PubMed Health⌕ Search

Biomedical subjects

H D Probeck

Publications and source records attributed to H D Probeck.

12 recordsLinked to original sources
PubMed1986

Karyotype and ultrastructure of a colony stimulating factor (CSF) producing cell line (5637) originated from a carcinoma of the human urinary bladder.

The cell line 5637 which originated from a human urinary bladder carcinoma is known to produce GM-CSF and Multi-CSF ectopically. Determination of cell surface antigens defined by monoclonal antibodies was recently reported. Here we report on the ultrastructure and karyology of this CSF secreting cell line. At the ultrastructural level the monolayer in vitro culture and the solid tumors formed in nude mice showed all characteristics consistent with a well-differentiated transitional cell carcinoma (TCC). A subclone was found to grow in suspension and did not secrete any CSF activity. High resolution chromosome analysis revealed chromosomal abnormalities which agreed only in few particulars with nonrandom chromosomal aberrations usually found in TCC. Analysis of the cytogenetic results showed that nearly all structural abnormalities present are known to be associated with acute or chronic human leukemia. The possibility that the ectopic production of CSF in this cell line may be correlated to one or more of the described chromosomal aberrations is discussed.

Animals↗
PubMed1983

Chromosome anomalies in 136 couples with a history of recurrent abortions.

Cytogenetic studies were performed on 136 couples with a history of two or more abortions referred to us after gynaecological causes of the abortions had been excluded. Fifteen (11%) of the couples were found to have a chromosome anomaly, and when the couples were subdivided according to number of abortions, surprisingly 6 (10%) of the 59 couples with a history of only two abortions had a chromosome anomaly. An increased frequency of mosaicism for X-chromosome aneuploidy (2.2%) in the women from the 136 couples was also found. A review of the literature shows that translocations of some chromosomes (e.g. nos. 1, 7 or 22) preferentially lead to fetal wastage, while those involving, for example, chromosome nos. 5, 9, 14 or 21 are more likely to result in the birth of a handicapped child. Couples with a history of two abortions should be investigated cytogenetically. Other causes of miscarriages must, however, be excluded first.

Abortion, Habitual↗
PubMed1983

The genetic significance of accessory bisatellited marker chromosomes.

Ten new cases of accessory bisatellited marker chromosomes examined in different laboratories are reported. As a basis for genetic counseling in the context of prenatal diagnosis a cytogenetic categorization of such marker chromosomes is proposed and an estimation of the genetic risk associated with each category is carried out. The results are as follows: There is no increased risk for offspring with abnormal phenotype born to a healthy carrier of an accessory bisatellited marker chromosome with either a single or two closely adjacent C-bands (Category AI or AII). The unbiased sample of cases with de novo accessory bisatellited marker chromosomes of categories AI and AII is too small to allow a satisfactory estimation of the actual risk that, in case of such a prenatal finding, the foetus may not show a normal phenotype as a consequence of the marker chromosome. There is, however, evidence that this risk may be lower than 10%. Accessory bisatellited marker chromosomes showing a discrete pattern of G- and R-bands situated between two distant C-bands (Category AIII) usually indicate a chromosomal imbalance giving rise to an abnormal phenotype. Mosaic carriers of such dicentric marker chromosomes may, however, present a normal phenotype.

Abortion, Spontaneous↗
PubMed1983

Low doses of X-rays decrease the risk of diploidy in mouse oocytes.

Females from the NMRI/Han mouse strain ovulate a high number of diploid oocytes (about 12%) after gonadotrophin-stimulated ovulation. These oocytes can be fertilized and develop into triploid embryos subsequently. The exposure of such gonadotrophin-primed females to X-ray doses of 0.05, 0.10, 0.20 or 0.40 Gy during the preovulatory period (2 h after the HCG dose) significantly decreased the percentage of diploid oocytes. After the highest dose used, i.e. 0.80 Gy, however, the incidence was on the level from unirradiated females, again. We suggest that the observed negative hump-shaped dose response of diploidy is not caused by secondary modifications induced by irradiation, such as a selective killing of diploid oocytes before ovulation, or a (compensatory) super-ovulation of only normal oocytes, but rather is caused by a direct radiobiological interference of low doses in protecting from gonadotrophin-induced aneuploidy.

