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Biomedical subjects

S Britton

Publications and source records attributed to S Britton.

At least 127 records · Page 7Linked to original sources
PubMed1982

The nosocomial component of medical care. A prospective study on the amount, spectrum and costs of medical disturbances in a department of infectious diseases.

During a nine month period all patients admitted to a department of infectious diseases were prospectively studied regarding nosocomial reactions defined as any unwanted or unexpected negative effect of medical treatment or care. Eleven percent of 1271 patients were admitted because of complications to previous medical treatment. Twenty-seven percent of the patients developed adverse reactions during the hospital stay. Only four percent of these resulted in a prolonged hospital stay. Six patients (0.5%) died from complications to medical care. We deduce that medical complications are not a major factor in prolonging hospital stay, but rather that the longer the hospital stay the greater the risk for developing nosocomial symptoms. The estimated cost for the whole of the nosocomial matter was seventeen percent of the budget of the department.

Age Factors↗
PubMed1981

Characteristics of Epstein-Barr virus activation of human B lymphocytes.

Epstein-Barr virus (EBV) will infect at least every third cell if exposed in vitro to an extensively purified B cell population from human peripheral blood. About 10% of such infected cells will be driven into immunoglobulin synthesis and secretion, as judged by the indirect protein A plaque assay. The appearance of EB nuclear antigen, de novo DNA synthesis, and immunoglobulin secretion are linked phenomena accompanying infection as judged by viral dilution experiments, which yield kinetics of a one-hit order. Induction of immunoglobulin secretion in B cells by EBV requires de novo synthesis of DNA, and consequently, nontransforming EBV (P3HR1) will not induce immunoglobulin secretion and will also specifically block such induction from subsequently added EBV. The termination of immunoglobulin induction by EBV in short-term cultures appears to be T cell dependent.

Antibody Formation↗
PubMed1981

Cyclosporin A promotes spontaneous outgrowth in vitro of Epstein-Barr virus-induced B-cell lines.

Cyclosporin A (CSA) is a fungal metabolite which exerts profound effects on the immune system and has potential as a selective immuno-suppressive agent. Clinical trials with human renal allograft recipients have confirmed this potential but there have been disturbing reports of lymphoma in a significant number of patients. Despite extensive animal studies, the specificity of this drug for human lymphocyte subpopulations is largely unknown. We demonstrate here that in vitro CSA has no apparent effect on Epstein-Barr virus (EBV)-induced B-lymphocyte activation, but totally inhibits the T-cell dependent pokeweed mitogen (PWM) B-cell response. In addition, CSA markedly facilitates the outgrowth of B-lymphoblastoid cell lines from both EBV-infected and non-infected lymphocytes of EBV immune donors cultured in vitro. These results indicate that CSA can interfere with the lymphocytes normally responsible for maintaining the life-long carrier state initiated by primary infection with EBV, allowing outgrowth of the persistently infected cells circulating in the peripheral blood.

B-Lymphocytes↗
PubMed1981

A sequential study of human B lymphocyte function from birth to two years of age.

The immunoglobulin synthesizing capacity of individual lymphocytes from newborns and infants aged 2, 6, 12 and 24 months respectively has been studied. The technique has been to expose purified lymphocytes to a T lymphocyte dependent (pokeweed mitogen) or a T lymphocyte independent (Epstein-Barr virus) activator of B lymphocytes. Activation has been measured as immunoglobulin secretion of individual B lymphocytes using a hemolytic plaque assay. B lymphocytes from newborns can be made to synthesize IgM at adult levels, but not IgG and IgA. Within 24 months from birth the secretion of IgG has reached adult capacity whereas IgA formation is still diminished. Lymphocytes synthesizing IgG subclasses appear at different times insofar as IgG1 and IgG3 are well demonstrable within 12 months from birth whereas IgG2 and IgG4 has not at all reached adult levels even 24 months after birth. The T lymphocyte dependent activator (pokeweed mitogen) fails to induce immunoglobulin synthesis in peripheral blood lymphocytes from newborns because of a defect helper T cell function. Such T cell capacity appears at the age of 6 months. The data unequivocally demonstrate restricted but definite B lymphocyte functional capacity already at birth and a gradual but partial acquisition of adult competence until the age of 2 years.

Age Factors↗
PubMed1981

Polyclonal human T lymphocyte activation results in the secondary functional activation of the human B lymphocyte.

