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Biomedical subjects

S S Cross

Publications and source records attributed to S S Cross.

At least 109 records · Page 6Linked to original sources

Computer-assisted learning in morbid anatomy. A stimulation of autopsy procedures and death certification.

This article describes the objectives, design and performance of a computer program which provides a textual simulation of autopsies. The benefits of using this program to teach medical students about the procedures of autopsy diagnosis is discussed. This form of computer-assisted learning is also useful in introducing medical students to correct death certification: a neglected area of medical education.

Autopsy↗

Is there any justification for the routine examination of bowel resection margins in colorectal adenocarcinoma?

The proximal and distal bowel resection margins of 339 specimens of colorectal adenocarcinoma were examined for the presence of tumour. In only five cases was tumour found in a resection margin. In four of these cases macroscopic examination showed that the tumour extended to the resection margin. In the fifth case the tumour was present in the pericolic fat. These results and reported data on the intramural spread of colorectal cancer suggest that examination of bowel resection margins is unnecessary unless the tumour extends to within 2 cm of the resection margin. Examination of the deep radial margins of the tumour and slides to show other prognostic indicators would be a more effective use of histopathological resources.

Adenocarcinoma↗

Endocrine cell hyperplasia and appendiceal carcinoids.

As endocrine tumours in a number of organs may arise in a background of hyperplasia, the density of endocrine cells in appendices from ten patients with carcinoid tumours was compared with that in appendices from ten age- and sex-matched control patients. Crypt and lamina propria endocrine cells were quantified separately. The density of argentaffin endocrine cells in the crypts was significantly higher in appendices with carcinoid tumours when compared with the controls. No difference was found in non-argentaffin endocrine cells, and no difference was found in either argentaffin or argyrophil endocrine cells in the lamina propria. While it is possible that carcinoid tumours induce an increase in the number of enterochromaffin (EC) cells in the background mucosa, it is considered more likely that EC cell hyperplasia predisposes to the development of carcinoid tumours of the appendix.

Adolescent↗

Pseudosarcoma of the oesophagus.

The presentation, histology and management of a pseudosarcoma (or polypoid carcinoma) of the oesophagus are presented. Historical and modern theories of pathogenesis are discussed. Though rare, ENT surgeons should be aware of these tumours, as patients with such tumours present early and potentially have a much better prognosis than those with the more common oesophageal malignancies.

Aged↗

Immunoperoxidase in lymphomas induced by host-versus-graft (HVG) reaction.

It appears that the development and type of lymphoid neoplasm in mice depends on the ratio of T cell subsets and the repeated stimulation of the lymphoid systems as well as a genetic predisposition. Mice with HVG disease developed lymphomas in an average of 462 days versus 567 days for normal mice. Murine leukemia virus was detected in the HVG mice perinatally at 3 weeks of age and three months earlier in the noninjected mice. The immunoglobulins were IgA and IgM or IgM alone and IgG in three cases. No IgA was detected.

Animals↗

Expression of murine leukemia viruses in RFM mice with host versus graft disease after perinatal inoculation of (T6 X RFM)F1 lymphohemopoietic cells.

Host versus graft disease is the fatal syndrome of altered immunity that follows the perinatal inoculation of related F1 hybrid spleen cells to susceptible strains of inbred mice. The allogenic reaction results in severe depletion of T-lymphocytes, but causes hyperplasia and hypersecretion of B-cells. Among the long-term survivors of acute host versus graft reactions, there is a high incidence of nonthymic lymphomas associated with ecotropic murine leukemia virus that may be of donor F1 origin. The present studies were done to determine whether ecotropic murine leukemia virus played any role in the pathogenesis of acute host versus graft disease in RFM mice perinatally inoculated with (T6 X RFM)F1 spleen cells. In RFM/(T6 X RFM)F1 chimeras, N-tropic murine leukemia virus can be detected as early as 3 days. The progression of the disease was accompanied by increasing viral expression. The inoculation of N-tropic virus of F1 donor origin into RFM neonates failed to induce disease, although the virus proliferated. Detection of progressively rising titers of antibody to murine leukemia virus linked the virus to the development of hyperimmunoglobulinemia by virtue of its ability to serve as a replicating source of antigens. These and other studies provided evidence that the seemingly paradoxical appearance of hyperimmunoglobulinemia in T-cell-deficient mice with the host versus graft syndrome is due, at least in part, to the stimulation of presensitized F1 donor B-cells, which are not destroyed in the allogenic reaction, as are the T-cells. Another unusual finding was the detection of polytropic murine leukemia virus in 25-day-old RFM/(T6 X RFM)F1 chimeras. It is suggested that the allogenic host versus graft reaction favored the formation of recombinants.

