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Lipids have been found to modulate tumor biology, including proliferation, survival, and metastasis. With the new understanding of tumor immune escape that has developed in recent years, the influence of lipids on the cancer–immunity cycle has also been gradually discovered. First, regarding antigen presentation, cholesterol prevents tumor antigens from being identified by antigen presenting cells. Fatty acids reduce the expression of major histocompatibility complex class I and costimulatory factors in dendritic cells, impairing antigen presentation to T cells. Prostaglandin E2 (PGE2) reduce the accumulation of tumor-infiltrating dendritic cells. Regarding T-cell priming and activation, cholesterol destroys the structure of the T-cell receptor and reduces immunodetection. In contrast, cholesterol also promotes T-cell receptor clustering and relative signal transduction. PGE2 represses T-cell proliferation. Finally, regarding T-cell killing of cancer cells, PGE2 and cholesterol weaken granule-dependent cytotoxicity. Moreover, fatty acids, cholesterol, and PGE2 can improve the activity of immunosuppressive cells, increase the expression of immune checkpoints and promote the secretion of immunosuppressive cytokines. Given the regulatory role of lipids in the cancer–immunity cycle, drugs that modulate fatty acids, cholesterol and PGE2 have been envisioned as effective way in restoring antitumor immunity and synergizing with immunotherapy. These strategies have been studied in both preclinical and clinical studies. Lipids regulate cancer immunity cycle by affecting antigen presentation, T-cell priming and activation and T-cell killing of tumor, which in turn promotes immune surveillance escape. [Display omitted] [ABSTRACT FROM AUTHOR]

Phallus rubrovolvatus (P. rubrovolvatus) is a large and rare fungus widely consumed and used for medicinal purposes in East Asian countries, earning the reputation of "plant meat". We created a reference genome for P. rubrovolvatus , with an assembly length of 33.39 Mb and 144 overlapping groups. We identified 9,204 coding genes on the genome, of which 231 gene clusters are related to amino acid synthesis and transport. In this study, via integrating the flavor-related metabolite and transcriptome data of five different developmental stages of P. rubrovolvatus , we produced a global map of the alterations in flavor-related metabolites throughout the entire development process of P. rubrovolvatus. With this dataset, we constructed a complex regulatory network, thereby identifying the key structural genes and metabolites for the regulation of free amino acids in the flavor formation of P. rubrovolvatus , and glutathione and 5′-nucleotides possess a strong synergistic fresh-enhancing effect. In the five different developmental stages of P. rubrovolvatus , the regulation of the identified genes related to the synthesis of amino acids and derivatives on flavor metabolism has been confirmed, which demonstrates that our dataset offers a suitable instrument for elucidating the regulatory substances that control the flavor biosynthetic pathways, which were previously not elucidated. Overall, our research findings not only provide novel insights into the metabolic regulation of flavor during the mycelia developmental process of P. rubrovolvatus , but also lay the groundwork for enhancing the flavor of P. rubrovolvatus. [Display omitted] • The genome of Phallus rubrovolvatus has been assembled. • Amino acids grant Phallus rubrovolvatu s a unique flavor. • Glutathione and 5′-nucleotide play an enhancing role in flavor formation. • The molecular mechanism of the formation of the unique flavor of Phallus rubrovolvatu s. [ABSTRACT FROM AUTHOR]

Compared with a disordered network, the ordered framework is more beneficial to improving the multifunctional properties (including thermal, electrical, and mechanical properties) of epoxy-based composites. However, current methods for building aligned structures are both energy and time-consuming on account of the tedious and lengthy lyophilization process. Herein, a new strategy is proposed to obtain low-density graphene aerogels (GAs) with long-range oriented structures through a lyophilization-free processes. Due to the minimum thermal boundary resistance, the prepared aligned graphene/epoxy composite exhibits an ultrahigh thermal conductivity of ∼11.6 W/(m·K) at a graphene content of 1.84 vol%, i.e., an enhancement efficiency of 3640% per 1 vol%. In addition, the compressive strength of the composite is increased by 2.6 times compared to epoxy (from 0.29 MPa to 0.76 MPa). Because the composite shows a modulus as low as 0.5–1.0 MPa, it has excellent deformability and compression performance. Moreover, the obtained 3-mm-thick composite achieves an electromagnetic interference shielding effectiveness (EMI SE) of 40 dB due to the interconnected graphene network structure, which meets the requirements of commercial EMI shielding applications. Hence, this strategy can be used to synthesize aligned graphene/epoxy composites with excellent multifunctional performances, which can be simultaneously used as elastic thermal interface materials (TIMs) and EMI shielding materials in the fields of advanced electronic packaging. [Display omitted] • Aligned graphene aerogel (GA) was fabricated by a lyophilization-free approach. • The compressive strength of the composite is increased by 2.6 times compared to epoxy (0.29 MPa to 0.76 MPa) and the composite shows a modulus as low as 0.48–1.0 MPa, exhibiting excellent deformability and compression performance. • The vertical pathways and high-quality give composite an ultrahigh thermal conductivity (∼11.6 W/m·K) with ultralow graphene loading (1.84 vol%), i.e., an enhancement efficiency of 3640% per 1 vol%. • The obtained 3-mm-thick composite achieves an electromagnetic interference shielding effectiveness of 40 dB due to the interconnected network structure. [ABSTRACT FROM AUTHOR]

