Aimed at reducing deficiencies in representing the Madden-Julian oscillation (MJO) in general circulation models (GCMs), a global model evaluation project on vertical structure and physical processes of the MJO was coordinated. In this paper, results from the climate simulation component of this project are reported. It is shown that the MJO remains a great challenge in these latest generation GCMs. The systematic eastward propagation of the MJO is only well simulated in about one fourth of the total participating models. The observed vertical westward tilt with altitude of the MJO is well simulated in good MJO models but not in the poor ones. Damped Kelvin wave responses to the east of convection in the lower troposphere could be responsible for the missing MJO preconditioning process in these poor MJO models. Several process-oriented diagnostics were conducted to discriminate key processes for realistic MJO simulations. While large-scale rainfall partition and low-level mean zonal winds over the Indo-Pacific in a model are not found to be closely associated with its MJO skill, two metrics, including the low-level relative humidity difference between high-and low-rain events and seasonal mean gross moist stability, exhibit statistically significant correlations with the MJO performance. It is further indicated that increased cloud-radiative feedback tends to be associated with reduced amplitude of intraseasonal variability, which is incompatible with the radiative instability theory previously proposed for the MJO. Results in this study confirm that inclusion of air-sea interaction can lead to significant improvement in simulating the MJO.

The Australian Community Climate and Earth System Simulator coupled model (ACCESS-CM) has been developed at the Centre for Australian Weather and Climate Research (CAWCR), a partnership between CSIRO 1 and the Bureau of Meteorology. It is built by coupling the UK Met Office atmospheric unified model (UM), and other sub-models as required, to the ACCESS ocean model, which consists of the NOAA/GFDL 2 ocean model MOM4p1 and the LANL 3 sea-ice model CICE4.1, under the CERFACS 4 OASIS3.2-5 coupling framework. The primary goal of the ACCESS-CM development is to provide the Australian climate community with a new generation fully coupled climate model for climate research, and to participate in phase five of the Coupled Model Inter-comparison Project (CMIP5). This paper describes the ACCESS-CM framework and components, and presents the control climates from two versions of the ACCESS-CM, ACCESS1.0 and AC-CESS1.3, together with some fields from the 20 th century historical experiments, as part of model evaluation. While sharing the same ocean sea-ice model (except different setups for a few parameters), ACCESS1.0 and ACCESS1.3 differ from each other in their atmospheric and land surface components: the former is configured with the UK Met Office HadGEM2 (r1.1) atmospheric physics and the Met Office Surface Exchange Scheme land surface model version 2, and the latter with atmospheric physics similar to the UK Met Office Global Atmosphere 1.0 including modifications performed at CAWCR and the CSIRO Community Atmosphere Biosphere Land Exchange land surface model version 1.8. The global average annual mean surface air temperature across the 500-year preindustrial control integrations show a warming drift of 0.35 °C in ACCESS1.0 and 0.04 °C in AC-CESS1.3. The overall skills of ACCESS-CM in simulating a set of key climatic fields both globally and over Australia significantly surpass those from the preceding CSIRO Mk3.5 model delivered to the previous coupled model inter-comparison. However, ACCESS-CM, like other CMIP5 models, has deficiencies in various aspects, and these are also discussed.

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The outbreak of the pandemic caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) calls for an urgent unmet need for developing a facial and cost-effective detection method. The requirement of well-trained personnel and sophisticated instrument of current primary mean (reverse transcription polymerase chain reaction, RT-PCR) may hinder the practical application worldwide. In this regard, a reverse transcription recombinase polymerase amplification (RT-RPA) coupled with CRISPR-Cas12a colorimetric assay is proposed for the SARS-CoV-2 detection. The methodology we have described herein utilizes DNA-modified gold nanoparticles (AuNPs) as a universal colorimetric readout and can specifically target ORF1ab and N regions of the SARS-CoV-2 genome. After the virus genome is amplified through RT-RPA, the resulting abundant dsDNA will bind and activate Cas12a. Under trans-cleavage degradation, the capped DNA substrate will be hydrolyzed gradually from AuNPs, demonstrating a change in the surface plasmon resonance (SPR), which can be facially monitored by UV–vis absorbance spectroscopy and naked eye observation. The high amplification efficiency from RT-RPA and Cas12a trans-cleavage process bring the sensitivity of our method to 1 copy of viral genome sequence per test. Notably, under the dual variations inspecting from the isothermal amplification and Cas12a activation process, the false positive events from other beta coronavirus members can be effectively avoided and thus significantly improve the specificity. Furthermore, the reliability of this colorimetric assay is validated by standard clinical samples from the hospital laboratory department. Through integration of the inherently high sensitivity and specificity from an RPA-coupled Cas12a system with the intrinsic simplicity of AuNP-based colorimetric assay, our method increases the practical testing availability of SARS-CoV-2.

Inflammatory mediators, many of which activate the signaling of nuclear factor kappa B (NFκB), have received increasing attention in the field of neurogenesis. NFκB signaling regulates neurite outgrowth and neural plasticity as well as the proliferation/apoptosis and terminal differentiation of neural stem cells (NSCs). Early neurogenesis from NSCs produces identical progeny through symmetric division and committed daughter cells through asymmetric division. Here, we show that NFκB signaling is required for NSC initial differentiation. The canonical IKKβ/IκBα/ p65 pathway is activated during the initial stages of neural differentiation induced by treatment with TNFα or with- drawal of epidermal growth factor/basic fibroblast growth factor. NSC-specific inhibition of NFκB in transgenic mice causes an accumulation of Nestin+/Sox2+/glial fibrillary acidic protein+ NSCs. Inhibition of NFκB signaling in vitro blocks differentiation and asymmetric division and maintains NSCs in an undifferentiated state. The induction of initial differentiation and asymmetry by NFκB signaling occurs through the inhibition of C/EBPβ expression. Our data reveal a novel function of NFκB signaling in early neurogenesis and provide insight into the molecular mechanisms underlying neurodevelopmental disorders and neurodegenerative diseases.