Peckbennett0232

To analyse the impact of a medication reconciliation toolkit (OCM) which details all the treatment at the admission, intra-hospital therapeutic adjustment and their justifications, on the transmission and quality of extra-hospital follow-up of prescribing recommendations.

The OCM was fulfilled with the prescriptions of patient aged ≥75 years admitted to a geriatric short-stay unit and sent to general practitioners (GPs) upon discharge. Drug discrepancies (DD) and exposure to polypharmacy after intra-hospital medication conciliation and the ambulatory repeat prescribing (1 month after discharge) were measured. GPs' satisfaction was investigated.

The medication list of 173 patients (1242 molecules; median 8 molecules/day) were reconciled, optimized, and transmitted using the OCM to the 89 GPs of the 103 patients who were returned home. Intra-hospital conciliation identified 779 DD (4.6 ± 2.3) of which 39.0% were missed treatment additions. After renewal of the discharge order, only 1.6 ± 1.6 DD were measured. Between admission, discharge, and repeat prescribing, exposure to polypharmacy was reduced from 83.2 to 74.6 and 67.7% (p<0.05). Despite a 31.5% response rate to the mail questionnaire, 79.3% of physicians thought the OCM facilitated continuity of care and 75.5% wanted it generalized.

This study shows that the OCM is a useful tool and of interest for documenting the process of intra-hospital therapeutic optimization and in the rapid transmission and the follow-up of recommendations by partners in the community.

This study shows that the OCM is a useful tool and of interest for documenting the process of intra-hospital therapeutic optimization and in the rapid transmission and the follow-up of recommendations by partners in the community.The Coronarovirus disease 2019 (Covid-19) outbreak strongly affected nursing and was responsible for a high mortality rate. During the pandemic of March-May 2020, 17 French nursing homes organized staff confinement periods with residents 24 hours a day and 7 days a week, to reduce the risk of entry of the SARS-CoV-2 virus into their facilities, in a context where visits to residents were prohibited. By means of a telephone survey of their directors, we observed that 16 nursing homes (94%) had no cases of COVID-19 among the residents, and that mortality from COVID-19 was very low compared to that recorded at the national level by Santé publique France (p less then 10-4). Moreover, the number of cases of Covid-19 among the staff of these nursing homes was also lower than that recorded by Santé publique France (p less then 10-4). These establishments experienced certain difficulties which the directors managed to overcome and the investment of these teams was widely appreciated by the families of the residents and through the press.Drug treatment of 3D cancer spheroids more accurately reflects in vivo therapeutic responses compared to adherent culture studies. In EGFR-mutated lung adenocarcinoma, EGFR-TKIs show enhanced efficacy in spheroid cultures. Simultaneous inhibition of multiple parallel RTKs further enhances EGFR-TKI effectiveness. We show that the common RTK signaling intermediate SOS1 was required for 3D spheroid growth of EGFR-mutated NSCLC cells. Using two distinct measures of pharmacologic synergy, we demonstrated that SOS1 inhibition strongly synergized with EGFR-TKI treatment only in 3D spheroid cultures. FTY720 Combined EGFR- and SOS1-inhibition markedly inhibited Raf/MEK/ERK and PI3K/AKT signaling. Finally, broad assessment of the pharmacologic landscape of drug-drug interactions downstream of mutated EGFR revealed synergy when combining an EGFR-TKI with inhibitors of proximal signaling intermediates SOS1 and SHP2, but not inhibitors of downstream RAS effector pathways. These data indicate that vertical inhibition of proximal EGFR signaling should be pursued as a potential therapy to treat EGFR-mutated tumors.Fibrodysplasia ossificans progressiva (FOP) is a rare human genetic disorder characterized by altered skeletal development and extraskeletal ossification. All cases of FOP are caused by activating mutations in the type I BMP/TGFβ cell surface receptor ACVR1, which over-activates signaling through phospho-Smad1/5 (pSmad1/5). To investigate the mechanism by which FOP-ACVR1 enhances pSmad1/5 activation, we used zebrafish embryonic dorsoventral (DV) patterning as an assay for BMP signaling. We determined that the FOP mutants ACVR1-R206H and -G328R do not require their ligand binding domain to over-activate BMP signaling in DV patterning. However, intact ACVR1-R206H has the ability to respond to both Bmp7 and Activin A ligands. Additionally, BMPR1, a type I BMP receptor normally required for BMP-mediated patterning of the embryo, is dispensable for both ligand-independent signaling pathway activation and ligand-responsive signaling hyperactivation by ACVR1-R206H. These results demonstrate that FOP-ACVR1 is not constrained by the same receptor/ligand partner requirements as WT-ACVR1.DNA replication is needed to duplicate a cell's genome in S phase and segregate it during cell division. Previous work in Leishmania detected DNA replication initiation at just a single region in each chromosome, an organisation predicted to be insufficient for complete genome duplication within S phase. Here, we show that acetylated histone H3 (AcH3), base J and a kinetochore factor co-localise in each chromosome at only a single locus, which corresponds with previously mapped DNA replication initiation regions and is demarcated by localised G/T skew and G4 patterns. In addition, we describe previously undetected subtelomeric DNA replication in G2/M and G1-phase-enriched cells. Finally, we show that subtelomeric DNA replication, unlike chromosome-internal DNA replication, is sensitive to hydroxyurea and dependent on 9-1-1 activity. These findings indicate that Leishmania's genome duplication programme employs subtelomeric DNA replication initiation, possibly extending beyond S phase, to support predominantly chromosome-internal DNA replication initiation within S phase.

The pathological feigning of disease can be seen in all medical disciplines. It is associated with variegated symptom presentations, self-inflicted injuries, forced but unnecessary interventions, unusual and protracted recoveries, and frequent changes of treating physician. Factitious illness is often difficult to distinguish from functional or dissociative disorders on the one hand, and from malingering on the other. Many cases, even fatal ones, probably go unrecognized. The suspicion that a patient's problem may be, at least in part, factitious is subject to a strong taboo and generally rests on supportive rather than conclusive evidence. The danger of misdiagnosis and inappropriate treatment is high.

On the basis of a selective review of current literature, we summarize the phenomenology of factitious disorders and present concrete strategies for dealing with suspected factitious disorders.

Through the early recognition and assessment of clues and warning signs, the clinician will be able to judge whether a factitious disorder should be considered as a differential diagnosis, as a comorbid disturbance, or as the suspected main diagnosis.