Substantial evidence has linked short-term exposure to ambient fine particulate matter (PM 2.5 ) with increased cardiovascular mortality, however, the specific chemical constituent and emission source responsible for this effect remained largely unclear. A time series Poisson model was employed to quantify the association of cardiovascular mortality with two sets of shipping pollution emission: nickel (Ni), vanadium (V) (the indices of shipping emission) and estimated shipping emission using a source apportionment approach in Guangzhou, China in 2014. We observed that Ni, V, and estimated shipping emission in PM 2.5 were associated with increased cardiovascular mortality, an inter-quartile range (IQR) increase in lag 2 Ni was associated with 4.60% (95% CI: 0.14%, 9.26%) increase in overall cardiovascular mortality, and 13.35% (95% CI: 5.54%, 21.75%) increase in cerebrovascular mortality; each IQR increase of lag 1 V was correlated with 6.01% (95% CI: 1.83%, 10.37%) increase in overall cardiovascular mortality, and 11.02% (95% CI: 3.15%, 19.49%) increase in cerebrovascular mortality; and each IQR increase in lag 1 shipping emission was associated with 5.55% (95% CI: 0.78%, 10.54%) increase in overall cardiovascular mortality, and 10.39% (95% CI: 1.43%, 20.14%) increase in cerebrovascular mortality. The results remained robust to adjustment for PM 2.5 mass and gaseous air pollutants. This study suggests that shipping emission is an important detrimental factor of cardiovascular mortality, and should be emphasized in air pollution control and management in order to protect the public health in Guangzhou, China. [ABSTRACT FROM AUTHOR]

While increasing evidence suggested that PM 2.5 is the most harmful fraction of the particle pollutants, the health effects of coarse particles (PM 10–2.5 ) have been inconclusive, especially on cerebrovascular diseases, we thus evaluated the effects of PM 10 , PM 2.5 , and PM 10–2.5 on stroke mortality in six Chinese subtropical cities using generalized additive models. We also conducted random-effects meta-analyses to estimate the overall effects across the six cities. We found that PM 10 , PM 2.5 , and PM 10-2.5 were significantly associated with stroke mortality. Each 10 μg/m 3 increase of PM 10 , PM 2.5 and PM 10-2.5 (lag03) was associated with an increase of 1.88% (95% CI: 1.37%, 2.39%), 3.07% (95% CI: 2.35%, 3.79%), and 5.72% (95% CI: 3.82%, 7.65%) in overall stroke mortality. Using the World Health Organization's guideline as reference concentration, we estimated that 3.21% (95% CI: 1.65%, 3.01%) of stroke mortality (corresponding to 1743 stroke mortalities, 95% CI: 896, 1633) were attributed to PM 10 , 5.57% (95% CI: 0.50%, 1.23%) stroke mortality (3019, 95% CI: 2286, 3777) were attributed to PM 2.5 , and 2.02% (95% CI: 1.85%, 3.08%) of stroke mortality (1097, 95% CI: 1005, 1673) could be attributed to PM 10-2.5 . Our analysis indicates that both PM 2.5 and PM 10-2.5 are important risk factors of stroke mortality and should be considered in the prevention and control of stroke in the study area. [ABSTRACT FROM AUTHOR]