Animals↗

Neonatal infection with mouse thymic virus: spleen and lymph node necrosis.

Mouse thymic virus (TA) is a naturally occurring herpesvirus of laboratory and wild mice, which produces massive thymic necrosis when inoculated into newborn mice. Our histopathological study showed necrosis not only of the thymus but also of the spleen and lymph nodes which was noticeable by day 7 and complete by day 14. Both spleen and lymph nodes regenerated to an almost normal histological pattern by day 70. The results show that TA infects multiple lymphoid tissues causing massive necrosis in all, and is not limited to a single site, the thymus. TA infection was found to be a persistent herpesvirus infection in both the lymph nodes and spleen. During the period of acute infection, as necrosis increased, the response of cell suspensions of lymph nodes to the T cell mitogens concanavalin A and phytohaemagglutinin was virtually non-existent. Activity returned to normal as the histological repair progressed.

Animals↗

Biology of mouse thymic virus, a herpesvirus of mice, and the antigenic relationship to mouse cytomegalovirus.

Mouse thymic virus (TA) is a herpesvirus which produces extensive necrosis of the thymus of newborn mice 7 to 14 days after infection. Infectious virus can be recovered from the thymus for only 10 days after infection, with highest titers occurring between days 5 and 7. In mice 5 days old or less, TA infects thymus cells and produces massive necrosis. TA also infects the salivary glands and persists as a chronic infection. Newborn mice infected with TA have no detectable humoral immune response. Infected adult mice respond, and humoral antibody is detected 7 days after infection. Titers are maintained for months thereafter. Regardless of the age of the mice inoculated with TA, persistent infection was established in the salivary glands, but no evidence for thymus involvement was observed when adults were infected. TA does not cross-react serologically by immunofluorescent, complement fixation, or virus neutralization tests with mouse cytomegalovirus; however, interestingly, the epidemiology of the two herpesviruses are similar. Both mouse cytomegalovirus and TA were isolated from the same animals in populations of laboratory and wild mice. Evidence of infection with mouse cytomegalovirus and TA were most apparent by virus isolations, since humoral antibody responses are rarely observed. All strains of mice tested were susceptible to TA infection. However, in some strains maximum necrosis occurred at 7 days, compared with 10 to 14 days for other strains. The difference in age susceptibility and the target tissue of thymus in newborn mice suggests that TA is a model herpesvirus for studying the effects of viral infections on humoral and cell-mediated immunological functions.

Animals↗

Maturation of regulatory factors influencing magnitude of antibody response to capsular polysaccharide of type III Streptococcus pneumoniae.

Mice of different ages were evaluated for their ability to give a plaque-forming cell response to the capsular polysaccharide of Streptococcus pneumoniae (SSS-III). The response of amplifier and suppressor thymus-derived (T-) cells was also evaluated. The responses to an optimally immunogenic dose of SSS-III for two-and three-week-old mice were only 7% and 14%, respectively, of that produced by adult mice; values comparable to those of adult mice were attained by four weeks of age. Activity of amplifier T-cells, which was minimal at two to four weeks of age, matured slowly and did not reach a maximum until eight to 10 weeks of age. However, activity of suppressor T-cells was found to be fully developed as early as two weeks of age. These findings indicate that the inhibitory effects of suppressor T-cells are predominant in young mice and that such cells may play an active role in determining the ease with which immunological unresponsiveness is induced in neonates.

Aging↗

Regulation of the antibody response to type III pneumococcal polysaccharide. V. Ontogeny of factors influencing the magnitude of the plaque-forming cell response.

