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951.
952.
Lea Brader Lars Rejnmark Carsten Carlberg Ursula Schwab Marjukka Kolehmainen Fredrik Rosqvist Lieselotte Cloetens Mona Landin-Olsson Ingibjorg Gunnarsdottir Kaisa S. Poutanen Karl-Heinz Herzig Ulf Risérus Markku J. Savolainen Inga Thorsdottir Matti Uusitupa Kjeld Hermansen 《European journal of nutrition》2014,53(4):1145-1145
953.
954.
This article argues that home-care policy in Ireland was ambiguous throughout the first decade of the 21st century: policy-makers expanded home care, but failed to develop policies to govern this expanded provision. As a result, home care became more widely available in the absence of a framework to govern access to services and to regulate care providers. We analysed official policy documents, statistics and policy critiques published between 2000 and 2010 in order to understand this incongruity between the expansion of home-care services and the failure to develop policies to govern access to and quality of services. The key factors that motivated home-care expansion in the Irish case were: (1) problems in the acute hospital sector and the perception of home care as a partial solution to these (political blame avoidance) and (2) significant GDP growth (until 2007) that provided politicians with the means to fund expansion in home-care services (political credit claiming). The key factors that inhibited the development of a policy framework to govern home-care services were: (1) weak governance structures in health services and decision-making at national level based on short-term political gain; (2) Ireland's adherence to the liberal welfare state model and concern about uncontrollable care costs in the face of population ageing; (3) until 2010, paucity of attention to home-care issues in the Irish media and (4) weak provider interest representation. The recent budgetary cutbacks in Ireland bring into sharp relief the political expediency of an unregulated domiciliary care sector and absence of entitlements to home care. We conclude that the forces that drive expanded provision are different from drivers of policy to govern home care and that weakness of governance structures and political advantages of the absence of regulation are the main reasons for the lack of standards and entitlement rules. 相似文献
955.
Elena Puris Markku Pasanen Veli‐Pekka Ranta Mikko Gynther Aleksanteri Petsalo Pirjo Kkel Ville Mnnist Jussi Pihlajamki 《Basic & clinical pharmacology & toxicology》2019,125(2):123-132
There is a lack of information about the changes in drug pharmacokinetics and cytochrome P450 (CYP) metabolism after bariatric surgery. Here, we investigated the effects of laparoscopic Roux‐en‐Y gastric bypass (LRYGB) surgery on pharmacokinetics of nine drugs given simultaneously which may reveal changes in the activities of the main CYPs. Eight obese subjects undergoing LRYGB received an oral cocktail containing nine drugs, substrates of various CYPs: melatonin (CYP1A2), nicotine (CYP2A6), bupropion (CYP2B6), repaglinide (CYP2C8), losartan (CYP2C9), omeprazole (CYP2C19/CYP3A4), dextromethorphan (CYP2D6), chlorzoxazone (CYP2E1) and midazolam (CYP3A). The 6‐hours pharmacokinetic profiles in serum and urine of each drug or corresponding metabolite as well as their metabolic ratios were compared before surgery with those at a median 1 year later. LRYGB exerted variable effects on the pharmacokinetics of these drugs. The geometric mean AUC0‐6 (90% confidence interval) of melatonin, bupropion, repaglinide, chlorzoxazone and midazolam after LRYGB was 27 (19%‐41%), 54 (43%‐67%), 44 (29%‐66%), 160 (129%‐197%) and 74 (62%‐90%) of the pre‐surgery values, respectively. The pharmacokinetics of losartan, omeprazole and dextromethorphan did not change in response to surgery. Nicotine was not detected in serum, while geometric mean of AUC0‐6 of its metabolite, cotinine, increased by 1.7 times after surgery. There were 3.6‐ and 1.3‐fold increases in the AUC ratios of 6‐hydroxymelatonin/melatonin and hydroxybupropion/bupropion, respectively. The cocktail revealed multiple pharmacokinetic changes occurring after LRYGB with the greatest effects observed for CYP1A2, CYP2C8 and CYP2E1 substrates. Future studies should be focused on CYP1A2, CYP2A6, CYP2C8 and CYP2B6 to clarify the changes in activities of these enzymes after LRYGB. 相似文献
956.
Ileana Montoya Perez Ivan Jambor Tapio Pahikkala Antti Airola Harri Merisaari Jani Saunavaara Saeid Alinezhad Riina‐Minna Vnnen Terhi Tallgrn Janne Verho Aida Kiviniemi Otto Ettala Juha Knaapila Kari T. Syvnen Markku Kallajoki Paula Vainio Hannu J. Aronen Kim Pettersson Peter J. Bostrm Pekka Taimen 《Journal of magnetic resonance imaging : JMRI》2020,51(5):1540-1553
957.
Ileana Montoya Perez Ivan Jambor Tommi Kauko Janne Verho Otto Ettala Ugo Falagario Harri Merisaari Aida Kiviniemi Pekka Taimen Kari T. Syvnen Juha Knaapila Marjo Seppnen Antti Rannikko Jarno Riikonen Markku Kallajoki Tuomas Mirtti Tarja Lamminen Jani Saunavaara Tapio Pahikkala Peter J. Bostrm Hannu J. Aronen 《Journal of magnetic resonance imaging : JMRI》2020,51(5):1556-1567
958.