Until menopause, women have a lower propensity to develop metabolic diseases than men, suggestive of a protective role for sex hormones. Although a functional synergy between central actions of estrogens and leptin has been demonstrated to protect against metabolic disturbances, the underlying cellular and molecular mechanisms mediating this crosstalk have remained elusive. By using a series of embryonic, adult-onset, and tissue/cell-specific loss-of-function mouse models, we document an unprecedented role of hypothalamic Cbp/P300-interacting transactivator with Glu/Asp-rich carboxy-terminal domain 1 (Cited1) in mediating estradiol (E2)-dependent leptin actions that control feeding specifically in pro-opiomelanocortin (Pomc) neurons. We reveal that within arcuate Pomc neurons, Cited1 drives leptin's anorectic effects by acting as a co-factor converging E2 and leptin signaling via direct Cited1-ERα-Stat3 interactions. Together, these results provide new insights on how melanocortin neurons integrate endocrine inputs from gonadal and adipose axes via Cited1, thereby contributing to the sexual dimorphism in diet-induced obesity. [Display omitted] • Global and hypothalamic Cited1 loss exacerbates diet-induced obesity in female mice • Cited1 is highly enriched in estradiol-sensitive melanocortin neurons • Hypothalamic Cited1 molecularly links the effects of E2 and leptin on food intake • Cited1 in PomcARC neurons acts as a downstream co-factor for E2-leptin signaling Estradiol regulates energy homeostasis by altering feeding behavior, but how this sex hormone converges with the melanocortin system is not fully understood. Here, González-García et al. discover that Cited1 acts as a crucial hypothalamic co-factor mediating the anti-obesity effects of estradiol through potentiation of leptin's anorectic actions. This neuroendocrine mechanism represents a mode by which melanocortin neurons integrate energy stores with reproductive signals for metabolic adaptation in diet-induced obesity. [ABSTRACT FROM AUTHOR]

Though significant associations between particulate matter (PM) air pollution and cardiovascular diseases have been widely reported, it remains unclear what characteristics, such as particle size and chemical constituents, may be responsible for the effects. A time-series model was applied to examine the cardiovascular effects of particle size (for the period of 2009–2011) and chemical constituents (2007–2010) in Guangzhou, we controlled for potential confounders in the model, such as time trends, day of the week, public holidays, meteorological factors and influenza epidemic. We found significant associations of cardiovascular mortality with PM 10 , PM 2.5 and PM 1 ; the excess risk (ER) was 6.10% (95% CI: 1.76%, 10.64%), 6.11% (95% CI: 1.76%, 10.64%) and 6.48% (95% CI: 2.10%, 11.06%) for per IQR increase in PM 10 , PM 2.5 and PM 1 at moving averages for the current day and the previous 3 days (lag 03 ), respectively. We did not find significant effects of PM 2.5-10 and PM 1-2.5 . For PM 2.5 constituents, we found that organic carbon, elemental carbon, sulfate, nitrate and ammonium were significantly associated with cardiovascular mortality, the corresponding ER for an IQR concentration increase at lag 03 was 1.13% (95% CI: 0.10%, 2.17%), 2.77% (95% CI: 0.72%, 4.86%), 2.21% (95% CI: 1.05%, 3.38%), 1.98% (95% CI: 0.54%, 3.44%), and 3.38% (95% CI: 1.56%, 5.23%), respectively. These results were robust to adjustment of other air pollutants and they remained consistent in various sensitivity analyses by changing model parameters. Our study suggests that PM 1 and constituents from combustion and secondary aerosols might be important characteristics of PM pollution associated with cardiovascular mortality in Guangzhou. [ABSTRACT FROM AUTHOR]

The short-term effects of ambient temperature on mortality have been widely investigated. However, the epidemiological evidence on the long-term effects of temperature on mortality is rare. In present study, we conducted a nationwide quasi-experimental design, which based on a variant of difference-in-differences (DID) approach, to examine the association between long-term exposure to ambient temperature and mortality risk in China, and to analyze the effect modification of population characteristics and socioeconomic status. Data on mortality were collected from 364 communities across China during 2006–2017, and environmental data were obtained for the same period. We estimated a 2.93 % (95 % CI: 2.68 %, 3.18 %) increase in mortality risk per 1 °C decreases in annual temperature, the greater effects were observed on respiratory diseases (5.16 %, 95 % CI: 4.53 %, 5.79 %) than cardiovascular diseases (3.43 %, 95 % CI: 3.06 %, 3.80 %), and on younger people (4.21 %, 95 % CI: 3.73 %, 4.68 %) than the elderly (2.36 %, 95 % CI: 2.06 %, 2.65 %). In seasonal analysis, per 1 °C decreases in average temperature was associated with 1.55 % (95 % CI: 1.23 %, 1.87 %), −0.53 % (95 % CI: −0.89 %, −0.16 %), 2.88 % (95 % CI: 2.45 %, 3.31 %) and 4.21 % (95 % CI: 3.98 %, 4.43 %) mortality change in spring, summer, autumn and winter, respectively. The effects of long-term temperature on total mortality were more pronounced among the communities with low urbanization, low education attainment, and low GDP per capita. In total, the decrease of average temperature in summer decreased mortality risk, while increased mortality risk in other seasons, and the associations were modified by demographic characteristics and socioeconomic status. Our findings suggest that populations with disadvantaged characteristics and socioeconomic status are vulnerable to long-term exposure of temperature, and targeted policies should be formulated to strengthen the response to the health threats of temperature exposure. [Display omitted] • Long-term effect of temperature on health was assessed by a quasi-experiment study. • The decreased summer temperature was associated with decreased mortality risks. • The average winter temperature is negatively correlated with mortality risks. • People with respiratory diseases and the young are more susceptible to temperature. • The temperature risk are more prominent in areas with low socioeconomic status. [ABSTRACT FROM AUTHOR]

