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Biomedical subjects

M Bond

Publications and source records attributed to M Bond.

At least 73 records · Page 4Linked to original sources
PubMed1995

Altered subcellular Ca2+ regulation in papillary muscles from cardiomyopathic hamster hearts.

To investigate whether cardiac dysfunction in prefailure cardiomyopathic (CM) hamster hearts is due to Ca2+ overload or alternatively to decreased availability of Ca2+ in the sarcoplasmic reticulum (SR), the Ca2+ channel agonist, BAY K 8644, was used to compare the effects of increased Ca2+ influx on function and subcellular Ca2+ distribution in papillary muscles from hearts of 110-day-old CM and normal hamsters. A band, mitochondrial, and junctional SR Ca2+ were measured by electron probe microanalysis in CM and normal papillary muscles, which were either untreated or pretreated with BAY K 8644. Muscles were then rapidly frozen during contraction or relaxation. The results showed decreased tension development and decreased inotropic response to BAY K 8644 in CM muscles versus normals. There was no elevation of mitochondrial or A-band Ca2+ in BAY K 8644-treated or untreated CM muscles frozen during contraction or relaxation compared with similarly treated normals. In muscles frozen during relaxation, junctional SR Ca2+ was lower in both untreated and BAY K 8644-treated CM muscles versus comparably treated normals. These results do not support the hypothesis of an increased sensitivity to Ca2+ in hypertrophied, prefailure CM hearts but do indicate that less Ca2+ is available in the SR for activation of contraction.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1995

Arachidonic acid-dependent phosphorylation of troponin I and myosin light chain 2 in cardiac myocytes.

Recent evidence has suggested that arachidonic acid (AA) may be an important signaling molecule in cardiac excitation-contraction coupling. We previously showed that AA and endothelin-1 (ET) inhibit distinct K+ channels via protein kinase C-dependent pathways in rat ventricular myocytes. In addition, we demonstrated that Ca2+ transients in populations of fura 2-loaded myocytes were potentiated by AA and ET via activation of protein kinase C. In this study, we have used suspensions of [32P]orthophosphate (32Pi)-labeled rat ventricular myocytes to study the effects of AA and ET at the level of the myofilaments. After a 10-minute incubation of the labeled cells with phorbol 12-myristate 13-acetate (PMA), AA, or ET in the presence or absence of the protein kinase C inhibitor calphostin C, the myofibrillar proteins were separated by PAGE. Measurement of unloaded cell shortening using video edge detection in single electrically stimulated myocytes was also used to assess the effects of AA and ET on myocyte contractility. Incubation with either PMA, AA, or ET resulted in similar increases in 32Pi incorporation into troponin I (TnI) and myosin light chain 2 (MLC2), which was inhibited by preincubation with the protein kinase C antagonist calphostin C. In addition, the ability of these agonists to stimulate phosphorylation of TnI or MLC2 did not require extracellular Ca2+ or intact intracellular Ca2+ stores. The effects of AA and ET together on phosphorylation of TnI or MLC2 were not additive.(ABSTRACT TRUNCATED AT 250 WORDS)

Actin Cytoskeleton↗
PubMed1995

Effect of lovastatin on cholesterol content of cardiac and red blood cell membranes in normal and cardiomyopathic hamsters.

Lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A, is used therapeutically to lower plasma cholesterol levels. However, the effect of this therapy on cell membrane cholesterol in vivo is not known. The goal of this study was to investigate whether lovastatin treatment of hamsters decreases cholesterol in cardiac cell membranes and in red blood cell (RBC) membranes. Because abnormal cellular Ca++ regulation has been associated with altered membrane cholesterol in hearts of cardiomyopathic (CM) hamsters, we also measured the cholesterol content of cardiac and RBC membranes from lovastatin-treated and untreated Bio 14.6 CM hamsters to determine whether any differences existed with respect to normals. Sarcolemma-enriched cardiac membranes and RBC membranes were obtained from 42 to 45-day normal and CM hamsters after 13 days of lovastatin treatment (0.1% of food/day) and from untreated normal and CM hamsters. Plasma cholesterol, membrane cholesterol/phospholipid (C/PL) ratio and cholesterol per milligram of membrane protein (C/prot) were determined. In hearts from untreated CM hamsters, C/prot was significantly lower (P < .05) than in untreated normals. Lovastatin decreased plasma cholesterol by 76% and 81% in normal and CM hamsters, respectively (P < .001), but after lovastatin treatment, there was no significant change in C/PL or C/prot in cardiac membranes from either strain; there was also no significant decrease in C/prot or in C/PL of RBC membranes from normals or C/PL of CM hamster RBC membranes. However, lovastatin feeding resulted in a significant (P < .01) 24% decrease in C/prot of CM RBC membranes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

The violence management team. An approach to aggressive behaviour in a general hospital.

OBJECTIVES: To describe the establishment of a violence management team (VMT) to manage patients who exhibit violent behaviour in a general hospital (Flinders Medical Centre), and to review data collected in the first 44 months of operation. METHODS: The VMT consisted of a doctor, a senior nurse and four orderlies. Calls to the team were recorded and audited. Data were collected from patient case notes and supplemented, where necessary, with information from medical and nursing staff. RESULTS: There were 282 calls for the VMT during the study period, most often to patients with organic mental disorders (45%), substance abuse disorders (18%) and personality disorders (15%). In 30% of calls, verbal placation alone was sufficient to manage the patient; however, 62% of patients needed physical restraint (i.e., were physically held by team members) and 53% were administered a sedative medication. CONCLUSIONS: Violent behaviour in patients in a general hospital is an important problem, often caused by organic mental disorders. This, and the need to restrain aggressive patients so that they can receive essential medical care, suggest that such behaviour should be treated as a clinical problem rather than one for security guards or the police. The VMT provides a mechanism for dealing with aggressive patients which ensures good patient management, as well as protecting the health and safety of staff. It is also a monitor for quality assurance purposes, and provides data to determine the causes of patient violence and to implement prevention programs.

Diagnosis-Related Groups↗
PubMed1994

Infection with Pseudomonas cepacia in chronic granulomatous disease: role of nonoxidative killing by neutrophils in host defense.

Pseudomonas aeruginosa and Pseudomonas cepacia are catalase-producing bacteria, but only P. cepacia causes infections in patients with chronic granulomatous disease (CGD). The in vitro killing of P. aeruginosa and P. cepacia by polymorphonuclear leukocytes (PMNL) from patients with CGD and from healthy adults was assessed. Of 6 patients with CGD who developed severe infections with P. cepacia, 4 died. PMNL from the 2 survivors and 6 other patients with CGD killed P. aeruginosa strains efficiently and P. cepacia strains poorly. PMNL from 2 patients with autosomal recessive CGD and from 2 carriers for X-linked CGD killed P. cepacia intermediately between normal controls and patients with X-linked CGD. When superoxide anion and hydrogen peroxide were scavenged with superoxide dismutase and catalase, normal PMNL killed P. aeruginosa but not P. cepacia. Thus, P. cepacia, but not P. aeruginosa, is a pathogen in patients with CGD, because it resists neutrophil-mediated nonoxidative bactericidal effects.

Burkholderia cepacia↗
PubMed1994

Measurement of subcellular Ca2+ redistribution in cardiac muscle in situ: time resolved rapid freezing and electron probe microanalysis.

