Neuroinflammation plays a role in the etiology of these diseases and caffeine may provide protection through the modulation of inflammation. Adenosine has a known role in the propagation of inflammation and caffeine may reduce microglia activation directly by blocking adenosine receptors on microglia. Chronic neuroinflammation is associated with an increase in extracellular
levels of glutamate and drugs that limit the effects of glutamate at neuronal receptors have been shown to indirectly reduce the neuroinflammatory response of microglia cells. A1 and A2A receptors have been shown to regulate the pre-synaptic release of glutamate, therefore, caffeine may also reduce neuroinflammation via its ability to regulate glutamate release. Caffeine was
administered at various doses to young rats with experimentally induced neuroinflammation by chronic infusion of lipopolysaccharide PF299804 order (LPS) over two or four weeks into the 4th ventricle click here and to aged rats with naturally elevated levels of microglia activation. Caffeine attenuated the number of activated microglia within the hippocampus of animals with LPS-induced and age-related inflammation. (C) 2010 Elsevier Ireland Ltd. All rights reserved.”
“Objective: To demonstrate the efficacy of a minimally invasive, nonoperative, catheter-based approach to the treatment of traumatic chyle leak.
Methods: A retrospective review of 109 patients was conducted to assess the efficacy of thoracic duct embolization or interruption for the treatment of high-output chyle leak caused by injury to the thoracic duct.
Results: A total of 106 patients presented with chylothorax, 1 patient presented with chylopericardium, and 2 patients presented with cervical lymphocele. Twenty patients (18%) had previous failed thoracic duct ligation. In 108 of 109 patients, a lymphangiogram was successful. Catheterization of the thoracic duct was achieved in 73 patients
(67%). In 71 of these 73 patients, embolization of the thoracic duct was performed. Endovascular coils or liquid embolic agent was used to occlude the thoracic duct. In 18 of 33 cases of unsuccessful catheterization, thoracic duct needle interruption was attempted below the diaphragm. Resolution of the chyle leak was observed in 64 of 71 patients (90%) post-embolization. Needle interruption of the thoracic duct was successful PDK4 in 13 of 18 patients (72%). In 17 of the 20 patients who had previous attempts at thoracic duct ligation, embolization or interruption was attempted and successful in 15 (88%). The overall success rate for the entire series was 71% (77/109). There were 3 (3%) minor complications.
Conclusion: Catheter embolization or needle interruption of the thoracic duct is safe, feasible, and successful in eliminating a high-output chyle leak in the majority (71%) of patients. This minimally invasive, although technically challenging, procedure should be the initial approach for the treatment of a traumatic chylothorax.