Allgemeines,Genetik, Cytologie,Physiologie

Ohne Zusammenfassung     

Zur Physiologie und Cytologie der Fettbildung bei Endomyces vernalis

Ohne ZusammenfassungD 93.—Als vorläufige Mitteilung erschien: M. Steiner, Ernährung und Fettbildung bei Endomyces vernalis. Ber. d. Deutsch. bot. Ges. 56, 73, 1938.     

Zur Cytologie der Triticumarten

Ohne Zusammenfassung     

Cytologie vonThamnidium elegans Link

Zusammenfassung Mitochondrien (gefärbt mit Hilfe des Succinat-Dehydrogenase-Mediums und durch Janusgrün B), Lipide sowie das Enzym saure Phosphatase sind beiThamnidium elegans in besonderem Maße an Orten intensiver Differenzierungsprozesse zu finden, so im Spitzenbereich von Sporangiophoren im Stadium I, in Sporangien und in Sporangiolen bildenden Seitenästen. Die Sporangiolen zeigen im Gegensatz zu den meisten Sporangiosporen positive cytochemische Reaktionen, was offenbar auf Unterschiede in der Wandstruktur und damit in der Permeabilität beruht. Im Spitzenbereich von Hyphen läßt sich phasenkontrastmikroskopisch ein scharf abgegrenztes Gebilde nachweisen, das möglicherweise mit dem Spitzenkörper identisch ist.

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Cytology ofThamnidium elegans linkI. Cytochemical and phase contrast microscope investigations of hyphae, sporangia, and sporangiola

Summary Mitochondria (stained by succinate dehydrogenase medium and Janusgreen B), lipids, and acid phosphatase are found in high degree at sites of pronounced differentiation: in the tips of sporangiophores at stage I, in sporangia and in sporangiola producing side-branches. In contrast to most of the sporangiospores the sporangiola show positive cytochemical reactions; this is very probably due to differences in cell wall composition and subsequently in permeability. In the apex of hyphae a distinct structure can be detected by phase contrast microscopy which is perhaps identical with a Spitzenkörper.

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Frau Prof. Dr. B.Haccius danke ich für die Überlassung der Pilzkultur.     

Zur Cytologie von Crepis

Ohne Zusammenfassung Mit 8 Textabbildungen     

Genetik des Hafers

Ohne Zusammenfassung     

Beitrag zur Cytologie von Melandrium

Ohne Zusammenfassung     

Genetik und Abstammungslehre

Ohne Zusammenfassung     

Genetik des Prostatakarzinoms

Prostate cancer is the most frequent malignancy in males and its etiology is strongly influenced by genetic factors. Nevertheless, no mutated genes which could be used for diagnosis have been identified in a major proportion of familial cases. Three genes with germline mutations have been identified after linkage analysis (ELAC2, RNASEL, MSR1), but these mutations are very rare and their penetrance is not well defined. The association of most genes with genetic variants is weak, and only BRCA2/familial breast cancer is of clinical relevance. As a consequence of the extreme genetic heterogeneity, diagnostic tools are not available and genetic counseling has to rely on risk estimates from pedigree data in which a single affected first degree relative indicates a relevant risk.     

Genetik der Psoriasis

Psoriasis is a complex inflammatory and cutaneous disorder with complex inheritance. Currently, the most important risk factor is HLA-CW0602 (and/or a factor in strong linkage disequilibrium with it). This risk allele particularly predisposes to early manifestation (<40 years) and affects the clinical course. To date, genome-wide linkage studies have provided 11 susceptibility loci, while only a few candidate genes have been identified, which bear comparably small odd ratios. Immunological approaches, therapeutic studies with antibodies against immunologic molecules, and candidate-gene-oriented association studies could delineate more aspects of the complex etiology of psoriasis. Increasingly, pathophysiologic and genetic findings converge, giving evidence that psoriasis can be characterized by misdirected immunologic regulation processes of keratinocytes and cells of the inborn and adaptive immune system.     

Beitrag zur Cytologie der Charales

Ohne ZusammenfassungMit 22 Textabbildungen.     

Genetik der Parkinson-Krankheit

In addition to the nine well-defined monogenic forms of Parkinson’s disease, there are numerous known genetic risk and protective variants that modulate the risk of Parkinson’s disease. Among the monogenic forms, three (PARK1/PARK4, PARK8, PARK17) follow an autosomal dominant mode of inheritance, whereas six are recessively inherited (PARK2, PARK6, PARK7, PARK9, PARK14, PARK15). Six forms have clinical characteristics very similar to those of idiopathic Parkinson’s disease (PARK1/PARK4, PARK2, PARK6, PARK7, PARK8, PARK17). Among the latter forms, late-onset PARK8 with mutations in the LRRK2 gene and early-onset PARK2 caused by mutations in the Parkin gene are by far the most common. Both the monogenic and the idiopathic forms of Parkinson’s disease share common pathophysiological mechanisms involving oxidative modification, impaired protein degradation and mitochondrial dysfunction. Therefore, monogenic forms of Parkinson’s disease can serve as human model diseases for the idiopathic forms.