To directly assess the physiological roles of sarcoplasmic reticulum (SR) and mitochondria (MT), we have utilized energy dispersive electron probe microanalysis (EPMA) on ultrathin freeze-dried cryosections from isolated papillary muscles, rapidly frozen at precise time points of the contractile cycle. Using this approach, we can detect redistribution of subcellular Ca2+ during the cardiac contractile cycle. Changes in Ca2+ of less than 1.0 mmol/kg dry wt can be detected. By determining the variability of the Ca2+ measurements in preliminary experiments, we have also demonstrated that it is possible to optimize experimental design, i.e., to predict the number of animals per treatment group and the number of X-ray spectra per animal that are required in order to detect a specified Ca2+ difference. Quantitative EPMA of rapidly frozen contracting papillary muscle has also allowed us to correlate the Ca2+ content of SR and MT with the contractile state of the muscle. Our results show a decrease of 40% in the amount of Ca2+ stored in the junctional SR during a cardiac muscle twitch, thus providing direct evidence for a role of the SR as a primary site of Ca2+ release. In addition, we have demonstrated dissociation between MT Ca2+ uptake and activation of regulatory enzymes, such as pyruvate dehydrogenase, indicating that MT Ca2+ uptake is not required for activation of MT metabolism.

Animals↗
PubMed1994

Knee-joint proprioception during 30-day 6 degrees head-down bed rest with isotonic and isokinetic exercise training.

To determine if daily isotonic exercise or isokinetic exercise training coupled with daily leg proprioceptive training, would influence leg proprioceptive tracking responses during bed rest (BR), 19 men (36 +/- SD 4 years, 178 +/- 7 cm, 76.8 +/- 7.8 kg) were allocated into a no-exercise (NOE) training control group (n = 5), and isotonic exercise (ITE, n = 7) and isokinetic exercise (IKE, n = 7) training groups. Exercise training was conducted during BR for two 30-min periods.d-1, 5 d.week-1. Only the IKE group performed proprioceptive training using a new isokinetic procedure with each lower extremity for 2.5 min before and after the daily exercise training sessions; proprioceptive testing occurred weekly for all groups. There were no significant differences in proprioceptive tracking scores, expressed as a percentage of the perfect score of 100, in the pre-BR ambulatory control period between the three groups. Knee extension and flexion tracking responses were unchanged with NOE during BR, but were significantly greater (*p < 0.05) at the end of BR in both exercise groups when compared with NOE responses (extension: NOE 80.7 +/- 0.7%, ITE 82.9* +/- 0.6%, IKE 86.5* +/- 0.7%; flexion: NOE 77.6 +/- 1.5%, ITE 80.0 +/- 0.8% (NS), IKE 83.6* +/- 0.8%). Although proprioceptive tracking was unchanged during BR with NOE, both isotonic exercise training (without additional proprioceptive training) and especially isokinetic exercise training when combined with daily proprioceptive training, significantly improved knee proprioceptive tracking responses after 30 d of BR.

Adult↗
PubMed1994

Developmental supervision in health visiting.

Although supervision is supposed to be a helpful and supportive process, it is often seen as negative and critical. Meg Bond and Stevie Holland describe a developmental model of supervision, which can enhance health visitors' personal and professional development.

Community Health Nursing↗
PubMed1994

Isokinetic strength and endurance during 30-day 6 degrees head-down bed rest with isotonic and isokinetic exercise training.

The purpose of our study was to determine if an intensive, intermittent, isokinetic, lower extremity exercise training program would attenuate or eliminate the decrease of muscular strength and endurance during prolonged bed rest (BR). The 19 male subjects (36 +/- 1 yr, 178 +/- 2 cm, 76.5 +/- 1.7 kg) were allocated into a no exercise (NOE) training group (N = 5), an isotonic (lower extremity cycle ergometer) exercise (ITE) training group (N = 7), and an isokinetic (isokinetic knee flexion-extension) exercise (IKE) training group (N = 7). Peak knee (flexion and extension) and shoulder (abduction-adduction) functions were measured weekly in all groups with one 5-repetition set. After BR, average knee extension total work decreased by 16% with NOE, increased by 27% with IKE, and was unchanged with ITE. Average knee flexion total work and peak torque (strength) responses were unchanged in all groups. Force production increased by 20% with IKE and was unchanged with NOE and ITE. Shoulder total work was unchanged in all groups, while gross average peak torque increased by 27% with ITE and by 22% with IKE, and was unchanged with NOE. Thus, while ITE training can maintain some isokinetic functions during BR, maximal intermittent IKE training can increase other functions above pre-BR control levels.

