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The optimal approaches to managing diabetic foot infections remain a challenge for clinicians. Despite an exponential rise in publications investigating different treatment strategies, the various agents studied generally produce comparable results, and high-quality data are scarce. In this systematic review, we searched the medical literature using the PubMed and Embase databases for published studies on the treatment of diabetic foot infections as of June 2018. This systematic review is an update of previous reviews, the first of which was undertaken in 2010 and the most recent in 2014, by the infection committee of the International Working Group of the Diabetic Foot. We defined the context of literature by formulating clinical questions of interest, then developing structured clinical questions (PICOs) to address these. We only included data from controlled studies of an intervention to prevent or cure a diabetic foot infection. Two independent reviewers selected articles for inclusion and then assessed tnfection related outcomes of the diabetic foot. In general, the quality of more recent trial designs are better in past years, but there is still a great need for further well-designed trials to produce higher quality evidence to underpin our recommendations. © 2020 John Wiley & Sons Ltd.AIM We aimed to determine systematic bias and the range of random error in tongue pressure measurements among young healthy adults and elderly patients with certification of requiring long-term care or support, considering sex, and to establish a measurement method. METHODS Subjects were 226 adults (88 young healthy adults and 138 elderly patients with certification of requiring long-term care or support). Tongue pressure was measured thrice. Bland-Altman analysis was performed for the first and second trials, and second and third trials. RESULTS Fixed bias was revealed for the first and second trials among young healthy adults. Systematic bias was not found for the second and third trials. Fixed bias was revealed for the first and second trials among elderly patients, with a proportional bias with a negative slope for the second and third trials. For young healthy adults, the minimal detectable change was 6.0 and 5.4 kPa in males and females, respectively. For elderly patients, the limit of agreement ranged from -5.9 to 8.6 and from -5.4 to 8.8 kPa in males and females, respectively. CONCLUSIONS There was a difference in systematic bias in tongue pressure measurement between young healthy adults and elderly patients with certification of needing long-term care or support. In young healthy adults, the third trial results showed stability, whereas they decreased in elderly patients. In elderly patients, it was suggested that the number of measurements reduced from three to two when a maximum value was adopted. No differences were observed among sexes in either young or elderly patients. Geriatr Gerontol Int 2020; •• ••-••. © 2020 Japan Geriatrics Society.INTRODUCTION The exact mechanisms underlying the development and maintenance of phantom limb pain are still unclear. This study aimed to identify the factors affecting pain intensity in chronic, lower limb, traumatic phantom limb pain patients. METHODS This is a cross-sectional analysis of patients with phantom limb pain. learn more We assessed amputation-related, pain-related clinical and demographic variables. We performed univariate and multivariate models to evaluate the associated factors modulating phantom limb pain and residual limb pain intensity. RESULTS We included 71 unilateral traumatic lower limb amputees. Results showed that (i) amputation related perceptions were experienced by a large majority of the chronic phantom limb pain patients (sensations 90.1%, N=64; residual pain 81.7%, N=58); (ii) phantom limb pain intensity has two significant protective factors phantom limb movement and having effective treatment for phantom limb pain previously and two significant risk factors phantom limb sensation intensity and age; (iii) on the other hand, for residual limb pain, risk factors are different presence of pain before amputation and level of amputation (in addition to the same protective factors). CONCLUSION These results suggest different neurobiological mechanisms to explain phantom limb and residual limb pain intensity. While phantom limb pain risk factors seem to be related to maladaptive plasticity as phantom sensation and older age are associated with more pain, residual limb pain risk factors seem to have factors leading to neuropathic pain such as the amount of neural lesion and previous history of chronic pain. Interestingly, the phantom movement appears to be protective for both phenomena. This article is protected by copyright. All rights reserved.Staphylococcus aureus, a versatile Gram-positive bacterium, is the main cause of bone and joint infections (BJI), which are prone to recurrence. The inflammasome is an immune signaling platform that assembles after pathogen recognition. It activates proteases, most notably caspase-1 that proteolytically matures and promotes the secretion of mature IL-1β and IL-18. The role of inflammasomes and caspase-1 in the secretion of mature IL-1β and in the defence of S. aureus-infected osteoblasts has not yet been fully investigated. We show here that S. aureus-infected osteoblast-like MG-63 but not caspase-1 knock-out CASP1-/- MG-63 cells, which were generated using CRISPR-Cas9 technology, activate the inflammasome as monitored by the release of mature IL-1β. The effect was strain-dependent. The use of S. aureus deletion and complemented phenole soluble modulins (PSMs) mutants demonstrated a key role of PSMs in inflammasomes-related IL-1β production. Furthermore, we found that the lack of caspase-1 in CASP1-/- MG-63 cells impairs their defense functions, as bacterial clearance was drastically decreased in CASP1-/- MG-63 compared to wild-type cells. Our results demonstrate that osteoblast-like MG-63 cells play an important role in the immune response against S. aureus infection through inflammasomes activation and establish a crucial role of caspase-1 in bacterial clearance. This article is protected by copyright. All rights reserved. This article is protected by copyright. All rights reserved.