Search PubMed⌕ Search

Biomedical subjects

W Gilmore

Publications and source records attributed to W Gilmore.

32 records · Page 2Linked to original sources
PubMed1991

Aspergillus flavus and aflatoxins B1, B2, and M1 in corn associated with equine death.

Corn from an Arkansas farm, where three horses died and others became sick, was investigated for causative principles. Necropsy of the three horses revealed what appeared to be severe hepatic necrosis. Histopathological examination indicated a pattern of hepatic lesions that was suggestive of aflatoxin contamination of the feed. Mycological examination of the corn by dilution plating revealed 95% of the colonies as Aspergillus flavus. Chemical analysis of the corn for mycotoxins was positive for aflatoxin B1, B2, and M1 at concentrations of 114, 10, and 6 micrograms/Kg, respectively. Cyclopiazonic acid, sterigmatocystin, and the Fusarium toxins, vomitoxin (deoxynivalenol), T-2 toxin, and diacetoxyscirpenol, were not detected. The presence of aflatoxin metabolites in the moldy corn and the presence of appropriate lesions were compatible with the diagnosis, equine aflatoxicosis.

Aflatoxins↗
PubMed1990

Stressor induced variations of intracranial self-stimulation from the mesocortex in several strains of mice.

Intracranial self-stimulation (ICSS) from the mesocortex was assessed in BALB/cByJ, C57BL/6J and DBA/2J mice immediately, 24 h and again 168 h following stressor application. Stressor exposure failed to influence ICSS performance in C57BL/6J mice, while self-stimulation performance was reduced among BALB/cByJ mice only in the immediate post-stressor interval. In contrast, DBA/2J mice exhibited reduced rates of responding for brain stimulation at each of the post-stressor intervals. The potential contribution of DA alterations to the strain-dependent variations of ICSS performance induced by uncontrollable footshock are discussed.

Animals↗
PubMed1990

The enhancement of polyclonal T cell proliferation by beta-endorphin.

Beta-endorphin (beta-end) is a naturally occurring opioid peptide that has been implicated as a modulator of immune function. In this communication, data are presented to illustrate that beta-end enhances proliferation of murine splenocytes stimulated by the T cell mitogen, Con A. The T cell sensitivity of this effect was demonstrated in cell preparations enriched for T cells by nylon wool separation. The opioid specificity of the enhancement indicates that the C-terminus of the 31 amino acid peptide contributed significantly to the effect. In addition, the magnitude and the incidence of the enhancement was highly dependent on the concentration of Con A, the density of the tested cells and the timing of the addition of beta-end relative to that of Con A. These observations suggest that the state of activation of the T cell is a principal determinant of its sensitivity to beta-end. Overall, the data provide compelling evidence for the existence of an immunomodulatory role for beta-end.

Animals↗
PubMed1989

Evidence for a subpopulation of antigen-presenting cells specific for the induction of the delayed-type hypersensitivity response.

Young adult SJL mice (8 weeks of age or younger) do not mount a delayed-type hypersensitivity (DTH) response due to the failure of a macrophage antigen-presenting cell (APC) to induce TDTH effector cells. SJL mice that are 10 weeks of age or older produce a normal DTH response. This genetic defect provides a model for the investigation of functional subpopulations of APC which interact with specific subpopulations of T cells. In this study, we used this model to examine whether macrophage APC impairment involves APC-dependent immune responses other than DTH. No age-dependent differences were found in the ability of spleen cells from SJL mice to proliferate and synthesize interleukin-2 in response to concanavalin A; nor was the proliferative response to a variety of antigenic stimuli affected. In addition, no differences were observed in the contact sensitivity response or in the in vitro generation of allogeneic cytotoxic T lymphocytes (CTL). In contrast, the in vivo generation of allogeneic CTL was significantly depressed in 6-week-old SJL and could not be restored to normal by the adoptive transfer of macrophages from DTH responsive 12-week-old SJL mice. Finally, examination of the humoral response of 6-week-old SJL indicated no impairment in IgM or IgG serum antibody levels or in the induction of splenic B cells. Thus, the macrophage APC regulating the induction of TDTH effector cells does not appear to participate in the induction of T helper cells for other cellular and humoral responses. These data support the hypothesis that distinct subpopulations of APC may regulate the induction of specific immune effector mechanisms.

Animals↗
PubMed1988

Antigenic assessment of coronaviruses isolated from patients with multiple sclerosis.

