The next widespread bamboo flowering poses a massive risk to the giant panda

The IUCN Red List has downgraded several species from “endangered” to “vulnerable” that still have largely unknown extinction risks. We consider one of those downgraded species, the giant panda, a bamboo specialist. Massive bamboo flowering could be a natural disaster for giant pandas. Using scenario analysis, we explored possible impacts of the next bamboo flowering in the Qinling and Minshan Mountains that are home to most giant pandas. Our results showed that the Qinling Mountains could experience large-scale bamboo flowering leading to a high risk of widespread food shortages for the giant pandas by 2020. The Minshan Mountains could similarly experience a large-scale bamboo flowering with a high risk for giant pandas between 2020 and 2030 without suitable alternative habitat in the surrounding areas. These scenarios highlight thus-far unforeseen dangers of conserving giant pandas in a fragmented habitat. We recommend advance measures to protect giant panda from severe population crashes when flowering happens. This study also suggests the need to anticipate and manage long-term risks to other downgraded species

Long Non-Coding RNA Expression Profiles for the Characterization of Different Bladder Cancer Grade

Background/Aims: Bladder cancer (BC) is one of the most frequent urologic tumors worldwide. However, long non-coding RNA(lncRNA) expression profiles in BC progression remain unclear. This study aimed to explore lncRNA expression profiles in different grades of bladder cancer and normal urothelium tissues. Methods: We performed high-throughput sequencing in BC tissues of different grade and obtained the expression profiles of its lncRNAs. Then, aberrantly expressed lncRNAs were validated by quantitative reverse transcription polymerase chain reaction (RT-PCR). Gene Ontology (GO) and pathway analyses were used to investigate the potential function of these lncRNAs. Co-expresson network was constructed to explore the relationship between lncRNAs and target mRNAs. Results: We identified 252 aberrantly expressed lncRNAs in high-grade BC while compared to low-grade BC, and 269 lncRNAs in high-grade BC while compared to normal urothelium. Notably, we found 33 overlapped lncRNAs. Subsequently, 7 lncRNAs were selected from the overlapped part and confirmed by RT-PCR. GO and pathway analyses showed that these dysregulated lncRNAs participated in cell migration, cell adhesion, as well as Ras signaling pathway. Co-expression network and The Cancer Genome Atlas (TCGA) data showed LUCAT1 and CCNB1 had positive relationship in regulating the progress of bladder cancer. Conclusion: Our findings revealed the significant role of lncRNAs in the development process of bladder cancer

Follicular Oocytes Better Support Development in Rabbit Cloning Than Oviductal Oocytes

This study was conducted to determine the effect of rabbit oocytes collected from ovaries or oviducts on the developmental potential of nuclear transplant embryos. Donor nuclei were obtained from adult skin fibroblasts, cumulus cells, and embryonic blastomeres. Rabbit oocytes were flushed from the oviducts (oviductal oocytes) or aspirated from the ovaries (follicular oocytes) of superovulated does at 10, 11, or 12-h post-hCG injection. The majority of collected oocytes were still attached to the sites of ovulation on the ovaries. We found that follicular oocytes had a significantly higher rate of fusion with nuclear donor cells than oviductal oocytes. There was no difference in the cleavage rate between follicular and oviductal groups, but morula and blastocyst development was significantly higher in the follicular group than in the oviductal group. Two live clones were produced in follicular group using blastomere and cumulus nuclear donors, whereas one live clone was produced in the oviductal group using a cumulus nuclear donor. These results demonstrate that cloned rabbit embryos derived from follicular oocytes have better developmental competence than those derived from oviductal oocytes.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90481/1/cell-2E2011-2E0030.pd

Liquefaction structures induced by the M5.7 earthquake on May 28, 2018 in Songyuan, Jilin Province, NE China and research implication

Acknowledgements Many thanks to Yang Wang, Wei Chen and Dong-Hao Peng from Jilin Oilfield for their help in the field investigation. We thank Dr. Lv Wang from Monash University and Dr. Gail Maxwell from the University of Aberdeen for their valuable advice on sedimentology, and we also thank Dr. Gui-Dong Ping and Dr. Zhao-Han Xie for the discussion we had about the regional tectonic stress field. We are grateful to Professor Zeng-Zhao Feng, editors and two anonymous reviewers for their editorial work and many constructive comments and suggestions that greatly improved this manuscript. Funding This study is supported by the “Natural Science Foundation of Heilongjiang Province (No. JJ2016ZR0573)”, “Youth Foundation of Northeast Petroleum University (No. NEPUBS201503)”, “Northeast Petroleum University Scientific Research Start-up Fund”, “Shandong Provincial Key Laboratory of Depositional Mineralization and Mineral Foundation (No. DMSMZO17009)”, and “Natural Science Foundation of Shandong Province (No. ZR2016DB15)”. Authors’ contributions ZFS applied for the funding, performed the research, analyzed the data, compiled a few figures and wrote the manuscript. JHZ designed the work, took part in the field trip and interpreted the data. JH interpreted part of the data and revised the manuscript. BH took part in the field trip, collected data and compiled Fig. 5. XWL interpreted part of the data and revised the manuscript. ZXL collected papers and completed some figures. WMR collected some data and compiled Fig. 2. YFZ, HQY, and JLL interpreted some of the data. LTN and GXS took part in fieldwork and collected data. JJL, WXZ and BZ interpreted some data and compiled some figures. All authors approved the final manuscript. Availability of data and materials All data generated or analyzed during this study are included in this published article. Additional data related to this paper can be requested from the corresponding author.Peer reviewedPublisher PD

Activation of the Dormant Secondary Metabolite Production by Introducing Gentamicin-Resistance in a Marine-Derived Penicillium purpurogenum G59

