Bushfranck9761

Altogether, our findings suggest that, in muscle cells, MOTS-c interacts with STAT3 via the putative SH2 binding motif in the YIFY region to reduce STAT3 transcriptional activity, which enhances myotube formation. This newly discovered mechanism of action highlights MOTS-c as a potential therapeutic target against muscle-wasting in several diseases.The present article provides a narrative review on how language communicates sensory information and how knowledge of sight and sound develops in individuals born deaf or blind. Studying knowledge of the perceptually inaccessible sensory domain for these populations offers a lens into how humans learn about that which they cannot perceive. We first review the linguistic strategies within language that communicate sensory information. Highlighting the power of language to shape knowledge, we next review the detailed knowledge of sensory information by individuals with congenital sensory impairments, limitations therein, and neural representations of imperceptible phenomena. We suggest that the acquisition of sensory knowledge is supported by language, experience with multiple perceptual domains, and cognitive and social abilities which mature over the first years of life, both in individuals with and without sensory impairment. We conclude by proposing a developmental trajectory for acquiring sensory knowledge in the absence of sensory perception.We report the clinical case of AB, a right-handed 19-year-old woman who presents severe developmental topographical disorientation, a relatively rare syndrome, leading to difficulties in navigating in familiar (and novel) environments. This symptomatology appears without acquired cerebral damage (MRI described as normal) nor more global cognitive disability (high degree of education achieved). An extensive assessment of spatial cognition with different aspects of underlying cognitive processes is first presented. Second, the patient's preserved cognitive abilities and her major difficulties in calculation, as well as her attention deficit, as seen in a detailed neuropsychological assessment, are reported. For the first time to our knowledge, we show that developmental topographical disorientation can be associated with other developmental cognitive disorders affecting number processing (dyscalculia) and attention (Attention Deficit-Hyperactivity Disorder (ADHD)). We discuss the links between these different cognitive processes in relation to visuo-spatial working memory and magnitude representation, which could represent common denominators for all these syndromes. This case report highlights the importance of thoroughly assessing potentially associated neurocognitive disorders in developmental topographical disorientation. In addition, it highlights the necessity to keep in mind the prevalence of spatial difficulties in the assessment of children and adolescents with other neurodevelopmental syndromes. Finally, this case study raises a new question about the nosology of developmental disorders affecting the visuo-spatial and spatial domains.Action monitoring is crucial to the successful execution of an action and understanding the actions of others. It is often impaired due to brain lesions, in particular after stroke. This systematic review aims to map the literature on the neurophysiological correlates of action monitoring in patients with brain lesions. Eighteen studies were identified and divided into two groups studies on monitoring of one's own actions and studies on monitoring of the actions of others. The first group included EEG studies on monitoring of self-performed erroneous and correct actions. Impaired error detection (decreased error-related negativity) was observed in patients with lesions in the performance-monitoring network, as compared to healthy controls. Less consistent results were shown for error positivity and behavioral error monitoring performance. The second group of studies on monitoring of others' actions reported decreased mu frequency suppression, impaired readiness potential in the affected hemisphere and decreased EEG indices of error observation (observed error positivity and theta power) in stroke patients. As a whole, these results indicate distinct patterns of impaired neurophysiological activity related to monitoring one's own versus others' actions in patients with brain lesions. EEG recordings of this dissociation in the same patients might be a useful index of motor recovery, and therefore, potentially also beneficial in rehabilitation protocols.The endothelium is the critical barrier that controls transendothelial communications. Blood vessels in cancer tissue are poorly developed and highly permeable. However, it is poorly understood how circulating cancer cells released through these "leaky" vessels break the intact vasculature of remote organs to metastasize. We investigated the roles of cancer cell-derived extracellular vesicles (CEVs) in regulating cancer metastasis by analyzing samples from gastric cancer patients, performing in vitro experiments, and studying mouse models. We made several novel observations. First, the rate of metastasis was closely associated with plasma levels of CEVs in patients with gastric cancer. Second, cultured endothelial cells endocytosed CEVs, resulting in cytoskeletal rearrangement, low expression of the junction proteins cadherin and CD31, and forming large intercellular gaps to allow the transendothelial migration of cancer cells. The dynamin inhibitor Dynasore prevented these CEV-induced changes of endothelial cells by blocking CEVs endocytosis. Third, CEVs disrupted the endothelial barrier of cancer-bearing mice to promote cancer metastasis. Finally, lactadherin promoted the clearance of circulating CEVs to reduce metastasis. These results demonstrate the essential role of CEVs in promoting the metastasis of gastric cancer.

Methamphetamine (METH) is one of the most widely used addictive drugs, and addiction to it is on the rise all over the world. METH abuse has long-term damaging effects that reduce memory and impair cognitive functions. According to studies, the observed effects are strongly related to the nerve cell damage caused by METH, which leads to neurotoxicity. Some of these intra-neuronal events include dopamine oxidation, excitotoxicity, and oxidative stress. Erythropoietin (EPO) is a hormone produced primarily by the kidneys and, in small quantities, by the liver. Studies have shown that EPO exhibits considerable neuroprotective effects. This study aimed to investigate the protective effects of EPO on METH neurotoxicity.