Adult↗
PubMed1993

Arachidonic acid and endothelin potentiate Ca2+ transients in rat cardiac myocytes via inhibition of distinct K+ channels.

The release of arachidonic acid by phospholipases in response to cell surface receptor activation may be an important step in the initiation of inotropic events in cardiac muscle. Endothelin has been shown to activate phospholipase A2 and release arachidonic acid in isolated rat hearts. Endothelin also has a positive inotropic effect in cardiac muscle, suggesting that endothelin increases Ca2+ influx or the amount of Ca2+ released from the sarcoplasmic reticulum. We used suspensions of adult rat ventricular myocytes loaded with fura-2/AM to compare the effects of arachidonic acid and endothelin on Ca2+ transients evoked by extracellular ATP. We showed recently (Damron, D.S., and Bond, M. (1993) Circ. Res. 72, 376-386) that pretreatment of cardiac myocytes with arachidonic acid significantly potentiated the amplitude of the ATP-triggered Ca2+ transient. We now report that endothelin also enhances the ATP-triggered Ca2+ transient and that the effect of the combination of maximal doses of endothelin and arachidonic acid is additive. Neither endothelin nor arachidonic acid was found to affect the size of the sarcoplasmic reticulum Ca2+ store. The potentiating effects of both arachidonic acid and endothelin were sensitive to inhibitors of protein kinase C. Endothelin was also found to stimulate phospholipase C but not phospholipase A2. Application of arachidonic acid to individual cardiac muscle cells resulted in inhibition of the transient outward K+ current, whereas application of endothelin inhibited the delayed rectifier current. These effects of arachidonic acid and endothelin were additive, and both effects could be blocked by the protein kinase C inhibitor, staurosporine. Similarly, staurosporine inhibited endothelin-induced increases in isometric contractions in ventricular papillary muscle. We conclude that arachidonic acid and endothelin may be involved in the modulation of inotropic activity in cardiac muscle by means of protein kinase C-dependent inhibition of two distinct K+ channels. This would result in a prolongation of action potential duration and thus an increase in Ca2+ influx across the sarcolemma.

4-Aminopyridine↗
PubMed1993

The Defense Style Questionnaire.

The Defense Style Questionnaire has proven of interest as the first questionnaire to reliably describe defense styles. The 72-item DSM-III-R-labeled Defense Style Questionnaire was administered to 388 controls and 324 patients. Eight statistical and two a priori criteria were used in choosing two items to represent each of the 20 defenses. A new 40-item Defense Style Questionnaire is published together with normative and reliability data on a normal population, patients with anxiety disorders, and child-abusing parents. The scores are unaffected by the sex of the respondent, but the endorsement of immature defense styles decreases with age.

Adolescent↗
PubMed1993

Modulation of Ca2+ cycling in cardiac myocytes by arachidonic acid.

It is believed that inotropic agents exert their effects in cardiac muscle via a modulation of Ca2+ cycling; however, the involvement of phospholipase activation and the biochemical pathways participating in inotropic responsiveness remain unclear. The aim of the current study was to determine whether arachidonic acid and/or eicosanoids participate in inotropic responses by modulating Ca2+ cycling in cardiac myocytes. Experiments were performed with populations of freshly isolated, fura-2-loaded adult rat ventricular myocytes. Arachidonic acid stimulated a transient increase in cytosolic free Ca2+, which was still present after addition of EGTA but was significantly reduced by pretreatment with caffeine. Addition of arachidonic acid to either electrically stimulated or quiescent myocytes enhanced the amplitude of the ATP-induced Ca2+ transient. This effect was still observed in the presence of inhibitors of cyclooxygenase, lipoxygenase, and epoxygenase pathways but was significantly diminished after pretreatment with inhibitors of protein kinase C. In contrast, arachidonic acid attenuated the amplitude of electrically induced Ca2+ transients. This effect was mimicked by eicosatetraynoic acid and by the K+ channel agonist pinacidil. The inhibitory effect of eicosatetraynoic acid and arachidonic acid was reversed by addition of fatty acid-free bovine serum albumin. Together, these results suggest that arachidonic acid may play a physiological role in cardiac muscle excitation-contraction coupling as a modulator of sarcolemmal ion channels and/or Ca2+ release from the sarcoplasmic reticulum.

