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Biomedical subjects

W Braund

Publications and source records attributed to W Braund.

6 recordsLinked to original sources
PubMed2001

Rural intern training.

In recent times, legislative initiatives in Australia have changed the method by which doctors enter general practice. One result of this tightening has been to restrict the access of junior doctors to medical experiences outside the hospital environment, and force a closer examination of the 'generalist training' provided to junior doctors. The Australian Medical Training Review Panel, created as part of these legislative changes, developed a series of recommendations about general training in 1996, one of which was to provide for rural and community experiences for junior doctors. This article describes the experience of a 'rural intern' rotation from Flinders Medical Centre to the rural community of Jamestown, in South Australia.

Journal Article↗
PubMed1995

Regulation of the insulin-like growth factors and their binding proteins by glucocorticoid and growth hormone in nonislet cell tumor hypoglycemia.

Hypoglycemia in patients with nonislet cell tumors is often secondary to overexpression of tumor insulin-like growth factor (IGF) II. In these patients the formation of serum complexes between IGFs, IGF binding protein-3 (IGFBP-3), and the acid-labile subunit (ALS) is impaired. An 87-yr-old woman with nonislet cell tumor hypoglycemia resulting from a localized fibrous tumor of the pleura was treated for 97 days with graded doses of prednisolone (30, 10, and 5 mg/day) followed by GH (1, 4, 8, 4, and 2 U/day). Both prednisolone and GH alleviated the hypoglycemia, concomitantly with increases in IGF-I, IGFBP-3, and ALS levels. Pretreatment serum IGFBP-2 and IGFBP-6 levels were greatly elevated, but as glucose normalized with treatment, only IGFBP-2 decreased, showing an inverse correlation with glucose (r = 0.716). IGFBP-1 gave a variable pattern not clearly related to blood glucose. Both treatments caused a redistribution of serum IGFBP-3 from binary- to ternary-complexed forms. However, only prednisolone improved the ability of IGFBP-3 to bind ALS in vitro. Prednisolone also suppressed IGF-II, the effect being confined to pro-IGF-II forms. Compared with normal IGF-II, pro-IGF-II inhibited ALS binding to IGFBP-3 in vitro. Although prednisolone and GH reverse hypoglycemia by different mechanisms, with only prednisolone suppressing tumor IGF-II secretion, both increase the formation of ternary IGF-IGFBP-3 complexes. We conclude that the failure of serum IGFBP-3 and tumor IGF-II to complex with ALS is a primary cause of hypoglycemia in nonislet cell tumor hypoglycemia.

Aged↗
PubMed1989

Prevalence of genetic haemochromatosis among diabetic patients.

Since diabetes mellitus is a frequent manifestation of haemochromatosis the prevalence of the disease was investigated in 418 patients attending a diabetic clinic. 21 (5%) patients had a persistently high serum ferritin (men, over 400 micrograms/l; women, over 300 micrograms/l) and 5 of these had transferrin saturations consistently over 55%. Idiopathic haemochromatosis was confirmed by liver biopsy in 4 patients, all of whom had a hepatic iron index greater than 2.0. The prevalence rate of previously unrecognised idiopathic haemochromatosis was thus 9.6 per 1000 (general population prevalence 1 in 250), suggesting that screening of diabetic patients for this genetic disease may be more cost-effective than screening in the general population.

Adult↗
PubMed1986

Regulation of pulsatile secretion of progesterone during the human luteal phase.

This study was designed to evaluate the role of luteinizing hormone (LH) and prolactin (PRL) in regulating pulsatile progesterone secretion in the human. This was done first by correlating the frequency of progesterone, LH and PRL pulses during the mid-luteal phase of normal cycles. Second, by increasing the frequency of LH pulses with naloxone and GnRH injections and examining the impact on progesterone pulse frequency. Third, by abolishing PRL pulsatility with metoclopramide and looking at the effect on progesterone pulsatility. Nine normal subjects in the mid-luteal phase (4-10 days after the initial postovulatory rise in progesterone) were studied for 8 h with blood samples taken at 15 min intervals. Each sample was assayed for progesterone, LH and PRL and the pulse frequency (number of pulses in 8 h) determined for each hormone. The mean pulse frequencies were 2.3 (s.e.m. = 0.4) for progesterone, 1.3 (s.e.m. = 0.4) for LH, and 2.1 (s.e.m. = 0.3) for PRL. Cross-correlation analysis showed that there was no significant synchrony between pulses of progesterone and pulses of LH and PRL. When naloxone was given to six normal subjects in the mid-luteal phase, the mean LH pulse frequency (number of pulses in 6 h) was increased from 2.2 (s.e.m. = 0.3) during a saline infusion to 3.2 (s.e.m. = 0.5) during the naloxone infusion (P less than 0.05). However, the mean pulse frequency for progesterone remained unchanged during the saline and naloxone studies. There was no significant difference between the mean serum LH in the saline and naloxone groups, and the mean serum progesterone concentration was not significantly altered.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1984

Synchronous secretion of luteinizing hormone and prolactin in the human luteal phase: neuroendocrine mechanisms.

Studies of normal luteal phase women have shown that increases in serum LH and PRL are commonly synchronous. This study was designed to investigate the possible neuroendocrine mechanism(s) underlying this phenomenon. Six normal women were studied during the midluteal phase of 2 cycles. In the first cycle, they had blood samples collected at 15-min intervals for 6 h on 3 occasions during which time they received an infusion of normal saline or naloxone (1 mg/h) or a bolus of metoclopramide (10 mg, iv). In a second cycle, they received GnRH in increasing iv doses of 1, 10, and 50 micrograms at 2-h intervals. During the saline infusion, 11 of the 16 serum LH pulses (69%) were accompanied by an increase in serum PRL, and in 5 of the subjects, the first pulse of LH was synchronous with that of PRL (P = 0.0015). Naloxone increased the number of LH pulses from 16 to 20 and the number of PRL pulses from 12 to 16, all of which were synchronous with LH pulses. Administration of metoclopramide caused a substantial increase in PRL and a loss of further PRL pulsatility; however, LH pulsatility remained unaffected. Even after the smallest dose of GnRH (1 microgram), there was an increase in serum PRL [basal level, 11.8 +/- 2.1 (+/- SE) micrograms/liter; peak level, 16.5 +/- 3.3 micrograms/liter] as well as LH and FSH. The increase in serum PRL was, unlike the gonadotropin response, maximal after the 10-microgram dose of GnRH (peak level, 23.2 +/- 6 micrograms/liter) and did not increase further after the 50-micrograms dose (peak level, 18.5 +/- 2.4 micrograms/liter). These studies demonstrate that there is a PRL response to GnRH in the luteal phase and suggest that the observed synchrony in LH and PRL secretion at this time results from a physiological response of both the gonadotrope and the lactotrope to endogenous GnRH.

Adolescent↗