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Biomedical subjects

M A Fisher

Publications and source records attributed to M A Fisher.

At least 19 recordsLinked to original sources

An evaluation of abamectin given at turnout and six weeks after turnout for the control of nematode infections in calves.

Two groups of 16 set-stocked calves were used to evaluate a new strategy for the prevention of parasitic bronchitis and parasitic gastroenteritis. One group was left untreated while the calves in the other were treated with abamectin at 0.2 mg/kg at turnout and again six weeks later. The treatment prevented the output of nematode eggs and lungworm larvae in faeces for at least 70 days. The number of infective larvae subsequently appearing on the pasture was reduced by 90.2 per cent and the infectivity of the pasture (as monitored by tracer calves) by 96.0 to 99.8 per cent in the case of Dictyocaulus viviparus, 88.2 to 99.2 per cent for Ostertagia ostertagi and 69.3 to 98.1 per cent for Cooperia oncophora. Parasitic bronchitis occurred in the control calves and both bronchitis and gastroenteritis in the tracer calves grazing the paddock grazed by the control calves, but no disease occurred either in any of the calves treated with abamectin or in the tracer calves grazing the paddock grazed by these calves.

Animal Feed

Vrms/T quantitation: usefulness in patients with neuropathies.

This study evaluates the sensitivity of root mean square voltage (Vrms)/turns (T) ratios in neuropathies. Data were recorded with concentric needle electrodes from the biceps brachii, first dorsal interosseous, tibialis anterior, and calf muscles. Recordings were analyzed from 35 normal subjects as well as 24 consecutive patients referred for evaluation of neuropathic disorders. Direct tension measurements were not required. Reasoning from studies in normal subjects in which Vrms/T values were related to measurements of relative tension, the data were recorded during strong muscle contractions of less than 80% of maximum tension as monitored by mean amplitude values. For all 5 muscles, mean Vrms/T values > or = 1.0 calculated from four separate needle sites were significantly more frequent in the patients than controls (p < 0.012-0.0001). There were 13 muscles in which relevant conduction studies were abnormal and Vrms/T > or = 1.0 were the only abnormality of the needle EMG examination. In addition, a Vrms/T of > or = 1.0 was present in 10/14 muscles in which abnormalities might have been expected but where other needle EMG parameters were unremarkable and relevant nerve conductions normal. This study indicates that Vrms/T measurements can add meaningfully to the electrodiagnostic evaluation of neurogenic dysfunction.

Adult

Cytokine-induced upregulation of hepatic intercellular adhesion molecule-1 messenger RNA expression and its role in the pathophysiology of murine endotoxin shock and acute liver failure.

Neutrophil-induced liver injury during endotoxemia is dependent on the adhesion molecule Mac-1 (CD11b/CD18) on neutrophils. The potential involvement of its counterreceptor, intercellular adhesion molecule-1 (ICAM-1), in the pathogenesis was investigated after administration of 100 micrograms/kg Salmonella abortus equi endotoxin (ET) in galactosamine-sensitized mice (Gal). In ET-sensitive mice (C3Heb/FeJ), which generated large amounts of tumor necrosis factor-alpha (TNF-alpha), massive neutrophil infiltration and severe liver injury were observed. In an ET-resistant strain (C3H/HeJ), which did not generate TNF-alpha Gal/ET failed to cause neutrophil accumulation or injury. ICAM-1 messenger RNA (mRNA), negligible in control livers, was selectively induced by Gal/ET in ET-sensitive mice. Intravenous injection of murine TNF-alpha, interleukin-1 alpha (IL-1 alpha) or IL-I beta (13 to 23 micrograms/kg) strongly induced the ICAM-1 message in both strains, showing a comparable capacity for ICAM-1 mRNA synthesis. All cytokines caused similar neutrophil accumulation in the liver; however, only Gal/TNF-alpha also caused upregulation of Mac-1 on circulating neutrophils and liver injury. The anti-murine ICAM-1 monoclonal antibody YN.1 (3 mg/kg) attenuated liver injury in ET-sensitive mice by 67% to 90% compared with isotype-matched control antibody-treated animals but did not reduce neutrophil accumulation in hepatic sinusoids. Our data suggest that the cytokines TNF-alpha and IL-1 are the main mediators responsible for upregulation of ICAM-1 mRNA in the liver during endotoxemia. The upregulation of both adhesion molecules, ICAM-1 and Mac-1, is necessary for a neutrophil-induced liver injury to occur. (ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Activation of Kupffer cells and neutrophils for reactive oxygen formation is responsible for endotoxin-enhanced liver injury after hepatic ischemia.

