Revisit to the yield ratio of triton and 3^3He as an indicator of neutron-rich neck emission

The neutron rich neck zone created in heavy ion reaction is experimentally probed by the production of the $A=3$ isobars. The energy spectra and angular distributions of triton and $^3$He are measured with the CSHINE detector in $^{86}$Kr +$^{208}$Pb reactions at 25 MeV/u. While the energy spectrum of $^{3}$He is harder than that of triton, known as "$^{3}$He-puzzle", the yield ratio $R({\rm t/^3He})$ presents a robust rising trend with the polar angle in laboratory. Using the fission fragments to reconstruct the fission plane, the enhancement of out-plane $R({\rm t/^3He})$ is confirmed in comparison to the in-plane ratios. Transport model simulations reproduce qualitatively the experimental trends, but the quantitative agreement is not achieved. The results demonstrate that a neutron rich neck zone is formed in the reactions. Further studies are called for to understand the clustering and the isospin dynamics related to neck formation

Observation of the electromagnetic doubly OZI-suppressed decay J/ψ→ϕπ0J/\psi \rightarrow \phi \pi^{0}

Using a sample of $1.31$ billion $J/\psi$ events accumulated with the BESIII detector at the BEPCII collider, we report the observation of the decay $J/\psi \rightarrow \phi\pi^{0}$, which is the first evidence for a doubly Okubo-Zweig-Iizuka suppressed electromagnetic $J/\psi$ decay. A clear structure is observed in the $K^{+} K^{-}$ mass spectrum around 1.02 GeV/$c^2$, which can be attributed to interference between $J/\psi \rightarrow \phi\pi^{0}$ and $J/\psi \rightarrow K^{+}K^{-}\pi^{0}$ decays. Due to this interference, two possible solutions are found. The corresponding measured values of the branching fraction of $J/\psi \to \phi\pi^{0}$ are $[2.94 \pm 0.16\text{(stat.)} \pm 0.16\text{(syst.)}] \times 10^{-6}$ and $[1.24 \pm 0.33\text{(stat.)} \pm 0.30\text{(syst.)}] \times 10^{-7}$.Comment: 7 pages, 4 figures, published in Phys. Rev.

Brn2 Is a Transcription Factor Regulating Keratinocyte Differentiation with a Possible Role in the Pathogenesis of Lichen Planus

Terminal differentiation of skin keratinocytes is a vertically directed multi-step process that is tightly controlled by the sequential expression of a variety of genes. In this study, we investigated the role of the POU domain-containing transcription factor Brn2 in keratinocyte differentiation. Immunohistochemical analysis showed that Brn2 is expressed primarily in the upper granular layer. Consistent with its epidermal localization, Brn2 expression was highly induced at 14 days after calcium treatment of cultured normal human epidermal keratinocytes. When Brn2 was overexpressed by adenoviral transduction, Brn2 led to increased expression of the differentiation-related genes involucrin, filaggrin, and loricrin in addition to inhibition of their proliferation. Chromatin immunoprecipitation demonstrated that Brn2 bound to the promoter regions of these differentiation-related genes. We injected the purified Brn2 adenovirus into rat skin, which led to a thickened epidermis with increased amounts of differentiation related markers. The histopathologic features of adenovirus-Brn2 injected skin tissues looked similar to the features of lichen planus, a human skin disease showing chronic inflammation and well-differentiated epidermal changes. Moreover, Brn2 is shown to be expressed in almost all cell nuclei of the thickened epidermis of lichen planus, and Brn2 also attracts T lymphocytes. Our results demonstrate that Brn2 is probably a transcriptional factor playing an important role in keratinocyte differentiation and probably also in the pathogenesis of lichen planus lesions

Does or did the supernova remnant Cassiopeia A operate as a PeVatron?

For decades, supernova remnants (SNRs) have been considered the prime sources of Galactic Cosmic rays (CRs). But whether SNRs can accelerate CR protons to PeV energies and thus dominate CR flux up to the knee is currently under intensive theoretical and phenomenological debate. The direct test of the ability of SNRs to operate as CR PeVatrons can be provided by ultrahigh-energy (UHE; $E_\gamma \geq 100$~TeV) $\gamma$-rays. In this context, the historical SNR Cassiopeia A (Cas A) is considered one of the most promising target for UHE observations. This paper presents the observation of Cas A and its vicinity by the LHAASO KM2A detector. The exceptional sensitivity of LHAASO KM2A in the UHE band, combined with the young age of Cas A, enabled us to derive stringent model-independent limits on the energy budget of UHE protons and nuclei accelerated by Cas A at any epoch after the explosion. The results challenge the prevailing paradigm that Cas A-type SNRs are major suppliers of PeV CRs in the Milky Way.Comment: 11 pages, 3 figures, Accepted by the APJ

Measurement of ultra-high-energy diffuse gamma-ray emission of the Galactic plane from 10 TeV to 1 PeV with LHAASO-KM2A

The diffuse Galactic $\gamma$-ray emission, mainly produced via interactions between cosmic rays and the interstellar medium and/or radiation field, is a very important probe of the distribution, propagation, and interaction of cosmic rays in the Milky Way. In this work we report the measurements of diffuse $\gamma$-rays from the Galactic plane between 10 TeV and 1 PeV energies, with the square kilometer array of the Large High Altitude Air Shower Observatory (LHAASO). Diffuse emissions from the inner ($15^{\circ}<l<125^{\circ}$, $|b|<5^{\circ}$) and outer ($125^{\circ}<l<235^{\circ}$, $|b|<5^{\circ}$) Galactic plane are detected with $29.1\sigma$ and $12.7\sigma$ significance, respectively. The outer Galactic plane diffuse emission is detected for the first time in the very- to ultra-high-energy domain ($E>10$~TeV). The energy spectrum in the inner Galaxy regions can be described by a power-law function with an index of $-2.99\pm0.04$, which is different from the curved spectrum as expected from hadronic interactions between locally measured cosmic rays and the line-of-sight integrated gas content. Furthermore, the measured flux is higher by a factor of $\sim3$ than the prediction. A similar spectrum with an index of $-2.99\pm0.07$ is found in the outer Galaxy region, and the absolute flux for $10\lesssim E\lesssim60$ TeV is again higher than the prediction for hadronic cosmic ray interactions. The latitude distributions of the diffuse emission are consistent with the gas distribution, while the longitude distributions show clear deviation from the gas distribution. The LHAASO measurements imply that either additional emission sources exist or cosmic ray intensities have spatial variations.Comment: 12 pages, 8 figures, 5 tables; accepted for publication in Physical Review Letters; source mask file provided as ancillary fil

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1.

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field