Preservation Of Connectivity Research Articles

A novel Android malware detection method with API semantics extraction

Due to the continuous evolution of both the Android framework and malware, conventional malware detection methods that have been trained using outdated apps are inadequate in effectively identifying sophisticated evolved malware. To address this issue, in this paper, we propose a novel Android malware detection method with API semantics extraction (AMDASE), it can effectively identify evolved malware instances. Firstly, AMDASE performs API clustering to obtain cluster centers representing API functions before malware detection. We design API sentence to summarize API features and employ natural language processing (NLP) tools to acquire embeddings of API sentence for clustering. With the help of API sentence, it becomes possible to effectively extract the semantics of API contained in features like method name that accurately represents its intended functionality, which also makes the clustering results more accurate. Secondly, AMDASE extracts call graph from each app and optimizes the call graph by removing nodes corresponding to unknown functions, while ensuring the preservation of connectivity between their predecessor and successor nodes. The optimized call graph can extract more robust API contextual information that accurately represents the behavior of each app. Thirdly, in order to maintain resilience against the evolution of Android malware, AMDASE extracts function call pairs from the optimized call graph and abstracts the APIs in function call pairs into cluster centers obtained in API clustering. Finally, feature vectors are generated using one-hot mapping and machine learning classifiers are used for malware detection. We evaluate AMDASE on a dataset of 42,154 benign and 42,450 malicious apps developed over a seven-year period. The experimental results demonstrate that AMDASE greatly outperforms the existing state-of-the-art methods and has a significantly slower aging speed.

Screening of Crucial Cytosolicproteins Interconnecting the Endoplasmic Reticulum and Mitochondria in Parkinson's Disease and the Impact of Anti-Parkinson Drugs in the Preservation of Organelle Connectivity.

Mitochondrial dysfunction is well-established in Parkinson's disease (PD); however, its dysfunctions associating with cell organelle connectivity remain unknown. We aimed to establish the crucial cytosolic protein involved in organelle connectivity between mitochondria and the endopalmic reticulum (ER) through a computational approach by constructing an organelle protein network to extract functional clusters presenting the crucial PD protein connecting organelles. Then, we assessed the influence of anti-parkinsonism drugs (n = 35) on the crucial protein through molecular docking and molecular dynamic simulation and further validated its gene expression in PD participants under, istradefylline (n = 25) and amantadine (n = 25) treatment. Based on our investigation, D-aspartate oxidase (DDO )protein was found to be the critical that connects both mitochondria and the ER. Further, molecular docking showed that istradefylline has a high affinity (-9.073 kcal/mol) against DDO protein, which may disrupt mitochondrial-ER connectivity. While amantadine (-4.53 kcal/mol) shows negligible effects against DDO that contribute to conformational changes in drug binding, Successively, DDO gene expression was downregulated in istradefylline-treated PD participants, which elucidated the likelihood of an istradefylline off-target mechanism. Overall, our findings illuminate the off-target effects of anti-parkinsonism medications on DDO protein, enabling the recommendation of off-target-free PD treatments.

Structural preservation does not ensure function at sensory Ia - motoneuron synapses following peripheral nerve injury and repair.

