Can China's carbon generalized system of preferences reduce urban residents' carbon emissions? Evidence from a quasi-natural experiment.

The carbon generalized system of preferences (CGSP) is an innovative incentive mechanism implemented by the Chinese government, which has also become an important part of carbon emission reduction at the living end, and it is of great significance to study whether the Pilot Policy can reduce the carbon emissions of residents. This study firstly accounts for the total carbon emissions and per capita carbon emissions of the residents of 284 cities in China, and on this basis, adopts the SCM method to quantitatively study and analyze the overall and local implementation effects of CGSP in China by taking the first batch of CGSP pilots in China as an example, and further applies the mediation effect model to test the pathways of the role of CGSP. The main findings of the study are as follows: (1) During the period of 2010-2020, the total carbon emissions from urban residents' living in China showed a yearly growth trend, from 36,623.98 ×10-2Mt in 2010-85,241.20 ×10-2Mt in 2020, an increase of 8.83%. Total carbon emissions present a structural difference of "electricity consumption > central heating > private transport > gas (oil, natural gas) consumption". (2) Overall, the implementation of the CGSP had a robust positive impact on the overall carbon emission reduction in the pilot cities, with an average annual emission reduction effect value of 36.53 ×10-2Mt. Locally, the annual net policy effect values of Dongguan, Zhongshan, Heyuan, and Guangzhou are 6169.79 ×10-2, 26,600.17 ×10-2, 17,081.34 ×10-2 and 9393.36 ×10-2Mt respectively. (3) CGSP has a good carbon emission reduction effect by suppressing the impact on residents' carbon emissions through enhancing the city's innovation capacity and promoting electricity saving and consumption reduction, while the mediating effect played by the promotion of green and low-carbon travel in the pilot policy is not significant. Finally, based on the research findings, relevant suggestions are targeted.

High Catalytic Activity of C60 Pdn Encapsulated in Metal-Organic Framework UiO-67, for Tandem Hydrogenation Reaction.

Metal nanoparticles (NPs) stabilized by MOFs are very promising for catalysis, whereas introduction of C60 into MOFs has been very rarely used, and there was no report for their cooperative catalysis in organic syntheses. In this work, C60 @UiO-67 was synthesized by a one-pot method, so that C60 is uniformly distributed on UiO-67 in molecular form. Pd NPs coordinating with C60 have been successfully embedded into the framework. The obtained multifunctional C60 Pdn @UiO-67 catalyst exhibits remarkable synergistic catalytic activity in cascade reactions under mild conditions, where UiO-67 affords Lewis acidity and C60 Pdn offers higher hydrogenation activity relative to solely Pd NPs.

Single-cell RNA sequencing reveals immune cell dysfunction in the peripheral blood of patients with highly aggressive gastric cancer.

Highly aggressive gastric cancer (HAGC) is a gastric cancer characterized by bone marrow metastasis and disseminated intravascular coagulation (DIC). Information about the disease is limited. Here we employed single-cell RNA sequencing to investigate peripheral blood mononuclear cells (PBMCs), aiming to unravel the immune response of patients toward HAGC. PBMCs from seven HAGC patients, six normal advanced gastric cancer (NAGC) patients, and five healthy individuals were analysed by single-cell RNA sequencing. The expression of genes of interest was validated by bulk RNA-sequencing and ELISA. We found a massive expansion of neutrophils in PBMCs of HAGC. These neutrophils are activated, but immature. Besides, mononuclear phagocytes exhibited an M2-like signature and T cells were suppressed and reduced in number. Analysis of cell-cell crosstalk revealed that several signalling pathways involved in neutrophil to T-cell suppression including APP-CD74, MIF-(CD74+CXCR2), and MIF-(CD74+CD44) pathways were increased in HAGC. NETosis-associated genes S100A8 and S100A9 as well as VEGF, PDGF, FGF, and NOTCH signalling that contribute to DIC development were upregulated in HAGC too. This study reveals significant changes in the distribution and interactions of the PBMC subsets and provides valuable insight into the immune response in patients with HAGC. S100A8 and S100A9 are highly expressed in HAGC neutrophils, suggesting their potential to be used as novel diagnostic and therapeutic targets for HAGC.

Single-cell analysis reveals transcriptomic and epigenomic impacts on the maternal-fetal interface following SARS-CoV-2 infection.

