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Biomedical subjects

D J Cooper

Publications and source records attributed to D J Cooper.

At least 19 recordsLinked to original sources
PubMed1998

A smoking cessation programme conducted through dental practices in the UK.

OBJECTIVES: To assess the feasibility of using primary care dentists and the dental team providing smoking cessation advice in practice. DESIGN: A prospective study to examine the success of a smoking cessation programme. SETTING: 54 primary care dental practices in the UK. METHOD: Training and educational materials were supplied to members of the dental team and to potential recruits smoking 10 or more cigarettes a day. Recruitment was over 6 months and subjects were followed up for 9 months. In addition to dentists' counselling, nicotine patches were made available, on request, at cost price. Salivary cotinine assay was used for validation of smoking levels at initial counselling and 9 months after recruitment. RESULTS: 54 practices were enrolled but only 22 recruited patients. Records of 154 eligible patients were evaluated. Compliance to attend follow up clinics was poor--only 74 reported at 9 months. Among them 17 (11%) were successful in giving-up tobacco for 9 months as validated by patient histories and salivary cotinine assay. A large variation performance of the dental practices was noted. CONCLUSIONS: Motivated dentists with staff support and access to information on smoking counselling are able to contribute to tobacco control measures in the community. The success of this programme closely parallels those reported in general medical practice settings. In view of the very considerable attrition rates found at all levels of the programme in the present study and the uneven performance of the participating practices the quit rate reported here may not accurately reflect what could be achieved in an individual primary care setting.

Adult↗
PubMed1998

Quality assessment of the management of road traffic fatalities at a level I trauma center compared with other hospitals in Victoria, Australia. Consultative Committee on Road Traffic Fatalities in Victoria.

OBJECTIVES: Since 1992, the Consultative Committee on Road Traffic Fatalities in Victoria, Australia, has identified problems including those contributing to death and the potential preventability of deaths in road fatalities who survived until at least the arrival of ambulance services. The present analysis examines the outcomes at a Level I trauma center compared with other hospital groups in Victoria. METHODS: Between 1992 and 1994, 257 consecutive eligible fatalities were evaluated. Problems in management and preventable deaths were identified at the trauma center (TC) and in pooled data from other hospital groups, i.e., specialist teaching (Level II), other metropolitan (Level III), large regional (Level III), and small regional hospitals. RESULTS: Mean problems identified and those contributing to death (controlled for the number of areas of care), were less frequent at TC (1.7 and 0.6) than at other hospital groups (specialist teaching, 1.9 and 1.1*; metropolitan, 3.1* and 1.6*; large regional, 3.8* and 1.8*; small regional, 5.1* and 2.6*) (*p < 0.05 compared with TC). Preventable and potentially preventable deaths were also less common at TC (20%) than at the other hospital groups (specialist teaching, 40%*; metropolitan, 41%*; large regional, 53%*; small regional, 62%*) (*p < 0.05 compared with TC). When a Trauma and Injury Severity Score of 75% or more was used to define preventable death, a similar trend was identified. CONCLUSION: Management of patients with major trauma at a Level I trauma center was associated with fewer problems contributing to death and fewer preventable and potentially preventable deaths than at the different hospital groups. A trauma system in Victoria, including bypass of major trauma patients to designated hospitals with 24-hour trauma services, is likely to decrease the frequency of problems, including the preventable death rates.

Accidents, Traffic↗
PubMed1998

Optimal assessment of cervical spine trauma in critically ill patients: a prospective evaluation.

There is no uniformly accepted protocol for the radiological assessment of the cervical spine in critically ill trauma patients. The Alfred Trauma Centre receives about 40% of Victorian patients with major trauma. A protocol was developed for cervical spine evaluation, comprising three plain X-rays and a swimmer's view added when necessary to visualize C7-T1, CT and/or MRI for abnormal regions, and functional (flexion/extension) X-rays to exclude cervical spine instability due to soft tissue trauma. Functional X-rays were performed "actively" in conscious patients and "passively" in unconscious patients. One hundred consecutive patients were prospectively evaluated and 91 survived to complete data collection. Six (6.6%) had unstable cervical spine injuries--five detected with plain X-rays and one (1.1%) detected only with passive functional X-rays. Static cervical X-rays cost $93.00 per patient. Functional cervical X-rays added $42.00 per patient and were uncomplicated. Collar complications were common when collars remained on for more than 72 hours. This low detection rate is clinically important because of the enormous potential social and economic costs of missed unstable cervical spine fractures.

