Biomedical subjects

Gudrun Edgren

Publications and source records attributed to Gudrun Edgren.

4 recordsLinked to original sources

PubMed2006

Developing a competence-based core curriculum in biomedical laboratory science: a Delphi study.

In this study the Delphi technique has been used to develop a core curriculum for education of the biomedical scientist. The rapid development in biomedicine and the corresponding changes in methodology in biomedical laboratories demand careful planning of the education of biomedical scientists. The Delphi technique uses an anonymous panel of experts for suggestions and assessments aiming at consensus. Twenty-six experts from different kinds of hospital and university laboratories took part in the investigation. They suggested and assessed necessary competences for a recently graduated biomedical scientist, and if 75% or more of the participants agreed on a competence, it was included in the core curriculum. The final list consisted of 66 competences of varying depth, in three categories. This list contained several generic competences, concerning for example basic laboratory methods, handling of samples, dealing with apparatus and applying relevant rules and laws; basic knowledge in chemistry, preclinical medicine and laboratory methods; and finally attitudes that the panel expected in the recently graduated person. The core was sufficiently restricted to be used in a three-year programme and still leave space for about one year of electives/special study modules. It became rather traditional, e.g. it did not include competences that many recent reports consider important for the future professional.

Biomedical Research↗

PubMed2006

Portfolio as a method for continuous assessment in an undergraduate health education programme.

A portfolio assessment system has been introduced into a biomedical science programme to promote both continuous learning and deep approaches to learning. Attention has been focused on creating harmony between the assessment system and the PBL curriculum of the programme. Biomedicine and laboratory work are central in the curriculum. The portfolio included evidence of laboratory work, personal reflections and certificates from the PBL tutor. The portfolio was assessed on three occasions over 20 weeks. The grades were 'pass' or 'fail'. The tutor certificate appeared to be a crucial part of the portfolio since a 'fail' in this part usually led to an overall 'fail'. Both students and teachers were concerned about ensuring that enough factual knowledge, as measured by a traditional test, had been achieved. The agreement was good enough for the pass or fail level but some expected differences were found at the detailed level. The course, including the portfolio, was evaluated orally during weekly whole-group meetings and using a questionnaire at the end. The students felt comfortable with the portfolio system and preferred it to a traditional test. The teachers felt that they needed to develop their teacher-student discussion skills and to improve their feedback on the reflections. Peer assessment between students is proposed as a line of action to enhance the credibility of the crucial tutor certificate. The portfolio might be an efficient tool for the students to concentrate their efforts on the most central concepts of medical laboratory work. The model will be developed through further discussions and better consensus among faculty.

Adult↗

PubMed2004

VPAC2-R mediates the lipolytic effects of pituitary adenylate cyclase-activating polypeptide/vasoactive intestinal polypeptide in primary rat adipocytes.

The neuropeptides pituitary adenylate cyclase-activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) are structurally and functionally related. Their actions have been shown to be mediated by three different receptor subtypes: PAC1-R, which has exclusive affinity for PACAP, and VPAC1-R and VPAC2-R, which have equal affinity for PACAP and VIP. We recently showed that PACAP38 induces lipolysis in rat adipocytes, and in the present study we examined whether VIP has similar effects and which of the three receptors mediates this PACAP/VIP action. We showed by RT-PCR that all three receptor subtypes are present in rat adipocytes. We demonstrated that VIP (1-100 nm), like PACAP38, stimulates lipolysis in isolated adipocytes, as determined by glycerol release. By a pharmacological approach, using antagonists and agonists specific for the receptor subtypes, we elucidated the mechanisms by which PACAP38 and VIP mediate their lipolytic effects. We found that antagonists of PAC1-R [PACAP(6-38)] and VPAC1-R (PG97-269) did not affect lipolysis induced by 0.1-100 nm PACAP38 or VIP, and that a VPAC1-R agonist [K15, R16, L27VIP(1-7)GRF(8-27)] did not affect lipolysis at 1-1000 nm. However, two different VPAC2-R agonists [Hexa-VIP(1-28) and Ro25-1553] clearly mimicked the lipolytic effect of PACAP38 and VIP. In addition, the VPAC2-R antagonist PG99-465 (100 nm) caused right-shifted dose-response curves of PACAP38- and VIP-induced lipolysis. These results therefore provide evidence that all three PACAP/VIP receptor subtypes are expressed in primary rat adipocytes, but that the VPAC2-R subtype is responsible for mediating the lipolytic effects induced by PACAP38 and VIP.

Adipocytes↗

PubMed2003

Dual effects of pituitary adenylate cyclase-activating polypeptide and isoproterenol on lipid metabolism and signaling in primary rat adipocytes.

Pituitary adenylate cyclase-activating peptide (PACAP) is a neuropeptide that exerts its effects throughout the body by elevating the intracellular amounts of cAMP. In adipocytes, an increased amount of cAMP is associated with increased lipolysis. In this work we evaluated the effects of PACAP38 on triglyceride metabolism in primary rat adipocytes. Stimulation of adipocytes with PACAP (0.1-100 nm) resulted in stimulation of lipolysis to the same extent as isoproterenol. Lipolysis was blocked by 25 microm of the protein kinase A inhibitor H-89 and potentiated in the presence of 10 microm OPC3911, a phosphodiesterase 3 inhibitor. In addition, PACAP38 induced activation of protein kinase A. Insulin efficiently inhibited PACAP38-induced lipolysis in a phosphatidyl inositol 3-kinase and phosphodiesterase 3-dependent manner. Interestingly, we also found that PACAP38, as well as isoproterenol, induced potentiation of lipogenesis in the presence of insulin. These results show that PACAP38 and isoproterenol mediate catabolic as well as anabolic effects in adipocytes, depending on the concentration of insulin present. We speculate that in the early postprandial state and during fasting, when insulin levels are low, PACAP and beta-adrenergic catecholamines induce lipolysis, whereas when higher levels of insulin are present, these agents potentiate the anabolic effect of insulin, i.e. storage of triglycerides.

Adipocytes↗