UB2/UB3/TSH4-anchored transcriptional networks regulate early maize inflorescence development in response to simulated shade.

Increasing planting density has been adopted as an effective means to increase maize (Zea mays) yield. Competition for light from neighbors can trigger plant shade avoidance syndrome, which includes accelerated flowering. However, the regulatory networks of maize inflorescence development in response to high-density planting remain poorly understood. In this study, we showed that shade-mimicking treatments cause precocious development of the tassels and ears. Comparative transcriptome profiling analyses revealed the enrichment of phytohormone-related genes and transcriptional regulators among the genes co-regulated by developmental progression and simulated shade. Network analysis showed that three homologous Squamosa promoter binding protein (SBP)-like (SPL) transcription factors, Unbranched2 (UB2), Unbranched3 (UB3), and Tasselsheath4 (TSH4), individually exhibited connectivity to over 2,400 genes across the V3-to-V9 stages of tassel development. In addition, we showed that the ub2 ub3 double mutant and tsh4 single mutant were almost insensitive to simulated shade treatments. Moreover, we demonstrated that UB2/UB3/TSH4 could directly regulate the expression of Barren inflorescence2 (BIF2) and Zea mays teosinte branched1/cycloidea/proliferating cell factor30 (ZmTCP30). Furthermore, we functionally verified a role of ZmTCP30 in regulating tassel branching and ear development. Our results reveal a UB2/UB3/TSH4-anchored transcriptional regulatory network of maize inflorescence development and provide valuable targets for breeding shade-tolerant maize cultivars.

The evening complex promotes maize flowering and adaptation to temperate regions.

Maize (Zea mays) originated in southern Mexico and has spread over a wide latitudinal range. Maize expansion from tropical to temperate regions has necessitated a reduction of its photoperiod sensitivity. In this study, we cloned a quantitative trait locus (QTL) regulating flowering time in maize and show that the maize ortholog of Arabidopsis thaliana EARLY FLOWERING3, ZmELF3.1, is the causal locus. We demonstrate that ZmELF3.1 and ZmELF3.2 proteins can physically interact with ZmELF4.1/4.2 and ZmLUX1/2, to form evening complex(es; ECs) in the maize circadian clock. Loss-of-function mutants for ZmELF3.1/3.2 and ZmLUX1/2 exhibited delayed flowering under long-day and short-day conditions. We show that EC directly represses the expression of several flowering suppressor genes, such as the CONSTANS, CONSTANS-LIKE, TOC1 (CCT) genes ZmCCT9 and ZmCCT10, ZmCONSTANS-LIKE 3, and the PSEUDORESPONSE REGULATOR (PRR) genes ZmPRR37a and ZmPRR73, thus alleviating their inhibition, allowing florigen gene expression and promoting flowering. Further, we identify two closely linked retrotransposons located in the ZmELF3.1 promoter that regulate the expression levels of ZmELF3.1 and may have been positively selected during postdomestication spread of maize from tropical to temperate regions during the pre-Columbian era. These findings provide insights into circadian clock-mediated regulation of photoperiodic flowering in maize and new targets of genetic improvement for breeding.

Gene expression and expression quantitative trait loci analyses uncover natural variations underlying the improvement of important agronomic traits during modern maize breeding.

Maize (Zea mays L.) is a major staple crop worldwide, and during modern maize breeding, cultivars with increased tolerance to high-density planting and higher yield per plant have contributed significantly to the increased yield per unit land area. Systematically identifying key agronomic traits and their associated genomic changes during modern maize breeding remains a significant challenge because of the complexity of genetic regulation and the interactions of the various agronomic traits, with most of them being controlled by numerous small-effect quantitative trait loci (QTLs). Here, we performed phenotypic and gene expression analyses for a set of 137 elite inbred lines of maize from different breeding eras in China. We found four yield-related traits are significantly improved during modern maize breeding. Through gene-clustering analyses, we identified four groups of expressed genes with distinct trends of expression pattern change across the historical breeding eras. In combination with weighted gene co-expression network analysis, we identified several candidate genes regulating various plant architecture- and yield-related agronomic traits, such as ZmARF16, ZmARF34, ZmTCP40, ZmPIN7, ZmPYL10, ZmJMJ10, ZmARF1, ZmSWEET15b, ZmGLN6 and Zm00001d019150. Further, by combining expression quantitative trait loci (eQTLs) analyses, correlation coefficient analyses and population genetics, we identified a set of candidate genes that might have been under selection and contributed to the genetic improvement of various agronomic traits during modern maize breeding, including a number of known key regulators of plant architecture, flowering time and yield-related traits, such as ZmPIF3.3, ZAG1, ZFL2 and ZmBES1. Lastly, we validated the functional variations in GL15, ZmPHYB2 and ZmPYL10 that influence kernel row number, flowering time, plant height and ear height, respectively. Our results demonstrates the effectiveness of our combined approaches for uncovering key candidate regulatory genes and functional variation underlying the improvement of important agronomic traits during modern maize breeding, and provide a valuable genetic resource for the molecular breeding of maize cultivars with tolerance for high-density planting.

