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Biomedical subjects

G Mitchell

Publications and source records attributed to G Mitchell.

At least 73 records · Page 4Linked to original sources
PubMed1998

Assessment of GP management of symptoms of dying patients in an Australian community hospice by chart audit.

BACKGROUND: With specialist palliative care services becoming widespread, and the place of the GP in palliative care being examined, audit of patient care delivered by GPs is required in order to ensure adequate standards of care. OBJECTIVE: We aimed to evaluate symptomatic care delivered to palliative care patients by GPs in an Australian community hospice with a developed quality assurance programme. METHODS: The study was set in a newly established community-based, GP-run hospice in a provincial city in Queensland, Australia. A chart audit was carried out of the first 20 patients admitted to a community-based hospice, in order to establish (i) whether attempts were made by the treating doctor to find the direct cause of symptoms before initiating management; and (ii) whether management accorded with developed consensus-based guidelines. RESULTS: Twenty patients were treated by 14 GPs; 135 new symptoms were identified in the records of these patients. Of the 125 symptoms for which guidelines could be identified in the literature, in 87 (70%) an attempt by the treating GP to find a direct cause could be demonstrated. Of the 114 symptoms with treatments defined in the guidelines, 107 (90%) treatments conformed to the guidelines. Constipation, nausea/vomiting, anorexia and back pain were the conditions for which there were the fewest attempts at establishing a direct cause before treatment. In most cases these conditions were treated in accordance with the guidelines. CONCLUSION: Quality assurance mechanisms present in an in-patient palliative care setting appear to be associated with high-quality care by GPs.

Aged↗
PubMed1998

Learning disability care staff's emotional reactions to aggressive challenging behaviours: development of a measurement tool.

OBJECTIVES: To describe the development of a rating scale measure of caregivers' emotional reactions to aggressive challenging behaviour, and to report preliminary psychometric data for the scale. DESIGN: Using previous research on staff working with people with learning disabilities, a range of likely emotional reactions to challenging behaviours were selected for possible inclusion in a rating scale measure. METHODS: A total of 83 care staff from 23 community residences for people with learning disabilities rated their recent emotional reactions to aggressive challenging behaviour using 18 emotion items. A further sample of 18 care staff participated in a test-retest study after the initial stages of scale development. RESULTS: A rating scale was developed on the basis of a factor analysis and further item analysis. The measure has two subscales: feelings of depression/anger (10 items), and feelings of fear/anxiety (5 items). The subscales have a high internal consistency, good test-retest reliability and are relatively unaffected by social desirability biases. CONCLUSIONS: The emotional reactions to aggressive challenging behaviour scale has excellent face and construct validity, and other preliminary psychometric data are promising. The scale has a number of potential research and clinical applications.

Activities of Daily Living↗
PubMed1997

An electrophysiological method for measuring the potassium permeability of the nerve perineurium.

An electrophysiological method is described for measuring the potassium permeability (PK) of the perineurium of the sciatic nerve of the frog. The method is based on the principle of grease-gap recording, in which an insulating compartment separates two surface recording electrodes. The sciatic nerves of frogs Rana temporaria and R. pipiens were isolated and mounted across a five compartment chamber, with Vaseline grease seals on the partitions between compartments. Compartments #1, #2 and #5 contained frog Ringer solution, #4 was filled with Vaseline and formed the grease gap, and #3 was the test compartment in which solutions could be changed. The nerve was stimulated via platinum electrodes in compartments #1 and #2, and DC potentials and compound action potentials (CAP) were recorded between Ag/AgCl electrodes connected through Ringer-agar bridges to compartments #3 and #5. In nerves with undamaged perineurium, changing from normal Ringer to high [K+] Ringer (100 mM, KCl replacing NaCl) for 2 min caused negligible change in DC potential or CAP, indicating that raised [K+] was not reaching the axon surface, and hence that the perineurium was exerting a diffusional restriction on K+ entry. In nerves damaged by stretching or drying, K+ pulses caused a depolarising change in DC potential (delta DC), and corresponding decline in CAP amplitude, consistent with a leaky perineurium allowing K+ entry and axonal depolarisation. Ringer made hypertonic by the addition of 2.5 M sucrose or 5 M NaCl caused increased perineurial permeability to K+. The method was calibrated by measuring the delta DC in response to raised [K+] in the range 5-100 mM [K+] in desheathed nerves; from this calibration curve relating delta DC to endoneurial [K+] it was possible to calculate the change in endoneurial [K+] occurring in intact preparations. The calculations showed that the undamaged perineurium had a PK of < 6.3 x 10(-7) cm.s-1, similar to the value calculated for in situ nerves using radioisotopic techniques, but less than the value reported for isolated perineurial cylinders. The method gives real-time information on the K+ permeability of the nerve perineurium and its modulation by experimental treatments.

