Dangerousness, stress, and mental health evaluations.
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Adolescent↗
Biomedical subjects
G Ramsay
Publications and source records attributed to G Ramsay.
The role of transcriptional activation in the function of the Drosophila myb gene.
Vertebrate myb genes encode DNA-binding proteins that regulate transcription and have been implicated in regulation of cell proliferation, differentiation, and apoptosis. We have demonstrated that the single myb gene in Drosophila melanogaster, Dm myb, is required for the G(2)/M transition of the cell cycle and for suppression of endoreduplication. Recently, it has become apparent that the family of proteins containing Myb-related DNA-binding domains is much larger than originally believed and that the biochemical properties and functions of these proteins are diverse. We undertook studies to characterize the biochemical properties of the Drosophila Myb protein (DMyb). We now provide evidence that in addition to having homology with the vertebrate Myb proteins, the Drosophila Myb protein (DMyb) shares its biochemical properties. DMyb binds to a similar consensus sequence and activates transcription from a reporter construct regulated by vertebrate Myb proteins. We also show that DMyb proteins carrying mutations corresponding to previously isolated mutant alleles of Dm myb are less active as transcriptional activators than wild-type DMyb, indicating that a decrease in transcriptional activation ability is likely to cause the mutant phenotypes.
Animals↗
Intraabdominal infection: pulmonary failure.
Since its first description in 1967, the mortality of the adult respiratory distress syndrome (ARDS) has remained unchanged despite the increasing sophistication of supportive techniques. Few patients now die of refractory hypoxemia, the majority succumbing to the multiple systems organ failure syndrome, commonly due to sepsis. Sepsis is both the most common cause of ARDS, usually involving the abdomen, and the most frequent complication, usually affecting the lungs. ARDS is, thus, increasingly seen as the pulmonary component of multiple systems organ failure, triggered by the systemic response to sepsis. In critically ill patients, impairment of hepatic function and of the barrier function of the gut mucosa allows translocation of endotoxin derived from the aerobic Gram-negative bacteria within the gut. This releases mediators which are responsible for the activation of cellular and humoral cascades, resulting in the pathological changes seen in ARDS. This sequence of events underlines the importance of therapies directed at abnormal colonization of the gastrointestinal tract and elimination of the gut endotoxin pool. Selective decontamination of the digestive tract is attractive in that it attacks the problem from 2 sides: first, by eliminating colonization, it appears effective in preventing secondary infection and, second, it may also play a role in reducing the enteric endotoxin pool. Recent descriptions of pathological oxygen supply dependency in both ARDS and septic patients emphasize the similarity of pathophysiological abnormalities in the 2 conditions. Intensive supportive therapy to achieve adequate oxygen transport and aggressive investigation and surgical management of septic foci are the cornerstones of management of the established syndrome.
Humans↗
Identification of nuclear proteins encoded by viral and cellular myc oncogenes.
The myelocytomatosis viruses are a family of replication-defective avian retroviruses that cause a variety of tumours in chickens and transform both fibroblasts and macrophages in culture through the activity of their oncogene v-myc. A closely related gene (c-myc) is found in vertebrate animals and is thought to be the progenitor of v-myc. Changes in the expression and perhaps the structure of c-myc have been implicated in the genesis of avian, murine and human tumours (for a review, see ref. 15). Elucidation of the mechanisms by which v-myc and c-myc might elicit tumorigenesis requires identification of the proteins encoded by these genes. To this end, we have expressed a portion of v-myc in a bacterial host and used the resulting protein to raise antisera that react with myc proteins. We report here that v-myc and c-myc encode closely related proteins with molecular weights (MWs) of approximately 58,000. Integration of retroviral DNA near or within c-myc in avian lymphomas apparently enhances expression of the gene. Here we have used cells from one such tumour to identify the protein encoded by c-myc and find that the coding domain for the gene is probably intact.
Avian Leukosis Virus↗
Amplification and enhanced expression of the c-myc oncogene in mouse SEWA tumour cells.
SEWA tumour cells are derived from an osteosarcoma induced in an A.SW mouse by infection with polyoma virus. Cytogenetic analyses have revealed three different characteristic chromosomal abnormalities diagnostic for the presence of amplified genes: 'double minutes' (DMs), homogeneously staining chromosomal regions (HSRs) and C-bandless chromosomes (CMs; for review see ref. 2). DMs may undergo fluctuation in number depending on the conditions in which the cells grow. Their number usually increases after injection of cells into a mouse and often is reduced to undetectable levels when the cells are explanted back into tissue culture; when the cells are re-introduced into the mouse, they again acquire multiple DMs. We show here that cells of SEWA lines carrying DMs, HSRs or CMs contain amplified copies of the proto-oncogene c-myc and enhanced levels of c-myc messenger RNA and c-myc protein. DMs or CMs are the sites of c-myc amplification in two different SEWA lines.
Animals↗