Injury that severs peripheral nerves often results in long-lasting motor behavioral deficits and in reorganization of related spinal motor circuitry, neither of which reverse even after nerve regeneration. Stretch areflexia and gait ataxia, for example, emerges from a combination of factors including degeneration of Ia - motoneuron synapses between peripherally damaged Ia muscle spindle afferents and motoneurons. Based on evidence that nerve injury acts through immune responses to induce synapse degeneration, we hypothesized that suppressing inflammatory responses would preserve Ia - motoneuron connectivity and aid in restoring normal function. We tested our hypothesis by administering the anti-inflammatory agent minocycline in male and female rats following axotomy of a peripheral nerve. The connectivity of Ia - motoneuron synapses was then assessed both structurally and functionally at different time points. We found that minocycline treatment overcame the physical loss of Ia contacts on motoneurons which are otherwise lost after axotomy. While necessary for functional recovery, synaptic preservation was not sufficient to overcome functional decline expressed as smaller than normal stretch-evoked synaptic potentials (SSP) evoked monosynaptically at Ia - motoneuron connections and an absence of the stretch reflex. These findings demonstrate a limited capacity of minocycline to rescue normal sensorimotor behavior, illustrating that structural preservation of synaptic connectivity does not ensure normal synaptic function.Significance Statement:Here we demonstrate that acute treatment with the semisynthetic tetracycline anti-inflammatory agent minocycline permanently prevents the comprehensive loss of synaptic contacts made between sensory neurons and spinal motoneurons following peripheral nerve injury and eventual regeneration. Treatment failed, however, to rescue normal function of those synapses or the reflex circuit they mediate. These findings demonstrate that preventing synaptic disconnection alone is not sufficient to restore neural circuit operation and associated sensorimotor behaviors.

Chlorophyll a fluorescence during flag leaf senescence of field‐grown winter wheat plants under drought conditions

AbstractImproving wheat grain yield plays a significant role in ensuring global food security. Wheat production could be increased by the genetic improvement of wheat genotypes where delayed senescence with enhanced post‐anthesis capacity and staygreen traits could have an important role. In this study, chlorophyll a fluorescence (ChlF) rise kinetics from the early until late senescence of flag leaves, grain yield and other agro‐morphological characteristics were compared for three winter wheat advanced lines (Osk.4.312/10‐18, Osk.4.330/6‐18 and Osk.4.354/12‐18) under natural drought conditions. The differences between lines were observed when considering the heading date which was 1 and 4 days earlier for the line Osk.4.354/12‐18, than lines Osk.4.312/10‐18 and Osk.4.330/6‐18, respectively. Furthermore, line Osk.4.354/12‐18 had the highest test weight (kg hl−1), while line Osk.4.330/6‐18 showed a tendency of decreased grain yield, compared to the other two lines. Analysis of ChlF transients and several JIP‐test parameters indicated that all three lines had a generally similar course of changes in the photosynthetic performance of flag leaves during senescence under drought conditions. However, at the point when a decrease in photosynthetic performance was initiated, it was slightly less intensive in line Osk.4.354/12‐18 accompanied by longer preservation of functionality and connectivity of PSII units, than in the other two lines, which contributed to its better agronomical performance. These results indicated that even delicate variations in the functioning of the photosynthetic apparatus of the flag leaf during grain filling were agronomically important, especially when plants were exposed to drought stress, and could be used to differentiate otherwise similar wheat genotypes. Even small genotype‐specific differences in the photosynthetic performance of senescing flag leaves, along with earlier heading dates, could assist in the selection of genotypes with a better ability to cope with unfavourable environmental conditions.

Intravenous immunoglobulin (IVIG) promotes brain repair and improves cognitive outcomes after traumatic brain injury in a FcγRIIB receptor-dependent manner

Intravenous immunoglobulin (IVIG) is a promising immune-modulatory therapy for limiting harmful inflammation and associated secondary tissue loss in neurotrauma. Here, we show that IVIG therapy attenuates spatial learning and memory deficits following a controlled cortical impact mouse model of traumatic brain injury (TBI). These improvements in cognitive outcomes were associated with increased neuronal survival, an overall reduction in brain tissue loss, and a greater preservation of neural connectivity. Furthermore, we demonstrate that the presence of the main inhibitory FcγRIIB receptor is required for the beneficial effects of IVIG treatment in TBI, with our results simultaneously highlighting the role of this receptor in reducing secondary damage arising from brain injury.

Vulnerability of the Neonatal Connectome following Postnatal Stress.

