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The results showed that the positive rates of ASFV, CSFV and APPV were 43.75 %, 13.28 % and 4.17 %, respectively, and the coinfection rates of ASFV/CSFV, ASFV/APPV and CSFV/APPV were 5.47 %, 1.83 % and 1.30 %, respectively. To understand the epidemiological characteristics of APPV, the newly discovered virus, in Guangxi Province, the clinical samples from APPV-positive animals were selected randomly for amplification and sequencing, and the complete genomic sequences of four APPV strains were obtained. Phylogenetic analysis demonstrated that APPV strains from Guangxi Province had a high degree of genetic diversity. This study provides an important tool for rapid detection and accurate diagnosis of ASFV, CSFV and APPV.Living systems are subject to the arrow of time; from birth, they undergo complex transformations (self-organization) in a constant battle for survival, but inevitably ageing and disease trap them to death. Can ageing be understood and eventually reversed? What tools can be employed to further our understanding of ageing? The present article is an invitation for biologists and clinicians to consider key conceptual ideas and computational tools (known to mathematicians and physicists), which potentially may help dissect some of the underlying processes of ageing and disease. Specifically, we first discuss how to classify and analyse complex systems, as well as highlight critical theoretical difficulties that make complex systems hard to study. Subsequently, we introduce Topological Data Analysis - a novel Big Data tool - which may help in the study of complex systems since it extracts knowledge from data in a holistic approach via topological considerations. These conceptual ideas and tools are discussed in a relatively informal way to pave future discussions and collaborations between mathematicians and biologists studying ageing.Vascular cognitive impairment, the second most common cause of dementia, profoundly affects hippocampal-dependent functions. However, while the growing literature covers complex neuronal interactions, little is known about the sustaining hippocampal microcirculation. Here we examined vasoconstriction to physiological pressures of hippocampal arterioles, a fundamental feature of small arteries, in a genetic mouse model of CADASIL, an archetypal cerebral small vessel disease. Using diameter and membrane potential recordings on isolated arterioles, we observed both blunted pressure-induced vasoconstriction and smooth muscle cell depolarization in CADASIL. This impairment was abolished in the presence of voltage-gated potassium (KV1) channel blocker 4-aminopyridine, or by application of heparin-binding EGF-like growth factor (HB-EGF), which promotes KV1 channel down-regulations. Interestingly, we observed that HB-EGF induced a depolarization of the myocyte plasma membrane within the arteriolar wall in CADASIL, but not wild-type, arterioles. Collectively, our results indicate that hippocampal arterioles in CADASIL mice display a blunted contractile response to luminal pressure, similar to the defect we previously reported in cortical arterioles and pial arteries, that is rescued by HB-EGF. Hippocampal vascular dysfunction in CADASIL could then contribute to the decreased vascular reserve associated with decreased cognitive performance, and its correction may provide a therapeutic option for treating vascular cognitive impairment.
The electroencephalograph (EEG) pattern of burst suppression with identical bursts (BSIB), with or without myoclonus, occurs often after resuscitation from cardiac arrest. These patterns are associated with severe brain injury but their neuropathological basis is unknown. learn more Using EEG source localization, we tested whether post-cardiac arrest myoclonus was associated with specific anatomical distribution of BSIB.

We performed a single center, case-control study of EEG-monitored post-cardiac arrest patients with BSIB. We determined the presence of myoclonus from clinical notes and video recordings. We generated normalized source density maps (sLORETA) for the first 0.5 s of each burst projected onto a standard anatomic model, and compared proportion of EEG power in the precentral gyrus (motor cortex) to the rest of the brain.

We included 20 patients, 10 with and 10 without myoclonus. Patients with myoclonus had greater electrical activation localized to the precentral gyrus compared to those without (median 3.25 [IQR 2.74-3.59] vs 2.68 [IQR 2.66-2.71], P = 0.04). There was no difference between groups in region of burst origin.

Among patients with BSIB after cardiac arrest, those with clinical myoclonus have more electrocortical activation in the precentral gyrus.
Among patients with BSIB after cardiac arrest, those with clinical myoclonus have more electrocortical activation in the precentral gyrus.
To explore if electrographic status epilepticus (ESE) after cardiac arrest causes additional secondary brain injury reflected by serum levels of two novel biomarkers of brain injury neurofilament light chain (NfL) originating from neurons and glial fibrillary acidic protein (GFAP) from glial cells.

Simplified continuous EEG (cEEG) and serum levels of NfL and GFAP, sampled at 24, 48 and 72 h after cardiac arrest, were collected during the Target Temperature Management (TTM)-trial. Two statistical methods were used multivariable regresssion analysis; and a matched control group of patients without ESE matched for early predictors of poor neurological outcome.

128 patients had available biomarkers and cEEG. Twenty-six (20%) patients developed ESE, the majority (69%) within 24 h. ESE was an independent predictor of elevated serum NfL (p < 0.001) but not of serum GFAP (p = 0.16) at 72 h after cardiac arrest. Compared to a control group matched for early predictors of poor neurological outcome, patients who developed ESE had higher levels of serum NfL (p = 0.03) and GFAP (p = 0.04) at 72 h after cardiac arrest.

ESE after cardiac arrest is associated with higher levels of serum NfL which may suggest increased secondary neuronal injury compared to matched patients without ESE but similar initial brain injury. Associations with GFAP reflecting glial injury are less clear. The study design cannot exclude imperfect matching or other mechanisms of secondary brain injury contributing to the higher levels of biomarkers of brain injury seen in the patients with ESE.
ESE after cardiac arrest is associated with higher levels of serum NfL which may suggest increased secondary neuronal injury compared to matched patients without ESE but similar initial brain injury. Associations with GFAP reflecting glial injury are less clear. The study design cannot exclude imperfect matching or other mechanisms of secondary brain injury contributing to the higher levels of biomarkers of brain injury seen in the patients with ESE.
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