Treatment of GH3 cells with thyrotropin-releasing hormone (TRH) for periods up to 60 min resulted in a prolonged reduction in the cellular content of phosphatidylinositol (PtdIns) with no lasting change in the levels of the other inositol-containing phospholipids. Accompanying this was a maintained increase in the GH3 cell 1,2-diacylglycerol content and a slower decline in the level of cellular triacylglycerol. When the cells were suspended in lithium-containing balanced salt solution for 30 min (in the absence of exogenous myo-inositol), there was a 15% decrease in GH3 cell inositol levels. This was associated with a small, but significant, increase in the cellular content of phosphatidylinositol 4,5-bisphosphate (PtdIns4,5P2) and 1,2-diacylglycerol. Addition of TRH to cells suspended in lithium-containing medium depleted cellular inositol levels by around 65% within 30 min. By this time, there was also a 50% reduction in the cellular content of PtdIns and a 20% reduction in phosphatidylinositol 4-phosphate (PtdIns4P). Control levels of PtdIns4,5P2 were maintained in the combined presence of TRH and lithium. Under those conditions, TRH no longer depleted cellular triacylglycerol and there was a marked increase in the ability of TRH to elevate the GH3 cell content of 1,2-diacylglycerol. The effect of TRH on the cellular content of phosphatidic acid was not altered by the presence of lithium. The results show, firstly, that when PtdIns resynthesis is inhibited by lithium-induced inositol depletion, its glycerol backbone accumulates, at least in part, in 1,2-diacylglycerol and, secondly, that GH3 cells preserve their cellular levels of PtdIns4,5P2 in the face of a considerable reduction in the cellular content of PtdIns.
TWENTY-EIQHT cases of papillary tumours of the heart valves have been reported hitherto (Prichard, 1951), nine of them on the aortic valve, nine on the tricuspid, five on the mitral and five on the pulmonary. Many of these are very incompletely described and this fact, together with their apparent rarity, is the justification for the publication of two further cases.
Case 1A female infant, previously in good health, died from an attack of gastroenteritis at the age of nine months. At the post-mortem examination, idammation of the alimentary tract and fatty change in the liver were present, and in the substance of the aortic cusp of the mitral valve was a firm, apparently fibrous nodule measuring 0.5 by 0.3 cm. The nodule projected mainly on the auricular surface of the valve cusp and the endocardium covering this surface was of velvety texture. There was no other cardiac lesion.Histology. The sections show a papillary nodule, completely covered by endothelium, with villi protruding in the direction of the auricle and composed of a central fibrous core surrounded by delicate collagenous and elastic fibres separated from each other by rnucinous material. The central collagenous zone contains areas of fibrinoid degeneration and of vacuolation due to the mucinous substance.Close beneath the endothelium are coarse elastic fibres, then there is a zone of delicate open collagenous tissue with scattered fibroblasts, and finally a central area of dense collagen fibres. Elastic fibres are present throughout and tend to be arranged in the long axis of the valve cusp ( figs. 1 and 2). The mid-zone has a foamy appearance due to the presence of stromal mucin which stains feebly with Southgate's mucicarmine and by the periodic acid-Schiff technique, and metachromatically with toluidine blue.The villi are avascular but a few large capillaries are present in the solid portion. Iron pigment and glycogen are absent.
Case 2A woman aged 80 died from hypertensive cardiac failure and at post-mortem examination a papillary tumour measuring 1.5 by 1.0 cm. waa found on the ventricular surface of the right anterior cusp of the pulmonary valve. It was composed entirely of delicate fronds radiating from a short pedicle arising from an otherwise normal valve cusp (fig. 3). There was no evidence of endocarditis.The basal part of the nodule is solid.It is removed by the action of hyaluronidase.
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