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Biomedical subjects

J G Davis

Publications and source records attributed to J G Davis.

At least 19 recordsLinked to original sources
PubMed1992

Carboxyl-terminal deletion and point mutations decrease the transforming potential of the activated rat neu oncogene product.

The rat neu oncogene encodes a constitutively activated growth factor receptor/transmembrane tyrosine kinase, p185Tneu, that is structurally similar to yet distinct from the epidermal growth factor receptor. To explore the role of the carboxyl-terminal region and of putative autophosphorylation sites in regulating the activity of the rat p185Tneu (T, transforming) protein, we used site-directed mutagenesis to generate a p185Tneu mutant in which a putative tyrosine autophosphorylation site (residue 1253) at the extreme carboxyl terminus was replaced by a phenylalanine residue and a mutant in which the carboxyl-terminal 122 amino acids were deleted. These proteins were expressed in NIH 3T3 cells at comparable levels and exhibited similar autophosphorylation activity, exogenous substrate phosphorylation ability, oligomerization levels, and responsiveness to a partially purified neu-activating factor. However, the mutant p185Tneu proteins displayed a decreased transforming capacity both in vitro and in vivo. This analysis demonstrated that the carboxyl-terminal domain and at least one putative tyrosine autophosphorylation site of p185Tneu play a role in positively regulating the cell growth-regulating properties of the neu protein.

3T3 Cells↗
PubMed1992

Expression of the neu proto-oncogene by Schwann cells during peripheral nerve development and Wallerian degeneration.

The neu gene, which encodes a putative tyrosine kinase growth factor receptor termed p185neu, was originally identified as a dominant transforming gene in neurogliomas and schwannomas induced by transplacental treatment of rat embryos with ethylnitrosourea. The present studies were undertaken to determine the expression pattern of the neu gene in peripheral nerve. Northern blot analysis of total RNA isolated from rat sciatic nerves demonstrated prominent neu mRNA expression on postnatal days 1 and 7, with substantially lower expression up to adulthood. Immunohistochemical studies confirmed expression of p185neu by Schwann cells (SC) in developing sciatic nerve and minimal p185neu immunoreactivity in adult nerves. However, neu mRNA and p185neu protein progressively increased following sciatic nerve transection in adult animals. In addition, neu mRNA and p185neu were found in neonatal rat sciatic nerve SC and several SC-derived cell lines. In resting SC, neu mRNA was expressed at a low level, but was greatly increased by treatment with forskolin and glial growth factor. These studies demonstrate that the neu gene and its protein product, p185neu, are expressed by SC both in vivo and in vitro and suggest that p185neu plays a role in the regulation of SC proliferation or differentiation.

Animals↗
PubMed1992

Neonatal alloimmune thrombocytopenia due to anti-HPA-5b (Br(a), Zav(a), Hca): the importance of third-generation platelet antibody detection techniques, a case report.

Investigation of the maternal serum in a case of suspected alloimmune neonatal thrombocytopenia by conventional, second-generation platelet serological assays (platelet radioactive antiglobulin test [PRAT], platelet suspension immunofluorescence test [PSIFT] and solid-phase adherence assay (SPAA, 'Capture-P') demonstrated only the presence of HLA class-I antibodies of limited specificities: no platelet-specific antibodies were detectable. The use of a third generation, glycoprotein capture assay (monoclonal antibody-specific immobilization of platelet antigens, MAIPA) revealed the additional presence of anti-HPA-5b with a titre of 1 in 32. Despite this relatively high titre, and the fact that it was able to induce a prolonged thrombocytopenia, this antibody was not detectable by conventional assays. In view of these findings we conclude that the use of MAIPA is essential when investigating cases of suspected alloimmune neonatal thrombocytopenia.

Abnormalities, Multiple↗
PubMed1992

Fanconi anemia: a model for genetic causes of abnormal brain development.