Unraveling Prevalence and Effects of Deleterious Mutations in Maize Elite Lines across Decades of Modern Breeding.

Future breeding is likely to involve the detection and removal of deleterious alleles, which are mutations that negatively affect crop fitness. However, little is known about the prevalence of such mutations and their effects on phenotypic traits in the context of modern crop breeding. To address this, we examined the number and frequency of deleterious mutations in 350 elite maize inbred lines developed over the past few decades in China and the United States. Our findings reveal an accumulation of weakly deleterious mutations and a decrease in strongly deleterious mutations, indicating the dominant effects of genetic drift and purifying selection for the two types of mutations, respectively. We also discovered that slightly deleterious mutations, when at lower frequencies, were more likely to be heterozygous in the developed hybrids. This is consistent with complementation as a potential explanation for heterosis. Subsequently, we found that deleterious mutations accounted for more of the variation in phenotypic traits than nondeleterious mutations with matched minor allele frequencies, especially for traits related to leaf angle and flowering time. Moreover, we detected fewer deleterious mutations in the promoter and gene body regions of differentially expressed genes across breeding eras than in nondifferentially expressed genes. Overall, our results provide a comprehensive assessment of the prevalence and impact of deleterious mutations in modern maize breeding and establish a useful baseline for future maize improvement efforts.

Genome-Wide Identification and Expression Analyses of the FAR1/FHY3 Gene Family Provide Insight into Inflorescence Development in Maize.

As transcription factors derived from transposase, FAR-RED IMPAIRED RESPONSE1 (FAR1) and its homolog FHY3 play crucial roles in the regulation of light signaling and various stress responses by coordinating the expression of downstream target genes. Despite the extensive investigation of the FAR1/FHY3 family in Arabidopsis thaliana and other species, a comprehensive examination of these genes in maize has not been conducted thus far. In this study, we employed a genomic mining approach to identify 16 ZmFAR1 genes in the maize inbred line B73, which were further classified into five subgroups based on their phylogenetic relationships. The present study characterized the predicted polypeptide sequences, molecular weights, isoelectric points, chromosomal distribution, gene structure, conserved motifs, subcellular localizations, phylogenetic relationships, and cis-regulatory elements of all members belonging to the ZmFAR1 family. Furthermore, the tissue-specific expression of the 16 ZmFAR1 genes was analyzed using RNA-seq, and their expression patterns under far-red light conditions were validated in the ear and tassel through qRT-qPCR. The observed highly temporal and spatial expression patterns of these ZmFAR1 genes were likely associated with their specific functional capabilities under different light conditions. Further analysis revealed that six ZmFAR1 genes (ZmFAR1-1, ZmFAR1-10, ZmFAR1-11, ZmFAR1-12, ZmFAR1-14, and ZmFAR1-15) exhibited a response to simulated shading treatment and actively contributed to the development of maize ears. Through the integration of expression quantitative trait loci (eQTL) analyses and population genetics, we identified the presence of potential causal variations in ZmFAR1-14 and ZmFAR1-9, which play a crucial role in regulating the kernel row number and kernel volume weight, respectively. In summary, this study represents the initial identification and characterization of ZmFAR1 family members in maize, uncovering the functional variation in candidate regulatory genes associated with the improvement of significant agronomic traits during modern maize breeding.

High-throughput screening identified pacritinib as a promising therapeutic approach to overcome lenvatinib resistance in hepatocellular carcinoma by targeting IRAK1.

