations of lower activation thresholds for cathodic stimulation. However, cathodic and anodic pulses induced artifact patterns that were equivalent but opposite. The proposed artifact removal technique enhances prior approaches by allowing direct measurement of local tissue responses without requirements for stimulus polarity reversal, template scaling, or specialized filters. This approach could be integrated into future neuromodulation systems to visualize stimulus-evoked neural potentials that would otherwise be obscured by stimulus artifacts.

Role of Amniotic Fluid Toxicity in the Pathophysiology of Myelomeningocele: A Narrative Literature Review.

Myelomeningocele is a birth defect whose clinical manifestations are due both to incomplete neural tube closure and the progressive destruction of exposed neuroepithelium during pregnancy. Two hypotheses have been formulated to explain the spinal cord damage in utero: mechanical trauma and chemical factors. The objective of this review was to summarize the current insights about the potential role of amniotic fluid in spinal cord damage in myelomeningocele. Numerous histological and clinical data on animals and humans strongly suggest a progressive degeneration of neural tissue including loss of neural cells, astrogliosis, inflammation, and loss of normal architecture. However, few data have been published about the direct toxicity of amniotic fluid in this neural degeneration, including the potentially toxic effect of meconium. Finally, the chemical and cellular modifications of amniotic fluid composition in myelomeningocele could reflect both the process (toxic effect of meconium) and the consequences of neuroepithelium destruction (release of neural cells). Fetal surgery not only stops the leakage of the cerebrospinal fluid but also reduces the toxic effect of amniotic fluid by restoring the intrauterine environment. Identification of amniotic fluid neurotoxic factors could lead to the development of therapeutic agents designed to protect spinal tissue and improve fetal myelomeningocele outcomes.

The influence of temperature and β-1,3-glucans on the occurrence of white spot syndrome virus and white spot disease in post-larvae of Penaeus vannamei shrimp

Penaeus vannamei is the main species of shrimp farmed worldwide, and for Ecuador it is the first non-oil economic sector. However, various pathogens, including white spot syndrome virus (WSSV), threaten the sustainability of shrimp farming. P. vannamei larvae are susceptible to WSSV infection via vertical or horizontal transmission. To decrease the incidence of WSSV in PLs, a bioassay was performed by exposing P. vannamei shrimp (PL25), which were negative for WSSV and white spot disease (WSD), to two protective factors, water temperature (T = 24 °C and T = 31 °C), and immunestimulation using β-1,3-glucans (BG) (with and without BG added to the food), using a crossed two-factor design, for 20 days. The incidence of WSSV and WSD was modeled using generalized linear model (GLM). The strength of the association between the response and explanatory variables was estimated using the odds ratio [Exp (Beta)] and interpreted as the level of risk for the incidence of WSSV or WSD in one of the categories compared to the baseline category in the GLM. Odds ratios were considered significant if their 95 % confidence interval did not include the value 1. The results showed that BG had a significant negative effect on the number of WSSV-positive animals. In addition, a lower probability of WSSV infection was determined by combining 31 °C and BG. In this treatment, the WSD injuries were almost undetectable. Most larvae shrimps affected by WSD exhibited injuries to the antennal gland and connective tissue. In situ hybridization analysis revealed that 29 % of shrimp, initially negative by histology, were positive for WSSV. The virus was detected mainly in the nervous tissue of the head, epithelium, connective tissue of the head appendages, and the oral region surrounding the integumental glands. Apoptosis analysis showed a weak signal in nerve tissue but was more intense in epithelial cells of the head appendages, in association with cuticular damage. According to the findings, WSSV could disseminate among shrimp populations by infecting them through the TG and epithelium of the head appendage, followed by connective tissue and nervous tissue. However, applying BG at 31 °C may serve as a protective measure to reduce WSD injuries and restrict WSSV dissemination.

Electrostatic Mapping of Rabies Anti-idiotype Antibody Compared to Rabies Virus Glycoprotein

Rabies is a lethal viral animal disease that assaults the central nervous system. Its glycoprotein is a viral protein that is essential for viral pathogenicity. Initially, the rabies vaccine was produced from nerve tissue, but it is no longer recommended since it causes adverse effects and is less effective. The anti-idiotype antibody vaccination is one option that functions as homologous artificial antigens to the glycoprotein of the rabies virus. The CDR is the structure of anti-idiotypic antibodies that play a role in mimicking epitopes. It may resemble or be identical to epitopes seen in rabies virus glycoproteins. The objective of this study is to determine the affinity of the CDR anti-idiotype antibody for the rabies virus glycoprotein epitope by studying the CDR electrostatic value. This electrostatic value was analyzed by bioinformatics approaches using a webPIPSA server. The findings revealed an electrostatic resemblance between the structure of anti-idiotype antibodies and the rabies virus glycoprotein. Further study will be aimed at collecting electrostatic values from each structure to create an anti-rabies vaccine. Keywords: anti-idiotype antibodies, CDR, electrostatic, rabies, glycoprotein, webPIPSA

Central nervous tissue in ovarian mature teratoma: A neuropathological study of 101 resected tumors.

