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Biomedical subjects

J Searle

Publications and source records attributed to J Searle.

At least 73 records · Page 4Linked to original sources
PubMed1979

The nature of piecemeal necrosis in chronic active hepatitis.

On the basis of histological studies, it is proposed that the type of liver-cell death in piecemeal necrosis is apoptosis. The characteristic inconspicuousness of apoptosis explains why the mode of hepatocyte elimination in piecemeal necrosis has hitherto remained obscure. Cell-mediated immune attack induces apoptosis, not classical necrosis, and the occurrence of apoptosis in piecemeal necrosis links the observed morphological changes in chronic active hepatitis with the other evidence for an autoimmune pathogenesis. It is significant that apoptosis does not evoke inflammation or fibroplasia. In attempting to elucidate the cause of the fibrosis that accompanies progression to cirrhosis in chronic hepatitis, it may thus be more relevant to study the effect on fibroblasts of substances liberated during lymphocyte-hepatocyte interactions than the death of the hepatocytes.

Autoimmune Diseases↗
PubMed1979

Apoptosis. Its nature and implications for dermatopathology.

Apoptosis is a distinctive mode of cell death with characteristic morphologic features which serves as a balance to mitosis in regulating the size of animal tissues. In contrast to coagulative necrosis, the cytologic features of apoptosis suggest active self-destructive rather than progressive disintegration. It typically affects scattered individual cells which condense and bud to produce many membrane-bounded fragments in which organelles appear intact when viewed by the electron microscope. These apoptotic bodies are then phagocytosed and digested by cells resident in the tissue. Apoptosis, unlike coagulative necrosis, does not itself evoke an inflammatory response. Apoptosis is a feature of such diverse processes as deletion of phylogenetic vestiges during normal embryonic development, involution of endocrine-dependent organs after withdrawal of trophic hormones, cell-mediated immune attack on tissues, and therapeutically induced regression of neoplasms. Apoptosis has received scant attention in dermatopathology. However, it is now known to be an important feature of lichen planus, certain drug eruptions, the skin lesions of graft-versus-host reactions, the regression of plane warts, and the effects of ultraviolet damage. It is also involved in the kinetics of cutaneous neoplasms. In some of these situations, apoptotic bodies have, in the past, been given names such as Civatte bodies, colloid bodies, single-cell necrobiosis, sunburn cells, and dyskeratotic cells without their basic nature having been recognized.

Animals↗
PubMed1978

Differential radiation response amongst proliferating epithelial cells.

Tissue irradiation results in both reproductive and histologically evident cell death. The correlation between these is poor. Irrespective of dose and fraction sterilized, many cells behave as if unirradiated (cell cycle and maturation activity). The fraction of histologically observable dead cells is usually less than 0.1, with most in the intestine being positioned in the presumptive stem cell region. The data strongly suggest different epithelial sub-populations with differing radioresponses. These may be the stem and differentiated proliferative cells.

Animals↗
PubMed1977

An electron microscopic study of the mode of donor cell death in unmodified rejection of pig liver allografts.

The only type of cell death found in pig liver allografts 1 week after technically successful operation was apoptosis. Its extent paralleled the degree of mononuclear cell infiltration of the liver parenchyma, and mononuclear cells were found applied to the surfaces of hepatocytes showing early stages of the process. The results suggest that cellular immune attack induces apoptosis of donor cells, and that the action is a direct one. However, implication of other factors such as vascular damage in the induction of apoptosis in the grafts could not be excluded.

Animals↗
PubMed1977

Circadian rhythms of presumptive stem cells in three different epithelia of the mouse.

Variation in the percentage of labelled cells (LI), mitoses (MI) and apoptosis (AI: i.e. shrinkage necrosis) have been studied throughout a 24 hr period (40 min after labelling with 3H-TdR) for tongue epithelium, epidermis and intestinal epithelium in the mouse. A room with reversed light cycle was used to obtain data for half of the 24 hr period. All three tissues showed marked variations in LI with peak values between 24.00 and 03.00 hours. In the intestine a maximum value for MI was observed 3-6 hr after that for LI and with a maximum value for AI slightly later. In all three epithelia the circadian rhythm was most striking in cells at positions which can be correlated with presumptive stem cell activity; e.g. in the crypts the labelling and mitotic peaks reflecting a circadian rhythm were most clearly distinguishable at the basal part of the crypts. These observations are discussed in relation to the validity of various proliferative models.

Animals↗
PubMed1975

An electron-microscope study of the mode of cell death induced by cancer-chemotherapeutic agents in populations of proliferating normal and neoplastic cells.

Deletion of scattered single cells by ultrastructurally typical apoptosis was observed to take place continuously in the lining of the small intestinal crypts of normal mice, and in untreated Crocker mouse ascites tumours. Injection of the cancer-chemotherapeutic agents actinomycin D, mitomycin C, cytosine arabinoside and cycloheximide massively enhanced the rate of apoptosis in each situation, the morphology of cell death induced by these drugs being fundamentally different from that of coagulative necrosis, which developed without treatment in the centres of solid nodules that grew after subcutaneous inoculation of the tumour. In the crypt lining, where the predominant cell type affected appeared to be epithelial, the apoptotic bodies were either extruded into the lumen or rapidly phagocytosed and degraded by adjacent viable cells. But bodies in the ascites tumour were rarely ingested by uninvolved cells, presumably because of their wide dispersal in a fluid medium, and the stages in their development were seen more clearly than has been possible in solid tissues, where phagocytosis is ususlly rapid: they eventually underwent a change resembling coagulative necrosis or in-vitro autolysis. Reports suggesting that cancer-chemotherapeutic agents enhance autophagy in solid malignant neoplasms require confirmation, for secondary lysosomes of any sort were found to be uncommon in the treated ascites tumours, and there is little doubt that phagocytosed apoptotic bodies have been mistaken for autophagic vacuoles in the past. The significance of the fact that cancer-chemotherapeutic agents induce a type of cell death that is found in normal tissues is at present unknown.

Animals↗
PubMed1975

Letter: Cytolysis.

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Antineoplastic Agents↗