CS nerve growth factor regulates sevoflurane anesthesiainduced nerve injury in nerve cells

Purpose: Sevoflurane is the most commonly used anesthetic agent for surgery. However, it is associated with deficiency in learning and memory abilities. The study was aimed at investigating the role of nerve growth factor (NGF) in sevoflurane anesthesia-induced nerve injury.Methods: RT-qPCR assay was applied to measure expressions of NGF, miR-98-5p and other factors related to apoptosis. CCK-8 assay was used for detecting cell viability while luciferase reporter assay was employed to measure binding condition between miR-98-5p and NGF. Expressions of proteins in PI3K/AKT/mTOR signaling pathway was measured with western blot.Results: Sevoflurane reduced cell viability of RGC-5 cells, promoted apoptosis and reduced the expression of NGF. In sevoflurane-induced RGC-5 cells, over-expression of NGF promoted cell viability with reduced apoptosis. Also, there was reduction in the protein expression of PI3K/AKT/mTOR signaling pathway by sevoflurane, while up-regulation of NGF promoted the expressions of these proteins. In the presence of PI3K inhibitor, reduction cell viability was reduced but apoptosis increased. Luciferase reporter assay detected MiR-98-5p as the target gene of NGF and its overexpression restored high cell viability in the over-expressed NGF. The rate of apoptosis and expressions of proteins was also restored with up-regulation of miR-98-5p.Conclusion: Sevoflurane caused damage to nerve cells, while over-expression of NGF reduced the injury through PI3K/AKT/mTOR signaling pathway and suppression of miR-98-5p. Keywords: Nerve growth factor, Sevoflurane, Nerve injury, Anesthesia, miR-98-5

Electrical tuning of robust layered antiferromagnetism in MXene monolayer

A-type antiferromagnetism, with an in-plane ferromagnetic order and the interlayer antiferromagnetic coupling, owns inborn advantages for electrical manipulations but is naturally rare in real materials except in those artificial antiferromagnetic heterostructures. Here, a robust layered antiferromagnetism with a high N\'eel temperature is predicted in a MXene Cr$_2$CCl$_2$ monolayer, which provides an ideal platform as a magnetoelectric field effect transistor. Based on first-principles calculations, we demonstrate that an electric field can induce the band splitting between spin-up and spin-down channels. Although no net magnetization is generated, the inversion symmetry between the lower Cr layer and the upper Cr layer is broken via electronic cloud distortions. Moreover, this electric field can be replaced by a proximate ferroelectric layer for nonvolatility. The magneto-optic Kerr effect can be used to detect this magnetoelectricity, even if it is a collinear antiferromagnet with zero magnetization

Involvement of potential pathways in malignant transformation from Oral Leukoplakia to Oral Squamous Cell Carcinoma revealed by proteomic analysis

<p>Abstract</p> <p>Background</p> <p>Oral squamous cell carcinoma (OSCC) is one of the most common forms of cancer associated with the presence of precancerous oral leukoplakia. Given the poor prognosis associated with oral leukoplakia, and the difficulties in distinguishing it from cancer lesions, there is an urgent need to elucidate the molecular determinants and critical signal pathways underlying the malignant transformation of precancerous to cancerous tissue, and thus to identify novel diagnostic and therapeutic target.</p> <p>Results</p> <p>We have utilized two dimensional electrophoresis (2-DE) followed by ESI-Q-TOF-LC-MS/MS to identify proteins differentially expressed in six pairs of oral leukoplakia tissues with dysplasia and oral squamous cancer tissues, each pair was collected from a single patient. Approximately 85 differentially and constantly expressed proteins (> two-fold change, P < 0.05) were identified, including 52 up-regulated and 33 down-regulated. Gene ontological methods were employed to identify the biological processes that were over-represented in this carcinogenic stage. Biological networks were also constructed to reveal the potential links between those protein candidates. Among them, three homologs of proteosome activator PA28 a, b and g were shown to have up-regulated mRNA levels in OSCC cells relative to oral keratinocytes.</p> <p>Conclusion</p> <p>Varying levels of differentially expressed proteins were possibly involved in the malignant transformation of oral leukoplakia. Their expression levels, bioprocess, and interaction networks were analyzed using a bioinformatics approach. This study shows that the three homologs of PA28 may play an important role in malignant transformation and is an example of a systematic biology study, in which functional proteomics were constructed to help to elucidate mechanistic aspects and potential involvement of proteins. Our results provide new insights into the pathogenesis of oral cancer. These differentially expressed proteins may have utility as useful candidate markers of OSCC.</p

Multi-source adversarial transfer learning for ultrasound image segmentation with limited similarity

Lesion segmentation of ultrasound medical images based on deep learning techniques is a widely used method for diagnosing diseases. Although there is a large amount of ultrasound image data in medical centers and other places, labeled ultrasound datasets are a scarce resource, and it is likely that no datasets are available for new tissues/organs. Transfer learning provides the possibility to solve this problem, but there are too many features in natural images that are not related to the target domain. As a source domain, redundant features that are not conducive to the task will be extracted. Migration between ultrasound images can avoid this problem, but there are few types of public datasets, and it is difficult to find sufficiently similar source domains. Compared with natural images, ultrasound images have less information, and there are fewer transferable features between different ultrasound images, which may cause negative transfer. To this end, a multi-source adversarial transfer learning network for ultrasound image segmentation is proposed. Specifically, to address the lack of annotations, the idea of adversarial transfer learning is used to adaptively extract common features between a certain pair of source and target domains, which provides the possibility to utilize unlabeled ultrasound data. To alleviate the lack of knowledge in a single source domain, multi-source transfer learning is adopted to fuse knowledge from multiple source domains. In order to ensure the effectiveness of the fusion and maximize the use of precious data, a multi-source domain independent strategy is also proposed to improve the estimation of the target domain data distribution, which further increases the learning ability of the multi-source adversarial migration learning network in multiple domains.Comment: Submitted to Applied Soft Computing Journa