Lenvatinib resistance presents a significant challenge in the clinical management of advanced hepatocellular carcinoma (HCC). To address this issue, we established lenvatinib resistant HCC cells and performed high-throughput screening using FDA-approved anti-cancer drug library. Through quantitative selective drug sensitivity scoring (sDSS), pacritinib, a well-known JAK inhibitor, emerged as the top candidate, displaying the highest sDSS score among 219 compounds. We further demonstrated that pacritinib reduced the viability of a panel of HCC cell lines in a dose-dependent manner, while exhibiting minimal effects on normal liver cells. Interestingly, pacritinib, but not other JAK inhibitors such as ruxolitinib, upadacitinib, or filgotinib, acted synergistically with lenvatinib in HCC cells. In lenvatinib-resistant HCC cells, pacritinib significantly decreased proliferation and induced apoptosis. Rescue studies using IL-1 receptor-associated kinase 1 (IRAK1) overexpression and knockdown revealed that pacritinib's effects are mediated through IRAK1, with minimal impact on normal liver cells. In a xenograft model of lenvatinib-resistant HCC, oral administration of pacritinib significantly reduced tumor size without affecting body weight. Immunohistochemical analysis of tumor sections revealed that pacritinib reduced Ki67 staining and phosphorylated IRAK1. Our findings suggest that pacritinib may be a promising therapeutic option for the treatment of advanced HCC, particularly in patients who have developed resistance to lenvatinib.

ZmELF3.1 integrates the RA2-TSH4 module to repress maize tassel branching.

Tassel branch number (TBN) is a key agronomic trait for adapting to high-density planting and grain yield in maize. However, the molecular regulatory mechanisms underlying tassel branching are still largely unknown. Here, we used molecular and genetic studies together to show that ZmELF3.1 plays a critical role in regulating TBN in maize. Previous studies showed that ZmELF3.1 forms the evening complex through interacting with ZmELF4 and ZmLUX to regulate flowering in maize and that RA2 and TSH4 (ZmSBP2) suppresses and promotes TBN in maize, respectively. In this study, we show that loss-of-function mutants of ZmELF3.1 exhibit a significant increase of TBN. We also show that RA2 directly binds to the promoter of TSH4 and represses its expression, thus leading to reduced TBN. We further demonstrate that ZmELF3.1 directly interacts with both RA2 and ZmELF4.2 to form tri-protein complexes that further enhance the binding of RA2 to the promoter of TSH4, leading to suppressed TSH4 expression and consequently decreased TBN. Our combined results establish a novel functional link between the ELF3-ELF4-RA2 complex and miR156-SPL regulatory module in regulating tassel branching and provide a valuable target for genetic improvement of tassel branching in maize.

Decoding the microbiota metabolome in hepatobiliary and pancreatic cancers: Pathways to precision diagnostics and targeted therapeutics.

We delve into the critical role of the gut microbiota and its metabolites in the pathogenesis and progression of hepatobiliary and pancreatic (HBP) cancers, illuminating an urgent need for breakthroughs in diagnostic and therapeutic strategies. Given the high mortality rates associated with HBP cancers, which are attributed to aggressive recurrence, metastasis, and poor responses to chemotherapy, exploring microbiome research presents a promising frontier. This research highlights how microbial metabolites, including secondary bile acids, short-chain fatty acids, and lipopolysaccharides, crucially influence cancer cell behaviors such as proliferation, apoptosis, and immune evasion, significantly contributing to the oncogenesis and progression of HBP cancers. By integrating the latest findings, we discuss the association of microbial alterations with HBP cancers, key metabolites, and their implications, and how metabolomics and microbiomics can enhance diagnostic precision. Furthermore, the paper explores strategies for targeted therapies through microbiome metabolomics, including the direct therapeutic effects of microbiome metabolites and potential synergistic effects on conventional therapies. We also recognize that the field of microbial metabolites for the diagnosis and treatment of tumors still has a lot of problems to be solved. The aim of this study is to pioneer microbial metabolite research and provide a reference for HBP cancer diagnosis, treatment, and prognosis.

VmsR, a LuxR-Type Regulator, Contributes to Virulence, Cell Motility, Extracellular Polysaccharide Production and Biofilm Formation in Xanthomonas oryzae pv. oryzicola.

