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Scholars in scientific disciplines face unique challenges in the creation of visualizations, especially in publications that require insights derived from analyses to be visually displayed. The literature on visualizations describes different techniques and best practices for the creation of graphs. However, these techniques have not been used to evaluate the impact of visualizations in academic publications. In the field of ecology, as in other scientific fields, graphs are an essential part of journal articles. Little is known about the connections between the kind of data presented and domain in which the researchers conducted their study that together produces the visual graphics. This study focused on articles published in the Journal of Ecology between 1996 and 2016 to explore possible connections between data type, domain, and visualization type. Specifically, this study asked three questions: How many of the graphics published between 1996 and 2016 follow a particular set of recommendations for best practices? What can Pearson correlations reveal about the relationships between type of data, domain of study, and visual displays? Can the findings be examined through an inter-reliability test lens? Out of the 20,080 visualizations assessed, 54% included unnecessary graphical elements in the early part of the study (1996–2010). The most common type of data was univariate (35%) and it was often displayed using line graphs. Twenty-one percent of the articles in the period studied could be categorized under the domain type “single species.” Pearson correlation analysis showed that data type and domain type was positively correlated ( r = 0.08; p ≤ 0.05). Cohen’s kappa for the reliability test was 0.86, suggesting good agreement between the two categories. This study provides evidence that data type and domain types are equally important in determining the type of visualizations found in scientific journals.

Spreading depolarization (SD) and seizures are pathophysiological events associated with cerebral ischemia. Here, we investigated their role for injury progression in the cerebral cortex. Cerebral ischemia was induced in anesthetized male Wistar rats using the photothrombosis (PT) stroke model. SD and spontaneous neuronal activity were recorded in the presence of either urethane or ketamine/xylazine anesthesia. Blood–brain barrier (BBB) permeability, cerebral perfusion, and cellular damage were assessed through a cranial window and repeated intravenous injection of fluorescein sodium salt and propidium iodide until 4 h after PT. Neuronal injury and early lesion volume were quantified by stereological cell counting and manual and automated assessment of ex vivo T2-weighted magnetic resonance imaging. Onset SDs originated at the thrombotic core and invaded neighboring cortex, whereas delayed SDs often showed opposite propagation patterns. Seizure induction by 4-aminopyridine caused no increase in lesion volume or neuronal injury in urethane-anesthetized animals. Ketamine/xylazine anesthesia was associated with a lower number of onset SDs, reduced lesion volume, and neuronal injury despite a longer duration of seizures. BBB permeability increase inversely correlated with the number of SDs at 3 and 4 h after PT. Our results provide further evidence that ketamine may counteract the early progression of ischemic injury.

Focal cerebral ischemia is among the main causes of death and disability worldwide. The ischemic core often progresses, invading the peri-ischemic brain; however, assessing the propensity of the peri-ischemic brain to undergo secondary damage, understanding the underlying mechanisms, and adjusting treatment accordingly remain clinically unmet challenges. A significant hallmark of the peri-ischemic brain is dysfunction of the blood-brain barrier (BBB), yet the role of disturbed vascular permeability in stroke progression is unclear. Here we describe a longitudinal in vivo fluorescence imaging approach for the evaluation of cortical perfusion, BBB dysfunction, free radical formation and cellular injury using the photothrombosis vascular occlusion model in male Sprague Dawley rats. Blood-brain barrier dysfunction propagated within the peri-ischemic brain in the first hours after photothrombosis and was associated with free radical formation and cellular injury. Inhibiting free radical signaling significantly reduced progressive cellular damage after photothrombosis, with no significant effect on blood flow and BBB permeability. Our approach allows a dynamic follow-up of cellular events and their response to therapeutics in the acutely injured cerebral cortex.

Spreading depolarizations (SD) are waves of abrupt, near-complete breakdown of neuronal transmembrane ion gradients, are the largest possible pathophysiologic disruption of viable cerebral gray matter, and are a crucial mechanism of lesion development. Spreading depolarizations are increasingly recorded during multimodal neuromonitoring in neurocritical care as a causal biomarker providing a diagnostic summary measure of metabolic failure and excitotoxic injury. Focal ischemia causes spreading depolarization within minutes. Further spreading depolarizations arise for hours to days due to energy supply-demand mismatch in viable tissue. Spreading depolarizations exacerbate neuronal injury through prolonged ionic breakdown and spreading depolarization-related hypoperfusion (spreading ischemia). Local duration of the depolarization indicates local tissue energy status and risk of injury. Regional electrocorticographic monitoring affords even remote detection of injury because spreading depolarizations propagate widely from ischemic or metabolically stressed zones; characteristic patterns, including temporal clusters of spreading depolarizations and persistent depression of spontaneous cortical activity, can be recognized and quantified. Here, we describe the experimental basis for interpreting these patterns and illustrate their translation to human disease. We further provide consensus recommendations for electrocorticographic methods to record, classify, and score spreading depolarizations and associated spreading depressions. These methods offer distinct advantages over other neuromonitoring modalities and allow for future refinement through less invasive and more automated approaches.

