Plasma and tissue histamine in equine grass sickness.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J M Hunt.
Explore the source record for details and available documents.
The acute change in pulmonary artery pressure in response to oxygen may have prognostic value for patients with chronic obstructive pulmonary disease treated with long term domiciliary oxygen. A study was carried out to elucidate the mechanism of the acute cardio-respiratory response to oxygen in such patients and to determine whether it can be quantified non-invasively. The effects of acute oxygen administration (100% for 20 minutes and 28% oxygen for 24 hours) were assessed by non-invasive means and right heart catheterisation in 17 patients with severe stable hypoxaemic chronic obstructive pulmonary disease. Measurements included change in the ratio of dead space to tidal volume (VD/VT), effective pulmonary capillary blood flow (by rebreathing and single breath soluble gas uptake: QRB, QSB), left ventricular ejection fraction (radionuclide ventriculography), and M mode echocardiographic estimates of ventricular diameters and fractional shortening. These values were compared with those obtained from right heart catheter measurements of pulmonary artery pressure, cardiac index (thermodilution and direct carbon dioxide Fick: QTD, QFICK), and pulmonary vascular resistance. Oxygen administration resulted in a significant fall in pulmonary artery pressure, QTD, and QRB and a significant increase in VD/VT. The fall in QRB after 100% oxygen breathing for 20 minutes correlated strongly with the fall in pulmonary artery pressure (r = 0.86). There was no correlation between the fall in pulmonary artery pressure and the fall in QSB or the risen in VD/VT. Left ventricular ejection fraction did not change significantly. Echocardiography was technically unsatisfactory because of lung hyperinflation. Apart from a possible relation between VO2max and fall in pulmonary artery pressure after 24 hours of 28% oxygen breathing (r = 0.49, p less than 0.1) none of the baseline respiratory function measurements predicted the fall in pulmonary artery pressure or QRB. It is concluded that the cardiopulmonary response to acute oxygen breathing in patients with hypoxic chronic obstructive pulmonary disease includes a reduction in pulmonary artery pressure and cardiac output and a redistribution of pulmonary blood flow, and that rebreathing measurements of effective pulmonary blood flow can be used to quantify this response non-invasively.
Formation of the N-(deoxyguanosin-8-yl)-aminofluorene adduct was studied in enzyme-altered foci induced by four different liver carcinogenesis models. Foci were detected and scored for enzyme phenotype by a computer-aided image overlay technique. Localization of the enzymes gamma-glutamyl transpeptidase, canalicular ATPase and glucose-6-phosphatase was performed by enzyme histochemistry, allowing identification of foci of seven different phenotypes. Patterns of foci obtained by image overlay were compared to in situ 2-acetylaminofluorene--DNA adduct distribution obtained by immunofluorescence. Foci were induced by the following models: (1) chronic feeding of 0.02% 2-acetylaminofluorene (2-AAF) for 8 weeks; (2) intubation of diethylnitrosamine (DEN) (10 mg/kg) 24 h after a 70% partial hepatectomy (PH), followed 8 weeks later by a diet containing 0.05% phenobarbital for 9 months; (3) intubation of DEN (10 mg/kg) 24 h after PH, followed by a diet containing 0.01% ciprofibrate for 5 months, and after an additional 4 months a diet containing 0.05% phenobarbital for 2 months; (4) maintenance for 7.5, 16.5 or 19.5 months after transplantation of DEN/2-AAF/PH ('Solt-Farber' protocol) donor liver cells into host rats receiving a brief 2-AAF/PH selective regimen then no further treatment until sacrifice. To test the capacity of both foci and morphologically normal livers to form DNA adducts, the animals in models 2-4 received a diet containing 0.02% 2-AAF for 5 or 6 days before sacrifice. In all of the enzyme-altered foci identified in models 1-3 there were no DNA adducts visible by immunofluorescence. Scattered groups of positive cells were occasionally seen in the otherwise dark foci induced by model 4. For technical reasons some enzyme-altered foci were not identifiable on the fluorescence-stained slides. In liver serial sections from rats in models 1-4, there were 75, 304, 125 and 68 enzyme-altered foci of seven different phenotypes which were identified as AF-DNA negative. In models 1 and 4 there were some additional adduct-negative foci not associated with any of the seven identified focus phenotypes. These studies demonstrate that loss of the ability to form DNA adducts in hepatic enzyme-altered foci is a common and very early biochemical adaptation to xenobiotic exposure in different hepatocarcinogenesis models. This adaptation also is retained by the majority of foci in later stages of hepatocarcinogenesis.
