Vascular injury and orthopaedics.
Ontology highlight
ABSTRACT:
SUBMITTER: Parvizi J
PROVIDER: S-EPMC6287961 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description: Not available
| S-EPMC6977530 | biostudies-literature
Project description:There is a growing interest in the application of artificial intelligence (AI) to orthopaedic surgery. This review aims to identify and characterise research in this field, in order to understand the extent, range and nature of this work, and act as springboard to stimulate future studies. A scoping review, a form of structured evidence synthesis, was conducted to summarise the use of AI in orthopaedics. A literature search (1946-2019) identified 222 studies eligible for inclusion. These studies were predominantly small and retrospective. There has been significant growth in the number of papers published in the last three years, mainly from the USA (37%). The majority of research used AI for image interpretation (45%) or as a clinical decision tool (25%). Spine (43%), knee (23%) and hip (14%) were the regions of the body most commonly studied. The application of artificial intelligence to orthopaedics is growing. However, the scope of its use so far remains limited, both in terms of its possible clinical applications, and the sub-specialty areas of the body which have been studied. A standardized method of reporting AI studies would allow direct assessment and comparison. Prospective studies are required to validate AI tools for clinical use.
| S-EPMC8610245 | biostudies-literature
Project description:The novel Coronavirus (COVID-19) pandemic has placed an immense strain on health care systems and orthopedic surgeons across the world. To limit the spread, federal and state governments mandated the cancellation of all nonurgent surgical cases to address surging hospital admissions and manage workforce and resource reallocation. During the pandemic surge, thousands of surgical cancellations have been required. We outline our experience through the onset and advance of the surge, detail our incident response and discuss the transition toward recovery. Level of Evidence: Level V.
| S-EPMC7245196 | biostudies-literature
Project description:The global burden of ischaemic strokes is almost 4-fold greater than haemorrhagic strokes. Current evidence suggests that 25-30% of ischaemic stroke survivors develop immediate or delayed vascular cognitive impairment (VCI) or vascular dementia (VaD). Dementia after stroke injury may encompass all types of cognitive disorders. States of cognitive dysfunction before the index stroke are described under the umbrella of pre-stroke dementia, which may entail vascular changes as well as insidious neurodegenerative processes. Risk factors for cognitive impairment and dementia after stroke are multifactorial including older age, family history, genetic variants, low educational status, vascular comorbidities, prior transient ischaemic attack or recurrent stroke and depressive illness. Neuroimaging determinants of dementia after stroke comprise silent brain infarcts, white matter changes, lacunar infarcts and medial temporal lobe atrophy. Until recently, the neuropathology of dementia after stroke was poorly defined. Most of post-stroke dementia is consistent with VaD involving multiple substrates. Microinfarction, microvascular changes related to blood-brain barrier damage, focal neuronal atrophy and low burden of co-existing neurodegenerative pathology appear key substrates of dementia after stroke injury. The elucidation of mechanisms of dementia after stroke injury will enable establishment of effective strategy for symptomatic relief and prevention. Controlling vascular disease risk factors is essential to reduce the burden of cognitive dysfunction after stroke. This article is part of a Special Issue entitled: Vascular Contributions to Cognitive Impairment and Dementia edited by M. Paul Murphy, Roderick A. Corriveau and Donna M. Wilcock.
