Certain low pathogenic avian influenza viruses can mutate to highly pathogenic viruses when they circulate in domestic poultry, at which point they can cause devastating poultry diseases and severe economic damage. The H7N9 influenza viruses that emerged in 2013 in China had caused severe human infections and deaths. However, these viruses were nonlethal in poultry. It is unknown whether the H7N9 viruses can acquire additional mutations during their circulation in nature and become lethal to poultry and more dangerous for humans. Here, we evaluated the evolution of H7N9 viruses isolated from avian species between 2013 and 2017 in China and found 23 different genotypes, 7 of which were detected only in ducks and were genetically distinct from the other 16 genotypes that evolved from the 2013 H7N9 viruses. Importantly, some H7N9 viruses obtained an insertion of four amino acids in their hemagglutinin (HA) cleavage site and were lethal in chickens. The index strain was not lethal in mice or ferrets, but readily obtained the 627K or 701N mutation in its PB2 segment upon replication in ferrets, causing it to become highly lethal in mice and ferrets and to be transmitted efficiently in ferrets by respiratory droplet. H7N9 viruses bearing the HA insertion and PB2 627K mutation have been detected in humans in China. Our study indicates that the new H7N9 mutants are lethal to chickens and pose an increased threat to human health, and thus highlights the need to control and eradicate the H7N9 viruses to prevent a possible pandemic.
With regards to developing miniaturized coherent light sources, the temperature-insensitivity in gain spectrum and threshold is highly desirable. Quantum dots (QDs) are predicted to possess a temperature-insensitive threshold by virtue of the separated electronic states; however, it is never observed in colloidal QDs due to the poor thermal stability. Besides, for the classical II-VI QDs, the gain profile generally redshifts with increasing temperature, plaguing the device chromaticity. Herein, this paper addresses the above two issues simultaneously by embedding ligands-free CsPbBr nanocrystals in a wider band gap Cs PbBr matrix by solution-phase synthesis. The unique electronic structures of CsPbBr nanocrystals enable temperature-insensitive gain spectrum while the lack of ligands and protection from Cs PbBr matrix ensure the thermal stability and high temperature operation. Specifically, a color drift-free stimulated emission irrespective of temperature change (20-150 °C) upon two-photon pumping is presented and the characteristic temperature is determined to be as high as ≈260 K. The superior gain properties of the CsPbBr /Cs PbBr perovskite nanocomposites are directly validated by a vertical cavity surface emitting laser operating at temperature as high as 100 °C. The results shed light on manipulating optical gain from the advantageous CsPbBr nanocrystals and represent a significant step toward the temperature-insensitive frequency-upconverted lasers.
Influence of light exposure on cesium lead halide nanostructures has been explored. A discovery of photon driven transformation (PDT) in 2D CsPbBr nanoplatelets is reported, in which the quantum-confined few-monolayer nanoplatelets will convert to bulk phase under very low irradiation intensity (≈20 mW cm ). Benefiting from the remarkable emission color change during PDT, the multicolor luminescence photopatterns and facile information photo-encoding are established.
for the battery technologies. However, the main impediment for the practical application of lithium metal batteries is the lithium dendrite formation.  It not only penetrates the separator to induce the short circuit of the batteries,  but also generates high surface area in the anode to accelerate the unwanted side reactions between electrolytes and lithium metal, resulting in the electrolyte depletion and the subsequent battery failure.  Up to now, many strategies targeting lithium dendrites suppression rely on the "internal strategies," i.e., the modification or optimization of the components inside the cells. Those strategies include electrolyte optimization, artificial solid electrolyte interphase (SEI) design, and synthesis of 3D current collector.  Electrolyte additives such as LiF,  LiNO 3 ,  and Li 2 S x  were chosen to form stable SEI on the surface of Li anode to suppress the dendrite growth.  For creating artificial SEI layer on the anode, gas treatment  (N 2 , O 2 , CO 2 , or SO 2 ), liquid treatment (Li 3 PO 4 and Cu 3 N/styrene−butadiene rubber  ), and physical deposition of nanofilm (Al 2 O 3 ,  carbon,  and organic polymer  ) are the three typical methods by accessing the internal interface of the battery. The rational design of 3D current collectors also helps to inhibit dendritic growth.  One type of 3D current collectors is lithiophilic matrix such as lithiophilic-lithiophobic gradient interfacial layer,  N-doped graphene,  and metal−organic framework,  which redistributes Li-ions to the anode surface through chemical bonding interactions to achieve uniform lithium deposition. The other type is conductive matrix including porous carbon,  graphene matrix,  3D-ordered macroporous Cu,  and fibrous metal felt  that reduces dendritic growth by reducing the current density with a large surface area. [27,28] Although these "internal strategies" could effectively suppress the dendrite formation, cell stability becomes a concern due to the change of the cell environment such as the use of additives and the modification of the electrode.Introducing an "external strategy," by using external magnetic field to rearrange the Li + concentration on the anode surface, could achieve a uniform lithium deposition. The latest study shows that the growth of Li dendrites stems from the nonuniform Li + concentration on the electrode surface.  Lithium metal is the most attractive anode material due to its extremely high specific capacity, minimum potential, and low density. However, uncontrollable growth of lithium dendrite results in severe safety and cycling stability concerns, which hinders the application in next generation secondary batteries. In this paper, a new and facile method imposing a magnetic field to lithium metal anodes is proposed. That is, the lithium ions suffering Lorentz force due to the electromagnetic fields are put into spiral motion causing magnetohydrodynamics (MHD) effect. This MHD effect can effecti...