Adult↗
PubMed1998

The effect of manual lung hyperinflation and postural drainage on pulmonary complications in mechanically ventilated trauma patients.

This study questioned whether manual lung hyperinflation (MHI) and postural drainage reduced the incidence of nosocomial pneumonia or improved other outcome variables in mechanically ventilated trauma patients. Patients were withdrawn from the study if they developed nosocomial pneumonia according to a predetermined definition or on the clinical suspicion of nosocomial pneumonia by the attending intensivist. Of the 46 patients who fulfilled all the inclusion criteria and were enrolled into the study, 22 patients were randomized to group A (physiotherapy) and 24 patients to group B (control group). Twice as many patients were withdrawn in group B (8/24) compared with group A (4/22), although the differences were not statistically significant, [X2(1, 1) = 1.36, P = 0.24]. The length of time receiving mechanical ventilation and in the ICU was similar between the two groups and there were no differences in pulmonary dysfunction ("worst" daily PaO2/FiO2 ratio) between the two groups. There were no ICU deaths in either group. Physiotherapy as used in this study was not associated with a reduced incidence of nosocomial pneumonia based on standard clinical criteria. Nevertheless the trend to more frequent nosocomial pneumonia in the control patients suggests that a larger study in more severely injured patients with stricter clinical criteria for the definition of nosocomial pneumonia is indicated.

Adult↗
PubMed1997

A 16S rRNA gene oligonucleotide probe for identification of Bacillus thuringiensis isolates from sheep fleece.

Larvae of the Australian sheep blowfly Lucilia cuprina are susceptible to some strains of Bacillus thuringiensis, including some isolates from sheep fleeces from South Australia and Western Australia. Larvicidal strains of B. thuringiensis include var. thuringiensis, tolworthi, darmstadiensis, morrisoni, and toumanoffi. As part of an ecological study, a large number of B. thuringiensis fleece isolates from untreated sheep and sheep previously treated with larvicidal B. thuringiensis were screened for larvicidal activity. A ribotyping method to distinguish larvicidal B. thuringiensis jetted (sprayed) onto sheep from the natural B. thuringiensis flora of the fleece was developed. A cloned fragment of the 16S rRNA gene used as a probe for B. thuringiensis DNA digested with restriction endonucleases enables separation of B. thuringiensis serovars and separation within the serovars thuringiensis, tolworthi, and kurstaki. The 16S gene probe method is useful for distinguishing between reisolates of larvicidal B. thuringiensis jetted onto sheep and the background B. thuringiensis population present prior to jetting.

Animals↗
PubMed1997

Myocardial anaerobic metabolism occurs at a critical coronary venous PO2 in pigs.

We tested the hypothesis that the onset of myocardial anaerobic metabolism is fundamentally different from the whole body and other organs, where the onset of anaerobic metabolism occurs at a critical oxygen extraction ratio--not at a critical venous PO2. We measured oxygen saturation and PO2 of arterial and coronary venous blood at the onset of global myocardial anaerobic metabolism during progressive hypoxic hypoxia (n = 7) compared with carbon monoxide hypoxia (n = 7), which left-shifted the oxygen-hemoglobin dissociation curve. The onset of global myocardial anaerobic metabolism was defined by decreased myocardial lactate consumption and left ventricular contractility. Coronary venous PO2 was no different during hypoxic hypoxia and carbon monoxide hypoxia at equivalent arterial oxygen saturations, particularly at the onset of myocardial anaerobic metabolism (PO2 17.0 +/- 1.7 torr versus 15.9 +/- 2.2 torr, p = NS). However, the myocardial oxygen extraction ratio was significantly greater during hypoxic hypoxia than during carbon monoxide hypoxia at the onset of myocardial anaerobic metabolism (0.88 +/- 0.02 versus 0.65 +/- 0.04, p < 0.01). Thus, in contrast to the whole body where the onset of anaerobic metabolism occurs at a critical oxygen extraction ratio, the onset of myocardial anaerobic metabolism occurs at a critical coronary venous PO2.

