bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of leguminous green manure–crop rotation on soil enzyme activity and stoichiometry
Authors: Liu Meixia , Hu Zonghao , Fan Yi , Hua Bin , Yang Wei , Pang Shuang , Mao Rong , Zhang Yang , Bai Keyu , Fadda Carlo , De Santis Paola , Bergamini Nadia , Usmankulova Aziza , Samedjanovich Buriyev Salimjan , Zhang Ximei 
Published: July 2024

Abstract
As a crucial strategy for sustainable agricultural production, green manure–crop rotation can regulate soil nutrient cycling and decrease the reliance on nitrogen fertilizers. However, we still lack a comprehensive understanding of the changes in soil eco-enzyme activities, microbial metabolism and nutrient limitations caused by leguminous green manure–crop rotation. Here, we conducted field experiments of leguminous green manure–crop rotation across China to analyze soil extracellular enzyme activities, specifically β-glucosidase (BG), N-acetyl-β-d-glucosaminidase (NAG), leucine aminopeptidase (LAP) and acid phosphatase (AP). The study revealed that long-term green manure–crop rotation increased carbon and nitrogen accumulation in farmland, with a significant average increase of 20.1% and 36.4% in BG, AP enzyme activities in topsoil, while showing a decrease in ln(NAG + LAP):ln(AP) ratios. The ratios of ln(BG):ln(NAG + LAP) and ln(NAG + LAP):ln(AP) in soil across various regions were typically below 1:1, indicating that soil microbial activity is more constrained by nitrogen and phosphorus nutrients rather than by carbon. Precipitation, temperature, soil total carbon (TC) and total nitrogen (TN) were identified as key environmental factors for extracellular enzyme activities and stoichiometric ratios. Our study highlights that the green manure–crop rotation alleviates nitrogen limitation while enhancing phosphorus limitation, and is closely related to the accumulation of TC and TN in the soil.
A case of bone tumor-induced compartment syndrome
Authors: Chaudhry Nadeem , Qureshi Abid , Sultana Mosammath , Pawanarkar Meehika , Rizwan Muhammad 
Published: July 2024

Abstract
Compartment syndrome is a rare critical condition that can arise in individuals with cancer, presenting with significant challenges in diagnosis and management. Compartment syndrome occurs when the pressure within a closed fascial space rises to a point that restricts circulation. A 56 year-old male patient presented with 2 days of pain and swelling in the right upper extremity pain. Physical examination was remarkable for right upper extremity erythema swelling and tense compartments, concerning for compartment syndrome. Humerus X-ray showed moth eaten appearance of mid humerus with periosteal reaction and fracture. Patient was taken to the operating room for anterior and posterior compartment fasciotomies. Compartment syndrome is a surgical emergency, for which fasciotomy is generally performed. Pathology has rarely been linked to malignancy, with seldom reports examining causation. More research regarding pathophysiology of cancer in relation to compartment syndrome needs to be conducted.
Epilepsy Genomics
Authors: Delgado-Escueta Antonio V. 
Published: July 2024

Abstract
Approximately 1% of 25,000 genes and 25 million single-nucleotide polymorphisms in the genome of modern humans are epilepsy variants. Epilepsy variants are the molecular basis of fatal progressive myoclonus epilepsies, epileptic encephalopathies, and other genetic epilepsies. This chapter annotates the early success and key turning points in the quest to cure fatal epilepsies. The first key turning point occurred in 2018 when “every-2-weeks” intraventricular infusion of cerliponase alfa, enzyme replacement therapy, halted progression of an early childhood progressive myoclonus epilepsy (CLN2 Batten disease), as reported by Schulz et al. In 2021, Schaeffer et al. reported 2 years of intraventricular cerliponase alfa delayed or prevented onset of symptoms in presymptomatic CLN2 infants. Earlier, in 2017, the Food and Drug Administration (FDA) and European Medicines Agency approved Nusinersen, an antisense oligonucleotide, and AVXS-101 (Zolgensma), a viral-mediated gene replacement therapy, as disease halting and potential cures for Werdnig Hoffmann type I spinal muscular atrophy of infancy (SMN1). Even now, breakthrough advances by others include (1) ex vivo HSPC transduction gene therapy in metachromatic keukodystrophy, and (2) genome editing with zinc finger nuclease opening DNA strands and inserting a correct alpha-L-iduronidase into the genome of Hurler mucopolysaccharidoses patients. Recently, the FDA proclaimed that they expect to approve 10–20 cell and gene therapies a year from 2025 onward. As clinical trials raise hopes for cures, vigilance for adverse effects and ethical concerns must not waiver.
Role of the Subiculum in Focal Epilepsy
Authors: Evstratova Alesya , Diaz-Fernandez Belén , Lévesque Maxime , Avoli Massimo , Huberfeld Gilles 
Published: July 2024

