On DWI of seven nodules, all nodules (100%) were isointense. None of seven nodules (0%) examined using postcontrast MRI showed enhancement. None of eight nodules (0%) examined using serial MRI (range, 4-60 months) showed changes in morphology over time.

These nodules were incidentally encountered and shared similar MRI features. Although pathological confirmation was lacking in our cases, these

nodules may be of nonaggressive nature.”
“Background: Alterations in pulmonary GSK621 in vivo blood flow are often associated with the initiation and progression of pulmonary vascular disease. However, the cellular mechanisms involved in mediating flow effects in the pulmonary circulation remain unclear. Depending on the disease condition, flow may be extremely low or high. We therefore examined effects of pathologically low and high flow on endothelial production of factors capable of affecting pulmonary vascular tone and structure as well as on potential underlying

mechanisms. Methods: Flow effects on pulmonary endothelial release of NO, PGF(1a), ET-1 and TxB(2), on expression of total and phosphorylated eNOS as well as Akt, and on VEGF were examined. Additionally, in a coculture system, effects of flow-exposed endothelial cells on smooth muscle (SM) proliferation and contractile protein were studied. Results: Compared to physiological flow, pathologically high and low flow attenuated endothelial release of NO and PGF(1a), and enhanced release of ET-1. Physiological flow CRT0066101 in vivo activated the Akt/eNOS pathway, while pathological flow depressed it. Pathologically high flow altered VE-cadherin expression. Pathologically high flow on the endothelium upregulated alpha-SM-actin and SM-MHC without affecting SM proliferation. Conclusion:

Physiological flow leads to production of mediators which favor vasodilation. Pathological flow alters the balance of mediator production which favors vasoconstriction. Copyright (C) 2009 S. Karger AG, Basel”
“Transient peri-ictal changes on imaging had been described following status epilepticus (SE), but its cause is not very well understood. We analyzed the magnetic resonance imaging ADAMTS5 (MRI) findings in SE patients in order to elucidate such changes including peri-ictal signal.

This prospective study involved 34 patients (M/F 23:11, mean age 25.8 +/- 17.2 years) who experienced SE. MRI was performed during or within 96 h of cessation of seizures. Twenty-five patients had generalized convulsive status epilectus (GCSE; ten secondary GCSE and 15 primary GCSE). Seven patients had epilepsia partialis continua and two patients non-convulsive SE. Eight patients had a history of seizures and three patients previous SE. The mean duration of SE prior to MRI was 89.2 +/- 105.3 h (range 2-360 h). MRI provided diagnosis in 17 patients, and in 13 patients, no structural cause was identified.

Peri-ictal focal signal changes with restricted diffusion on apparent diffusion coefficient maps were present in seven (20.