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A Gropp

Publications and source records attributed to A Gropp.

At least 19 recordsLinked to original sources
PubMed1992

Cholinesterase activity in the chondrocranium of normal and exencephalic mouse fetus with trisomy 12.

Cholinesterase (ChE) activity in the chondrocranium of normal and exencephalic trisomy 12 mouse fetuses was studied. Non-specific cholinesterase activity was found strongly in the developing bone cells at the central zone and weakly in the more maturely developed bone cells at the peripheral zone of the chondrocranium of both normal and exencephalic trisomy 12 mouse fetuses. In exencephalic mouse fetuses, the ChE-activity was lesser than in the normal ones which corresponded to hypoplastic chondrocranium. The centrifugal direction of the maturity of individual bone cells could be demonstrated by the activity of cholinesterase. The young bone cells showed strong ChE-activity while the more matured cells showed weak ChE-activity. The enzyme activity disappeared when the definite tissue structure was well developed. From this study, it may be concluded that ChE plays a role in chondrocranium development which is different from its known function in the adult tissue.

Anencephaly↗
PubMed1988

Restriction fragment polymorphism in the sex-determining region of the Y chromosomal DNA of European wild mice.

Using 32P-labeled probe consisting mainly of (GATA)n we have shown that a male specific Alu1 DNA blot pattern which defines the Y chromosome sex-determining locus in inbred mice is highly polymorphic in wild mice, indicating substantial sequence evolution in this region under field conditions. In all cases examined by in situ hybridization, the region concerned is paracentromeric. In contrast, the blot pattern of another probe (M 34) which detects repeated sequences specific to the mouse Y chromosome but outside the sex-determining locus, remains constant between different isolates.

Animals↗
PubMed1985

Susceptibility of mice reconstituted with trisomy 19 hematopoietic cells to infection with Rauscher leukemia virus.

Radiation chimeras with trisomy 19 hematopoietic cells were constructed to test the sensitivity of the trisomic hematopoietic system to infection with Rauscher leukemia virus: Hematopoietic cells from livers of trisomic fetuses were rescued by transplantation into lethally irradiated adult mice. These Ts 19 radiation chimeras show a stable and sufficiently long-lived trisomic hematopoiesis to allow experimental induction of Rauscher leukemia. Rauscher leukemia virus (RLV) induced a marked proliferation of erythroblasts in the spleens of Ts 19 mice and control chimeras within 3 weeks. The onset of erythroblast proliferation was significantly delayed in the Ts 19 mice, suggesting a smaller number of target cells for the RLV and/or reduced susceptibility of the target cells to RLV. Both Ts 19 and control chimeras developed nonlymphocytic leukemia 2-4 months after RLV injection. The course of leukemogenesis was similar in the two experimental groups. No numerical chromosome abnormalities associated with leukemogenesis were detectable in Ts 19 or control cells. The numbers of chromosomal sister chromatid exchanges 2 weeks after RLV injection were elevated to the same degree in both Ts 19 and control cells. Thus, cells with constitutional trisomy do not show increased chromosomal instability due to leukemogenesis.

Animals↗
PubMed1985

Drug-induced liver injury in liver biopsies of the years 1981 and 1983, their prevalence and type of presentation.

Based on the histological picture of liver biopsies examined in the years 1981 and 1983, drug-induced liver injury has been suspected in 131 and 170 cases. In relation to the total number of the examined liver biopsies this accounted for 6 and 9.6%, respectively. In only 20 (i.e. 15%), respectively 17 (i.e. 10%) of the cases, a drug-induced injury could be clinically excluded. However, a drug-induced injury was doubtlessly secured in 21 (16%) and 28 (16.5%) of the cases. The histological phenotype seen in association with the incriminated drug is presented. In 90 (68.7%) and 125 (73.5%) of the cases it was neither possible to secure nor to exclude the drug as cause of this damage, either because in 32/72 cases the clinical work-up was incomplete or because the drug-induced damage was clinically suspected, but not sufficiently documented by follow-up examinations after drug-withdrawal.

Adolescent↗
PubMed1985

Quantitative histology of human fetal testes in chromosomal disease.

