[Experience with immunosuppressive treatment of autoimmune myocarditis proven by myocardial biopsy].
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Biomedical subjects
Publications and source records attributed to T Forster.
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A family is presented in which there is a high incidence of hypertrophic cardiomyopathy and congenital deaf-mutism. The two abnormalities occurred together in 2 cases, and the syndrome was strongly suspected in a third individual. Hypertrophic cardiomyopathy without deaf-mutism was observed in a further 2 cases. Hypertrophic cardiomyopathy is inherited by an autosomal dominant mode; that occurring together with deaf-mutism is also probably inherited dominantly.
The echocardiographic data on 14 junior and 15 senior players in a first-division basketball club were compared. No difference was found between the senior and junior players as regards the thickness of the interventricular septum (11.47 vs 11.21 mm) or the thickness of the posterior wall of the left ventricle (9.8 vs 9.86 mm). The adults displayed a larger left ventricular end-diastolic diameter (56.8 vs 53.6 mm, P less than 0.05), end-diastolic volume (194 vs 164 ml, P less than 0.05), stroke volume (142 vs 116 ml, P less than 0.05), right ventricular diameter (27.9 vs 23.2, P less than 0.01), aortic root diameter (35.0 vs 32.0, P less than 0.05), and left atrial diameter (42.7 vs 37.2, P less than 0.01). However, among these, only the stroke volume and right ventricular diameter remained significantly different after normalization to body surface area. A significant difference could not be demonstrated in the linear ejection fraction, the ejection fraction, or the fractionated interventricular septum and posterior wall thicknesses. The examinations indicated that left ventricular hypertrophy had fully developed by the age of 18 years in the basketball players and that there was no further enhancement in adults. However, the left ventricular, right ventricular, and left atrial volume were larger in the adults than in the junior players.
The echocardiographic parameters were followed for 3 years in 15 boys aged 13 years on average, who were beginning competitive canoe race training, and were compared with the corresponding data on 17 boys of the same age who did not take part in sports. As compared to non-sporting boys the 13-year-old canoeist boys had a larger left ventricular end-diastolic diameter (46.13 +/- 4.64 mm vs 44.35 +/- 3.06 mm), a thicker left ventricular posterior wall (7.47 +/- 0.74 mm vs 6.47 +/- 1.18 mm) and particularly a thicker interventricular septum (8.33 +/- 1.18 mm vs 7.59 +/- 1.6 mm) just after they began sport, in spite of the fact there were no significant differences between the two groups in age, height, weight and body surface area. The preexisting difference in left ventricular hypertrophy between the two groups increased significantly during the 3-year follow-up period. The thickness of the left ventricular posterior wall in diastole increased to 9.20 +/- 1.01 mm vs 8.24 +/- 0.83 mm (p = 0.006), and that of the interventricular septum to 10.73 +/- 1.58 mm vs 9.59 +/- 1.18 (p = 0.025). The hypertrophic index and the left ventricular mass corresponded to the data given above (9.97 +/- 1.25 mm vs 8.91 +/- 0.94 mm, p = 0.01; and 261 +/- 50.7 g vs 202.83 +/- 45.8, p = 0.002, respectively). The canoeist boys had a slightly larger aortic root diameter at the beginning, and this difference increased and became more significant during the 3 years (29.4 +/- 2.39 mm vs 27.18 +/- 1.88 mm, p = 0.006). There were no significant differences between the two groups in the size of the left atrium, the fractional shortening of the left ventricle and the calculated ejection fraction and stroke volume.
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Twenty-five developmentally delayed or neurologically impaired nonverbal children, aged 2 to 15 years, referred for visual acuity assessment, were beyond the age at which standard preferential-looking techniques are considered to be effective and none could be tested with Snellen letters, illiterate Es, or Allen pictures. Our method, in which the children learn to point to grating stimuli, enabled us to obtain monocular visual acuity estimates in 19 of the 25 patients. When indicated, patching therapy was begun and was monitored with this method. Similar testing of 31 unimpaired children showed good prediction of recognition visual acuities except in patients with visual acuities worse than 20/160. The grating method accurately identified or excluded amblyopia in 26 of 31 children (84%). We consider this a clinically useful test of visual acuity in nonverbal impaired children.
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The sensitivity of 3 bleeding time techniques to an aspirin-induced defect of platelet function has been assessed in 35 normal volunteers. A carefully standardised Ivy technique was compared with 2 commercial devices for a template bleeding time, the Simplate II and the Thrombolette. The standardised Ivy and the Simplate II were found to have a similar sensitivity; the Thrombolette tended to be less sensitive but the difference was not significant.
