Charissa N. Kahue

Bio: Charissa N. Kahue is an academic researcher from Chaminade University of Honolulu. The author has contributed to research in topics: Otorhinolaryngology & Autophagy. The author has an hindex of 1, co-authored 1 publications receiving 461 citations.

Varicella Zoster Virus Reactivation Involving the Vagus Nerve

Abstract: Objectives: To characterize the presentation, clinical course and functional outcomes of patients with varicella zoster virus (VZV) reactivation involving the vagus nerve. To highlight the role of otolaryngology in acute and long-term management of laryngopharyngeal VZV and its sequelae. Methods: Retrospective review of 3 patients with laryngopharyngeal VZV, managed at a tertiary referral center. Results: All cases presented with vesicular lesions involving mucosa of the laryngopharynx. Each experienced vocal fold hypomobility, among other otolaryngologic sequelae. All were treated with systemic antivirals and corticosteroids. Mucosal lesions resolved within 7 days of treatment initiation; functional deficits persisted for months to years. Dysphonia improved to a plateau at 3 months, while dysphagia took longer to resolve. One patient with disseminated disease experienced bilateral vocal fold paralysis requiring temporary tracheostomy. Conclusions: Vagal neuropathy secondary to VZV reactivation is a rare clinical entity with a variety of laryngeal manifestations. Early initiation of systemic therapy and serial endoscopic evaluations are critical components of acute management when laryngopharyngeal involvement is suspected. Otolaryngologists should plan for long-term phonatory and deglutitive therapy in these cases, as neurologic sequelae can persist for months to years following initial insult. Level of Evidence: Level 4 (Case-series).

Autophagy fights disease through cellular self-digestion

Abstract: Autophagy, or cellular self-digestion, is a cellular pathway involved in protein and organelle degradation, with an astonishing number of connections to human disease and physiology. For example, autophagic dysfunction is associated with cancer, neurodegeneration, microbial infection and ageing. Paradoxically, although autophagy is primarily a protective process for the cell, it can also play a role in cell death. Understanding autophagy may ultimately allow scientists and clinicians to harness this process for the purpose of improving human health.

Regulation Mechanisms and Signaling Pathways of Autophagy

Abstract: Autophagy is a process of self-degradation of cellular components in which double-membrane autophagosomes sequester organelles or portions of cytosol and fuse with lysosomes or vacuoles for breakdown by resident hydrolases. Autophagy is upregulated in response to extra- or intracellular stress and signals such as starvation, growth factor deprivation, ER stress, and pathogen infection. Defective autophagy plays a significant role in human pathologies, including cancer, neurodegeneration, and infectious diseases. We present our current knowledge on the key genes composing the autophagy machinery in eukaryotes from yeast to mammalian cells and the signaling pathways that sense the status of different types of stress and induce autophagy for cell survival and homeostasis. We also review the recent advances on the molecular mechanisms that regulate the autophagy machinery at various levels, from transcriptional activation to post-translational protein modification.

Role of autophagy in cancer

Abstract: Autophagy is a cellular degradation pathway for the clearance of damaged or superfluous proteins and organelles. The recycling of these intracellular constituents also serves as an alternative energy source during periods of metabolic stress to maintain homeostasis and viability. In tumour cells with defects in apoptosis, autophagy allows prolonged survival. Paradoxically, autophagy defects are associated with increased tumorigenesis, but the mechanism behind this has not been determined. Recent evidence suggests that autophagy provides a protective function to limit tumour necrosis and inflammation, and to mitigate genome damage in tumour cells in response to metabolic stress.

Eaten alive: a history of macroautophagy.

Abstract: Macroautophagy (hereafter autophagy), or 'self-eating', is a conserved cellular pathway that controls protein and organelle degradation, and has essential roles in survival, development and homeostasis. Autophagy is also integral to human health and is involved in physiology, development, lifespan and a wide range of diseases, including cancer, neurodegeneration and microbial infection. Although research on this topic began in the late 1950s, substantial progress in the molecular study of autophagy has taken place during only the past 15 years. This review traces the key findings that led to our current molecular understanding of this complex process.

Deconvoluting the context-dependent role for autophagy in cancer

Abstract: Autophagy (also known as macroautophagy) captures intracellular components in autophagosomes and delivers them to lysosomes, where they are degraded and recycled. Autophagy can have two functions in cancer. It can be tumour suppressive through the elimination of oncogenic protein substrates, toxic unfolded proteins and damaged organelles. Alternatively, it can be tumour promoting in established cancers through autophagy-mediated intracellular recycling that provides substrates for metabolism and that maintains the functional pool of mitochondria. Therefore, defining the context-specific role for autophagy in cancer and the mechanisms involved will be important to guide autophagy-based therapeutic intervention.