Abstract
The subiculum has for a long time been neglected and solely considered as the output region of the hippocampus, conducting or relaying inputs to the entorhinal cortex. However, significant evidence does not support such a passive role. The subiculum is a three-layer cortex structured associated with highly organized substructures. Preeminent bursting neuronal behavior and local microcircuits favor the production of strong neuronal activities. All hippocampal rhythms such as theta, gamma, sharp-wave ripples, and ripples can be generated by the subiculum. As a result, the subiculum is an important limbic structure involved in spatial location and memory. The role of the subiculum in epilepsy was highlighted by studies on human postoperative tissues, showing that it is a major and autonomous site of genesis of epileptic interictal and ictal activities. In these studies, a leading role of interneurons in the buildup of epileptic activities was suggested, and chloride dysregulation leading to depolarizing and potentially excitatory effects of GABAA signaling was unraveled. Evidence indicates that the subiculum not only anatomically “supports” hippocampal outputs, but that it also actively participates to the generation of epileptic activities in the temporal lobe.
A Classification of Seizures Based on Dynamics
Authors: Sheheitli Hiba , Wang Huifang , Lemarechal Jean-Didier , Bernard Christophe , Jirsa Viktor K. 
Published: July 2024

Abstract
Patient stratification according to seizure types is a pivotal step in the diagnosis and treatment of epilepsy. Great progress has been made in the understanding of the pathology and physiological substrates of epilepsy, leading to formal classification schemes based on empirical clinical features. However, much remains elusive regarding the mechanisms underlying seizures and the heterogeneity of its manifestations, which formal classification schemes attempt to capture. In the pursuit of a fundamental theory of seizure dynamics, dynamical systems theory provides the mathematical framework for a mechanistic understanding for the underlying dynamical processes. Within this framework, the need for a classification of seizures based on dynamics becomes evident. The diverse types of seizure onset and offset patterns are shown to be captured mathematically by different types of bifurcations that exhibit canonical invariant dynamical features. A seizure can then be classified into a corresponding “dynamotype” consisting of its onset and offset pair of bifurcations. Sixteen dynamotypes arise as combinations of the simplest relevant bifurcations, resulting in an organizational taxonomy of seizure dynamics (TSD). The current chapter provides a brief introduction into the mathematical theory upon which this taxonomy is built before presenting the different seizure dynamotypes. It then describes how TSD can be implemented as a classification scheme for the analysis of clinical stereo electroencephalographic data, along with sample results that summarize the observed prevalence of the different dynamotypes in a sample clinical dataset. The chapter ends with a discussion of the clinical ramifications of TSD and its implications for seizure control.
A Crucial Role for Astrocytes in Epileptogenesis
Authors: Bedner Peter , Peterson Allison R. , Binder Devin K. , Steinhäuser Christian 
Published: July 2024

Abstract
A growing body of evidence suggests that astrocytes are crucial actors in the initiation and progression of epilepsy. Reactive astrocytes in human and experimental epilepsy display marked morphological, transcriptional, and functional changes, but it is still often unclear whether this represents a causative factor, a consequence, or an adaptive response in epileptogenesis. A distinctive feature of astrocytes is their extensive intercellular coupling via gap junction channels. This allows them to form large syncytium-like functional networks that play essential roles in ion and neurotransmitter homeostasis, gliotransmission, nutrient supply to neurons, and regulation of the extracellular space volume. The first part of this chapter summarizes current knowledge on the role of gap junction channels in epilepsy, their expression and activity in human and experimental epilepsy, and the consequences of their genetic and pharmacological modulation on neuronal excitability and epileptogenesis. Astrocytes also regulate and respond to extracellular glutamate levels in the central nervous system via the Na+-dependent glutamate transporters glutamate transporter-1 (GLT-1) and glutamate aspartate transporter (GLAST) and the metabotropic glutamate receptors (mGluR) 3 and mGluR5. Both impaired astrocytic glutamate clearance and changes in mGluR signaling could contribute to the development of epilepsy. The second part of this chapter summarizes the changes in astrocyte glutamate receptors and transporters in epilepsy. Overall, both astrocytic gap junction channels and glutamate transporters and receptors could serve as novel therapeutic targets for epilepsy.
Brain Mosaicism in Epileptogenic Cortical Malformations
Authors: Ribierre Théo , Baulac Stéphanie 
Published: July 2024

