Biomedical subjects
A Gropp
Publications and source records attributed to A Gropp.
[Chromosome abnormalities, tumours and developmental disorders (author's transl)].
Clonal chromosome disorders occurring or acquired at any postnatal age are often closely related with the origin of tumours. In man the Ph1-chromosome (9; 22) anomaly in CML or the 8; 14 translocation in the African malignant Burkitt Non-Hodgkin lymphoma are, among other cases, prominent examples. On the other hand, constitutive, inherited or novel chromosome anomalies conveyed from the zygote to all tissues of the organism may cause a higher risk for the origin of tumours. Rarely, inheritable minor structural chromosome mutations are known to determine the occurrence of dysontogenetic tumours, as e.g., nephroblastoma, but it is assumed that more such cases will become elucidated in the future. As a special phenomenon, true hydatiform mole is a tumour of the placental tissue due to a disorder of intragenome regulation. Constitutive or numerical structural chromosome anomalies of man are a frequent cause of early or late abortion or of abnormal development and malformation. Despite the predominating principle of selective fetal elimination, a few anomalies such as Down's syndrome, may escape to longer survival due to the relatively mild effects of chromosome 21 triplication. Trisomies which represent in man the most frequent type of chromosome disorders, can be induced, and systematically studied in an experimental model of the mouse. This allows the elaboration of the developmental profiles of all trisomies (and monosomies) of the mouse. Also, the above mentioned principle of selective elimination of abnormal implants can be analysed experimentally. Although the developmental span of a trisomic zygote is limited, there is evidence that cells and tissues isolated from the chromosomally abnormal organism can survive much longer. Thus, haemopoietic stem cells, at least in Ts 12 and 19 of the mouse, can be rescued from trisomic fetuses by transferring them to lethally irradiated adult mice, whose blood forming organs may eventually become permanently repopulated by the trisomic cell lineage. This type of experiments is suited for closer analyses of potential functions vs. defects of chromosomally abnormal cellular systems, e.g., with regard to growth and development.
Trisomic hemopoietic stem cells of fetal origin restore hemopoiesis in lethally irradiated mice.
Autosomal trisomy in the mouse is invariably associated with fetal or early postnatal death. Hemopoietic stem cells from fetuses trisomic for chromosome 12 or 19 can be rescued by transplantation into lethally irradiated mice. These trisomic cells restore hemopoiesis, including lymphopoiesis, in the irradiated mice and establish a permanent and almost complete engraftment. There is no evidence that hemopoietic cells with trisomy 12 or 19 are cytogenetically unstable.
Chromosome rearrangements involved in the origin of trisomy 15 in spontaneous leukemia of AKR mice.
Trisomy 15, known to be the predominant chromosome abnormality in leukemic cells of the AKR strain, develops even in animals of the subline AKR/Rb1Ald with two constitutive Robertsonian translocation chromosomes (6.15). Among 10 leukemic animals of this subline exhibiting chromosomal anomalies, 6 showed trisomy of the whole Robertsonian translocation chromosome with the expression of combined trisomy 6 and 15 as the most frequent abnormality. Besides this, rearrangements were observed in five animals, most of them resulting from centric fission of the Rb(6.15) translocation chromosome. Trisomy 15 with two Rb(6.15) and an extra acrocentric 15 was found in 44% of spleen cells in one animal, and a new Rb translocation of chromosomes 11 and 15 was seen in 50% of spleen and thymus cells of another animal. In both cases trisomy 15 without simultaneous trisomy 6 resulted. Thus, the triplication of a whole Rb(6.15) is frequent in leukemic AKR/Rb(6.15)1Ald, and ensuing double trisomy 6 + 15 is tolerated by the leukemic cell. But the development of trisomy 15 combined with centric fission of Rb(6.15) without simultaneous trisomy 6 is another principle realized in leukemogenesis.
Descriptive neuropathology of chromosomal disorders in man.
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Sex determination and phenotype in wood lemmings with XXY and related karyotypic anomalies.
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A comparison between trisomy 12 and vitamin A induced exencephaly and associated malformations in the mouse embryo.
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Variable positions of NORs in Mus musculus.
Silver-NOR staining has been applied to mouse (Mus musculus) chromosomes of different feral populations from Italy, Yougoslavia, and Germany and to chromosomes of M. spretus, a closely related species, from Portugal. In addition to the known pattern of proximal sites on smaller autosomes, terminal sites with silver-NORs on chromosomes 4 and 13 were detected. In M. spretus only terminal NORs were present on chromosomes 4, 13, and 19. Thus, the location of silver-NORs within the genus Mus and M. musculus subspecies shows wide variation.
