The results indicate that ETV is a most effective treatment in cases of obstructive hydrocephalus that is caused by aqueductal stenosis and space-occupying lesions. For patients with infections or intraventricular bleeding, ETV has considerable effects in selected cases with confirmed CSF dynamic studies. Early clinical and cine phase-contrast MR imaging findings after the operation play an important role in predicting patient outcomes after ETV. The predictive value of an alteration in ventricle size, especially during the early stage following ETV, is unsatisfactory. Seventy-five percent of ETV failures occur within 6 months after surgery. A repeated ventriculostomy should be considered to be a sufficient treatment option in cases in which stoma dysfunction is suspected.

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The new hydrodynamic concept of hydrocephalus opens the possibility that ETV may be an effective treatment for communicating hydrocephalus. It thus constitutes an interchangeable alternative to shunting. Patient age, analysis of the causes of hydrocephalus, and mental state evaluation play important roles in outcome prediction in patients with communicating hydrocephalus who undergo ETV. Randomized clinical studies are needed to explore further the role of this treatment in communicating hydrocephalus therapy.

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The potential effect of icariside II on dexamethasone-induced osteoblast cell damages was evaluated here. In MC3T3-E1 osteoblastic cells and the primary murine osteoblasts, co-treatment with icariside II dramatically attenuated dexamethasone- induced cell death and apoptosis. Icariside II activated Akt signaling, which is required for its actions in osteoblasts. Akt inhibitors (LY294002, perifosine and MK-2206) almost abolished icariside II-induced osteoblast cytoprotection against dexamethasone. Further studies showed that icariside II activated Nrf2 signaling, downstream of Akt, to inhibit dexamethasone-induced reactive oxygen species (ROS) production in MC3T3-E1 cells and primary osteoblasts. On the other hand, Nrf2 shRNA knockdown inhibited icariside II-induced anti-dexamethasone cytoprotection in MC3T3-E1 cells. Finally, we showed that icariside II induced heparin-binding EGF (HB-EGF) production and EGFR trans-activation in MC3T3-E1 cells. EGFR inhibition, via anti-HB-EGF antibody, EGFR inhibitor AG1478 or EGFR shRNA knockdown, almost blocked icariside II-induced Akt-Nrf2 activation in MC3T3-E1 cells. Collectively, we conclude that icariside II activates EGFR-Akt-Nrf2 signaling and protects osteoblasts from dexamethasone. Icariside II might have translational value for the treatment of dexamethasone-associated osteoporosis/osteonecrosis.