The authors analyzed by transmission electron microscopy (TEM) neurosurgical samples obtained from patients with cerebral tumors, neurotrauma, cerebral ischemia, Moyamoya disease, encephalitis, etc. Their observations concern a variety of dying cell types by different programmed death pathways, including apoptosis, paraptosis, autophagy, autoschizis, programmed necrosis, as well as combined and coexisting forms. This ample work pointed out not only the role of TEM in cell death diagnosis, but the biological differences in cell behavior and beneficial or detrimental effects of suicides for homeostasis, survival, or normal functioning of a tissue, like the integrated vascular tissue and brain parenchyma.
This study is based on data analysis by light and transmission electron microscopy of the surgical cases in cerebral tumors, cerebrovascular malformations, thromboses in the carotid system, and other injuries such as perivascular hemorrhage. We examined cortical arteries and veins, perivascular areas with old hematic masses, vasculogenic foci, and broken large vessels. We identified, characterized, and compared both undifferentiated cells and well-differentiated cordocytes within periadventitial areas where these cells cooperate very well with precursor/stem cells to perform vital functions for cerebral vasculature with immediate effect on brain parenchyma. This useful cellular cooperation was observed by serial sections pointing out the main role of cordocytes during the entire process of collateral vessel formation after thrombosis and, respectively, in vascular wall repair after ruptures. This is the first cytohistopathological study which illustrates and explains some facets of cordocytes-stem cells cooperation around the vessels of human brain with emphasis on the fundamental role of cordocytes in response to vascular injuries. Our pioneering study will be completed for both basic science and modern medical care by further studies.
Light microscopy and transmission electron microscopy were used to investigate surgical cases in a variety of pathological conditions (thromboses, tumors, cerebrovascular malformations, Moyamoya disease) to identify and characterize different phenotypes belonging to a new interstitial cell recently described ultrastructurally in the brain and here named "cordocyte." Also, this work is an attempt to identify and characterize precursor/stem cells for cordocytic lineage in the perivascular areas, within perivascular nerves and pia mater (now considered a cordocytic-vascular tissue). Unexpected relationships and functions emerge from observations concerning these phenotypes, almost ubiquitous, but not yet fully studied in the brain.
We have evidence that methamphetamine (METH)-induced neuronal death is morphologically necrotic, not apoptotic, as is currently believed, and that electrographic seizures may be responsible. We administered 40 mg/kg i.p. to 12 male C57BL/6 mice and monitored EEGs continuously and rectal temperatures every 15 min, keeping rectal temperatures <41.0 °C. Seven of the 12 mice had repetitive electrographic seizure discharges (RESDs) and 5 did not. The RESDs were often not accompanied by behavioral signs of seizures-i.e., they were often not accompanied by clonic forelimb movements. The 7 mice with RESDs had acidophilic neurons (the H&E lightmicroscopic equivalent of necrotic neurons by ultrastructural examination) in all of 7 brain regions (hippocampal CA1, CA2, CA3 and hilus, amygdala, piriform cortex and entorhinal cortex), the same brain regions damaged following generalized seizures, 24 h after METH administration. The 5 mice without RESDs had a few acidophilic neurons in 4 of the 7 brain regions, but those with RESDs had significantly more in 6 of the 7 brain regions. Maximum rectal temperatures were comparable in mice with and without RESDs, so that cannot explain the difference between the two groups with respect to METH-induced neuronal death. Our data show that METH-induced neuronal death is morphologically necrotic, that EEGs must be recorded to detect electrographic seizure activity in rodents without behavioral evidence of seizures, and that RESDs may be responsible for METH-induced neuronal death.
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