PubMed Health⌕ Search

Biomedical subjects

R M Morgan

Publications and source records attributed to R M Morgan.

At least 19 recordsLinked to original sources
PubMed1995

Thoracic deformation and velocity analysis in frontal impact.

The objective of the present study was to measure dynamic chest deformations and compute chest velocity and viscous criterion during real world frontal impacts conducted on a horizontal sled. Four unembalmed human cadavers were restrained using a three-point belt restraint in the driver seat of a sled buck. Two chest bands (each with a 24 gauge capability) were placed on the thorax to record the temporal deformation patterns during impact. All tests were conducted at a velocity of approximately 50 kph. Biomechanical data were gathered digitally at a sampling rate of 12,500 Hz. Multiple rib fractures were identified in all specimens at autopsy. Analysis of approximately 800 temporal deformation contours of the thorax demonstrated regional differences. The overall mean maximum normalized chest deflections, maximum chest compression velocities, and peak viscous response variables ranged from 0.15 to 0.51, 1.79 to 4.87 m/s, and 0.15 to 1.95 m/s, respectively. These findings clearly illustrate the potential use of the chest band output to correlate injury with biomechanical variables and establish thoracic impact tolerance.

Accidents, Traffic↗
PubMed1995

Virulence of a Porphyromonas gingivalis W83 mutant defective in the prtH gene.

In a previous study we cloned and determined the nucleotide sequence of the prtH gene from Porphyromonas gingivalis W83. This gene specifies a 97-kDa protease which is normally found in the membrane vesicles produced by P. gingivalis and which cleaves the C3 complement protein under defined conditions. We developed a novel ermF-ermAM antibiotic resistance gene cassette, which was used with the cloned prtH gene to prepare an insertionally inactivated allele of this gene. This genetic construct was introduced by electroporation into P. gingivalis W83 in order to create a protease-deficient mutant by recombinational allelic exchange. The mutant strain, designated V2296, was compared with the parent strain W83 for proteolytic activity and virulence. Extracellular protein preparations from V2296 showed decreased proteolytic activity compared with preparations from W83. Casein substrate zymography revealed that the 97-kDa proteolytic component as well as a 45-kDa protease was missing in the mutant. In in vivo experiments using a mouse model, V2296 was dramatically reduced in virulence compared with the wild-type W83 strain. A molecular survey of several clinical isolates of P. gingivalis using the prtH gene as a probe suggested that prtH gene sequences were conserved and that they may have been present in multiple copies. Two of 10 isolates did not hybridize with the prtH gene probe. These strains, like the V2296 mutant, also displayed decreased virulence in the mouse model. Taken together, these results suggest an important role for P. gingivalis proteases in soft tissue infections and specifically indicate that the prtH gene product is a virulence factor.

Alleles↗
PubMed1993

Calcium antagonists and Bay K8644 promote depolarization of the rat heart mitochondrial membrane potential. Further evidence for a role in alteration of oxidative metabolism.

Studies were carried out using a tetraphenylphosphonium (TPP+)-selective electrode to monitor the effect of selected calcium (Ca2+) antagonists and the dihydropyridine Ca2+ agonist Bay K8644 on membrane potential (psi) associated with isolated rat heart mitochondria. Verapamil and diltiazem (10-500 microM), standard Ca2+ antagonists, produced a depolarization of both liver and heart mitochondria at concentrations > 150 microM. In contrast, nitrendipine (10-200 microM), a dihydropyridine compound, produced a concentration-related inhibition of psi in mitochondria from both sources, effects which were statistically significant at concentrations > 50 microM. Cinnarizine (10-100 microM) and bepridil (10-100 microM) also produced inhibition of heart psi, these effects being particularly noted in the presence of bepridil, where depolarization of the membrane was statistically significant with only 10 microM drug. The results indicate the complexity of action of these drugs at the mitochondrial level. In general, drug actions on psi appear to be correlated with previously reported effects on Ca2+ transportation rather than oxidative phosphorylation associated with rat heart mitochondria. The findings also illustrate that the mitochondrial actions of cardiovascular compounds may be of relevance in situ, particularly during ischaemia/reperfusion when mitochondria become loaded with Ca2+.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1992

Timing relationships for secondary ischemia in rodents: the effect of venous obstruction.

In a previous study, timing relationships were studied for flaps subjected to secondary ischemia by total pedicle interruption. In the current paper, using a rodent epigastric flap, a similar study for flaps subjected to secondary ischemia by venous obstruction was performed. These conditions were designed to mimic a venous thrombosis following flap transfer, as would be performed clinically. In Experiment 1, the time interval between primary and secondary ischemia was varied. When the interval was 72 hr, flaps with secondary ischemia had similar survival to those with primary ischemia. However, when the time interval was 24 hr, flap survival after secondary ischemia was significantly worse than after primary ischemia (p less than 0.01). In Experiment 2, the duration of primary ischemia was varied (15 min, 30 min or 1.5 hr), prior to a fixed interval between primary and secondary ischemia and 5 hr of secondary ischemia. These conditions produced significantly more necrosis than 5 hr of primary ischemia. Thus, even short periods of primary ischemia may have detrimental effects on flap survival after a subsequent period of secondary ischemia. This may have important clinical ramifications.