| S-EPMC4827373 | biostudies-literature
Project description:Traumatic microbleeds are small foci of hypointensity seen on T2*-weighted MRI in patients following head trauma that have previously been considered a marker of axonal injury. The linear appearance and location of some traumatic microbleeds suggests a vascular origin. The aims of this study were to: (i) identify and characterize traumatic microbleeds in patients with acute traumatic brain injury; (ii) determine whether appearance of traumatic microbleeds predict clinical outcome; and (iii) describe the pathology underlying traumatic microbleeds in an index patient. Patients presenting to the emergency department following acute head trauma who received a head CT were enrolled within 48 h of injury and received a research MRI. Disability was defined using Glasgow Outcome Scale-Extended ≤6 at follow-up. All magnetic resonance images were interpreted prospectively and were used for subsequent analysis of traumatic microbleeds. Lesions on T2* MRI were stratified based on 'linear' streak-like or 'punctate' petechial-appearing traumatic microbleeds. The brain of an enrolled subject imaged acutely was procured following death for evaluation of traumatic microbleeds using MRI targeted pathology methods. Of the 439 patients enrolled over 78 months, 31% (134/439) had evidence of punctate and/or linear traumatic microbleeds on MRI. Severity of injury, mechanism of injury, and CT findings were associated with traumatic microbleeds on MRI. The presence of traumatic microbleeds was an independent predictor of disability (P < 0.05; odds ratio = 2.5). No differences were found between patients with punctate versus linear appearing microbleeds. Post-mortem imaging and histology revealed traumatic microbleed co-localization with iron-laden macrophages, predominately seen in perivascular space. Evidence of axonal injury was not observed in co-localized histopathological sections. Traumatic microbleeds were prevalent in the population studied and predictive of worse outcome. The source of traumatic microbleed signal on MRI appeared to be iron-laden macrophages in the perivascular space tracking a network of injured vessels. While axonal injury in association with traumatic microbleeds cannot be excluded, recognizing traumatic microbleeds as a form of traumatic vascular injury may aid in identifying patients who could benefit from new therapies targeting the injured vasculature and secondary injury to parenchyma.
| S-EPMC6821371 | biostudies-literature
Project description:The integrity of endothelial monolayer is a sine qua non for vascular homeostasis and maintenance of tissue-fluid balance. However, little is known about the signaling pathways regulating regeneration of the endothelial barrier after inflammatory vascular injury.Using genetic and pharmacological approaches, we demonstrated that endothelial regeneration selectively requires activation of p110?PI3K signaling, which thereby mediates the expression of the endothelial reparative transcription factor Forkhead box M1 (FoxM1). We observed that FoxM1 induction in the pulmonary vasculature was inhibited in mice treated with a p110?-selective inhibitor and in Pik3cg(-/-) mice after lipopolysaccharide challenge. Pik3cg(-/-) mice exhibited persistent lung inflammation induced by sepsis and sustained increase in vascular permeability. Restoration of expression of either p110? or FoxM1 in pulmonary endothelial cells of Pik3cg(-/-) mice restored endothelial regeneration and normalized the defective vascular repair program. We also observed diminished expression of p110? in pulmonary vascular endothelial cells of patients with acute respiratory distress syndrome, suggesting that impaired p110?-FoxM1 vascular repair signaling pathway is a critical factor in persistent leaky lung microvessels and edema formation in the disease.We identify p110? as the critical mediator of endothelial regeneration and vascular repair after sepsis-induced inflammatory injury. Thus, activation of p110?-FoxM1 endothelial regeneration may represent a novel strategy for the treatment of inflammatory vascular diseases.
| S-EPMC4792690 | biostudies-literature
Project description:BackgroundEndothelial cell (EC) regeneration is essential for inflammation resolution and vascular integrity recovery after inflammatory vascular injury. Cdc42 is a central regulator of cell survival and vessel formation in EC development. However, it is unknown that whether Cdc42 could be a regulating role of EC repair following the inflammatory injury in the lung. The study sought to test the hypothesis that Cdc42 is required for endothelial regeneration and vascular integrity recovery after LPS-induced inflammatory injury.Methods and resultsThe role of Cdc42 for the regulation of pulmonary vascular endothelial repair was tested in vitro and in vivo. In LPS-induced acute lung injury (ALI) mouse models, knockout of the Cdc42 gene in ECs increased inflammatory cell infiltration and pulmonary vascular leakage and inhibited vascular EC proliferation, which eventually resulted in more severe inflammatory lung injury. In addition, siRNA-mediated knockdown of Cdc42 protein on ECs disrupted cell proliferation and migration and tube formation, which are necessary processes for recovery after inflammatory vascular injury, resulting in inflammatory vascular injury recovery defects.ConclusionWe found that Cdc42 deficiency impairs EC function and regeneration, which are crucial in the post-inflammatory vascular injury repair process. These findings indicate that Cdc42 is a potential target for novel treatments designed to facilitate endothelial regeneration and vascular repair in inflammatory pulmonary vascular diseases, such as ALI/ARDS.
