BackgroundPatients undergoing pancreatic resection frequently require rehabilitation facilities after hospital discharge. We evaluated the predictive role of validated markers of frailty on rehabilitation facility placement to identify patients who may require this service.MethodsSingle-center retrospective cohort study of patients who underwent pancreatic resection from 2010 to 2015. 90-day morbidity and mortality were calculated. Postoperative validated markers of frailty (Activities of Daily Living scale, Braden scale [assesses pressure ulcer risk, lower scores = higher risk] and Morse fall scale) were evaluated via multivariate regression to identify predictors of discharge to rehabilitation facility.Results470 patients with complete data were included. Mean age was 62 and 49.2% were male. Postoperative median length of stay (LOS) was 8 (IQR 7–10). 92 (19.66%) patients were discharged to rehabilitation facilities and 138 (29.49%) patients were readmitted within 90 days. On multivariate analysis, age, sex, LOS > 8 days, inpatient Comprehensive Complication Index (CCI) and initial Braden scale were predictive of rehabilitation placement.ConclusionA marker of frailty routinely collected daily by nursing staff, the Braden scale, is available to help surgeons predict the need for postoperative rehabilitation placement after pancreatic resection. Engaging discharge planning services for at-risk patients may help prevent delayed hospital discharge and should be further evaluated. 相似文献
The global spread of antimicrobial resistance and the increasing number of immune‐compromised patients are major challenges in modern medicine. Targeting bacterial virulence or the human host immune system to increase host defence are important strategies in the search for novel antimicrobial drugs. We investigated the inflammatory response of the synthetic short antimicrobial peptide LTX21 in two model systems: a human whole blood ex vivo model and a murine in vivo peritoneum model – both reflecting early innate immune response. In the whole blood model, LTX21 increased the secretion of a range of different cytokines, decreased the level of tumour necrosis factor (TNF) and activated the complement system. In a haemolysis assay, we found 2.5% haemolysis at a LTX21 concentration of 500 mg/L. In the murine model, increased influx of white blood cells (WBCs) and polymorphonuclear neutrophils (PMNs) in the murine peritoneal cavity was observed after treatment with LTX21. In addition, LTX21 increased monocyte chemoattractant protein‐1 (MCP‐1). In conclusion, LTX21 affected the inflammatory response; the increase in cytokine secretion, complement activation and WBC influx indicates an activated inflammatory response. The present results indicate the impact of LTX21 on the host–pathogen interplay. Whether this will also affect the course of infection has to be investigated. 相似文献
Episodic memory is defined as the ability to recall events in a spatiotemporal context. Formation of such memories is critically dependent on the hippocampal formation and its inputs from the entorhinal cortex. To be able to support the formation of episodic memories, entorhinal cortex and hippocampal formation should contain a neuronal code that follows several requirements. First, the code should include information about position of the agent (“where”), sequence of events (“when”), and the content of the experience itself (“what”). Second, the code should arise instantly thereby being able to support memory formation of one‐shot experiences. For successful encoding and to avoid interference between memories during recall, variations in location, time, or in content of experience should result in unique ensemble activity. Finally, the code should capture several different resolutions of experience so that the necessary details relevant for future memory‐based predictions will be stored. We review how neuronal codes in entorhinal cortex and hippocampus follow these requirements and argue that during formation of episodic memories entorhinal cortex provides hippocampus with instant information about ongoing experience. Such information originates from (a) spatially modulated neurons in medial entorhinal cortex, including grid cells, which provide a stable and universal positional metric of the environment; (b) a continuously varying signal in lateral entorhinal cortex providing a code for the temporal progression of events; and (c) entorhinal neurons coding the content of experiences exemplified by object‐coding and odor‐selective neurons. During formation of episodic memories, information from these systems are thought to be encoded as unique sequential ensemble activity in hippocampus, thereby encoding associations between the content of an event and its spatial and temporal contexts. Upon exposure to parts of the encoded stimuli, activity in these ensembles can be reinstated, leading to reactivation of the encoded activity pattern and memory recollection. 相似文献
