Surgical landmarks of the glossopharyngeal nerve

Damage to the glossopharyngeal nerve can occur as a result of various Head and Neck surgeries. Associated with this damage are assorted side effects, such as dysphagia, xerostomia, and loss of taste. This study serves to create probabilistic maps of the glossopharyngeal nerve using quantitative data, and to identify different landmarks in order to locate the nerve. Eleven cadaveric heads were bilaterally dissected to expose and measure the glossopharyngeal nerve. The mastoid process is a more reliable marker for the location of the glossopharyngeal nerve as it stretches through the lateral neck. Additionally, distance landmark measurements from the nerve leaving the jugular foramen to it entering the pharyngeal space are offered. Furthermore, statistical probability equations for nerve location have been created. Measurements and models created by this study will aid in pre-operative identification of glossopharyngeal nerve landmarks that will lead to an increase in quality of life in Head and Neck surgery patients

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Coenzyme Q10 Alleviates Chronic Nucleoside Reverse Transcriptase Inhibitor-Induced Premature Endothelial Senescence.

Human immunodeficiency virus (HIV)-infected patients undergoing antiretroviral therapy are afforded an increased lifespan but also exhibit an elevated incidence of cardiovascular disease. HIV therapy uses a combination drug approach, and nucleoside reverse transcriptase inhibitors (NRTI) are a backbone of this therapy. Endothelial dysfunction is an initiating event in cardiovascular disease etiology, and in our prior studies, NRTIs induced an endothelial dysfunction that was dependent upon mitochondrial oxidative stress. Moreover, short-term NRTI administration induced a mitophagy-associated endothelial toxicity and increased reactive oxygen species (ROS) production that was rescued by coenzyme Q10 (Q10) or overexpression of a mitochondrial antioxidant enzyme. Thus, our objective was to examine mitochondrial toxicity in endothelial cells after chronic NRTI treatment and evaluate Q10 as a potential adjunct therapy for preventing NRTI-induced mitochondrial toxicity. Human aortic endothelial cells (HAEC) were exposed to chronic NRTI treatment, with or without Q10. ROS production, cell proliferation rate, levels of senescence, and mitochondrial bioenergetic function were determined. Chronic NRTI increased ROS production but decreased population doubling. In addition, NRTI increased the accumulation of ß-galactosidase, indicative of an accelerated rate of senescence. Moreover, ATP-linked respiration was diminished. Co-treatment with Q10 delayed the onset of NRTI-induced senescence, decreased ROS production and rescued the cells' mitochondrial respiration rate. Thus, our findings may suggest antioxidant enrichment approaches for reducing the cardiovascular side effects of NRTI therapy.