| S-EPMC5806471 | biostudies-literature
Project description:Carbapenemase resistant enterobacteriae (CPE) may be found in asymptomatic carriers. Its incidence is increasing worldwide. Surgical patients are at increased risk of immunocompromise and of carriage progressing to active infection. Active infection with CPE caries a high mortality rate, with the bacteria being resistant to many antibiotics. This article provides details on the epidemiology, screening and management of the orthopaedic patient with CPE. The guidelines advise orthopaedic staff on ways to avoid the spread of CPE amongst inpatients.
| S-EPMC6818357 | biostudies-literature
Project description:IntroductionTelemedicine is the delivery of healthcare across a distance using some form of communication technology. The COVID-19 pandemic has led to increased adoption of telemedicine with national orthopaedic governing bodies advocating its use, as evidence suggests that social distancing maybe necessary until 2022. This systematic review aims to explore evidence for telemedicine in orthopaedics to determine its advantages, validity, effectiveness and utilisation.MethodsDatabases of PubMed, Web of Science, Scopus and CINAHL were systematically searched and articles were included if they involved any form of telephone or video consultation in an orthopaedic population. Findings were synthesised into four themes: patient/clinician satisfaction, accuracy and validity of examination, safety and patient outcomes and cost effectiveness. Quality assessment was undertaken using Cochrane and Joanna Briggs Institute appraisal tools.ResultsTwenty-one studies were included consisting of nine randomised controlled trials (RCTs). Studies revealed high patient satisfaction with telemedicine for convenience, less waiting and travelling time. Telemedicine was cost effective particularly if patients had to travel long distances, required hospital transport or time off work. No clinically significant differences were found in patient examination nor measurement of patient-reported outcome measures. Telemedicine was reported to be a safe method of consultation.DiscussionEvidence suggests that telemedicine in orthopaedics can be safe, cost effective, valid in clinical assessment and with high patient/clinician satisfaction. However, more high-quality RCTs are required to elucidate long-term outcomes. This systematic review presents up-to-date evidence on the use of telemedicine and provides data for organisations considering its use during the COVID-19 pandemic and beyond.
| S-EPMC9124641 | biostudies-literature
Project description:To investigate the effects of peroxisome proliferator-activated receptor (PPAR)? in the cerebral vasculature following stroke-induced brain injury.Here, we report a novel finding that selective PPAR? genetic deletion in vascular smooth muscle cells (VSMCs) resulted in increased cerebrovascular permeability and brain infarction in mice after middle cerebral artery occlusion (MCAO). Mechanistically, we revealed for the first time that PPAR? expression is reduced, but matrix metalloproteinase (MMP)-9 activity is increased in cultured VSMCs after oxygen-glucose deprivation and also in the cerebral cortex of mice following MCAO. Moreover, gain- and loss of PPAR? function in VSMCs significantly reduces and increases oxygen-glucose deprivation-induced MMP-9 activity, respectively. We have further identified that MMP-9 is a direct target of PPAR?-mediated transrepression by chromatin immunoprecipitation and PPAR? transcriptional activity assays. Furthermore, inhibition of MMP-9 activity by lentiviral MMP-9 short hairpin RNA effectively improves cerebrovascular permeability and reduces brain infarction in VSMC-selective PPAR? conditional knockout mice after MCAO.Our data demonstrate that PPAR? in VSMCs can prevent ischemic brain injury by inhibition of MMP-9 activation and attenuation of postischemic inflammation. The pharmacological activation of PPAR? may provide a new therapeutic strategy to treat stroke-induced vascular and neuronal damage.
| S-EPMC3291895 | biostudies-other