Many studies have either supported or discounted the role of coronaviruses as etiologic agents in multiple sclerosis (MS). Two new approaches were applied to investigate this controversy. First, monoclonal antibodies specific for either murine coronaviruses (mouse hepatitis viruses) or human coronaviruses were used to characterize the antigenic features of MS-derived coronaviruses SK and SD. Both isolates were found to have a mouse hepatitis virus-type profile. Second, serum and cerebrospinal fluid antibodies to different coronaviruses, including SD, were measured in MS and control groups. No significant difference in antibody level to coronaviruses was found between MS and control samples. The results of these antigenic studies do not support a specific association between MS and coronaviruses.

Adult↗
PubMed1988

The effects of pertussis toxin and cholera toxin on mitogen-induced interleukin-2 production: evidence for G protein involvement in signal transduction.

GTP-binding proteins, known as G proteins, play important roles in transducing signals generated by the binding of specific ligands to cell surface receptors. We examined the possibility that a G protein is involved in transducing the concanavalin A (Con A) signal for IL-2 production using a T-cell hybridoma, FS6-14.13, and the bacterial toxins, pertussis toxin (PTX) and cholera toxin (CTX). These toxins are known to interact with and modify the functions of G proteins. High concentrations of PTX (25-50 micrograms/ml) stimulated IL-2 production in the FS-6 cells in the absence of Con A, presumably due to the ability of its B subunit to crosslink membrane proteins. However, in the presence of Con A, PTX inhibited IL-2 production at concentrations ranging from 0.05 to 50 micrograms/ml. It is unlikely that this inhibition was due to a competitive interaction between Con A and PTX for binding sites at the cell surface, since high concentrations of PTX only minimally reduced Con A-FITC binding, evaluated by FACS analysis. In addition, concentrations of PTX which were not able to stimulate IL-2 production in the absence of Con A, retained their ability to inhibit IL-2 production in the presence of Con A. These data suggest the involvement of the PTX A subunit in this activity. In support of this possibility, PTX catalyzed ADP-ribosylation of a Mr = 41,000-Da protein in FS-6 membranes. This strongly suggests that a PTX substrate is involved in transducing the Con A signal for IL-2 production in FS-6 cells. CTX also inhibited Con A-induced IL-2 production, an effect mimicked by the addition of dibutyryl-cAMP. This suggests that a CTX substrate linked to the adenylyl cyclase-cAMP pathway is probably not involved in transducing the stimulatory Con A signal, but may play a role in downregulating T-cell activation.

Adenosine Diphosphate Ribose↗
PubMed1988

Beta-endorphin enhances interleukin-2 (IL-2) production in murine lymphocytes.

Beta-endorphin has been reported to enhance T lymphocyte proliferation and cytolytic activity. In this report, it is demonstrated that beta-endorphin enhances the production of the T cell lymphokine, interleukin-2, from mitogen-stimulated, unfractionated murine splenocytes, as well from a cloned T cell line. The enhancement is naloxone irreversible and dependent on the integrity of the C-terminal amino acids, though the N-terminal amino acids appear to contribute to the potency of the enhancement. The data suggest that beta-endorphin interacts with a nonopioid receptor that has specificity characteristics similar to a nonopioid beta-endorphin receptor described in the central nervous system.

Adjuvants, Immunologic↗
PubMed1988

Oral melanoma with oral squamous carcinoma: report of a case.

A case of an oral melanoma occurring simultaneously with an oral squamous carcinoma has been presented. This combination is not thought to have been reported in the literature before. The histologic diagnosis is discussed as are the incidence, prognosis, and possible treatment of oral melanoma.

Carcinoma, Squamous Cell↗
PubMed1987

Characterization of the structural proteins of the murine coronavirus strain A59 using monoclonal antibodies.

Monoclonal antibodies reacting with the A59 strain of mouse hepatitis virus (MHV-A59) were characterized and those specific to the E2 major envelope glycoprotein were studied in detail. Antibodies were tested for their ability to neutralize viral infectivity (N+ characteristic) and prevent viral-induced cell-to-cell fusion (F+ characteristic). All four possible combinations of activities reflecting E2 functions were found, i.e., N+F+, N-F-, N+F-, and N-F+. In addition, competitive binding studies with these monoclonal antibodies revealed two nonoverlapping antigenic regions. The first region, designated A, was recognized by antibodies which included each of the four functional types. Region B was identified by a single monoclonal antibody with N-F- activities. The existence of antibodies which only neutralize virus or only block viral-induced fusion implies that the structures on E2 which serve as targets for neutralization and which induce fusion are not identical. The critical determinants for neutralization and fusion must be closely related topographically on E2 since both N+F- and N-F+ antibodies recognize the same antigenic region.