Abstract
This chapter focuses on focal cortical dysplasia type II (FCDII) and mild malformation of cortical development with oligodendroglial hyperplasia in epilepsy (MOGHE), a mild malformation of cortical development, for which genetic advances have been remarkable in recent years. There is now clear evidence that FCDII is caused by brain somatic mutations in genes belonging to the mTOR pathway, and that MOGHE, a mild malformation of cortical development, is due to somatic mutations in the SLC35A2 gene, encoding the major Golgi-localized UDP-galactose transporter. Numerous rodent models using the in utero electroporation procedure have been used to model FCDII and recapitulate most neuropathological and clinical features. This chapter discusses the recent advances in using cerebral organoids to model neurodevelopmental disorders.
GABAA Receptors, Seizures, and Epilepsy
Authors: Olsen Richard W. , Wallner Martin , Rogawski Michael A. 
Published: July 2024

Abstract
GABAA receptors (GABARs), the main inhibitory neurotransmitter receptors in the mammalian brain, exist in a multitude of subtypes, including forms that predominantly mediate fast inhibitory synaptic transmission and other highly GABA-sensitive extrasynaptic forms that mediate tonic inhibition. GABARs are heteropentameric proteins formed by three different, yet homologous, subunits. Synaptic and extrasynaptic GABARs are targets of some medications used clinically in the treatment of seizures and epilepsy, including the barbiturates phenobarbital, primidone, and pentobarbital; propofol, and the neuroactive steroid ganaxolone. Synaptic GABARs are the targets of benzodiazepines, including diazepam, lorazepam, midazolam, and clobazam. Other epilepsy medications may also interact with GABARs in addition to affecting other antiseizure targets. This chapter gives a brief history of the GABAR involvement in the epilepsies and then describes developments since the publication of the last volume in this series in 2012. Greater understanding of the roles of GABAR isoforms has suggested strategies to target subpopulations of GABAR to more effectively treat various types of epilepsy and its comorbidities. Subtype specific GABAR positive modulators that selectively act on α2, α3, and α5 GABAR isoforms, and may have enhanced efficacy and reduced tolerance liability, are under investigation.
Strategies on Gene Therapy in Progressive Myoclonus Epilepsies
Authors: Kayani Saima , Gumusgoz Emrah , Minassian Berge A. , Dolce Alison 
Published: July 2024

Abstract
Progressive myoclonus epilepsies (PMEs) are a group of genetically and clinically heterogeneous diseases characterized by an invariable neurodegenerative decline leading to devastating disabilities and often fatal outcomes. Although there is a broad range of clinical manifestations, the shared features are encompassed within the name. Typically beginning in childhood and adolescence, patients present with very frequent myoclonus in addition to other types of epileptic seizures that very soon become refractory to medication. This is accompanied by a progressive neurocognitive decline along with other devastating changes including, but not limited to, vision loss, neuropathy, myopathy, and ataxia in a child that was otherwise previously normal. This chapter will review the potential therapeutic strategies for various PMEs.
Attention-Deficit Disorders and Epilepsy
Authors: Maheshwari Atul 
Published: July 2024

