A student-centred feedback model for educators.

Background: Effective feedback is instrumental to effective learning. Current feedback models tend to be educator driven rather than learner-centred, with the focus on how the supervisor should give feedback rather than on the role of the learner in requesting and responding to feedback.

Context: An alternative approach emphasising the theoretical principles of student-centred and self-regulated learning is offered, drawing upon the literature and also upon the experience of the authors.

Conducting the symphony: a qualitative study of facilitation in problem-based learning tutorials.

Context: Tutors in problem-based learning (PBL) tutorials have a complex role to play in facilitating students' learning. This includes providing support for students' acquisition of content knowledge and skills in critical thinking, coaching of group processes and modelling of reflective practice. Few studies which investigate the key role of tutors in the PBL tutorial process are qualitative in design.

Diastolic ventricular interaction in chronic heart failure: relation to heart rate variability and neurohumoral status.

It is likely that abnormal baroreflex control mechanisms are at least partially responsible for autonomic dysfunction in chronic heart failure. We recently demonstrated that diastolic ventricular interaction is associated with impaired baroreflex control of vascular resistance in heart failure. We reasoned that by constraining left ventricular filling, such interaction would decrease baroreflex activity and, thereby, increase sympathetic and decrease parasympathetic outflow.

Association study of the 5' flanking regions of endothelial-nitric oxide synthase and endothelin-1 genes in familial primary open-angle glaucoma.

1. Endothelium-derived substances are important regulators of the microcirculation. Endothelium-derived nitric oxide (NO), which is catalysed by nitric oxide synthase (NOS), is a potent modulator of vascular tone in the human ophthalmic artery, which is normally in a state of constant vasodilation due to the actions of NO.

Evidence for persistent dysfunction of wild-type aldosterone synthase gene in glucocorticoid-treated familial hyperaldosteronism type I.

Background: In familial hyperaldosteronism type I (FH-I), glucocorticoid treatment suppresses adrenocorticotrophic hormone-regulated hybrid gene expression and corrects hyperaldosteronism.

Objective: To determine whether the wild-type aldosterone synthase genes, thereby released from chronic suppression, are capable of functioning normally.

Methods: We compared mid-morning levels of plasma potassium, plasma aldosterone, plasma renin activity (PRA) and aldosterone: PRA ratios, measured with patients in an upright position, and responsiveness of aldosterone levels to infusion of angiotensin II (AII), for 11 patients with FH-I before and during long-term (0.

In familial hyperaldosteronism type I, hybrid gene-induced aldosterone production dominates that induced by wild-type genes.

We compared the aldosterone-producing potency of the angiotensin II-sensitive wild-type aldosterone synthase genes and the ACTH-sensitive hybrid 11 beta-hydroxylase/aldosterone synthase gene by examining aldosterone, PRA, and cortisol day-curves (2-hourly levels over 24 h) in patients with familial hyperaldosteronism type I, before and during long-term (0.8-13.5 yr) glucocorticoid treatment.

PCR-SSCP analysis of the glucocorticoid-responsive element of the atrial natriuretic peptide gene in familial primary open-angle glaucoma.

1. Familial primary open-angle glaucoma (POAG) is a heterogeneous disease of unknown aetiology and the elucidation of the underlying genetic mechanisms contributing to phenotypic expression will be essential if earlier diagnosis of at-risk individuals and more specific medical treatment can be achieved. In a significant percentage of patients with POAG, intraocular pressure increases in response to topical ocular glucocorticoids.

Insertion/deletion polymorphism of the angiotensin-converting enzyme gene and loss of the insertion allele in aldosterone-producing adenoma.

The genetic mechanisms responsible for the formation of adrenocortical adenomas which autonomously produce aldosterone are largely unknown. The adrenal renin-angiotensin system has been implicated in the pathophysiology of these tumours. Angiotensin-converting enzyme (ACE) catalyses the generation of angiotensin II, and the insertion/deletion (I/D) polymorphism of the ACE gene regulates up to 50% of plasma and cellular ACE variability in humans.

