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Biomedical subjects

D Isaac

Publications and source records attributed to D Isaac.

10 recordsLinked to original sources
PubMed2004

Child safety education and the world wide web: an evaluation of the content and quality of online resources.

The purpose of this study was to assess the content, quality, and type of internet resources available for safety education. Using 19 search engines with search strings targeting major forms of injury, identified resources were classified by audience group, accessibility, and authorship. Two independent reviewers rated each resource on the basis of its content and a set of quality criteria using a three point scale. Overall, 10 (18.2%) resources were of highest quality, four (7.3%) were intermediate, and 41 (74.5%) were not recommended. Eighteen months after the original search, 67.3% of all resources and 90% of the highest quality resources were still on the internet. This study provides a methodology for evaluating child safety resources on the world wide web and demonstrates that most internet resources for safety education are of dubious quality. A rating system such as the one developed for this study may be used to identify valuable internet materials.

Accident Prevention↗
PubMed2003

Failure of immunotherapy to prevent, arrest or reverse diabetic lumbosacral plexopathy.

Three patients are described who had severe and progressive diabetic lumbosacral plexopathy despite active immunosuppressive therapy. One patient developed the condition while immunosuppressed for a cardiac transplant and two others progressed while receiving intravenous gamma globulin. The cases raise questions about current unsupported practices of treatment for this condition. Robust clinical trial evidence is required before immunosuppression can be recommended.

Adult↗
PubMed2000

Comparison of vasopeptidase inhibitor, omapatrilat, and lisinopril on exercise tolerance and morbidity in patients with heart failure: IMPRESS randomised trial.

BACKGROUND: We aimed to assess in patients with congestive heart failure whether dual inhibition of neutral endopeptidase and angiotensin-converting enzyme (ACE) with the vasopeptidase inhibitor omapatrilat is better than ACE inhibition alone with lisinopril on functional capacity and clinical outcome. METHODS: We did a prospective, randomised, double-blind, parallel trial of 573 patients with New York Heart Association (NYHA) class II-IV congestive heart failure, left-ventricular ejection fraction of 40% or less, and receiving an ACE inhibitor. Patients were randomly assigned omapatrilat at a daily target dose of 40 mg (n=289) or lisinopril at a daily target dose of 20 mg (n=284) for 24 weeks. The primary endpoint was improvement in maximum exercise treadmill test (ETT) at week 12. Secondary endpoints included death and comorbid events indicative of worsening heart failure. FINDINGS: Week 12 ETT increased similarly in the omapatrilat and lisinopril groups (24 vs 31 s, p=0.45). The two drugs were fairly well tolerated, but there were fewer cardiovascular-system serious adverse events in the omapatrilat group than in the lisinopril group (20 [7%] vs 34 [12%], p=0.04). There was a suggestive trend in favour of omapatrilat on the combined endpoint of death or admission for worsening heart failure (p=0.052; hazard ratio 0.53 [95% CI 0.27-1.02]) and a significant benefit of omapatrilat in the composite of death, admission, or discontinuation of study treatment for worsening heart failure (p=0.035; 0.52 [0.28-0.96]). Omapatrilat improved NYHA class more than lisinopril in patients who had NYHA class III and IV (p=0.035), but not if patients with NYHA class II were included. INTERPRETATION: Our findings suggest that omapatrilat could have some advantages over lisinopril in the treatment of patients with congestive heart failure. Thus use of vasopeptidase inhibitors could constitute a potentially important treatment for further improving the prognosis and well being of patients with this disorder.

Angiotensin II↗
PubMed1999

Ascorbic acid is neuroprotective against global ischaemia in striatum but not hippocampus: histological and voltammetric data.

