62 research outputs found
Hypothetical granulin-like molecule from Fasciola hepatica identified by bioinformatics analysis
Lipopolysaccharide-induced blood-brain barrier disruption: roles of cyclooxygenase, oxidative stress, neuroinflammation, and elements of the neurovascular unit
Background: Disruption of the blood-brain barrier (BBB) occurs in many diseases and is often mediated by inflammatory and neuroimmune mechanisms. Inflammation is well established as a cause of BBB disruption, but many mechanistic questions remain. Methods: We used lipopolysaccharide (LPS) to induce inflammation and BBB disruption in mice. BBB disruption was measured using 14C-sucrose and radioactively labeled albumin. Brain cytokine responses were measured using multiplex technology and dependence on cyclooxygenase (COX) and oxidative stress determined by treatments with indomethacin and N-acetylcysteine. Astrocyte and microglia/macrophage responses were measured using brain immunohistochemistry. In vitro studies used Transwell cultures of primary brain endothelial cells co- or tri-cultured with astrocytes and pericytes to measure effects of LPS on transendothelial electrical resistance (TEER), cellular distribution of tight junction proteins, and permeability to 14C-sucrose and radioactive albumin. Results: In comparison to LPS-induced weight loss, the BBB was relatively resistant to LPS-induced disruption. Disruption occurred only with the highest dose of LPS and was most evident in the frontal cortex, thalamus, pons-medulla, and cerebellum with no disruption in the hypothalamus. The in vitro and in vivo patterns of LPS-induced disruption as measured with 14C-sucrose, radioactive albumin, and TEER suggested involvement of both paracellular and transcytotic pathways. Disruption as measured with albumin and 14C-sucrose, but not TEER, was blocked by indomethacin. N-acetylcysteine did not affect disruption. In vivo, the measures of neuroinflammation induced by LPS were mainly not reversed by indomethacin. In vitro, the effects on LPS and indomethacin were not altered when brain endothelial cells (BECs) were cultured with astrocytes or pericytes. Conclusions: The BBB is relatively resistant to LPS-induced disruption with some brain regions more vulnerable than others. LPS-induced disruption appears is to be dependent on COX but not on oxidative stress. Based on in vivo and in vitro measures of neuroinflammation, it appears that astrocytes, microglia/macrophages, and pericytes play little role in the LPS-mediated disruption of the BBB
Hydronephrosis Secondary to an Ectopic Decidual Reaction in the Urinary Bladder.
A 28-year-old pregnant woman at 19 weeks gestation presented with dysuria as well as lower abdominal and left flank pain. Imaging revealed left-sided hydronephrosis and a mass invading the posterior bladder wall. Management included placement of a left nephrostomy tube and transurethral resection of ~25% of the mass. Microscopy showed an ectopic decidual reaction within the muscularis propria. The patient improved symptomatically and continued prenatal care. Complete resolution of her ureteral obstruction was demonstrated during the postpartum period. Ectopic decidual reactions involving the urinary bladder are extremely rare, and ureteral obstruction secondary to this phenomenon has not yet been reported
Multiple Aneurysmen der Netzhautgefäße mit Circinataherden und Blutungen an beiden Augen bei einer 65jährigen Patientin
Remarks on the Use of Continuum Damage Models and on the Limitations of their Applicability in Ductile Fracture Mechanics
Effect of the cationic polypeptide polylysine on neutral amino acid transport in isolated brain microvessels
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