Rationale: Pyroptosis is a morphologically and mechanistically distinct form of cell death and is characterized by gasdermin D (GSDMD) or gasdermin E (GSDME)-mediated necrosis with excessive inflammatory factor release. Cardiomyocyte necrosis and inflammation play key roles in the pathophysiology of myocardial ischemia/reperfusion (I/R) injury. However, whether cardiomyocytes undergo pyroptosis and the underlying mechanism in myocardial I/R injury remain unclear. Objective: We aimed to investigate the role of pyroptosis in myocardial I/R injury. Methods and Results: In vivo and in vitro experiments were used to investigate pyroptosis of cardiomyocyte and the associated mechanisms during I/R injury. Wild-type (WT), Myh6-Cre and cardiomyocyte-specific GSDMD-deficient (GSDMD-CKO) male mice were subjected to I/R. Human peripheral blood samples were collected from STEMI (acute ST-segment-elevation myocardial infarction) patients or control patients at 0, 1 and 24 h after PCI (percutaneous coronary intervention) in our department. The serum levels of GSDMD were measured by ELISA. H/R (hypoxia/reoxygenation) induced cardiomyocyte pyroptosis and the release of mature IL-18 but not IL-1β, which mechanistically resulted from GSDMD cleavage by caspase-11 in cardiomyocytes. Furthermore, GSDMD gene deletion blocked H/R-induced cardiomyocyte pyroptosis and IL-18 release. GSDMD and its pyroptosis-inducing N-terminal fragment (GSDMD-N) were upregulated in myocardial tissues after I/R injury. Immunofluorescence analysis showed that GSDMD was mainly localized in cardiomyocytes. GSDMD deficiency in cardiomyocytes significantly reduced the I/R-induced myocardial infarct size. Moreover, increased GSDMD serum levels were detected in patients exhibiting I/R injury 1 h after PCI for STEMI. Conclusions: Our results show that GSDMD-mediated cardiomyocyte pyroptosis is a key event during myocardial I/R injury and that the caspase-11/GSDMD pathway may be essential to this process. Additionally, GSDMD inhibition significantly reduces cardiomyocyte pyroptosis and I/R-induced myocardial injury.
Rationale: Targeting inflammation has been shown to provide clinical benefit in the field of cardiovascular diseases. Although manipulating regulatory T-cell function is an important goal of immunotherapy, the molecules that mediate their suppressive activity remain largely unknown. IL (interleukin)-35, an immunosuppressive cytokine mainly produced by regulatory T cells, is a novel member of the IL-12 family and is composed of an EBI3 (Epstein-Barr virus–induced gene 3) subunit and a p35 subunit. However, the role of IL-35 in infarct healing remains elusive. Objective: This study aimed to determine whether IL-35 signaling is involved in healing and cardiac remodeling after myocardial infarction (MI) and, if so, to elucidate the underlying molecular mechanisms. Methods and Results: IL-35 subunits (EBI3 and p35), which are mainly expressed in regulatory T cells, were upregulated in mice after MI. After IL-35 inhibition, mice showed impaired infarct healing and aggravated cardiac remodeling, as demonstrated by a significant increase in mortality because of cardiac rupture, decreased wall thickness, and worse cardiac function compared with wild-type MI mice. IL-35 inhibition also led to decreased expression of α-SMA (α-smooth muscle actin) and collagen I/III in the hearts of mice after MI. Pharmacological inhibition of IL-35 suppressed the accumulation of Ly6C low and major histocompatibility complex II low /C-C motif chemokine receptor type 2 − (MHC II low CCR2 − ) macrophages in infarcted hearts. IL-35 activated transcription of CX3CR1 (C-X3-C motif chemokine receptor 1) and TGF (transforming growth factor) β1 in macrophages by inducing GP130 signaling, via IL12Rβ2 and phosphorylation of STAT1 (signal transducer and activator of transcription family) and STAT4 and subsequently promoted Ly6C low macrophage survival and extracellular matrix deposition. Moreover, compared with control MI mice, IL-35–treated MI mice showed increased expression of α-SMA and collagen within scars, correlating with decreased left ventricular rupture rates. Conclusions: IL-35 reduces cardiac rupture, improves wound healing, and attenuates cardiac remodeling after MI by promoting reparative CX3CR1 + Ly6C low macrophage survival.
As a single-element nanomaterial, sulfur nanodots are emerging as a kind of heavy-metal-free nanomaterials which are believed to excel over traditional undesirable compound semiconductor nanocrystals in practical applications. Attaining their potential shall rest on the facile fabrication of high quality samples. Yet, so far the reported fabrication techniques for fluorescent sulfur nanodots have been time-consuming and cost-ineffective. Instead, we employed a strategy of hydrothermal reaction to synthesize sulfur nanodots, which reduces the synthesis time remarkably from generally required 125 h to 4 h. As-synthesized sulfur nanodots (without any post-treatment) manifest good monodispersity and a reasonable photoluminescence quantum yield up to 4.02%. The fission-aggregation mechanism has been proposed to account for the reaction dynamics in the formation of sulfur nanodots. Optical spectroscopic analysis indicates the existence of tail states in the electronic structures of sulfur nanodots, and the photoluminescence properties are governed by both the core and surface states of the sulfur nanodots, which may provide usable hints for manipulating and harnessing the luminescence properties. Besides the insight into both the synthesis and emission mechanism of luminescent sulfur nanodots, our findings pave the way to the bio-related expedite exploitation of these materials.
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