Highlights d cDC2 initiate activation but not differentiation of antitumor CD4 + T conv d T reg depletion relieves cDC2 suppression driving antitumor CD4 + T conv differentiation d Human equivalent of mouse cDC2 are present in the tumor and draining lymph node d The balance of human cDC2/T reg in the TME dictates T cell quality and prognosis

4. Laryngoscope, 124:1204-1208, 2014.

Importance As the limits of advanced skull base malignancies that can be managed through an endoscopic endonasal approach continue to be expanded, the resultant anterior skull base defects are of increasing size and complexity. In the absence of nasoseptal or turbinate flaps, the vascularized pericranial flap has been employed at our institution with excellent results. Objective The study aimed to review the outcomes of patients who underwent endonasal anterior craniofacial resection with anterior skull base reconstruction using a vascularized pericranial flap. Design Retrospective chart review of patients treated by the University of California – San Francisco minimally invasive skull base service from the years 2011 to 2017. Average duration of follow-up was 16.4 months. Setting This study was conducted at Academic tertiary referral center. Participants A total of nine patients with advanced anterior cranial base malignancies were identified who were treated with a minimally invasive, endoscopic anterior craniofacial resection from the years 2011 to 2017. Due to the nature of the resection in these patients, nasoseptal flaps and inferior/middle turbinate flaps were unavailable or insufficient for anterior skull base defect repair. Each patient underwent reconstruction of the anterior cranial base defect using an anteriorly based pericranial flap harvested by bicoronal incision, and tunneled anteriorly to the nasal cavity through a frontoethmoidal incision.

No abstract

Objectives: To present a novel location in which neurosarcoidomatous inflammation is identified and its accompanying presentation. Methods: The authors present a case of bilateral vocal fold paresis associated with non-caseating granulomatous inflammation of the cervical and intra-axial portions of the vagus nerve masquerading as a cranial nerve tumor. Results: Examination revealed bilateral vocal fold paresis and asymmetric palate elevation. MRI demonstrated enhancing bilateral jugular foramen masses, and neck ultrasound demonstrated bilateral thickened appearance of the vagus nerves. Vagus nerve biopsy demonstrated non-caseating granulomas. Conclusions: Neurosarcoidosis may contribute to variable cranial neuropathies. Vocal fold paresis is usually thought to arise from mediastinal compression of the left recurrent laryngeal nerve. Rarely, though, lesions may arise in other parts of the vagus nerve. Failure of response to steroids does not rule out the diagnosis, making tissue diagnosis important in some cases.