摘要:

AbstractThere is now persuasive evidence that osteoclasts are formed by the fusion of mononuclear phagocytes. The presence of osteoclasts on bone thus infers the phagocytic recognition of bone by mononuclear phagocytes. I compared the phagocytic recognition by macrophages of hydroxyapatite, and native, demineralised and deproteinated bone powder. Removal of mineral resulted in loss of phagocytic recognition by macrophages, while removal of the organic component resulted in avid binding of bone fragments to a similar degree to that observed for hydroxyapatite crystals. The organic component of bone therefore protects the hydroxyapatite crystals of the mineral component from phagocytic recognition by macrophages. A simple model for bone resorption would be that resident bone‐lining cells (active and resting osteoblasts) remove the organic protection under appropriate stimuli and thus allow phagocytic recognition of the underlying mineral by macrophages, which accumulate, fuse and commence digestio

ISSN:0022-3417    

DOI:10.1002/path.1711350102

出版商:John Wiley&Sons, Ltd.    

年代:1981

数据来源: WILEY

摘要:

AbstractHyperthyroid and hypothyroid states were induced in rats by administration of triiodothyronine or surgical thyroparathyroidectomy. The anti‐inflammatory activity of Indomethacin, Oxametacine and Phenylbutazone was evaluated in these animals using paw oedema provoked by carrageenan granulomas induced by cotton pellets and polyarthritis induced by Freund complete adjuvant.Our results indicate that the hyperthyroid state leads to a significant inhibition of the acute inflammatory response to carrageenan, while hypothyroidism has no effect. There was a marked increase in the anti‐inflammatory activity of Indomethacin and Phenylbutazone in hyperthyroid rats. By contrast, in thyroparathyroidectomised animals the anti‐inflammatory effect of these drugs appeared less than in euthyroid rats.The hyperthyroid state slightly inhibited the development of the cotton pellet‐induced granuloma, while hypothyroidism enhanced it. Treatment of hypothyroid animals with the anti‐inflammatory drugs resulted in a significant decrease in the size of the granuloma. In the hyperthyroid state, the activity of the compounds appeared similar to that detected in euthyroid rats.Neither hyperthyroidism, nor hypothyroidism affected the inflammatory response to mycobacterial adjuvant, or the effect of anti‐inflammatory drugs on the response.These results suggest that thyroid hormones may influence, to various degrees the development of acute inflammation due to carrageenan, and chronic inflammation due to implanted cotton pellets. Our results indicate also that hyper‐ and hypothyroid states can modify the response of the rat to some non‐steroidal anti‐i

ISSN:0022-3417    

DOI:10.1002/path.1711350103

出版商:John Wiley&Sons, Ltd.    

年代:1981

数据来源: WILEY

摘要:

AbstractSudden death in cattle, especially calves, is a common problem of farm practice. Some cases are associated with significant cardiac lesions; in others, although necropsy suggests cardiac failure to be the cause of death, histological examination of H&E sections fails to demonstrate conclusively the site and nature of the lesion. We have studied 26 animals which died suddenly and in which the only pathological abnormalities detected were definite or equivocal myocardial necrosis. Three types of necrosis were identified: myodegeneration, contraction band necrosis and coagulation necrosis. Vacuolation of myocytes occurred in control hearts only in the sub‐endocardial myocardium, but was found more extensively in diseased hearts. Paraffin sections of myocardium stained by von Kòssa's method or by haematoxylin‐basic fuchsin‐picric acid improved the detection of myocardial necrosis. Some myocardium was examined by electron microscopy which detected early myocardial necrosis in some equivocal cases and defined the nature of the lesion in more advanced cases. Early changes were an increase in the number of type A mitochondrial inclusions which did not contain significant quantities of calcium but which increased in number after death, albeit to a lesser degree, even in control material. This was followed by deposition of electron‐dense granules and spicules (Type B inclusions) and totally electron‐opaque mitochondria in association with contraction band necrosis. X‐ray microanalysis showed type B inclusions and electron‐opaque mitochondria to have peaks for calcium. It is suggested that myocardial cell death in animals having such lesions resulted from mitochondrial calcium overload. The findings are discussed in relation to nutritional myopathies of ruminants and human myocardial disease associated with sudden death, and to experimental myocar

ISSN:0022-3417    

DOI:10.1002/path.1711350104

出版商:John Wiley&Sons, Ltd.    

年代:1981

数据来源: WILEY

ISSN:0022-3417    

DOI:10.1002/path.1711350105

出版商:John Wiley&Sons, Ltd.    

年代:1981

数据来源: WILEY

摘要:

AbstractSecretory piece of immunoglobulin A, a product of normal breast tissue, and beta1pregnancy‐specific glycoprotein, a product of syncytiotrophoblast of placenta, have been demonstrated in breast carcinomas by an indirect immunoperoxidase method. A close relationship has been found between the site of staining within cells and tumour structure for both secretory piece, the appropriate protein, and beta1pregnancy‐specific glycoprotein, the inappropriate protein. The reaction was at the periphery of cells in areas of tubular differentiation and was diffusely intracytoplasmic in solid groups of tumour cells.The poorly differentiated carcinomas have a low incidence of detection for both antigens but the tumours showing good histological differentiation appear to be functionally heterogeneous with some being negative for both proteins, some staining for the appropriate secretory piece of immunoglobulin A and the inappropriate beta1pregnancy‐specific glycoprotein and only one out of 12 producing the appropriate protein

ISSN:0022-3417    

DOI:10.1002/path.1711350106

出版商:John Wiley&Sons, Ltd.    

年代:1981

数据来源: WILEY

ISSN:0022-3417    

DOI:10.1002/path.1711350101

出版商:John Wiley&Sons, Ltd.    

年代:1981

数据来源: WILEY