Biomedical subjects

M Bundy

Publications and source records attributed to M Bundy.

11 recordsLinked to original sources

PubMed1994

Ursodeoxycholic acid modifies gut-derived endotoxemia in neonatal rats.

We developed a model for the translocation of intraluminal endotoxin in the neonatal animal and used it to examine the capacity of a nonhepatotoxic bile acid, ursodeoxycholic acid (UDCA), to modify endotoxin translocation and cytokine response. Three-d-old Sprague-Dawley rats were randomized to receive enterally either no drug, lipopolysaccharide (LPS, 1 mg/animal), or UDCA (400 micrograms/animal) alone, or UDCA followed by LPS 1 h later. One h after LPS administration, the rats were killed and plasma endotoxin and tumor necrosis factor (TNF) were measured. Control animals had low circulating endotoxin (21.2 +/- 7.6 endotoxin units) and TNF (0.06 +/- 0.02 ng/mL). Enteral administration of LPS 1 h before the rats were killed resulted in significant elevation of endotoxin (249.5 +/- 71.3, p = 0.008) and TNF (3.6 +/- 1.3, p = 0.019). UDCA alone did not alter endotoxin levels (8.7 +/- 2.1). UDCA 1 h before LPS prevented the rise in endotoxin (38.9 +/- 11.2 endotoxin units) and TNF (0.2 +/- 0.05) significantly. Chenodeoxycholic acid was studied in a similar group of experiments and prevented neither the translocation of LPS nor the development of increased TNF levels in animals receiving LPS. In conclusion, LPS can cross the intestinal barrier in the normal neonatal rat. UDCA, administered before LPS, can decrease the translocation of LPS and prevent the cytokine response as measured by TNF levels. We speculate that UDCA, administered prophylactically, might reduce morbidity in clinical conditions leading to gut-derived endotoxemia.

Animals↗

PubMed1990

Occupational disease surveillance of an aircraft rework facility.

Analysis of the 1987-1988 morbidity data of an aircraft rework facility's 6,672 employees identified 118 patients with occupational diseases. In our study, 61 cases (52%) involved eye and skin conditions. This was comparable to the State of California occupational diseases report. However, systemic conditions appeared to be higher (24% vs. 7%) in the study group, and this finding may need further investigation to clarify its significance. Patients employed as craftworkers accounted for nearly half of all reported occupational diseases. Federal workers in this facility appeared to have a higher percentage (70%) of "no time lost" when compared with that of the State of California report (54%). The utility of morbidity data in the prevention of occupational diseases is discussed.

Adolescent↗

PubMed1986

Production of monoclonal antibodies against human growth hormone releasing hormone and their use in an enzyme-linked immunosorbent assay (ELISA)

Two murine monoclonal antibodies (mAbs) specific for human growth hormone releasing hormone (GHRH-44-NH2) were produced from a fusion of spleen cells from a BALB/c mouse immunized with GHRH-conjugated BSA with SP 2/0 myeloma cells. The antibodies were of the IgG1 kappa, and IgG2b-kappa isotypes. The binding of both antibodies to GHRH-coated plates was inhibited by a 30-44 amino acid fragment but not by a 1-26 fragment. Thus, both antibodies are directed against the carboxy terminus of the peptide. Furthermore, both antibodies bind to the same epitope on the 30-44 amino acid portion since they cross-inhibit each other's binding to intact GHRH. Using these mAbs, a direct binding GHRH enzyme-linked immunosorbent assay (ELISA) was developed which had a least detectable dose of 30 pg. The availability of these antibodies and their use in ELISA methodology permits consistent and specific detection of GHRH in a non-isotope assay. They should prove of value in screening acromegalic patients for ectopic sources of GHRH secretion and in studies of ontogenic analysis of GHRH production.

Animals↗

PubMed1981

When are studies adequate for regulatory purposes? View of one regulated.

The question of adequacy of studies for regulatory purposes has been debated for years. Nine questions need answers to determine adequacy: (1) Does the study deal with a defined problem or a defined segment of it? (2) Do the study data justify the conclusions drawn? (3) Were appropriate statistical analyses used? Is there evidence of bias versus objectivity in the collection or analysis of data? (4) Does the study support, supplement (or complement) or refute information in the literature? Is the study truly new information? (5) Does the study conform to the Interagency Regulatory Liaison Group (IRLG) guidelines for documentation of Epidemiologic Studies? (6) Does the study stand up to peer review? (7) Have other investigators been able to confirm the findings by duplicating the study? (8) Is the study acceptable or can it be made acceptable for publication in a reputable scientific journal? (9) Is the problem of such magnitude or significance that regulation is required? Because there is no such thing as a risk-free environment or absolute safety and there is no definitive "yes" answer to each of the questions, the regulated would hope--yes, insist--that the regulators exercise judgement with great skill in promulgation of rules or regulations. The application of safety factors and the determination of acceptable levels of risk should be social decisions. A discussion of instances where the "regulated" believes that studies have not been adequate, or others habe been ignored, or misinterpreted for regulatory purposes in included.A method of settling controversial questions to eliminate the litigation route is proposed. Judgment which is so often eliminated by regulation needs to find its way back into the regulatory process. The regulated recognize the need for regulations. However, when these regulations are based on less than good scientific judgment, harm will be done to the regulatory process itself in the long run.

Air Pollutants↗

PubMed1976