We report a case of tracheal papillomatosis in a 69-year-old woman who presented with stridor and functional evidence of large airway obstruction. She was successfully treated by endobronchial resection using a Neodymium Yag laser. This provided lasting symptomatic relief of dyspnea. Respiratory papillomatosis is a disease predominantly of the childhood larynx and its presentation with predominant tracheal involvement late in life is extremely uncommon. Laser therapy provides an extremely effective treatment modality for this condition.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Rat epoxide hydrolase (EH) (EC 3.3.2.3) is elevated in cells of premalignant liver lesions, and variable EH activity has been reported for hepatocellular carcinomas. To facilitate detection of altered EH levels in liver cells, an immunoblotting method was devised. Rabbit antiserum specific for rat EH was prepared and used to detect EH extracted from suspensions of normal liver cells and from hepatoma cell lines. Compared with normal liver cells, 3 rat hepatoma cell lines, 7777, HTC and 17X, showed virtually undetectable EH levels by immunoblotting. The immunoblotting results rule out the possibility that very low EH enzymatic activity in the hepatoma cells results from production of normal amounts of non-functional enzyme protein.
The cellular, biochemical, and genetic changes that occur in the liver of rats exposed to chemical hepatocarcinogens are reviewed. Multiple new cell types appear in the liver of carcinogen-treated rats including foci, nodules, ducts, oval cells, and atypical hyperplastic areas. The application of phenotypic markers for these cell types suggests that hepatocellular carcinomas may arise from more than one cell type, including a putative liver stem cell that proliferates following carcinogen exposure. Study of DNA, RNA, and proteins produced by hepatocellular carcinomas and putative premalignant cells has so far failed to identify a gene or gene product clearly associated with the malignant or premalignant phenotype. Understanding the cellular lineage from normal cell through putative premalignant cell to cancer is critical to understanding the process of carcinogenesis. Application of new immunological (monoclonal antibody, transplantation) and molecular biological (gene cloning, oncogene identification) approaches to this problem holds promise that the process of hepatocarcinogenesis will be better known in the near future.
The lethality of Listeria isolates was determined with normal adult mice and mice that were immunocompromised by treatment with 20 mg of carrageenan per kg. The mean 50% lethal doses (LD50s) of the pathogenic isolates were significantly lower (alpha = 0.05) in the immunocompromised mice than in the untreated mice, with an average reduction of 5.8 log10 units. In contrast, the mean LD50s of the nonpathogenic isolates were lower in the immunocompromised mice by an average of only 0.4 log10 unit, a difference that was not significant (alpha = 0.05). When immunocompromised mice were used, the LD50s of pathogenic Listeria monocytogenes isolates were lower than those of nonpathogenic L. innocua and L. seeligeri isolates by greater than or equal to 6 log10 units and lower than those of nonpathogenic L. ivanovii isolates by greater than or equal to 4 log10 units. Pathogenic L. monocytogenes isolates could be distinguished from nonpathogenic isolates by their ability to cause deaths in immunocompromised mice in 3 days at a dose of approximately 10(4) CFU per mouse. An alternative procedure using iron-overloaded mice failed to effectively differentiate pathogenic Listeria isolates.
