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B L Hamilton

Publications and source records attributed to B L Hamilton.

At least 37 records · Page 2Linked to original sources
PubMed1987

Inhibitory control of proximal colonic motility by the sympathetic nervous system.

The purpose of this study is to determine whether or not the sympathetic nervous system provides a tonic inhibitory input to the colon in chloralose-anesthetized cats. Proximal and midcolonic motility were monitored using extraluminal force transducers. An intravenous bolus injection of 5 mg of phentolamine in 14 animals elicited a pronounced increase in proximal colon contractility. The minute motility index changed from 0 +/- 0 to 26 +/- 4 after phentolamine administration. Midcolonic motility also increased in response to phentolamine. Specific blockade of alpha 2-receptors, but not alpha 1-receptors, caused the same response seen with phentolamine. alpha-Adrenergic blockade increased colon contractility after spinal cord transection but not after ganglionic blockade. Blockade of alpha-adrenergic receptors was also performed before vagal and pelvic nerve stimulation and in both cases increased colonic motility. Vagal stimulation alone had no effect on colonic contractility, while pelvic nerve stimulation increased motility at the midcolon. alpha-Receptor blockade did not alter the ineffectiveness of vagal stimulation but did unmask excitatory effects of pelvic nerve stimulation on the proximal colon. All excitatory colonic responses were prevented by blocking muscarinic cholinergic receptors. These data indicate that tonic sympathetic nervous system activity exerts an inhibitory effect on colonic motility. The inhibitory effect is mediated through alpha 2-adrenergic receptors. Based on these findings, we suggest that alterations in sympathetic nervous system activity may be extremely important for the regulation of circular muscle contractions in the colon.

Acetylcholine↗
PubMed1987

Effect of maternal-fetal histoincompatibility on the weight of the feto-placental unit in mice: the role of minor histocompatibility antigens.

Female mice from four congenic strains were bred to males of the same four strains to determine the effect of maternal-fetal disparity at major histocompatibility complex (MHC) and the effect of non-MHC minor histocompatibility antigens on the weight of the feto-placental unit. An increase in feto-placental weights was found in all three of the four strains that could be evaluated when mother and fetus differed at multiple minor histocompatibility loci, irrespective of whether disparity at the MHC was present. No increase in feto-placental weights was found when mother and fetus differed at the MHC alone. The fact that these results were found in all strains studied suggests that the effect of maternal-fetal disparity at multiple minor histocompatibility antigens (minor HA) on the weight of the feto-placental unit is biologically significant. We conclude that if the increase in weight of the feto-placental unit results from immunostimulation, then minor histocompatibility antigens are the primary target of the maternal immune response to the histocompatibility antigens of the fetus.

Animals↗
PubMed1985

Maternal-fetal disparity at multiple minor histocompatibility loci affects the weight of the feto-placental unit in mice.

Inbred mice from selected unrelated and congenic strains were mated to determine the relative effects of maternal-fetal disparity at major histocompatibility complex (H-2) and non-H-2 minor histocompatibility antigens on the feto-placental unit at 14 days of gestation. A significant increase in weight of the feto-placental unit was observed only when mother and fetus differed at multiple minor histocompatibility loci. No increase in the weight of the feto-placental unit was observed when mother and fetus differed only at H-2. These results suggest that immunostimulation of the fetus results from a maternal response to minor histocompatibility antigens and not to H-2 antigens.

Animals↗
PubMed1985

Prevention of graft-versus-host disease using antibody to Thy 1. A role for complement in vivo.

An in vitro assay was used to determine whether mouse complement (C') was able to lyse T cells coated with a monoclonal IgM anti-Thy-1 antibody. Using lymph node cells (LNC) as targets, it was found that antibody-coated mature T cells were efficiently lysed by serum from C57BL/6, but inefficiently lysed by serum from BALB/c mice. Serum from both strains lysed antibody-coated thymocytes, demonstrating that BALB/c serum is not deficient in one of the C' components. The lytic activity of BALB/c serum could be improved by increasing the concentration of monoclonal anti-Thy-1 used to coat the target LNC. In contrast, serum from C5-deficient A/HeJ mice was unable to lyse either of the antibody-coated target cells in vitro. These in vitro results were confirmed in vivo using a model of lethal graft-versus-host disease (GVHD) induced to minor histocompatibility antigens. In this model, GVHD occurs when lethally irradiated mice are transplanted with bone marrow plus spleen cells from H-2-identical donor mice. GVHD is prevented when T cells are removed from the cells by in vitro treatment with anti-Thy-1 antibody plus rabbit C'. As predicted by the in vitro data, C57BL/6 mice were protected from GVHD when transplanted with LP cells treated with a 1:100 dilution of anti-Thy-1 antibody, but without complement, but BALB/c recipients of antibody-coated B10.D2/nSN cells were not. When the concentration of anti-Thy-1 used to coat the donor cells was increased to 1:50, 8 of 9 recipients were protected from GVHD. In contrast, none of the C5-deficient DBA/2 recipients of anti-Thy-1 (1:50 dilution) treated B10.D2 cells were protected from GVHD. Complement-mediated lysis appears to be the primary mechanism by which T cells coated with a monoclonal IgM anti-Thy-1 antibody are functionally inactivated in vivo.