Anaerobiosis↗
PubMed1997

Acute weakness syndromes in critically ill patients--a reappraisal.

Over the last twenty years, increasing numbers of critically ill, mechanically ventilated patients who develop acute profound muscle weakness have been described. These acute weakness syndromes have not been well understood and they have been given many names including: acute steroid myopathy, acute quadriplegic myopathy, the floppy person syndrome, critical illness polyneuropathy, critical illness polyneuromyopathy, and prolonged neurogenic weakness. Many of these "syndromes" either overlap or represent the same disease process in different patients. Many have been incompletely diagnosed. During this review it became evident that the acute weakness syndromes currently recognized in critically ill patients could be categorized into four major groups: myopathy, neuromuscular junction abnormalities, neuropathy and polyneuromyopathy. Each had different possible aetiologies. "Myopathy" includes acute necrotizing myopathy and disuse atrophy. Neuromuscular junction abnormalities are subdivided into myasthenia-like syndromes and prolonged neuromuscular blockade. Neuropathies are divided into critical illness polyneuropathy and acute motor neuropathy. The anterior horn cell injury in Hopkins syndrome should also be considered in this group. Polyneuromyopathies include various combinations of neuropathy and myopathy in the same patients.

Acute Disease↗
PubMed1995

Mass spectrometry of the humanized monoclonal antibody CAMPATH 1H.

Two mass spectrometric techniques, electrospray ionization (ESI) and matrix-assisted laser desorption ionization (MALDI) have been used to study the intact humanized monoclonal antibody CAMPATH 1H, its fully and partially deglycosylated species, and 13 fragments prepared from it. The transformed ESI mass spectra of the glycosylated species gave complex patterns of molecular masses (M(r's). These have been substantially assigned to the presence of a mixture of glycoforms, each resulting from the combination of a single protein species with specific glycans of four distinct masses. The MALDI mass spectra of the glycosylated species, with the exception of that of the smallest fragment Fc/2, which indicated the presence of three of the glycans, gave single M(r) values comparable to the mean M(r) calculated from the ESI results. The M(r) values for the 10 prepared nonglycosylated species support the validity of the published amino acid sequence for the antibody and define the cleavage sites for the enzymic fragmentations. It is concluded that mass measurement of the Fc/2 fragment using ESI techniques provides a convenient means of preliminary assessment of the major glycosylated entities.

Amino Acid Sequence↗
PubMed1995

Different effects of histamine H1 and H2 stimulation on left ventricular contractility in pigs.

Histamine decreases ventricular contractility in some settings but increases it in others. To better understand these apparently discrepant results, we measured hemodynamics and left ventricular pressure (Millar catheter) and volume (ultrasonic crystals) in atrially paced, alpha- and beta-antagonist-treated pigs. Histamine was infused (0.5-10 micrograms.kg-1.min-1) before and after H2-antagonist (ranitidine) pretreatment. Changes in left ventricular contractile function were measured as shift of the end-systolic pressure-volume relationship (delta ESPVR) at a pressure of 100 mmHg. We found that at low doses (0.5 and 1 micrograms.kg-1.min-1), histamine significantly decreased delta ESPVR (-1.1 +/- 1.4 ml, P < 0.05) after H2-antagonist pretreatment. At doses above 1 micrograms.kg-1.min-1, histamine increased contractility in a dose-response fashion [maximum effect: 5.1 +/- 3.3 ml, dose resulting in 50% effect (ED50): 0.75 +/- 1.79 micrograms.kg-1.min-1] that was best described using a Hill coefficient of 2. Ranitidine increased the ED50 by approximately one order of magnitude (0.75 +/- 1.79 to 9.50 +/- 2.60 micrograms.kg-1.min-1, P < 0.05). We conclude that in vivo, at higher doses, histamine increases left ventricular contractility via H2-receptor stimulation, whereas at low doses histamine decreases left ventricular contractility, probably via H1-receptor stimulation.

