Rare variations of cephalic vein drainage: two case reports.

Throughout the years, anatomic studies have demonstrated numerous variations in the course of the cephalic vein (CV). There are, however, very rare cases of uncommon formation, course, or termination of the vein to which our attention should be drawn. During routine dissections conducted in the Department of Anatomy and Neurobiology, in 2 formalin-fixed cadavers, very rare anatomical variants were found.

Accelerated Extracellular Nucleotide Metabolism in Brain Microvascular Endothelial Cells in Experimental Hypercholesterolemia.

Hypercholesterolemia affects the neurovascular unit, including the cerebral blood vessel endothelium. Operation of this system, especially in the context of energy metabolism, is controlled by extracellular concentration of purines, regulated by ecto-enzymes, such as e-NTPDase-1/CD39, ecto-5'-NT/CD73, and eADA. We hypothesize that hypercholesterolemia, via modulation of the activity of nucleotide metabolism-regulating ecto-enzymes, deteriorates glycolytic efficiency and energy metabolism of endothelial cells, which may potentially contribute to development of neurodegenerative processes.

The Effect of Simvastatin on the Dynamics of NF-κB-Regulated Neurodegenerative and Neuroprotective Processes in the Acute Phase of Ischemic Stroke.

Statins are lipid-lowering drugs that act by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase, a rate-limiting enzyme in cholesterol biosynthesis. Animal studies have shown neuroprotective effects of statins in cerebral stroke. However, the underlying mechanisms are not fully understood.

The extent of damage to the blood-brain barrier in the hypercholesterolemic LDLR/Apo E double knockout mice depends on the animal's age, duration of pathology and brain area.

One of the effects of hypercholesterolemia (Hch) exerted on the central nervous system (CNS) is damage to the blood-brain barrier (BBB). Increased permeability of BBB results from structural changes in the vascular wall, loss of the tight junctions and barrier function, as well as alterations in the concentration of proteins located in the layers of the vascular wall. These changes occur in the course of metabolic and neurodegenerative diseases.

Transient cerebral ischemia induces the neuroglial proliferative activity and the potential to redirect neuroglial differentiation.

Brain injury triggers a complex response involving morphological changes, cellular proliferation, and differentiation of newly formed neuroglial subpopulations. These processes have been extensively studied in animal stroke models with permanent large vessel occlusion. However, less is known about neuroglial response after transient cerebral ischemia.