Animals↗
PubMed1997

Chromosomal localization of the human liver form cytochrome c oxidase subunit VIIa gene.

The chromosomal loci corresponding to human cytochrome c oxidase (COX) subunit VIIa Liver (VIIa-L) isoform genes were determined utilizing a combined approach of genomic cloning, in situ hybridization, and somatic hybrid genetics. In contrast to the proposal of E. Arnaudo et al. (Gene (Amst.), 119: 299-305, 1992) that COX VIIa-L sequences are located on chromosomes 4 and 14, we found that COX VIIa-L related sequences reside on chromosome 6, while an additional COX VIIa-L cross-reacting sequence psi-gene) was located on chromosome 4.

Animals↗
PubMed1997

Selective brain cooling: role of angularis oculi vein and nasal thermoreception.

We have measured blood flows in the angularis oculi (AOV), facial, and jugular veins and temperatures in the carotid artery and near the hypothalamus in three lightly anesthetized sheep while body and nasal mucosal (Tnm) temperatures were varied independently. Above a threshold hypothalamic temperature (Thyp) of 39 degrees C both selective brain cooling (SBC) and AOV blood flow increased. For a given Thyp, the increase in AOV flow and SBC was inversely proportional to Tnm: low Tnm resulted in high AOV flow and SBC, whereas increasing Tnm attenuated both AOV flow and SBC. This decrease in AOV flow results in submaximal SBC, which does not concur with the hypothesis that SBC functions to protect a thermally vulnerable brain. The trigger for these changes in AOV blood flow was Tnm. Occlusion of the AOV during SBC showed that AOV flow accounted for over 80% of SBC. We conclude that SBC is not only a mechanism for reducing brain temperature but may also be a means of adjusting Thyp to facilitate the appropriate thermoregulatory responses.

Animals↗
PubMed1996

Do actions reported by physicians in training conflict with consensus guidelines on ethics?

OBJECTIVE: To assess the extent to which actions reported by internal medicine trainees conflict with published guidelines on ethics. METHODS: A confidential survey was sent to a random sample (N = 1000) of associate members of the American College of Physicians (ACP). Questions were asked about ethical decision making in areas addressed by the guidelines in the ACP Ethics Manual. Quoted manual guidelines were provided, followed by 55 yes or no questions, such that a yes answer represented an action that conflicted with a guideline. There were two follow-up mailings to nonresponders. RESULTS: Forty percent (n = 397) completed the questionnaire; 17% indicated they were aware of the guidelines on ethics. On average, associates responded yes to 16% of questions where a yes response indicated they have acted outside guidelines on ethics one or more times. The mean number of responses (n = 55) that conflicted with a guideline was 7.6 per person (SD, 4.7 responses; range, 0 to 33 responses). Ninety-eight percent of respondents reported actions falling outside a guideline one or more times and 80% did so four or more times. The most frequently reported reason (965/3219 [30%]) from a list of four choices for acting outside a guideline was "I was aware of the guideline, but this did not represent an ethical dilemma to me." CONCLUSIONS: Few responding ACP associates indicated awareness of the ACP guidelines on ethics. Physicians in training nevertheless reported acting according to the presented guidelines most of the time, although nearly all respondents acted outside a guideline at least once, and some did so many times. Reported behaviors were sometimes inconsistent with consensus ethical standards that apply to internists. Physicians in training need to know more about ethical standards that apply to their own practice and should be aware when their actions deviate from ethical norms. Before acting outside guidelines on ethics, trainees should discuss their conflicts with others, such as attending physicians, clinical ethicists, or hospital ethics committees.

