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Biomedical subjects

M J Walker

Publications and source records attributed to M J Walker.

At least 217 records · Page 12Linked to original sources
PubMed1980

Presence of steroid receptors in human soft tissue sarcomas of diverse histological origin.

The incidence of cytosol receptors for androgen, estrogen, glucocorticoid, and progesterone was determined in a series of histologically diverse soft tissue sarcomas. Receptor binding was characterized in tumor specimens from 29 adult patients (14 female, 15 male) obtained during surgery. Nineteen (66%) tumor cytosols bound at least one steroid. Seven (24%) had more than one receptor. Ten of 23 (43%) cytosols assayed for androgen binding were positive (Kd 0.97 +/- 0.23 X 10(-9) M; 60.6 +/- 25.9 fmol/mg protein), 7 of 29 (24%) for estrogen (Kd 1.00 +/- 0.19 X 10(-9) M; 33.2 +/- 10.9 fmol/mg protein), 9 of 26 (35%) bound glucocorticoid (Kd 4.22 +/- 1.77 X 10(-9) M; 231.0 +/- 155.0 fmol/mg protein), and 1 of 28 (4%) bound progesterone (Kd 0.41 X 10(-9) M; 18.7 fmol/mg protein). Density gradient analysis suggested that androgen and estrogen binding was located predominantly in the 6S and 7 to 8S regions, respectively, whereas receptor for glucocorticoid sedimented at 8S. Steroid binding was not related to patient age. Estrogen-positive (71%) and glucocorticoid-positive (78%) cytosols appeared predominantly in tumors from female patients. Receptor distribution also appeared to be correlated to tumor histogenetic origin.

Adult↗
PubMed1979

Prostaglandins have limited actions on abnormalities of beating induced in cultured heart cells.

Prostaglandins are antiarrhythmic in a variety of situations including ischaemic arrhythmias, but the mechanisms involved are not known. In view of this, the protective actions of prostaglandins A2, E2, F1 alpha, F2 beta, and I2 against abnormalities of beating induced in cultured heart cells were investigated. Abnormalities of beating were induced in single cells by variety of agents including ouabain Ca++, K+, dinitrophenol (DNP), and toxic material from the jellyfish Cyanea. Abnormalities were assessed in terms of rate, rate range, subjective arrhythmic behaviour and percent cells beating. The prostaglandins (at 10(-7)-10(-5) M) were added with the arrhythmogenic agent to test for their ability to modify agent-induced beating abnormalities and were compared with lidocaine and quinidine. Prostaglandins alone had minimal direct effects on the cells and only minimally reduced responses to arrhythmogenic agents. The most protective prostaglandins, PGE2 and PGF1 alpha, tended to normalise beating behaviour most noticeably in DNP-treated cells, unlike lidocaine and quinidine which were effective against Ca++-induced changes while worsening those of K+. Thus, a general ability to protect disturbed cardiac cells is not seen with high concentrations of prostaglandins.

Animals↗
PubMed1979

The actions of prostaglandins I2 and E2 on arrhythmias produced by coronary occlusion in the rat and dog.

Prostaglandins E2 and I2 were compared with known antiarrhythmics for their actions against arrhythmias produced by occlusion of the left anterior descending coronary artery in the anaesthetised rat while PGI2 was also examined in the dog. PGI2 in the dog suppressed early arrhythmias produced during occlusion but did not influence those produced by occlusion-release or those occurring 24 hours after a permanent occlusion; none of the A,B,C or D series prostaglandins tested markedly reduced 24 hour arrhythmias. In the rat PGE2 was antiarrhythmic against early occlusion arrhythmias (30 minutes occlusion) in a dose related manner (infusions of 1-4 microgram/kg/min) whereas PGI2 infusions potentiated the arrhythmogenic effect of occlusion. PGE2 was as effective an antiarrhythmic as 10mg/kg Org. 6001 which was more effective in this test situtation than dl-propranolol. No obvious mechanisms for the actions of PGE2 or PGI2 were apparent although both agents lowered blood pressure and reduced the size of the occluded zone produced by ligation.

