Cell-type-specific whole-brain direct inputs to the anterior and posterior piriform cortex

The piriform cortex (PC) is a key region in the brain that is involved in both processing and coding of olfactory information. It is implicated in various brain disorders, such as epilepsy, Alzheimer’s disease and autism. The PC consists of anterior (APC) and posterior (PPC) parts, which are largely different both in their anatomy and functions. However, the monosynaptic input networks to specific neural populations within APC and PPC remain poorly understood. Here, we mapped the whole-brain monosynaptic inputs to the two major neural populations, the excitatory glutamatergic principal neurons and the inhibitory γ-aminobutyric acid (GABA)-ergic interneurons within the APC and PPC using the rabies virus-mediated retrograde trans-synaptic tracing system. We found that for both types of neurons, APC and PPC share some similarities in input networks, with dominant inputs originating from the olfactory areas (OLF), followed by the isocortex, hippocampal formation (HPF), cortical subplate (CTXsp), cerebral nuclei (CNU) and interbrain (IB), whereas the midbrain (MB) and hindbrain (HB) were either blank or sporadically labeled. However, APC and PPC also showed distinct features in their input distribution patterns. For both types of neurons, the APC was innervated more heavily by bilateral OLF and cortical areas compared to the PPC; whereas the input proportions from the HPF to the PPC were higher than to the APC. Overall, our results revealed that monosynaptic input networks to both excitatory and inhibitory neural populations of different PC subdivisions, may provide the structural architecture for revealing the diverse functions of the PC

Coulomb effects on the formation of proton halo nuclei

The exotic structures in the 2s_{1/2} states of five pairs of mirror nuclei ^{17}O-^{17}F, ^{26}Na-^{26}P, ^{27}Mg-^{27}P, ^{28}Al-^{28}P and ^{29}Si-^{29}P are investigated with the relativistic mean-field (RMF) theory and the single-particle model (SPM) to explore the role of the Coulomb effects on the proton halo formation. The present RMF calculations show that the exotic structure of the valence proton is more obvious than that of the valence neutron of its mirror nucleus, the difference of exotic size between each mirror nuclei becomes smaller with the increase of mass number A of the mirror nuclei and the ratios of the valence proton and valence neutron root-mean-square (RMS) radius to the matter radius in each pair of mirror nuclei all decrease linearly with the increase of A. In order to interpret these results, we analyze two opposite effects of Coulomb interaction on the exotic structure formation with SPM and find that the contribution of the energy level shift is more important than that of the Coulomb barrier for light nuclei. However, the hindrance of the Coulomb barrier becomes more obvious with the increase of A. When A is larger than 34, Coulomb effects on the exotic structure formation will almost become zero because its two effects counteract with each other.Comment: 9 pages, 6 figures. One colum

Fermions tunnelling from the charged dilatonic black holes

Kerner and Mann's recent work shows that, for an uncharged and non-rotating black hole, its Hawking temperature can be exactly derived by fermions tunnelling from its horizons. In this paper, our main work is to improve the analysis to deal with charged fermion tunnelling from the general dilatonic black holes, specifically including the charged, spherically symmetric dilatonic black hole, the rotating Einstein-Maxwell-Dilaton-Axion (EMDA) black hole and the rotating Kaluza-Klein (KK) black hole. As a result, the correct Hawking temperatures are well recovered by charged fermions tunnelling from these black holes.Comment: 16 pages, revised version to appear in Class. Quant. Gra

Tunnelling Methods and Hawking's radiation: achievements and prospects

The aim of this work is to review the tunnelling method as an alternative description of the quantum radiation from black holes and cosmological horizons. The method is first formulated and discussed for the case of stationary black holes, then a foundation is provided in terms of analytic continuation throughout complex space-time. The two principal implementations of the tunnelling approach, which are the null geodesic method and the Hamilton-Jacobi method, are shown to be equivalent in the stationary case. The Hamilton-Jacobi method is then extended to cover spherically symmetric dynamical black holes, cosmological horizons and naked singularities. Prospects and achievements are discussed in the conclusions.Comment: Topical Review commissioned and accepted for publication by "Classical and Quantum Gravity". 101 pages; 6 figure

Thickness-Dependent Morphologies of Gold on N-Layer Graphenes

We report that gold thermally deposited onto n-layer graphenes interacts differently with these substrates depending on the number layer, indicating the different surface properties of graphenes. This results in thickness-dependent morphologies of gold on n-layer graphenes, which can be used to identify and distinguish graphenes with high throughput and spatial resolution. This technique may play an important role in checking if n-layer graphenes are mixed with different layer numbers of graphene with a smaller size, which cannot be found by Raman spectra. The possible mechanisms for these observations are discussed

CRISPR-Cas9 screens in human cells and primary neurons identify modifiers of C9ORF72 dipeptide-repeat-protein toxicity.

