bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of maternal inflammation on growth performance, carcass characteristics, and meat quality of offspring pigs
Authors: Johnson Danielle C , Bryan Erin E , Burris Elli S , Dilger Ryan N , Harsh Bailey N , Dilger Anna C 
Published: July 2024

Abstract
The objective of this research was to determine the effects of mid-gestational maternal inflammation on performance, carcass characteristics, and meat quality of offspring. Pregnant gilts were administered either lipopolysaccharide (LPS; n = 7) or saline (CON, n = 7) from days 70 to 84 of gestation. Gilts assigned to the LPS treatment were administered an intravenous injection of reconstituted LPS every other day with a beginning dose of 10 μg LPS/kg body weight and subsequent doses increasing by 12%, while CON gilts received intravenous injections of comparable volumes of saline. Gilts farrowed naturally, and at day 66 of age, a total of 59 pigs, both barrows and gilts began a 3-phase feeding regimen designed to meet or exceed nutrient requirements for growing-finishing pigs. Pigs were weighed on days 0, 35, 70, and 105 of the finishing trial to determine average daily gain, average daily feed intake, and gain-to-feed ratio (G:F). On day 106, pigs were slaughtered under the supervision of the U.S. Department of Agriculture Food Safety Inspection Service. Ending live weight, hot carcass weight, and dressing percentage were determined. The left side of carcasses was weighed and fabricated to determine carcass cutting yields. The semitendinosus was collected for histological samples. Fresh belly characteristics and loin quality were measured. Two chops were collected for Warner–Bratzler shear force and proximate analysis. No differences (P ≥ 0.13) between LPS and CON pigs were observed for growth performance in phases 1, 2, 3, or overall (days 0 to 105) performance with the exception of overall G:F reduced in CON pigs compared with LPS pigs (P = 0.03). There was a tendency for carcass yield to be reduced (P = 0.06; 0.82% units) in LPS pigs compared with CON pigs. Additionally, longissimus muscle area tended to be reduced (P = 0.10) 2.27 cm2 in LPS compared with CON pigs. Loin chop quality traits including instrumental color, subjective color, marbling, firmness, pH, and drip loss were not different (P ≥ 0.09) between LPS and CON pigs. Fresh belly characteristics were not different (P ≥ 0.22) between LPS and CON pigs. There were no differences in primal and subprimal weights, except that LPS pigs tended to have a reduction (P ≥ 0.07) in tenderloin and Canadian back weights compared with CON pigs. Furthermore, LPS pigs had no differences (P ≥ 0.25) in muscle fiber composition or size; however, LPS pigs tended (P = 0.10) to have a 13% reduction in estimated muscle fibers number compared with CON pigs. In summary, mid-gestational inflammation did not result in reduced meat quality, growth performance, or carcass yields of offspring.
Habitat integrity and interspecific relationships affect the diversity of freshwater crabs (Decapoda: Brachyura: Pseudothelphusidae, Trichodactylidae) in eastern Amazon streams
Authors: Rivera-Pérez Juan Mateo , Cruz Gabriel Martins , Penha Izabella Cristina da Silva , Juen Leandro 
Published: July 2024

ABSTRACT
Freshwater crabs play a crucial role in aquatic ecosystems by contributing to decomposition of organic matter and facilitating energy flow in food webs. They also serve as sensitive indicators of habitat modification, pollution, and other anthropogenic activities. We assessed the relationship between the integrity of Amazonian stream habitats and the abundance and interspecific competition among species of freshwater crab species in Pará, Brazil. Our findings, based on surveys across 35 streams of varying habitat integrity and employing generalized linear models for data analysis, revealed that the loss of riparian vegetation and increased streambank erosion negatively impacted the abundance of freshwater crabs of the family Trichodactylidae. Interactions between species also influenced the abundance of species of Pseudothelphusidae and Trichodactylidae, where their co-occurrence in the streams was analyzed. Our findings underscore the importance of understanding how environmental changes affect the diversity of freshwater crabs and that such changes can be valuable in identifying and mitigating long-term environmental impacts on streams.
Exploring the efficacy of pyrethroid incorporated nets for the control of stored product moth species: immediate and delayed effects onEphestia kuehniellaandPlodia interpunctella(Lepidoptera: Pyralidae)
Authors: Altunç Yunus Emre , Sakka Maria K , Gourgouta Marina , Morrison William R , Güncan Ali , Athanassiou Christos G 
Published: July 2024