Ovarian mature teratomas frequently contain central nervous system (CNS) tissue that often exhibits a variety of neuropathologic alterations. The author systematically examined the changes seen in CNS tissue from a series of 251 cases of resected ovarian mature teratomas. A total of 101 (40.2%) samples contained CNS tissue in varying amounts. The principal pathologic findings in the CNS tissue from ovarian mature teratomas were as follows: (i) CNS tissue tended to form a relatively thin, undulating, plate-like structure that comprised the walls or septa of cystic tumors; (ii) most neurons were small or medium sized, and no CD34-positive "ramifying cells" were observed; (iii) cytoplasmic processes of some astrocytes closely surrounded the walls of capillaries, suggesting formation of a blood-brain barrier; (iv) some ependymal cells exhibited a columnar shape and showed a pseudostratified arrangement, and these cells extended thick basal cytoplasmic processes into the neuropil; (v) a few choroid plexus epithelial cells showed melanin deposition, tubular transformation, or oncocytic changes; (vi) hamartoma-like hyperplasia of arachnoid cells was noted beneath skin tissue; (vii) some CNS tissue showed formation of cerebral cortical structures exhibiting "gyration" with incompletely layered structures, and disruption of the glia limitans with spillage of cortical tissue into the "subarachnoid" space was also observed; and (viii) in the well-formed cerebellar cortex, dendrites of Purkinje cells exhibited varied dysmorphic changes. These neuropathologic observations should lead to a deeper understanding of the pathogenesis of various lesions in the brain.

Reconciliation of weak pairwise spike-train correlations and highly coherent local field potentials across space.

Multi-electrode arrays covering several square millimeters of neural tissue provide simultaneous access to population signals such as extracellular potentials and spiking activity of one hundred or more individual neurons. The interpretation of the recorded data calls for multiscale computational models with corresponding spatial dimensions and signal predictions. Multi-layer spiking neuron network models of local cortical circuits covering about $1\,{\text{mm}^{2}}$ have been developed, integrating experimentally obtained neuron-type-specific connectivity data and reproducing features of observed in-vivo spiking statistics. Local field potentials can be computed from the simulated spiking activity. We here extend a local network and local field potential model to an area of $4\times 4\,{\text{mm}^{2}}$, preserving the neuron density and introducing distance-dependent connection probabilities and conduction delays. We find that the upscaling procedure preserves the overall spiking statistics of the original model and reproduces asynchronous irregular spiking across populations and weak pairwise spike-train correlations in agreement with experimental recordings from sensory cortex. Also compatible with experimental observations, the correlation of local field potential signals is strong and decays over a distance of several hundred micrometers. Enhanced spatial coherence in the low-gamma band around $50\,\text{Hz}$ may explain the recent report of an apparent band-pass filter effect in the spatial reach of the local field potential.

Intracranial injuries in the autopsy material of the Department of Forensic Medicine of the Medical University of Lodz with analysis of anatomical lesions caused by traumatic brain injuries

BackgroundIn 2022, 408 autopsies were performed in the Department of Forensic Medicine of the Lodz Medical University, of which as many as 82 concerned deaths with intracranial injuries, which represents about 20 % of all performed autopsies. AimThe article presents a comparative analysis of deaths of people with intracranial injuries in terms of frequency, the structure of victims (gender, age, sobriety), type of injury (intracranial bleeding, bruises of nerve tissue, nerve tissue tears, posttraumatic brain oedema, etc.), causes and circumstances of death, place of death (house, hospital, street) survival time, type of tool/object used, and the obtained data were compared with publications from other departments of forensic medicine. ResultsThe victims were definitely male. Regarding age, deaths mainly concerned people between 31 and 70. The most common cause of death was multi-organ injuries, craniocerebral, intracranial and the least other injuries. Regarding the circumstances of the deaths, most of the cases were accidents; the fewest were homicides.