Decreased actin and tubulin synthesis in 3T3 cells after transformation by SV40 virus.
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Biomedical subjects
Publications and source records attributed to L Taylor.
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A prospective screening program was undertaken at the Royal Free Hospital, London, to ascertain the incidence of alpha-1-antitrypsin (AAT) deficiency in patients with liver disease. Quantitative determinations of serum alpha-1-antitrypsin were performed on 469 patients with hepatobiliary disease and 98 subjects with no known liver disease. Sera with low values of AAT were phenotyped. The homozygous state was rare and comprised only 1% of the patients with liver disease. All of the 5 homozygous deficient (ZZ phenotype) patients had a history of neonatal liver disease. Other phenotypes (partial deficiency) were found in 4.7% of patients with liver disease and 6.1% of subjects with normal liver function. Types of liver disease in the patients with other phenotypes were widely varied. Routine determination of serum AAT level and phenotype and special staining for AAT in liver biopsies in all adults with liver disease appears unnecessary. Investigation of possible AAT deficiency should be carried out, however, in children and young adults, in those with a history of neonatal liver disease, and possibly in all patients with liver disease of unknown aetiology.
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A series of 29 femoropopliteal bypass operations is described. The patients were selected carefully to exclude those with clinical and aortographic evidence of aorto-iliac disease. A pulsatility index was calculated from the velocity waveforms recorded over the common femoral and popliteal arteries. The pulsatility index is the ratio of the amplitude of the waveform to its mean height over one cardiac cycle. There was a highly significant difference in the result of the operation between patients with a pulsatility index of 4 or more in the common femoral artery and patients with a pulsatility index of less than 4. We concluded that calculation of this pulsatility index provides useful additional evidence when selecting patients suitable for a femoropopliteal bypass.
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A controlled prospective survey of women taking oestrogen-progestogen oral contraceptives showed increases in mean systolic and diastolic blood pressure of 14.2 mm Hg and 8.5 mm Hg respectively after four years. The largest increases in individual cases were 36 mm Hg systolic and 20 mm Hg diastolic. Blood pressure returned to pretreatment levels within three months after oral contraceptives had been stopped. These changes in blood pressure were unrelated to the progestogenic potencies of the preparations being taken.
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Inhibition of growth and DNA synthesis was observed in WI 38 cells incubated with 8-methylthioadenosine 3':5'-cyclic monophosphate or prostaglandin E(1). The effect of both compounds on cell growth was reversible. On removal of these compounds from culture media the cells initiated DNA synthesis and divided. In addition, prostaglandin E(1) stimulated cyclic AMP formation in these cells to over 40 times the normal basal value. The increase in cyclic AMP concentration in WI 38 cells after addition of prostaglandin E(1) showed a marked variation. Cells that had recently been treated with trypsin and plated at a lower cell density exhibited a smaller response to addition of prostaglandin E(1) than cells that had divided and reached confluence.
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