Histological studies using paired immunofluorescence staining and peroxidase-anti-peroxidase staining were performed on sections of rat livers with an antiserum specific for the 2-acetylaminofluorene (AAF)-DNA adduct N-deoxyguanosin-(8-yl)-aminofluorene (dG-8-AF). This is the predominant adduct in rat liver DNA at 5 (80%) and 28 (100%) days of AAF feeding. Nuclear staining was observed in livers of male Fischer rats fed 0.02% AAF for these time periods, and was not present in livers of animals fed control diet or detected when specific antiserum, first absorbed with the immunogen adduct, was utilized. In addition, nuclear staining was unchanged after incubation with RNase and abolished after incubation with DNase. Adducts were not readily detectable when whole-liver adduct concentrations were less than an average of 10(5) adducts per cell (30-50 fmol/micrograms DNA). The overall pattern of adduct distribution in livers of AAF-fed animals was distinctly non-uniform. A predominance of nuclear staining was found in the periportal areas by both immunofluorescence and immunoperoxidase procedures. In contrast, staining was very weak in the centrilobular areas. When animals were fed AAF for 28 days and control diet subsequently for 7, 14, 21 or 28 days, the overall intensity of the immunohistochemical staining decreased with time on control diet. However, the pattern of localization remained the same as in livers of rats fed AAF for 28 days, with the predominance of adducts being in the periportal areas. In male rats fed 0.02% AAF for 8 weeks, foci positive for gamma-glutamyltranspeptidase (GGT) became apparent, and the nuclei in these areas showed no immunofluorescence, indicating the absence of detectable levels of the dG-8-AF adduct. Twenty adduct-negative areas in the median lobes of three rat livers were positive for GGT, which suggests that loss of ability to form adducts in these regions occurs concomitantly with early phenotypic changes.
Explore the source record for details and available documents.
An experimental model of postoperative ileus was developed in ponies using trauma to, and exposure of, a length of small intestine which gave rise to a reproducible and reversible set of changes in gut activity. This was assessed by recordings of electrical and mechanical activity and by propulsion of spheres from stomach to anus. Activity was depressed, especially in the stomach and colon, and transit was slowed. All drugs given increased electromechanical activity but propranolol was the least effective and did not alter the delayed transit of spheres. Yohimbine was more effective and the addition of bethanechol produced a little extra propulsive action. Metoclopramide had the best effect, virtually returning transit to normal and was the only drug fully restoring coordination of gastric and small intestinal activity which was disrupted by the ileus procedure. Loss of gastroduodenal coordination is probably the central lesion in equine ileus and may be mediated by dopamine.
A survey of 259 surgical colic cases revealed that over 50 per cent of fatalities occurred in the postoperative period. Postoperative ileus and circulatory/endotoxaemic shock accounted for 70 per cent of these deaths. Other less important complications were salmonellosis, long bone fracture, adhesions, haemorrhage, laminitis, wound infection and ischaemic muscle damage. Close monitoring of postoperative progress is necessary to enable early diagnosis and treatment. Recent developments in understanding of the pathophysiology of endotoxic shock and ileus may lead to more successful treatment regimes. The possibilities include the use of cyclooxygenase inhibitors, anti-endotoxin hyperimmune serum and dopamine antagonists.
Explore the source record for details and available documents.
Prostaglandin E1 was infused intravenously (25, 50 and 75 ng/kg/min) in three ponies. Changes in gastrointestinal mechanical and electrical activity were recorded from chronically implanted strain-gauge force transducers and electrodes. Dose-dependent responses were obtained: there were significant decreases in electrical spiking activity in the stomach, left large colon and small colon, with a corresponding decrease of activity in the left dorsal colon mechanogram. The small intestine was also affected, showing a decrease in both contraction rate and amplitude, which was more marked in the proximal jejunum than in the ileum. There was an association between these changes in gastrointestinal activity and the presence of discomfort and diminished gut sounds.
Explore the source record for details and available documents.
The method of Doyle and Roman (Appl. Environ. Microbiol. 43:1343-1353, 1982) was compared with that of Lovett et al. (Appl. Environ. Microbiol. 46:459-462, 1983) for the ability to recover Campylobacter jejuni strains inoculated into raw milk at a concentration of less than 1 cell per g. The method of Lovett et al. gave significantly greater recovery proportions.