Tumour Seeding Following Core Biopsy of a Mucoepidermoid Carcinoma of the Parotid: Radiological Evidence and a Surgical Approach to En-Bloc Dissection of the Mass and Tract.

Tumour seeding along the needle tract following core needle biopsy of the parotid is a recognised complication. We present a unique case of mucoepidermoid carcinoma of the parotid in an 18-year-old patient with associated tumour seeding within the core needle biopsy tract. Tumour seeding was confirmed both histologically and radiologically on magnetic resonance imaging as early as 35 days post-biopsy. The patient was treated successfully with a combination of surgery and adjuvant proton beam therapy. This case also visually demonstrates a surgical approach to en-block excision of the mass and tract.

Submucosal Intraglossal Fish Bone Extraction: A Case for the Multidisciplinary Team.

Most impacted fish bones in the aerodigestive tract are easily removed or managed in the emergency department. Occasionally, they present as a diagnostic and surgical challenge. We present a case of a submucosal intraglossal fish bone extraction in a 38-year-old male who presented with localized pain in his tongue. This case highlights several key factors contributing to the successful outcome, including multidisciplinary input from anaesthesiology, radiology, and the oral and maxillofacial surgical team. The use of a pre-operative computed tomography (CT) scan, nasal intubation, and intra-operative ultrasound scan potentially minimised the risk of associated complications.

Loss of clusterin shifts amyloid deposition to the cerebrovasculature via disruption of perivascular drainage pathways.

Alzheimer's disease (AD) is characterized by amyloid-ß (Aß) peptide deposition in brain parenchyma as plaques and in cerebral blood vessels as cerebral amyloid angiopathy (CAA). CAA deposition leads to several clinical complications, including intracerebral hemorrhage. The underlying molecular mechanisms that regulate plaque and CAA deposition in the vast majority of sporadic AD patients remain unclear. The clusterin (CLU) gene is genetically associated with AD and CLU has been shown to alter aggregation, toxicity, and blood-brain barrier transport of Aß, suggesting it might play a key role in regulating the balance between Aß deposition and clearance in both brain and blood vessels. Here, we investigated the effect of CLU on Aß pathology using the amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of AD amyloidosis on a Clu+/+ or Clu-/- background. We found a marked decrease in plaque deposition in the brain parenchyma but an equally striking increase in CAA within the cerebrovasculature of APP/PS1;Clu-/- mice. Surprisingly, despite the several-fold increase in CAA levels, APP/PS1;Clu-/- mice had significantly less hemorrhage and inflammation. Mice lacking CLU had impaired clearance of Aß in vivo and exogenously added CLU significantly prevented Aß binding to isolated vessels ex vivo. These findings suggest that in the absence of CLU, Aß clearance shifts to perivascular drainage pathways, resulting in fewer parenchymal plaques but more CAA because of loss of CLU chaperone activity, complicating the potential therapeutic targeting of CLU for AD.