On the surgery of the profunda femoris artery.
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Biomedical subjects
Publications and source records attributed to C Stephenson.
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We have investigated the expression of the DNA-repair enzyme O6-methylguanine-DNA methyltransferase in the Burkitt's lymphoma cell line Raji. An existing mutant Raji cell line which lacks thymidine kinase activity had previously been shown to be Mex- and to no longer express O6-methylguanine-DNA methyltransferase. We report here that in addition to the methyltransferase and thymidine kinase, a third enzyme with an unrelated function, galactokinase, is also not expressed in Raji cells. The control of thymidine kinase expression is post-transcriptional and it is possible that galactokinase and methyltransferase can share a common post-transcriptional regulation with thymidine kinase.
The Mex- (Mer-) phenotype of human cells is characterised by a sensitivity to agents such as N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and N-methyl-N-nitrosourea (MNU). The hypersensitivity of Mex- cells is a consequence of their failure to express the DNA-repair enzyme m6-Gua-DNA methyltransferase. Resistance to MNNG and MNU may be acquired by Mex- cells either by reexpression of a methyltransferase function or by an ill-defined process of tolerance in which the cytotoxic potential of m6-Gua is circumvented without the altered base being removed from DNA. It has been suggested that tolerance might involve an altered mismatch correcting function. We have investigated proteins which recognise and bind specifically to DNA fragments containing single-base mismatches. Cell-free extracts of a Burkitt's lymphoma cell line (Raji) contain two such mismatch binding activities. Neither protein appears to have a high affinity for m6-Gua-containing base pairs. The data indicate that m6-Gua-containing base pairs might be poor substrates for mismatch repair processes in human cells.
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BACKGROUND AND OBJECTIVES: Bradycardia occurs during 9%-13% of spinal anesthetics and may lead to cardiac arrest. Several risk factors for the development of bradycardia have been identified, but the risk conferred by presence of abnormalities detected on preoperative electrocardiogram (ECG) has not been examined. The authors undertook the study to correlate abnormal ECG findings with the incidence of bradycardia. METHODS: The data-base was previously collected from 952 patients undergoing spinal anesthesia. Patient records were reviewed and 537 had ECGs performed within 6 months of surgery. Intraoperative bradycardia was defined as a heart rate < 50 bpm (plus > 10% decrease from baseline). Abnormalities recorded from the ECG were prolonged PR interval (PR > 0.2 sec), atrial-ventricular conduction abnormalities, evidence of chamber hypertrophy, ischemia, and infarction. The findings were compared with incidence of bradycardia using contingency tables. Significant correlations were then evaluated with logistic regression. Significance was defined as P < .05. RESULTS: The incidence of bradycardia in this population was 12%. Patients with a prolonged PR interval had an increased incidence of bradycardia (25%, P = .01). Other ECG abnormalities did not correlate with increased incidence of bradycardia. Duration of PR interval did correlate significantly (P = .001) but poorly (r2 = 0.014) with baseline heart rate. However, logistic regression demonstrated that prolonged PR interval was a significant and independent predictor for bradycardia (odds ratio = 3.2, P = .01). CONCLUSIONS: Risk factors previously identified for the development of bradycardia during spinal anesthesia include: baseline heart rate < 60 bpm, ASA physical status 1 versus 3 or 4, use of beta-blocking drugs, sensory block height > or = T5, and age < 50. The results demonstrate that prolonged PR interval on the preoperative ECG is another significant and independent predictor for bradycardia.