17 research outputs found
A literature review on surgery for cervical vagal schwannomas
Cervical vagal schwannoma is a benign, slow-growing mass, often asymptomatic, with a very low lifetime risk of malignant transformation in general population, but diagnosis is still a challenge. Surgical resection is the treatment of choice even if its close relationship with nerve fibres, from which it arises, threats vagal nerve preservation. We present a case report and a systematic review of literature. All studies on surgical resection of cervical vagal schwannoma have been reviewed. Papers matching the inclusion criteria (topic on surgical removal of cervical vagal schwannoma, English language, full text available) were selected. Fifty-three patients with vagal neck schwannoma submitted to surgery were identified among 22 studies selected. Female/male ratio was 1.5 and median age 44 years. Median diameter was 5 cm (range 2 to 10). Most schwannoma were asymptomatic (68.2%) and received an intracapsular excision (64.9%). Postoperative symptoms were reported in 22.6% of patients. Cervical vagal schwannoma is a benign pathology requiring surgical excision, but frequently postoperative complications can affect patients lifelong, so, surgical indications should be based carefully on the balance between risks and benefits
Acute and chronic mitochondrial respiratory chain deficiency differentially regulate lysosomal biogenesis
Mitochondria are key cellular signaling platforms, affecting fundamental processes such as cell
proliferation, differentiation and death. However, it remains unclear how mitochondrial signaling
affects other organelles, particularly lysosomes. Here, we demonstrate that mitochondrial respiratory
chain (RC) impairments elicit a stress signaling pathway that regulates lysosomal biogenesis via
the microphtalmia transcription factor family. Interestingly, the effect of mitochondrial stress over
lysosomal biogenesis depends on the timeframe of the stress elicited: while RC inhibition with
rotenone or uncoupling with CCCP initially triggers lysosomal biogenesis, the effect peaks after few
hours and returns to baseline. Long-term RC inhibition by long-term treatment with rotenone, or
patient mutations in fibroblasts and in a mouse model result in repression of lysosomal biogenesis. The
induction of lysosomal biogenesis by short-term mitochondrial stress is dependent on TFEB and MITF,
requires AMPK signaling and is independent of calcineurin signaling. These results reveal an integrated
view of how mitochondrial signaling affects lysosomes, which is essential to fully comprehend the
consequences of mitochondrial malfunction, particularly in the context of mitochondrial diseases.Open-Access-Publikationsfonds 2017peerReviewe