Animals↗
PubMed1992

Laparoscopic cholecystectomy: an initial community experience.

The initial 950 consecutive laparoscopic cholecystectomies performed in one city at four hospitals by 30 general surgeons are reported, covering a period from April 4, 1990 to April 3, 1991. There were two operative deaths (0.2%), three common bile duct lacerations (0.3%), two subhepatic abscesses, two bowel perforations, and three bile leaks, two requiring laparotomy. Seven episodes of bleeding occurred, of which five required laparotomy, but none involved a major vessel. Sixty-five procedures were converted to open (6.7%). The mean operative time was 85.4 min. Intraoperative cholangiography was adequately completed in 49.8% and not attempted in 30.3%. Thirteen patients (2.7%) were found to have common duct stones. The pathologic diagnoses were chronic cholecystitis in 784 patients (82.5%), acute cholecystitis in 145 (15.3%), and cancer of the gallbladder in one (0.1%). Hospital stays ranged from 4 h to 31 days (mean 49.5 h). This procedure can be learned and performed safely in a community setting.

Age Factors↗
PubMed1992

Treating cancer-related pain in the emergency department: the emergency nurse's role.

Ask for and believe the patient's report of pain, use a preventive approach, combine opioids and nonopioids when possible, and consider adjuvant drugs for neuropathic pain not relieved by an adequate trial of opioids and NSAID. Remain a patient advocate through careful assessment and reassessment of the patient and informative collaboration with the physician and other colleagues. Anticipate and treat side effects, and identify and address pain myths held by patients and families that interfere with sound pain management practices. Establish mutually set goals and direct the patient to necessary follow up. Emergency nurses can do much to alleviate unnecessary suffering and improve quality of life for patients with cancer who come to the emergency department for help.

Emergency Nursing↗
PubMed1991

Collaborative study of the International Office of Cocoa, Chocolate and Sugar Confectionery on Salmonella detection from cocoa and chocolate processing environmental samples.

A comparative collaborative study was performed in 13 laboratories to evaluate the use of motility enrichment on Modified Semisolid Rappaport-Vassiliadis medium for rapid Salmonella detection from food-processing environmental samples. Artificially contaminated chocolate scrapings and naturally contaminated cocoa bean dust samples were used in the study. Pre-enrichment was performed in buffered peptone water with added casein and malachite green oxalate. Motility enrichment was compared with a conventional cultural procedure using Rappaport-Vassiliadis broth and selenite cystine broth as selective enrichment. The productivity of motility enrichment was 93.5% compared to a productivity of the cultural procedure of 92%. Statistical analysis showed that there was no significant difference between the two procedures. Modified Semisolid Rappaport-Vassiliadis medium is a sensitive and simple diagnostic tool for the microbiological safety evaluation of food-processing environments.

Cacao↗
PubMed1991

Timing relationships for secondary ischemia in rodents: the effect of arteriovenous obstruction.

The first ischemic insult a tissue suffers is primary (1 degree) ischemia. A second ischemic episode, such as thrombosis after free tissue transfer, may be regarded as secondary (2 degrees) ischemia. Timing relationships were studied in a rodent epigastric-flap model. In a first experiment, the interval between 1 degree ischemia and 2 degrees ischemia was varied. Flaps which had 2 degrees ischemia 12 and 36 hr after the 1 degree episode, had decreased ischemic tolerance, compared with 1 degree ischemic flaps; 2 degrees ischemic flaps, after an interval of 72 hr, had an ischemic tolerance similar to 1 degree ischemic flaps. In a second experiment, the length of the 1 degree ischemia was varied. It was found that as little as 5 min of 1 degree ischemia significantly decreased the subsequent tolerance of 2 degrees ischemia. The possible clinical significance of these results is discussed.

Animals↗
PubMed1991

Ca2+ ion sequestration by guinea-pig tracheal cartilage: its influence on trachealis reactivity to KCl.