LuxR-type regulators play pivotal roles in regulating numerous bacterial processes, including bacterial motility and virulence, thereby exerting a significant influence on bacterial behavior and pathogenicity. Xanthomonas oryzae pv. oryzicola, a rice pathogen, causes bacterial leaf streak. Our research has identified VmsR, which is a response regulator of the two-component system (TCS) that belongs to the LuxR family. These findings of the experiment reveal that VmsR plays a crucial role in regulating pathogenicity, motility, biofilm formation, and the production of extracellular polysaccharides (EPSs) in Xoc GX01. Notably, our study shows that the vmsR mutant exhibits a reduced swimming motility but an enhanced swarming motility. Furthermore, this mutant displays decreased virulence while significantly increasing EPS production and biofilm formation. We have uncovered that VmsR directly interacts with the promoter regions of fliC and fliS, promoting their expression. In contrast, VmsR specifically binds to the promoter of gumB, resulting in its downregulation. These findings indicate that the knockout of vmsR has profound effects on virulence, motility, biofilm formation, and EPS production in Xoc GX01, providing insights into the intricate regulatory network of Xoc.

Microring structure for flexible polymer waveguide-based optical pressure sensing.

Flexible pressure sensors provide a promising platform for artificial smart skins, and photonic devices provide a new technique to fabricate pressure sensors. Here, we present a flexible waveguide-based optical pressure sensor based on a microring structure. The waveguide-based optical pressure sensor is based on a five-cascade microring array structure with a size of 1500 µm × 500 µm and uses the change in output power to linearly characterize the change in pressure acting on the device. The results show that the device has a sensing range of 0-60 kPa with a sensitivity of 23.14 µW/kPa, as well as the ability to detect pulse signals, swallowing, hand gestures, etc. The waveguide-based pressure sensors offer the advantages of good output linearity, high integration density and easy-to-build arrays.

"Urban Respiration" Revealed by Atmospheric O2 Measurements in an Industrial Metropolis.

Urban regions, which "inhale" O2 from the air and "exhale" CO2 and atmospheric pollutants, including harmful gases and fine particles, are the largest sinks of atmospheric O2, yet long-term O2 measurements in urban regions are currently lacking. In this study, we report continuous measurements of atmospheric O2 in downtown Lanzhou, an industrial metropolis in northwestern China. We found declines in atmospheric O2 associated with deteriorated air quality and robust anticorrelations between O2 and gaseous oxides. By combining O2 and pollutants measurements with a Lagrangian atmospheric transport model, we quantitatively break down "urban respiration" (ΔO2URB) into human respiration (ΔO2RES) and fossil fuel combustion (ΔO2FF). We found increased ΔO2FF contribution (from 66.92% to 72.50%) and decreased ΔO2RES contribution (from 33.08 to 27.50%) as O2 declines and pollutants accumulate. Further attribution of ΔO2FF reveals intracity transport of atmospheric pollutants from industrial sectors and suggests transportation sectors as the major O2 sink in downtown Lanzhou. The varying relationships between O2 and pollutants under different conditions unfold the dynamics of urban respiration and provide insights into the O2 and energy consumption, pollutant emission, and intracity atmospheric transport processes.

Pan-Cancer Analysis Reveals PPRC1 as a Novel Prognostic Biomarker in Ovarian Cancer and Hepatocellular Carcinoma.

Background and Objectives: As is well understood, peroxisome proliferator-activated receptor gamma cofactor-related 1 (PPRC1) plays a central role in the transcriptional control of the mitochondrial biogenesis and oxidative phosphorylation (OXPHOS) process, yet its critical role in pan-cancer remains unclear. Materials and Methods: In this paper, the expression levels of PPRC1 in different tumor tissues and corresponding adjacent normal tissues were analyzed based on four databases: The Genotype-Tissue Expression (GTEx), Cancer Cell Line Encyclopedia (CCLE), The Cancer Genome Atlas (TCGA), and Tumor Immune Estimation Resource (TIMER). Meanwhile, the prognostic value of PPRC1 was inferred using Kaplan-Meier plotter and forest-plot studies. In addition, the correlation between PPRC1 expression and tumor immune cell infiltration, immune checkpoints, and the tumor-stemness index was analyzed using TCGA and TIMER databases. Results: According to our findings, the expression level of PPRC1 was found to be different in different cancer types and there was a positive correlation between PPRC1 expression and prognosis in several tumor types. In addition, PPRC1 expression was found to be significantly correlated with immune cell infiltration, immune checkpoints, and the tumor-stemness index in both ovarian and hepatocellular carcinoma. Conclusions: PPRC1 demonstrated promising potential as a novel biomarker in pan-cancer due to its potential association with immune cell infiltration, expression of immune checkpoints, and the tumor-stemness index.