Hexanucleotide-repeat expansions in the C9ORF72 gene are the most common cause of amyotrophic lateral sclerosis and frontotemporal dementia (c9ALS/FTD). The nucleotide-repeat expansions are translated into dipeptide-repeat (DPR) proteins, which are aggregation prone and may contribute to neurodegeneration. We used the CRISPR-Cas9 system to perform genome-wide gene-knockout screens for suppressors and enhancers of C9ORF72 DPR toxicity in human cells. We validated hits by performing secondary CRISPR-Cas9 screens in primary mouse neurons. We uncovered potent modifiers of DPR toxicity whose gene products function in nucleocytoplasmic transport, the endoplasmic reticulum (ER), proteasome, RNA-processing pathways, and chromatin modification. One modifier, TMX2, modulated the ER-stress signature elicited by C9ORF72 DPRs in neurons and improved survival of human induced motor neurons from patients with C9ORF72 ALS. Together, our results demonstrate the promise of CRISPR-Cas9 screens in defining mechanisms of neurodegenerative diseases

Hypoxia leads to significant changes in alternative splicing and elevated expression of CLK splice factor kinases in PC3 prostate cancer cells

© 2018 The Author(s). Background: Mounting evidence suggests that one of the ways that cells adapt to hypoxia is through alternative splicing. The aim of this study was firstly to examine the effect of hypoxia on the alternative splicing of cancer associated genes using the prostate cancer cell line PC3 as a model. Secondly, the effect of hypoxia on the expression of several regulators of splicing was examined. Methods: PC3 cells were grown in 1% oxygen in a hypoxic chamber for 48 h, RNA extracted and sent for high throughput PCR analysis at the RNomics platform at the University of Sherbrooke, Canada. Genes whose exon inclusion rate PSI (ψ) changed significantly were identified, and their altered exon inclusion rates verified by RT-PCR in three cell lines. The expression of splice factors and splice factor kinases in response to hypoxia was examined by qPCR and western blotting. The splice factor kinase CLK1 was inhibited with the benzothiazole TG003. Results: In PC3 cells the exon inclusion rate PSI (ψ) was seen to change by >25% in 12 cancer-associated genes; MBP, APAF1, PUF60, SYNE2, CDC42BPA, FGFR10P, BTN2A2, UTRN, RAP1GDS1, PTPN13, TTC23 and CASP9 (caspase 9). The expression of the splice factors SRSF1, SRSF2, SRSF3, SAM68, HuR, hnRNPA1, and of the splice factor kinases SRPK1 and CLK1 increased significantly in hypoxia. We also observed that the splice factor kinase CLK3, but not CLK2 and CLK4, was also induced in hypoxic DU145 prostate, HT29 colon and MCF7 breast cancer cell lines. Lastly, we show that the inhibition of CLK1 in PC3 cells with the benzothiazole TG003 increased expression of the anti-apoptotic isoform caspase 9b. Conclusions: Significant changes in alternative splicing of cancer associated genes occur in prostate cancer cells in hypoxic conditions. The expression of several splice factors and splice factor kinases increases during hypoxia, in particular the Cdc-like splice factor kinases CLK1 and CLK3. We suggest that in hypoxia the elevated expression of these regulators of splicing helps cells adapt through alternative splicing of key cancer-associated genes. We suggest that the CLK splice factor kinases could be targeted in cancers in which hypoxia contributes to resistance to therapy

Improved measurements of the Dalitz decays η/η′→γe+e−\eta/\eta'\rightarrow\gamma e^{+}e^{-}

Based on a data sample of 10 billion $J/\psi$ events collected with the BESIII detector, improved measurements of the Dalitz decays $\eta/\eta'\rightarrow\gamma e^+e^-$ are performed, where the $\eta$ and $\eta'$ are produced through the radiative decays $J/\psi\rightarrow\gamma \eta/\eta'$. The branching fractions of $\eta\rightarrow\gamma e^+e^-$ and $\eta'\rightarrow\gamma e^+e^-$ are measured to be $(7.07 \pm 0.05 \pm 0.23)\times10^{-3}$ and $(4.83\pm0.07\pm0.14)\times10^{-4}$, respectively. Within the single pole model, the parameter of electromagnetic transition form factor for $\eta\rightarrow\gamma e^+e^-$ is determined to be $\Lambda_{\eta}=(0.749 \pm 0.027 \pm 0.007)~ {\rm GeV}/c^{2}$. Within the multi-pole model, we extract the electromagnetic transition form factors for $\eta'\rightarrow\gamma e^+e^-$ to be $\Lambda_{\eta'} = (0.802 \pm 0.007\pm 0.008)~ {\rm GeV}/c^{2}$ and $\gamma_{\eta'} = (0.113\pm0.010\pm0.002)~ {\rm GeV}/c^{2}$. The results are consistent with both theoretical predictions and previous measurements. The characteristic sizes of the interaction regions for the $\eta$ and $\eta'$ are calculated to be $(0.645 \pm 0.023 \pm 0.007 )~ {\rm fm}$ and $(0.596 \pm 0.005 \pm 0.006)~ {\rm fm}$, respectively. In addition, we search for the dark photon in $\eta/\eta^\prime\rightarrow\gamma e^{+}e^{-}$, and the upper limits of the branching fractions as a function of the dark photon are given at 90\% confidence level