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C Hedinger

Publications and source records attributed to C Hedinger.

At least 127 records · Page 7Linked to original sources

Quantitative and ultrastructural study of germinal epithelium in testicular biopsies with "mixed atrophy".

In 17 cases of male sterility with so-called "mixed atrophy" in testicular biopsies, the germinal epithelium was investigated by quantitative as well as by ultrastructural means. In 13 cases, the number of spermatids only was reduced, in 2 cases earlier stages of germinal cells were diminished also. Normal quantitative data were found in biopsies of 2 patients. Among ultrastructural alterations various disturbances of the acrosome were dominant. Additional ultrastructural findings in spermatids included binucleate forms and lack of mitochondrial sheaths in the middle-piece. The largely uniform changes in the tunica propria (fibrosis of the innermost layers, extensive changes of the basement membrane) were considered to be at least one of the cofactors responsible for the alterations of the germinal epithelium.

Adult↗

Motile components in spermatids as related to transport of spermatids and spermatozoa.

Two distinctly different components of motility were detected in living early spermatids of the rat using phase contrast microscopy and video-analysis: the primary flagellum (a 9 + 2 axonema) executes wave-like motion in three dimensions. At the same time the flagellum displays alternatively in clockwise and counter-clockwise directions partial torsion, whereas shortening and elongation can also be observed. The second component is based on rhythmical movements of the spermatid cytoplasm at identical stages. During differentiation the capacity for motion reduces progressively. For instance, late spermatids are only capable of bending their now thickened flagellum. Spermatozoa were found immotile. Germ cells during differentiation are thought to contribute themselves to their transfer through the germinal epithelium. Reduction of motility in the differentiating flagellum is due to growing accessory structures surrounding the axonema, whereas motility of the cytoplasm is reduced by its resorption. In man, some forms of hypofertility and sterility, such as the immotile-cilia syndrome, might already be caused by imperfect motile components present in spermatids.

Animals↗

Mosaicism of dynein in spermatozoa and cilia and fibrous sheath aberrations in an infertile man.

Male patients displaying an immotile or almost immotile sperm population are the object of an interdisciplinary study concerning a ciliary mutant that induces the "Immotile-Cilia Syndrome". Development and function of both sperm flagella and cilia are normally affected because of disturbances of the 9 + 2-arrangement. During this program, clinical, physiological, genetical and ultrastructural investigations were done. The ultrastructure of immotile spermatozoa of an infertile man did not reveal inner and outer dynein arms. Lack of the ATPase dynein which is essential for movement of the 9 + 2-axoneme, is typical for the above syndrome. In addition, symmetry of the fibrous sheath of the spermatozoa was very abnormal. The pneumologist examined normal lung function, where the ultrastructure of the cilia of the nasal mucosa displayed the dynein arms. Analysis of family tree and chromosomes by the geneticist also gave a normal result. As revealed by this infertile patient it seems likely that expression of dynein must not be identical in both germ cells and somatic cells. Such variations are therefore regarded as additional forms of the "Immotile-Cilia syndrome". Asymmetric fibrous sheaths are thought to be a result of immotile spermatid flagella, leading to an abnormal arrangement of the accessory axonemal structures. Normal early spermatid flagella of man and rat show specific movements.

Adenosine Triphosphatases↗