Fanconi anemia is an autosomal recessive disease resulting in bone-marrow failure, phenotypical abnormalities and predisposition to malignancy. The authors reviewed 257 clinical and neuropathology results from the International Fanconi Anemia Registry at The Rockefeller University. Two patients had hydrocephalus and ventriculoperitoneal shunts. Of 15 neuropathology reports, 10 found CNS abnormalities, with the most common--ventriculomegaly--seen in six, two of whom required shunts. Aqueductal stenosis, agenesis of the corpus callosum and septum pellucidum, and holoprosencephaly were found. The authors conclude that neurological derangements are probably more common in Fanconi anemia than previously recognised. Fanconi anemia cells in culture are highly sensitive to oxidative stress and alkylating agents; Fanconi anemia may provide a model for a genetic disorder potentially predisposing to environmental insults.

Abnormalities, Multiple↗
PubMed1979

Inhibition of degradation of insulin by ophthalamic acid and by a bovine pancreatic proteinase inhibitor.

We have previously observed that, on subcutaneous administration, a significant proportion of insulin is degraded at the site of injection. The present paper reports that the degradative activity of slices of rat adipose tissue can be inhibited in vitro by ophthalmic acid, a natural analogue of glutathione, and by bovine pancreatic proteinase inhibitor, whereas it is increased by the addition of reduced glutathione.

Adipose Tissue↗
PubMed1979

Prenatal diagnosis of trisomy 20 mosaicism.

Three cases of trisomy 20 mosaicism in amniotic fluid cell cultures are described. Two of the pregnancies resulted in normal full-term infants. The third pregnancy was terminated and revealed a phenotypically normal fetus. A review of five previously reported cases is presented. Explanations of these findings include in vitro nondisjunction, culture of extraembryonic tissue, and true fetal mosaicism. The diagnostic dilemma this presents is discussed.

Adult↗
PubMed1977

De novo trisomy 9pter leads to q13.

A case of de novo trisomy 9p was observed. Cytogenetic analysis of G-, R-, Q-, and C-banded preparations revealed a karyotypic description of 47,XY,+del(9)(pter leads to q13). In addition to the principal characteristics of the 9p trisomy syndrome, the child presented with skeletal and urogenital abnormalities. It appears that certain clinical abnormalities are due to trisomy of 9q1.

Abnormalities, Multiple↗
PubMed1977

The high-risk perinatal registry. A systematic approach for reducing perinatal mortality.

A systematic and comprehensive review of all 320 perinatal deaths occurring in Nassau County in 1973 reveals that one-quarter of these deaths might have been prevented if modalities of care that were known and available at that time had been utilized appropriately. Preventability--the presence or absence of avoidable factors which might have materially lessened the risk of death --was determined for each perinatal death. Preventable deaths were disproportionately higher among postmature (P less than .01) and large-for-gestational-age (P less than .05) perinatal deaths, neonatal deaths after the first day of life (P less than .05), intrapartum fetal deaths (P less than .01), and perinatal deaths secondary to anoxia and idiopathic respiratory distress syndrome (P less than .01). The study concludes that rigorous application of currently available medical knowledge, the establishment of local perinatal mortality review committees, and vigorous outreach to practitioners are urgently needed to bridge the time gap between the development of new modalities of care and their application.

Adult↗
PubMed1976

A child with presumptive monosomy 21 (45,XY,-21) in a family in which some members are Gq-.

Presumptive monosomy for chromosome 21 was found in a male child with multiple malformations and severe psychomotor retardation. Chromosome analyses of cells from blood and skin samples were performed at intervals during the first few years of his life. In preparations stained with nonbanding was well as quinacrine, Giemsa, and reverse acridine orange banding techniques, only one No. 21 chromosome could be detected with no apparent abnormalities of the other chromosomes. The proband's phenotypically normal father, paternal grandfather, brother, and paternal aunt have a deletion for a short segment of the long arm of a G-group chromosome. Genetic-marker studies allow the exclusion of a number of blood groups as being associated with No 21. There is inconclusive evidence suggesting that expression of the Duffy blood group, which has been mapped to chromosome 1, may be influenced by genetic information on chromosome 21. This family is of potential value for further gene-mapping studies.

Abnormalities, Multiple↗