Aneuploidy↗
PubMed1982

Nondisjunction and chromosome breakage in mouse oocytes after various x-ray doses.

The effect of varying X-ray doses (0.05-0.80 Gy) on preovulatory mouse oocytes was studied by measuring nondisjunction during the first meiotic division, as well as structural chromosome anomalies in ovulated oocytes at metaphase stage II. The incidence of nondisjunction (0.1% hyperploid oocytes) found in oocytes from nonirradiated NMRI-Han female mice was in accordance with the results previously obtained with the same strain. Significantly (P less than 0.05) more hyperploid oocytes (0.9%) were ovulated following irradiation with 0.8 Gy. There was no statistically significant increase of nondisjunction after low doses. Structural chromosome anomalies occurred, however, even after an irradiation dose as low as 0.05 Gy. The dose response for structural chromosome anomalies is altogether different from that of radiation-induced hyperploidy. We consider that irradiation of mature oocytes might well be less hazardous with regard to its potency for increasing nondisjunction during the first meiotic division when compared with the effect of chemical mutagens.

Animals↗
PubMed1979

Chromosomal imbalance in ovulated oocytes from Syrian hamsters (Mesocricetus auratus) and Chinese hamsters (Cricetulus griseus).

Chromosomes were studied in ovulated oocytes from Syrian hamsters (Mesocricetus auratus) and Chinese hamster (Cricetulus griseus) to assess the degree of chromosomal imbalance after first meiotic division of oogenesis. Only one hyperploid oocyte among 307 studied was detected in the former, and none in oocytes from the latter species. Structural chromosome alterations, single chromatids due to presegregation, and diploid chromosome sets resulting from meiotic blockage were not observed. The hormones which were used to stimulate ovulation apparently did not enhance first meiotic cleavage errors in these hamster oocytes. The low figures of chromosomal anomalies in hamster oocytes are compared to those from a large sample of mouse oocytes obtained from three different strains and prepared under identical conditions. The relevance of these findings to the obviously higher impact of chromosomal aneuploidy in man is discussed.

Aneuploidy↗
PubMed1979

Detection of nondisjunction in mammals.

Methods have been developed in the past to assess spontaneous and induced chromosomal aneuploidy in germ cells and in early pre- and postimplantation mammalian embryos. Some of these methods yield still more information when combined with chromosome banding techniques. Various chemicals and x-rays have been tested in mammalian oogenesis and x-rays in spermatogenesis. The inference may be drawn from these studies that spontaneous nondisjunction is considered to occur only rarely in mouse and hamster oogenesis and spermatogenesis. X-rays induce nondisjunction during male and femlae meiosis, thus giving rise to significantly more aneuploid oocytes and F1 embryos. The alkylating agents trenimone and cyclophosphamide induce chromosomal missegregation in oocytes; the incidence depends on the dose injected. Hormones used as oral contraceptives did cause aneuploidy in oocytes, but only after daily treatment with high doses. Hormones used for stimulated ovulation did not interfere with chromosome segregation in the mouse and Chinese and Syrian hamsters. The following problems may be considered in futre studies: the problem of a species-specificity for induced nondisjunction; the question of a stage sensitivity (transplacental treatment); what happens after chronic exposure, also at low doses; the presence of a threshold; the existence of a dose-effect relation; the nature of cellular target(s) responsible for induced nondisjunction (spindle, regulatory proteins for polymerization of microtubules and ther depolymerization, centrioles, centromeres, RNA, or gene expression); whether DNA is involved and whether repair capacity plays a role.

Alkylating Agents↗