Androstanols↗
PubMed1979

Phosphorylation of a ribosomal protein and of virus-specific proteins in cells infected with herpes simplex virus.

In cells infected with herpes simplex virus a protein associated with the small subunit of ribosomes became phosphorylated. It was not detectably labelled with 14C-amino acids added after infection and is therefore probably a cellular protein. The phosphorylated ribosomal proteins from HSV-1- and HSV-2-infected cells were indistinguishable electrophoretically and had an apparent mol. wt. of about 48 000. Phosphorylation of the 48K protein was detected 2 to 3 h after infection and reached a maximum rate at 4 to 5 h. It was prevented by adding cycloheximide at 2 h, or actinomycin at 1.5 h p.i., or azetidine at the beginning of infection. The phosphorylation did not occur on reversal of a cycloheximide block in the presence of actinomycin, confirming that it is not caused by a virus alpha-polypeptide. Virus that had been irradiated with u.v. light, although still able to suppress synthesis of cellular protein and DNA, did not induce phosphorylation of the 48K ribosomal protein. Therefore the phosphorylation is not responsible for the suppression of host synthesis. The alpha polypeptides ICP 4, 0, 22 and 27 are also phosphorylated but, in contrast to that of the ribosomal protein, their phosphorylation does not depend on the synthesis of beta and gamma polypeptides. It is probably mediated by a host enzyme.

Animals↗
PubMed1978

The action of prostaglandin E2 and F1alpha on myocardial ischaemia-infarction arrhythmias in the dog.

Prostaglandin E2 and F1alpha infusions have been tested for their ability to reduce the arrhythmias associated with occlusion of the left descending coronary artery in the anaesthetised dog. At 1 microgram/kg/min both PGs reduced the incidence of premature ventricular contractions occurring during 25-min occlusions, while not reducing the incidence of ventricular fibrillation occurring on occlusion release. When infused for 5-min periods at 1 to 16 microgram/kg/min, neither PGE2 nor PGF1alpha effectively reduced the frequency of ventricular arrhythmias occurring 24 hr after a permanent coronary occlusion.

Animals↗
PubMed1978

On the association of virus proteins with the nuclei of cells infected with herpes simplex virus.

In cells infected with herpes simplex virus, HSV-I, newly synthesized polypeptides accumulated in the nucleus at different rates, which did not change during the first 6 h after infection. Canavanine, an arginine analogue, prevented the nuclear accumulation of ICP (infected cell polypeptides) 5 and 8 and azetidine, a proline analogue, prevented that of ICP 5 and 7. The transfer of polypeptides to the nucleus was inhibited at 4 degrees C but not by dinitrophenol. Some of the nuclear polypeptides could be released by washing isolated nuclei with hypertonic salt solutions. ICP 17 was particularly sensitive to high salt treatment while ICP 5 and II were resistent. ICP 4b, a modified form of the alpha polypeptide ICP 4, was released by EDTA, and the detergent NP40 removed ICP II. Treatment of nuclei with DNase selectively reduced the amount of bound alpha polypeptides ICP 4c (the second modified form of ICP 4), 0 and 27 as well as ICP 8 and 25. Nuclei isolated from infected or uninfected cells and incubated in labelled cytoplasmic extracts took up primarily ICP 8 and 32. Alpha polypeptides were taken up to a lesser extent and ICP 6 and 10 were excluded. It is concluded that affinities for various constituents of host cell nuclei are likely to determine the nuclear accumulation of specific virus polypeptides.

Azetidines↗
PubMed1978

Suppression of the synthesis of cellular macromolecules by herpes simplex virus.

