Real-time demonstration of two-aperture coherent digital combining free-space optical transmission with a real-valued MIMO adaptive equalizer.

Compared with the single-aperture system, the multi-aperture coherent digital combining system has the technical advantage of the effective mitigation of deep fading under strong turbulence, ease of scalability, and potential higher collected optical power. However, the tricky problem of a multi-aperture system is to efficiently combine multiple branch signals with a static skew mismatch and with time-varying characteristics of received power scintillation. In this Letter, a real-valued massive array multiple-input multiple-output (MIMO) adaptive equalizer is proposed for the first time to our knowledge to realize multi-aperture channel equalization and combining, simultaneously. In the proof-of-principle system, the feasibility of the combining technique is verified based on a MIMO 4 × 2 equalizer in a 2.5-GBaud data rate QPSK modulation FPGA-based two-aperture coherent receiver with a dynamic turbulence simulator. The results show that no reduction in combining efficiency is observed under static turbulence conditions at the hard-decision forward error correction (HD-FEC) limit of 3.8 × 0-3, and combining efficiencies of 95% and 88% are obtained for the dynamic moderate and strong turbulence.

Association Between Air Pollution and Cardiovascular Disease Hospitalizations in Lanzhou City, 2013-2020: A Time Series Analysis.

Extensive evidence has shown that air pollution increases the risk of cardiovascular disease (CVD) admissions. We aimed to explore the short-term effect of air pollution on CVD admissions in Lanzhou residents and their lag effects. Meteorological data, air pollution data, and a total of 309,561 daily hospitalizations for CVD among urban residents in Lanzhou were collected from 2013 to 2020. Distributed lag non-linear model was used to analyze the relationship between air pollutants and CVD admissions, stratified by gender, age, and season. PM2.5, NO2, and CO have the strongest harmful effects at lag03, while SO2 at lag3. The relative risks of CVD admissions were 1.0013(95% CI: 1.0003, 1.0023), 1.0032(95% CI: 1.0008, 1.0056), and 1.0040(95% CI: 1.0024, 1.0057) when PM2.5, SO2, and NO2 concentrations were increased by 10 µg/m³, respectively. Each 1 mg/m3 increase in CO concentration was associated with a relative risk of cardiovascular hospitalization of risk was 1.0909(95% CI: 1.0367, 1.1479). We observed a relative risk of 0.9981(95% CI: 0.9972, 0.9991) for each 10 µg/m³ increase in O3 for CVD admissions at lag06. We found a significant lag effects of air pollutants on CVD admissions. NO2 and CO pose a greater risk of hospitalization for women, while PM2.5 and SO2 have a greater impact on men. PM2.5, NO2, and CO have a greater impact on CVD admissions in individuals aged <65 years, whereas SO2 affects those aged ≥65 years. Our research indicates a possible short-term impact of air pollution on CVD. Local public health and environmental policies should take these preliminary findings into account.

Astragalus polysaccharide protects experimental colitis through an aryl hydrocarbon receptor-dependent autophagy mechanism.

BACKGROUND AND PURPOSE: Disruption of intestinal barriers plays a vital role in the pathogenesis of colitis. The aryl hydrocarbon receptor (AhR) is a recognition sensor that mediates intestinal immune homeostasis and minimizes intestinal inflammation. Astragalus polysaccharide (APS) exerts pharmacological actions in colitis; however, the mechanism has not been elucidated. We investigated whether APS protects through AhR-dependent autophagy. EXPERIMENTAL APPROACH: The symptoms of dextran sulfate sodium (DSS)-induced colitis in mice involving intestinal barrier function and inflammatory injury were evaluated after APS administration. Intestinal-specific Becn1 conditional knockout (Becn1 cKO) mice were constructed and compared with wild-type mice. Autophagy and the effects of APS were investigated after the deactivation of AhRs. The relationship between APS-induced AhRs and autophagic Becn1 was investigated using a dual-luciferase reporter system and chromatin immunoprecipitation (ChIP)-quantitative polymerase chain reaction assay. Caco-2 cells were used to investigate inflammatory responses and AhR-dependent autophagy. KEY RESULTS: APS improved intestinal barrier function in inflammatory injury in colitis mice. APS triggered autophagic flow; however, knockout of Becn1 in the gut increased susceptibility to colitis, leading to diminished epithelial barrier function and severe intestinal inflammation, impairing the protective effects of APS. Mechanistically, APS-triggered autophagy depends on AhR expression. Activated AhR binds to the promoter Becn1 to operate transcription of genes involved in anti-inflammation and intestinal barrier repair, while deactivation of AhR correlated with intestinal inflammation and the therapeutic function of APS. CONCLUSIONS AND IMPLICATIONS: APS protects colitis mice by targeting autophagy, especially as the AhR stimulates the repair of damaged intestinal barrier functions.

