Early Neurosurgical Education in the Era of Distance Learning: Incorporating Virtual Reality and Cadaveric Specimen Demonstrations.

Background: Virtual reality (VR) has emerged as a powerful tool for neuroanatomy education of postgraduate medical trainees. However, its use in early training in neurosurgery, such as of undergraduate, medical, and physician assistant students, has not been evaluated. We also have limited insight into how VR may be integrated with traditional teaching methods.

Intraoperative augmented reality fiber tractography complements cortical and subcortical mapping.

Augmented reality (AR) has been found to be advantageous in enhancing visualization of complex neuroanatomy intraoperatively and in neurosurgical education. Another key tool that allows neurosurgeons to have enhanced visualization, namely of white matter tracts, is diffusion tensor imaging (DTI) that is processed with high-definition fiber tractography (HDFT). There remains an enduring challenge in the structural-functional correlation of white matter tracts that centers on the difficulty in clearly assigning function to any given fiber tract when evaluating them through separated as opposed to integrated modalities.

Vertebrae segmentation in reduced radiation CT imaging for augmented reality applications.

Purpose: There is growing evidence for the use of augmented reality (AR) navigation in spinal surgery to increase surgical accuracy and improve clinical outcomes. Recent research has employed AR techniques to create accurate auto-segmentations, the basis of patient registration, using reduced radiation dose intraoperative computed tomography images. In this study, we aimed to determine if spinal surgery AR applications can employ reduced radiation dose preoperative computed tomography (pCT) images.

Patient-specific virtual reality technology for complex neurosurgical cases: illustrative cases.

Background: Virtual reality (VR) offers an interactive environment for visualizing the intimate three-dimensional (3D) relationship between a patient's pathology and surrounding anatomy. The authors present a model for using personalized VR technology, applied across the neurosurgical treatment continuum from the initial consultation to preoperative surgical planning, then to intraoperative navigation, and finally to postoperative visits, for various tumor and vascular pathologies.

Observations: Five adult patients undergoing procedures for spinal cord cavernoma, clinoidal meningioma, anaplastic oligodendroglioma, giant aneurysm, and arteriovenous malformation were included.

Microvesicles but Not Exosomes from Pathfinder Cells Stimulate Functional Recovery of the Pancreas in a Mouse Streptozotocin-Induced Diabetes Model.

Pathfinder cells (PCs), a novel cell type derived from the pancreas of adult rats, have been demonstrated to stimulate recovery of tissue structure and function in two animal models of acute tissue damage to date-streptozotocin (STZ)-induced diabetes and ischemia-reperfusion damage to the kidney. In repaired tissue, PCs and their progeny typically represent only 0.02% of the repaired tissue, suggesting that they act via a paracrine mechanism on native cells in the damaged area.

Mitotic activation of the DISC1-inducible cyclic AMP phosphodiesterase-4D9 (PDE4D9), through multi-site phosphorylation, influences cell cycle progression.

In Rat-1 cells, the dramatic decrease in the levels of both intracellular cyclic 3'5' adenosine monophosphate (cyclic AMP; cAMP) and in the activity of cAMP-activated protein kinase A (PKA) observed in mitosis was paralleled by a profound increase in cAMP hydrolyzing phosphodiesterase-4 (PDE4) activity. The decrease in PKA activity, which occurs during mitosis, was attributable to PDE4 activation as the PDE4 selective inhibitor, rolipram, but not the phosphodiesterase-3 (PDE3) inhibitor, cilostamide, specifically ablated this cell cycle-dependent effect. PDE4 inhibition caused Rat-1 cells to move from S phase into G2/M more rapidly, to transit through G2/M more quickly and to remain in G1 for a longer period.

Exploiting paracrine mechanisms of tissue regeneration to repair damaged organs.

Stem cells have been studied for many years for their potential to repair damaged organs in the human body. Although many different mechanisms have been suggested as to how stem cells may initiate and facilitate repair processes, much remains unknown. Recently, there has been considerable interest in the idea that stem cells may exert their effects in vivo via paracrine actions.

Elucidation of a structural basis for the inhibitor-driven, p62 (SQSTM1)-dependent intracellular redistribution of cAMP phosphodiesterase-4A4 (PDE4A4).

A survey of PDE4 inhibitors reveals that some compounds trigger intracellular aggregation of PDE4A4 into accretion foci through association with the ubiquitin-binding scaffold protein p62 (SQSTM1). We show that this effect is driven by inhibitor occupancy of the catalytic pocket and stabilization of a "capped state" in which a sequence within the enzyme's upstream conserved region 2 (UCR2) module folds across the catalytic pocket. Only certain inhibitors cause PDE4A4 foci formation, and the structural features responsible for driving the process are defined.

Phosphorylation of cAMP-specific PDE4A5 (phosphodiesterase-4A5) by MK2 (MAPKAPK2) attenuates its activation through protein kinase A phosphorylation.

cAMP-specific PDE (phosphodiesterase) 4 isoforms underpin compartmentalized cAMP signalling in mammalian cells through targeting to specific signalling complexes. Their importance is apparent as PDE4 selective inhibitors exert profound anti-inflammatory effects and act as cognitive enhancers. The p38 MAPK (mitogen-activated protein kinase) signalling cascade is a key signal transduction pathway involved in the control of cellular immune, inflammatory and stress responses.

p62 (SQSTM1) and cyclic AMP phosphodiesterase-4A4 (PDE4A4) locate to a novel, reversible protein aggregate with links to autophagy and proteasome degradation pathways.

Chronic challenge of cyclic AMP phosphodiesterase-4A4 (PDE4A4) with certain PDE4 selective inhibitors causes it to reversibly form intracellular aggregates that are not membrane-encapsulated. These aggregates are neither stress granules (SGs) nor processing bodies (PBs) as they contain neither PABP-1 nor Dcp1a, respectively. However, the PDE4 inhibitor rolipram decreases arsenite-induced SGs and increases the amount of PBs, while arsenite challenge ablates rolipram-induced PDE4A4 aggregates.

Interaction of calcium/calmodulin-dependent protein kinase IIdeltaC with sorcin indirectly modulates ryanodine receptor function in cardiac myocytes.

Calcium/calmodulin dependent protein kinase II delta C (CaMKIIdelta(C)) and the EF-hand Ca(2+)-binding protein, sorcin have both been shown to regulate the excitation-contraction coupling process. This study explores the possibility that these two proteins interact directly and, as a result of this interaction, modulate cardiac calcium handling. Two independent methods (surface plasmon resonance (SPR) and overlay assays) were used to determine whether CaMKIIdelta(C) and sorcin interacted in a direct manner.