Stress following preterm birth can disrupt the emerging foundation of the neonatal brain. The current study examined how structural brain development is affected by a stressful early environment and whether changes in topological architecture at term-equivalent age could explain the increased vulnerability for behavioral symptoms during early childhood. Longitudinal changes in structural brain connectivity were quantified using diffusion-weighted imaging (DWI) and tractography in preterm born infants (gestational age <28 weeks), imaged at 30 and/or 40 weeks of gestation (N = 145, 43.5% female). A global index of postnatal stress was determined based on the number of invasive procedures during hospitalization (e.g., heel lance). Higher stress levels impaired structural connectivity growth in a subnetwork of 48 connections (p = 0.003), including the amygdala, insula, hippocampus, and posterior cingulate cortex. Findings were replicated in an independent validation sample (N = 123, 39.8% female, n = 91 with follow-up). Classifying infants into vulnerable and resilient based on having more or less internalizing symptoms at two to five years of age (n = 71) revealed lower connectivity in the hippocampus and amygdala for vulnerable relative to resilient infants (p < 0.001). Our findings suggest that higher stress exposure during hospital admission is associated with slower growth of structural connectivity. The preservation of global connectivity of the amygdala and hippocampus might reflect a stress-buffering or resilience-enhancing factor against a stressful early environment and early-childhood internalizing symptoms.SIGNIFICANCE STATEMENT The preterm brain is exposed to various external stimuli following birth. The effects of early chronic stress on neonatal brain networks and the remarkable degree of resilience are not well understood. The current study aims to provide an increased understanding of the impact of postnatal stress on third-trimester brain development and describe the topological architecture of a resilient brain. We observed a sparser neonatal brain network in infants exposed to higher postnatal stress. Limbic regulatory regions, including the hippocampus and amygdala, may play a key role as crucial convergence sites of protective factors. Understanding how stress-induced alterations in early brain development might lead to brain (re)organization may provide essential insights into resilient functioning.

Promoting regeneration while blocking cell death preserves motor neuron function in a model of ALS.

Amyotrophic lateral sclerosis (ALS) is a devastating and fatal neurodegenerative disease of motor neurons with very few treatment options. We had previously found that motor neuron degeneration in a mouse model of ALS can be delayed by deleting the axon damage sensor MAP3K12 or dual leucine zipper kinase (DLK). However, DLK is also involved in axon regeneration, prompting us to ask whether combining DLK deletion with a way to promote axon regeneration would result in greater motor neuron protection. To achieve this, we used a mouse line that constitutively expresses ATF3, a master regulator of regeneration in neurons. Although there is precedence for each individual strategy in the SOD1G93A mouse model of ALS, these have not previously been combined. By several lines of evidence including motor neuron electrophysiology, histology and behaviour, we observed a powerful synergy when combining DLK deletion with ATF3 expression. The combinatorial strategy resulted in significant protection of motor neurons with fewer undergoing cell death, reduced axon degeneration and preservation of motor function and connectivity to muscle. This study provides a demonstration of the power of combinatorial therapy to treat neurodegenerative disease.

Dispersal and Survival of Captive-Reared Threatened Fishes in a Tonle Sap Lake Reserve