Abstract
Attention-deficit/hyperactivity disorder (ADHD) is a common comorbidity in patients with epilepsy. A polygenic predisposition likely interacts with environmental factors to determine the ultimate likelihood and severity of comorbid attention deficits. Epilepsy syndromes such as Dravet syndrome, juvenile myoclonic epilepsy, childhood absence epilepsy, and fragile X syndrome all have a high prevalence of ADHD. Many of these epilepsy syndromes are associated with monogenic mutations that have been implicated in inhibitory neurotransmission (Scn1a, GABRA1, Cacna1a, SNAP25, and FMR1, respectively). Monogenic rodent models carrying these genetic mutations have recapitulated varying degrees of epilepsy, hyperactivity, and attention deficits. Specifically testing various aspects of attention in rodents has been performed with validated procedures such as the Attention Set-Shifting task (ASST) or the 5-Choice Serial Reaction Time task (5-CSRTT). Recent studies have found cell-type-specific dysfunction in subsets of inhibitory neurons, most prominently in parvalbumin-expressing neurons. This underlying dysfunction likely leads to the symptomatic expression of both seizures and attention deficits. Both can be treated independently with antiseizure drugs and stimulant therapy, respectively. However, there remain no specific therapies for the underlying epileptogenic insult. Further studies should aim to combine the pathophysiological insight gained from monogenic models with targeted therapies on the genetic, molecular, cellular, and/or network levels. These therapies can then be screened on mutant rodent models using the ASST or 5-CSRTT to identify therapies with the greatest chance of improving quality of life in patients with comorbid epilepsy and ADHD.
Gene Therapy for Epilepsy
Authors: Goodspeed Kimberly , Armstrong Dallas , Boitnott Andrea , Dolce Alison , Ling Qinglan , Gray Steven J. 
Published: July 2024

Abstract
Epilepsy is a disease with diverse etiology; however, greater than 70%–80% of epileptic syndromes are thought to be associated with some genetic abnormality. Because of our fast-expanding genetic knowledge in epilepsy, we are approaching a new era of clinical management. We have an increased understanding of the underlying pathogenesis of genetic epilepsy as well as novel targets for precision therapies. Gene therapy, including gene transfer therapy, gene silencing, and gene editing, are promising new approaches to genetic epilepsy which have the potential to treat more than just the seizure manifestation of these devastating disorders. This chapter briefly reviews the role of genetic testing in epilepsy and introduces the application of gene therapy to genetic epilepsy syndromes as well as epileptogenesis more broadly.
Gene Therapy for Refractory Epilepsy
Authors: Kullmann Dimitri M. 
Published: July 2024

Abstract
Pharmacoresistance in epilepsy is common and represents a substantial unmet need. Of the advanced therapies for focal epilepsy in preclinical development, gene delivery using viral vectors to alter neuronal or circuit excitability in epileptogenic zones is arguably the closest to clinical translation. Monogenic disorders underlying severe childhood-onset epilepsies are also candidates for such treatments, because the genetic defect may be amenable to correction, although the brain areas that need to be targeted are less clearly defined. Several gene therapies have been validated in experimental rodent models, mainly based on the delivery of DNA or RNA encoding ion channels, neurotransmitters, or receptors. Some ion channel genes, however, are too big to package into adeno-associated or lentiviral vectors, and alternative approaches to manipulate gene expression have been proposed. Current obstacles to clinical translation center on optimizing delivery to defined brain areas, determining the correct dosage, and evaluating the long-term safety and efficacy of irreversible modification of the genetic makeup of neurons.
Environmental effects on low surface brightness galaxies in the IllustrisTNG simulation
Authors: Pérez-Montaño Luis Enrique , Cervantes Sodi Bernardo , Rodriguez-Gomez Vicente , Zhu Qirong , Ogiya Go 
Published: July 2024

ABSTRACT
Employing the TNG100 run of the IllustrisTNG project, we characterize the environment of low surface brightness galaxies (LSBGs) across varying scales, from their associated dark matter haloes to their distribution within the broader cosmic structure. We find no significant differences in the halo concentration index $c_{200}$ between LSBGs and their high surface brightness galaxy (HSBG) counterparts, with LSBGs residing in haloes with higher spin parameter $\lambda$ and slightly more spherical shapes than HSBGs. LSBGs show a stronger alignment between the dark and stellar angular momentum vectors than their high surface brightness counterparts. The relative abundance of LSBGs within groups and clusters displays a central deficit, hinting at potential destruction upon reaching these core regions. Studying the density field, we find a preference for rotation-dominated LSBGs to reside in low-density environments, while dispersion-dominated LSBGs thrive in high-density regions where galaxy interactions govern their evolution, an observation corroborated by our analysis of the two-point correlation function $\xi (r)$. Our examination of the cosmic web reveals no significant differences in the distance to the closest large-scale structure, barring a few exceptions. This suggests a limited impact of large-scale spatial distribution on mechanisms driving LSBG evolution. All together, we conclude that the halo vicinity and local environment at the scale of galaxy clusters, where mechanisms such as galaxy mergers and tidal stripping, as well as stellar and gas accretion take place, is the most likely environment that favour the emergence of LSBGs with different morphologies, mostly driven by the presence or absence of important local interaction phenomena.
Parallel Evolution at the Regulatory Base-Pair Level Contributes to Mammalian Interspecific Differences in Polygenic Traits
Authors: Okamoto Alexander S , Capellini Terence D 
Published: July 2024