Abstract: Many previous studies have suggested a link between alcohol outlets and assaultive violence rates. In 1997 the City of New Orleans adopted a series of policies, e.g., increased license fee, additional enforcement staff, and expanded powers for the alcohol license board. The policies were specifically enacted to address the proliferation of problem alcohol outlets believed to be the source of a variety of social problems including assaultive violence. In this research, we evaluate the impact of a city level policy in New Orleans to address the problem alcohol outlets and their influence on assaultive violence. The spatial association between rates of assaultive violence at the census tract level (n=170) over a ten year period raises a challenge in statistical analysis. To meet this challenge we developed a hierarchical change-point model that controls for important covariates of assaultive violence and accounts for unexplained spatial and temporal variability. While our model is somewhat complex, its hierarchical Bayesian analysis is accessible via the WinBUGS software program. Keeping other effects fixed, the implementation of the new city level policy was associated with a decrease in the positive association between census tract level rates of assaultive violence and alcohol outlet density. Comparing several candidate change-point models using the DIC criterion, the positive association began decreasing the year of the policy implementation. The magnitude of the association continued to decrease for roughly two years and then stabilized. We also created maps of the fitted assaultive violence rates in New Orleans, as well as spatial residual maps which, together with Moran’s I’s, suggest that the spatial variation of the data is well accounted for by our model. We reach the conclusion that the implementation of the policy is associated with a significant decrease in the positive relationship between assaultive violence and the off-sale alcohol outlet density. [Copyright &y& Elsevier]

Abstract: Objective: To describe the epidemiological characteristics of nonfatal child pedestrian injuries and provide information to help understand an important public-health problem. Methods: This was a school-based, cross-sectional questionnaire survey. The sample (42 750 children) was obtained from two urban cities of Guangdong Province, China, using multi-stage randomized sampling. Information was collected by the respondents self-reporting in the classroom. Results: The incidence rate of nonfatal child pedestrian injuries in the cities was 2.0%. Boys had a higher incidence rate (2.6%) than girls (1.4%). Compared to other children, those aged 10 years are at the highest risk. The primary places of occurrence were sidewalks, residential roads, and crosswalks. High-risk behavior of the children immediately prior to injury included mid-block crossings, playing on roads, and crossing on red lights. The major vehicles that caused pedestrian injuries were bicycles, car or vans, and motorcycles. Bruises, fractures, and injuries to the internal organs were the top three types of injuries. Almost 40% of victims were hospitalized, and nearly 30% of the victims suffered long-term disabilities. Conclusion: This study shows that nonfatal child pedestrian injuries are a very serious public-health problem in the urban cities of Guangdong. Based on the epidemiological characteristics, prevention strategies and further research should be carried out to reduce the occurrence of injuries. [Copyright &y& Elsevier]

Abstract: The creep behavior of bagasse-based composites with virgin and recycled polyvinyl chloride (B/PVC) and high density polyethylene (B/HDPE) as well as a commercial wood and HDPE composite decking material was investigated. The instantaneous deformation and creep rate of all composites at the same loading level increased at higher temperatures. At a constant load level, B/PVC composites had better creep resistance than B/HDPE systems at low temperatures. However, B/PVC composites showed greater temperature-dependence. Several creep models (i.e., Burgers model, Findley’s power law model, and a simpler two-parameter power law model) were used to fit the measured creep data. Time–temperature superposition (TTS) was attempted for long-term creep prediction. The four-element Burgers model and the two-parameter power law model fitted creep curves of the composites well. The TTS principle more accurately predicted the creep response of the PVC composites compared to the HDPE composites. [Copyright &y& Elsevier]