The Tonle Sap Lake in Cambodia supports several species of threatened megafish and contains one of the largest networks of freshwater fish reserves in the world. Despite these traits, this system remains understudied in terms of its utility for endangered fish conservation and restoration. This study was the first of a series of planned fish releases designed to test the effectiveness of conservation supplementation programs in the Tonle Sap Lake. In March 2022 (during the dry season), 1582 captive-reared fishes, including 1538 striped catfish Pangasianodon hypopthalmus, 42 giant barb Catlocarpio siamensis, and two Mekong giant catfish Pangasianodon gigas, were tagged and released into a 986-hectare fish reserve to assess post-release dispersal and survival. Brightly colored external tags with unique identification numbers were used to facilitate tag returns. A high-profile release event was held to raise awareness about the activity, bringing attention to the importance of fish reserves and endangered species conservation, and disseminating information about the research and tag return and reward program. This, in concert with other efforts, served to be an important education and outreach tool and increased tag return rates. We found that mortality from fishing was rapid and very high. Nineteen percent of released fishes were recaptured in the first 2 days after the fish release, and 46% were recaptured by day 83 after the release, indicating intense fishing pressure on the Tonle Sap Lake fisheries. Eighty percent of recaptured fishes were caught in stationary gill nets, most within 10 km of the release site. Fishing mortality rates were independent of fish size or source (pond-reared or cage-reared). Environmental DNA (eDNA) was found to be capable of detecting each of these species’ presence in the water at the release site and could prove to be a useful tool for endangered species monitoring and restoration. Future research should explore alternative release timing, release location, and other methods of increasing post-release survival. Ultimately, underlying sources of mortality, especially fishing, will need to be addressed for conservation supplementation programs to succeed in the Tonle Sap Lake. Conservation supplementation should not be viewed as a substitute for more fundamental conservation measures, such as maintenance of environmental flows, preservation of ecological connectivity, and science-based fisheries management.

POSTINJURY FECAL MICROBIOME TRANSPLANT DECREASES LESION SIZE AND NEUROINFLAMMATION IN TRAUMATIC BRAIN INJURY.

Background: Traumatic brain injury (TBI) is an underrecognized public health threat. The constitutive activation of microglia after TBI has been linked to long-term neurocognitive deficits and the progression of neurodegenerative disease. Evolving evidence indicates a critical role for the gut-brain axis in this process. Specifically, TBI has been shown to induce the depletion of commensal gut bacteria. The resulting gut dysbiosis is associated with neuroinflammation and disease. Hypothesis: We hypothesized that fecal microbiota transplantation would attenuate microglial activation and improve neuropathology after TBI. Methods: C57Bl/6 mice were subjected to severe TBI (n = 10) or sham injury (n = 10) via an open-head controlled cortical impact. The mice underwent fecal microbiota transplantation (FMT) or vehicle alone via oral gavage once weekly for 4 weeks after injury. At 59 days after TBI, mice underwent three-dimensional, contrast-enhanced magnetic resonance imaging. Following imaging, mice were killed, brains harvested at 60 DPI, and CD45+ cells isolated via florescence-activated cell sorting. cDNA libraries were prepared using the 10x Genomics Chromium Single Cell 3' Reagent kit followed by sequencing on a HiSeq4000 instrument, and computational analysis was performed. Results: Fecal microbiota transplantation resulted in a &gt;marked reduction of ventriculomegaly (P &lt; 0.002) and preservation of white matter connectivity at 59 days after TBI (P &lt; 0.0001). In addition, microglia from FMT-treated mice significantly reduced inflammatory gene expression and enriched pathways involving the heat-shock response compared with mice treated with vehicle alone. Conclusions: We hypothesized that restoring gut microbial community structure via FMT would attenuate microglial activation and reduce neuropathology after TBI. Our data demonstrated significant preservation of cortical volume and white matter connectivity after an injury compared with mice treated with vehicle alone. This preservation of neuroanatomy after TBI was associated with a marked reduction in inflammatory gene expression within the microglia of FMT-treated mice. Microglia from FMT-treated mice enriched pathways in the heat-shock response, which is known to play a neuroprotective role in TBI and other neurodegenerative disease processes.

Towards Ecological Management and Sustainable Urban Planning in Seoul, South Korea: Mapping Wild Pollinator Habitat Preferences and Corridors Using Citizen Science Data.