Animals↗
PubMed1985

Reduction of lethal graft-versus-host disease: transplantation of cultured murine bone marrow across minor histocompatibility differences.

The murine bone marrow culture technique was used to prepare donor marrow for bone marrow transplantation across minor histocompatibility complex differences. Previous studies have shown that theta-positive cells are rapidly lost from such cultures and that transplantation of cultured marrow across major histocompatibility complex differences results in a delay in the development of lethal graft-v-host disease (GVHD). In this study, a total of 1 to 2 X 10(7) nonadherent cells (740 to 1560 CFUs [colony-forming units]) from three-day-old cultures were used as a source of donor marrow. Three strain combinations were evaluated; LP/J into C57BL/6; BIO.BR into CBA/J; and C57BL/6 into LP/J. Donor mice were immunized with recipient spleen cells prior to culture in order to increase the graft-v-host response. For LP/J marrow into C57BL/6 mice, 5 X 10(7) donor spleen cells transplanted along with the marrow were needed to induce lethal GVHD. However, lethal GVHD was seen without the addition of spleen cells for BIO.BR into CBA/J and C57BL/6 into LP/J strain combinations. Most animals receiving fresh marrow were dead of GVHD five weeks after transplantation. With the use of cultured marrow the three-month survival was 80%, 51%, and 93%, respectively, for LP/J into C57BL/6, BIO.BR into CBA/J, and C57BL/6 into LP/J strain combinations. Long-term donor engraftment in all recipient animals receiving cultured marrow was confirmed by analyzing hemoglobin polymorphisms between the strain combinations. These results demonstrate that in contrast to transplantation across major histocompatibility complex differences, the use of cultured cells for bone marrow transplantation across minor histocompatibility complex differences allows for engraftment while reducing the risk of lethal GVHD.

Animals↗
PubMed1984

Absence of correlation between cytolytic T lymphocytes and lethal murine graft-versus-host disease in response to minor histocompatibility antigens.

Lethally irradiated mice were transplanted with bone marrow plus spleen cells from H-2 identical donor mice. Five of the six recipient strains developed lethal GVHD, but the sixth strain did not develop any signs of GVHD. Spleen cells from all six transplanted strains were cytotoxic to recipient strain target cells in a short-term chromium release assay. The cytotoxic spleen cells were antigen-specific for recipient strain target cells, Thy-1+ and Lyt-2+--and some were also Lyt-1+. These data demonstrate for the first time that the presence of antirecipient cytotoxic T lymphocytes (CTL) does not correlate with lethal GVHD. Although CTL may contribute to the pathogenesis of GVHD in response to minor histocompatibility antigens, they do not appear to be the primary effector mechanism.

Animals↗
PubMed1983

Acute and chronic graft-versus-host disease induced by minor histocompatibility antigens in mice.

We have developed a murine model of acute and chronic forms of graft-versus-host disease (GVHD) as defined by clinical features that develop in response to minor histocompatibility antigen (minor HA) differences. C57BL/6J (B6) and LP/J mice were selected for serologic identity at H-2 and for mutual nonreactivity in mixed lymphocyte culture (MLC). Lethally irradiated B6 recipients were transplanted with anti-Thy-1.2-treated LP bone marrow cells plus various numbers of untreated LP spleen cells. The B6 recipient mice developed acute and chronic forms of GVHD that showed clinical and histological similarities to the acute and chronic forms of GVHD seen in human recipients of bone marrow transplants from HLA-identical and MLC-nonreactive donors. The definition of acute and chronic GVHD by clinical criteria appears to have biological significance in predicting subsequent survival patterns of recipient mice with GVHD. The incidence of acute and chronic GVHD in the mouse model was a function of the number of donor spleen cells transplanted. Using this model, we demonstrate that both acute and chronic forms of GVHD are initiated by donor lymphocytes. Based on these results, acute and chronic forms of GVHD induced to minor HA appear to be two manifestations of the same T-cell-mediated disease process rather than two different diseases.

Acute Disease↗
PubMed1983

Murine graft-versus-host skin disease: a chronologic and quantitative analysis of two histologic patterns.

Human graft-versus-host disease (GVHD) has several cutaneous manifestations, including a lichenoid and a sclerotic injury pattern. A versatile animal model of graft-versus-host skin disease (GVHSD) would facilitate study of the pathophysiology of these two cutaneous injury patterns. We have examined two murine chimeras histologically and have found two distinct patterns. Allogeneically transplanted B1/6 mice show a prolonged lichenoid-interface dermatitis that eventuates in clinical alopecia, whereas LP/J recipients of allogeneic cells do not show hair loss. Their histopathology consists of an early lichenoid phase that abates and is replaced by dermal sclerosis. Because of the versatility of the mouse as a laboratory animal, we feel that this model provides an excellent opportunity to define the immunopathologic mechanisms responsible for skin injury in GVHD. In addition, an understanding of the pathogenesis of the T cell-dependent, lichenoid, and sclerotic patterns of tissue injury in GVHSD might well provide insight into the pathogenesis of the GVHSD analogs, cutaneous lupus erythematosus and scleroderma.

