To investigate the effects of the Wii Fit rehabilitation program in addition to a standard physical therapy program (SPTP) on lower extremity functional status and functional mobility in adults with severe burns after hospital discharge.

A single-blinded, parallel groups randomized controlled trial.

Outpatient rehabilitation center.

Thirty-four patients, 31.3±7.3 years old, with lower extremity deep partial-thickness and full-thickness burn and total body surface area of more than 40% were allocated randomly into two equal groups.

The Wii Fit group received the Wii Fit program for thirty minutes in addition to SPTP for sixty minutes, while the SPTP group received SPTP only. The intervention was three sessions a week for 12 weeks.

The primary outcome measurements were functional status and functional mobility, which were assessed by the high mobility assessment tool, Lower Limb Functional Index, and Timed-up and go test. The secondary outcomes included exercise capacity, muscle strength, and balancnctional mobility, exercise capacity, muscle strength and balance than patients who received SPTP alone. The Wii fit program was a useful adjunctive therapy in rehabilitating adults with lower extremity burn injury.

The implementation of efficient health and vigilance strategy is one of the essential aspects of the health policy of public and private health establishments, in order to reduce the risk of incidents due to medical devices.

The objective of this study is to demonstrate the importance of user notification and to recognize the role of nursing staff in the materiovigilance process.

This is a retrospective study of materiovigilance cases notified for three years (2016, 2017, and 2018) at the National Institute of Oncology. The evaluation of the incidents was carried out with the aim of taking the necessary measures to prevent and minimize risk.

7308 cases of materiovigilance during the 3 years were collected. A spontaneous collection of reports was predominant (70%). The distribution of the number of incidents by the profile of notifiers shows that reports come from surgeons and much more from nurses. The surgical block (35.7%) and medical oncology services (14.3%) were the services that reported more; the majority of the observed adverse events were attributed to infusion sets (n=7105).4 serious cases of materiovigilance. reported during these 3 years at the level of the vigilance unit considered the most relevant were detailed with examples of immediate actions taken and risk minimization actions.

This study highlights the characteristics of incidents reported. The role of the nursing staff and the strong presence of nurses in the vigilance system has been well demonstrated, thus reducing the risk of side effects due to medical devices.

