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Biomedical subjects

G M Cooper

Publications and source records attributed to G M Cooper.

At least 181 records · Page 10Linked to original sources
PubMed1979

Analgesic effects of sublingual buprenorphine.

The analgesic effects of sublingually administered buprenorphine 0.4 mg have been compared with morphine 10 mg given intramuscularly in patients following operation. The results indicate a slower onset of action for buprenorphine but of much longer duration than morphine. There were no serious side effects or difference in their incidence between the two drugs.

Administration, Oral↗
PubMed1979

Redistribution of body heat during anaesthesia. A comparison of halothane, fentanyl and epidural anaesthesia.

Epidural anaesthesia and high dose fentanyl (50 micrograms/kg) when used to supplement nitrous oxide and oxygen anaesthesia for a standard lower abdominal operation were associated with a mean fall in deep body temperature, as measured in the external auditory meatus, of 0.46 degrees C and 0.6 degrees C/hr respectively. This is significantly different from the mean values of 0.14 degrees C and 0.2 degrees C/hr which were recorded when moderate dose fentanyl (10 micrograms/kg) or 0.5% halothane were used to supplement anaesthesia. When mean skin temperature is combined with the core temperature to provide an estimate for total body heat, there is no difference between the groups. Redistribution of body heat occurs and this may be related to reduced adrenergic stimulation and altered regional blood flow. Where the facilities and environments are inadequate for the maintenance of normothermia, care should be taken in the choice of anaesthetic technique. In the recovery period mean body heat gain showed a wide scatter of results but those patients receiving epidural anaesthesia were slow to rewarm despite a high incidence of shivering in this group. The implications of this are discussed.

Adult↗
PubMed1978

Linkage of the endogenous avian leukosis virus genome of virus-producing chicken cells to inhibitory cellular DNA sequences.

The endogenous avian leukosis virus genome of uninfected virus-producing(V+) chicken embryo fibroblasts appears to be inefficiently transcribed and is noninfectious in transfection assays of high molecular weight DNA. We previously proposed that the endogenous virus genome was linked to a cis-acting control element which inhibited its transcription and, consequently, interfered with transfection by endogenous viral DNA. We now report that DNA of uninfected V+ cells is infectious at a low level when sheared to the approximate size of the virus genome. These results suggest that the endogenous virus genome of uninfected V+ chicken cells can be converted to an infectious form by separating it from adjacent cellular DNA sequences, as predicted by the cis-acting control element model.

Animals↗
PubMed1978

Marker rescue of endogenous cellular genetic information related to the avian leukosis virus gene encoding RNA-directed DNA polymerase.

Endogenous cellular genetic information related to the avian leukosis virus gene encoding RNA-directed DNA polymerase was studied, using a marker rescue assay to detect biological activity of subgenomic fragments of virus-related DNAs of uninfected avian cells. Recipient cultures of chicken embryo fibroblasts were treated with sonicated DNA fragments and were infected with a temperature-sensitive mutant of Rous sarcoma virus that encoded a thermolabile DNA polymerase. Wild-type progeny viruses were isolated by marker rescue with fragments of DNA of uninfected chicken, pheasant, quail, and turkey cells. The DNAs of these uninfected avian cells, therefore, appeared to contain endogenous genetic information related to the avian leukosis virus DNA polymerase gene.

Animals↗
PubMed1978

Mechanism of transfection of chicken embryo fibroblasts by Rous sarcoma virus DNA.

The mechanism of transfection by Rous sarcoma virus DNA was investigated by assaying DNA-mediated transformation under conditions which restricted secondary virus infection. Chicken embryo fibroblasts which were genetically resistant to virus infection as a result of the absence of receptors for virus penetration were also resistant to transformation by integrated or unintegrated Rous sarcoma virus DNA. In addition, DNA of replication-defective Bryan hightiter Rous sarcoma virus was noninfectious, and transformation by DNA of a temperature-sensitive DNA polymerase mutant was temperature sensitive. These results indicated that secondary virus infection was necessary for transformation by Rous sarcoma virus DNA. Since transformation was assayed by colony formation in soft agar, as well as by focus formation, the requirement for secondary virus infection was not an artifact of potential difficulty in detection of foci formed by division of single transformed cells. Therefore, it appeared that donor DNA did not stably transform recipient cells by direct integration. Instead, the results were consistent with the hypothesis that transfection of chicken embryo fibroblasts by Rous sarcoma virus DNA proceeded by transcription of donor DNA, formation of extracellular progeny virus, and secondary virus infection of sensitive cells.

Animals↗
PubMed1977

Assay of noninfectious fragments of DNA of avian leukosis virus-infected cells by marker rescue.

