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Background: The term dermatoporosis (DP) is used to describe the clinical signs and functional consequences of age‐related extreme skin fragility. It is associated with potentially severe complications, including deep dissecting hematomas and extended skin lacerations. No studies have evaluated the prevalence and risk factors of DP in adults aged 75 and older. Methods: The aim of our study was to assess the prevalence, complications, and risk factors of DP in a cohort of older patients hospitalized in a rehabilitation center. A case–control, single‐center study was conducted between September and October 2020 in our rehabilitation ward, Rothschild Hospital, Paris, France. A senior dermatologist and a resident in geriatric medicine performed a systematic dermatological examination. The presence of DP, its stage, its location, and complications were collected, as were demographical data, comorbidities, past sun exposure, skin phototype, treatments, and biological data. Results: A total of 101 patients (62 women, median age 86 years [extreme values 75–104]) were included. The overall prevalence of DP was 27%. Stage 1 was the most frequent. DP was mainly located on the upper limbs. Ten (37%) patients had a DP complication: eight (30%) skin lacerations and two (7%) deep dissecting hematomas. Multivariate analysis revealed a significant association between DP and age (odds ratio [OR] 5.82, 95% confidence interval [CI] 1.67–24.92, p = 0.009), smoking (OR 8.67, 95% CI 2.59–34.85, p = 0.001), recreational sun exposure (OR 4.23, 95% CI 1.30–15.21, p = 0.02), and anticoagulant therapy (OR 4.53, 95% CI 1.32–17.26, p = 0.02). Conclusion: Our study is the first to analyze the prevalence and risk factors of DP in older adults in rehabilitation. Frequency of DP makes it relevant for the geriatrician and should be described more to prevent potential severe complications. A multicentric study, with inpatients and outpatients, could evaluate the prevalence of DP in a more representative older adult population. [ABSTRACT FROM AUTHOR]

Sedative‐use disorder can occur in elderly individuals, but remains a taboo subject. France is the second top‐consuming country of benzodiazepines (BZDs) and Z drugs in Europe, with 38% of women >80 years old using these drugs. Despite the recommendations of the French National Authority for Health (HAS) to general practitioners, deprescription remains rare. The aim of this study was to understand the perception of healthcare providers towards BZD or Z drug withdrawal within a psychogeriatric unit and to provide insights from advanced practice nurses (APRNs) on this topic. Eight healthcare providers from different professions in a psychogeriatric unit were interviewed. The interviews were recorded and transcribed verbatim, and the data were analysed following the interpretive phenomenological approach. The COREQ statement was used as a guide in the reporting of the study. Four themes were identified in the interview transcripts: (i) problems specific to the elderly; (ii) problems specific to BZD or Z drug consumption; (iii) present care; and (iv) envisioned practice. While the healthcare providers interviewed appeared to have knowledge on the adverse effects of BZDs, it appears difficult to taper the use of BZDs outside crisis periods of behaviour disorders in elderly patients. Caregivers recommend an evolution of practices, such as introducing BDZ and Z drug withdrawal programs that could involve the emerging profession of APRNs in general practice in France. APRNs could be a valuable resource to screen for BZD‐related disorders and to manage withdrawal strategies in complex cases. [ABSTRACT FROM AUTHOR]

Adult neurogenesis in the subventricular zone of the lateral ventricle decreases with age. In the subventricular zone, the specialized extracellular matrix structures, known as fractones, contact neural stem cells and regulate neurogenesis. Fractones are composed of extracellular matrix components, such as heparan sulfate proteoglycans. We previously found that fractones capture and store fibroblast growth factor 2 (FGF-2) via heparan sulfate binding, and may deliver FGF-2 to neural stem cells in a timely manner. The heparan sulfate (HS) chains in the fractones of the aged subventricular zone are modified based on immunohistochemistry. However, how aging affects fractone composition and subsequent FGF-2 signaling and neurogenesis remains unknown. The formation of the FGF-fibroblast growth factor receptor-HS complex is necessary to activate FGF-2 signaling and induce the phosphorylation of extracellular signalregulated kinase (Erk1/2). In this study, we observed a reduction inHS6-O-sulfation, which is critical for FGF-2 signal transduction, and failure of the FGF-2-induced phosphorylation of Erk1/2 in the aged subventricular zone. In addition, we observed increased HS 6-O-endo-sulfatase, an enzyme that may be responsible for the HS modifications in aged fractones. In conclusion, the data revealed that heparan sulfate 6-O-sulfation is reduced and FGF- 2-dependent Erk1/2 signaling is impaired in the aged subventricular zone. HS modifications in fractones might play a role in the reduced neurogenic activity in aging brains. [ABSTRACT FROM AUTHOR]

Objectives: Fractones are extracellular matrix structures that form a niche for neural stem cells and their immediate progeny in the subventricular zone of the lateral ventricle (SVZa), the primary neurogenic zone in the adult brain. We have previously shown that heparan sulphates (HS) associated with fractones bind fibroblast growth factor-2 (FGF-2), a powerful mitotic growth factor in the SVZa. Here, our objective was to determine whether the binding of FGF-2 to fractone-HS is implicated in the mechanism leading to cell proliferation in the SVZa. Materials and methods: Heparitinase-1 was intracerebroventricularly injected with FGF-2 to N-desulfate HS proteoglycans and determine whether the loss of HS and of FGF-2 binding to fractones modifies FGF-2 effect on cell proliferation. We also examined in vivo the binding of Alexa-Fluor-FGF-2 in relationship with the location of HS immunoreactivity in the SVZa. Results: Heparatinase-1 drastically reduced the stimulatory effect of FGF-2 on cell proliferation in the SVZa. Alexa-Fluor-FGF-2 binding was strictly co-localized with HS immunoreactivity in fractones and adjacent vascular basement membranes in the SVZa. Conclusions: Our results demonstrate that FGF-2 requires HS to stimulate cell proliferation in the SVZa and suggest that HS associated with fractones and vascular basement membranes are responsible for activating FGF-2. Therefore, fractones and vascular basement membranes may function as a HS niche to drive cell proliferation in the adult neurogenic zone. [ABSTRACT FROM AUTHOR]

