Focus on Form : J. J. Tikkanen, Giotto and Art Research in the 19th Century

My doctoral dissertation is on Johan Jakob Tikkanen (1857 1930), the first professor of art history in Finland, and his significance and methods in the context of late 19th and early 20th-century European art history. Tikkanen was one of the pioneering scholars in the field of medieval art research, and, along with Anton Springer, Heinrich Wölfflin, Aloïs Riegl, Adolfo Venturi, Franz Wickhoff, Julius von Schlosser, Aby Warburg, Emile Mâle and others, one of the scholars who defined art history as an independent academic discipline. Tikkanen s scholarly interests and his methods resemble those of many formalistically oriented German and Austrian art historians of his time. He became well known throughout Europe, mainly for his studies on illustrated medieval manuscripts. Tikkanen s dissertation, Der Malerische Styl Giotto s Versuch zu einer Characteristik Desselben, from 1884 was regarded in its day as the best form-analytical study on the painter. It has a central position in the present thesis, as it already included nearly all the methods that Tikkanen used and elaborated upon throughout his career. Giotto also gives a good perspective for comparing Tikkanen s ideas with a long art-historical tradition. Tikkanen was profoundly interested in artistic creativity. In his own words, he wanted to study das künstlerische Können , artistic ability, instead of das künstlerische Wollen or artistic will, which was an important theoretical issue in art history in the late 19th century. This starting point led him to the history of style and iconographical research. Along with the Danish art historian, Julius Lange, he was one of the first scholars who began to study the meaning of gestures and postures in art. In my dissertation I have emphasized the importance of Tikkanen s personal art education. I regard it as having influenced both his scholarly argumentation and his working methods. I have also written a short overview of the situation of art history in Finland and in Northern Countries before Tikkanen s time in order to give an idea of his scientific background. My thesis is a critical and historiographical study on J. J. Tikkanen s role in the development of art history and its methodology.

Joseph Ritter von Wertheimer, Moritz Lazarus and Abraham Geiger; Officers of the first Jewish Council of Leipzig Portraits; Groups; Men

"Praesidium der ersten israelitischen Synode zu Leipzig. II Vicepraesident Ritter V. Wertheimer aus Wien. Praesident Prof. Dr. M. Lazarus aus Berlin. I Vicepraesident Dr. A. Geiger aus Frankfurt a/M."

Studio portrait of Erich von Kahler; Munich.

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Outdoor portrait of Emil Preetorius, Erich von Kahler and Friedrich Gundolf.

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Ambassador von Staden and Secretary Califano signing the U.S.-German Social Security Agreement; Washington, D.C.

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Rudolf and Antoinette von Kahler in living room; Vienna-Doebling Architecture; Residences

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Painting of Freiherr Martin von Magnus Family Portraits Family

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Genetic Mechanisms of Tumourigenesis in von Hippel-Lindau-Associated Tumours with the Emphasis on Capillary Hemangioblastoma

The von Hippel-lindau (VHL) disease is a dominantly inherited neoplastic disorder which predisposes patients to multiple tumours including capillary haemangioblastomas (CHBs), pheochromocytomas (PCCs), renal cell carcinomas (RCCs). CHBs are the most common manifestations of VHL disease, occurring sporadically or as a manifestation of VHL disease. Inactivation of the VHL gene at 3p25-26 is believed to cause both familial and sporadic VHL-associated tumours and germ-line mutation of the VHL gene have been detected in 100% of the CHBs studied. However, a limited number of sporadic CHBs, PCCs display VHL inactivation. Other molecular alterations involved in tumourigenesis of sporadic CHBs, PCCs remain largely unknown. The purpose of the present work was to search for genetic alterations, or other mechanisms of inactivation, in addition to the VHL gene, that may be important in the development of VHL-associated tumours. Though less satisfactory than cure, prevention and early detection are the most promising and feasible means reducing cancer morbidity and mortality. This work is based on the view that increasing knowledge about the molecular events underlying tumour development will eventually aid in early detection and lead to improved treatment. We evaluated a large set of VHL-associated patients, searched for a clinical and radiologic signs of the disease. We succesfully performed a germ-line mutation analysis and characterised three patient groups, VHL, suspect VHL and sporadic, a germ-line mutation analysis revealed a 50% mutation rate only in the VHL groups, no sporadic or suspect cases displayed any mutation. We also utilized comparative genomic hybridization (CGH) to screen for DNA copy number changes in both sporadic and VHL-associated CHB. Our analysis revealed (27%) DNA copy number losses. The most common finding was loss of chromosomal arm 6q, seen in (23%) cases, No differences were noted between VHL-associated and sporadic tumours. Furthermore a loss of heterozygosity (LOH) study on chromosome 3p and 6q was done with the purpose to determine allele losses not observable by CGH, and to uncover the location of putative tumour suppressor genes important in CHB and PCC tumourigenesis. We identified loss of chromosome 6q and a minimal deleted area at 6q23-24 in CHBs. We also showed LOH at 6q23-24 in PCCs and identified the ZAC1 (6q24-25) as a candidate gene, ZAC1 is a maternally imprinted tumour suppressor gene with anti proliferative properties. To study further the role of ZAC inactivation in CHBs, we investigated LOH, promoter hypermethylation and expression status of the ZAC1 gene in mainly sporadic CHBs. Our LOH analysis revealed that the majority of the tumours with allele loss. The gene promoter methylation analysis similarly detected predominance of the methylated ZAC sequence in almost all tumours. Immunohistochemistry exhibited a strongly reduced expression of ZAC in stromal cells of all CHBs studied. Our current results indicate that the absence of the unmethylated, ZAC1 promoter sequence was highly concurrent with LOH for the ZAC1 region or 6q loss. This observation together with lack of ZAC expression, points to preferential loss of the non imprinted, expressed ZAC allele in CHB, in summary, our series of studies reveal a new chromosomal region 6q, emphasizes the importance of ZAC1 gene in the development of CHB and PCC, particularly in non-VHL associated cases.

Outdoor portrait of Erich von Kahler.

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