Association Between Air Pollution and Coronary Heart Disease Hospitalizations in Lanzhou City, 2013-2020: a Time Series Analysis.

Coronary heart disease (CHD) is one of the most serious public health problems. However, few studies have focused on the effects of exposure to particulate matter and gaseous air pollutants on CHD. This study aimed to explore the relationship between air pollutants and the number of hospitalized patients with CHD in Lanzhou, and we collected daily data on the number of hospitalized patients with CHD, daily air pollutants, and meteorological factors from 2013 to 2020. A distributed lag nonlinear model (DLNM) combined with a quasi-Poisson regression model was applied to evaluate the relationship between air pollutants and the number of hospitalized patients with CHD. The results indicated that the hysteresis effect of all pollutants except O38h reached its maximum at lag3, and the relative risk of coronary heart disease admission was 1.0014 (95%CI: 1.0004, 1.0023), 1.0003 (95%CI: 1.0000, 1.0006), 1.0020 (95%CI: 1.0004, 1.0035), and 1.0053 (95%CI: 1.0026, 1.0080) when PM2.5, PM10, NO2, and SO2 concentrations were increased by 10 µg/m3, respectively. Each 1 mg/m3 increase in CO concentration was associated with a relative risk of coronary heart disease; hospitalization risk was 1.1076 (95%CI: 1.0530, 1.1650). We observed a relative risk of 0.9991 (95%CI: 0.9986, 0.9999) for each 10 µg/m3 increase in O38h for coronary heart disease admission at lag1. Women and elderly were more susceptible to the impact of air pollution, and the impact was greater during cold seasons. Our results indicate that air pollution increased the risk of hospitalization for CHD in a short term. The research findings can provide strategic insights into the impact of current and future air pollution on CHD.

Astragaloside trigger autophagy: Implication a potential therapeutic strategy for pulmonary fibrosis.

Pulmonary fibrosis is an abnormal wound-healing response to repeated alveolar injury, characterized by continuous inflammation and abnormal collagen deposition. Its treatment is problematic. Astragaloside (AST) is an active component of Astragalus membranaceus with anti-inflammatory and anti-tumor properties. Although the underlying mechanisms are unknown, AST is also used to treat fibrotic diseases. This study aimed to investigate the mechanisms of action of AST in pulmonary fibrosis treatment. We found that AST significantly improved restrictive ventilatory impairment, compliance, total lung capacity, and functional residual capacity. In mice with pulmonary fibrosis, extracellular matrix deposition in the pulmonary parenchyma and intemperate inflammation were reversed. This therapeutic effect can be attributed to autophagy, activating the genes for autophagy flux and autophagic vacuoles. Impaired autophagy increased susceptibility to pulmonary fibrosis by exacerbating collagen deposition in vitro and in vivo. Using a combination of molecular docking and network pharmacology, the Ras/Raf/MEK/ERK signaling pathway was identified as a possible candidate for the pharmacologic target of AST. Functional dephosphorylation of MEK and ERK inhibited the Ras/Raf/MEK/ERK signaling pathway, which converges at the rapamycin switch to initiate autophagy. Inhibitors of Ras and MEK regulated autophagy. These findings suggest that AST might treat pulmonary fibrosis by modulating the Ras/Raf/MEK/ERK signaling pathway mediated by depression.

Induction of autophagy via the TLR4/NF-κB signaling pathway by astragaloside â £ contributes to the amelioration of inflammation in RAW264.7 cells.

