OFP-13-006 Dopamine and alpha synuclein interplay in neurodegeneration: A rat animal model G. Stoica * , G. Lungu, N. Bjorklund * Texas A&M University, Veterinary Pathobiology, College Station, USA Objective: A spontaneous autosomal recessive rat model for neurodegeneration was developed in our laboratory. These rats demonstrate progressive increases in alpha synuclein (α-syn) in the brain mesencephalon followed by loss of dopaminergic terminals in the basal ganglia and motor impairments. Method: Histology, immunohistochemistry, transmission electron microscopy were used for morphological analyses. For α-syn assessment real-time PCR and western blot were used. Dopamine measurements were performed by ion mobility mass spectral (IMMS). Results: The severity of pathology is directly related to the overexpression of α-syn and parallel decrease in dopamine (DA) level in the striatum (ST) of affected rats. The neurodegeneration in this model is characterized by the presence of perikarya and neurites Lewis bodies (LB) and diffuse marked accumulation of perikaryal α-syn in the substantia nigra (SN), brain stem, and striatum along with neuronal loss. Light and ultrastructural analyses revealed that the process of neuronal degeneration is a "dying back" type. The disease process is accompanied by gliosis and release of inflammatory cytokines. Conclusion: Decrease dopamine and overexpression of α-syn in the brain mesencephalon may provide a naturally occurring animal model for Parkinson's disease and other synucleinopathies that reproduces significant pathological, neurochemical, and behavioral features of the human disease. Sunday, 9 September 2012, 14.15 -16.15 Objective: The mitotic index in thin primary melanomas replaced Clark level in the 2009 staging system of the AJCC. However, the recommended quantification of proliferation by hot spots on HE stains is criticized. An alternative may be the immunohistochemical proliferation marker phosphohistone H3 (PHH3) visualizing all mitotic cells. And, when combined with the melanocytic marker MART1, PHH3 insures quantification of proliferating melanocytes, only. Method: 153 primary melanomas with a median follow-up of 12 years for patients with event-free melanoma were included. PHH3/MART1 stains were performed by an indirect sequential immunoenzymatic technique. The number of PHH3/MART1 positive cells was counted in a fixed 1-mm2 frame in the dermal area with the highest concentration of positive cells (hot spots). Results: In multivariate analysis, PHH3 in hot spots was a strong independent prognostic marker for recurrent disease (HR=3.7, 95 % CI, 1.4 to 9.6; P=.008) and melanoma-specific death (HR=3.4, 95 % CI, 1.3 to 9.0; P=.013), when corrected for primary tumor thickness and ulceration. Conclusion: Cellular proliferation is an independent prognostic marker in primary cutaneous melanoma. However, accurate quantification is crucial for correct clinical staging. For this purpose, proliferation indices of the novel PHH3/MART1 double stains seem very promising. Objective: Some of the more common benign vocal fold lesions are polyps, nodules and polypoid corditis (Reinke's edema). The majority of vocal fold pathology develops in the mucosal layer of the vocal fold, precisely in Reinkes space. Basic science and clinical research over past decades has led to advances in our understanding of benign laryngeal lesions. The aim of our study was compared contact telescopy findings with histological analyzes in a patients with Reinke's edema. Method: The our study included 80 consecutive patients with clinical diagnosis of Reinke's edema. Videoassisted contact telescopy was performed in all cases under general anesthesia and mucosa was stained by methylene blue. Tissue biopsies were taken from areas exhibiting visible pathological changes and sent to routine histopathology and immunohistochemical analyses. We analyzed expression of pancytokeratin antibodies, vimentin and CD 34. Results: In the all case of Reinke's edema, contact telescopic scans showed a change of direction or a disappearance of regular distribution and morphology of blood vessels (irregular shapes, positions, and patterns, apparently running in random directions) in vocal fold mucosa. Marked pathological changes were noted by contact telescopic scans, confirmed with histopathology analyses. Conclusion: Contact telescopy is a useful additional diagnostic tool regarding Reinke's edema.