A novel four-dimensional prediction model of soil heavy metal pollution: Geographical explanations beyond artificial intelligence "black box".

The current artificial intelligence (AI)-based prediction approaches of soil pollutants are inadequate in estimating the geospatial source-sink processes and striking a balance between the interpretability and accuracy, resulting in poor spatial extrapolation and generalization. In this study, we developed and tested a geographically interpretable four-dimensional AI prediction model for soil heavy metal (Cd) contents (4DGISHM) in Shaoguan city of China from 2016 to 2030. The 4DGISHM approach characterized spatio-temporal changes in source-sink processes of soil Cd by estimating spatio-temporal patterns and the effects of drivers and their interactions of soil Cd at local to regional scales using TreeExplainer-based SHAP and parallel ensemble AI algorithms.

PTPRN Serves as a Prognostic Biomarker and Correlated with Immune Infiltrates in Low Grade Glioma.

Background: Glioma is one of the most common malignant tumors of the central nervous system. Immune infiltration of tumor microenvironment was associated with overall survival in low grade glioma (LGG). However, effects of Tyrosine phosphatase receptor type N (PTPRN) on the progress of LGG and its correlation with tumor infiltration are unclear.

Spatiotemporal Patterns of Spreading Depolarization and its Correlation with Brain Injury During the Acute Stage of Subarachnoid Hemorrhage in Mice.

Objective: Spreading depolarization (SD) has been regarded as one cause of neuronal injury in subarachnoid hemorrhage (SAH). However, SD in the hyperacute phase of SAH is still unclear. The objective of this study was to detect real-time spatial-temporal patterns of SD, assess the effect of SD on cerebral blood flow, and test the relationship between SD and brain injury in the acute phase of SAH.

Minimally Invasive Surgery for Intracerebral and Intraventricular Hemorrhage.

Spontaneous intracerebral hemorrhage (ICH), especially related to intraventricular hemorrhage (IVH), is the most devastating type of stroke and is associated with high mortality and morbidity. Optimal management of ICH remains one of the most controversial areas of neurosurgery and no effective treatment exists for ICH. Studies comparing conventional surgical interventions with optimal medical management failed to show significant benefit.

Loss of Kir6.1 facilitates peri-infarct depolarizations in focal cerebral ischemia.

Objective: Peri-infarct depolarizations (PIDs) are spontaneous waves that propagate slowly across the penumbra region following stroke, contributing to secondary infarct growth and negatively affecting stroke outcomes. K channels are generally spread in the brain. Under conditions of ischemia and/or hypoxia, K channels play a cytoprotective role in neurons.

Safety profile of the transcription factor EB (TFEB)-based gene therapy through intracranial injection in mice.

Transcription factor EB (TFEB)-based gene therapy is a promising therapeutic strategy in treating neurodegenerative diseases by promoting autophagy/lysosome-mediated degradation and clearance of misfolded proteins that contribute to the pathogenesis of these diseases. However, recent findings have shown that TFEB has proinflammatory properties, raising the safety concerns about its clinical application. To investigate whether TFEB induces significant inflammatory responses in the brain, male C57BL/6 mice were injected with phosphate-buffered saline (PBS), adeno-associated virus serotype 8 (AAV8) vectors overexpressing mouse TFEB (pAAV8-CMV-mTFEB), or AAV8 vectors expressing green fluorescent proteins (GFPs) in the barrel cortex.

Loss of GFAP and Vimentin Does Not Affect Peri-Infarct Depolarizations after Focal Cerebral Ischemia.

Peri-infarct depolarization (PID), one kind of spreading depolarization, contributes to infarct volume enlargement after ischemic stroke. Astrocytes participate in PIDs by various mechanisms. The roles of glial fibrillary acidic protein (GFAP) and vimentin (Vim), intermediate filament proteins in astrocytes, however, in PIDs induction and propagation remain unknown.

Spreading Depolarization during the Acute Stage of Experimental Subarachnoid Hemorrhage in Mice.

Spreading depolarization (SD) has been suggested as a pathomechanism for delayed cerebral ischemia after subarachnoid hemorrhage (SAH). However, the role of SD during the acute phase of SAH is still unclear. The objective of this study was to investigate (a) the occurrence of SD with intrinsic optical signal (IOS) imaging, (b) the effect of ketamine on SD, and (c) the resulting brain edema (brain water content (BWC)) during the acute stage of experimental SAH in mice.

Large field-of-view movement-compensated intrinsic optical signal imaging for the characterization of the haemodynamic response to spreading depolarizations in large gyrencephalic brains.

Haemodynamic responses to spreading depolarizations (SDs) have an important role during the development of secondary brain damage. Characterization of the haemodynamic responses in larger brains, however, is difficult due to movement artefacts. Intrinsic optical signal (IOS) imaging, laser speckle flowmetry (LSF) and electrocorticography were performed in different configurations in three groups of in total 18 swine.

Pharmacological modulation of spreading depolarizations.

Spreading depolarization (SD) is a wave of almost complete depolarization of the neuronal and glial cells. Nowadays there is sufficient evidence demonstrating its pathophysiological effect in migraine with aura, transient global amnesia, stroke, subarachnoid hemorrhage, intracerebral hemorrhage, and traumatic brain injury. In these cases, occurrence of SD has been associated with functional neuronal damage, neuronal necrosis, neurological degeneration, and poor clinical outcome.

The effect of ketamine on optical and electrical characteristics of spreading depolarizations in gyrencephalic swine cortex.

Spreading depolarization (SD) is a wave of mass neuronal and glial depolarization that propagates across the cerebral cortex and has been implicated in the pathophysiology of brain injury states and migraine with aura. Analgesics and sedatives seem to have a significant effect on SD modulation. Studies have shown that ketamine, an NMDA receptor blocker, has the capacity to influence SD occurrence.

Delayed cerebral ischemia after subarachnoid hemorrhage: from vascular spasm to cortical spreading depolarizations.

Non-traumatic subarachnoid hemorrhage (SAH) represents about 5 to 6% of the overall incidence of stroke and is associated with high morbidity and mortality. Despite the substantial research and clinical efforts, delayed cerebral ischemia (DCI) is still the major complication after SAH and represents an important factor for severe neurological deficits. Cerebral vasospasm (VSP) has been recognised for a long time as an important underlying pathophysiologic cause of DCI, but it is now clearer that the mechanisms underlying DCI are multifactorial.

'Long' pressure reactivity index (L-PRx) as a measure of autoregulation correlates with outcome in traumatic brain injury patients.

Background: Cerebral autoregulation and, consequently, cerebrovascular pressure reactivity, can be disturbed after traumatic brain injury (TBI). Continuous monitoring of autoregulation has shown its clinical importance as an independent predictor of neurological outcome. The cerebral pressure reactivity index (PRx) reflects that changes in seconds of cerebrovascular reactivity have prognostic significance.