Laparoscopic adrenalectomy.

Using the transperitoneal, laparoscopic approach, we performed 67 successful adrenalectomies between June 1993 and July 1995 at Greenslopes Hospital, Brisbane. There were 30 women and 37 men. Syndromes of primary adrenal hormone overproduction--primary aldosteronism (n = 52), pheochromocytoma (n = 6), and hypercortisolism (n = 1)--were present in 59 patients and apparently nonfunctioning adrenal tumors (of which one was malignant) in 8 patients.

The atrial natriuretic peptide gene in patients with familial primary open-angle glaucoma.

Family history is a major risk factor in the development of primary open-angle glaucoma. The atrial natriuretic peptide system has been implicated in the underlying pathophysiology of the disease. This study looked for any alterations in the ANP gene and 5' proximal promoter regions of the ANP gene, in 53 patients from familial primary open-angle glaucoma families.

Different allelic patterns at chromosome 11q13 in paired aldosterone-producing tumours and blood DNA.

1. We previously reported loss of heterozygosity (LOH) at region q13 of chromosome 11 in five aldosterone-producing tumours (APT) using restriction fragment length polymorphism (RFLP) analysis, including two from patients with familial hyperaldosteronism. 2.

Production of 18-oxo-cortisol in subtypes of primary aldosteronism.

1. In familial hyperaldosteronism type I (FH-I), expression of an adrenocorticotropic hormone (ACTH)-dependent hybrid 11 beta-hydroxylase/aldosterone synthase gene causes excessive 'hybrid steroid' (18-hydroxy- and 18-oxo-cortisol) production. In order to study the mechanism of elevated 'hybrid steroid' levels in angiotensin-unresponsive (AII-U) aldosterone-producing adenoma (APA), we compared responses of 24 h urinary 18-oxo-cortisol, aldosterone and cortisol to dexamethasone (0.

PCR-SSCP analysis of the promoter region of the renin gene in patients with aldosterone-producing adenomas.

1. Aldosterone-producing adenomas (APA) of the adrenal gland may be responsive or un-responsive to the renin-angiotensin system. 2.

PCR-SSCP analysis of the p53 gene in tumours of the adrenal gland.

1. Mutations of the p53 tumour suppressor gene are relatively common in the aetiology of a wide spectrum of tumour types, both sporadic and familial. 2.

Clinical, biochemical and genetic approaches to the detection of familial hyperaldosteronism type I.

Aim: Since detection of familial hyperaldosteronism type I (glucocorticoid-suppressible hyperaldosteronism) allows specific treatment of hypertension with dexamethasone, we compared clinical, biochemical and genetic approaches to detection.

Patients And Methods: We studied 22 affected patients, 21 from a single, large family and an additional adopted male. Plasma aldosterone, plasma renin activity and urinary 18-oxo-cortisol were measured by radioimmunoassay.

Long-PCR of the ANP gene and PCR-SSCP analysis of the proximal promoter region of the ANP gene in patients with aldosterone producing adenoma.

Previous studies have shown a significant association between allelic frequencies at the ANP gene locus and aldosterone responsiveness to angiotensin in aldosterone-producing adenoma (APA). We searched for any gross insertions or deletions in the ANP gene in APA and any associations between allelic frequencies at the Hpa II and Sca I RFLP sites within the ANP gene and angiotensin-responsive and unresponsive APA and normal subjects. We also searched for possible point mutations in the promoter region of the ANP gene (-595 to transcription start site) in peripheral blood and tumor DNA from 59 patients with APA and in peripheral blood DNA from 39 normal subjects by polymerase chain reaction and single strand conformation polymorphism (PCR-SSCP) analysis.

Reduced renal extraction of atrial natriuretic peptide in primary aldosteronism.

