Biomedical subjects

E C Ebert

Publications and source records attributed to E C Ebert.

61 records · Page 4Linked to original sources

PubMed1986

Examination of the low proliferative capacity of human jejunal intraepithelial lymphocytes.

The proliferation of human jejunal intraepithelial lymphocytes (IEL) was examined to determine how it differed from that of peripheral blood (PB) T lymphocytes. The IEL were mainly T lymphocytes of the cytotoxic-suppressor (T8+) phenotype. They demonstrated lower proliferative responses to various stimuli (2,501 +/- 565 ct/min with phytohaemagglutinin; PHA) compared to unseparated PB T lymphocytes (73,678 +/- 2,495) or the T8+ subset (68,939 +/- 10,053 ct/min) (P less than 0.001). This low proliferative response was also a characteristic of the T8+ T lymphocytes in the lamina propria (4,606 +/- 1,226 ct/min) but not the T4+ subset (43,447 +/- 10,188 ct/min) (P less than 0.05). These findings were not due to isolation techniques or to differences in kinetics. Mixing experiments revealed that the IEL did not contain cells which suppressed proliferation. In addition, the IEL could be stimulated by mitogens, as they produced the same amount of interleukin 2 (IL-2) and IL-2 receptors as did PB T lymphocytes. Although the lectin-induced proliferative response of IEL was unaltered by the addition of autologous macrophages and minimally increased by IL-2, it was markedly enhanced by the addition of sheep red blood cells (SRBC). The enhancing effect of SRBC was not due to T cell recognition of xenogenic antigens on the erythrocytes since neither allogeneic non-T lymphocytes nor other xenogenic erythrocytes produced the same effect. Both intact SRBC and membrane fragments from osmotically lysed cells augmented lymphocyte proliferation. Thus, jejunal IEL could be activated by mitogen and proliferated as much as PB T lymphocytes if exposed to a membrane component found on SRBC.

Adult↗

PubMed1986

Effects of tumor type and burden on carcass lipid depletion in mice.

Cancer bearing is frequently accompanied by weight loss, yet the factors causing cancer cachexia remain unclear. This study compares how tumor type and tumor burden affect host carcass fat depletion. Nude mice were inoculated with human malignant melanoma, human colon adenocarcinoma, or murine sarcoma cells, or were noninjected controls. Body weights, tumor burdens, and carcass lipid contents were measured. Carcass weights of melanoma-bearing mice were significantly lower than those of sarcoma-bearing mice, mice exposed to colon cancer antigens but without tumor growth, or control mice (all p less than 0.02). The degree of carcass lipid loss in melanoma-bearing mice (mean tumor burden 3.5% of total body weight [TBW]) was almost three times that of sarcoma-bearing mice (p less than 0.05), which had more than twice the tumor burden (mean tumor burden 7.8% TBW). Exposure to colon cancer antigens without tumor growth resulted in essentially no carcass lipid depletion compared with control mice. These findings argue against a mass effect of tumor as being solely responsible for host fat mobilization and suggest that carcass lipid depletion in tumor-bearing nude mice is more a function of tumor type than of tumor burden.

Adenocarcinoma↗

PubMed1985

Diminished interleukin 2 production and receptor generation characterize the acquired immunodeficiency syndrome.

The Acquired Immunodeficiency Syndrome (AIDS) is a disease found primarily in homosexual men, consisting of opportunistic infections and tumors, and is due to an acquired T-cell defect. In the present report, we studied various T-cell functions which might serve to distinguish homosexuals with a symptom complex including lymphadenopathy from those with AIDS. T lymphocytes from the lymphadenopathy and AIDS patients had markedly depressed proliferative responses in the autologous (auto) and allogeneic (allo) mixed lymphocyte reaction (MLR) compared to healthy homosexuals or heterosexual controls (P less than 0.001). Since proliferation in the MLR depends upon interleukin 2 (IL-2), a T-cell growth factor, we studied the production of and response to IL-2 in various groups of homosexuals and heterosexual controls. IL-2 production was markedly depressed in the lymphadenopathy and AIDS patients, 1.0 and 0.1 U/ml, respectively, compared to the healthy homosexual or heterosexual controls, both 5.0 U/ml (P less than 0.05 and P less than 0.01, respectively). Although the auto MLR of the lymphadenopathy patients rose to control values with the addition of exogenous IL-2, the auto MLR of the AIDS patients did not (P less than 0.01). This lack of responsiveness to IL-2 in the AIDS group was due to their inability to generate IL-2 receptors as shown by the absence of IL-2 absorption by activated cells and the absence of the Tac antigen (IL-2 receptor) on these same cells. The T4+ and T8+ T-cell subsets from the AIDS patients each demonstrated depressed IL-2 production and responsiveness following activation with autologous cells or mitogen, as well as the absence of Tac antigen. The diminished T-cell proliferation in the auto MLR in the lymphadenopathy group is associated with one defect, low IL-2 production, while the depressed proliferation in the AIDS group is associated with two defects, low IL-2 production and a lack of IL-2 receptor generation. These studies demonstrate that IL-2 receptor generation helps distinguish homosexuals with lymphadenopathy from those with AIDS, and that in addition to T-cell defects in the OKT4+ T-cell subset there are significant abnormalities in the OKT8+ T-cell subset in AIDS patients.