A marker rescue assay of noninfectious fragments of avian leukosis virus DNAs is describe. DNA fragments were prepared either by sonication of EcoRI-digestion of DNAs of chicken cells infected with wild-type Rous sarcoma virus, with a nontransforming avian leukosis virus, and with a mutant of Rous sarcoma virus temperature sensitive for transformation. Recipient cultures of chicken embryo fibroblasts were treated with noninfectious DNA fragments and infected with temperature-sensitive mutants of Rous sarcoma virus defective in DNA polymerase or in an internal virion structural protein. Wild-type progeny viruses which replicated at the nonpermissive temperature were isolated. Some of the wild-type progeny acquired both the wild-type DNA polymerase and the subgroup specificity of the Rous sarcona virus strain used for preparation of sonicated or EcoRI-digested DNA fragments. Therefore the genetic markers for DNA polymerase and envelope were linked and appeared to be located on the same EcoRi fragment of the DNA of Rous sarcoma virus-infected cells.

Animals↗
PubMed1976

Lack of infectivity of the endogenous avian leukosis virus-related genes in the DNA of uninfected chicken cells.

The infectivity of the avian leukosis virus-related genes in the DNA of four genetically distinct types of chicken cells was determined. Infectious DNA of Rous-associated virus-O(RAV-O) was obtained from V- chicken cells which were experimentally infected with RAV-O and from V+tvbs chicken cells, which spontaneously produced RAV-O and were sensitive to exogenous RAV-O infection. However, infectious DNA of RAV-O was not obtained from uninfected V- chicken cells or from V+tvbr chicken cells, which spontaneously produced a low titer of RAV-O but were resistant to exogenous RAV-O infection. No detectable amplification of the RAV-O related DNA sequences in the V+tvbs cells was found by hybridization of RAV-O 125I-labeled RNA to the DNAs of V+tvbs and uninfected V- cells. These results indicate that the endogenous avian leukosis virus-related genes in uninfected V- and V+tvbr cells differ from the RAV-O proviruses in RAV-O-infected V- and V+tvbs cells. The lack of infectivity of the DNA of V+tvbr cells is consistent with the hypothesis that the endogenous RAV-O genome in V+tvbr cells is linked to a cis-acting control element, which results in its inefficient expression.

Animals↗
PubMed1975

Infectious DNA from cells infected with Rous sarcoma virus, reticuloendotheliosis virus or Rous-associated virus-O.

We have described an efficient and quantitative assay for infectious DNA of the avian ribodeoxyviruses and have applied this method to study the possible existence of infectious viral DNAs in uninfected cells. Infectious DNA from cells infected with RSV or REV consisted of a single unit of DNA with a specific infectivity of 10(-5)-10(-6). The minimum molecular weight of RSV DNA required for infection of chicken cells was about 6 million, while the minimum molecular weight of infectious REV DNA was about 20 million. This difference may reflect complementation of the RSV DNA by endogenous avian leukosis virus-related DNA in uninfected chicken cells. Uninfected chicken cells do not contain infectious DNA for an REV, nor for a strongly transforming or a nontransforming avian leukosis virus.

Animals↗
PubMed1974

Infectious rous sarcoma virus and reticuloendotheliosis virus DNAs.

An efficient and quantitative assay for infectious Rous sarcoma virus and reticuloendotheliosis virus DNAs is described. The specific infectivities of viral DNA corresponded to one infectious unit per 10(5) to 10(6) viral DNA molecules. Infection with viral DNA followed one-hit kinetics. The minimal size of infectious Rous sarcoma virus DNA was approximately 6 million daltons, whereas the minimal size of infectious reticuloendotheliosis virus DNA was larger, 10 to 20 million daltons.

Animals↗
PubMed1973

Phosphorylation of 5-bromodeoxycytidine in cells infected with herpes simplex virus.

5-Bromodeoxycytidine is phosphorylated to 5-bromodeoxycytidine 5'-monophosphate in extracts of cells infected with herpes simplex virus but not in extracts of uninfected cells. The conversion of 5-bromodeoxycytidine to nucleotides and its utilization for DNA synthesis in uninfected cells occurs by deamination of 5-bromodeoxycytidine to 5-bromodeoxyuridine followed by phosphorylation of 5-bromodeoxyuridine to 5-bromodeoxyuridine 5'-monophosphate. In contrast, in cells infected with herpes simplex virus, 5-bromodeoxycytidine is phosphorylated directly to 5-bromodeoxycytidine 5'-monophosphate, which can then be deaminated to 5-bromodeoxyuridine 5'-monophosphate and incorporated into DNA. These results indicate a difference in the substrate specificity of nucleoside kinases induced by herpes simplex virus and the enzymes present in uninfected cells. It is suggested that this difference in substrate specificity between virus-induced and host-cell enzymes may allow selective chemotherapy of herpes simplex infections with 5-bromo- or 5-iododeoxycytidine.

Adult↗