After either acute psychological stress or exposure to acetylcholinesterase (AChE) inhibitors, long-lasting deleterious changes of a similar nature occur in the mammalian brain. We explored the molecular and neurophysiological mechanisms preceding these convergent delayed consequences in vivo and in perfused hippocampal brain slices. In stressed mice, we observed a disruption of the blood-brain barrier, which leads to efficient brain penetrance of anti-AChEs. This increase in penetrance of anti-AChEs, and consequently in acetylcholine (ACh) levels, induces a cascade of c-fos-mediated transcriptional responses dependent on intracellular Ca2+ accumulation. Consequently, the capacity for synthesis and vesicle packaging of ACh is suppressed simultaneously with enhanced AChE production that potentiates ACh hydrolysis. This bimodal decrease in ACh bioavailability, which is independent of the hypothalamic-pituitary-adrenal axis, then ter minates the initial neurophysiological excitation. In vivo, this AChE overexpression leads to enzyme accu mulation that is evident for more than 80 hr. The overexpressed enzyme can protect the brain from sustained hyperexcitability and from increased susceptibility to seizure activity and neuronal toxicity. However, exper imental accumulation of AChE in brain neurons through transgenic manipulations leads to a slowly pro gressive deterioration in cognitive and neuromotor faculties. The transcriptional consequences of stress and anti-AChEs may therefore be beneficial in the short term but deleterious in the long term. NEURO SCIENTIST 5:173-183, 1999

SD is a depolarization wave propagating at a rate of about 3 mm/min in the cerebral cortex. It is characterized by an amplitude reduction of the electrocorticographic activity, a rise of the extracellular potassium to 60 mM and a reduction of the extracellular volume. Typical changes of cerebral blood flow (CBF) accompany SD, which consist of a short lasting "spreading hyperemia" followed by a long lasting "spreading oligemia". SD is triggered by electrical, mechanical or toxic factors and is probably involved in the pathogenesis of migraine, focal ischemia, head trauma and cerebral hemorrhage. SD is assumed to be the pathophysiological correlate of the migraine aura. We have recently observed a patient with familial hemiplegic migraine (FHM) type II and a long-lasting migraine aura with fluctuating neurological symptoms. Quantitative analysis of early gadolinium-enhanced MR images revealed a left-hemispheric, cortical blood brain-barrier (BBB) disruption preceding delayed cortical edema in this ATP1A2 mutation carrier. As we know from the work by Strong et al. repetitive SDs can occur in the human brain tissue, which could explain the fluctuating symptoms in our FHM patient. Additionally, a recent publication by Gursoy-Ozdemir et al. showed a delayed enhancement of BBB permeability and subsequent cortical oedema following a single SD. Based on these observations, we studied here whether recurrent SD causes early BBB disruption in the rat cortex in vivo. We triggered SD with artificial cerebrospinal fluid (ACSF) containing a potassium concentration ([K+]ACSF) of 130 mM at an open parietal cranial window. SDs were monitored with an intracortical potassium sensitive microelectrode and laser-Doppler flowmetry. We also recorded the propagation of SDs to a distant closed frontal cranial window using an epidural Ag-AgCl electrode. BBB integrity was evaluated quantitatively by analyzing fluorescence in brain sections following the peripheral injection of Evan's Blue or Lucifer yellow. At the occipital window, [K+]ACSF evoked several SDs in all animals. In the first group (n = 10), one or more SDs propagated to the frontal window. In contrast, in the second group (n = 9), pretreatment with MK-801 (5 mg/kg BW i.v.), abolished SD propagation. Within two hours after the onset of the first SD, significantly enhanced fluorescence intensity at the frontal cortex was only measured in animals from group 1 with multiple propagated SDs. In conclusion, we provide evidence that repetitive SDs significantly increase blood-brain barrier permeability within two hours after the onset.