Acquired Immunodeficiency Syndrome↗

PubMed1985

Sheep red blood cells enhance T-lymphocyte proliferation.

Small numbers of sheep red blood cells (SRBC) markedly augmented the proliferation of T lymphocytes activated by antigens or mitogens. This effect occurred with as few as one SRBC per T lymphocyte and with intact or osmotically lysed red cells. When increasing numbers of SRBC was added to T lymphocyte cultures stimulated with PHA or autologous cells, T lymphocyte proliferation peaked sharply at 10 to 50 SRBC per T cell. The SRBC did not influence resting T-lymphocytes. Rather, the effect occurred after T lymphocyte activation during cell division. There was a detectable increase in interleukin 2 (IL-2) receptor generation but not in IL-2 production by activated T lymphocytes cultured with SRBC versus medium alone. Finally, anti-T11 antibody could inhibit the SRBC enhancing effect on T-lymphocyte function, suggesting that an empty erythrocyte (E) receptor on the T lymphocyte was necessary for the SRBC action.

Animals↗

PubMed1984

Does early diagnosis and delivery in acute fatty liver of pregnancy lead to improvement in maternal and infant survival?

Two cases of acute fatty liver of pregnancy resulting in maternal and infant survival are described. There have only been six such cases reported previously. The two described here are unique because the diagnosis was made prepartum by an oil red O stain of a frozen section of a liver biopsy, and the patients were promptly delivered by cesarean section under spinal anesthesia. The role of early diagnosis and delivery in this disease is discussed.

Acute Disease↗

PubMed1984

T-cell abnormalities in inflammatory bowel disease are mediated by interleukin 2.

Inflammatory bowel disease (IBD) may be an immunologically mediated disorder in which T cells are unable to respond appropriately to cell surface-associated antigens. To test this possibility, 37 patients with IBD, 24 with Crohn's disease and 13 with ulcerative colitis who were not being treated with immunosuppressive therapy were studied. The ability of T cells to proliferate in response to autologous or allogeneic cells, i.e., the autologous or allogeneic mixed-lymphocyte reaction (MLR) was tested. The autologous MLR was depressed using patient cells compared to control cells, regardless of disease type or activity (1564 +/- 223 cpm versus 3300 +/- 381 cpm, P less than 0.05) while the allogeneic MLR was depressed in patients with active disease only (29,833 +/- 2871 cpm versus 46,799 +/- 3340 cpm, P less than 0.01). The ability of T cells to recognize and lyse allogeneic cells, allogeneic cell-mediated lympholysis (CML), was also low in patients with active disease (24 +/- 4% versus 37 +/- 3%, P less than 0.05). Since T-cell proliferation and cytotoxicity depend upon adequate production of and response to a T-cell growth factor, interleukin 2 (IL-2), IL-2 production and responsiveness in IBD were studied. IL-2 production by patient T cells in response to phytohemagglutinin was only 39% of control values, P less than 0.05. The response to IL-2 was measured by the increase in T-cell proliferation in the autologous MLR in medium alone or medium supplemented with IL-2. Control T-cell proliferation rose from 3300 +/- 381 cpm to 10,761 +/- 428 cpm with exogenous IL-2 (P less than 0.001). Patient T-cell proliferation rose from 1564 +/- 223 cpm to 6817 +/- 771 cpm with IL-2 (P less than 0.001) but did not reach the level of the IL-2-supplemented control autologous MLR (P less than 0.05). In addition, the percentage of activated patient T cells having Tac antigen (IL-2 receptor) was depressed (P less than 0.05). These findings did not vary with disease type or activity. It is concluded from these data that peripheral blood T lymphocytes from patients with IBD have a diminished response to cell surface antigens which is associated with a decrease in IL-2 production and receptor generation. These defects may be responsible for the depressed T-cell proliferation and cytotoxicity that accompany IBD.

Adolescent↗

PubMed1983

Pneumatic dilatation in patients with symptomatic diffuse esophageal spasm and lower esophageal sphincter dysfunction.

Nine patients with severe symptoms of diffuse esophageal spasm and lower esophageal sphincter dysfunction who were unresponsive to medical therapy and bougienage dilatation were treated by forceful pneumatic dilatation. Treatment with pneumatic dilatation in eight of the nine patients produced a marked improvement in dysphagia and regurgitation (average follow-up of 37.4 months). Esophageal motility performed up to three years (average 12.4 months) after clinically successful pneumatic dilatation revealed a decrease in lower esophageal sphincter pressure from 34.0 +/- 4.0 mm Hg (mean +/- standard error) to 19.2 +/- 2.7 mm Hg (P less than 0.01). There were no significant changes in either the percentage of lower esophageal sphincter relaxation or the type of esophageal motor pattern. We conclude from this study that pneumatic dilatation is an effective form of therapy for a select group of patients with severe symptomatic diffuse esophageal spasm with lower esophageal sphincter dysfunction who are unresponsive to conventional medical therapy.

Adult↗