Contemporary Russian Women Authors: Rejecting Definition in Literary Rebellion

Russia’s women have had a difficult time finding a voice in literature until as recently as the 1980s. With this new voice, many women writers have countered the widespread gender assumptions inherent in patriarchal Russian culture. This essay explores how four contemporary Russian women authors— Ludmilla Petrushevskaya, Nina Sadur, Tatyana Tolstaya, and Ludmila Ulitskaya—challenge binary gender stereotypes, particularly those concerning women. Each author has uniquely rejected a prescribed definition of ‘woman’ in her prose, and together the four authors form a literary rebellion against stereotypical notions of femininity

Rewriting results sections in the language of evidence

Despite much criticism, black-or-white null-hypothesis significance testing with an arbitrary P-value cutoff still is the standard way to report scientific findings. One obstacle to progress is likely a lack of knowledge about suitable alternatives. Here, we suggest language of evidence that allows for a more nuanced approach to communicate scientific findings as a simple and intuitive alternative to statistical significance testing. We provide examples for rewriting results sections in research papers accordingly. Language of evidence has previously been suggested in medical statistics, and it is consistent with reporting approaches of international research networks, like the Intergovernmental Panel on Climate Change, for example. Instead of re-inventing the wheel, ecology and evolution might benefit from adopting some of the ‘good practices’ that exist in other fields.Rewriting results sections in the language of evidencepublishedVersio

Pathogenic SCN2A variants cause early-stage dysfunction in patient-derived neurons

Pathogenic heterozygous variants in SCN2A, which encodes the neuronal sodium channel NaV1.2, cause different types of epilepsy or intellectual disability (ID)/autism without seizures. Previous studies using mouse models or heterologous systems suggest that NaV1.2 channel gain-of-function typically causes epilepsy, whereas loss-of-function leads to ID/autism. How altered channel biophysics translate into patient neurons remains unknown. Here, we investigated iPSC-derived early-stage cortical neurons from ID patients harboring diverse pathogenic SCN2A variants [p.(Leu611Valfs*35); p.(Arg937Cys); p.(Trp1716*)], and compared them to neurons from an epileptic encephalopathy patient [p.(Glu1803Gly)] and controls. ID neurons consistently expressed lower NaV1.2 protein levels. In neurons with the frameshift variant, NaV1.2 mRNA and protein levels were reduced by ~ 50%, suggesting nonsense-mediated decay and haploinsufficiency. In other ID neurons, only protein levels were reduced implying NaV1.2 instability. Electrophysiological analysis revealed decreased sodium current density and impaired action potential (AP) firing in ID neurons, consistent with reduced NaV1.2 levels. By contrast, epilepsy neurons displayed no change in NaV1.2 levels or sodium current density, but impaired sodium channel inactivation. Single-cell transcriptomics identified dysregulation of distinct molecular pathways including inhibition of oxidative phosphorylation in neurons with SCN2A haploinsufficiency, and activation of calcium signaling and neurotransmission in epilepsy neurons. Together, our patient iPSC-derived neurons reveal characteristic sodium channel dysfunction consistent with biophysical changes previously observed in heterologous systems. Additionally, our model links the channel dysfunction in ID to reduced NaV1.2 levels and uncovers impaired AP firing in early-stage neurons. The altered molecular pathways may reflect a homeostatic response to NaV1.2 dysfunction and can guide further investigations

Preliminary assessment of the feasibility of using AB words to assess candidacy in adults

Background: Adult cochlear implant (CI) candidacy is assessed in part by the use of speech perception measures. In the United Kingdom the current cut-off point to fall within the CI candidacy range is a score of less than 50% on the BKB sentences presented in quiet (presented at 70 dBSPL). Goal: The specific goal of this article was to review the benefit of adding the AB word test to the assessment test battery for candidacy. Results: The AB word test scores showed good sensitivity and specificity when calculated based on both word and phoneme scores. The word score equivalent for 50% correct on the BKB sentences was 18.5% and it was 34.5% when the phoneme score was calculated; these scores are in line with those used in centres in Wales (15% AB word score). Conclusion: The goal of the British Cochlear Implant Group (BCIG) service evaluation was to determine if the pre-implant assessment measures are appropriate and set at the correct level for determining candidacy, the future analyses will determine whether the speech perception cut-off point for candidacy should be adjusted and whether other more challenging measures should be used in the candidacy evaluation

Pathogenic SCN2A variants cause early-stage dysfunction in patient-derived neurons

Pathogenic heterozygous variants in SCN2A, which encodes the neuronal sodium channel NaV1.2, cause different types of epilepsy or intellectual disability (ID)/autism without seizures. Previous studies using mouse models or heterologous systems suggest that NaV1.2 channel gain-of-function typically causes epilepsy, whereas loss-of-function leads to ID/autism. How altered channel biophysics translate into patient neurons remains unknown. Here, we investigated iPSC-derived early-stage cortical neurons from ID patients harboring diverse pathogenic SCN2A variants [p.(Leu611Valfs*35); p.(Arg937Cys); p.(Trp1716*)], and compared them to neurons from an epileptic encephalopathy patient [p.(Glu1803Gly)] and controls. ID neurons consistently expressed lower NaV1.2 protein levels. In neurons with the frameshift variant, NaV1.2 mRNA and protein levels were reduced by ~ 50%, suggesting nonsense-mediated decay and haploinsufficiency. In other ID neurons, only protein levels were reduced implying NaV1.2 instability. Electrophysiological analysis revealed decreased sodium current density and impaired action potential (AP) firing in ID neurons, consistent with reduced NaV1.2 levels. By contrast, epilepsy neurons displayed no change in NaV1.2 levels or sodium current density, but impaired sodium channel inactivation. Single-cell transcriptomics identified dysregulation of distinct molecular pathways including inhibition of oxidative phosphorylation in neurons with SCN2A haploinsufficiency, and activation of calcium signaling and neurotransmission in epilepsy neurons. Together, our patient iPSC-derived neurons reveal characteristic sodium channel dysfunction consistent with biophysical changes previously observed in heterologous systems. Additionally, our model links the channel dysfunction in ID to reduced NaV1.2 levels and uncovers impaired AP firing in early-stage neurons. The altered molecular pathways may reflect a homeostatic response to NaV1.2 dysfunction and can guide further investigations

