PubMed Health⌕ Search

Biomedical subjects

P Buck

Publications and source records attributed to P Buck.

At least 73 records · Page 4Linked to original sources
PubMed1980

Experimental approach to the pathogenesis of the anomalies of amniotic disease.

By intra-adnexal injection of glucose in the rabbit embryo, we were able to stimulate all the anomalies associated with "Amniotic Disease". Since we were even able to obtain amniotic bands, this study provides an excellent experimental model of this disease. Resulting lesions occur early in development, corresponding to the first trimester of human gestation. All of the anomalies can ultimately be explained by the destruction of the most superficial cells: epiblastic cells of the embryo and the amnion, subjacent mesenchyme, and endothelial cells. The subsequent lack of interaction between these cells and the importance of the anatomical localizations of resulting hematomas can lead to the pathogenetic approach to this disease. In light of the present study, the disease appears to be caused by an external factor within the amniotic fluid. The exact nature of the destructive agent(s) remains a mystery in man.

Abnormalities, Drug-Induced↗
PubMed1980

Hay fever plants in Oklahoma.

More than 181 species of Oklahoma hay fever plants were identified. These are listed with their relative allergenicity and distribution within six major botanical zones of the state.

Oklahoma↗
PubMed1979

Abnormal children of a 47,XYY father.

Abnormal children of two 47,XYY men were studied. One of these men had 2 normal daughters and a child, 45,X/46,XY, with gonadal dysgenesis. The other man had 2 normal sons and a child with Down's syndrome. The extra chromosome 21 of this child came from the mother. Another 47,XYY man had 4 normal children.

Adult↗
PubMed1978

Abnormalities resulting from intra-adnexal injection of glucose in the rabbit embryo--an experimental model of "amniotic disease".

Intra-adnexal injections of glucose into the rabbit embryo have induced amputations of digits or segments of limbs, congenital grooves, amniotic bands, club feet, syndactyly, hare lip, anencephaly, and ulcerations of the scalp. We have thus reproduced all the anomalies which are encountered in the clinical syndrome of "amniotic disease." These anomalies result from destruction of the cutaneous epithelium and the subjacent mesenchymatous cells, and extravasation of blood with hematoma formation around the superficial vessels. This general mechanism explains most of these anomalies. Intra-adnexal injections of glucose thus constitute an external trauma for the embryo and is good experimental model of amniotic disease.

Abnormalities, Drug-Induced↗
PubMed1977

Forceps delivery.

Explore the source record for details and available documents.

Extraction, Obstetrical↗
PubMed1977

[Reduction of glucose embryotoxicity by intra-ovulary injection of insulin].

The injection of 10 mg glucose and 0.4 U.I. of insulin in the ovulary fluid of 14th day rabbit embryo, produces less anomalies than the injection of the same concentration of glucose alone. This result shows that the insulin receptor is probably present in the 14th day rabbit embryo, before the differentiation of B cells in the pancreas.

Abnormalities, Drug-Induced↗
PubMed1976

[Period of sensitivity of the rabbit fetus to the embryopathic and lethal action of D-glucose in intraovular injection].

We studied the effect of injection of D-glucose in rabbit foetus ovulary liquid at the 14th, 16th and 18th day of pregnancy. Injection of 14th and 16th day determined a high percentage of foetal death and limb necrosis. On and after the 18th day of pregnancy, the foetus is insensible to the treatment. The 18th day is, in the rabbit, the period of a new hormonal equilibre establishment.

Abnormalities, Drug-Induced↗
PubMed1975

Lack of development, factor of congenital ureterohydronephrosis.

Female Swiss mice (25-30 g) received a single subcutaneous injection of 200 mug nucleotoxic substance (chloraminophen) on day 11 of pregnancy. The fetuses taken from the treated mother on day 18 show a significant lack of development and urinary anomalies, such as ureterohydronephrosis (26%) and renal agenesis (few cases). Ureterohydronephrosis seems to be caused by lacking development of the ureterovesical junction region.

Abnormalities, Drug-Induced↗
PubMed1971

The potential cell population doubling time in neuroblastoma and nephroblastoma.

Estimates are presented of the median potential cell population doubling time in five neuroblastomas and six nephroblastomas. The median time in the neuroblastomas was 4·2 days (101 hours) and in the nephroblastomas was 7·8 days (188 hours). Estimates of the duration of metaphase in the two kinds of tumour are also offered, based on the natural mitotic index in six neuroblastomas and five nephroblastomas. The findings are set in the context of a brief review of other studies on the cell population kinetics of human tumours. A more detailed but frankly speculative analysis is made of one nephroblastoma which suggests that cells are produced at the rate of at least 5 per 1000 tumour cells per hour, of which about 3 are lost.

Biopsy↗