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Scalp lacerations are frequently seen in both living trauma victims and at post-mortem examination. In clinical circles, it is well known that even “trivial” lacerations of blood-rich areas such as the scalp may bleed profusely and persistently. It is less well known, however, that hemorrhage even from simple scalp lacerations may be fatal. We present seven cases in which hemorrhage from simple scalp lacerations was considered to be the principle cause of death. Chronic alcohol misuse, alcoholic liver disease, and the co-existence of other pathologies such as ischemic heart disease were frequently contributory factors. [ABSTRACT FROM AUTHOR]

In the long term, administration of dimethylhydrazine (DMH) to rats results in the development of tumours in both small intestine and colon. This study has been undertaken in order to document the sequence of changes occurring in the intestinal mucosa in the first 108 h following a single subcutaneous injection of DMH. After a lag of several hours there is evidence of damage to cells in the proliferation zone of the intestinal crypts, and a brief reduction in tritiated thymidine labelling index. A phase of compensatory regenerative activity emerges from the setting of continuing cell damage, resulting in restoration of the mucosa to normal. The severity of the toxic damage to the intestinal mucosa at various sites mirrors the vulnerability of the mucosa to the long term carcinogenic effects of DMH, suggesting that inherent properties of the mucosa may be of more importance than other cocarcinogenic influences in the ultimate development of tumours. [ABSTRACT FROM AUTHOR]

In a population of cells that proportion which is actively engaged in the proliferative cycle is often estimated from the ratio of the observed labelling index to an expected labelling index, calculated, on the basis of all cells being in cycle, from the cell cycle phase durations and the age distribution. Ignoring the variability in cell cycle times may lead to large overestimates or underestimates in the expected labelling index. A method is given of obtaining a more accurate estimate of this variable, and hence of the proliferative proportion. [ABSTRACT FROM AUTHOR]

This study has been undertaken in order to compare in detail cell proliferation in the mucosal crypts at several sites along the length of the large bowel of the rat. The techniques which have been used include simple morphometry, calculation of mitotic and tritiated thymidine labelling indices, metaphase arrest with vincristine, and the fraction of labelled mitoses method. Major differences exist in the size and shape of the crypts at different sites. In particular the distribution of the proliferating cells within the crypt varies. Mean cell cycle time ranges from 58 h in the descending colon to 25 h in the caecum; this variation appears to be brought about largely by changes in the duration of G, the other phase durations remaining relatively constant. There is also variation in cell cycle time and growth fraction at different levels within the crypt; throughout the bowel cells appear to cycle more slowly at the bottom of the crypt, but changes in growth fraction do not display a similarly consistent pattern. Clearly the organisation of cell proliferation in the normal rat colon is very complex, and strict definition of anatomical location is required in any study of cell proliferation whether in normal or in diseased animals. [ABSTRACT FROM AUTHOR]

The parenteral administration of 1,2-dimethylhydrazine to rats caused the development of colonic neoplasms in about 90% of animals by 24-30 weeks of treatment. Usually there were multiple tumours with a mean of 2.7 per rat. The lesions have been classified histologically into adenomata (26% of all tumours) and carcinomata, the latter showing varying degrees of differentiation. No completely anaplastic tumours were seen, and there were none originating in connective tissue. The distributions of the different tumour types along the length of the colon varied. The more benign lesions were situated predominantly in the distal half of the colon, while the poorly differentiated adenocarcinomata were concentrated in the proximal third of the colon. There was good evidence to suggest that adenomata often progressed to frank malignancy in the distal colon. In the proximal part, however, it appeared that tumours frequently developed de novo as poorly differentiated carcinomata. Perhaps regional variations in the kinetic organisation of the normal colonic mucosa somehow influence the nature of the neoplastic change induced by DMH, thus accounting for the differences in tumor distribution. After 24 weeks of DMH treatment there was only a small increase in the mean number of tumours per rat. [ABSTRACT FROM AUTHOR]

In the present study we have used a variety of techniques in order to investigate cell proliferation in the mucosal crypts at a strictly defined site in the descending colon of the mouse. The mean crypt length was 31.1 cells, and the mean crypt circumference 22.5 cells, giving a total crypt population of about 700 cells. The corrected mitotic index for the whole crypt column was 1.33%; the labelling index was 11.7% with peak values of about 27% occurring at the bottom of the crypt. Metaphase accumulation following vincristine showed that the birth rate in the whole crypt was 26.5 cells/1000 cells/h. From a consideration of cumulative mitotic index and cumulative birth rate a mitotic duration of 0.39 h was obtained. Analysis of FLM data gave a cell cycle time for the whole crypt of 15.5 h: from FLM data and observed labelling index a growth fraction for the whole crypt of 29% was obtained. Analysis of FLM data for individual cell position groups at different sites within the crypt indicated that the mean cell cycle time showed little variability and was about 15 to 16 h, whereas the duration of DNA synthesis fell with rising cell positions. Growth fraction too appeared to fall with rising cell position within the crypt. [ABSTRACT FROM AUTHOR]

The present study was undertaken in order to try to define some of the kinetic parameters in the colonic mucosa of normal Wistar rats. Preliminary observations showed considerable morphological differences in the mucosa from site to site along the length of the colon. In particular the height of the crypts (measured in cells) was variable. In addition labelling index studies demonstrated dramatic variations in the distribution of labelling along the length of the crypts from site to site in the bowel. A single site in the descending colon was selected for more detailed study using a stathmokinetic agent, vincristine, and the continous labelling technique with tritiated thymidine. The results of these investigations suggest that there exists at the base of the crypt a subpopulation of cells cycling more slowly than the cells in the rest of the proliferative compartment. Growth fraction appears to fall with rising cell positions within the crypt. [ABSTRACT FROM AUTHOR]