Initially, 48 male Wistar rats, weighing 250-300g, were randomly assigned to four groups control (n=12), METH (n=12), and METH+EPO (2500, 5000 IU/kg/IP- n=12). METH was injected intraperitoneally at a dose of 40mg per kg of body weight (four injections of 10mg every two hours) to induce neurotoxhave great neuroprotective effects on METH neurotoxicity due to its anti-inflammatory, antioxidant, and antiapoptotic properties.Early and rapid detection of Japanese encephalitis virus (JEV) is necessary for timely preventive and control measures. However, JEV RNA detection remains challenging due to the low level of viremia. In this study, a RApid VIsual CRISPR (RAVI-CRISPR) assay based on reverse transcription loop-mediated isothermal amplification (RT-LAMP) and CRISPR/Cas12a targeting was developed for easy detection of JEV in the field. We showed successful detection of 8.97 or more copies of the C gene sequence of JEV RNA within approximately 60 min. This assay also displayed no cross-reactivity with other porcine pathogens. We applied our one-tube RAVI-CRISPR assay to 18 brain tissue sample for JE diagnosis. The results from both fluorescence intensity measurements and directly naked-eye visualization were consistent with those from real-time PCR analysis. Taken together, our results showed that one-tube RAVI-CRISPR assay is robust, convenient, sensitive, specific, affordable, and potentially adaptable to on-site detection or surveillance of JEV in clinical and vector samples.

Steady-state visual evoked potential (SSVEP) is a prevalent paradigm of brain-computer interface (BCI). Recently, deep neural networks (DNNs) have been employed for SSVEP target recognition. However, current DNN models can not fully extract information from SSVEP harmonic components, and ignore the influence of non-target stimuli.

To employ information of multiple sub-bands and non-target stimulus data, we propose a DNN model for SSVEP target detection, i.e., FB-EEGNet, which fuses features of multiple neural networks. Additionally, we design a multi-label for each sample and optimize the parameters of FB-EEGNet across multi-stimulus to incorporate the information from non-target stimuli.

Under the subject-specific condition, FB-EEGNet achieves the average classification accuracies (information transfer rate (ITR)) of 76.75% (50.70 bits/min) and 89.14% (70.45 bits/min) in a time widow of 0.7s under the public 12-target dataset and our experimental 9-target dataset, respectively. Under the cross-subject condition, FB-EEGNet achieved mean accuracies (ITRs) of 81.72% (67.99 bits/min) and 92.15% (76.12 bits/min) on the public and experimental datasets in a time window of 1s, respectively.

FB-EEGNet shows superior performance than CCNN, EEGNet, CCA and FBCCA both for subject-dependent and subject-independent SSVEP target recognition.

FB-EEGNet can effectively extract information from multiple sub-bands and cross-stimulus targets, providing a promising way for extracting deep features in SSVEP using neural networks.

FB-EEGNet can effectively extract information from multiple sub-bands and cross-stimulus targets, providing a promising way for extracting deep features in SSVEP using neural networks.Autophagy-dependent selective degradation of excess or damaged mitochondria, termed mitophagy, is a tightly regulated process necessary for mitochondrial quality and quantity control. Mitochondria are highly dynamic and major sites for vital cellular processes such as ATP and iron‑sulfur cluster biogenesis. Due to their pivotal roles for immunity, apoptosis, and aging, the maintenance of mitochondrial function is of utmost importance for cellular homeostasis. In yeast, mitophagy is mediated by the receptor protein Atg32 that is localized to the outer mitochondrial membrane. CDK2-IN-73 Upon mitophagy induction, Atg32 expression is transcriptionally upregulated, which leads to its accumulation on the mitochondrial surface and to recruitment of the autophagic machinery via its direct interaction with Atg11 and Atg8. Importantly, post-translational modifications such as phosphorylation further fine-tune the mitophagic response. This review summarizes the current knowledge about mitophagy in yeast and its connection with mitochondrial dynamics and the ubiquitin-proteasome system.The extracellular matrix (ECM) plays critical roles in breast cancer development. Whether ECM composition is regulated by the phosphorylation of eIF4E on serine 209, an event required for tumorigenesis, has not been explored. Herein, we used proteomics and mouse modeling to investigate the impact of mutating serine 209 to alanine on eIF4E (i.e., S209A) on mammary gland (MG) ECM. The proteomic data have been deposited to the ProteomeXchange Consortium via the PRIDE partner repository with the dataset identifier PXD028953. We discovered that S209A knock-in mice, expressing a non-phosphorylatable form of eIF4E, have less collagen-I deposition in native and tumor-bearing MGs, leading to altered tumor cell invasion. Additionally, phospho-eIF4E deficiency impacts collagen topology; fibers at the tumor-stroma boundary in phospho-eIF4E-deficient mice run parallel to the tumor edge but radiate outwards in wild-type mice. Finally, a phospho-eIF4E-deficient tumor microenvironment resists anti-PD-1 therapy-induced collagen deposition, correlating with an increased anti-tumor response to immunotherapy.