The working models of LCoS (Liquid Crystal on Silicon) were optimized in parameter space by simulation. Two modes were selected, which were suitable for phase modulation. One was the RTN-52° mode, the other was parallel alignment ECB mode. Phase changes were measured when various voltages are applied to LCoS. In addition, we showed some results when the LCoS was used as a Fresnel lens. [Copyright &y& Elsevier]

Insecticidal proteins from the bacterium Bacillus thuringiensis (Bt) can provide safe and effective control of some major pests, but evolution of resistance by pests diminishes these benefits. Better understanding of the genetics and mechanisms of resistance is urgently needed to improve methods for monitoring, managing, and countering pest resistance to Bt toxins. Here we used CRISPR-mediated knockouts to evaluate the role of five genes encoding candidate Bt toxin receptors in Spodoptera exigua (beet armyworm), a devastating pest of vegetable, field and flower crops. We compared susceptibility to Bt toxins Cry1Ac, Cry1Fa, and Cry1Ca between the parent susceptible strain and each of five strains homozygous for the knockout of one of the candidate genes (SeAPN1, SeCad1, SeABCC1, SeABCC2 or SeABCC3). The results from the 15 pairwise comparisons reveal that SeABCC2 has a major role and SeCad1 a minor role in mediating toxicity of Cry1Ac and Cry1Fa. SeABCC2 also has a minor role in toxicity of Cry1Ca. In addition, the results imply little or no role for the other three candidate receptors in toxicity of Cry1Ac or Cry1Fa; or for the four candidate receptors other than SeABCC2 in toxicity of Cry1Ca. Image 1 • CRISPR-mediated knockouts used to evaluate the role of five genes encoding candidate Bt receptors in Spodoptera exigua. • SeABCC2 has a major role and SeCad1 a minor role in mediating toxicity of Cry1Ac and Cry1Fa. • SeABCC2 also has a minor role in toxicity of Cry1Ca. [ABSTRACT FROM AUTHOR]

The small naphthoquinone molecules modified reduced-graphene oxide with chemical absorption of polysulfides based on the abundant keto functional groups, leads to the significantly improved cycling performance for Li-S batteries. • Organic NQ molecule-decorated rGO was applied as host for Li-S batteries. • Chemical absorption of polysulfides/sulfur can be achieved. • The S/NQ-rGO electrode delivers outstanding electrochemical performance. Graphene-based materials are explored to be promising candidates for lithium-sulfur batteries based on their unique two-dimensional geometry structure and excellent electric conductivity. However, the inferior ability to confine polysulfides results in quick capacity fading and poor cycling stability of graphene-related electrode materials. Herein, small organic naphthoquinone (NQ) molecules with redox active properties are introduced to the reduced graphene oxide (rGO) as an advanced sulfur host to significantly prolong cycle life for Li-S batteries. The effective combination between small NQ organic molecules and rGO successfully leads to the conductive composite network, where the keto groups from NQ play the key role in promoting the chemical absorption of polysulfides/sulfur by forming the S O interaction. Notably, the NQ-rGO composite shows superior lithium polysulfides absorptivity with a sulfur loading of 65.3%. The S/NQ-rGO displays outstanding electrochemical performances for lithium-sulfur batteries, in terms of large reversible capacities with excellent cycling stability (936 mAh g−1 after 200 cycles at 0.1C and 670 mAh g−1 after 500 cycles at 1C) and superior rate ability (525 mAh g−1 at 5C). [ABSTRACT FROM AUTHOR]