A new approach to activate silent gene clusters for dormant secondary metabolite production has been developed by introducing gentamicin-resistance to an originally inactive, marine-derived fungal strain Penicillium purpurogenum G59. Upon treatment of the G59 spores with a high concentration of gentamicin in aqueous DMSO, a total of 181 mutants were obtained by single colony isolation. In contrast to the strain G59, the EtOAc extracts of nine mutant cultures showed inhibitory effects on K562 cells, indicating that the nine mutants had acquired capability to produce antitumor metabolites. This was evidenced by TLC and HPLC analysis of EtOAc extracts of G59 and the nine mutants. Further isolation and characterization demonstrated that four antitumor secondary metabolites, janthinone (1), fructigenine A (2), aspterric acid methyl ester (3) and citrinin (4), were newly produced by mutant 5-1-4 compared to the parent strain G59, and which were also not found in the secondary metabolites of other Penicillium purpurogenum strains. However, Compounds 1–4 inhibited the proliferation of K562 cells with inhibition rates of 34.6% (1), 60.8% (2), 31.7% (3) and 67.1% (4) at 100 μg/mL, respectively. The present study demonstrated the effectiveness of a simple, yet practical approach to activate the production of dormant fungal secondary metabolites by introducing acquired resistance to aminoglycoside antibiotics, which could be applied to the studies for eliciting dormant metabolic potential of fungi to obtain cryptic secondary metabolites

Real-Time Observation of Iodide Ion Migration in Methylammonium Lead Halide Perovskites

Organic-inorganic metal-halide perovskites (e.g. CH3NH3PbI3-xClx) emerged as a promising opto-electronic material. However, the Shockley–Queisser Limit for the power conversion efficiency (PCE) of perovskite-based photovoltaic devices has still not been reached, which was attributed to non-radiative recombination pathways, as suggested by photoluminescence (PL) inactive (or dark) areas on perovskite films. Although these observations have been related to the presence of ions/defects, the underlying fundamental physics and detailed microscopic processes, concerning trap/defect status, ion migration, etc., still remain poorly understood. Here we utilize correlated wide-field PL microscopy and impedance spectroscopy (IS) on perovskite films to in-situ investigate both the spatial and temporal evolution of these PL inactive areas under external electrical fields. We attribute the formation of PL inactive domains to the migration and accumulation of iodine ions under external fields. Hence we are able to characterize the kinetic processes and determine the drift velocities of these ions. In addition, we show that I2 vapor directly affects the PL quenching of a perovskite film, which provides evidence that the migration/segregation of iodide ions plays an important role in the PL quenching and consequently limits the PCE of organometal halide based perovskite photovoltaic devices

Persistent sulfate formation from London Fog to Chinese haze

Sulfate aerosols exert profound impacts on human and ecosystem health, weather, and climate, but their formation mechanism remains uncertain. Atmospheric models consistently underpredict sulfate levels under diverse environmental conditions. From atmospheric measurements in two Chinese megacities and complementary laboratory experiments, we show that the aqueous oxidation of SO2 by NO2 is key to efficient sulfate formation but is only feasible under two atmospheric conditions: on fine aerosols with high relative humidity and NH3 neutralization or under cloud conditions. Under polluted environments, this SO2 oxidation process leads to large sulfate production rates and promotes formation of nitrate and organic matter on aqueous particles, exacerbating severe haze development. Effective haze mitigation is achievable by intervening in the sulfate formation process with enforced NH3 and NO2 control measures. In addition to explaining the polluted episodes currently occurring in China and during the 1952 London Fog, this sulfate production mechanism is widespread, and our results suggest a way to tackle this growing problem in China and much of the developing world

Protein Disulfide Isomerase Regulates Endoplasmic Reticulum Stress and the Apoptotic Process during Prion Infection and PrP Mutant-Induced Cytotoxicity

<div><h3>Background</h3><p>Protein disulfide isomerase (PDI), is sorted to be enzymatic chaperone for reconstructing misfolded protein in endoplasmic reticulum lumen. Recently, PDI has been identified as a link between misfolded protein and neuron apoptosis. However, the potential for PDI to be involved in the pathogenesis of prion disease remains unknown. In this study, we propose that PDI may function as a pleiotropic regulator in the cytotoxicity induced by mutated prion proteins and in the pathogenesis of prion diseases.</p> <h3>Methodology/Principal Findings</h3><p>To elucidate potential alterations of PDI in prion diseases, the levels of PDI and relevant apoptotic executors in 263K infected hamsters brain tissues were evaluated with the use of Western blots. Abnormal upregulation of PDI, Grp78 and Grp58 was detected. Dynamic assays of PDI alteration identified that the upregulation of PDI started at the early stage and persistently increased till later stage. Obvious increases of PDI and Grp78 levels were also observed in cultured cells transiently expressing PrP mutants, PrP-KDEL or PrP-PG15, accompanied by significant cytotoxicities. Excessive expression of PDI partially eased ER stress and cell apoptosis caused by accumulation of PrP-KDEL, but had less effect on cytotoxicity induced by PrP-PG15. Knockdown of endogenous PDI significantly amended cytotoxicity of PrP-PG15, but had little influence on that of PrP-KDEL. A series of membrane potential assays found that apoptosis induced by misfolded PrP proteins could be regulated by PDI via mitochondrial dysfunction. Moreover, biotin-switch assays demonstrated active <em>S</em>-nitrosylted modifications of PDI (SNO-PDI) both in the brains of scrapie-infected rodents and in the cells with misfolded PrP proteins.</p> <h3>Conclusion/Significance</h3><p>Current data in this study highlight that PDI and its relevant executors may function as a pleiotropic regulator in the processes of different misfolded PrP proteins and at different stages during prion infection. SNO-PDI may feed as an accomplice for PDI apoptosis.</p> </div