Animals↗
PubMed1994

On the analysis of bovine trypsin by electrospray-mass spectrometry.

In this paper the results obtained from an electrospray mass spectrometric (ES-MS) analytical study of commercial grade bovine trypsin are presented and discussed. It is proven, somewhat contrary to an earlier report, that ES-MS analysis may be performed routinely on a triple quadrupole mass spectrometer using the normal ES-MS raw data transformation procedures to identify and quantify the three forms of trypsin, namely, beta, alpha and psi, present in the samples. Further, it was found that all of the samples analysed contained small amounts of two peptides of M(r) = 5447 and 17,882 Da, which are postulated to originate from catalytic cleavage of alpha-trypsin by beta-trypsin.

Animals↗
PubMed1994

Decrease in left ventricular contractility after tumor necrosis factor-alpha infusion in dogs.

Whether systolic contractility or diastolic compliance changes soon after tumor necrosis factor-alpha (TNF-alpha) exposure is not known. Accordingly, we measured hemodynamics, left ventricular contractility using the slope of the end-systolic pressure-volume relationship, and diastolic pressure-volume relationships in six control dogs and in six dogs receiving 60 micrograms.kg-1.h-1 i.v. of TNF-alpha. Mean aortic pressure decreased by 22% 1 h after TNF-alpha infusion and remained decreased (P < 0.05). Cardiac output increased by 19% 1 h after TNF-alpha infusion and remained significantly greater than control values (P < 0.05). Left ventricular contractility decreased by 23% (P < 0.05) 1 h after TNF-alpha infusion and decreased by 52% (P < 0.01) 5 h after TNF-alpha infusion. The diastolic pressure-volume relationship did not change in the TNF-alpha group or the control group. Ejection fraction did not change after TNF-alpha infusion despite the decrease in contractility because afterload decreased. We conclude that TNF-alpha is important in causing the hypotensive, hyperdynamic circulation of sepsis. The new finding that left ventricular contractility is decreased shortly after TNF-alpha infusion suggests that TNF-alpha, or another mediator released very soon after TNF-alpha, is an important myocardial depressant factor.

Animals↗
PubMed1994

Tumor necrosis factor alpha decreases in vivo diaphragm contractility in dogs.

In this study, we hypothesized that tumor necrosis factor alpha (TNF alpha) is an important mediator of sepsis-related impairment in diaphragm contractility (1-2). In 12 anesthetized, ventilated dogs, bipolar stimulating electrodes were placed on the phrenic nerves and diaphragm electromyographic activity (EMG) and shortening were recorded with needle electrodes and piezoelectric crystals, respectively. Transdiaphragmatic pressure (Pdi) was also recorded using esophageal (Pes) and abdominal balloon catheters (Pdi = Pab-Pes). Dogs were randomized to receive saline injection (n = 6), or TNF alpha 60 micrograms/kg (n = 6). All parameters were recorded hourly for 6 h. Mean arterial blood pressure decreased 1 h after infusion in TNF alpha animals (p < 0.05) with no significant change thereafter. Cardiac output increased early after TNF alpha infusion (p < 0.05) and remained at greater than baseline values at study termination. Diaphragm pressure generation and costal shortening decreased progressively from 3 to 6 h post TNF alpha infusion (p < 0.05) with no significant change in control animals. Compound diaphragm action potential in response to supramaximal phrenic stimulation decreased in TNF alpha animals (p < 0.01) with no significant change in control animals 3 and 6 h postinfusion. We conclude that TNF alpha infusion was associated with significant declines in isotonic and quasi-isometric diaphragm contraction and that this could be explained, at least in part, by impaired neuromuscular transmission.

Action Potentials↗