Background & Aims We aimed to identify long noncoding RNAs (lncRNAs) that are up-regulated in gastric cancer tissues from patients and study their function in gastric tumor metastasis. Methods We collected gastric tumor and nontumor tissues from patients in China and analyzed levels of lncRNAs by microarray analysis, proteins by immunohistochemistry, and RNAs by quantitative reverse-transcription polymerase chain reaction; we compared these with survival times of patients and tumor progression. RNA levels were knocked down or knocked out in BGC-823, SGC-7901, and MKN45 cell lines using small interfering or short hairpin RNAs or clustered regularly interspaced short palindromic repeats (ie, CRISPR)/CRISPR associated protein 9 (ie, Cas9) vectors. Genes were overexpressed from transfected plasmids in HGC-27 cells. Cells were analyzed by Northern blot and immunoblot, polysome profiling assay, and cell invasion assay. Cells were injected into the tail veins or spleens of nude mice or SCID mice; lung and liver tissues were collected, and metastases were counted. lncRNAs were cloned by using rapid amplification of complementary DNA ends. Their interactions with other genes were determined by RNA pulldown and mapping assays. Results In microarray analyses, we identified 151 lncRNAs expressed at significantly higher levels in gastric tumor vs nontumor tissues. Levels of an lncRNA that we called gastric cancer metastasis associated long noncoding RNA (GMAN) were increased in gastric tumor tissues, compared with nontumor tissues; its up-regulation was associated with tumor metastasis and shorter survival times of patients. The GMAN gene overlaps with the ephrin A1 gene (EFNA1) and was highly expressed in BGC-823 and MKN45 cells. Knockdown of GMAN in these cells did not affect proliferation, colony formation, or adhesion but did reduce their invasive activity in Transwell assays. Ectopic expression of GMAN increased the invasive activity of HGC-27 cells. BGC-823 and MKN45 cells with knockdown of GMAN formed fewer metastases after injection into tail veins of nude mice. Knockdown or knockout of GMAN also reduced levels of ephrin A1 protein in cells. We found that GMAN promoted translation of ephrin A1 messenger RNA into protein by binding to the antisense GMAN RNA (GMAN-AS)—this antisense sequence is also complementary to that of ephrin A1 mRNA. Levels of ephrin A1 protein were also increased in gastric tumors from patients with metastases than in those without metastases. Knockout of ephrin A1 in BGC-823 cells reduced their invasive activity in Transwell assays and ability to form metastases after injection into SCID mice. Ectopic expression of ephrin A1 in BGC-823 cells with knockdown or knockout of GMAN restored their invasive activities and ability form metastases in nude or SCID mice. A CRISPR/Cas9-based strategy to disrupt the GMAN gene significantly reduced the numbers of metastases formed from SGC-7901 cells in mice. Conclusions We identified an lncRNA, which we call GMAN , that is increased in gastric tumors from patients and associated with survival and formation of metastases. It regulates translation of ephrin A1 mRNA by binding competitively to GMAN-AS. Knockdown or knockout of GMAN or ephrin A1 in gastric cancer cell lines reduces their invasive activity and ability to form metastases after injection into mice. These genes might be targeted to prevent or reduce gastric cancer metastasis. [ABSTRACT FROM AUTHOR]

Abstract The World Health Organization sets up the Ambient Air Quality Guidelines mainly based on short-term and long-term health effects of air pollution. Previous studies, however, have generally revealed a non-threshold concentration-response relationship between air pollution and health, making it difficult to determine a concentration, below which no obvious health effects can be observed. Here we proposed a novel approach based on the concept of "number needed to treat", specifically, we calculated the reduction in air pollution concentrations needed to avoid one death corresponding to different hypothetical concentration standards; the one with the smallest value would be the most practical concentration standard. As an example, we applied this approach to the daily standard of ambient PM 2.5 (particulate matter with aerodynamic diameter ≤2.5 μm) in four Chinese cities. The calculation was based on the association between daily mortality and ambient PM 2.5 , which was examined by a generalized additive model with adjustment of important covariates. Significant associations were observed between PM 2.5 and mortality. Our analyses suggested that it is appropriate to have 50 μg/m3 as the daily standard of ambient PM 2.5 for the study area, compared to the current standard of which were directly adopted from the national standard of 75 μg/m3. This novel approach should be considered when planning and/or revising the ambient air quality guidelines/standards. Highlights • There is limited method for air pollution standard formulation. • The "number needed to treat" was proposed as one potential method. • We examined the acute association between PM 2.5 and mortality in four Chinese cities. • We then calculated the reduction in air pollution concentrations needed to avoid one death. • Finally, we suggested that 50 μg/m3 should be considered as daily standard of ambient PM 2.5 in the study area. Capsule This study proposes a new "number needed to treat" approach to help establish or revise daily ambient air quality standards. [ABSTRACT FROM AUTHOR]

