Transposition Island Pedicle Flap to Repair the Nasal Ala.

Reconstruction of the nasal ala presents surgical challenges, including loss of the nasofacial junction and vasculature compromise, in addition to achieving a cosmetically satisfactory result. The reconstructive surgeon has a variety of closure techniques to employ, but few allow for acceptable cosmesis in a single-stage procedure. The objective of this study is to discuss a novel approach to alar reconstruction using a melolabial-based transposition island pedicle flap, an alternative to traditional interpolated melolabial flaps and inferiorly based interpolated paranasal flap methods. Our reconstruction method utilizes an island pedicle flap harvested from the nasolabial fold and rotated 165˚ medially and superiorly into a surgical defect on the adjacent ala. The pedicle is placed within the alar facial sulcus for a slight trap-dooring effect, recreating the sulcus. The harvest site is closed linearly, resulting in a fusiform scar line to take advantage of the nasolabial fold. Although delicate care is required while dissecting and positioning the flap, it is an otherwise straightforward procedure. The ideal candidate for this technique presents with loss of the alar subunit with an intact alar rim. The only limitation to this style of flap is that the patient has undergone prior procedures involving the ipsilateral nasolabial fold. The transposition island pedicle flap is a well-tolerated alternative to patient cases that require grafting or more involved multi-step reconstructions to efficiently repair nasal alar defects. This technique provides the patient with a presentable cosmetic result using local tissue with minimal post-surgical complications and alar compromise.

Association of Cognitive Function with Amyloid-ß and Tau Proteins in the Vitreous Humor.

BACKGROUND: The eye may serve as source for diagnostic testing for early detection of Alzheimer's disease (AD). Examination of amyloid-ß (Aß) and tau protein content in human vitreous and its correlation to neuro-cognition may improve ocular-based AD detection methods. OBJECTIVE: To evaluate levels of Aß and tau protein in human vitreous humor and investigate the clinical predictive role of these proteins as early diagnostic markers of AD. METHODS: A prospective, single-center, multi-surgeon cohort study. Vitreous humor samples from 80 eyes were measured quantitatively for Aß40-42, pTau, and tTau. Linear regression was used to test associations between AD biomarker levels, Mini-Mental State Exam (MMSE), and serum apolipoprotein E (APOE) allele status, with adjustment for age, sex, and education level of patients. RESULTS: Lower MMSE scores were significantly associated with lower levels of vitreous Aß40 (p = 0.015), Aß42 (p = 0.0066), and tTau (p = 0.0085), and these biomarkers were not associated with any pre-existing eye conditions. Presence of the ɛ4 allele and the ɛ2 allele approached significance with reduced Aß40 level (p = 0.053) and increased p-Tau level (p = 0.056), respectively. CONCLUSION: Patients with poor cognitive function have significantly lower vitreous humor levels of AD-related biomarkers Aß40, Aß42, and tTau. These biomarkers do not correlate with underlying eye conditions, suggesting their specificity in association with cognitive change. This is the first study to our knowledge to correlate cognition with AD-related proteins in the vitreous humor. Results suggest ocular proteins may have a role for early dementia detection in individuals at risk for AD.