Carte de la Grèce ancienne pour servir à l'histoire des Juifs de Mr. Prideaux / G. par L. Borde

Échelle(s) : [1:2 900 000 environ], Echelle, Stades grecs a 600 au D. [600 = 3,8 cm]

Prédiction des durées de séjour en réadaptation en fonction du status fonctionnel

Objectif : En Suisse, la réadaptation est financée en partie par l'assureur qui fixe préalablement à l'admission un nombre de jours (durée garantie) qu'il s'engage à rembourser. Lorsqu'une durée garantie est trop courte, une demande de prolongation est nécessaire, induisant des démarches administratives. Les objectifs de cette étude étaient a) d'étudier le lien entre durées garanties et caractéristiques du patient ; b) d'estimer les coûts liés aux demandes de prolongation ; c) d'évaluer l'impact de l'introduction d'un modèle d'attribution de durée garantie basé sur l'état fonctionnel du patient.¦Méthodes : Les corrélations entre état fonctionnel, durée effective et durée garantie ont été testées sur 208 séjours représentatifs. Des durées garanties fictives ont été calculées à partir de la médiane de durée de séjour de 2 335 patients, groupés selon leur niveau fonctionnel (score des activités de base de la vie quotidienne (BAVQ) 0-1 vs 2-4 vs 5-6), puis comparées aux durées de séjour effectives et garanties.¦Résultats : L'état fonctionnel du patient n'est pas corrélé à la durée garantie, et 69 % des séjours nécessitent au moins une demande de prolongation, représentant 2,6 équivalents temps plein en temps administratif projeté sur le canton. L'application du modèle proposé réduirait de 28 % les demandes de prolongation, et n'augmenterait que marginalement la proportion de jours garantis en surplus (11,2 % contre 6,5 % actuellement).¦Conclusion : L'utilisation systématique d'un modèle d'attribution de durées garanties basées sur l'état fonctionnel du patient permettrait de réduire sensiblement les coûts administratifs liés aux demandes de prolongation, sans entraîner de risque accru d'une augmentation de la durée de séjour.

A 338-bp proximal fragment of the glucose transporter type 2 (GLUT2) promoter drives reporter gene expression in the pancreatic islets of transgenic mice.

The high Km glucose transporter GLUT2 is a membrane protein expressed in tissues involved in maintaining glucose homeostasis, and in cells where glucose-sensing is necessary. In many experimental models of diabetes, GLUT2 gene expression is decreased in pancreatic beta-cells, which could lead to a loss of glucose-induced insulin secretion. In order to identify factors involved in pancreatic beta-cell specific expression of GLUT2, we have recently cloned the murine GLUT2 promoter and identified cis-elements within the 338-bp of the proximal promoter capable of binding islet-specific trans-acting factors. Furthermore, in transient transfection studies, this 338-bp fragment could efficiently drive the expression of the chloramphenicol acetyl transferase (CAT) gene in cell lines derived from the endocrine pancreas, but displayed no promoter activity in non-pancreatic cells. In this report, we tested the cell-specific expression of a CAT reporter gene driven by a short (338 bp) and a larger (1311 bp) fragment of the GLUT2 promoter in transgenic mice. We generated ten transgenic lines that integrated one of the constructs. CAT mRNA expression in transgenic tissues was assessed using the RNAse protection assay and the quantitative reverse transcribed polymerase chain reaction (RT-PCR). Overall CAT mRNA expression for both constructs was low compared to endogenous GLUT2 mRNA levels but the reporter transcript could be detected in all animals in the pancreatic islets and the liver, and in a few transgenic lines in the kidney and the small intestine. The CAT protein was also present in Langerhans islets and in the liver for both constructs by immunocytochemistry. These findings suggest that the proximal 338 bp of the murine GLUT2 promoter contain cis-elements required for the islet-specific expression of GLUT2.