Diamide insecticides selectively activate insect ryanodine receptors (RyRs), inducing uncontrolled release of calcium ions, and causing muscle contraction, paralysis and eventually death. The RyR G4946E substitution associated with diamide resistance has been identified in three lepidopteran pests, Plutella xylostella , Tuta absoluta and Chilo suppressalis . Recently, the T. absoluta RyR G4946V mutation was knocked into the model insect Drosophila melanogaster by CRISPR/Cas9 mediated genome editing and provided in vivo functional confirmation for its role in diamide resistance. In the present study, we successfully introduced the RyR G4946E mutation with CRISPR/Cas9 technology into a lepidopteran pest of global importance, Spodoptera exigua . The genome-edited strain (named 4946E) homozygous for the SeRyR G4946E mutation exhibited 223-, 336- and >1000-fold resistance to chlorantraniliprole, cyantraniliprole and flubendiamide, respectively when compared to the wild type strain (WHS) of S. exigua . Reciprocal crossing experiments revealed that the target-site resistance in strain 4946E underlies an autosomal and almost recessive mode of inheritance for anthranilic diamides, whereas it was completely recessive for flubendiamide. Our results not only provided in vivo functional validation of the RyR G4946E mutation in conferring high levels of resistance to diamide insecticides for the first time in a controlled genetic background of a lepidopteran pest, but also revealed slight differences on the level of resistance between anthranilic diamides (chlorantraniliprole and cyantraniliprole) and flubendiamide conferred by the SeRyR G4946E mutation. [ABSTRACT FROM AUTHOR]

Highlights: [•] MiR-215 is frequently up-regulated in gastric cancer and may serve as a biomarker for diagnosis. [•] Inhibition of miR-215 suppresses gastric cancer cell proliferation via G1 arrest. [•] MiR-215 targets RB1 through its 3′-UTR in gastric cancer cells. [•] RB1 is involved in the role of miR-215 in modulating gastric cancer cell proliferation. [Copyright &y& Elsevier]

Abstract: Currently flower color in Hosta is limited to purple and white with some variation across species and cultivars in patterning of the two colors. This study was undertaken to determine the contributions of anthocyanins to current Hosta flower colors and to investigate the potential for increasing color diversity. Eighty-six hostas (6 species and 80 cultivars) were used in this study to investigate the composition and content of anthocyanins by high-performance liquid chromatography coupled with diode array detection (HPLC-DAD) and high-performance liquid chromatographic with electro spray ionization and mass spectrometry (HPLC–ESI–MS). The results showed that the color variation was low in the tepals of the genus of Hosta. Nine anthocyanins were initially identified using a typical purple cultivar (H. ‘Nakaimo’) and a white species (Hosta montana) The anthocyanins were delphinidin 3,5-O-diglucoside (Dp3G5G), cyanidin 3,5-O-diglucoside(Cy3G5G), petunidin 3,5-O-diglucoside (Pt3G5G), peonidin 3-O-rutinoside-5-O-glucoside (Pn3Ru5G), malvidin 3-O-rutinoside-5-O-glucoside (Mv3Ru5G), malvidin 3,5-O-diglucoside (Mv3G5G), petunidin 3-O-rutinoside (Pt3Ru), peonidin 3-O-rutinoside (Pn3Ru) and malvidin 3-O-rutinoside (Mv3Ru). Anthocyanin types and content were different between the purple flowered hostas (PFH) and the white flowered hostas (WFH, including white flower with purple spots or streaks): PFH had higher levels of anthocyanins and were correlated with the pigments Mv3Ru5G, Mv3G5G, Pt3G5G and Dp3G5G; WFH had lower levels of anthocyanins and were correlated with the pigments Pt3Ru, Pn3Ru, Mv3Ru and Pn3Ru5G. The dominance of Mv3G5G and Mv3Ru5G was responsible for flowers of simplex purple. Path analysis showed that Mv3G5G had the highest direct effect on lightness (L*), and color balance (a* and b*), while Pt3G5G had the highest direct effect on saturation (C*). [Copyright &y& Elsevier]

Abstract: Concise synthesis of a 6-deoxy-α-l-talose tetrasaccharide, 6-deoxy-α-l-Talp-(1→3)-6-deoxy-α-l-Talp-(1→2)-6-deoxy-α-l-Talp-(1→3)-6-deoxy-α-l-Talp, the dimer of the disaccharide repeating unit of the OPS from Aggregatibacter actinomycetemcomitans serotype c, has been accomplished through suitable protecting group manipulations and stereoselective glycosylation starting from commercially available l-rhamnose. The target oligosaccharide in the form of its p-methoxyphenyl glycoside is suitable for further glycoconjugate formation via selective cleavage of this group. [Copyright &y& Elsevier]