Francesco Sambo Alberto Malovini Niina Sandholm Monica Stavarachi Carol Forsblom Ville-Petteri Mäkinen Valma Harjutsalo Raija Lithovius Daniel Gordin Maija Parkkonen Markku Saraheimo Lena M. Thorn Nina Tolonen Johan Wadén Bing He Anne-May Österholm Jaako Tuomilehto Maria Lajer Rany M. Salem Amy Jayne McKnight Lise Tarnow Nicolae M. Panduru Nicola Barbarini Barbara Di Camillo Gianna M. Toffolo Karl Tryggvason Riccardo Bellazzi Claudio Cobelli Per-Henrik Groop 《Diabetologia》2014,57(8):1611-1622
Aims/hypothesis
Diabetic nephropathy is a major diabetic complication, and diabetes is the leading cause of end-stage renal disease (ESRD). Family studies suggest a hereditary component for diabetic nephropathy. However, only a few genes have been associated with diabetic nephropathy or ESRD in diabetic patients. Our aim was to detect novel genetic variants associated with diabetic nephropathy and ESRD.Methods
We exploited a novel algorithm, ‘Bag of Naive Bayes’, whose marker selection strategy is complementary to that of conventional genome-wide association models based on univariate association tests. The analysis was performed on a genome-wide association study of 3,464 patients with type 1 diabetes from the Finnish Diabetic Nephropathy (FinnDiane) Study and subsequently replicated with 4,263 type 1 diabetes patients from the Steno Diabetes Centre, the All Ireland-Warren 3-Genetics of Kidneys in Diabetes UK collection (UK–Republic of Ireland) and the Genetics of Kidneys in Diabetes US Study (GoKinD US).Results
Five genetic loci (WNT4/ZBTB40-rs12137135, RGMA/MCTP2-rs17709344, MAPRE1P2-rs1670754, SEMA6D/SLC24A5-rs12917114 and SIK1-rs2838302) were associated with ESRD in the FinnDiane study. An association between ESRD and rs17709344, tagging the previously identified rs12437854 and located between the RGMA and MCTP2 genes, was replicated in independent case–control cohorts. rs12917114 near SEMA6D was associated with ESRD in the replication cohorts under the genotypic model (p?<?0.05), and rs12137135 upstream of WNT4 was associated with ESRD in Steno.Conclusions/interpretation
This study supports the previously identified findings on the RGMA/MCTP2 region and suggests novel susceptibility loci for ESRD. This highlights the importance of applying complementary statistical methods to detect novel genetic variants in diabetic nephropathy and, in general, in complex diseases. 相似文献959.
Niina Sandholm Carol Forsblom Ville-Petteri Mäkinen Amy Jayne McKnight Anne-May Österholm Bing He Valma Harjutsalo Raija Lithovius Daniel Gordin Maija Parkkonen Markku Saraheimo Lena M. Thorn Nina Tolonen Johan Wadén Jaakko Tuomilehto Maria Lajer Emma Ahlqvist Anna Möllsten M. Loredana Marcovecchio Jason Cooper David Dunger Andrew D. Paterson Gianpaolo Zerbini Leif Groop Lise Tarnow Alexander P. Maxwell Karl Tryggvason Per-Henrik Groop 《Diabetologia》2014,57(6):1143-1153
Aims/hypothesis
An abnormal urinary albumin excretion rate (AER) is often the first clinically detectable manifestation of diabetic nephropathy. Our aim was to estimate the heritability and to detect genetic variation associated with elevated AER in patients with type 1 diabetes.Methods
The discovery phase genome-wide association study (GWAS) included 1,925 patients with type 1 diabetes and with data on 24 h AER. AER was analysed as a continuous trait and the analysis was stratified by the use of antihypertensive medication. Signals with a p value <10?4 were followed up in 3,750 additional patients with type 1 diabetes from seven studies.Results
The narrow-sense heritability, captured with our genotyping platform, was estimated to explain 27.3% of the total AER variability, and 37.6% after adjustment for covariates. In the discovery stage, five single nucleotide polymorphisms in the GLRA3 gene were strongly associated with albuminuria (p?<?5?×?10?8). In the replication group, a nominally significant association (p?=?0.035) was observed between albuminuria and rs1564939 in GLRA3, but this was in the opposite direction. Sequencing of the surrounding genetic region in 48 Finnish and 48 UK individuals supported the possibility that population-specific rare variants contribute to the synthetic association observed at the common variants in GLRA3. The strongest replication (p?=?0.026) was obtained for rs2410601 between the PSD3 and SH2D4A genes. Pathway analysis highlighted natural killer cell mediated immunity processes.Conclusions/interpretation
This study suggests novel pathways and molecular mechanisms for the pathogenesis of albuminuria in type 1 diabetes. 相似文献960.
Merja K. Laine Johan G. Eriksson Urho M. Kujala Niko S. Wasenius Jaakko Kaprio Heli M. Bäckmand Markku Peltonen Tuomas H. Mertsalmi Seppo Sarna 《Diabetologia》2014,57(2):270-274