1. The contractile response of guinea-pig isolated trachealis to KCl has been studied in the presence and absence of cartilage. 2. Dissection of cartilage from the trachealis resulted in both a rightward displacement of the concentration-response curve to KCl (EC50 value: intact strip, 26.9 +/- 3.7 mM n = 5; dissected strip, 38.7 +/- 2.6 mM n = 5; P less than 0.05), and a reduction in the contractile response to KCl (30 mM) observed in a nominally Ca(2+)-free medium. 3. Removal of cartilage from the trachealis did not alter the responsiveness of the tissue to CaCl2 (2.5 mM) when added to K+ depolarized tissues. 4. Muscle-denuded cartilage rings were prepared by surgical removal of the trachealis muscle. Autoradiographic studies, and a direct comparison of Ca2+ (2.5 mM) uptake with that of sorbitol (2.5 mM) showed that cartilage per se had a high capacity to accumulate Ca2+ ions by a process which was resistant to iodoacetate (100 microM), diflunisal (100 microM) and boiling. 5. The uptake of 45Ca into isolated cartilage was unaltered by the addition of orthovanadate (500 microM), verapamil (10 microM), diltiazem (10 microM) or Bay K 8644 (10 microM), but was significantly reduced (P less than 0.05) in the presence of LaCl3 (1-10 mM). 6. We conclude, like previous studies, that cartilage may supply a pool of Ca2+ ions to airway smooth muscle during the generation of tension in a noninally Ca(2+)-free medium, and that LaCl3 may provide an experimental tool to elucidate further the role of non-muscle Ca(2+)-depots in smooth muscle contraction.

Animals↗
PubMed1990

Bay K 8644, modifier of calcium transport and energy metabolism in rat heart mitochondria: a new intracellular site of action.

1. The dihydropyridine Ca2+ channel agonist Bay K 8644 (10-200 microM) produced a concentration-dependent increase in State 4 respiration in the rat heart mitochondria with the highest concentration (200 microM) increasing the rate from 33.1 +/- 0.7 to 187.0 +/- 13.3 ng atoms O2 consumed min-1 mg-1 protein. 2. Bay K 8644 (200 microM) reduced State 3 respiration from 247.2 +/- 11.7 to 174.4 +/- 0.06 ng atoms O2 min-1 mg-1 protein, reduced the respiratory control index (RCI) from 5.3 +/- 0.45 to 1.1 +/- 0.03 and reduced the ADP:O ratio from 2.75 +/- 0.03 to 1.3 +/- 0.15. 3. A similar, but smaller, stimulation of State 4 respiration was seen with nitrendipine (25-200 microM), the rate increasing from 22.6 +/- 1.0 to 33.1 +/- 1.8 ng atoms O2 consumed min-1 mg-1 protein in the presence of 200 microM nitrendipine. 4. Bay K 8644 (10-60 microM) increased the total Ca2+ uptake into rat heart mitochondria, the total increasing from 248.8 +/- 8.4 to 406.9 +/- 17.6 ng Ca2+ mg-1 protein at 60 microM Bay K 8644 (EC50 = 18.9 +/- 1.4 microM). 5. Bay K 8644 (10-60 microM) produced a concentration-dependent reduction in the Ca2+ influx rate (IC50 = 52.5 +/- 2.8 microM). Similar effects were seen with (+)-Bay K 8644 and (-)-Bay K 8644. 6. Nitrendipine (40-120 microM) stimulated Ca2+ efflux from mitochondria preloaded with the ion; the efflux rate increasing from 2.9 +/- 0.05 to 114.2 +/- 6.2 nmol Ca2+ min-1 mg-1 protein (EC50 = 57.3 +/- 1.3 microM). 7. These data indicate dihydropyridine-induced changes in the activity of the mitochondrial Na+/Ca2 . antiporter pathway; nitrendipine causing stimulation and Bay K 8644 causing inhibition.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

Determination of the extent of ischemic damage and the effect of the calcium antagonist, verapamil following coronary artery ligation in the rat.

Apart from pharmacological interventions, four methods can be used to induce myocardial damage in the isolated, perfused heart. These are (i) total global ischemia, where perfusion is stopped completely; (ii) partial ischemia where perfusion is restricted; (iii) regional ischemia, produced by occlusion of the coronary circulation, and (v) hypoxia where the oxygenated buffer is replaced with a buffer bubbled with nitrogen. Using rat hearts, coronary artery occlusion was found to have potential as a screening device for antiischemic compounds. In these studies 45Ca uptake and enzyme release were found to increase with ligation time. The inclusion of the Ca2+ antagonist verapamil (0.01 to 1 microM) resulted in a concentration-dependent inhibition of 45Ca uptake (IC50 = 68 nM); however the proportion of tissue damaged remained unchanged. Similar findings were obtained in the presence of the dihydropyridine Ca2+ antagonist nicardipine (0.1 or 1 microM). Measurement of enzyme release during the reperfusion period confirmed significant correlations between levels of either lactate dehydrogenase (LDH) or creatine kinase (CK) and 45Ca uptake. Studies involving LDH show that cation uptake precedes enzyme release (r = 0.93; p = less than 0.001).

Animals↗
PubMed1988

Palmitoyl carnitine: an endogenous promotor of calcium efflux from rat heart mitochondria.