Animals↗
PubMed1982

Kinetics of the anti-recipient cytotoxic cell response of mice with minor histocompatibility antigen graft-vs-host disease.

The kinetics of the anti-recipient cytotoxic cell response of spleen cells from mice undergoing graft-vs-host disease (GVHD) induced to minor histocompatibility antigens were studied. Two population of cytotoxic cells were identified. Cytotoxic T lymphocytes (CTL) were present in recipient spleens 2 and 3 wk after transplantation but disappeared from the spleens before the onset of clinical disease. Cytotoxic T lymphocyte precursors (CTLp) were first detected in recipient spleens 2 wk after transplantation and were present during clinical disease. CTL may function as effectors in GVHD induced to minor histocompatibility antigens.

Animals↗
PubMed1981

Angiomatous lymphoid hamartoma: inhibitory effects on erythropoiesis, growth, and primary hemostasis.

An 11-year-old boy was noted to have microcytic anemia, growth retardation, polyclonal hypergammaglobulinemia, and abnormal platelet function. An angiomatous lymphoid hamartoma was removed from the retroperitoneal space. Postoperatively the child exhibited a dramatic growth spurt and complete resolution of the abnormal laboratory measurements. Studies were performed before and after tumor removal to investigate the nature of the associated anemia, growth retardation, and altered hemostasis. There was no evidence of iron deficiency, thalassemia, or an antierythropoietin factor. Prolonged bleeding time and impaired ristocetin-induced platelet aggregation normalized following tumor resection. Serum obtained before surgery inhibited lymphocyte proliferation in mixed lymphocyte culture as well as fibroblast growth in vitro. Detailed study of growth regulatory hormones failed to reveal significant alterations except for significantly reduced somatomedin which normalized after surgery. The factor(s) which inhibit in vitro cellular growth and lower in vivo plasma somatomedin concentration remain unknown.

Adolescent↗
PubMed1981

Anti-recipient cytotoxic T lymphocyte precursors are present in the spleens of mice with acute graft versus host disease due to minor histocompatibility antigens.

A model for bone marrow transplantation across minor histocompatibility barriers was developed by using mouse strains that were H-2 identical and mutually non-reactive in MLC. Acute graft-vs-host disease was induced only when donor lymphoid cells were included in the marrow inoculum, in both C57BL/6 recipients of LP cells and BALB/c recipients of B10.D2/nSN cells. GVHD was prevented by treating the lymphoid cells with anti-Thy 1.2 and C before transplantation. Spleen cells from mice with acute GVHD were not directly cytotoxic to recipient strain target cells. However, when spleen cells from mice with GVHD were boosted in vitro to recipient strain stimulator cells they generated a specific anti-recipient cytotoxic response. Spleen cells from mice without GVHD did not generate a cytotoxic response in vitro. The cytotoxic effector cells and their precursors were shown to be T lymphocytes. This model and the in vitro method described may be useful in further studies of the immunobiology of GVHD due to minor histocompatibility antigens and of transplantation tolerance.

Acute Disease↗
PubMed1980

Neurons of the periaqueductal gray matter as revealed by Golgi study.

Neurons of the periaqueductal gray matter of the normal adult cat are classified into seven general types, Ia, Ib, II, IIIa, IIIb, IIIc, and IIId, based on the Golgi-Cox impregnated materials. Types Ia and Ib are spindle shaped bipolar neurons with one straight dendritic process forming varicosities and short stemmed spines. Type Ia is small in size and Ib is larger. The axon of each neuron emerges from another pole and projects beyond the PAG region. Occasionally it may share the origin with a dendrite or a tuft of dendrites. Type II, triangular shaped, had an apical dendrite that traverses a long distance within the PAG and an axon emerging from the basal portion and projecting beyond the PAG. Type IIIa, b, c, and d are pleomorphic multipolar neurons. Type IIIa has a rhomboid-shaped soma and dichotomically branching dendrites. Type IIIb has a spheroidal soma and short axons that terminate within the PAG. Type IIIc has a piriform soma and spiny dendrites that ramify perfusely and an axon which terminates within the PAG. Type IIId has the largest soma of all these neurons and the structure resembles an undifferentiated motor neuron of the CNS. Axons of the types IIIa and IIId are projecting in nature. Type Ia is found exclusively in the area immediately surrounding the aqueduct, the nucleus medialis. Types IIIc and IIId are found exclusively in the lateral region of the PAG which corresponds to the nucleus lateralis while the remaining cell types are found mostly in nuclei lateralis and dorsalis.

Animals↗