Pseudoepitheliomatous Hyperplasia of the Larynx Requiring Total Laryngectomy.

BACKGROUND Pseudoepitheliomatous hyperplasia (PEH) is a reactive epithelial proliferation occurring secondary to infection, neoplasm, injury, and inflammation. The histopathological characteristics of PEH may lead to it being confused with well-differentiated squamous cell carcinoma (SCC). CASE REPORT We present here the case of a 57-year-old male patient, who was diabetic and a smoker, who presented with dysphonia. Although nasal endoscopy suggested SCC, morphological and immunophenotypical study of biopsy tissue ruled out malignancy. CONCLUSIONS As the prognosis worsened, the patient required several urgent surgical interventions due to bleeding abscesses and dyspnea. A total laryngectomy was performed.

BARHL1 Is Downregulated in Alzheimer's Disease and May Regulate Cognitive Functions through ESR1 and Multiple Pathways.

The Transcription factor BarH like homeobox 1 (BARHL1) is overexpressed in medulloblastoma and plays a role in neurogenesis. However, much about the BARHL1 regulatory networks and their functions in neurodegenerative and neoplastic disorders is not yet known. In this study, using a tissue microarray (TMA), we report for the first time that BARHL1 is downregulated in hormone-negative breast cancers and Alzheimer's disease (AD). Furthermore, using an integrative bioinformatics approach and mining knockout mouse data, we show that: (i) BARHL1 and Estrogen Receptor 1 (ESR1) may constitute a network that regulates Neurotrophin 3 (NTF3)- and Brain Derived Neurotrophic Factor (BDNF)-mediated neurogenesis and neural survival; (ii) this is probably linked to AD pathways affecting aberrant post-translational modifications including SUMOylation and ubiquitination; (iii) the BARHL1-ESR1 network possibly regulates ß-amyloid metabolism and memory; and (iv) hsa-mir-18a, having common key targets in the BARHL1-ESR1 network and AD pathway, may modulate neuron death, reduce ß-amyloid processing and might also be involved in hearing and cognitive decline associated with AD. We have also hypothesized why estrogen replacement therapy improves AD condition. In addition, we have provided a feasible new mechanism to explain the abnormal function of mossy fibers and cerebellar granule cells related to memory and cognitive decline in AD apart from the Tau and amyloid pathogenesis through our BARHL1-ESR1 axis.