AbstractInsect pests pose a significant threat to stored commodities, necessitating the exploration of alternative pest management strategies. Long-lasting insecticide-incorporated nets (LLINs) have emerged as a promising tool, offering selectivity and reduced ecological impact compared to conventional chemical approaches. However, their efficacy against Ephestia kuehniella Zeller and Plodia interpunctella (Hübner) (Lepidoptera: Pyralidae), cosmopolitan stored product moth species, has remained underexplored. This study investigated the immediate and delayed effects of 2 commercial pyrethroid-incorporated nets, Carifend (0.34% α-cypermethrin) and D-Terrence (0.4% deltamethrin), on the adult and larval stages. Both LLINs demonstrated high efficacy in controlling E. kuehniella and P. interpunctella, with mortality rates reaching up to 100% depending on exposure and post-exposure durations. Particularly, rapid knockdown was observed with D-Terrence net inducing 100% of adults in P. interpunctella after 30 min exposure. LLINs achieved almost 100% immediate mortality rate against adults after just 1 day of exposure. In addition, immediate rates of affected individuals reached as high as 81% and 91% in E. kuehniella and P. interpunctella larvae, respectively, following just 5 h of exposure to the D-Terrence. Different responses were observed between the adult and larval stages, with larvae exhibiting higher tolerance and potential for recovery from the affected phase after short exposures. There were increasing mortality rates after greater exposure to LLIN. Findings highlight the potential of LLINs as a pest management tool in storage facilities against these important stored product moths. Understanding the responses between life stages and the significance of delayed effects is crucial for optimizing LLIN deployment strategies.
Towards a polarized semantics for assertion and denial
Authors: Carrara Massimiliano , Chiffi Daniele , De Florio Ciro 
Published: July 2024

Abstract
Recent logic and linguistic literature suggest that certain forms of denial cannot be reduced to a simple assertion of negation. In particular, the existence of mathematical and empirical conjectures offers a basis for refuting Frege’s thesis of equivalence between denial and assertion of negation. Following this line of thought we develop a formal framework with two primitive illocutionary operators for assertion and denial, where denial is not a simple negation of assertion. We introduce a semantics for the operators mentioned above. Finally, we discuss the relations between asserted and denied contents.
Cerebral Cortical Dysplasia or Dysgenesis
Authors: Sarnat Harvey B. , Flores-Sarnat Laura 
Published: July 2024

Abstract
Embryonic and fetal ontogenesis of the central nervous system is realized by genetically programmed developmental processes with precise timing of onset. Both anatomical development and timing are altered in brain malformations. Keratan sulfate (KS) proteoglycan is a key axonal pathfinding guide and insulator of tracts and fascicles within the central nervous system and an essential determinant of the equilibrium of excitation and inhibition at the level of the individual neuron during development. KS is selective by repelling glutamatergic axons and facilitating GABAergic axons at sites of synapse formation. Its demonstration by immunocytochemistry provides another perspective for understanding epileptogenesis at the cellular level in brain resections for epilepsy and at autopsy, including fetal tissues. Examples of malformations in which epileptogenesis is influenced by KS are polymicrogyria, schizencephaly, focal cortical dysplasias, holoprosencephaly, and Down syndrome.
Excitation-Inhibition Balance in Absence Seizure Ictogenesis
Authors: Lőrincz Magor L. , Crunelli Vincenzo , David Francois 
Published: July 2024

