[Teleophthalmology Using Whole Slide Imaging (WSI): Clinical-Pathological Correlation Even Without Own Histological Laboratory]. / Teleophthalmopathologie mittels Whole Slide Imaging (WSI): klinisch-pathologische Korrelation auch ohne eigenes histologisches Labor.

Telepathology has experienced enormous growth over the last two decades due to significant advances in IT and has led to the introduction of innovative solutions for digital imaging in ophthalmology. Whole Slide Imaging (WSI), where conventional glass slides are fully scanned, offers a wide range of applications, including remote (conciliary) diagnostics, second opinions, (remote) teaching and research and presentation. In addition to qualified and experienced personnel, a comparatively expensive basic equipment has so far also been an essential requirement. The focus ophthalmology at the Eye Centre in Freiburg is able to involve a de facto unlimited number of users and consulting partners (also overseas) in the digital microscopy of identical sections independent of location, device and time. This is done simply by using the internet. This procedure has proven to be very successful and opens up completely new avenues, not only for correct diagnosis (clinical-pathological correlation), but also for education and training. Preparation and distribution of further histological slides in addition to the scanned slide is not required for small specimens with scant material, for example, nor is it necessary to purchase microscopes for the participants if funds are lacking or the infrastructure is unsuitable. When dealing with transferring data, it is essential to comply with data protection regulations.

Expression of ALDH1A1 and CD44 in primary head and neck squamous cell carcinoma and their value for carcinogenesis, tumor progression and cancer stem cell identification.

In head and neck squamous cell carcinoma (HNSCC), aldehyde dehydrogenase 1 family, member A1 (ALDH1A1) and hyaluronan receptor cluster of differentiation 44 (CD44) are often used as cancer stem cell (CSC) markers. The aim of the present study was to examine the relevance of these proteins for HNSCC in general and for the identification of CSCs. Tumors from 48 patients with primary HNSCC were analyzed for the expression of ALDH1A1 and CD44. Additionally, the association of the proteins with the proliferation rate and epidermal growth factor receptor (EGFR) expression was analyzed. ALDH1A1 was expressed in 54.2% of the carcinoma samples while CD44 was expressed in 89.6% of the carcinoma samples. Most notably, these proteins were often not expressed exclusively in a subpopulation, but also in the majority of tumor cells (ALDH1A1: 30.8% of ALDH1A1+ tumors; CD44: 65.1% of CD44+ tumors). Furthermore, patients with ALDH1A1+ tumors exhibited worse survival rates. CD44 and EGFR expression patterns were overlapping within the tumors and the expression rates were significantly connected. Ki-67+ tumor cells often expressed CD44. ALDH1A1 and CD44 expression patterns only partly overlapped. Consequently, ALDH1A1 and CD44 play significant roles in carcinogenesis and tumor progression. Within the present study, CD44 appeared to interact with EGFR and was more often expressed in primary HNSCC than the marker ALDH1A1. However, ALDH1A1 was a better marker to define a subpopulation of tumor cells. Finally, neither ALDH1A1 nor CD44, alone or combined, were sufficient to determine the CSC population in HNSCC.

Altered mucosal immune response after acute lung injury in a murine model of Ataxia Telangiectasia.

BACKGROUND: Ataxia telangiectasia (A-T) is a rare but devastating and progressive disorder characterized by cerebellar dysfunction, lymphoreticular malignancies and recurrent sinopulmonary infections. In A-T, disease of the respiratory system causes significant morbidity and is a frequent cause of death. METHODS: We used a self-limited murine model of hydrochloric acid-induced acute lung injury (ALI) to determine the inflammatory answer due to mucosal injury in Atm (A-T mutated)- deficient mice (Atm(-/-)). RESULTS: ATM deficiency increased peak lung inflammation as demonstrated by bronchoalveolar lavage fluid (BALF) neutrophils and lymphocytes and increased levels of BALF pro-inflammatory cytokines (e.g. IL-6, TNF). Furthermore, bronchial epithelial damage after ALI was increased in Atm(-/-) mice. ATM deficiency increased airway resistance and tissue compliance before ALI was performed. CONCLUSIONS: Together, these findings indicate that ATM plays a key role in inflammatory response after airway mucosal injury.