A comparison of the referral rates of trainees and trainers in an academic teaching practice

Objective: To compare the referral rates of trainee and trainer family physicians. Setting: The practice of the Department of Family Medicine at the Medical University of Southern Africa, Pretoria. Design: Analysis of 43 028 problem encounters selected from one in-service practice database. Participants: Thirteen junior registrars, seven senior registrars in a Master's programme and seven senior physicians. Main measure: Referral rates compared by the Generalised Linear Mixed Model to allow for case mix and variation between the three study groups. Results: Adjusted referral rates per thousand problem encounters were 97.7 for junior registrars (95% CI 79.4 - 120.7), 77.1 for senior registrars (95%CI 59.3 - 99.5) and 73.7 for senior physicians (95% CI 54.4 - 99.2). Differences between the groups were not statistically significant (Wald chi-square = 3.90; df = 2; P = 0.195). There was insufficient evidence to show that the large amount of variation in the referral rates of doctors within study groups was different between the three groups. Conclusions: Using a performance-oriented database and an advanced method for adjusting for case mix makes a difference to referral rates. There was no significant difference between the mean referral rates of trainees and trainers. There was a large amount of variation within all three groups. Together, these findings support the thesis that factors other than clinical diagnosis in the behaviour of doctors or their interaction with patients are determinants of the referral decision. This points to the value of peer reviewing of referral rates for both trainees and trainers during vocational training, as well as in group practices. Key Words: General practice, family medicine, referral, trainee For full text, click here: SA Fam Pract 2004;46(4):21-2

Causes of early neonatal respiratory distress in the former Venda - a community-based study

Objective: To determine in a rural black population the incidence of common forms of respiratory distress (RD) and low birth weight (LBW), the mortality from RD and the perinatal mortality rate (PMR). Design: A prospective study in a context in which about 90% of the community's births take place within the health service and unwell neonates are transferred to hospital. Setting: The Donald Fraser health ward, Northern Province (then Venda), which serves a population of about 180 000 through 21 clinics and health centres and a 450 bed hospital. Subjects: 7 539 infants born alive between 1 February 1992 and 31 January 1993, of whom 48 developed RD. Outcome measures: Hjalmarson's classification of RD, modified for local conditions. Criteria depended on clinical signs, chest radiography, neutrophil count in blood and gastric aspirate, blood cultures and postmortem examination. Results: RD 6.4/1 000 livebirths (95% Cl 4.6 - 8.2); infection 2.6/1 000 livebirths (95% Cl 1.4 - 3.7); hyaline membrane disease (HMD) 0.9/1 000 livebirths (95% Cl 0.2 - , .6); pulmonary maladaptation (transient tachypnoea) 0.8/1 000 livebirths (95% Cl 0.2 - 1.4); mortality from RD 2.1/1 000 livebirths (95% CILl - 3.2); incidence of LBW 7.9% (95% Cl 7.3 - 8.5); PMR 19.8/1 000 livebirths (95% Cl 17-23). Conclusion: A strikingly Jow incidence of neonatal AD in general and of HMD in particular was found in a rural black population, probably related to a low LBW incidence. Infection was the commonest cause of RD.S Afr Med J 1996; 86; 1413-1<i1

Estrogen regulation of apoptosis: how can one hormone stimulate and inhibit?

The link between estrogen and the development and proliferation of breast cancer is well documented. Estrogen stimulates growth and inhibits apoptosis through estrogen receptor-mediated mechanisms in many cell types. Interestingly, there is strong evidence that estrogen induces apoptosis in breast cancer and other cell types. Forty years ago, before the development of tamoxifen, high-dose estrogen was used to induce tumor regression of hormone-dependent breast cancer in post-menopausal women. While the mechanisms by which estrogen induces apoptosis were not completely known, recent evidence from our laboratory and others demonstrates the involvement of the extrinsic (Fas/FasL) and the intrinsic (mitochondria) pathways in this process. We discuss the different apoptotic signaling pathways involved in E2 (17β-estradiol)-induced apoptosis, including the intrinsic and extrinsic apoptosis pathways, the NF-κB (nuclear factor-kappa-B)-mediated survival pathway as well as the PI3K (phosphoinositide 3-kinase)/Akt signaling pathway. Breast cancer cells can also be sensitized to estrogen-induced apoptosis through suppression of glutathione by BSO (L-buthionine sulfoximine). This finding has implications for the control of breast cancer with low-dose estrogen and other targeted therapeutic drugs

Inducing Ni Sensitivity in the Ni Hyperaccumulator Plant Alyssum inflatum Nyárády (Brassicaceae) by Transforming with CAX1, a Vacuolar Membrane Calcium Transporter

The importance of calcium in nickel tolerance was studied in the nickel hyperaccumulator plant Alyssum inflatum by gene transformation of CAX1, a vacuolar membrane transporter that reduces cytosolic calcium. CAX1 from Arabidopsis thaliana with a CaMV35S promoter accompanying a kanamycin resistance gene was transferred into A. inflatum using Agrobacterium tumefaciens. Transformed calli were subcultured three times on kanamycin-rich media and transformation was confirmed by PCR using a specific primer for CAX1. At least 10 callus lines were used as a pool of transformed material. Both transformed and untransformed calli were treated with varying concentrations of either calcium (1–15 mM) or nickel (0– 500 lM) to compare their responses to those ions. Increased external calcium generally led to increased callus biomass, however, the increase was greater for untransformed callus. Further, increased external calcium led to increased callus calcium concentrations. Transformed callus was less nickel tolerant than untransformed callus: under increasing nickel concentrations callus relative growth rate was significantly less for transformed callus. Transformed callus also contained significantly less nickel than untransformed callus when exposed to the highest external nickel concentration (200 lM). We suggest that transformation with CAX1 decreased cytosolic calcium and resulted in decreased nickel tolerance. This in turn suggests that, at low cytosolic calcium concentrations, other nickel tolerance mechanisms (e.g., complexation and vacuolar sequestration) are insufficient for nickel tolerance. We propose that high cytosolic calcium is an important mechanism that results in nickel tolerance by nickel hyperaccumulator plants

Preparing for rural surgery: Procedure or skills?

No Abstract