Audiological results and quality of life of Sophono Alpha 2 transcutaneous bone-anchored implant users in single-sided deafness

Single-sided deafness (SSD) represents one of the most difficult audiological conditions to rehabilitate. The aim of this prospective study was to evaluate the audiological benefits and quality of life of patients affected by SSD who had previously been users of the Alpha 1® when upgrading them to the Sophono Alpha 2® external processor (Boulder, Colo., USA). Nine patients were included in the study. They underwent physical examination, free-field speech audiometry at 40 and 60 dB, a hearing-in-noise test (Hirsch's test and the squelch test), the Glasgow Benefit Inventory (GBI) questionnaire, and a specific questionnaire on patient satisfaction with Alpha 1. Afterwards, the Alpha 2 external processor was delivered to all patients, and the above-mentioned protocol was repeated after 1 month with the Alpha 2. A statistically significant improvement was found in the speech discrimination score at 40 dB and in the squelch test when using the Alpha 2 external processor compared to the Alpha 1. Alpha 2 had a good clinical tolerance and gave similar results in the specific questionnaire and the GBI to Alpha 1. In conclusion, the new Alpha 2 external processor represents a safe and effective device for the rehabilitation of SSD, and there is an audiological benefit to upgrading to the Alpha 2 external processor for patients who had previously been users of the Alpha 1. The improvement in quality of life is similar to that with other bone-anchored hearing devices

Effects of Angiotensin II on human endothelial cells survival signalling pathways and its angiogenic response

Reduced capillary density (rarefaction) is an early event of cardiovascular disease. The PI-3K-Akt pathway is a key player in anti-endothelial cells (ECs) apoptosis. VEGF is a key growth factor for angiogenesis. We investigated the effect of Angiotensin II (Ang II) on ECs survival signalling and angiogenesis in vitro. We found that Ang II had a biphasic effect on Akt phosphorylation by western blotting analysis. Low concentration Ang II caused a dose-dependent increase in Akt phosphorylation, while high concentration of Ang II led to a decrease of Akt phosphorylation. This effect was negative regulated by its type II receptor. Ang II 10(-4) M induced ECs apoptosis by its type H receptor was completely blocked by VEGF. Cell viability was increased by Ang II 10(-6) M and decreased by Ang II 10(-4) M. It was further decreased by pre-treatment with PI-3K/Akt inhibitor LY294002, but unaffected by p38-MAPK inhibitor SB202190. Ang II 10(-4) M reduced ECs' proliferation and vascular tube length, which were in part regulated by type II receptor. Our findings support a dose-dependent role of Ang II in effect on ECs survival and angiogenesis by PI-3K/Akt pathway. The anti-angiogenic effect of Ang H was mediated by its type II receptor

Apoptosis in vascular endothelial cells caused by serum deprivation, oxidative stress and transforming growth factor-?

Vascular endothelial cell apoptosis has previously been shown to play a role in the pathogenesis of hypertension-induced vessel deletion and damage. In the present in vitro study we analyse several possible relevant causative factors of vascular endothelial cell apoptosis, namely, serum deprivation and nutrient depletion, oxidative stress in the forms of hypoxia, hyperoxia or free radical damage, and altered levels of transforming growth factor-beta 1 (TGF-beta 1) protein. An established cell line, bovine aortic endothelial cells (BAEC), was maintained in complete growth medium (RPMI-1640 plus 15% fetal calf serum and antibiotics, abbreviated as RPMI) in 25cm(2) flasks or in 12-well plates on glass coverslips. Confluent but actively-growing cultures were treated with either hypoxia (PO2 of RPMI = 50mmHg), serum-free media (SFM), SFM plus hypoxia, hyperoxia (PO2 of RPMI = 450mmHg), hydrogen peroxide (H2O2, 1 mM) in SFM, or TGF-beta 1 protein (10ng/mL) in SFM. Appropriate control Cultures were used. BAEC were collected 48h or 72h after all treatments except for TGF-beta 1 and H2O2 treatments that were collected at 16-18h. Cell death was assessed using morphological characteristics or in situ end labeling (ISEL), cell proliferation assessed using proliferating cell nuclear antigen (PCNA), and TGF-beta 1 expression assessed using transcript levels or immunohistochemistry. All treatments significantly increased levels of apoptosis over control cultures (