Simple SummaryUrban landscapes, though a primary contributor to habitat fragmentation, have the potential to facilitate habitat connectivity for native pollinator species, especially with strategic green space planning. Citizen science data have been proven to be useful to address conservation issues in urban areas, especially where knowledge is lacking about species richness and habitat preferences. In this study, we used data collected by a citizen science program between 2016 and 2018 to determine which families of pollinators were the most frequently observed in Seoul, with which habitats pollinators had the highest affinities, and what parts of the city facilitated habitat connectivity. We found that the most suitable habitats for multiple families were located in public parks, university campuses, and Cultural Heritage sites. These results are directly applicable in order to better understand urban planning stakes for pollinators and wildlife in general and provide avenues for improvement to recreate functional greenways in a dense city like Seoul.The preservation and restoration of habitats and ecological connectivity inside cities is crucial to ensure wildlife can find suitable areas to forage, rest and reproduce, as well as to disperse, thereby allowing metapopulation functioning. In this study, we used data collected by a citizen science program between 2016 and 2018 to determine which families of pollinators were the most frequently observed in Seoul and with which habitats pollinators had the highest affinities. Using species distribution modeling and landscape graph approaches, we located the main habitats and corridors to reinforce connectivity for six pollinator families. Finally, we identified habitats and corridors where conservation actions should be prioritized. In total, 178 species belonging to 128 genera and 60 families were observed. Hymenopterans were the most recorded, followed by dipterans and lepidopterans. The most suitable habitats for pollinators were constituted of public parks, university campuses, and Cultural Heritage sites. In a dense city like Seoul, most of the conservation corridors are located in built-up areas. Innovative urban planning and architecture are therefore required as well as the setting-up of ecological management practices to lead to a more sustainable urbanism for pollinators and wildlife in general.

Dietary and Nutrient Patterns and Brain MRI Biomarkers in Dementia-Free Adults.

Cognitive impairment is a rapidly growing public health problem. As there is no curative treatment for dementia, the proactive management of modifiable risk factors and the identification of early biomarkers indicative of the cognitive decline are of great importance. Although nutrition is one of the most extensively studied lifestyle factor in relation to cognitive health, its association with brain magnetic resonance imaging (MRI) biomarkers is not well established. In the present work, we review available studies relating dietary or nutrient patterns with brain MRI biomarkers in dementia-free adults. Greater adherence to the Mediterranean diet has been associated with the preservation of structural connectivity and less brain atrophy in adults without dementia. In addition, specific nutrient patterns, characterized by a high intake of antioxidant vitamins, polyphenols and unsaturated fatty acids, have been related to larger brain volume. Although the results are encouraging regarding the role of dietary and nutrient patterns on imaging biomarkers, more well-designed observational longitudinal studies and clinical trials are needed in order to confirm potentially causal relationships and better understand underlying mechanisms.

Transcriptional preservation of serotonergic connectivity may shed light on neurodegeneration

In a recent study, Kitt, Tabuchi, and colleagues unveiled a novel function of an early-stage transcriptional network to maintain the adult integrity of serotonergic connectivity. Reported axonal and synaptic morphological alterations in serotonin (5-HT) neurons after selective inactivation of Lmx1b/Pet1 transcriptional networks may help to understand aging and neurodegenerative processes.

Preserved Electroencephalogram Power and Global Synchronization Predict Better Neurological Outcome in Sudden Cardiac Arrest Survivors.

Quantitative EEG (qEEG) delineates complex brain activities. Global field synchronization (GFS) is one multichannel EEG analysis that measures global functional connectivity through quantification of synchronization between signals. We hypothesized that preservation of global functional connectivity of brain activity might be a surrogate marker for good outcome in sudden cardiac arrest (SCA) survivors. In addition, we examined the relation of phase coherence and GFS in a mathematical approach. We retrospectively collected EEG data of SCA survivors in one academic medical center. We included 75 comatose patients who were resuscitated following in-hospital or out-of-hospital nontraumatic cardiac arrest between 2013 and 2017 in the intensive care unit (ICU) of National Taiwan University Hospital (NTUH). Twelve patients (16%) were defined as good outcome (GO) (CPC 1–2). The mean age in the GO group was low (51.6 ± 15.7 vs. 68.1 ± 12.9, p < 0.001). We analyzed standard EEG power, computed EEG GFS, and assessed the cerebral performance category (CPC) score 3 months after discharge. The alpha band showed the highest discrimination ability (area under curve [AUC] = 0.78) to predict GO using power. The alpha band of GFS showed the highest AUC value (0.8) to predict GO in GFS. Furthermore, by combining EEG power + GFS, the alpha band showed the best prediction value (AUC 0.86) in predicting GO. The sensitivity of EEG power + GFS was 73%, specificity was 93%, PPV was 0.67%, and NPV was 0.94%. In conclusion, by combining GFS and EEG power analysis, the neurological outcome of the nontraumatic cardiac arrest survivor can be well-predicted. Furthermore, we proved from a mathematical point of view that although both amplitude and phase contribute to obtaining GFS, the interference in phase variation drastically changes the possibility of generating a good GFS score.