Following reports that ascorbic acid (AA) blocks NMDA receptors, we examined its possible neuroprotective properties in vivo (gerbil bilateral carotid artery occlusion model: BCAO) and in vitro (ischaemia-induced dopamine (DA) release in brain slices). Five minutes of BCAO caused substantial cell loss of 90-95% and 40-50% in gerbil CA1 hippocampus and striatum, respectively, measured in haematoxylin and eosin-stained sections, 5 days post-insult. AA (500 mg kg(-1) day(-1) i.p. for 312 days, first dose 1 h before occlusion) significantly (P<0.05) reduced striatal cell loss (from 40 to 13%) while only reducing CA1 cell loss from 95 to 88%. A lower dose (250 mg kg(-1) day(-1) i.p. for 312 days) was ineffective in either region. AA (750 mg kg(-1) day(-1) i.p. for 312 days) caused significant striatal protection (cell loss reduced from 49 to 20%) if treatment was initiated 1 h before occlusion. Initiation of treatment immediately post occlusion did not cause significant protection. Neither treatment regime protected CA1 hippocampus. In separate experiments we examined the effect of AA on DA release, monitored by voltammetry, in an in vitro model of striatal ischaemia. Four DA release variables were measured: T(on)--time from initiation of ischaemia to the onset of DA release, T(pk)--the time from onset of DA release to maximum, deltaDA/deltat--the mean rate of DA release and [DA](max)-- the maximum extracellular DA concentration. Control values in drug-naive slices were: T(on)=193+/-8 s, T(pk) = 24 +/- 4 s, [DA](max) = 69 +/- 6 microM and deltaDA/deltat = 4.2 +/- 0.7 microM s(-1) (means+/-S.E.M., n=15). 212 h pretreatment with AA (0.4 to 10 mM) did not affect T(on) or [DA](max) but increased T(pk) and decreased deltaDA/deltat (P<0.05) with an EC50 of 1.66 mM. NMDA (100 microM) shortened T(on). N-ethylmaleimide (20 microM) had no effect on the response to AA but potentiated the action of NMDA on T(on). AA (2 or 10 mM) had no effect on the response to NMDA. We conclude that AA is neuroprotective against global ischaemia in the striatum and that some of this action may be due to attenuation of ischaemia-induced DA release. This action is mediated neither by blockade of the NMDA receptor nor modulation of its redox status.

Alkylating Agents↗
PubMed1996

Integrating general practice and hospital services.

OBJECTIVES: To evaluate a model of negotiations between six Divisions of General Practice and four teaching hospitals, aimed at creating formal agreements to improve the GP-hospital interface. METHOD: The evaluation examined the model's outcomes and participants' experiences. Outcomes were investigated via unstructured interviews with key informants, and analysis of relevant documentation. Participants' experiences were elicited via structured interviews with 11 Divisional members and 14 hospital representatives. RESULTS: Progress towards agreements was made in all cases, with a full agreement being reached at one hospital. Negotiations are continuing in the remaining hospitals. Additional outcomes were achieved during the process, and included resources and structural arrangements involving GPs. Participants were satisfied with the model, but certain key issues were identified. CONCLUSION: This evaluation suggests that for negotiations between GPs and hospitals to be successful, Divisions must be involved and be representative, hospitals must see value in formal agreements, their structure must be considered and the process must be collaborative. In the current policy context, which emphasises primary care, hospitals and GPs are increasingly likely to start working more cooperatively. This model has significant potential to improve the interface between the two parties, through its formal negotiation process, and could easily be adapted to other settings.

Australia↗
PubMed1993

Myocarditis masquerading as ischemic heart disease: the diagnostic utility of antimyosin imaging.

The diagnosis of myocarditis presents a diagnostic challenge due to its varied clinical presentation. In addition, criteria for myocarditis are varied. At present, the confirmation of myocarditis depends on an endomyocardial biopsy demonstrating myocardial inflammation and necrosis. Unfortunately, this invasive procedure is associated with some degree of risk and has significant limitations. This report discusses the case presentations of two patients with chest pain, electrocardiographic changes and elevated creatine kinase levels suggestive of myocardial infarction, who were subsequently found to have findings compatible with myocarditis based on indium-111 antimyosin antibody scanning. This noninvasive test therefore appears to have value in the differentiation of myocardial ischemia from myocarditis.

Adult↗