This study highlights the characteristics of incidents reported. The role of the nursing staff and the strong presence of nurses in the vigilance system has been well demonstrated, thus reducing the risk of side effects due to medical devices.The orphan nuclear receptor Nur77 is an immediate-early response gene that based on tissue and cell context is implicated in a plethora of cellular processes, including proliferation, differentiation, apoptosis, metabolism, and inflammation. Nur77 has a ligand-binding pocket that is obstructed by hydrophobic side-groups. Naturally-occurring, cell-endogenous ligands have not been identified and Nur77 transcriptional activity is thought to be regulated through post-translational modification and modulation of protein levels. To determine whether Nur77 is transcriptionally active in hematopoietic cells in vivo, we used an upstream activating sequence (UAS)-GFP transgenic reporter. We found that Nur77 is transcriptionally inactive in vivo in hematopoietic cells under basal conditions, but that activation occurs following cytokine exposure by G-CSF or IL-3. We also identified a series of serine residues required for cytokine-dependent transactivation of Nur77. Moreover, a kinase inhibitor library screen and proximity labeling-based mass spectrometry identified overlapping kinase pathways that physically interacted with Nur77 and whose inhibition abrogated cytokine-induced activation of Nur77. We determined that transcriptional activation of Nur77 by G-CSF or IL-3 requires functional JAK and mTor signaling since their inhibition leads to Nur77 transcriptional inactivation. Thus, intracellular cytokine signaling networks appear to regulate Nur77 transcriptional activity in mouse hematopoietic cells.The universally conserved P-loop ATPase Ola1 is implicated in various cellular stress response pathways, as well as in cancer and tumor progression. However, Ola1p functions are divergent between species and the involved mechanisms are only poorly understood. Here, we studied the role of Ola1p in the heat shock response of the yeast Saccharomyces cerevisiae using a combination of quantitative and pulse labeling-based proteomics approaches, in vitro studies and cell-based assays. Our data show that when heat stress is applied to cells lacking Ola1p, the expression of stress-protective proteins is enhanced. During heat stress Ola1p associates with detergent-resistant protein aggregates and rapidly forms assemblies that localize to stress granules. The assembly of Ola1p was also observed in vitro using purified protein and conditions, which resembled those in living cells. We show that loss of Ola1p results in increased protein ubiquitination of detergent-insoluble aggregates recovered from heat-shocked cells. When cells lacking Ola1p were subsequently relieved from heat stress, reinitiation of translation was delayed, whereas, at the same time, de novo synthesis of central factors required for protein refolding and the clearance of aggregates was enhanced when compared to wildtype cells. The combined data suggest that upon acute heat stress, Ola1p is involved in the stabilization of misfolded proteins, which become sequestered in cytoplasmic stress granules. This function of Ola1p enables cells to resume translation in a timely manner as soon as heat stress is relieved.Muscular dystrophies are a heterogeneous group of monogenic neuromuscular disorders which lead to progressive muscle loss and degeneration of the musculoskeletal system. The genetic causes of muscular dystrophies are well characterized, but no effective treatments have been developed so far. The discovery and application of the CRISPR/Cas system for genome editing offers a new path for disease treatment with the potential to permanently correct genetic mutations. The post-mitotic and multinucleated features of skeletal muscle provide an ideal target for CRISPR/Cas therapeutic genome editing because correction of a subpopulation of nuclei can provide benefit to the whole myofiber. In this review, we provide an overview of the CRISPR/Cas system and its derivatives in genome editing, proposing potential CRISPR/Cas-based therapies to correct diverse muscular dystrophies, and we discuss challenges for translating CRISPR/Cas genome editing to a viable therapy for permanent correction of muscular dystrophies.N4-methylcytosine (4 mC) is an important epigenetic modification that occurs enzymatically by the action of DNA methyltransferases. 4 mC sites exist in prokaryotes and eukaryotes while playing a vital role in regulating gene expression, DNA replication, and cell cycle. The efficient and accurate prediction of 4 mC sites has a significant role in the insight of 4 mC biological properties and functions. Therefore, a sequence-based predictor is proposed, namely 4 mC-RF, for identifying 4 mC sites through the integration of statistical moments along with position, and composition-dependent features. Relative and absolute position-based features are computed to extract optimal features. A popular machine learning classifier Random Forest was used for training the model. Validation results were obtained through rigorous processes of self-consistency, 10-fold cross-validation, Independent set testing, and Jackknife yielding 95.1%, 95.2%, 97.0%, and 94.7% accuracies, respectively. Our proposed model depicts the highest prediction accuracies as compared to existing models. Subsequently, the developed 4 mC-RF model was constructed into a web server. A significant and more accurate predictor of 4 mC Methylcytosine sites helps experimental scientists to gather faster, efficient, and cost-effective results.Pigment epithelium-derived factor (PEDF) is a non-inhibitory member of the serpin (serine protease inhibitor) family and is a well-known potent anti-tumor factor in a variety of cancers. It has been ascertained that PEDF regulates multiple metastatic processes through various plausible mechanisms, including inhibiting angiogenesis, inducing apoptosis, stimulating extracellular matrix (ECM) degradation, and suppressing the epithelial-to-mesenchymal transition (EMT) process. Although PEDF has been recognized as an anti-metastatic marker in most studies, its role remains controversial with conflicting reports of PEDF as a metastatic marker. The emerging insights into the mechanism(s) of PEDF in tumor progression and its therapeutic effects are discussed systematically in this review, aiming to improve our understanding in the context of metastasis and drug development.Epilepsy is a complex neurological syndrome characterized by seizures resulting from neuronal hyperexcitability and sudden and synchronized bursts of electrical discharges. Impaired astrocyte function that results in glutamate excitotoxicity has been recognized to play a key role in the pathogenesis of epilepsy. While there are 26 drugs marketed as anti-epileptic drugs no current treatments are disease modifying as they only suppress seizures rather than the development and progression of epilepsy. Excitatory amino acid transporters (EAATs) are critical for maintaining low extracellular glutamate concentrations and preventing excitotoxicity. When extracellular glutamate concentrations rise to abnormal levels, glutamate receptor overactivation and the subsequent excessive influx of calcium into the post-synaptic neuron can trigger cell death pathways. In this review we discuss targeting EAAT2, the predominant glutamate transporter in the CNS, as a promising approach for developing therapies for epilepsy. EAAT2 upregulation via transcriptional and translational regulation has proven successful in vivo in reducing spontaneous recurrent seizures and offering neuroprotective effects. Another approach to regulate EAAT2 activity is through positive allosteric modulation (PAM). Novel PAMs of EAAT2 have recently been identified and are under development, representing a promising approach for the advance of novel therapeutics for epilepsy.STING agonists are a new class of drugs for cancer immunotherapy that activate both innate and adaptive antitumor immunity. Recently, multiple clinical trials of STING agonists have been conducted in hematological malignancies and solid tumors. However, STING is commonly suppressed in melanoma via mechanisms that remain unclear. We found that STING expression was epigenetically suppressed by H3K27me3 in melanoma, and EZH2 inhibitor could induce an H3K27 shift from trimethylation to acetylation, resulting in increased expression of STING. Furthermore, a combination of STING agonist and EZH2 inhibitor upregulated major histocompatibility complex (MHC) class I expression and chemokines production. Whole-transcriptome analysis showed that type I interferon-related genes were significantly upregulated in the combination treatment group. In addition, the combination treatment synergistically reduced tumor growth and increased CD8+ T cell infiltration in a poorly immunogenic melanoma mouse model B16-F10. These results demonstrated a novel mechanism underlying the epigenetic regulation of STING expression in melanoma; combination of STING agonists and EZH2 inhibitors can boost the antitumor immune response and would be a promising treatment option for melanoma patients refractory to current immunotherapies.