Barriers to management of HCV in injection drug users are related to patients, health providers, and facilities. In a primary care drug user's addiction centre we studied access to HCV standard of care before and after using an onsite total care concept provided by a multidisciplinary team and noninvasive liver fibrosis evaluation. A total of 586 patients were seen between 2002 and 2004. The majority, 417 patients, were HCV positive and of these patients 337 were tested positive for HCV RNA. In 2002, patients were sent to the hospital. with the Starting of 2003, patients were offered standard of care HCV management in the center by a team of general practitioners, a consultant hepatologist, psychiatrists, nurses, and a health counsellor. Liver fibrosis was assessed by a non invasive method. In 2002, 6 patients had liver fibrosis assessment at hospital facilities, 4 patients were assessed with liver biopsy and 2 patients with Fibrotest-Actitest. 2 patients were treated for HCV at hospital. In 2003 and 2004, 224 patients were assessed with Fibrotest-Actitest on site. Of these, 85 were treated for HCV. SVR was achieved in 43%.We conclude that the combination of an onsite multidisciplinary team with the use of a noninvasive assessment method led to improved management of HCV infection in drug users' primary care facility. [ABSTRACT FROM AUTHOR]

Background Aim Study design Results Conclusion Relevance to Clinical Practice Most children admitted to a paediatric intensive care unit (PICU) now survive because of improvements in care. Many studies have identified the psychological, functional, cognitive and social impact of PICU admission on a child and their family. However, expert recommendations on follow‐up are lacking.To identify the strategies of clinical follow‐up after PICU discharge performed from 2001 to 2021.This scoping review was undertaken between January and April 2021 using three databases: PubMed, EMBASE and CINAHL. The search strategy consisted of a combination of keywords, including PICU, post‐PICU discharge and follow‐up in articles published between 2001 and 2021. The results are reported according to PRISMA‐ScR guidelines.Six‐hundred and fifty‐two articles were identified and 68 were analysed. Median age was 4.5 years and the two main reasons for PICU admission were cardiorespiratory failure and sepsis. Median length of PICU stay was 8 days. Most follow‐up was carried out by research units (88%), while 6% of studies reported follow‐up by a multidisciplinary PICU team. The most common follow‐up schedule included an assessment at PICU discharge, and then at 3, 6 and 12 months. Follow‐up for >1 year was reported in 20% of studies. One third of studies focused on follow‐up quality of life and neurological outcomes. Parental emotional impact was assessed in 7% of studies.Follow‐up after PICU discharge was highly heterogeneous regarding timing, health care professionals involved and assessment methods. There is an urgent need for standardization and coordination of PICU follow‐up because of the increasing number of patients impacted by a PICU stay.Although most patients admitted to a paediatric intensive care unit (PICU) now survive; they may develop paediatric post‐intensive care syndrome (PICS‐P). To our knowledge, there are currently no clinical guidelines regarding follow‐up after PICU discharge. This review summarizes current approaches to follow‐up after PICU discharge, including how it is carried out, who is involved and what the main aims of assessment are. [ABSTRACT FROM AUTHOR]

Familial Mediterranean fever (FMF) is the most frequent hereditary systemic autoinflammatory syndrome. FMF is usually caused by biallelic mutations in the MEFV gene, encoding Pyrin. Conclusive genetic evidence lacks for about 30% of patients diagnosed with clinical FMF. Pyrin is an inflammasome sensor maintained inactive by two kinases (PKN1/2). The consequences of MEFV mutations on inflammasome activation are still poorly understood. Here, we demonstrate that PKC superfamily inhibitors trigger inflammasome activation in monocytes from FMF patients while they trigger a delayed apoptosis in monocytes from healthy donors. The expression of the pathogenic p.M694V MEFV allele is necessary and sufficient for PKC inhibitors (or mutations precluding Pyrin phosphorylation) to trigger caspase‐1‐ and gasdermin D‐mediated pyroptosis. In line with colchicine efficacy in patients, colchicine fully blocks this response in FMF patients' monocytes. These results indicate that Pyrin inflammasome activation is solely controlled by Pyrin (de)phosphorylation in FMF patients while a second control mechanism restricts its activation in healthy donors/non‐FMF patients. This study paves the way toward a functional characterization of MEFV variants and a functional test to diagnose FMF. Synopsis: Familial Mediterranean fever (FMF) is a systemic auto‐inflammatory disease associated with MEFV mutations. MEFV encodes Pyrin, an inflammasome sensor. The link between MEFV mutations and the dysregulated activation of the Pyrin inflammasome observed in FMF patients is unclear. Pyrin dephosphorylation is insufficient to trigger full inflammasome activation in healthy donors'monocytes while it is sufficient in FMF patients monocytes.The pathogenic MEFV mutation most frequently observed in FMF patients triggers constitutive inflammasome activation only when combined to a phosphonull MEFV mutation.UCN‐01‐induced dephosphorylation of Pyrin triggers inflammasome activation in FMF patients' monocytes but not in monocytes from other patients paving the way to a functional diagnosis of FMF. [ABSTRACT FROM AUTHOR]