The polyclonal T lymphocyte activators Con A and PHA were demonstrated to induce secretion of IgM and IgG as well as IgA antibodies in cultures of human peripheral blood lymphocytes. A similar response was seen in one-way mixed lymphocyte cultures and the kinetics, dose-response characteristics and optimal culture conditions are presented. The presence of functional T lymphocytes is a prerequisite for in vitro B lymphocyte activation in response to T lymphocyte mitogens. A narrow dose-response profile is a characteristic for both Con A and PHA and polyclonal B cell activation occurred at what have been previously regarded as suboptimal concentrations of these agents. The use of higher doses of these activators failed to generate immunoglobulin-secreting cells despite the presence of early and optimal levels of DNA synthesis in the cultures.

Adult↗
PubMed1980

Cellular mechanisms of restricted immunoglobulin formation in the human neonate.

The functional capacity of human neonatal B lymphocytes has been investigated by in vitro methods using T lymphocyte-dependent (pokeweek mitogen, PWM) and -independent (Epstein-Barr virus, EBV) polyclonal B cell activators. B cell activation of single cells was detected by class-specific immunoglobulin (Ig) secretion using a reversed hemolytic plaque assay. It was found that neonatal B cells were triggered to secretion of IgM by EBV, with a magnitude comparable to adult levels, but that, in contrast to B cells from adults, they did not secret IgG. Cord lymphocytes did not secret Ig although they displayed a sizable DNA synthetic response to PWM. Using cell separation and culture experiments, it was shown that (allogeneic) adult T lymphocytes could restore cord B cell responsiveness to PWM and that cord T lymphocytes could not cooperate with adult B cells. In addition to this immaturity of cord T helper function for antibody synthesis, we found cells in the cord T cell-enriched fraction which inhibited the polyclonal response of adult lymphocytes to both PWM and EBV. These lymphocytes suppressed adult B lymphocytes directly but appeared ineffective against neonatal B lymphocytes themselves. The nature of these suppressing cells and their possible role in the fetal/maternal relationship are a matter of speculation.

Antibody-Producing Cells↗
PubMed1979

A live human B-cell activator operating in isolation of other cellular influences.

Using a reversed haemolytic plaque assay, we demonstrate that live but not inactivated Epstein-Barr (EB) virus can induce human blood lymphocytes to polyclonal Ig (IgM and IgG) secretion in vitro. Unlike pokeweed mitogen this B-cell-activating effect takes place in relative absence of T cells. EB virus thus promises to be a tool for study of B cell function isolated from other cellular influences, although its mechanism of activation appears to be different from that of previously known B cell activators.

Adult↗
PubMed1979

Pokeweed mitogen induced differentiation of human B cells: evaluation by a protein A haemolytic plaque assay.

Using the protein A plaque assay, the number of human cells secreting immunoglobulin of various classes after pokeweed mitogen stimulation was determined. At optimal response (on day 5-7) a mean of 58,354 IgM PFC/10(6), 34,207 IgG PFC/10(6) and 10,525 IgA PFC/10(6) cells was found when using peripheral blood lymphocytes. In spleen cells, peak values which were slightly higher than in blood, were obtained at day 4-6. The proportions of cells secreting light chains of either type were found to be comparable to those of unstimulated cells thus supporting the notion of the polyclonality of the response. Pokeweed mitogen stimulation of peripheral blood lymphocytes was found to be totally T-cell dependent whereas the response of spleen cells was not. When assayed for antigen-specific precursor cells in cultures stimulated by mitogen, the frequency of SRBC-specific IgM producing cells was found to be 1.3/1000 cells. This frequency was regularly found to be independent of medium supplement.

Antibody-Producing Cells↗
PubMed1978

Appearance of killer (K) cells in the mesenteric lymph nodes in Crohn's disease.

The local lymph node in Crohn's disease contains killer (K) cells which are able to lyse antibody-coated heterologous target cells. K cells are not found in mesenteric lymph nodes from control patients not suffering from Crohn's disease, whereas they are regularly found in similar amounts in the peripheral blood of both control and patients with Crohn's disease. Even mesenteric lymph node cells from areas not macroscopically affected by inflammatory disease show increased K cell activity as compared to control lymph node lymphocytes, suggesting a generalized mesenteric lymph node involvement with regard to K activity in Crohn's disease.

Adult↗
PubMed1976

Monocyte function in infectious mononucleosis: evidence for a reversible cellular defect.

Migration of blood monocytes from patients with acute infectious mononucleosis and from normal controls was measured against chemotactic factors in serum. Moncytes from patients with acute infectious mononucleosis showed decreased migration as compared with that of control monocytes. However, serum from patients with infectious mononucleosis contained normal or above normal amounts of chemotaxins for monocytes. The migratory defect of monocytes from patients with infectious mononucleosis was reversible within three months after the onset of diesease. The cause of this monocyte migration defect in infectious mononucleosis is though to be an in vivo blockade of receptors on monocytes for chemotaxins, and it is speculated that this defect can partially explain the explain the ablated delayed-hypersensitivity skin reactions in this disease.

Adult↗