The effects of the fatty acid ester palmitoyl carnitine (PC) on mitochondrial Ca2+ handling and ATP synthesis are described. At low concentrations (5-40 microM) PC was found to produce changes in mitochondrial Ca2+ handling, the most significant effect (P less than 0.05) being the promotion of Ca2+ efflux (EC25 = 1.19 +/- 0.11 microM). Studies on mitochondrial substrate oxidation in the presence of either glutamate plus malate, or succinate, confirmed the ability of PC (10-100 microM) to cause loss of respiratory control as shown by reductions in the Respiratory Control Index for each substrate. It was concluded that the effect of PC on Ca2+ transport was due to a direct action on the Na+-Ca2+ antiporter system, whilst the effect on respiration was due to an uncoupling action.

Animals↗
PubMed1986

The effects of cadmium on succinate and NADH-linked substrate oxidations in rat hepatic mitochondria.

Low concentrations of cadmium (3.3-40 microM) inhibited State 3 NADH-linked respiration in rat hepatic mitochondria, but failed to release oligomycin (1 microgram) inhibited State 3 respiration, or to significantly change the State 4 rate. In the presence of succinate, 40 microM cadmium inhibited State 3 respiration by 89%, while concentrations between 3.3 and 13.3 microM stimulated State 4 respiration. Higher concentrations caused marked inhibition. In the presence of succinate, cadmium released oligomycin inhibited State 3 respiration. Cadmium (0.001-1.0 mM) did not stimulate mitochondrial ATPase activity or inhibit ferricyanide reduction, but stimulated NAD+ linked mitochondrial dehydrogenase activities and NADH oxidation. These results indicate that cadmium interacts with either the NADH dehydrogenase complex or other NADH-dependent enzymes and not solely by an uncoupling action.

Adenosine Triphosphate↗
PubMed1986

Cadmium content in selected rat tissues following treatments with cadmium chloride and/or gamma radiation.

This study was conducted to determine concentrations of cadmium (Cd) in various rat tissues; radiation effectiveness on Cd concentrations in rat tissues; and Cd effectiveness when radiation was applied as the second insult. Animals were subjected to Cd over a 29-day period and on Day 30 were exposed to an acute dose of 60Co gamma-ray. Rats were killed on Day 1, 7, or 21 following irradiation. Cd concentrations were determined by flame spectroscopy. Rats injected with Cd alone or Cd in combination with radiation showed a dose-dependent accumulation and retention of the metal in the liver and kidney over the intervals to sacrifice. Significantly smaller amounts of the metal were seen in the spleen, intestine, stomach, heart, testis, lung, blood, brain, and muscle. Generally, Cd did not afford protection against radiation in the tissues studied. Radiation, when used singly or as a coinsult with Cd, did not significantly alter the concentrations of Cd in any of the tissues studied except the heart, in which it contributed to the clearance of Cd. No synergistic or antagonistic effects were observed between Cd and ionizing radiation in any of the other tissues studied.

Animals↗
PubMed1984

Interaction of cadmium chloride and gamma irradiation on blood parameters of the young adult rat.

Two hundred and sixteen male Sprague-Dawley (S-D) rats, 80 +/- 5 days old and weighing 220-250 g each, were assigned at random to nine groups of 24 rats each. Rats were injected with cadmium (Cd) intraperitoneally every 3 days for 29 days for a total of nine injections. Injections doses were 0, 1.0, or 2.5 mg Cd kg-1 body wt. Twenty-four hours after the last Cd injection (Day 30), each rat received an acute whole-body 60Co gamma radiation dose of 0, 3.62, or 5.43 Gray (Gy) at a dose rate of 33.04 Gy min-1. The irradiated groups exhibited significant decreases in the total number of white blood cells (WBCs) and the percentage of lymphocytes. Significant increases were seen in the percentage of polyneutrophils, serum triacylglycerols (TG), serum iron, and serum lactate dehydrogenase (LDH). Cd-treated groups had increased total WBCs, percentage of polyneutrophils, and serum glutamate oxaloacetate transaminase (SGOT). Significant decreases were observed in the percentage of lymphocytes, hemoglobin, total number of red blood cells (RBCs), and hematocrit. In the co-insult, significant decreases were seen in the total number of WBCs and RBCs, the percentage of lymphocytes, hemoglobin, and hematocrit. Significant increases were observed in the percentage of polyneutrophils and serum iron. In general, Cd acted as a debilitator which enhanced the overall effect of ionizing radiation when applied as the second insult. On the other hand, Cd also provided protection against radiation; that is, some parameters such as total WBCs, serum TG, serum iron, and serum LDH were not as adversely affected by the co-insult as when radiation only was used. The mechanism of this Cd anomaly is not known.

Analysis of Variance↗