An adult-stage transcriptional program for survival of serotonergic connectivity.

SUMMARYNeurons must function for decades of life, but how these non-dividing cells are preserved is poorly understood. Using mouse serotonin (5-HT) neurons as a model, we report an adult-stage transcriptional program specialized to ensure the preservation of neuronal connectivity. We uncover a switch in Lmx1b and Pet1 transcription factor function from controlling embryonic axonal growth to sustaining a transcriptomic signature of 5-HT connectivity comprising functionally diverse synaptic and axonal genes. Adult-stage deficiency of Lmx1b and Pet1 causes slowly progressing degeneration of 5-HT synapses and axons, increased susceptibility of 5-HT axons to neurotoxic injury, and abnormal stress responses. Axon degeneration occurs in a die back pattern and is accompanied by accumulation of α-synuclein and amyloid precursor protein in spheroids and mitochondrial fragmentation without cell body loss. Our findings suggest that neuronal connectivity is transcriptionally protected by maintenance of connectivity transcriptomes; progressive decay of such transcriptomes may contribute to age-related diseases of brain circuitry.

Occupancy models reveal potential of conservation prioritization for Central American jaguars

AbstractUnderstanding species‐environment relationships at large spatial scales is required for the prioritization of conservation areas and the preservation of landscape connectivity for large carnivores. This endeavour is challenging for jaguars (Panthera onca), given their elusiveness, and the local nature of most jaguar studies, precluding extrapolation to larger areas. We developed an occupancy model using occurrence data of jaguars across five countries of Central America, collected from camera‐trap studies of 2–12 months' duration, deployed over an area of 14 112 km2 from 2005 to 2018. Our occupancy model showed that habitat use of jaguars increased with primary net productivity and distance to human settlements, and distance to rivers. Detection of the species was related to survey effort and research team identity. Within the jaguar extent of occurrence, 73% was deemed suitable for the species, with 47% of it lying within Jaguar Conservation Units (JCU) and 59% of JCU land being legally protected. Suitable areas were divided into four distinct clusters of continuous habitat shared across country borders. However, large areas of predicted low habitat suitability may constrict connectivity in the region. The reliability of these spatial predictions is indicated by the model validation using an independent dataset (AUC = 0.82; sensitivity = 0.766, specificity = 0.761), and concordance of our results with other studies conducted in the region. Across Central America, we found that human influence has the strongest impact on jaguar habitat use and JCUs are the main reservoirs of habitat. Therefore, conservation actions must focus on preventing habitat loss and mitigating human pressure, particularly within the clusters of continuous areas of high suitability, and on restoring habitat to foster connectivity. The long‐term persistence of jaguars in the region will depend on strong international cooperation that secures jaguar populations and their habitat across Central American borders.

Corticothalamic Connectivity in Aneurysmal Subarachnoid Hemorrhage: Relationship with Disordered Consciousness and Clinical Outcomes.