Nearly-room-temperature ferromagnetism and tunable anomalous Hall effect in atomically thin Fe4CoGeTe2

Itinerant ferromagnetism at room temperature is a key ingredient for spin transport and manipulation. Here, we report the realization of nearly-room-temperature itinerant ferromagnetism in Co doped Fe5GeTe2 thin flakes. The ferromagnetic transition temperature TC (323 K - 337 K) is almost unchanged when thickness is down to 12 nm and is still about 284 K at 2 nm (bilayer thickness). Theoretical calculations further indicate that the ferromagnetism persists in monolayer Fe4CoGeTe2. In addition to the robust ferromagnetism down to the ultrathin limit, Fe4CoGeTe2 exhibits an unusual temperature- and thickness-dependent intrinsic anomalous Hall effect. We propose that it could be ascribed to the dependence of band structure on thickness that changes the Berry curvature near the Fermi energy level subtly. The nearly-room-temperature ferromagnetism and tunable anomalous Hall effect in atomically thin Fe4CoGeTe2 provide opportunities to understand the exotic transport properties of two-dimensional van der Waals magnetic materials and explore their potential applications in spintronics.Comment: 28 pages, 4 figures, 1 tabl

Glucagon-like peptide-2 protects the gastric mucosa via regulating blood flow and metabolites

IntroductionRefractory peptic ulcers lead to perforation and hemorrhage, which are fatal. However, these remain a therapeutic challenge. Gastric mucosal blood flow is crucial in maintaining gastric mucosal health. It’s reported that Glucagon-like peptide-2 (GLP-2), a gastrointestinal hormone, stimulated intestinal blood flow. However, the direct role of GLP-2 in gastric mucosal blood flow and metabolites remain unclear. Here, we speculated that GLP-2 might protect the gastric mucosa by increasing gastric mucosal blood flow and regulating metabolites. This study was conducted to evaluate the role of GLP-2 in gastric mucosal lesions and its underlying mechanism.MethodsWe analyzed endogenous GLP-2 during gastric mucosal injury in the serum. Rats were randomly divided into two groups, with 36 rats in each group as follows: (1) normal control group (NC1); (2) ethanol model group (EC1); rats in EC1 and NC1 groups were intragastrically administered ethanol (1 ml/200 g body weight) and distilled water (1 ml/200 g body weight). The serum was collected 10 min before intragastric administration and 15, 30, 60, 90, and 120 min after intragastric administration. Furthermore, additional male Sprague–Dawley rats were randomly divided into three groups, with six rats in each group as follows: (1) normal control group (NC); (2) ethanol model group (EC); (3) 10 μg/200 g body weight GLP-2 group (GLP-2). Rats in the NC and EC groups were intraperitoneally injected with saline. Those in the GLP-2 group were intraperitoneally injected with GLP-2. Thirty minutes later, rats in the EC and GLP-2 groups were intragastrically administered ethanol (1 ml/200 g body weight), and rats in the NC group were intragastrically administered distilled water (1 ml/200 g body weight). After the intragastric administration of ethanol for 1 h, the animals were anesthetized and gastric mucosal blood flow was measured. Serum were collected for ultra performance liquid chromatography/tandem mass spectrometry (UPLC-MS/MS) metabolomics.ResultsThere were no significant change in endogenous GLP-2 during gastric mucosal injury (P&lt;0.05). Pretreatment with GLP-2 significantly reduced ethanol-induced gastric mucosal lesions by improving the gastric mucosal blood flow, as examined using a laser Doppler flow meter, Guth Scale, hematoxylin-eosin staining, and two-photon microscopy. UPLC-MS/MS analyses showed that GLP-2 also maintained a steady state of linoleic acid metabolism.ConclusionsTaken together, GLP-2 protects the gastric mucosa against ethanol-induced lesions by improving gastric mucosa blood flow and affecting linoleic acid metabolism

Immune heterogeneity in cardiovascular diseases from a single-cell perspective

A variety of immune cell subsets occupy different niches in the cardiovascular system, causing changes in the structure and function of the heart and vascular system, and driving the progress of cardiovascular diseases (CVDs). The immune cells infiltrating the injury site are highly diverse and integrate into a broad dynamic immune network that controls the dynamic changes of CVDs. Due to technical limitations, the effects and molecular mechanisms of these dynamic immune networks on CVDs have not been fully revealed. With recent advances in single-cell technologies such as single-cell RNA sequencing, systematic interrogation of the immune cell subsets is feasible and will provide insights into the way we understand the integrative behavior of immune populations. We no longer lightly ignore the role of individual cells, especially certain highly heterogeneous or rare subpopulations. We summarize the phenotypic diversity of immune cell subsets and their significance in three CVDs of atherosclerosis, myocardial ischemia and heart failure. We believe that such a review could enhance our understanding of how immune heterogeneity drives the progression of CVDs, help to elucidate the regulatory roles of immune cell subsets in disease, and thus guide the development of new immunotherapies