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H Tschesche

Publications and source records attributed to H Tschesche.

229 records · Page 13Linked to original sources

On the teratogenesis of round-headed spermatozoa: investigations with antibodies against acrosin, an intraacrosomally located acrosin-inhibitor, and the outer acrosomal membrane.

Acrosin, the outer acrosomal membrane (OAM) and an acrosin inhibitor were studied in testicular cells and ejaculated spermatozoa of fertile men and in those of an infertile patient with exclusively round-headed spermatozoa in his ejaculates. The investigations were performed with the aid of immunohistochemical techniques using specific antibodies against the three acrosomal markers isolated from boar spermatozoa. The spermatozoa of fertile men exhibit staining for acrosin, the OAM and the acrosin inhibitor in the cap region while the round-headed spermatozoa of the patient are totally negative for the three markers, clearly supporting the conclusions of other authors that round-headed spermatozoa lack acrosomes. The lack of the acrosin system was further substantiated by the gelatin substrate film technique. In the course of normal human spermatogenesis acrosin, the OAM and the acrosin inhibitor we first demonstrable in early round spermatids, namely in identical compartments adjacent to the cell nucleus. During spermatid differentiation the staining for the three markers becomes flattened over the nucleus, resulting in a cap-like structure in testicular spermatozoa. In contrast to the ejaculated round-headed spermatozoa, the early round spermatids in the testis of the infertile patient exhibit fluorescent staining for the three markers in the region adjacent to the nuclear membrane. In the course of further spermiogenesis, the staining did not extend over the nuclear membrane, as was observed during normal spermiogenesis, but became separated from the nuclear membrane, as was observed during normal spermiogenesis, but became separated from the nuclear membrane, was translocated at various locations in the cytoplasm and was finally eliminated with the loss of the cytoplasm. These results are in accordance with the results of electron microscopically investigations on the teratogenesis of round-headed spermatozoa. Furthermore, the developmental pattern of the acrosin inhibitor during normal and abnormal spermiogenesis supports the intraacrosomal location of the acrosin inhibitor recently described by Tschesche et al. (1982).

Acrosin↗

Quantification of hemostatic proteins and activation products in synovial fluids from arthritic joints prior to and after induction of chemical synoviorthesis.

Synovial fluids drawn from joints of patients suffering from rheumatoid arthritis were investigated for their concentrations of proteins and activation markers of the complement, coagulation and fibrinolytic systems. A broad spectrum of plasmatic inhibitors and other hemostatic proteins were detectable by immunologic assays. Compared to normal plasma concentration ranges, levels of alpha 2-antiplasmin, antithrombin III, heparin-cofactor II, factor H, alpha 2-macroglobulin, inter-alpha-trypsin inhibitor, fibrinogen and particularly high molecular weight kininogen were found to be decreased when corrected for total protein content. However, highly elevated levels of C-reactive protein, factor XIII, PMN-elastase, prothrombin fragment F1+2, thrombin-antithrombin III, plasmin-antiplasmin and terminal complement-complexes as well as C5a were determined. Eight and 24 hours after induction of chemical synoviorthesis, a general increase in most of the parameters was observed. Statistically significant alterations were found for C1-inhibitor, factor H, alpha 1-antitrypsin, inter-alpha-trypsin inhibitor, factor XIII, protein C, thrombin-antithrombin III complexes and C5a.

Arthritis, Rheumatoid↗

Human keratinocyte cell lines differ in the expression of the collagenolytic matrix metalloproteinases-1,-8, and -13 and of TIMP-1.

We investigated cells and conditioned media of the three human keratinocyte cell lines HaCaT (non-tumorigenic), A5 (benign, tumorigenic) and II-4RT (malignant, tumorigenic) with regard to production and secretion of the collagenases-1 to -3 (MMP-1, MMP-8 and MMP-13) and TIMP-1 using semi-nested RT-PCR, Western blots, ELISA, immunocytochemistry and casein zymography. Transcripts of MMP-1, -8, -13 and TIMP-1 were detected in all cell lines by RT-PCR and the corresponding proteins were found in the cytoplasm of all three cell lines by Western blot analysis and/or immunocytochemistry. The conditioned media of the malignant II-4RT cells contain significantly more MMP-1 and MMP-8 than those of HaCaT or A5 as evidenced by immunoblotting and ELISA. In addition to the presence of latent MMP-1, zymography also detected the active form of this enzyme. TIMP-1 was found only in extracts of all three cell lines, predominantly in A5. This study clearly indicates that the epithelial tumor cells synthesize different collagenases and TIMP-1. The malignant clone secretes increased amounts of distinct collagenases compared to the non-tumorigenic cell line, thereby verifying a correlation between biological behaviour and the amount of collagenases. In addition, we provide clear evidence that MMP-8 is not exclusively found in polymorphonuclear granulocytes, but also in keratinocyte cell lines.

Base Sequence↗

The expression of angiogenin in tissue samples of different brain tumours and cultured glioma cells.

BACKGROUND: As a potential angiogenetic factor the 14.1 kDa polypeptide angiogenin induces neovascularisation. MATERIALS AND METHODS: We investigated the angiogenin expression by immunoblotting and an ELISA in 60 tissue specimens (40 gliomas, 20 other intracranial tumours), in 22 glioma cell cultures and in 4 supernantants of cultivated glioblastoma cells. RESULTS: We could show that angiogenin is detectable in different kinds of intracranial tumours with the highest amount in meningiomas and the lowest amount in low grade astrocytomas. In tissue specimens, a significantly higher angiogenin expression was measured in meningiomas compared to gliomas and metastases. Angiogenin could be detected in primary cultivated glioma cells, but not in the permanent cell lines. There was a significant correlation to the malignancy within the gliomas with an increase of angiogenin concentration according to the higher grade of malignancy. CONCLUSIONS: Our data suggest that angiogenin may contribute to the malignant transformation of gliomas and could perhaps advise that the physiological role of angiogenin is not restricted exclusively to angiogenesis. Based on these findings the clinical importance of angiogenin for therapeutic decisions in malignant brain tumours remains unclear and further analyses on m-RNA-levels are required.

Brain Neoplasms↗