The potential role of reactive oxygen species generated by Kupffer cells and neutrophils was investigated in a model of endotoxin-enhanced liver injury after hepatic ischemia. Male Fischer rats were subjected to 20 min ischemia and reperfusion of up to 24 h; .5 mg/kg Salmonella enteritidis endotoxin was injected at 30 min of reperfusion. The animals developed severe liver injury resulting in 50% hepatocellular necrosis at 24 h. Isolated Kupffer cells and neutrophils from the postischemic liver generated 10-fold more superoxide than cells from control livers. Treatment with gadolinium chloride (GdCl3) selectively reduced the capacity of Kupffer cells to generate superoxide by 65% and attenuated liver injury by 73% at 4 h and 58-69% at 24 h. Monoclonal antibodies against neutrophil adhesion molecules (CD11/CD18) had no effect on the early injury but reduced hepatocellular necrosis by 90-95% at 24 h. The antioxidant Trolox and the iron-chelator deferoxamine attenuated liver injury by 71 and 80%, respectively. It is concluded that Kupffer cells are mainly responsible for the initial injury, and neutrophils are the dominant cytotoxic cell type during the later phase. Reactive oxygen generated by both cell types is critical for this pathogenesis.

Animals

Normative F wave values and the number of recorded F waves.

F waves were recorded from the right abductor pollicis brevis of 11 normal subjects following 100 supramaximal stimuli. F wave data from sequential groups of 10 stimuli were analyzed. "True" values were considered those based on the results following all 100 stimuli. The F wave data evaluated were: minimal, mean, and median latencies; persistences (the percentage of F waves present in a series of stimuli); chronodispersion (CD) (the difference between minimal and maximal F latencies); mean F/M wave (mF/M) amplitudes; and repeater waves. F latencies appear normally distributed, and there is no statistical justification for using either median latencies or amplitudes. Following 10 stimuli, however, mean latencies are more reproducible than minimal values. In these normal data, results following 10 stimuli give latency measurements within 1 ms of "true" as well as for persistences; 20 stimuli will provide mean latencies within 0.5 ms of "true" as well as probable reasonable values (i.e., 80% of "true" or greater, for mF/M and the percentage of repeater waves; for CDs 80% of "true" or greater, 50-60 stimuli are needed; for the number of individual repeater waves, data from all 100 stimuli would be required. Analysis of repeater waves amplitudes would support a preferential activation of larger motor units in F waves.

Adult

Studies on the control of Toxocara canis in breeding kennels.

The control of Toxocara canis was investigated in naturally infected unweaned puppies. Anthelmintic treatments were administered to three litters of pups at 2, 4 and 6 weeks of age. When either a new combination anthelmintic containing febantel, pyrantel embonate and praziquantel or fenbendazole was used, the faecal egg output over the first 7 weeks of life was reduced by more than 80% and worm burdens by over 90%. In contrast, piperazine adipate had no appreciable effect on T. canis egg output, even though worm burdens were reduced by 86% by 7 weeks of age. In a further trial using three litters, the worm burden of pups treated with the combination anthelmintic was profiled before and after the 2 week dose and after the 4 week dose. Although worm numbers were substantially reduced by treatment, there was evidence of significant reinfection taking place throughout the control programme. It is concluded that more potent anthelmintics can provide longer term benefits by reducing the numbers of T. canis eggs shed into the environment, but that multiple dosing remains essential for this purpose.

Aging

Beneficial effects of extracellular glutathione against endotoxin-induced liver injury during ischemia and reperfusion.