Abstract
Parallel evolution occurs when distinct lineages with similar ancestral states converge on a new phenotype. Parallel evolution has been well documented at the organ, gene pathway, and amino acid sequence level but in theory, it can also occur at individual nucleotides within noncoding regions. To examine the role of parallel evolution in shaping the biology of mammalian complex traits, we used data on single-nucleotide polymorphisms (SNPs) influencing human intraspecific variation to predict trait values in other species for 11 complex traits. We found that the alleles at SNP positions associated with human intraspecific height and red blood cell (RBC) count variation are associated with interspecific variation in the corresponding traits across mammals. These associations hold for deeper branches of mammalian evolution as well as between strains of collaborative cross mice. While variation in RBC count between primates uses both ancient and more recently evolved genomic regions, we found that only primate-specific elements were correlated with primate body size. We show that the SNP positions driving these signals are flanked by conserved sequences, maintain synteny with target genes, and overlap transcription factor binding sites. This work highlights the potential of conserved but tunable regulatory elements to be reused in parallel to facilitate evolutionary adaptation in mammals.
Electronic perturbation of Cu nanowire surfaces with functionalized graphdiyne for enhanced CO2 reduction reaction
Authors: Zou Haiyuan , Cheng Dongfang , Tang Chao , Luo Wen , Xiong Huatian , Dong Hongliang , Li Fan , Song Tao , Shu Siyan , Dai Hao , Cui Ziang , Lu Zhouguang , Duan Lele 
Published: July 2024

ABSTRACT
Electronic perturbation of the surfaces of Cu catalysts is crucial for optimizing electrochemical CO2 reduction activity, yet still poses great challenges. Herein, nanostructured Cu nanowires (NW) with fine-tuned surface electronic structure are achieved via surface encapsulation with electron-withdrawing (–F) and -donating (–Me) group-functionalized graphdiynes (R-GDY, R = –F and –Me) and the resulting catalysts, denoted as R-GDY/Cu NW, display distinct CO2 reduction performances. In situ electrochemical spectroscopy revealed that the *CO (a key intermediate of the CO2 reduction reaction) binding affinity and consequent *CO coverage positively correlate with the Cu surface oxidation state, leading to favorable C–C coupling on F-GDY/Cu NW over Me-GDY/Cu NW. Electrochemical measurements corroborate the favorable C2H4 production with an optimum C2+ selectivity of 73.15% ± 2.5% observed for F-GDY/Cu NW, while the predominant CH4 production is favored by Me-GDY/Cu NW. Furthermore, by leveraging the *Cu–hydroxyl (OH)/*CO ratio as a descriptor, mechanistic investigation reveals that the protonation of distinct adsorbed *CO facilitated by *Cu–OH is crucial for the selective generation of C2H4 and CH4 on F-GDY/Cu NW and Me-GDY/Cu NW, respectively.
Coformulated Bictegravir/Emtricitabine/Tenofovir Alafenamide for Postexposure Prophylaxis After Sexual Assault: A Retrospective Real-World Study
Authors: Teresita de Jesús Cabrera-López , Edgar Pérez-Barragán , Carlos Ruben Nava-Campos , Marla Toiber-Rodríguez , Juan Carlos Rodríguez-Aldama , Raúl Adrián Cruz-Flores , Andrea González-Rodríguez 
Published: July 2024

Abstract
We report the experience of bictegravir/emtricitabine/tenofovir alafenamide for nonoccupational postexposure prophylaxis in sexual assault cases. Between June 2021 and October 2023, 39 individuals completed the 28-day follow-up; 41% experienced some side effects, and 1 person discontinued the drug because of a rash. No individuals seroconverted to HIV during the follow-up period.