G-1 Appeal Activity in the Public Assistance Programs, April 2006

Appeal Activity in the Public Assistance Programs April 2006

G-1, Appeal Activity in the Public Assistance Programs, May 2006

G-1, Appeal Activity in the Public Assistance Programs, May 2006

The influence of Bone Morphogenic Protein-2 on the consolidation phase in a distraction osteogenesis model.

We asked whether locally applied recombinant-Bone Morphogenic Protein-2 (rh-BMP-2) with an absorbable Type I collagen sponge (ACS) carrier could enhance the consolidation phase in a callotasis model. We performed unilateral transverse osteotomy of the tibia in 21 immature male rabbits. After a latency period of 7 days, a 3-weeks distraction was begun at a rate of 0.5mm/12h. At the end of the distraction period (Day 28) animals were randomly divided into three groups and underwent a second surgical procedure: 6 rabbits in Group I (Control group; the callus was exposed and nothing was added), 6 rabbits in Group II (ACS group; receiving the absorbable collagen sponge soaked with saline) and 9 rabbits in Group III (rh-BMP-2/ACS group; receiving the ACS soaked with 100μg/kg of rh-BMP-2, Inductos(®), Medtronic). Starting at Day 28 we assessed quantitative and qualitative radiographic parameters as well as densitometric parameters every two weeks (Days 28, 42, 56, 70 and 84). Animals were sacrificed after 8 weeks of consolidation (Day 84). Qualitative radiographic evaluation revealed hypertrophic calluses in the Group III animals. The rh-BMP-2/ACS also influenced the development of the cortex of the calluses as shown by the modified radiographic patterns in Group III when compared to Groups I and II. Densitometric analysis revealed the bone mineral content (BMC) was significantly higher in the rh-BMP-2/ACS treated animals (Group III).

New genetic loci implicated in fasting glucose homeostasis and their impact on type 2 diabetes risk.

Levels of circulating glucose are tightly regulated. To identify new loci influencing glycemic traits, we performed meta-analyses of 21 genome-wide association studies informative for fasting glucose, fasting insulin and indices of beta-cell function (HOMA-B) and insulin resistance (HOMA-IR) in up to 46,186 nondiabetic participants. Follow-up of 25 loci in up to 76,558 additional subjects identified 16 loci associated with fasting glucose and HOMA-B and two loci associated with fasting insulin and HOMA-IR. These include nine loci newly associated with fasting glucose (in or near ADCY5, MADD, ADRA2A, CRY2, FADS1, GLIS3, SLC2A2, PROX1 and C2CD4B) and one influencing fasting insulin and HOMA-IR (near IGF1). We also demonstrated association of ADCY5, PROX1, GCK, GCKR and DGKB-TMEM195 with type 2 diabetes. Within these loci, likely biological candidate genes influence signal transduction, cell proliferation, development, glucose-sensing and circadian regulation. Our results demonstrate that genetic studies of glycemic traits can identify type 2 diabetes risk loci, as well as loci containing gene variants that are associated with a modest elevation in glucose levels but are not associated with overt diabetes.

G-1 Appeal Activity in the Public Assistance Programs, February 2005

Appeal activity in the Public Assistance Programs

G-1 Appeal Activity in the Public Assistance Programs, June 2006

G-1 June 2006 - Appeal Activity in the Public Assistance Programs

G-1 Appeal Activity in the Public Assistance Programs, July 2006

G-1 July 2006 - Appeal Activity in the Public Assistance Programs

G-1 Appeal Activity in the Public Assistance Programs, August 2002

Monthly report from the Iowa Department of Human Services

G-1 Appeal Activity in the Public Assistance Programs, January 2002

Monthly report from the Iowa Department of Human Services

G-1 Appeal Activity in the Public Assistance Programs, April 2002

Monthly report from the Iowa Department of Human Services

G-1 Appeal Activity in the Public Assistance Programs, May 2002

Monthly report from the Iowa Department of Human Services

G-1 Appeal Activity in the Public Assistance Programs, June 2002

Monthly report from the Iowa Department of Human Services