The potential beneficial effect of hepatocellular glutathione against inflammatory liver damage was investigated in a model of endotoxin-enhanced ischemia-reperfusion injury. Animals were subjected to 20 min of hepatic ischemia, followed by 4 hr of reperfusion. The injection of 0.5 mg/kg Salmonella enteritidis endotoxin potentiated liver injury and the postischemic oxidant stress, as indicated by increased plasma levels of glutathione disulfide. Depletion of hepatic glutathione levels by > 90% with phorone and inhibition of glutathione synthesis with buthionine sulfoximine further increased liver injury in this model, as indicated by enhancement of plasma alanine aminotransferase activities from 2,234 +/- 122 U/L to 4,024 +/- 282 U/L. Continuous infusion of a glutathione (GSH) solution in GSH-depleted animals (22 mumol/kg/hr) attenuated reperfusion injury by 55%. In vitro experiments demonstrated the capability of GSH to react rapidly with reactive oxygen species, such as hydrogen peroxide (H2O2) and hypochlorous acid (HOCl). Only H2O2 oxidized GSH quantitatively to its disulfide; HOCl oxidized GSH to higher oxidation states. These data support the hypothesis that the enhanced release of hepatocellular GSH functions as a defense mechanism against reactive oxygen species generated by inflammatory cells during endotoxemia and reperfusion. This internal defense system of the liver may be of general importance in preventing, or at least limiting, liver damage by reactive oxygen generated in particular by Kupffer cells during their physiological function to remove gut-derived endotoxin and bacteria.

Animals

The 21-aminosteroid tirilazad mesylate protects against endotoxin shock and acute liver failure in rats.

The protective effect of the 21-aminosteroid tirilazad mesylate (U-74006F) was investigated in an experimental model of endotoxin shock and acute liver failure. In male Fischer rats subjected to 20 min of hepatic no-flow ischemia followed by reperfusion and injection of 0.5 mg/kg of Salmonella enteritidis endotoxin, severe hepatic injury developed, as indicated by a histological evaluation and liver enzyme release. Treatment with U-74006F (two bolus doses of 3 mg/kg each; the first dose was injected i.v. 30 min before ischemia and the second dose, at the time of reflow) reduced the hepatic injury by 60% at 4 hr of reperfusion, improved the survival rate from 18% to 55% and decreased the degree of hepatic injury at 48 hr of reperfusion. U-74006F treatment did not affect the extent of complement activation during reperfusion, the Kupffer cell-induced oxidant stress, or tumor necrosis factor-alpha formation in this model. U-74006F did not significantly reduce superoxide formation of Kupffer cells and neutrophils in vitro or in vivo. The substantial neutrophil infiltration in the liver during the pathogenesis was not affected at 4 hr of reperfusion but was attenuated by 70% at 48 hr. It was therefore concluded that, in the sequence of pathophysiological events, U74006F acted at a site distal to inflammatory cell activation and the generation of cytotoxic mediators. The protection against the initial endotoxin-enhanced reperfusion injury in the liver strongly inhibited the progression of the inflammatory response and subsequent liver failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Priming of phagocytes for reactive oxygen production during hepatic ischemia-reperfusion potentiates the susceptibility for endotoxin-induced liver injury.

Plasma levels of glutathione disulfide (GSSG) as an indicator of a vascular oxidant stress, tumor necrosis factor-alpha (TNF-alpha) formation, and liver injury (alanine aminotransferase activity, histology) were monitored in male Fischer rats after 30 min of hepatic ischemia followed by up to 4 hr of reperfusion. The injection of 1 mg/kg Salmonella enteritidis endotoxin at 30 min of reflow potentiated the postischemic oxidant stress and liver injury. TNF-alpha levels increased from 10 +/- 7 pg/ml (baseline) to 3,553 +/- 738 pg/ml after ischemia-reperfusion followed by endotoxin, or to 3,670 +/- 508 pg/ml after endotoxin alone. Depletion of serum complement before ischemia attenuated the endotoxin-mediated increase of reactive oxygen formation by 70% but did not affect TNF-alpha levels. Complement activation with cobra venom factor (CVF) during reperfusion had an effect similar to that of endotoxin on the oxidant stress and liver injury. CVF did not increase TNF-alpha formation during reperfusion. Kupffer cells and neutrophils isolated from the postischemic liver 2.5 hr after endotoxin injection generated 600% and 400% more superoxide, respectively, than cells isolated from control livers. The results demonstrate a substantial priming of hepatic phagocytes for reactive oxygen production but not TNF-alpha formation, even after short periods of hepatic ischemia, and the vulnerability of the postischemic liver to severe endotoxin-induced injury. Activated complement seems to be mainly responsible for the effects. These results may explain the high risk for hepatic failure after extensive liver resection and hypovolemic shock.

