Deep sequencing-based transcriptome analysis of Plutella xylostella larvae parasitized by Diadegma semiclausum

Background: Parasitoid insects manipulate their hosts' physiology by injecting various factors into their host upon parasitization. Transcriptomic approaches provide a powerful approach to study insect host-parasitoid interactions at the molecular level. In order to investigate the effects of parasitization by an ichneumonid wasp (Diadegma semiclausum) on the host (Plutella xylostella), the larval transcriptome profile was analyzed using a short-read deep sequencing method (Illumina). Symbiotic polydnaviruses (PDVs) associated with ichneumonid parasitoids, known as ichnoviruses, play significant roles in host immune suppression and developmental regulation. In the current study, D. semiclausum ichnovirus (DsIV) genes expressed in P. xylostella were identified and their sequences compared with other reported PDVs. Five of these genes encode proteins of unknown identity, that have not previously been reported

Programmed cell death and its role in inflammation

Cell death plays an important role in the regulation of inflammation and may be the result of inflammation. The maintenance of tissue homeostasis necessitates both the recognition and removal of invading microbial pathogens as well as the clearance of dying cells. In the past few decades, emerging knowledge on cell death and inflammation has enriched our molecular understanding of the signaling pathways that mediate various programs of cell death and multiple types of inflammatory responses. This review provides an overview of the major types of cell death related to inflammation. Modification of cell death pathways is likely to be a logical therapeutic target for inflammatory diseases

Revisiting the role of Zr doping in Ni-rich layered cathodes for lithium-ion batteries

The realization of high performance Ni-rich layered cathodes remains a challenge because of the multiple degradation factors that concurrently operate during battery cycling. In particular, depletion of oxygen charge and consequent lattice-oxygen instability at deep charge state accelerate the subsequent chemomechanical degradation mechanisms. Among the proposed methodologies, doping has proven to be effective in enhancing the cathode cycle life by stabilizing the layered structure. Herein, we achieved the electrochemically stabilized Ni-rich LiNi0.92Co0.04Mn0.04O2 through Zr doping, resulting in a 15% increase of the capacity retention after 100 cycles. In-depth investigations are conducted to unveil the effects of Zr doping on the layered cathode, and in particular, the critical role of Zr doping on the lattice oxygen stability is systematically studied. By combining state-of-the-art magnetometer characterization, X-ray analysis, and first-principles calculation, we reveal that Zr doping positively contributes the to lattice oxygen stability by alleviating the oxygen charge loss at deep charge, thereby improving the cathode electrochemical reversibility. Our findings provide an insight into the Zr doping mechanism and help to design Ni-rich layered oxides for future applications

Ca²⁺-signaling in airway smooth muscle cells is altered in T-bet knock-out mice

<p>Abstract</p> <p>Background</p> <p>Airway smooth muscle cells (ASMC) play a key role in bronchial hyperresponsiveness (BHR). A major component of the signaling cascade leading to ASMC contraction is calcium. So far, agonist-induced Ca²⁺-signaling in asthma has been studied by comparing innate properties of inbred rat or mouse strains, or by using selected mediators known to be involved in asthma. T-bet knock-out (KO) mice show key features of allergic asthma such as a shift towards T_H2-lymphocytes and display a broad spectrum of asthma-like histological and functional characteristics. In this study, we aimed at investigating whether Ca²⁺-homeostasis of ASMC is altered in T-bet KO-mice as an experimental model of asthma.</p> <p>Methods</p> <p>Lung slices of 100 to 200 μm thickness were obtained from T-bet KO- and wild-type mice. Airway contraction in response to acetylcholine (ACH) was measured by video-microscopy and Ca²⁺-signaling in single ASMC of lung slices was assessed using two-photon-microscopy.</p> <p>Results</p> <p>Airways from T-bet KO-mice showed increased baseline airway tone (BAT) and BHR compared to wild-type mice. This could be mimicked by incubation of lung slices from wild-type mice with IL-13. The increased BAT was correlated with an increased incidence of spontaneous changes in intracellular Ca²⁺-concentrations, whereas BHR correlated with higher ACH-induced Ca²⁺-transients and an increased proportion of ASMC showing Ca²⁺-oscillations. Emptying intracellular Ca²⁺-stores using caffeine or cyclopiazonic acid induced higher Ca²⁺-elevations in ASMC from T-bet KO- compared to wild-type mice.</p> <p>Conclusion</p> <p>Altered Ca²⁺-homeostasis of ASMC contributes to increased BAT and BHR in lung slices from T-bet KO-mice as a murine asthma model. We propose that a higher Ca²⁺-content of the intracellular Ca²⁺-stores is involved in the pathophysiology of these changes.</p