Commercial spruce plantations support a limited. canopy fauna: Evidence from a multi taxa comparison of native and plantation forests

Globally, the total area of plantation forest is increasing as deforestation and fragmentation of native forest continues. In some countries commercial plantations make up more than half of the total forested land. Internationally, there is growing emphasis on forestry policy for plantations to deliver biodiversity and ecosystem services. In Ireland, native forest now comprises just 1% of total land cover while non-native spruce forest makes up 60% of the plantation estate and approximately 6% of the total land cover. The majority of plantation invertebrate biodiversity assessments focus on ground-dwelling species and consequently a good understanding exists for these guilds, especially ground-active spiders and beetles. Using a technique of insecticide fogging, we examine the less well understood component of forest systems, the canopy fauna (Coleoptera, Araneae, Diptera and Hemiptera), in Irish spruce plantations (Sitka and Norway) and compare the assemblage composition, richness and abundance to that of remnant native forest (ash and oak). In addition, we examine the potential for accumulation of forest species in second rotation spruce plantations and identify indicator species for each forest type. From 30 sampled canopies, we recorded 1155 beetles and 1340 spiders from 144 species and over 142 000 Diptera and Hemiptera from 71 families. For all taxa, canopy assemblages of native forests were significantly different from closed-canopy plantation forests. No indicators for plantation forest were identified; those identified for native forest included species from multiple feeding guilds. Plantations supported approximately half the number of beetle species and half the number of Diptera and Hemiptera families recorded in native forests. Although assemblages in Norway spruce plantations were very different to those of native forest, they had consistently higher richness than Sitka spruce plantations. No differences in richness or abundance were found between first rotation and second rotation Sitka spruce plantations. Compared to other forest types, Sitka spruce plantations contained far greater total abundance of invertebrates, due to vast numbers of aphids and midges. Under current management, Sitka spruce plantations provide limited benefit to the canopy fauna typical of native forests in either first or second rotations. The large aphid populations may provide abundant food for insectivores but may also lead to reduced crop production through defoliation. Progressive forestry management should attempt to diversify the plantation canopy fauna, which may also increase productivity and resilience to pest species

Rewriting results sections in the language of evidence

Despite much criticism, black-or-white null-hypothesis significance testing with an arbitrary P-value cutoff still is the standard way to report scientific findings. One obstacle to progress is likely a lack of knowledge about suitable alternatives. Here, we suggest language of evidence that allows for a more nuanced approach to communicate scientific findings as a simple and intuitive alternative to statistical significance testing. We provide examples for rewriting results sections in research papers accordingly. Language of evidence has previously been suggested in medical statistics, and it is consistent with reporting approaches of international research networks, like the Intergovernmental Panel on Climate Change, for example. Instead of re-inventing the wheel, ecology and evolution might benefit from adopting some of the ‘good practices’ that exist in other fields

Pathogenic SCN2A variants cause early-stage dysfunction in patient-derived neurons

Pathogenic heterozygous variants in SCN2A, which encodes the neuronal sodium channel Na(V)1.2, cause different types of epilepsy or intellectual disability (ID)/autism without seizures. Previous studies using mouse models or heterologous systems suggest that Na(V)1.2 channel gain-of-function typically causes epilepsy, whereas loss-of-function leads to ID/autism. How altered channel biophysics translate into patient neurons remains unknown. Here, we investigated iPSC-derived early-stage cortical neurons from ID patients harboring diverse pathogenic SCN2A variants [p.(Leu611Valfs*35); p.(Arg937Cys); p.(Trp1716*)] and compared them with neurons from an epileptic encephalopathy (EE) patient [p.(Glu1803Gly)] and controls. ID neurons consistently expressed lower Na(V)1.2 protein levels. In neurons with the frameshift variant, Na(V)1.2 mRNA and protein levels were reduced by similar to 50%, suggesting nonsense-mediated decay and haploinsufficiency. In other ID neurons, only protein levels were reduced implying Na(V)1.2 instability. Electrophysiological analysis revealed decreased sodium current density and impaired action potential (AP) firing in ID neurons, consistent with reduced Na(V)1.2 levels. In contrast, epilepsy neurons displayed no change in Na(V)1.2 levels or sodium current density, but impaired sodium channel inactivation. Single-cell transcriptomics identified dysregulation of distinct molecular pathways including inhibition of oxidative phosphorylation in neurons with SCN2A haploinsufficiency and activation of calcium signaling and neurotransmission in epilepsy neurons. Together, our patient iPSC-derived neurons reveal characteristic sodium channel dysfunction consistent with biophysical changes previously observed in heterologous systems. Additionally, our model links the channel dysfunction in ID to reduced Na(V)1.2 levels and uncovers impaired AP firing in early-stage neurons. The altered molecular pathways may reflect a homeostatic response to Na(V)1.2 dysfunction and can guide further investigations.ISSN:0964-6906ISSN:1460-208