Adenosine Triphosphate

Prevalence of benzimidazole-resistance in equine cyathostome populations in south east England.

In order to study the prevalence of benzimidazole-resistance in equine cyathostomes, 30 stables in south east England were selected according to strict criteria but with minimum bias to provide three matched groups of 100 horses. One group was treated with fenbendazole, one with pyrantel embonate and the third was left untreated. The overall efficacies of fenbendazole and pyrantel embonate, as judged by the faecal egg-count reduction test, were 56.3 and 95.8 per cent, respectively. The numbers of horses at individual stables were too small to draw conclusions at each stable, but whereas efficacies greater than 85 per cent were recorded for pyrantel at 26 of 27 stables, the corresponding figure for fenbendazole was five of 27. Cyathostomes accounted for more than 90 per cent of the larvae cultured from faeces before and after treatment. Trichostrongylus axei was detected on 20 sites, but Strongylus species were present on only five. In the area of the survey, benzimidazole-resistance was very widespread in stables which used benzimidazole anthelmintics regularly and had more than nine horses per stable, but the benzimidazole-resistant cyathostome strains were adequately controlled with the non-benzimidazole anthelmintic pyrantel embonate.

Animals

AAEM Minimonograph #13: H reflexes and F waves: physiology and clinical indications.

Motoneurons can be activated both reflexly and antidromically following electrical stimulation of peripheral nerves. These H reflexes and F waves are clinically useful responses which interface at the level of the peripheral nerves and the spinal cord. Because these responses are commonly employed in the electrodiagnostic evaluation of patients, an understanding of their physiology and clinical applications is important. These are reviewed. Reasoning from the physiology, both the value and limitations of H-reflex and F-wave studies are considered for disorders of peripheral nerves, roots, and the central nervous system. Theoretical concepts about the physiology and pathophysiology of the nervous system based on H-reflex and F-wave data are also discussed.

Animals

Use of a triple-lumen catheter for umbilical venous access in the neonate.

We describe the use of a triple-lumen catheter inserted through the umbilical vein for infusion of vasoactive substances, fluids, and blood products, and also for withdrawal and exchange transfusion of blood and central venous pressure monitoring. Catheter malfunction occurred in 5 of 16 cases and was related to leaks or inability to draw blood via the desired port. No complications were attributable to catheter insertion or use.

Catheterization, Peripheral

Somatosensory evoked potential surgical monitoring. Observations during combined isoflurane-nitrous oxide anesthesia.

Somatosensory evoked potentials are used to monitor the integrity of the of the spinal cord during surgical procedures where the spinal cord is at risk. Changes in somatosensory evoked potential latencies and amplitudes can indicate impending structural damage. This use of somatosensory evoked potentials is complicated by the effects of nonsurgical factors, including anesthetics. Fifty patients were studied during surgery to determine the effects of coadministered isoflurane and nitrous oxide on cortical and subcortical somatosensory evoked potentials potentials following stimulation of the tibial and median nerves. Analysis revealed statistically significant correlations between expired isoflurane concentrations and prolongation of scalp and cervical latencies, and a negative correlation between nitrous oxide concentrations and scalp amplitudes. Scalp somatosensory evoked potential latencies were also positively correlated with procedure duration, unexplained by other variables. These data emphasize the complexity of interpreting somatosensory evoked potential changes during surgical monitoring, and indicate that separate, defined physiologic effects of an anesthetic can be manifest even when more than one anesthetic is administered.

Adolescent