Adenosine Triphosphate↗
PubMed1992

Effect of inotropic stimulation on mitochondrial calcium in cardiac muscle.

Ca(2+)-dependent activation of citric acid cycle enzymes has been demonstrated in isolated cardiac mitochondria. These observations led to the hypothesis that Ca2+ is the signal coupling myofibrillar energy use to mitochondrial energy production in vivo. To test this hypothesis we have measured mitochondrial Ca2+ content during increased energy demand, using electron probe microanalysis. Mitochondrial Ca2+ was measured in hamster papillary muscles rapidly frozen at the peak rate of tension rise under control conditions and after stimulation with the beta-adrenergic agonist isoproterenol (10(-6) M). A third group of muscles was frozen after incubation in low (46.5 mM) Na+ solution to Ca2+ load the cells. Pyruvate dehydrogenase activity was measured in each of the muscles. Isoproterenol caused a 39% increase in force and a 43% increase in pyruvate dehydrogenase activity but no change in mitochondrial Ca2+ (0.46 +/- 0.19 (S.E.) mmol of Ca2+/kg, dry weight) compared with control (0.54 +/- 0.12). In contrast, low Na+ increased pyruvate dehydrogenase activity by 56% and also elevated mitochondrial Ca2+ to 1.28 +/- 0.31 (p less than 0.02). These results demonstrate that mitochondrial Ca2+ is not elevated after inotropic stimulation of cardiac muscle by beta-adrenergic agonists although pyruvate dehydrogenase activity is increased. We conclude that Ca2+ uptake by mitochondria is not a requirement for activation of mitochondrial respiration after increased energy demand.

Animals↗
PubMed1992

Fast axonal transport is modulated by altering trans-axolemmal calcium flux.

Factors involved in fast axonal transport (motor proteins, microtubules, organelles, etc.) have been identified but the molecular mechanism controlling transport is unknown. We used video enhanced microscopy to directly evaluate the effect of calcium on fast axonal transport (FAxT). FAxT alterations included rapid speed decreases (within minutes) in Ca2+ free buffer and rapid speed increases (within seconds) when axons were treated with parathyroid hormone, BAY K 8644, or K+ depolarization. The speed increases were blocked by dihydropyridine Ca2+ channel antagonists. Ryanodine (20 microM), known to block calcium release from subcellular stores, caused a decrease in the rate of retrograde FAxT. Calcium ionophore A23187 (at 1 and 20 micrograms/ml) caused increases in FAxT, an effect also noted only in retrograde moving organelle traffic. Hyper- or hypo-tonic solutions produced no alterations making axoplasmic viscosity changes an unlikely explanation for the speed changes. Reproducible alteration of FAxT by manipulation of Ca2+ levels provides evidence that Ca2+ modulates fast axonal transport. Retrograde transport appears more sensitive to changes in Ca2+ and differential effects on antero- and retro-FAxT mechanisms suggest directional specificity for some of these signals which may be based upon the organelle size. Endogenous substances (e.g. PTH) that trigger axonal Ca2+ changes may rapidly modulate the rate of material delivery in axons. The results are discussed within the context of a Ca2+/calmodulin-dependent modification of the cytoskeletal matrix.

Animals↗