Codes of Ethics↗
PubMed1996

Evaluation of multiple sclerosis by 1H spectroscopic imaging at 4.1 T.

The authors report on high-field (4.1 T) magnetic resonance 1H spectroscopic imaging studies on eight patients with relapsing remitting multiple sclerosis (mean expanded disability status scale (EDSS) 1.0) and eight normal controls. Using T1-weighted imaging to determine lesion position, the authors found the ratios of choline/N-acetyl (NA) compounds and creatine/NA were increased significantly in the multiple sclerosis (MS) patients relative to controls in lesioned tissue, adjacent to lesion, far removed from lesions as well as in periventricular tissue. The gray matter creatine/NA was mildly increased (P < 0.01) in the MS patients, whereas the elevated gray-matter ratio of choline/NA was of borderline significance (P = 0.13). A more detailed comparison of white-matter and mean gray-matter metabolite values indicates that creatine is increased greatest in areas far from lesions. This is in contrast to choline, which was greatest in lesions, and NA, which was smallest in lesions. It is postulated that the creatine increase may reflect an astrocytic (gliotic) or oligodendrocytic remyelinating process. The increased choline most likely reflects varying levels of inflammation and membrane turnover, whereas the NA decrease is representative of axonal dysfunction or loss.

Adult↗
PubMed1996

Chronic sodium benzoate therapy in children with inborn errors of urea synthesis: effect on carnitine metabolism and ammonia nitrogen removal.

Sodium benzoate (SB) therapy is known to increase ammonia (NH3) nitrogen elimination via conjugation with glycine and excretion as urinary hippurate. In 16 children with inborn errors of urea synthesis we studied two issues: (1) the effect of chronic SB administration upon carnitine metabolism and (2) the efficacy of chronic SB therapy as measured by the molar ratio of hippurate excretion to SB intake. Measurements were performed during elective hospitalizations when the patients were in stable metabolic condition. We found that chronic SB therapy is not associated with a constant level of hippurate elimination and that interindividual and intraindividual variability may result in irregular removal of NH3 nitrogen. This variability may be due to various factors including the formation of small quantities of benzoylcarnitine, which was detected in the plasma of three of four patients receiving SB and carnitine therapy and in one of two patients on SB therapy without carnitine supplementation. The ratios of acyl to free carnitine were elevated in both plasma and urine in patients not receiving carnitine supplementation, but were normal in patients receiving supplementation.

Adolescent↗
PubMed1996

Inability of hyperglycemia to counter the ability of glucagon to increase net glucose output and activate glycogen phosphorylase in the perfused rat liver.

We examined the ability of hyperglycemia to alter the ability of glucagon to activate phosphorylase and stimulate glucose output in perfused rat livers. The livers were perfused with a Krebs-Henseleit buffer containing washed bovine erythrocytes and albumin at 37 degrees C for 90 or 120 minutes, In the first 60 minutes, the livers were perfused with insulin (10 microU/mL), glucagon (11 pg/mL), and glucose (105, 230, or 440 mg/dL). In the second 30 or 60 minutes, the glucagon concentration in the perfusate was elevated to 44, 88, 176 or 352 pg/mL or the infusion of glucagon was terminated. In the presence of glucose at 105 mg/dL, the termination of glucagon infusion decreased phosphorylase activity and glucose output. In contrast, the elevation of glucagon from 11 to 352 pg/mL activated phosphorylase and increased net glucose output in a dose-dependent manner. A linear correlation was observed between net glucose output and glycogen phosphorylase activity. An elevation of the glucose concentration from 105 to 230 or 440 mg/dL decreased net glucose output from 0.81 +/- 0.03 to 0.66 +/- 0.09 or -0.004 +/- 0.21 mg/min/100 g body weight, respectively, but did not cause significant change in phosphorylase-a activity (105 mg/dl, 50 +/- 11; 230 mg/dL, 40 +/- 2; 440 mg/dL, 69 +/ 3 mU/mg protein). The elevation of the glucagon concentration from 11 to 88 microU/mL in the presence of glucose at 105, 230, or 440 mg/dL increased net glucose output by 0.65 +/- 0.06, 0.61 +/- 0.08 or 0.64 +/- 0.26 mg/min 100 g body weight and raised phosphorylase-a activity by 65 +/- 5, 82 +/- 11, or 55 +/- 4 mU/mg protein, respectively. These results suggest that hyperglycemia decreases net hepatic glucose output without changing the activity of phosphory-lase-a. Further hyperglycemia does not alter the ability of glucagon to activate phosphorylase or to stimulate net hepatic glucose output.