Abstract
Thirty percent of children with absence seizures are pharmaco-resistant, and 60% suffer from neuropsychiatric comorbidities that often persist even after full pharmacological control of the seizures. This highlights the need for a detailed comprehension of the cellular and network mechanisms of these nonconvulsive seizures. Generally, network hyperexcitability and hypersynchrony underlying seizure ictogenesis are thought to originate from impaired inhibition or enhanced excitation. In absence seizures, there is a markedly enhanced synchrony in cortico-thalamic and cortico-basal ganglia-thalamic networks, but solid evidence from genetic animal models indicates that at the single-cell and neuronal population levels GABAergic inhibition is generally increased while excitation is mostly either unchanged or decreased. Here, recent results on intrinsic conductances and network mechanisms within cortico-thalamic and cortico-basal ganglia-thalamic circuits are highlighted that support this view.
Adult Neurogenesis in Epileptogenesis and Comorbidities
Authors: Cho Kyung-Ok , Hsieh Jenny 
Published: July 2024

Abstract
Epilepsy is a lifelong, devastating disease that affects all ages. Epileptic seizures generate abnormal adult-born granule cells (abGCs) in the dentate gyrus, which can contribute to the development of epilepsy and comorbidities. In this chapter, we present the characteristic features and potential significance of abGC abnormalities: increased proliferation and subsequent reduction of neural progenitors, persistent hilar basal dendrites, sprouting of mossy fibers, production of hilar ectopic granule cells, and dispersion of granule cells. We also describe several key molecules that regulate seizure-induced aberrant neurogenesis. We then discuss the role of reactive astrocytes and microglia in each step of hippocampal neurogenesis during the epileptogenesis. Finally, we review the crucial findings regarding the functional implications of abnormal abGCs in epileptogenesis and summarize comorbid illnesses such as cognitive impairment and mood disturbances. Seizure-generated abGCs represent an attractive target for treating epilepsy and associated psychiatric dysfunction. Therefore, developing novel and selective antiepileptic drugs will require more basic research on the molecular mechanisms governing aberrant hippocampal neurogenesis, as well as exploiting human and non-human primate models.
Adenosine Kinase
Authors: Murugan Madhuvika , Boison Detlev 
Published: July 2024

Abstract
Adenosine is an endogenous anticonvulsant, which is inversely linked to the expression levels of adenosine kinase (ADK), a ribokinase that metabolizes adenosine into AMP. ADK exists as two distinct isoforms, with unique cellular compartmentalization and functions. The short isoform (ADK-S) is localized primarily in the cytoplasm of astrocytes, where it controls, in conjunction with equilibrative adenosine transporters, the extracellular levels of adenosine and hence adenosine receptor-mediated mechanisms. On the other hand, the long isoform of ADK (ADK-L) is localized in the nucleus of astrocytes and a subset of neurons, where it regulates adenosine receptor independent epigenetic mechanisms. Overexpression of ADK-S was sufficient to generate spontaneous electrographic seizures, whereas increased ADK-L has been associated with epileptogenesis. Hence, targeting specific ADK isoforms is a rational approach for the suppression of seizures and the development of epilepsy. Systemic adenosine augmentation therapies are effective in seizure suppression, although accompanied by widespread cardiovascular side effects. The refinement of therapeutic administration strategies, the development of isoform-specific ADK inhibitors, or a combination of the two, will enable the formulation of more selective therapies for epilepsy and its prevention. Therapeutic tools to achieve focal adenosine augmentation, such as engineered stem cells and silk-based polymers, demonstrate robust protection from induced and spontaneous seizures. Metabolic therapies such as the ketogenic diet therapy have also been indicated to prevent disease progression via epigenetic mechanisms mediated by ADK. Small-molecule, ADK isoform-specific inhibitors are now in development with the goal to translate ADK-based therapies into clinical applications.
Inflammatory Astrocytic TGFβ Signaling Induced by Blood–Brain Barrier Dysfunction Drives Epileptogenesis
Authors: Yang Lynn T. , Anthony Giovanni , Kaufer Daniela 
Published: July 2024

