With the increasing demand for wound care and treatment worldwide, traditional dressings have been unable to meet the needs of the existing market due to their limited antibacterial properties and ...other defects. Electrospinning technology has attracted more and more researchers' attention as a simple and versatile manufacturing method. The electrospun nanofiber membrane has a unique structure and biological function similar to the extracellular matrix (ECM), and is considered an advanced wound dressing. They have significant potential in encapsulating and delivering active substances that promote wound healing. This article first discusses the common types of wound dressing, and then summarizes the development of electrospun fiber preparation technology. Finally, the polymers and common biologically active substances used in electrospinning wound dressings are summarized, and portable electrospinning equipment is also discussed. Additionally, future research needs are put forward.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, UILJ, UKNU, UL, UM, UPUK
Metamaterials have attracted considerable attention owing to their extraordinary ability in controlling the propagation of electromagnetic waves. These materials can be realized using artificial ...composites consisting of subwavelength metallic resonators, but losses of the metallic components may significantly degrade the performance of metamaterials, especially in the visible region. Here, we propose low-loss all-dielectric metasurfaces, comprised of a monolayer of titanium dioxide (TiO2) nanoparticles, to achieve perfect reflection band at visible wavelengths. Using the Mie scattering theory, we explore the electromagnetic scattering features of one single TiO2 nanosphere and show that both electric and magnetic dipole resonances can be excited inside the sphere in the visible range. Then, a semi-infinite medium of TiO2 nanospheres is studied using Lewin effective-medium model, and we find that the effective permeability or permittivity becomes negative around the magnetic or electric resonance wavelength, leading to the perfect reflection of light. On the basis of these results, we design a monolayer of TiO2 nanocylinder array to achieve a flat-top perfect reflection band by optimizing the wavelength interval between the magnetic and electric resonances. In addition, it is shown that the position of the perfect reflection band can be adjusted across the whole visible spectrum by changing the dimensions and lattice period of the TiO2 nanocylinder array. Our design of all-dielectric metamaterial reflectors may find applications in diverse fields such as filter, color printing, spectroscopy, and so on.
Type 2 diabetes (T2D) is characterized by insulin resistance along with pancreatic β cell failure. β cell factors are traditionally thought to control glucose homeostasis by modulating insulin ...levels, not insulin sensitivity. Exosomes are emerging as new regulators of intercellular communication. However, the role of β-cell-derived exosomes in metabolic homeostasis is poorly understood. Here, we report that microRNA-26a (miR-26a) in β cells not only modulates insulin secretion and β cell replication in an autocrine manner but also regulates peripheral insulin sensitivity in a paracrine manner through circulating exosomes. MiR-26a is reduced in serum exosomes of overweight humans and is inversely correlated with clinical features of T2D. Moreover, miR-26a is down-regulated in serum exosomes and islets of obese mice. Using miR-26a knockin and knockout mouse models, we showed that miR-26a in β cells alleviates obesity-induced insulin resistance and hyperinsulinemia. Mechanistically, miR-26a in β cells enhances peripheral insulin sensitivity via exosomes. Meanwhile, miR-26a prevents hyperinsulinemia through targeting several critical regulators of insulin secretion and β cell proliferation. These findings provide a new paradigm for the far-reaching systemic functions of β cells and offer opportunities for the treatment of T2D.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Doxorubicin is a valuable antineoplastic drug although its clinical use is greatly hindered by its severe cardiotoxicity with dismal target therapy available. Luteolin is a natural product extracted ...from vegetables and fruits with a wide range of biological efficacies including anti-oxidative, anti-tumorigenic, and anti-inflammatory properties. This study was designed to examine the possible effect of luteolin on doxorubicin-induced cardiotoxicity, if any, and the mechanism(s) involved with a focus on mitochondrial autophagy. Luteolin application (10 μM) in adult mouse cardiomyocytes overtly improved doxorubicin-induced cardiomyocyte contractile dysfunction including elevated peak shortening amplitude and maximal velocity of shortening/relengthening along with unchanged duration of shortening and relengthening. Luteolin alleviated doxorubicin-induced cardiotoxicity including apoptosis, accumulation of reactive oxygen species (ROS) and loss of mitochondrial membrane potential. Furthermore, luteolin attenuated doxorubicin-induced cardiotoxicity through promoting mitochondrial autophagy in association with facilitating phosphorylation of Drp1 at Ser
, and upregulating TFEB expression. In addition, luteolin treatment partially attenuated low dose doxorubicin-induced elongation of mitochondria. Treatment of Mdivi-1, a Drp1 GTPase inhibitor, negated the protective effect of luteolin on levels of TFEB, LAMP1, and LC3B, as well as loss of mitochondrial membrane potential and cardiomyocyte contractile dysfunction in the face of doxorubicin challenge. Taken together, these findings provide novel insights for the therapeutic efficacy of luteolin against doxorubicin-induced cardiotoxicity possibly through improved mitochondrial autophagy.
