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Biomedical subjects

M Smith

Publications and source records attributed to M Smith.

At least 1,081 records · Page 60Linked to original sources
PubMed1985

Anaesthesia for translumbar aortography.

Fifty patients presenting for elective translumbar aortography were randomly allocated to one of two groups receiving either enflurane or isoflurane. Premedication was with oral lorazepam. The patients' tracheas were intubated and they were allowed to breathe spontaneously in the prone position during the procedure. There was no significant difference in heart rate during the investigation but there was a statistically significant fall in the blood pressure from its pre-induction level. Arterial oxygenation was adequate throughout the procedure. Arterial carbon dioxide tension was significantly lower in the isoflurane group at the beginning and at end of the procedure (p less than 0.01), but there was no significant change in carbon dioxide tension within the groups during the procedure. Spontaneous ventilation with enflurane or isoflurane is a satisfactory anaesthetic technique for translumbar aortography.

Anesthesia, Inhalation↗
PubMed1985

Gene K of bacteriophage phi X174 codes for a protein which affects the burst size of phage production.

Site-directed mutagenesis has been used to produce a T----A change at nucleotide 70 of phi X174 genome. This generates an am codon, TAG, in the gene K reading frame without affecting the amino acid, leucine, encoded by the overlapping gene A. The gene K mutant produces small plaques on su- hosts. It has an identical latent period, but a more reduced burst size than that of the wild-type phi X174. The reduced burst size in the gene K mutant suggests that the gene K protein, although not essential, has a role in increasing infectivity by increasing the burst size three- to sixfold.

Bacteriophage phi X 174↗
PubMed1985

Saccharomyces cerevisiae CYC1 mRNA 5'-end positioning: analysis by in vitro mutagenesis, using synthetic duplexes with random mismatch base pairs.

Expression of the Saccharomyces cerevisiae CYC1 gene produces mRNA with more than 20 different 5' ends. A derivative of the CYC1 gene (CYC1-157) was constructed with a deletion of a portion of the CYC1 5'-noncoding region, which includes the sites at which many of the CYC1 mRNAs 5' ends map. A 54-mer double-stranded oligonucleotide homologous with the deleted sequence of CYC1-157 and which included a low level of random base pair mismatches (an average of two mismatches per duplex) was used to construct mutants of the CYC1 gene and examine the role of the DNA sequence at and immediately adjacent to the mRNA 5' ends in specifying their locations. The effect of these mutations on the site selection of mRNA 5' ends was examined by primer extension. Results indicate that there is a strong preference for 5' ends which align with an A residue (T in the template DNA strand) preceded by a short tract of pyrimidine residues.

Base Sequence↗
PubMed1985

Isolation and characterization of the SPT2 gene, a negative regulator of Ty-controlled yeast gene expression.

The his4-917 mutation of Saccharomyces cerevisiae results from the insertion of the Ty element Ty917 into the regulatory region of the HIS4 gene and renders the cell His-. The hist4-912 delta mutant, which carries a solo delta in the 5'-noncoding region of HIS4, is His+ at 37 degrees C but His- at 23 degrees C. Both these mutations interfere with HIS4 expression at the transcriptional level. The His- phenotype of both insertion mutations is suppressed by mutations at the SPT2 locus. The product of the wild-type SPT2 gene apparently represses HIS4 transcription in these mutant strains; this repression is relieved when the SPT2 gene is destroyed by mutation. The repression of transcription by SPT2 presumably results from an interaction between the SPT2+ gene product and Ty or delta sequences. In this paper, we report the cloning and DNA sequence analysis of the wild-type SPT2 gene and show that the gene is capable of encoding a protein of 333 amino acids in length. In addition, we show that a dominant mutation of the SPT2 gene results from the generation of an ochre codon which is presumed to lead to a shortened SPT2 gene product.

Amino Acid Sequence↗
PubMed1985

Taking blood from children causes no more than minimal harm.

The ethical question of whether taking blood from normal children for research purposes is justified, is determined in part at least, by whether or not the children are harmed. To try to assess the risks, the effects of venepuncture on a group of healthy subjects were studied, by means of a parental questionnaire completed approximately eighteen months after the venepuncture had taken place. Ninety-two healthy children aged between 6 and 8 had a blood sample taken for non-therapeutic reasons as part of a research study. Questionnaire responses reveal few negative effects, and in some cases positive effects.

Blood Specimen Collection↗
PubMed1985

Differential suppression of follicle-stimulating hormone and luteinizing hormone secretion in vivo by a gonadotropin-releasing hormone antagonist.

Because of some indication that FSH secretion is less dependent than LH secretion on GnRH in vivo, we performed experiments to examine the effects of a GnRH antagonist (antag) on LH and FSH secretion. We first showed that pituitary cells superfused with GnRH showed a similar pattern of suppressed secretion of both LH and FSH in response to addition of antag. In contrast, antag administration to ovariectomized rats had differing effects on LH and FSH secretion. Serum LH was suppressed in a dose-dependent fashion by 2 h (20-50% of control values). Recovery from the lower doses of antag was seen by 12 h, but the two highest doses maintained serum LH levels at 10% of control values for 72 h. In contrast, the effect on serum FSH was not manifested until 12 h. FSH was maximally decreased only to 40-60% of control values. The two highest doses maintained this effect for 72 h. These results reinforce previous suggestions that FSH secretion in vivo may occur independently of acute changes in GnRH secretion, and may have an GnRH-independent component.

Animals↗
PubMed1985

Refractoriness of platelets to prostaglandins after infusion in rabbits.

Continuous intravenous infusion of prostacyclin (prostaglandin I2, PGI2) in rabbits induced refractoriness to PGI2-induced inhibition of platelet function. Although inhibited during earlier stages, platelet response to adenosine diphosphate and thrombin became normal within 24 hours of PGI2 infusion. Cross-mixing experiments with platelets and plasma from infused and control animals suggested that the altered response to PGI2 was caused by a defect intrinsic in the platelets. PGI2-stimulated cyclic adenosine monophosphate (cAMP) production was reduced in platelets from infused rabbits as compared with those from controls. Platelets refractory to PGI2 were refractory to PGE1 and PGD2, as well. Because PGE1 but not PGD2 shares the same platelet receptor as PGI2, the phenomenon could not be ascribed to receptor-specific downregulation, which was also shown by refractoriness of platelets from infused rabbits to the nonprostanoid inhibitor of platelet function adenosine. Either increased concentrations of ineffective inhibitors or their combination with phosphodiesterase inhibitors overcame refractoriness of resistant platelets, which also responded to inhibition by dibutyryl cAMP, indicating residual activity of adenylate cyclase. That at least the catalytic subunit of the enzyme was still working in refractory platelets was shown by inhibition of aggregation induced by forskolin, a non-receptor-mediated activator of adenylate cyclase. Impairment of the adenylate cyclase regulatory subunit, possibly accompanied by multireceptor downregulation, may explain the paradoxical refractoriness of platelets to prolonged infusion of PGI2. Such an effect may limit the benefit of PGI2 in treatment of thromboembolic disease.

6-Ketoprostaglandin F1 alpha↗