Myocardial infarction is a frequent complication of cardiovascular disease leading to high morbidity and mortality worldwide. Elevated C-reactive protein (CRP) levels after myocardial infarction are associated with heart failure and poor prognosis. Cardiomyocyte microvesicles (CMV) are released during hypoxic conditions and can act as mediators of intercellular communication. MicroRNA (miRNA) are short non-coding RNA which can alter cellular mRNA-translation. Microvesicles (MV) have been shown to contain distinct patterns of miRNA from their parent cells which can affect protein expression in target cells. We hypothesized that miRNA containing CMV mediate hepatic CRP expression after cardiomyocyte hypoxia. H9c2-cells were cultured and murine cardiomyocytes were isolated from whole murine hearts. H9c2- and murine cardiomyocytes were exposed to hypoxic conditions using a hypoxia chamber. Microvesicles were isolated by differential centrifugation and analysed by flow cytometry. Next-generation-sequencing was performed to determine the miRNA-expression profile in H9c2 CMV compared to their parent cells. Microvesicles were incubated with a co-culture model of the liver consisting of THP-1 macrophages and HepG2 cells. IL-6 and CRP expression in the co-culture was assessed by qPCR and ELISA. CMV contain a distinct pattern of miRNA compared to their parent cells including many inflammation-related miRNA. CMV induced IL-6 expression in THP-1 macrophages alone and CRP expression in the hepatic co-culture model. MV from hypoxic cardiomyocytes can mediate CRP expression in a hepatic co-culture model. Further studies will have to show whether these effects are reproducible in-vivo.
X-linked adrenoleukodystrophy (X-ALD) is a devastating neurological disorder caused by mutations in the ABCD1 gene that encodes a peroxisomal ATP-binding cassette transporter (ABCD1) responsible for transport of CoA-activated very long-chain fatty acids (VLCFA) into the peroxisome for degradation. We used recombinant adenoassociated virus serotype 9 (rAAV9) vector for delivery of the human ABCD1 gene (ABCD1) to mouse central nervous system (CNS). In vitro, efficient delivery of ABCD1 gene was achieved in primary mixed brain glial cells from Abcd1−/− mice as well as X-ALD patient fibroblasts. Importantly, human ABCD1 localized to the peroxisome, and AAV-ABCD1 transduction showed a dose-dependent effect in reducing VLCFA. In vivo, AAV9-ABCD1 was delivered to Abcd1−/− mouse CNS by either stereotactic intracerebroventricular (ICV) or intravenous (IV) injections. Astrocytes, microglia and neurons were the major target cell types following ICV injection, while IV injection also delivered to microvascular endothelial cells and oligodendrocytes. IV injection also yielded high transduction of the adrenal gland. Importantly, IV injection of AAV9-ABCD1 reduced VLCFA in mouse brain and spinal cord. We conclude that AAV9-mediated ABCD1 gene transfer is able to reach target cells in the nervous system and adrenal gland as well as reduce VLCFA in culture and a mouse model of X-ALD. 相似文献
This document offers guidance to clinicians and facilities on the use of telemedicine to deliver medically necessary evaluation and management of change of condition for nursing home residents.
Settings and participants
Members of the telemedicine workgroup of AMDA—The Society for Post-Acute Long-Term Medicine-developed this guideline through both telephonic and face-to-face meetings between April 2017 and September 2018. The guideline is based on the currently available research, experience, and expertise of the workgroup's members, including a summary of a recently completed systematic mixed studies literature review to determine evidence for telemedicine to reduce emergency department visits or hospitalizations of nursing home residents.
Results
Research and experience to date support the use of telemedicine as a tool in change of condition assessment and management as a means of reducing unnecessary emergency department visits and hospitalization. Telemedicine-delivered care should be integrated into the primary care of the resident and delivered by providers with competency in post-acute long-term care. The development and sustainability of telemedicine programs is heavily dependent on financial implications. Quality measures should be defined for telemedicine programs in nursing homes.
Conclusions/Implications
Telemedicine programs in nursing homes can contribute to the delivery of timely, high quality medical care, which reduces unnecessary hospitalization. Reimbursement for telemedicine-driven care should be based upon medical necessity of visits to care and the maintenance of quality standards. More studies are needed to understand which telemedicine tools and processes are most effective in improving outcomes for nursing home residents. 相似文献
Journal of Neurology - Niemann–Pick disease type C1 (NPC1) is a rare autosomal-recessive lysosomal storage disorder presenting with a broad clinical spectrum ranging from a severe... 相似文献