Analysis of adequacy levels for human resources improvement within primary health care framework in Africa

Human resources in health care system in sub-Saharan Africa are generally picturing a lack of adequacy between expected skills from the professionals and health care needs expressed by the populations. It is, however, possible to analyse these various lacks of adequacy related to human resource management and their determinants to enhance the effectiveness of the health care system. From two projects focused on nurse professionals within the health care system in Central Africa, we present an analytic grid for adequacy levels looking into the following aspects: - adequacy between skills-based profiles for health system professionals, quality of care and service delivery (health care system /medical standards), needs and expectations from the populations, - adequacy between allocation of health system professionals, quality of care and services delivered (health care system /medical standards), needs and expectations from the populations, - adequacy between human resource management within health care system and medical standards, - adequacy between human resource management within education/teaching/training and needs from health care system and education sectors, - adequacy between basic and on-going education and realities of tasks expected and implemented by different categories of professionals within the health care system body, - adequacy between intentions for initial and on-going trainings and teaching programs in health sciences for trainers (teachers/supervisors/health care system professionals/ directors (teaching managers) of schools...). This tool is necessary for decision-makers as well as for health care system professionals who share common objectives for changes at each level of intervention within the health system. Setting this adequacy implies interdisciplinary and participative approaches for concerned actors in order to provide an overall vision of a more broaden system than health district, small island with self-rationality, and in which they operate

Association of warfarin dose with genes involved in its action and metabolism

We report an extensive study of variability in genes encoding proteins that are believed to be involved in the action and biotransformation of warfarin. Warfarin is a commonly prescribed anticoagulant that is difficult to use because of the wide interindividual variation in dose requirements, the narrow therapeutic range and the risk of serious bleeding. We genotyped 201 patients for polymorphisms in 29 genes in the warfarin interactive pathways and tested them for association with dose requirement. In our study, polymorphisms in or flanking the genes VKORC1, CYP2C9, CYP2C18, CYP2C19, PROC, APOE, EPHX1, CALU, GGCX and ORM1-ORM2 and haplotypes of VKORC1, CYP2C9, CYP2C8, CYP2C19, PROC, F7, GGCX, PROZ, F9, NR1I2 and ORM1-ORM2 were associated with dose (P < 0.05). VKORC1, CYP2C9, CYP2C18 and CYP2C19 were significant after experiment-wise correction for multiple testing (P < 0.000175), however, the association of CYP2C18 and CYP2C19 was fully explained by linkage disequilibrium with CYP2C9*2 and/or *3. PROC and APOE were both significantly associated with dose after correction within each gene. A multiple regression model with VKORC1, CYP2C9, PROC and the non-genetic predictors age, bodyweight, drug interactions and indication for treatment jointly accounted for 62% of variance in warfarin dose. Weaker associations observed for other genes could explain up to ∼10% additional dose variance, but require testing and validation in an independent and larger data set. Translation of this knowledge into clinical guidelines for warfarin prescription will be likely to have a major impact on the safety and efficacy of warfarin. ELECTRONIC SUPPLEMENTARY MATERIAL: Supplementary material is available in the online version of this article at http://dx.doi.org/10.1007/s00439-006-0260-8 and is accessible for authorized users

What cancer tells us about general practice. Birth of an hypothesis

We are presenting in this paper a study about general practitioners' behaviours and attitudes towards the cancer patients they take care of. To begin with, the approaching methods are presented in a critical way. The choice of these methods finds an explanation in the fact that we were looking for an information as near as possible to the real physicians' behaviours and supplying, at the same time, an important material, giving us the opportunity to undertake an interpretative analysis of the different medical cases about cancer patients (64) written by some (12) of the general practitioners (31) who had been interviewed before about cancer in their medical practice. We have tried, particularly, to point out and to illustrate with some examples the specific contribution of a chosen method compared with another one; for instance, the interviews compared to the written questionnaire, and the medical cancer cases written by the physicians compared to the interviews realized with the same general practitioners. In this paper we are also trying to report the preoccupations, the difficulties and the theoretical and methodological problems which appeared during the process of this research. Concerning the findings of this study, it is possible to assert that the main hypothesis seems coherent with the collected information: it really seems that cancer, with its social image in which fear for suffering and for dying prevail, is for the general practitioner a borderline situation in which his personal psychology and his feelings seem to play a more important part than his medical knowledge. In this 'drama', his previous relationship to his patient, the type of cancer involved, the patient's social and family background, the way in which he represents his profession, his medical experience, as well as his specialists network, also play an important part. If cancer is a challenge for the general practitioner, it seems that it is especially a challenge for the image he has of himself as a physician, but also as a human being, precisely because the part he can play concerning the therapeutics is very small. So, unlike the thesis of some authors, we think that the general practitioners (as a result also of a widely spread adhesion to values of a non-technical idea of his practice) can assume a determinant function, by advising the patient, by doing in the same time a good following up of the disease he suffers from, and by keeping with him a good relationship, which he often qualifies as 'interesting'.

Met 358 to Arg Mutation of Alpha1-Antitrypsin Associated with Protein C Deficiency in a Patient with Mild Bleeding Tendency) Key words: a1-antitrypsin Pitts- burgh -protein C * bleeding -DNA * mutation

Abstract The molecular defect responsible for a dramatic prolongation of all standard clotting tests discovered in a 15-yr-old boy has been identified. Initial investigations revealed the presence of an activated Factor X (Factor Xa) and thrombin inhibitor which copurified with alpha1-antitrypsin (a,-AT), thereby suggesting the occurrence of an a,-AT variant similar to a,-AT Pittsburgh. This was confirmed by dot-blot analysis and direct sequencing after amplification by the polymerase chain reaction. A G to T transition at nucleotide 10038 results in the substitution of Met to an Arg, converting a,-AT into an Arg-Ser protease inhibitor (serpin) that inhibited thrombin and Factor Xa more effectively than antithrombin III. Surprisingly, there was no bleeding history in the proband. The common mutation Z, which may explain a reduced expression of the allele bearing the Arg 358 Met mutation, was not observed in the propositus&apos; DNA. To exclude the presence of another mutation, the coding regions and intron/exon junctions were sequenced. No other mutation was found. Recently, the patient experienced his first hemorrhagic episode at the age of 17. The level ofthe abnormal inhibitor had increased twofold 2 mo before. The large decrease in protein C concentration may account for the mild bleeding tendency in this case, despite the presence of the a,-AT Pittsburgh mutation. An abnormal protein C pattern was observed in patient&apos;s plasma, suggesting that the circulating deficiency might be due to a deleterious effect of the abnormal inhibitor on both intracellular processing and catabolism of protein C. (J. Clin