Synthesis of cellular protein was substantially inhibited within 1 h of infection with herpes simplex virus, type 2, strain G (HSV-2). The inhibition also occurred, although no virus-specific protein synthesis was detected, after infection with u.v. irradiated virus and in cytoplasts that had been enucleated before infection. The inhibitory activity could not be distinguished from infectivity by dilution, sedimentation or reaction with gamma-globulin. HSV-2 also suppresssed the synthesis of Sendai virus proteins, but not those specified by HSV-1. Host protein synthesis was no more sensitive than virus protein synthesis to an increased concentration of NaCl in the medium, nor could the suppression of host synthesis be prevented by adding excess MgCl2 to the medium or by omitting CaCl2 or NaCl. It was accompanied by the breakdown of polyribosomes, which also occurred in the presence of cycloheximide but not at 4 degrees C. The breakdown yielded ribosomes that were sensitive to a high salt concentration, unlike those produced by treatment of polyribosomes with RNase. The synthesis of cellular DNA and RNA was also inhibited following infection with u.v.-inactivated virus. It is concluded that the suppression of host protein synthesis (and probably also of host DNA and RNA synthesis) is caused by a constituent of the infecting virus particles. The mechanism is obscure but probably does not depend on the leakage out of the cell of Mg2+ or into the cell or Ca2+ or Na+ ions, nor on the specific inhibition of initiation of host polypeptide chains, nor on RNase-like attack on host polyribosomes.

Cell Line↗
PubMed1978

Initial investigations into adrenaline accumulation and adrenergic responsiveness in cultured neonatal rat heart cells.

1 Accumulation of tritiated adrenaline (and/or its products) has been studied by a variety of techniques in viable, attached and free-floating myoblasts cultured from neonatal rat heart cells. 2 Accumulation increased with the number of cells used, the culture age of cells, incubation time and the concentration of adrenaline in the incubation mixture. 3 Accumulation-concentration data were not linearly correlated with dose-response data. 4 Accumulation did not correlate well with beta-adrenoceptor responsiveness in a number of situations of varying responsiveness. 5 Accumulation was not blocked by a variety of uptake blocking agents or alpha- and beta-adrenoceptor antagonists. 6 A much smaller accumulation process was observed in fibroblasts which respond to adrenaline with reversible morphological changes.

Animals↗
PubMed1977

Delayed appearance of propranolol sensitivity in cultured heart cells.

Examination of the appearance of adrenaline responsiveness and propranolol sensitivity with culture age in myoblasts cultured from neonatal rat hearts shows that propranolol sensitivity lags behind adrenergic responsiveness. Such a finding may illustrate subtle differences in sites for agonist and antagonist at the beta-receptor of these cells.

Animals↗
PubMed1977

The effects of prostaglandins on the beating activity of cultured heart cells.

The effects on the beating behavior of cultured rat heart cells of fourteen prostaglandins of the A, B, D, E, and F series were investigated, together with adrenaline and ouabain, at dose levels of 10-7 and 10-5M. Single heart cell beating activity was monitored photo-electrically and five parameters of beating behavior measured. Only PGF2alpha markedly increased rate while PGF2beta reduced it. Maintenance of a stable rate (rate range) was minimally affected by prostaglandins with PGF2beta possibly reducing, and PGF1alpha and 2-decarboxy E1 possibly increasing, rate range. PGF1alpha and F2alpha both statistically reduced the percentage of cells beating while the other prostaglandins had no effect. Most of the prostaglandins either produced no change, or reduced, indices of contractile force (optical density changes with contractions and its first derivative (dOD/dt)). Only the negative chronotropic agent PGF2beta produced a positive density effect. In conclusion, except for PGF2alpha, prostaglandins generally have limited actions on the beating activity of cultured heart cells.

Animals↗
PubMed1977

Bullous pemphigoid and rheumatoid arthritis with herpes simplex in the vesicular fluid.

Six cases of bullous perphigoid in association with rheumatoid arthritis have previously been reported in the literature. In the case reported in this paper, herpes simplex virus was found in the vesicular fluid. It is the first time this has been reported to this author's knowledge; this finding may contribute to the knowledge of the ultimate etiology of pemphigoid.

Arthritis, Rheumatoid↗