Abstract
Under healthy conditions, the brain is protected by the blood–brain barrier (BBB), a selective barrier function of the central nervous system vasculature restricting the passage of most macromolecules and cells from the blood into the brain. BBB dysfunction (BBBD) occurs in various epileptogenic conditions including stroke, traumatic injury, status epilepticus, and aging. This chapter summarizes recent findings which demonstrate that BBBD is sufficient to induce epileptogenesis, and identifies the epileptogenic cascade triggered by BBBD. This cascade includes (1) cross-BBB influx of albumin from the serum into the brain neuropil, (2) albumin binding to and activating astrocytic transforming growth factor beta (TGFβ) receptor ALK5, (3) mounting of inflammatory signaling and TGFβ1 positive feedback, (4) transcriptional changes in astrocytes that induce astrocytic decoupling and downregulation of K+ and glutamate buffering capacity, (5) degradation of extracellular matrix, and (6) growth of new excitatory synapses and reorganization of neural networks to favor excitatory activity. These changes epitomize the major hallmarks of epileptogenesis across animal models of acquired epilepsy and in tissue samples from patients, providing a “missing link” for how epileptogenic injuries trigger these pathological changes. Inhibition of TGFβR signaling blocks this cascade of events and prevents epileptogenesis. These findings highlight the potential of BBB-stabilizing treatments as an epilepsy-preventive therapeutic approach, and BBBD quantification as a biomarker for predicting postinjury epilepsy outcomes.
BDNF/TrkB Signaling and Epileptogenesis
Authors: Harward Stephen C. , Huang Yang Zhong , McNamara James O. 
Published: July 2024

Abstract
The epilepsies are one of the most common neurologic disorders with a diversity of etiologies. Despite tremendous advances in both medical and surgical therapies, availability of preventive and disease-modifying therapies is an important unmet medical need. Insight into the molecular and cellular mechanisms underlying epileptogenesis will hopefully provide novel targets for such therapies. To this end, multiple investigations using a variety of acquired epilepsy models deploying diverse etiologies (traumatic, ischemic, or seizure-induced) have identified the neurotrophin BDNF and its cognate receptor TrkB as key molecules in the pathogenesis. However, as detailed in this chapter, BDNF/TrkB signaling plays unique roles in each model. In addition to its contributions to epileptogenesis, BDNF/TrkB signaling contributes to neuronal survival following some epilepsy-inducing insults. Selective inhibition of distinct signaling pathways downstream of TrkB enables limiting TrkB-mediated epileptogenesis while preserving the protective functions. This chapter provides a critical review of the data supporting this diversity of roles for both BDNF and TrkB in the epilepsies and proposes strategies to disentangle these varying roles to develop therapies appropriate for clinical application.
EEG Biomarkers of Epileptogenesis
Authors: Kamintsky Lyna , Milikovsky Dan Z. , Friedman Alon 
Published: July 2024

Abstract
Insults to the brain (e.g., stroke, head trauma, infection, status epilepticus) can precipitate the development of epilepsy—months or even years after the initial insult. While not all patients with such injuries will go on to develop epilepsy, in a subgroup of individuals the injury will trigger epileptogenesis—a complex chain of events that transforms a nonepileptic brain into one that is prone to generating spontaneous seizures. To date, there are no clinically available tools capable of predicting which individuals are at high risk of post-insult epilepsy. A growing number of studies attempt to bridge this gap, by evaluating the utility of different diagnostic modalities (e.g., neuroimaging, molecular testing, electroencephalogram [EEG] analysis) in capturing changes reflective of the epileptogenic process. EEG holds particular promise as a modality for reflecting epileptogenic changes, due to its high temporal resolution and subsequent ability to capture a wide variety of brain-activity signatures. With the added advantages of portability, relative ease of use, safety, and low cost, a successful EEG-based biomarker is likely to become widely accessible in clinical settings. This chapter will discuss the most promising EEG signatures of epileptogenesis (interictal spikes, high-frequency oscillations, theta dynamics, and nonlinear dynamics), and the challenges of translating these biomarkers into clinically applicable tools. We conclude by highlighting the potential value of biomarker paradigms that (1) combine several signatures and (2) examine dynamic changes in these signatures over time.
Behavioral Biomarkers of Epileptogenesis and Epilepsy Severity
Authors: Ali Idrish , Casillas-Espinosa Pablo M. , Jones Nigel C. , O’Brien Terence J. 
Published: July 2024