Antibodies, Monoclonal↗
PubMed1981

The effect of 13-cis-retinoic acid on hamster buccal pouch carcinogenesis.

In order to determine whether 13-cis-retinoic acid, an analog of vitamin A, has antitumor activity in an oral cancer model system, the following study was undertaken. Fifty-three adult hamsters were divided into four groups. Group 1 was tested with a 0.5 percent solution of 9,10-dimethyl-1,2-benzanthracene (DMBA) in heavy mineral oil, which was painted on the right buccal pouch three times per week for 12 weeks. Group 2 received DMBA plus 13-cis-retinoic acid (RA) incorporated into gelatinized beadlets and mixed with a powdered commercial diet (dosage, 300 mg per kilogram of diet). Group 3 received only RA; Group 4 received a placebo. The animals were killed at 6, 12, and 18 weeks and tissues were studied clinically and histologically in a routine manner. Results show that all groups receiving DMBA developed epidermoid carcinomas. However, there were several other changes. In the RA-treated animals, particularly those treated with DMBA, there was an ingrowth of surface epithelium with development of ductal structures in the buccal pouch. There were changes in surface epithelium, and there were dense aggregates of lymphoid tissue with development of exophytic nodules suggestive of lymphoma. Animals fed RA showed a relative weight loss. The findings suggest that there was a hypervitaminosis A state yielding prominent epithelial metaplastic changes but not affecting the progression or production of carcinoma.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1980

Postsurgical hemorrhage resulting from a drug-induced circulating anticoagulant: report of case.

A case of circulating anticoagulant resulting in persistent postoperative bleeding has been reported. All clotting factors were normal when the patient's plasma was tested in a high dilution. Unlike previous reports of this type of coagulation inhibitor, the hemorrhagic diathesis was clinically severe in comparison with the mildly abnormal in vitro tests. Many unknowns remain: the chemical nature of this anticoagulant; the time needed to return to normal coagulation levels; the frequency and severity of drug-induced anticoagulation; and the dose and duration of usage of medications resulting in circulating anticoagulants. In retrospect, the only clinical evidence suggestive of a coagulation problem in this case was a marginally elevated partial thromboplastin time. In our opinion, a preoperative coagulation screening, consisting of prothrombin time, partial thromboplastin time, platelet count, and template bleeding time, may help to prevent serious postoperative hemostatic complications.

Antibodies, Antinuclear↗
PubMedDate not supplied

The opioid specificity of beta-endorphin enhancement of murine lymphocyte proliferation.

Beta-endorphin (beta-end) is a potent analgesic peptide which exhibits a variety of pharmacological activities in the central nervous system (CNS) following binding of its N-terminus to specific opioid receptors. Although C-terminal binding sites for this 31-amino-acid peptide have been characterized in CNS tissue, identification of their possible function has been facilitated by studies of beta-end effects on lymphocyte activities. In this communication, we report a detailed analysis of the opioid specificity of the ability of beta-end to enhance T cell mitogen-induced proliferation in unfractionated murine splenocytes. Intact 31-amino-acid beta-end peptides from several species, including human, camel and rat, enhanced concanavalin A-stimulated [3H]thymidine uptake 50-640% in a dose-dependent, naloxone-irreversible fashion. The presence of the C-terminal amino acids was required for the enhancement activity, since met-enkephalin, alpha- and gamma-endorphin, and human beta-end 1-27 were ineffective. Accordingly, the truncated peptides, human beta-end 6-31 and 18-31, were also able to enhance the Con A response. However, human beta-end 18-31 was consistently not as effective as beta-end 6-31 or the intact 31-residue peptide. These data suggest that although the C-terminus contains the primary active sequence, the N-terminus contributes to the overall potency of the effect. In support of this assertion, N-acetylation, which abolishes opioid binding activity, resulted in a reduced magnitude of enhancement. The data suggest that beta-end interacts with a non-opioid receptor which has specificity characteristics strikingly similar to non-opioid receptors characterized in CNS tissue.

Amino Acid Sequence↗