Neoplasms of the nasal cavity are rare in all species. They are almost always malignant and local invasion leads to destruction of the tissue. Metastases occur late in lymphnodes, lungs and liver. Clinical symptoms are unilateral nasal discharge, sneezing, epistaxis, stridor nasalis. Destruction of the nasal septum results in deformation of the skull, exophthalmus and epiphora. Diagnostics of nasal tumours include clinical investigations such as X-rays, CT and MRT as well as cytological and histological examination of smears or biopsies. In this study, nasal biopsies of 264 dogs and 126 cats were investigated. Inflammatory lesions were seen more often (dogs 66%, cats 62%) than neoplasms (dogs 34%, cats 38%). In dogs, adenocarcinoma (48%), squamous cell carcinoma (17%), transitional cell carcinoma (2%), esthesioblastoma (2%), lymphoma (6%), sarcoma (17%) and others (8%) were diagnosed. In cats, adenocarcinoma (30%), squamous cell carcinoma (14%), lymphoma (26%), sarcoma (20%) and others (10%) were found. In two thirds of the samples rhinitis was diagnosed exclusively. In cats, purulent rhinitis was the most common (64%). Bacteria were found in many cases but fungi were not detected. In dogs purulent rhinitis was less common (40%). In 11% of these cases fungi were identified as the cause for inflammation. Furthermore, lympho-plasmacytic rhinitis (dogs 20%, cats 8%) and mixed cellular rhinitis (dogs 40%, cats 28%) were found. Eosinophilic granulocytes were very common in dogs (90%) but less common in cats (23%). In addition to clinical examination techniques, histological investigation of representative biopsies is important for differentiation of neoplastic and inflammatory nasal diseases. Histological characterization is useful for prognosis and therapy.

Efficient strategies for labelling and delivery of bone marrow derived stem cells (BMCs) are required to elucidate the cellular kinetics and therapeutic effects after BMC transfer for myocardial infarction (MI). Lineage negative (lin-) BMCs, labelled ex vivo in a simple procedure with the cell tracker dye tetramethyl-rhodamine (TAMRA), were reliably detected by fluorescence microscopy with higher specificity than retroviral enhanced green fluorescence protein (EGFP) marking and detection. Only few cells entered the ischemic myocardium after intravenous (i.v.) application, but this number increased more than 18-fold after transcoronary delivery. Time course and kinetic analysis over 12 h revealed that myocardial colonization seems to be a biphasic process of first order decay with different elimination half-lives. Most cells are eliminated rapidly during the first 2 h (t1/2 40 min), but the remaining cells are retained significantly longer in the ischemic heart (t1/2 5.2 h). In contrast, BMC colonization of the spleen increased rather in a linear fashion. Although transcoronary BMC transfusion did not alter infarct size, it increased capillary density in the infarct border zone and improved LV function 4 weeks after MI. In conclusion, BMCs delivered by transcoronary injection increase capillary density and improve LV function after MI although homing to the ischemic heart is only transient.

MI is the most frequent cause of death in industrial countries. First clinical assays showed, that BMC could improve myocardial perfusion and cardiac function. To elucidate homing behaviour and therapeutic effects after cell transplantation for MI it is necessary to elaborate clinical approaches in experimental animal assays with corresponding ischemia/reperfusion and cell application as well as efficient strategies for cellular labelling. Lineage negative (lin-) BMCs, labeled ex vivo in a simple procedure with the cell tracker dye tetramethyl-rhodamine (TAMRA), were reliably detected by fluorescence microscopy with higher specificity than EGFP marking and detection. A newly established method of application near the coronary vessel in the murine ischemia/reperfusion model showed an 18-fold higher cellular homing in the ischemic myocardium compared with an intravenous application. Kinetic analysis over 12 h revealed that myocardial colonisation seem to be a biphasic process of first order decay with different elimination half-lifes. Most cells are eliminated rapidly during the first two hours (t1/2 40 min), but the remaining cells are retained significantly longer in the ischemic heart (t1/2 5.2 h). In contrast, BMC colonisation of the spleen increased in a linear fashion. Although transcoronary BMC transfusion did not alter infarct size, capillary density in the infarct border zone increased significantly and echocardiography showed an significant improvement of LV function 4 weeks after MI. Delivery of BMC by transcoronary injection after ischemia/reperfusion in the mouse model represents for the first time an minimal invasive clinical approach in which the applicated BMC increases capillary density and improve LV functions after MI, although homing to the ischemic heart is only transient.