Animals↗
PubMed1996

Mutation analysis in Canadian families with choroideremia.

Choroideremia (CHM) is an X-linked heritable progressive dystrophy of the choroid and retina. The condition predominantly affects males beginning in early childhood and eventually results in blindness after a period of 30-40 years. The CHM gene was localized to Xq21 and cloned in the past few years. The gene encodes for Rab escort protein-I, a protein involved in the isoprenylation of intracellular proteins. With the isolation of the gene, a number of mutations have been identified in patients affected by CHM using molecular techniques. Our group reports the characterization of mutations in four Canadian families affected by CHM. In addition, an intragenic polymorphism was identified in exon 5. Finding the mutations in these families will result in accurate predictive testing for carriers, avoid unnecessary repeated examination of at-risk individuals, and add to our understanding of the cause of this disorder.

Adaptor Proteins, Signal Transducing↗
PubMed1995

Effect of infarct artery patency on prognosis after acute myocardial infarction. The Survival and Ventricular Enlargement Investigators.

BACKGROUND: In patients with acute myocardial infarction (MI), early restoration of patency of the infarct-related artery (IRA) leads to preservation of left ventricular function and improved clinical outcome. However, there is evidence that the benefits associated with a patent IRA are out of proportion to the observed improvement in ventricular function and may result not only from salvage of ischemic myocardium but also from the opening of the IRA beyond a narrow postinfarct time window. The objectives of this study were (1) to assess the effect of IRA patency on outcome of patients after acute MI with left ventricular dysfunction while controlling for differences in left ventricular ejection fraction and the extent of coronary disease and (2) to determine the effect of angiotensin-converting enzyme (ACE) inhibitor therapy on patients with patent as well as occluded infarct arteries. METHODS AND RESULTS: The Survival and Ventricular Enlargement (SAVE) study consisted of 2231 patients with a documented MI and a left ventricular ejection fraction < or = 40%. They were randomized to the ACE inhibitor captopril (50 mg TID) or placebo 3 to 16 days after MI and were followed for an average of 3.5 years. Left ventricular ejection fraction, measured with radionuclide left ventriculography, was repeated at the end of the follow-up period. The 946 patients in whom the patency of the IRA was established before randomization form the basis of this study. At cardiac catheterization averaging 4.2 days after infarction, 30.7% of patients had an initially occluded IRA. After revascularization, 162 of the 946 patients (17.1%) were left with an occluded IRA at the time of randomization. The 162 patients with persistently occluded IRAs and 784 with patent IRAs had similar clinical baseline characteristics, but those with occluded arteries had a slightly lower ejection fraction than the 784 patients with patent infarct arteries (30% versus 32%, P = .01). Cox proportional-hazards analyses showed that the independent predictors of all-cause mortality were hypertension (relative risk [RR] 1.94, P < .001), number of diseased coronary arteries (RR 1.68, P < .001), occluded IRA (RR 1.49, P = .039), ejection fraction (RR 1.36, P < .001), age (RR 1.10, P = .030), and use of beta-adrenergic receptor blocking agents (RR 0.60, P = .007). Independent predictors of a composite end point consisting of cardiovascular mortality, morbidity, or reduction of ejection fraction of > or = 9 units were occluded IRA (odds ratio [OR] 1.73, P = .002), hypertension (OR 1.71, P < .001), number of diseased vessels (OR 1.38, P < .001), ejection fraction (OR 1.18, P = .003), use of beta-adrenergic receptor blocking agents (OR 0.67, P = .007), and randomization to captopril (OR 0.70, P = .009). CONCLUSIONS: IRA patency within 16 days after MI predicts a favorable clinical outcome, independent of the number of obstructed coronary arteries or of left ventricular function. The beneficial effect of ACE inhibition is independent of patency status of the IRA. These findings support the need for additional, prospective clinical trials of late reperfusion in MI patients.

Adrenergic beta-Antagonists↗