Icariin Ameliorates Alzheimer's Disease Pathology by Alleviating Myelin Injury in 3 × Tg-AD Mice.

Alzheimer's disease (AD) is a neurodegenerative disease characterized by excessive deposition of ß amyloid (Aß), hyperphosphorylation of tau protein, and neuronal cell death. Recent studies have shown that myelin cell damage, which leads to cognitive dysfunction, occurs before AD-related pathological changes. Here, we examine the effect of icariin (ICA), a prenylated flavonol glycoside, in improving cognitive function in AD model mice. ICA has been reported to exhibit cardiovascular protective functions and antiaging effects. In this study, we used 3 × Tg-AD mice as an AD model. The Morris water maze and Y maze tests were performed to assess the learning and memory of the mice. Immunofluorescence analysis of Aß1-42 deposition and myelin basic protein (MBP) expression in the mouse hippocampus was performed. Tau protein phosphorylation and MBP protein expression in the hippocampus were further analyzed by Western blotting. Myelin damage in the mouse optic nerve was evaluated by electron microscopy, and LFB staining was performed to assess myelin morphology in the mouse corpus callosum. MBP, Mpp5, and Egr2 transcript levels were quantified by qPCR. We observed that ICA treatment improved the learning and memory of 3 × Tg-AD mice and reduced Aß deposition and tau protein phosphorylation in the hippocampus. Moreover, this treatment protocol increased myelin-related gene expression and reduced myelin damage.

Adhesion and proliferation of bone marrow stromal cells on acellular spinal cord scaffolds.

OBJECTIVES: This study aimed to produce an acellular spinal cord scaffold-bone marrow stromal cell (ASCS-BMSC) complex in which the growth of BMSCs transplanted into the spinal cord of rats could be simulated in vitro, facilitating the observation and evaluation of the growth of BMSCs on the ASCS for the first time. METHODS: Freeze-thaw, chemical extraction and mechanical shaking approaches were used to remove the cellular components and prepare a rat ASCS containing only the extracellular matrix (ECM) structure from the rat spinal cord. BMSCs were embedded into ASCSs and freeze-dried agarose scaffolds (FASs), and cell migration and proliferation were observed via fluorescence microscopy and the MTT assay. RESULTS: Compared with the normal rat spinal cord, the ASCS had no cell structure and retained ECM components such as type IV collagen, fibronectin and laminin, showing a three-dimensional network structure with good voids. The growth and proliferation of BMSCs on the ASCS was good, as shown by the MTT assay. Scanning electron microscopy showed that BMSCs covered 65% of the ASCS surface, and the mitochondria of BMSCs were developed and adhered to collagen fibres, as demonstrated by transmission electron microscopy. HE staining showed that BMSCs could grow inside the ASCS, and immunohistochemical staining showed that BMSCs still expressed CD44 and CD90 on the ASCS and had stem cell characteristics. CONCLUSIONS: The results of the experiment indicate that the ASCS has the ability to improve cell adhesion and proliferation. Thus, the ASCS-BMSC combination may be used to treat spinal cord injury.

Chemical Composition, Antitumor Properties, and Mechanism of the Essential Oil from Plagiomnium acutum T. Kop.