Doxorubicin (DOX) is an effective anthracycline chemotherapeutic anticancer drug with its life-threatening cardiotoxicity severely limiting its clinical application. Mitochondrial damage-induced ...cardiomyocyte death is considered an essential cue for DOX cardiotoxicity. FUN14 domain containing 1 (FUNDC1) is a mitochondrial membrane protein participating in the regulation of mitochondrial integrity in multiple diseases although its role in DOX cardiomyopathy remains elusive. Here, we examined whether PANoptosis, a novel type of programmed cell death closely associated with mitochondrial damage, was involved in DOX-induced heart injury, and FUNDC1-mediated regulation of cardiomyocyte PANoptosis, if any. FUNDC1 was downregulated in heart tissues in patients with dilated cardiomyopathy (DCM) and DOX-challenged mice. FUNDC1 deficiency aggravated DOX-induced cardiac dysfunction, mitochondrial injury, and cardiomyocyte PANoptosis. Further examination revealed that FUNDC1 countered cytoplasmic release of mitochondrial DNA (mtDNA) and activation of PANoptosome through interaction with mitochondrial Tu translation elongation factor (TUFM), a key factor in the translational expression and repair of mitochondrial DNA, via its 96-133 amino acid domain. TUFM intervention reversed FUNDC1-elicited protection against DOX-induced mtDNA cytosolic release and cardiomyocyte PANoptosis. Our findings shed light toward a beneficial role of FUNDC1 in DOX cardiotoxicity and cardiomyocyte PANoptosis, thus offering therapeutic promises in DOX-induced cardiotoxicity.
Compared with natural scenes, aerial scenes are usually composed of numerous objects densely distributed within the aerial view, and thus, more key local semantic features are needed to describe ...them. However, when existing CNNs are used for remote sensing image classification, they typically focus on the global semantic features of the image, and especially for deep models, shallow and intermediate features are easily lost. This article proposes a channel-spatial attention mechanism based on a depthwise separable convolution (CSDS) network for aerial scene classification to solve these challenges. First, we construct a depthwise separable convolution (DS-Conv) and pyramid residual connection architecture. DS-Conv extracts features from each channel and merges them, effectively reducing the number of necessary calculations, and the pyramid residual connections connect the features from multiple layers and create associations. Then, the channel-spatial attention algorithm causes the model to obtain more effective features in the channel and spatial domains. Finally, an improved cross-entropy loss function is used to reduce the impact of similar categories on backpropagation. Comparative experiments on three public datasets show that the CSDS network can achieve results comparable to those of other state-of-the-art methods. In addition, visualization of feature extraction results by the Grad-CAM algorithm and ablation experiments for each module reflect the powerful feature learning and representation capabilities of the proposed CSDS network.
Plant responses to drought stress are complex due to various mechanisms of drought avoidance and tolerance to maintain growth. Traditional plant phenotyping methods are labor-intensive, ...time-consuming, and subjective. Plant phenotyping by integrating kinetic chlorophyll fluorescence with multicolor fluorescence imaging can acquire plant morphological, physiological, and pathological traits related to photosynthesis as well as its secondary metabolites, which will provide a new means to promote the progress of breeding for drought tolerant accessions and gain economic benefit for global agriculture production. Combination of kinetic chlorophyll fluorescence and multicolor fluorescence imaging proved to be efficient for the early detection of drought stress responses in the
ecotype Col-0 and one of its most affected mutants called
. Kinetic chlorophyll fluorescence curves were useful for understanding the drought tolerance mechanism of
. Conventional fluorescence parameters provided qualitative information related to drought stress responses in different genotypes, and the corresponding images showed spatial heterogeneities of drought stress responses within the leaf and the canopy levels. Fluorescence parameters selected by sequential forward selection presented high correlations with physiological traits but not morphological traits. The optimal fluorescence traits combined with the support vector machine resulted in good classification accuracies of 93.3 and 99.1% for classifying the control plants from the drought-stressed ones with 3 and 7 days treatments, respectively. The results demonstrated that the combination of kinetic chlorophyll fluorescence and multicolor fluorescence imaging with the machine learning technique was capable of providing comprehensive information of drought stress effects on the photosynthesis and the secondary metabolisms. It is a promising phenotyping technique that allows early detection of plant drought stress.