We present an exploratory analysis of the occurrence of early corticothalamic connectivity disruption after aneurysmal subarachnoid hemorrhage (SAH) and its correlation with clinical outcomes. We conducted a retrospective study of patients with acute SAH who underwent continuous electroencephalography (EEG) for impairment of consciousness. Only patients undergoing endovascular aneurysm treatment were included. Continuous EEG tracings were reviewed to obtain artifact-free segments. Power spectral analyses were performed, and segments were classified as A (only delta power), B (predominant delta and theta), C (predominant theta and beta), or D (predominant alpha and beta). Each incremental category from A to D implies greater preservation of corticothalamic connectivity. We dichotomized categories as AB for poor connectivity and CD for good connectivity. The modified Rankin Scale score at follow-up and in-hospital mortality were used as outcome measures. Sixty-nine patients were included, of whom 58 had good quality EEG segments for classification: 28 were AB and 30 were CD. Hunt and Hess and World Federation of Neurological Surgeons grades were higher and the initial Glasgow Coma Scale score was lower in the AB group compared with the CD group. AB classification was associated with an adjusted odds ratio of 5.71 (95% confidence interval 1.61-20.30; p < 0.01) for poor outcome (modified Rankin Scale score 4-6) at a median follow-up of 4months (interquartile range 2-6) and an odds ratio of 5.6 (95% confidence interval 0.98-31.95; p = 0.03) for in-hospital mortality, compared with CD. EEG spectral-power-based classification demonstrates early corticothalamic connectivity disruption following aneurysmal SAH and may be a mechanism involved in early brain injury. Furthermore, the extent of this disruption appears to be associated with functional outcome and in-hospital mortality in patients with aneurysmal SAH and appears to be a potentially useful predictive tool that must be validated prospectively.

Preserved structural connectivity mediates the clinical effect of thrombolysis in patients with anterior-circulation stroke

Thrombolysis with recombinant tissue plasminogen activator in acute ischemic stroke aims to restore compromised blood flow and prevent further neuronal damage. Despite the proven clinical efficacy of this treatment, little is known about the short-term effects of systemic thrombolysis on structural brain connectivity. In this secondary analysis of the WAKE-UP trial, we used MRI-derived measures of infarct size and estimated structural network disruption to establish that thrombolysis is associated not only with less infarct growth, but also with reduced loss of large-scale connectivity between grey-matter areas after stroke. In a causal mediation analysis, infarct growth mediated a non-significant 8.3% (CI95% [−8.0, 32.6]%) of the clinical effect of thrombolysis on functional outcome. The proportion mediated jointly through infarct growth and change of structural connectivity, especially in the border zone around the infarct core, however, was as high as 33.4% (CI95% [8.8, 77.4]%). Preservation of structural connectivity is thus an important determinant of treatment success and favourable functional outcome in addition to lesion volume. It might, in the future, serve as an imaging endpoint in clinical trials or as a target for therapeutic interventions.

Abnormal cerebellar function and tremor in a mouse model for non-manifesting partially penetrant dystonia type 6.

Loss-of-function mutations in the Thap1 gene cause partially penetrant dystonia type 6 (DYT6). Some non-manifesting DYT6 mutation carriers have tremor andabnormal cerebello-thalamo-cortical signalling. We show that Thap1 heterozygote mice have action tremor, a reduction in cerebellar neuron number, andabnormal electrophysiological signals in the remaining neurons. These results underscore the importance of Thap1 levels for cerebellar function. These results uncover how cerebellar abnormalities contribute to different dystonia-associated motor symptoms. Loss-of-function mutations in the Thanatos-associated domain-containing apoptosis-associated protein 1 (THAP1) gene cause partially penetrant autosomal dominant dystonia type 6 (DYT6). However, the neural abnormalities that promote the resultant motor dysfunctions remain elusive. Studies in humans show that some non-manifesting DYT6 carriers have altered cerebello-thalamo-cortical function with subtle but reproducible tremor. Here, we uncover that Thap1 heterozygote mice have action tremor that rises above normal baseline values even though they do not exhibit overt dystonia-like twisting behaviour. At the neural circuit level, we show using in vivo recordings in awake Thap1+/- mice that Purkinje cells have abnormal firing patterns and that cerebellar nuclei neurons, which connect the cerebellum to the thalamus, fire at a lower frequency. Although the Thap1+/- mice have fewer Purkinje cells and cerebellar nuclei neurons, the number of long-range excitatory outflow projection neurons is unaltered. The preservation of interregional connectivity suggests that abnormal neural function rather than neuron loss instigates the network dysfunction and the tremor in Thap1+/- mice. Accordingly, we report an inverse correlation between the average firing rate of cerebellar nuclei neurons and tremor power. Our data show that cerebellar circuitry is vulnerable to Thap1 mutations and that cerebellar dysfunction may be a primary cause of tremor in non-manifesting DYT6 carriers and a trigger for the abnormal postures in manifesting patients.