Plagiomnium acutum T. Kop. (P. acutum) has been used as a traditional Chinese medicine for thousands of years to treat cancer but lacks evidence. The objective of this work was to reveal the chemical composition of P. acutum essential oil (PEO) and explore its potential antitumor activity and molecular mechanism. PEO was prepared by the simultaneous distillation-extraction method and characterized by gas chromatography/mass spectroscopy. CCK8 assay, flow cytometry, western blot, and immunofluorescence techniques were used to analyze the effects and mechanism of PEO against cancer cells. A total of 74 constituents of PEO were identified, with diterpenes (26.5%), sesquiterpenes (23.89%), and alcohols (21.81%) being the major constituents. Two terpenoids, selina-6-en-4-ol and dolabella-3,7-dien-18-ol, were detected in PEO for the first time. PEO showed significant cell growth inhibitory activity on HepG2 and A549 cells by blocking the G1 phase and inducing apoptosis, which may be attributed to its upregulation of p21Cip1 and p27Kip1 proteins and interference with mitochondrial membrane potential effect. Dolabella-3,7-dien-18-ol accounts for 25.5% of PEO and is one of the main active components of PEO, with IC50 values in HepG2 and A549 cells of (25.820 ± 0.216) µg/mL and (23.597 ± 1.207) µg/mL, respectively. These results confirmed the antitumor medicinal value of P. acutum and showed great application potential in the pharmaceutical industry.

Expression of CAMK1 and its association with clinicopathologic characteristics in pancreatic cancer.

Calcium/calmodulin-dependent protein kinase (CAMKs) can control a wide range of cancer-related functions in multiple tumour types. Herein, we explore the expressions and clinical significances of calcium/calmodulin-dependent protein kinase 1 (CAMK1) in pancreatic cancer (PC). The expression of CAMK1 in PC was analysed by Gene Expression Profiling Interactive Analysis 2 (GEPIA 2) database and the Oncomine database. For further validation, the protein level of CAMK1 in PC tissues was also detected in the Human Protein Atlas (HPA) database and the tissue microarray (TMA)-based immunohistochemistry (IHC). GEPIA 2 and Kaplan-Meier Plotter (KM Plotter) databases were used to explore the prognostic significances of CAMK1 in overall survival (OS) and disease-free survival (DFS) of PC at mRNA level. The relationship between CAMK1 expression and the clinicopathological characteristics of PC was further explored. Additionally, the Search Tool for the Retrieval of Interacting Genes (STRING) database was used to analyse protein-protein interactions (PPI). We found CAMK1 was highly expressed in PC both in bioinformatics analyses and TMA-IHC results. The prognostic analyses from the public databases also showed consistent results with follow-up data. The PPI network suggested that CALM1, CALM3, CREB1, CALM2, SYN1, NOS3, ATF1, GAPDH, PPM1F and FBXL12 were important significant genes associated with CAMK1. Our finding revealed CAMK1 has prognostic value in PC patients, suggesting that CAMK1 may has a distinct role in PC patients and can be used as a candidate marker for investigating clinical prognosis of PC.

MIR210HG regulates glycolysis, cell proliferation, and metastasis of pancreatic cancer cells through miR-125b-5p/HK2/PKM2 axis.

Pancreatic cancer has the worst prognosis of all common cancers. Pancreatic cancer cells have a metabolic advantage due to their swiftly adaptive responses to hypoxic and low-nutrient medium. This advantage contributes to the aggressivity of pancreatic cancer. In this study, lncRNA MIR210HG was abnormally upregulated within pancreatic cancer. It acted as a key oncogenic regulator of pancreatic cancer aggressiveness and glycolysis. Knockdown of MIR210HG significantly inhibited the aggressive phenotype of pancreatic cancer cells and inhibited the growth of xenograft tumours. More importantly, MIR210HG knockdown inhibited pancreatic cancer cell glycolysis via regulating the glycolysis-related hexokinase 2 (HK2) and Pyruvate kinase muscle isozyme M2 (PKM2) expression. Compared with the MIR210HG knockdown group, miR-125b-5p inhibition promoted the aggressive phenotypes and glycolysis of pancreatic cancer cells. Furthermore, the effects of MIR210HG knockdown on HK2 and PKM2 expression, pancreatic cancer cell aggressive phenotypes, and glycolysis were significantly reversed by miR-125b-5p inhibition. In tissue samples, MIR210HG expression was negatively correlated with miR-125b-5p levels and positively correlated with HK2 and PKM2 expression. miR-125b-5p expression was negatively correlated with HK2 and PKM2 expression. In conclusion, MIR210HG affected the phenotypes of pancreatic cancer cells, including proliferation, invasion, migration, and glycolysis, via modulating the miR-125b-5p/HK2/PKM2 axis.

The role of seasonality in the spread of COVID-19 pandemic.