Drought is one of the major environmental stresses limiting crop growth and production. MYB family transcription factors play crucial roles in response to abiotic stresses. Previous studies found ...that
TaMYB31
is transcriptionally induced by drought stress. However, the biological functions of
TaMYB31
in drought stress responses remained unknown. In this study, three
TaMYB31
homoeologous genes from hexaploid wheat, designated
TaMYB31-A, TaMYB31-B
, and
TaMYB31-D
, were cloned and characterized. Expression analysis showed that
TaMYB31
genes have different tissue expression patterns, and
TaMYB31-B
has relatively high expression levels in most tested tissues. All the three homoeologs were up-regulated by polyethylene glycol (PEG) 6000 and abscisic acid (ABA) treatments. Subcellular localization analyses revealed that TaMYB31 is localized to the nucleus. Ectopic expression of the
TaMYB31-B
gene in
Arabidopsis
affected plants growth and enhanced drought tolerance. In addition, seed germination and seedling root growth of
TaMYB31-B
transgenic plants were more sensitive to exogenous ABA treatment compared to wild type control. RNA-seq analysis indicated that TaMYB31 functions through up-regulation of wax biosynthesis genes and drought-responsive genes. These results provide evidence that TaMYB31 acts as a positive regulator of drought resistance, and justify its potential application in genetic modification of crop drought tolerance.
SQUAMOSA promoter binding protein-like (SPL) family plays vital regulatory roles in plant growth and development. The SPL family in climacteric fruit Carica papaya has not been reported. This study ...identified 14 papaya SPLs (CpSPL) from papaya genome and analyzed their sequence features, phylogeny, intron/exon structure, conserved motif, miR156-mediated posttranscriptional regulation, and expression patterns. 14 CpSPLs were clustered into 8 groups, and two distinct expression patterns were revealed for miR156-targeted and nontargeted CpSPLs in different tissues and fruit development stages. The expression changes of CpSPLs in ethephon and 1-MCP treated fruit during ripening suggested that the CpSPLs guided by CpmiR156 play crucial roles in ethylene signaling pathway. This study sheds light on the new function of SPL family in fruit development and ripening, providing insights on understanding evolutionary divergence of the members of SPL family among plant species.
•14 SQUAMOSA promoter binding protein-like (SPL) family genes were identified in papaya genome.•7 CpSPLs contained the CpmiR156 binding site at the coding or 3′ UTR regions.•CpmiR156-targeted CpSPLs were highly expressed in stage IV (80 days).•1-MCP treatment significantly delayed the ripening process in papaya fruit at the early stages.•Expressions of several CpSPL genes and CpmiR156 were impacted by ETH and 1-MCP treatments.•CpSPL genes guided by CpmiR156 play crucial regulatory roles during papaya fruit ripening processes.
Rationale: Ischemic heart disease remains a primary threat to human health, while its precise etiopathogenesis is still unclear. TBC domain family member 15 (TBC1D15) is a RAB7 GTPase-activating ...protein participating in the regulation of mitochondrial dynamics. This study was designed to explore the role of TBC1D15 in acute myocardial infarction (MI)-induced cardiac injury and the possible mechanism(s) involved. Methods: Mitochondria-lysosome interaction was evaluated using transmission electron microscopy and live cell time-lapse imaging. Mitophagy flux was measured by fluorescence and western blotting. Adult mice were transfected with adenoviral TBC1D15 through intra-myocardium injection prior to a 3-day MI procedure. Cardiac morphology and function were evaluated at the levels of whole-heart, cardiomyocytes, intracellular organelles and cell signaling transduction. Results: Our results revealed downregulated level of TBC1D15, reduced systolic function, overt infarct area and myocardial interstitial fibrosis, elevated cardiomyocyte apoptosis and mitochondrial damage 3 days after MI. Overexpression of TBC1D15 restored cardiac systolic function, alleviated infarct area and myocardial interstitial fibrosis, reduced cardiomyocyte apoptosis and mitochondrial damage although TBC1D15 itself did not exert any myocardial effect in the absence of MI. Further examination revealed that 3-day MI-induced accumulation of damaged mitochondria was associated with blockade of mitochondrial clearance because of enlarged defective lysosomes and subsequent interrupted mitophagy flux, which were attenuated by TBC1D15 overexpression. Mechanistic studies showed that 3-day MI provoked abnormal mitochondria-lysosome contacts, leading to lysosomal enlargement and subsequently disabled lysosomal clearance of damaged mitochondria. TBC1D15 loosened the abnormal mitochondria-lysosome contacts through both the Fis1 binding and the RAB7 GAPase-activating domain of TBC1D15, as TBC1D15-dependent beneficial responses were reversed by interference with either of these two domains both in vitro and in vivo. Conclusions: Our findings indicated a pivotal role of TBC1D15 in acute MI-induced cardiac anomalies through Fis1/RAB7 regulated mitochondria-lysosome contacts and subsequent lysosome-dependent mitophagy flux activation, which may provide a new target in the clinical treatment of acute MI.