Mice of different ages were evaluated with respect to their ability to give a plaque-forming cell (PFC) response to Type III pneumococcal polysaccharide (SSSIII), as well as the degree of amplifier and suppressor thymus-derived(T) cell activity present. Although the magnitude of the PFC response to an optimally immunogenic dose of SSS-III for 2-and 3-week old mice was only 7% and 14%, respectively, of that produced by adult (8-week old) mice, values comparable to those of adult animals were attained by 4 weeks of age; no significant changes in the ability to respond to SSS-III occurred thereafter. Amplifier T cell activity, which was minimal at 2 to 4 weeks of age, matured slowly and did not reach a maximum until 8 to 10 weeks of age. By contrast, suppressor T cell activity appeared to be fully developed at least as early as 2 weeks of age; here, the inhibitory effects produced could by abrogated by depletion of T cells, indicating that the unresponsiveneness induced by such cells does not result in the depletion ot irreversible inactivation of B cells capable of responding to SSS-III. These findings suggest that the inhibitory effects of suppressor T cells are predominant in young mice and that such cells may play an important role in determining the ease with which unresponsiveness is induced in neonates, and in the prevention of autoimmune disease. Also, studies conducted with adult-thymectomized mice showed that both amplifier and suppressor T cells, once seeded to the periphery, are stable and do not depend upon the presence of intact thymus for the expression or renewal of their activity.

Aging↗

Neonatal infection with mouse thymic virus: effects on cells regulating the antibody response to type III pneumococcal polysaccharide.

Mice infected neonatally with mouse thymic virus (TA) were evaluated at different ages with respect to their ability to give a plaque-forming cell (PFC) response to type III pneumococcal polysaccharide (SSS-III), as well as the degree of amplifier and suppressor thymus-derived (T) cell activity present. B cell activity matured rapidly from 2 to 4 weeks of age and was not affected by TA infection. Amplifier T cell activity matured progressively over the first 8 weeks of life and was transiently suppressed in TA-infected mice at 4 weeks of age. Suppressor T cell activity measured at 2,4, and 6 weeks of age was unaffected by TA. The findings suggest that TA is highly tropic for T cells and has selective effects on subpopulations of T cells.

Aging↗

Neonatal infection with mouse thymic virus. Differential effects on T cells mediating the graft-versus-host reaction.

Neonatal infection with mouse thymic virus (TA), a murine herpes virus, produced extensive but temporary necrosis of the thymus which was maximal at 10 to 14 days of age. Studies of precursor and amplifier cells mediating graft-vs-host (GVH) reactivity of thymocytes, spleen cells (SC), and lymph node cells (LNC) of normal and TA-infected mice were made at 4 and 8 weeks of age. Infection with TA resulting in a profound reduction (70 to 80%) in the direct GVH reactivity of thymocytes at both ages; by comparison, the capacity of thymocytes to produce synergy when combined with normal LNC was normal at 8 weeks. Direct GVH reactivity of SC was depressed 90% 4 weeks after infection with TA but returned to near normal at 8 weeks. Direct GVH reactivity of LNC from TA-infected mice was normal at 4 and 8 weeks of age, but amplifier T cell activity in LNC was markedly depressed at 8 wekks. These results demonstrate that TA has highly selective effects upon subpopulations of T cells in thymus and lymph node.

Animals↗

Immunologic effects of neonatal infection with mouse thymic virus.

Mouse thymic virus is a herpesvirus that causes extensive thymic necrosis when given to newborn mice. During the time of acute infection spleen cells have markedly diminished reactivity to T cell phytomitogens and to allogeneic cells and are incapable of effecting a primary in vitro response to a "T-dependent" antigen; responses to B cell mitogens and to a T-independent antigen are unimpaired. Spleens from acutely infected mice have low theta antigen normal numbers of immunoglobulin-bearing cells. Surprisingly, despite widespread necrosis and cellular depletion, thymic cell reactivity to mitogens is unimpaired. However, the ability to thymocytes to proliferate and to generate cytotoxic killer cells in response to allogeneic cells is diminished.

Animals↗