It has been reported that the transmission of COVID-19 can be influenced by the variation of environmental factors due to the seasonal cycle. However, its underlying mechanism in the current and onward transmission pattern remains unclear owing to the limited data and difficulties in separating the impacts of social distancing. Understanding the role of seasonality in the spread of the COVID-19 pandemic is imperative in formulating public health interventions. Here, the seasonal signals of the COVID-19 time series are extracted using the EEMD method, and a modified Susceptible, Exposed, Infectious, Recovered (SEIR) model incorporated with seasonal factors is introduced to quantify its impact on the current COVID-19 pandemic. Seasonal signals decomposed via the EEMD method indicate that infectivity and mortality of SARS-CoV-2 are both higher in colder climates. The quantitative simulation shows that the cold season in the Southern Hemisphere countries caused a 59.71 ± 8.72% increase of the total infections, while the warm season in the Northern Hemisphere countries contributed to a 46.38 ± 29.10% reduction. COVID-19 seasonality is more pronounced at higher latitudes, where larger seasonal amplitudes of environmental indicators are observed. Seasonality alone is not sufficient to curb the virus transmission to an extent that intervention measures are no longer needed, but health care capacity should be scaled up in preparation for new surges in COVID-19 cases in the upcoming cold season. Our study highlights the necessity of considering seasonal factors when formulating intervention strategies.

Organic matter affects phosphorus recovery during vivianite crystallization.

Vivianite crystallization is a promising route for phosphorus (P) recovery from P-rich wastewater. However, organic matter (OM) in wastewater may influence vivianite formation. In this study, the effects of four representative OMs, glucose, bovine serum albumin (BSA), humic acid (HA) and sodium alginate (SA), on P recovery by vivianite were investigated. The results showed that P recovery efficiency was inhibited by HA and SA, declining by 3.7% and 12.1% under HA (100 mg/L) and SA (800 mg/L), respectively. BSA, HA and SA affected the aggregated form of vivianite crystals. Vivianite particle size decreased in the presence of HA and SA. Subsequent mechanistic exploration indicated that the complexation between the OM and Fe2+ was the main cause of P recovery efficiency reduction. The coprecipitation of HA and SA with vivianite could reduce the zeta potential on the crystal surface, resulting in a smaller particle size. The nucleation sites provided by BSA and SA could transfer vivianite from single plate-like agglomerate to multilayer plate-like agglomerate. This study provided a better understanding of P recovery by vivianite from OM-rich wastewater.

Protective effect of α-asarone and ß-asarone on Aß -induced inflammatory response in PC12 cells and its.

To investigate effects of α-asarone and ß-asarone on induced PC12 cell injury and related mechanisms. Aß toxic injury cell model was induced by Aß in PC12 cells. PC12 cells were divided into blank control group, model control group, α-asarone group (0.5, 1.0, ß-asarone group (6.3, 12.5, vasoactive intestinal peptide (VIP) group, and VIP antagonist control group. Cell survival rate was detected by CCK-8 kit; cell apoptosis rate was detected by flow cytometry. The levels of inflammatory cytokines interleukin (IL)-1, , tumor necrosis factor (TNF)-α, oxidation-related inducible nitric oxide synthase (iNOS), nitric oxide (NO), apoptosis factors caspase-3 and p53 were detected by ELISA method. The expressions of C-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38MAPK) were detected by Western blotting. Compared with model control group, cell survival rates of group, ß-asarone group and VIP group increased; the cell apoptosis rate decreased; levels of apoptosis-related factors caspase-3, p53, inflammatory factors IL-1, TNF-α decreased; IL-10 level increased; levels of oxidization-related factors iNOS and NO decreased; the expression of JNK and p38MAPK protein decreased (all <0.05). After VIP antagonist intervention, the survival rate of ß-asarone group decreased; apoptosis rate increased; apoptosis related factors caspase-3, p53, inflammatory factors IL-1, TNF-α increased; IL-10 decreased; oxidation related factors iNOS and NO increased; the expression of JNK and p38MAPK protein increased (all <0.05); while there were no significant changes in these indicators of α-asarone group (all >0.05). α-asarone and ß-asarone have protective effects on PC12 cell injury induced by Aß. ß-asarone may inhibit inflammatory factors and oxidation-related factors through promoting VIP secretion, regulating JNK/MAPK pathway, and reducing PC12 cell apoptosis; however, the effect of α-asarone may be not related to VIP secretion.