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The bleeding time by a modified Ivy technique was estimated on 128 normal volunteers, 59 men and 69 women. The bleeding time was found to be significantly longer in women than men (p < .001). This was not attributable to a difference in platelet count nor to any detectable difference in platelet aggregability. It is likely that a difference in blood vessels or supporting tissues is responsible for the observed difference.
The in-vivo sensitivity to heparin of activated partial thromboplastin time (aPTT) reagents is different from the in-vitro sensitivity. Equivalent therapeutic ranges for reagents of very different sensitivities may be determined from the regression line of aPTT against whole blood clotting time. The commonly used ratio of 1.5 to 2.5 times the normal control value is appropriate for some reagents, but for the other reagents a higher or lower range is appropriate. A suitable aPTT reagent for heparin control should be sensitive both to a threshold effect of heparin and to increasing dosage. Some reagents discriminate poorly at the threshold level.
Prostaglandin (PG) synthetase activity of rat kidney medulla microsomal fraction was determined in vitro using I-14C-arachidonic acid as substrate. Natural ACTH resulted in a dose dependent suppression of PGE2 formation in vitro. The biosynthesis of PGE2 alpha was enhanced in the presence of ACTH (cortrophin). ACTH4--10 (1-Phe7 or d-Phe7) resulted in decreased PGE2 synthesis. The ratio of PGF2 alpha/PGE2 increased in proportion to the concentration of natural ACTH. The increase in the ratio of PG-s was more pronounced when ACTH4--10 fragments were applied. Natural ACTH in a dose dependent manner inhibited the prostaglandin dehydrogenase activity of kidney cytosol fraction in vitro. Prostaglandin inactivation was suppressed only by high doses of ACTH4--10 (d-Phe7). The data indicate that the natural ACTH and ACTH4--10 fragments might have a physiological role in the regulation of the prostaglandin system of a non-steroidogenic tissue.
Increased vascular permeability was induced by prostaglandin E2 (PGE1), arachidonic acid and compound 48/80 in male rats. Natural ACTH in a dose-dependent manner inhibited Evans blue exudation elicited by arachidonic acid or compound 48/80, however, it was ineffective against PGE1. ACTH4--10 (d-Phe7 and 1-Phe7) injected together with the prophlogistic agents depressed the arachidonic acid and compound 48/80 induced vascular reaction. Indomethacin pretreatment inhibited the effect of arachidonic acid on vascular permeability suggesting that arachidonic acid evoked its vascular activity by means of affecting the endogenous synthesis of prostaglandins and, on the other hand, the prostaglandin system played a role in the vascular permeability inducing effect of compound 48/80. ACTH4--10 peptide fragments free of steroidogenic action and natural ACTH inhibited locally the in vivo formation of PGS from arachidonic acid in the rat skin, resulting in a nonspecific decrease of local inflammation.
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The effect of adrenal and gonadal hormones on vascular permeability induced by intradermal injection of prostaglandins (PGs) E1, F2alfa, arachidonic acid and compound 48/80 have been examined in the rate. PGE1, arachidonic acid and compound 48/80 produced an increase in local vascular permeability. PGF2alfa decreased the action of these vasoactive agents, when it was injected in a mixture intradermally with PGE1, arachidonic acid and compound 48/80. Vasoactive response induced by PGE1, arachidonic acid and compound 48/80 was inhibited by the removal of adrenals and testes, and it was restored to normal by injection either of cortisol, deoxycorticosterone (DOC) or testosterone. In adrenalectomized rats, no change was observed in the inhibition of vascular permeability elicited by PGF2alfa response to compound 48/80. The blocking effect of PGF2alfa on vascular permeability evoked by PGE1 and arachidonic acid showed a considerable decrease. After orchidectomy the inhibitory effect of PGF2alfa on the vascular permeability induced by arachidonic acid and compound 48/80 was completely blocked, while in the case of PGE1 the inhibition was partial. Testosterone treatment restored the anti-inflammatory effect of PGF2alfa against compound 48/80. Ovariectomy was without any effect on vascular response.
Six trromboplastins commonly used for prothrombin time determinations were studied. Prothrombin times of patients who were receiving oral anticoagulant therapy varied widely, depending on the origin of the thromboplastins. The therapeutic range which is recommended with one thromboplastin is often quite different from that recommended with another, and as a result, the therapeutic ranges of different institutions may show no overlap. Management of patients and comparison of therapeutic results would be facilitated if all thromboplastins in use in Australia were standardized by comparison with the Australian Reference Thromboplastin.
In clinical studies performed during 111 infusions of high dose methotrexate (MTX) we have evolved a clinical and laboratory protocol which permits such therapy without prohibitive risk to the patient. The plasma MTX data obtained indicate that pharmacokinetic disposition is dose related during these infusions and that such data are useful in identifying patients at risk from serious toxicity.