Bluegill Habitat Use in the Upper Mississippi River

Anthropogenic modifications to the environment have had damaging effects on the wildlife that depend on those natural ecosystems. Specific to Upper Mississippi River fishes, channelization, dams, and loss of floodplain connectivity have all been purported as deleterious. In the face of these habitat modifications, understanding habitat requirements of native species is needed to help guide management and restoration efforts. Furthermore, bluegill (Lepomis macrochirus) are an important indicator species that may provide insight to habitat needs of the broader fish community (e.g., “canary in a coal mine”). Prior research suggests bluegill require a mosaic of habitats throughout all life stages (e.g., main channel to backwater connection). As such, the objective of this study was to identify the habitat needs of bluegill in the Upper Mississippi River. We evaluated bluegill habitat use via electrofishing conducted by the U.S. Army Corps of Engineers’ Long-Term Resource Monitoring (LTRM) element. Electrofishing events (n = 4868) were conducted at three field sites throughout the Upper Mississippi River from 1993 to 2017. Our analysis of catch data (n = 83,352) indicates that bluegill prefer backwater macrohabitat over main channel and side channel habitats. Bluegill abundance varied between microhabitat characteristics. Bluegill catch rates were highest in low-flow areas, with velocities ranging from 0 to 0.09 m/sec. In general, catch rates were highest across all pools in moderately shallow depths (0–1.5 m) and in silty substrates. Management efforts that focus on the preservation of backwater habitat and connectivity to the main channel should help to sustain bluegill populations in the Upper Mississippi River. The information garnered in this study can be used to help direct management efforts that not only favor bluegill, but also other members of the Upper Mississippi River fish community.

Acute Mouse Brain Slicing to Investigate Spontaneous Hippocampal Network Activity.

Acute rodent brain slicing offers a tractable experimental approach to gain insight into the organization and function of neural circuits with single-cell resolution using electrophysiology, microscopy, and pharmacology. However, a major consideration in the design of in vitro experiments is the extent to which different slice preparations recapitulate naturalistic patterns of neural activity as observed in vivo. In the intact brain, the hippocampal network generates highly synchronized population activity reflective of the behavioral state of the animal, as exemplified by the sharp-wave ripple complexes (SWRs) that occur during waking consummatory states or non-REM sleep. SWRs and other forms of network activity can emerge spontaneously in isolated hippocampal slices under appropriate conditions. In order to apply the powerful brain slice toolkit to the investigation of hippocampal network activity, it is necessary to utilize an approach that optimizes tissue health and the preservation of functional connectivity within the hippocampal network. Mice are transcardially perfused with cold sucrose-based artificial cerebrospinal fluid. Horizontal slices containing the hippocampus are cut at a thickness of 450 μm to preserve synaptic connectivity. Slices recover in an interface-style chamber and are transferred to a submerged chamber for recordings. The recording chamber is designed for dual surface superfusion of artificial cerebrospinal fluid at a high flow rate to improve oxygenation of the slice. This protocol yields healthy tissue suitable for the investigation of complex and spontaneous network activity in vitro.