During pregnancy the maternal-fetal interface plays vital roles in fetal development. Its disruption is frequently found in pregnancy complications. Recent studies show increased incidences of adverse pregnancy outcomes in patients with COVID-19; however, the mechanism remains unclear. Here we analysed the molecular impacts of SARS-CoV-2 infection on the maternal-fetal interface. Generating bulk and single-nucleus transcriptomic and epigenomic profiles from patients with COVID-19 and control samples, we discovered aberrant immune activation and angiogenesis patterns in distinct cells from patients. Surprisingly, retrotransposons were also dysregulated in specific cell types. Notably, reduced enhancer activities of LTR8B elements were functionally linked to the downregulation of pregnancy-specific glycoprotein genes in syncytiotrophoblasts. Our findings revealed that SARS-CoV-2 infection induced substantial changes to the epigenome and transcriptome at the maternal-fetal interface, which may be associated with pregnancy complications.

Transposable Elements in Pluripotent Stem Cells and Human Disease.

Transposable elements (TEs) are mobile genetic elements that can randomly integrate into other genomic sites. They have successfully replicated and now occupy around 40% of the total DNA sequence in humans. TEs in the genome have a complex relationship with the host cell, being both potentially deleterious and advantageous at the same time. Only a tiny minority of TEs are still capable of transposition, yet their fossilized sequence fragments are thought to be involved in various molecular processes, such as gene transcriptional activity, RNA stability and subcellular localization, and chromosomal architecture. TEs have also been implicated in biological processes, although it is often hard to reveal cause from correlation due to formidable technical issues in analyzing TEs. In this review, we compare and contrast two views of TE activity: one in the pluripotent state, where TEs are broadly beneficial, or at least mechanistically useful, and a second state in human disease, where TEs are uniformly considered harmful.

Mouse strain-specific polymorphic provirus functions as cis-regulatory element leading to epigenomic and transcriptomic variations.

Polymorphic integrations of endogenous retroviruses (ERVs) have been previously detected in mouse and human genomes. While most are inert, a subset can influence the activity of the host genes. However, the molecular mechanism underlying how such elements affect the epigenome and transcriptome and their roles in driving intra-specific variation remain unclear. Here, by utilizing wildtype murine embryonic stem cells (mESCs) derived from distinct genetic backgrounds, we discover a polymorphic MMERGLN (GLN) element capable of regulating H3K27ac enrichment and transcription of neighboring loci. We demonstrate that this polymorphic element can enhance the neighboring Klhdc4 gene expression in cis, which alters the activity of downstream stress response genes. These results suggest that the polymorphic ERV-derived cis-regulatory element contributes to differential phenotypes from stimuli between mouse strains. Moreover, we identify thousands of potential polymorphic ERVs in mESCs, a subset of which show an association between proviral activity and nearby chromatin states and transcription. Overall, our findings elucidate the mechanism of how polymorphic ERVs can shape the epigenome and transcriptional networks that give rise to phenotypic divergence between individuals.

Replication timing maintains the global epigenetic state in human cells.

The temporal order of DNA replication [replication timing (RT)] is correlated with chromatin modifications and three-dimensional genome architecture; however, causal links have not been established, largely because of an inability to manipulate the global RT program. We show that loss of RIF1 causes near-complete elimination of the RT program by increasing heterogeneity between individual cells. RT changes are coupled with widespread alterations in chromatin modifications and genome compartmentalization. Conditional depletion of RIF1 causes replication-dependent disruption of histone modifications and alterations in genome architecture. These effects were magnified with successive cycles of altered RT. These results support models in which the timing of chromatin replication and thus assembly plays a key role in maintaining the global epigenetic state.

Enzyme-free strip biosensor for amplified detection of Pb2+ based on a catalytic DNA circuit.

A simple and enzyme-free strip biosensor for the amplified detection of Pb(2+) has been constructed based on a catalytic DNA circuit. This assay is ultrasensitive, enabling the visual detection of Pb(2+) concentrations as low as 10 pM without instrumentation.

A lateral flow biosensor for detection of single nucleotide polymorphism by circular strand displacement reaction.

A lateral flow biosensor for detection of single nucleotide polymorphism based on circular strand displacement reaction (CSDPR) has been developed. Taking advantage of high fidelity of T4 DNA ligase, signal amplification by CSDPR, and the optical properties of gold nanoparticles, this assay has reached a detection limit of 0.01 fM.