Abstract
Currently, there are no established biomarkers which predict the risk of epilepsy following an epileptogenic brain insult, or which predict outcomes of pharmacological or surgical interventions following epilepsy diagnosis. Epilepsy appears to share bidirectional mechanistic relationships with its associated behavioral comorbidities such as neuropsychiatric and cognitive impairments, with several pieces of evidence suggesting that behavioral abnormalities exist before the initial diagnosis of epilepsy. Here, we discuss the preclinical and clinical evidence of these relationships, and the potential for behavioral and cognitive disorders to be harnessed as predictive biomarkers for risk of epilepsy or treatment outcomes.
Potassium Channels in Genetic Epilepsy
Authors: Weston Matthew C. , Tzingounis Anastasios V. 
Published: July 2024

Abstract
The past 70 years have provided a foundation for understanding potassium channel function at the single-channel, cellular, and circuit levels. Basic science of epilepsy has implicated potassium channel dysfunction in the pathogenesis of acquired epilepsy, and, more recently, genetic studies have revealed a large number of variants in potassium channel–encoding genes that cause epilepsy in humans. Identification and functional assessment of these variants have demonstrated they alter protein function, generating several hypotheses for how potassium channel dysfunction leads to the hypersynchronous neural activity characteristic of seizures. However, appreciation of the developmental, cellular, and synaptic complexity of the brain has increased in parallel to our knowledge of potassium channels, complicating the most straightforward idea that potassium channel dysfunction merely leads to depolarization of principal neurons, which causes seizures. The fact that many potassium channel–related epilepsies remain treatment refractory underscores the lack of a mechanistic understanding of this process. This chapter reviews our current understanding of the genetic and functional changes in potassium channels that may lead to epilepsy, within the framework of features of the excitable neuronal membrane known to be controlled by potassium currents. From there, the chapter expands into cell-type-specific roles of potassium channels, their effects on circuit development, and novel molecular interactions, and the evidence that these factors may play a role in epileptogenesis. Finally, the chapter highlights newer experimental approaches that have the potential to clarify the mechanisms through which potassium channel dysfunction leads to epilepsy and pave the way for more effective treatments.
High-Voltage-Activated Calcium Channels in Epilepsy
Authors: Rossignol Elsa 
Published: July 2024

Abstract
Voltage-gated calcium channels support an array of fundamental biological processes in various systems. In the brain, they determine neuronal responses to stimulation, dendritic properties, neuronal firing mode, and synaptic release. They also regulate multiple critical developmental processes, including neuronal proliferation, migration, connectivity, and structural activity-dependent plasticity. For these reasons, mutations in voltage-gated calcium channels result in a variety of neurological disorders displaying epilepsy as a core feature. This chapter summarizes the molecular, cellular, and network mechanisms by which mutations in high-voltage-activated calcium channels result in epilepsy, with a particular focus on CaV1.2 (CACNA1C), CaV1.3 (CACNA1D), CaV2.1 (CACNA1A), and CaV2.3 (CACNA1E)-associated disorders.
Therapeutic Window for the Treatment of Lafora Disease
Authors: Varea Olga , Guinovart Joan J. , Duran Jordi 
Published: July 2024

Abstract
Lafora disease, a devastating form of myoclonus epilepsy, progresses swiftly with neurodegeneration and rapidly leads to dementia. It is caused by mutations in two genes, either laforin (EPM2A) or malin (NHLRC1 or EPM2B). The hallmark of the disease is the accumulation of intracellular insoluble aggregates of abnormal glycogen, called Lafora bodies. The identification of Lafora bodies as the underlying cause of the disease prompted the design of therapeutic strategies for this condition based on the prevention of glycogen accumulation. In this chapter, two therapeutic strategies are analyzed, namely the suppression of glycogen synthase expression and the restoration of malin in malin-deficient mice. Both strategies were tested in mice at different stages of the disease to determine the therapeutic window for treatment. Glycogen synthase suppression arrests the accumulation of Lafora bodies in the brain only when induced at an early stage of Lafora disease. In contrast, the restoration of malin not only arrests the accumulation of Lafora bodies even at an advanced stage of the disease but also induces changes in the composition of the preexisting Lafora bodies and, importantly, ameliorates the inflammatory response. Therefore, malin restoration is presented as a gene replacement therapy to be developed for future application in patients with malin-deficient Lafora disease. Both approaches are significantly more effective when implemented at early stages, thus highlighting the importance of early diagnosis for the successful treatment of the condition.