We investigated renal and peripheral forearm extraction of atrial natriuretic peptide in patients with primary aldosteronism to determine whether alterations in extraction may contribute to the elevated levels of circulating atrial natriuretic peptide observed in primary aldosteronism. We obtained simultaneous venous blood samples from the left renal vein and a peripheral vein and from the radial artery in 28 patients with primary aldosteronism and 10 patients with essential hypertension. Renal extraction of atrial natriuretic peptide was significantly (P < .

Effects of felodipine, metoprolol and their combination on blood pressure at rest and during exercise and on volume regulatory hormones in hypertensive patients.

The effects on blood pressure (BP) and heart rate (HR), at rest and during bicycle exercise, of the vascular selective calcium antagonist felodipine, the cardio-selective beta-blocker metoprolol, and of the two drugs in combination, were assessed in a double-blind, three-way cross-over study comprising 23 patients with essential, mild to moderate hypertension. All three treatment regimens were given to each patient in randomised order for 4 weeks after a 4 week placebo run-in period. Felodipine 10-20 mg daily, metoprolol 100-200 mg daily and the combination of felodipine 10-20 mg plus metoprolol 100 mg daily were all effective antihypertensive treatments both at rest and during exercise.

Laparoscopic adrenalectomy for adrenal tumours causing hypertension and for 'incidentalomas' of the adrenal on computerized tomography scanning.

1. In a 19 month period from June 1993 to December 1994, 60 patients (mean age 54.8 +/- 1.

Analysis of the renin gene in patients with aldosterone-producing adenomas by polymerase chain reaction-single stranded conformational polymorphisms and long polymerase chain reaction.

1. Angiotensin-responsive aldosterone-producing adenomas (AII-R-APA) have increased expression of renin mRNA compared with angiotensin-unresponsive aldosterone-producing adenomas (AII-U-APA) or normal adrenals. 2.

Plasma aldosterone response to ACTH in subtypes of primary aldosteronism.

1. Aldosterone responsiveness to ACTH was compared in eleven patients with angiotensin-unresponsive (AII-U) aldosterone-producing adenomas (APA), 16 with AII-responsive (AII-R) APA and 19 with bilateral adrenal hyperplasia (BAH). 2.

PCR-SSCP analysis of the angiotensin II type 1 receptor gene in patients with aldosterone-producing adenomas.

1. In patients with primary aldosteronism due to angiotensin-responsive and angiotensin-unresponsive aldosterone-producing adenomas, no differences in the coding region of the angiotensin II type 1 (AT1) receptor gene were observed compared to normal subjects in peripheral blood leucocyte DNA. 2.

Hybrid gene or hybrid steroids in the detection and screening for familial hyperaldosteronism type I.

1. Early diagnosis of Familial Hyperaldosteronism Type I (FH-I, glucocorticoid-suppressible hyperaldosteronism) in asymptomatic, affected individuals is essential if death from stroke is to be prevented. 2.

A new genetic test for familial hyperaldosteronism type I aids in the detection of curable hypertension.

In Familial Hyperaldosteronism Type I (FH-I, glucocorticoid-suppressible hyperaldosteronism), a curable form of hypertension inherited in an autosomal dominant fashion, the underlying genetic defect is a "hybrid gene" in which 11 beta-hydroxylase gene regulatory elements are fused to the coding region of the aldosterone synthase gene. The detection of this hybrid gene by Southern blotting is time consuming and involves the use of radioactive isotopes. We describe a new, long polymerase chain reaction-based method for detecting the hybrid gene which greatly reduces the time required to obtain a result, avoids exposure of laboratory workers to radioactive materials, and will thereby facilitate the screening of patients for the presence of FH-I.

Primary aldosteronism--some genetic, morphological, and biochemical aspects of subtypes.

Primary aldosteronism is the commonest cause of potentially curable hypertension when diagnosed in both florid and less florid forms. Genetic screening, so far available only for glucocorticoid-suppressible hyperaldosteronism, permits diagnosis from birth, before any biochemical or clinical abnormalities appear. Biochemical screening using the aldosterone-to-renin ratio permits diagnosis in the absence of raised aldosterone or of hypokalemia.