Three bacterial strains capable of transforming pyrazosulfuron-ethyl, designated as D61, D66, and D713, were isolated from pyrazosulfuron-ethyl contaminated soils. According to the sequence analysis of the partial 16S rRNA gene, it is found that the strains D61 and D66 belong to Pseudomonas sp., and the strain D713 belongs to Bacillus sp. The effects of pyrazosulfuron-ethyl concentration, pH and temperature on biodegradation were examined. At a concentration of 10.0mgL−1, pyrazosulfuron-ethyl was completely degraded by Pseudomonas sp. D61 after 2d and by Pseudomonas sp. D66 after 5d. At a concentration of 90.0mgL−1, pyrazosulfuron-ethyl can be completely degraded by Pseudomonas sp. D66 and D61 after 12d. More than 85.9% degradation rate was observed with Bacillus sp. D713 after 12d. The growth of these three strains was inhibited at low pH buffers. The abiotic degradation occurs much faster at low pH than at neutral and basic pH conditions. The degradation rate of pyrazosulfuron-ethyl at 28°C was faster than those at 20°C and 37°C by these strains, except the highest degradation rate of Bacillus sp. D713 was obtained at 37°C. The pyrazosulfuron-ethyl biodegradation products were identified by liquid chromatography–mass spectroscopy with positive/negative modes and tandem MS–MS techniques. The main degradation product was detected and identified as 5-(N-(4,6-dimethoxypyrimidin-2-ylcarbamoyl)sulfamoyl)-1-methyl-1H-pyrazole-4-carboxylic acid based on mass spectral data and fragmentation patterns. [Copyright &y& Elsevier]

The hypothesis for this research is that only in some brain areas, regional cerebral blood flow (rCBF) after tobacco smoking is correlated with arterial plasma nicotine concentrations. Twenty-one healthy adult tobacco smokers of both genders were studied after overnight tobacco abstinence. H215O water was used to measure rCBF. Six separate scans were taken about 12 min apart with the subjects'' eyes closed and relaxed. Research tobacco cigarettes smoked were of average (1.0 mg) and low (0.08 mg) nicotine but similar tar yield (9.5 and 9.1 mg). Increases in normalized rCBF were obtained in the occipital cortex, cerebellum, and thalamus, and decreases in the anterior cingulate, nucleus accumbens, amygdala, and hippocampus immediately after smoking the first average nicotine yield cigarette of the morning. After smoking the second average nicotine yield cigarette, the effects were less than smoking the first. Low-nicotine cigarettes produced fewer changes in rCBF than those after the first average cigarette. As expected, statistically significant correlations were found between increases in arterial plasma nicotine and HR. Correlations with arterial nicotine on rCBF were statistically significant in brain areas with the greatest changes in relative blood flow such as the cerebellum and occipital cortex. Nicotine delivery by tobacco smoking is only one of the factors, which contribute to changes in rCBF. [Copyright &y& Elsevier]

Although the effect of ambient temperature on cardiovascular disease (CVDs) has been well explored, studies using years of life lost (YLLs) as the outcome especially evaluating the average life loss per death attributable to temperatures were rare. We examine the associations between ambient temperature and YLLs of CVDs, and further quantify temperature-related life loss per death. Daily YLL rates were calculated using death data from 364 locations across China during 2006–2017, and meteorological data were collected for the same period. A distributed-lag nonlinear model and meta-regression were applied to examine the relationships between temperature and YLL rates of CVDs. Subgroup analyses by age, gender, region, and cause-specific CVDs were investigated. The total YLLs and average YLLs per death attributable to temperature were further quantified to assess life loss caused by non-optimal temperature. Both high and low temperatures significantly increased YLL rates of CVDs, with greater effects for cold than heat. Cerebrovascular diseases (CEDs) account for the largest proportion (47.17%) of total YLLs of CVDs attributable to non-optimal temperature. On average, life loss per CVD death attributable to non-optimal temperatures was 1.51 (95% eCI: 1.33, 1.69) years, with 1.07 (95% eCI: 1.00, 1.15) years from moderate cold. Average life losses per death were observed higher for males (1.71, 95% eCI: 1.43, 1.99), younger population (3.82, 95% eCI: 2.86, 4.75), central China (1.62; 95% eCI: 1.41, 1.83) and hemorrhagic stroke (2.86, 95% eCI: 2.63, 3.10) than their correspondents. We found that non-optimal temperature significantly aggravated premature death of CVD, with CEDs being the most affected, and most of temperature-related life loss of CVD was attributed to moderate cold. Our findings imply that peoples with CEDs in moderate cold days are vulnerable populations, which may contribute to a better understanding the adverse effects and pathogenesis of temperature on CVDs. Unlabelled Image • This study examines the health effects of non-optimal temperature, and quantify temperature-related life loss per death. • Life loss per CVD death attributable to non-optimal temperatures was 1.51. • Most of temperature-related life loss of CVD was attributed to moderate cold. [ABSTRACT FROM AUTHOR]