Morphometric studies on male gonads were performed in 35 midterm fetuses aborted after prenatal diagnosis of a chromosome anomaly and in 11 chromosomally normal controls. A significant reduction of the number and volume percentage of premeiotic germ cells was observed in the chromosomally abnormal cases. Germ cell depletion was correlated with the severity of the chromosomal disease. It was least expressed in the XYY condition. In trisomy 13 and 18, depletion lead to values of less than a half or even a fourth the values of controls. Complex anomalies with XXY or XYY in addition to an autosomal disorder showed a moderate effect on germ cell reduction. No morphological differences were observed in germ cells or in Sertoli cells in a comparative electron microscopic study. Paucity of fetal germ cells can result from impaired colonization of the gonadal ridge, from low mitotic activity, or from increased premeiotic cell loss. All three factors seem to contribute to the above findings.

Cell Count↗
PubMed1983

Murine trisomy: developmental profiles of the embryo, and isolation of trisomic cellular systems.

Many questions related to the development and the phenotypic expression of trisomy (Ts) are amenable to systematic investigation in a mouse model that allows the induction of Ts 1 to 19 by a breeding design of mice heterozygous for Robertsonian metacentric chromosomes. Some Ts do not survive the first critical phase of organogenesis on days 11 to 12 of fetal development; others as Ts 12, 14, 16, 18, and 19, have a life span until or beyond birth. Model type studies of the morphogenesis of developmental anomalies (e.g. craniocerebral, cardiovascular, or placental) are possible in Ts with a longer developmental span, and Ts 16 of the mouse is considered as a natural model of human trisomy 21. The eventual breakdown and death of the trisomic organism are inevitable. There is considerable interest to find ways for rescue and longer survival of Ts in competitive developmental systems, as e.g., in Ts in equilibrium with 2n blastocyst chimeras, or by isolation of trisomic cellular or tissue systems. Thus, the transfer of Ts hemopoietic stem cells of the fetal liver to irradiated adult recipients is a means of studying the functional capacities and maturation of trisomic hemopoiesis and lymphopoiesis. Both are almost completely restored by Ts 12, 14, 18, and 19 stem cell transplantation with survival periods of more than 6 months. But in other Ts, as of chromosomes 13 or 16, such capacity of reconstitution is impaired. The stepwise analysis of the effects of chromosome triplication on the cell level, in isolated functional systems and in the embryonic organism, is a promising way to understand the phenotypic expression of genome anomalies in complex developmental processes.

Animals↗
PubMed1983

Down's syndrome in the male. Reproductive pathology and meiotic studies.

Studies on testicular histology and meiosis were carried out by the use of light and electron microscopy in an 18-year-old Down's syndrome male in an attempt to follow the fate of the extra chromosome 21 and to evaluate the effects of this condition on spermatogenesis and the reproductive functions. The histological changes in the testes corresponded to spermatogenic arrest. Electron microscopic whole-mount spreadings of meiotic cells in the pachytene stage showed that in most nuclei an extra chromosome 21 was not detectable. Only in a small number of nuclei, univalents or trivalents with segmental pairing structures of an extra chromosome could be discovered. In contrast, the great majority of (C-banded) diakinesis figures showed the presence of a supernumerary G (no. 21) chromosome. The absence of a traceable extra chromosome 21 in most pachytene cells is explained by the assumption that it is intimately connected with and hidden in the sex vesicle, whose complex structure does not allow the identification of single elements. Strong support for this assumption is seen (a) in the general tendency of narrow spatial association of unpaired segments with the XY complex and (b) in close structural similarities occurring between univalents or nonsynapsed segments of trivalents and the nonpaired segments of the sex chromosomes. It is suggested that the association or connection of an extra chromosome with the XY complex during pachytene interferes with the phenomenon of X inactivation. In animal systems such abnormal interference is related with spermatogenic breakdown and, in a general way, with male hybrid type sterility. So far, the range of sterility vs. fertility in cases of male Down's syndrome is not yet fully clear, but it appears that impairment of fertility, and sterility are most frequent. If so, it is proposed that the effect of the trisomy 21 condition on spermatogenesis (and fertility) is a consequence of the behavior of the extra chromosome in the meiotic prophase.

Adolescent↗
PubMed1980

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.

Animals↗
PubMed1979

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.

Animals↗
PubMed1979

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.

Animals↗