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Biomedical subjects

C A Michie

Publications and source records attributed to C A Michie.

At least 37 records · Page 2Linked to original sources
PubMed1997

Modeling the lifespan of human T lymphocyte subsets.

T lymphocytes may be classified as naive or memory cells, depending on whether they possess immunological memory. The central tenet of this work is that memory lymphocytes revert to naive lymphocytes in vivo. This phenomenon is modeled by a mechanism qualitatively similar to Demoivre's law of human mortality. Additionally, both lymphocyte subsets undergo decay. Model parameters and their standard errors are estimated by maximizing a likelihood function constructed by Kalman filtering of the experimental data on the assumption that it is contaminated by measurement noise of constant relative error.

Cell Death↗
PubMed1996

Lymphocyte dynamics, apoptosis and HIV infection.

Death of HIV-infected CD4+ cells and HIV-induced death of uninfected CD4+ cells by apoptosis have been suggested to be important factors in causing the gradual progressive decline of CD4+ cells in the blood of HIV-positive patients. Recent advances in our knowledge of the dynamics of infection and the mechanism of apoptosis are reviewed with the aid of a mathematical model.

Apoptosis↗
PubMed1995

In vivo estimates of division and death rates of human T lymphocytes.

We present data on the decay, after radiotherapy, of naive and memory human T lymphocytes with stable chromosome damage. These data are analyzed in conjunction with existing data on the decay of naive and memory T lymphocytes with unstable chromosome damage and older data on unsorted lymphocytes. The analyses yield in vivo estimates for some life-history parameters of human T lymphocytes. Best estimates of proliferation rates have naive lymphocytes dividing once every 3.5 years and memory lymphocytes dividing once every 22 weeks. It appears that memory lymphocytes can revert to the naive phenotype, but only, on average, after 3.5 years in the memory class. The lymphocytes with stable chromosome damage decay very slowly, yielding surprisingly low estimates of their death rate. The estimated parameters are used in a simple mathematical model of the population dynamics of undamaged naive and memory lymphocytes. We use this model to illustrate that it is possible for the unprimed subset of a constantly stimulated clone to stay small, even when there is a large population of specific primed cells reverting to the unprimed state.

Cell Death↗
PubMed1995

The effect of treatment on lymphokine-secreting cells in the intestinal mucosa of children with Crohn's disease.

BACKGROUND: Recent studies have shown both interleukin 2 (IL-2) and interferon gamma (IFN) to be elevated in patients with active Crohn's disease compared to ulcerative colitis or non-inflammatory bowel disease controls. However the effect of treatment on these lymphokines has not been studied. PATIENTS AND METHODS: Using a reverse haemolytic plaque assay the percentage of lymphokine-secreting cells was determined in the intestinal mucosa of children with Crohn's disease before and after 8 weeks of treatment with either enteral nutrition, cyclosporin or steroids. RESULTS: Before treatment, a high percentage of cells isolated from mucosal biopsies secreted IL-2 or interferon-gamma. Eight weeks' treatment with the immunosuppressive agents cyclosporin, or with corticosteroids, produced a significant reduction in the percentage of IL-2 secreting cells, although only for the former was there also a reduction in interferon-gamma secreting cells. Enteral nutrition however, produced a reduction in lymphokine-secreting cells equivalent to cyclosporin and produced the best histological and clinical improvement. CONCLUSION: Enteral nutrition and cyclosporin can down-regulate lymphokine secretion in the gut in Crohn's disease.

Adolescent↗
PubMed1995

Selective recruitment of lymphocyte subsets to the inflamed appendix.

Total lymphocyte counts and the distribution of lymphocyte subsets were determined in peripheral venous blood and appendiceal mononuclear cells from 60 patients who underwent appendicectomy for the clinical diagnosis of appendicitis. A significant peripheral lymphopenia was observed in the 46 patients with histologically confirmed acute appendicitis which was accompanied by an increase in the appendiceal lymphocyte concentration. There was an even greater depletion of CD45RO+ (memory) T lymphocytes in peripheral blood and an increase in the inflamed appendix. Reciprocal changes were observed in the CD45RA+ (naive) T lymphocyte subset. These changes were reflected in the local arterial and venous CD45RA and CD45RO T lymphocyte subsets. Proliferation studies showed an expanded functional repertoire of T lymphocytes in the inflamed appendix. Selective recruitment of memory T lymphocytes from the peripheral blood to the inflamed appendix was demonstrated.

Acute Disease↗
PubMed1995

Group B streptococcal infection: when does vertical transmission take place?

Expression of CD45 isoforms was used to estimate when group B streptococci had infected a child born with low Apgar scores who subsequently died. The measure suggested that infection was present more than 24 hours before delivery, thus distinguishing perinatal infection as the primary event which preceded intrapartum asphyxia in this case.

Adult↗
PubMed1994

Tumor necrosis factor alpha-producing cells in the intestinal mucosa of children with inflammatory bowel disease.

BACKGROUND/AIMS: Cytokines are thought to be important in mediating tissue damage in inflammatory bowel disease (IBD). Many of the in vivo activities of tumor necrosis factor alpha (TNF-alpha) match the changes found in IBD, but its importance is controversial. METHODS: A sensitive, reverse hemolytic plaque assay was used to determine the frequency of TNF-alpha secreting cells isolated from mucosal biopsy specimens of children with Crohn's disease or ulcerative colitis (UC) and non-IBD controls before and after medical treatment. RESULTS: Frequency of TNF-alpha secreting cells was significantly increased in biopsy specimens from children with mild, nonspecific inflammation compared with those with histologically normal intestine. Frequency did not increase in UC compared with children with nonspecific inflammation but was significantly greater in Crohn's disease than in UC. After treatment, the frequency of TNF-alpha secreting cells was reduced in patients receiving cyclosporin A, not reduced in patients with steroids or enteral nutrition, and not changed with treatment in UC. CONCLUSIONS: TNF-alpha secreting cells are increased in the mucosa of inflamed intestine, regardless of pathogenesis. In patients with IBD, higher levels are seen in Crohn's disease than in UC, probably reflecting the extensive T-cell activation in Crohn's disease. No relation existed between histological healing and the frequency of TNF-alpha-secreting cells.

Adolescent↗