Condensation of all human chromosomes in phase G2 and early mitosis can be drastically inhibited by 33258-Hoechst treatment.
Condensation of human chromosomes in phase G2 and early mitosis is inhibited by the fluorochrome 33258-Hoechst. This inhibitory effect is most apparent in primary diploid fibroblasts and lymphoblasts and least pronounced in peripheral blood lymphocytes. Condensation of the human Y chromosome, which contains a large heterochromatic region rich in A-T base pairs, is drastically inhibited by 33258-Hoechst treatment of fibroblasts and lymphoblasts. The difference in sensitivity of human chromosomes in different cell types to 33258-Hoechst probably reflects differences in the cell-membrane permeabilities to 33258-Hoechst.
Inhibition of condensation of human Y chromosome by the fluorochrome Hoechst 33258 in a mouse-human cell hybrid.
The fluorochrome Hoechst 33258 which binds preferentially to A-T base pairs, drastically inhibits the condensation of A-T-rich centromeric heterochromatin regions in mouse cell lines. The condensation of all other regions of these chromosomes is also inhibited to some extent. The human Y chromosome contains a large heterochromatic region, which is also rich in A-T base pairs. This chromosome is not affected by Hoechst 33258 in human leukocyte cell cultures. On the other hand, condensation of the multiple copies of human Y chromosome in the mouse-human cell hybrid RH-28Y-23 is inhibited and the chromosomes appear distorted in Hoechst 33258-treated cells.
Pattern of condensation of mouse and Chinese hamster chromosomes in G2 and mitosis of 33258-Hoechst-treated cells.
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Localization of NORs in chromosomes of mouse cell lines by a combined 33258-Hoechst and Ag-staining technique.
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[Pathological and embryological studies on abortion cases related to the Seveso accident].
After the explosion accident on July 10, 1976 in Seveso (Italy), material from 30 interrupted pregnancies and from 4 spontaneous abortions was investigated by embryological and histomorphological studies. No indications of mutagenic, teratogenic or fetotoxic effects of TCDD could be found. The cases of spontaneous abortion, albeit more suspect for dioxin damage, showed different morphological alterations obviously due to a variety of causative factors independent of TCDD. On the other hand it is not possible to exclude entirely an embryotoxic effect of TCDD because in the majority of cases the fetal tissues were incomplete.
[Teratospermia from the human- and veterinary-medicine viewpoints].
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Gene dosage for isocitrate dehydrogenase in mouse embryos trisomic for chromosome 1.
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H-Y antigen and the origin of XY female wood lemmings (Myopus schisticolor).
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Robertsonian metacentrics in the mouse.
A survey is given on the occurrence, the geographic origin and the arm composition of 27 Robertsonian fusion metacentric chromosomes of wild populations of the mouse. Their study is of twofold interest: a) it is possible to introduce these naturally occuring metacentrics in laboratory strains for experimental use. At present, altogether 34 metacentric chromosomes of different composition are available including 7 cases of metacentrics known form laboratory strains of the mouse. b) With the search for metacentrics in the mouse and with their identification insights are permitted in the role of Robertsonian changes in the course of mammalian evolution--Several separate populations of the mouse with different sets of multiple (up to 9) metacentrics have been found in Switzerland and Italy. Some of the individual metacentrics may occur in different populations. The participation of an acrocentric autosome in the formation of metacentrics seem to be at random, but the sex chromosomes are never included in a metacentric.--Homology of the arms involved in metacentrics is conserved, so that in meiosis of interpopulation hybrids is due to mechanisms of segregational imbalance and subsequent prenatal elimination of fetal offspring, but it follows also the pattern of male limited hybrid sterility.--From an evolutionary view point, karyotype rearrangements of Robertsonian type may initiate reproductive isolation, which prepares the ground for further genetic diversification and, as in the case of the mouse, of incipient speciation.
Fine structure of 33 258 H-treated chromosomes.
Metaphase chromosomes of mouse strain L cells show strikingly uncondensed pericentric heterochromatic regions after treatment of living cells with the benzimidazol-derivative 33 258 Hoechst. In electron micrographs of total preparations after G-band staining the chromosomes are seen to be made up of irregularly folded fibrils of 200-400 A in diameter. In the uncondensed regions only very few fibrils laid loose loops are present, making it probable that only one fibril forms one chromatid.