Cigarette smoking-related lung injury is one of the most common and fatal etiologies of many respiratory diseases, for which no effective interventions are available. Astragaloside Ⅳ (ASⅣ) is an active component extracted from Astragalus membranaceus. It is prescribed as a treatment for upper respiratory tract infections. Here, we report the potential anti-inflammatory effects and mechanisms of ASⅣ on cigarette smoking extract- (CSE)-exposed RAW264.7 cells. Murine macrophages were exposed to CSE, followed by administration of ASⅣ at 25-100 µg/mL for 24 h. ASⅣ significantly rescued CSE-induced cell death by inhibition of release pro-inflammatory cytokines. We measured autophagy as an intracellular scavenger by analyzing autophagic flux using tandem mRFP-GFP-LC3 fluorescence microscopy. Following administration with ASⅣ in CSE-exposed RAW264.7 cells, there was a notable increase in autophagosomes and a range of autophagic vacuoles were generated, as seen with transmission electron microscopy. Loss of autophagy following transfection siRNA aggravated inflammatory injury and release of inflammatory cytokines. Mechanistically, ASⅣ-triggered autophagy is mediated by the TLR4/NF-κB signaling pathway to reduce inflammation. Taken together, our findings suggest that ASⅣ acts stimulates autophagy, and that ASⅣ induces autophagy by inhibiting the TLR4/NF-κB signaling pathway, contributing to alleviation of inflammation.

Comparative transcriptome analysis of Trichoderma reesei reveals different gene regulatory networks induced by synthetic mixtures of glucose and ß-disaccharide.

The mixture of glucose and ß-disaccharide (MGD) synthesized by transglycosylation of glucose as a low-cost soluble carbon source can efficiently induce cellulase production in Trichoderma reesei, which holds potential for the biorefining of lignocellulosic biomass. However, it is not yet fully understood how MGD induces T. reesei cellulase. In this study, transcriptomic analyses were conducted to investigate the molecular basis of MGD for lignocellulose-degrading enzyme production of T. reesei Rut C30 compared with that on lactose. Particular attention was paid to CAZymes, transcription factors, transporters and other protein processing pathways related to lignocellulose degradation. As a result, MGD can elicit transcription of GH5-, GH6- and GH7-encoding cellulases that is up to 1.4-fold higher than that induced by lactose, but GH11- and GH74-encoding xylanases are downregulated by 1.7- and 4.4-fold, respectively. Gene expression profiles suggest that the transcription activators xyr1 and vib1 are significantly upregulated and that the mitogen-activated protein kinase pathway is strengthened compared to the case of lactose induction. In addition, hac1-encoding UPR-specific transcription factors are significantly upregulated by MGD, which may be enhanced due to proper folding and processing of nascent proteins. These findings provide a theoretical basis for further understanding the characterization of efficient cellulase production using MGD as an inducer in T. reesei and offer potential strategies for strain improvement.

Bacterial association and comparison between lung and intestine in rats.

The association between lung and intestine has already been reported, but the differences in community structures or functions between lung and intestine bacteria yet need to explore. To explore the differences in community structures or functions, the lung tissues and fecal contents in rats were collected and analyzed through 16S rRNA sequencing. It was found that intestine bacteria was more abundant and diverse than lung bacteria. In intestine bacteria, Firmicutes and Bacteroides were identified as major phyla while Lactobacillus was among the most abundant genus. However, in lung the major identified phylum was Proteobacteria and genus Pseudomonas was most prominent genus. On the other hand, in contrast the lung bacteria was more concentrated in cytoskeleton and function in energy production and conversion. While, intestine bacteria were enriched in RNA processing, modification chromatin structure, dynamics and amino acid metabolism. The study provides the basis for understanding the relationships between lung and intestine bacteria.

Antifibrotic action of Yifei Sanjie formula enhanced autophagy via PI3K-AKT-mTOR signaling pathway in mouse model of pulmonary fibrosis.

Pulmonary fibrosis (PF) is a crippling disease characterized by progressive dyspnea and associated with a high mortality rate, but its origin is unknown and there is no effective treatment. Yifei Sanjie formula (YFSJF) is a Chinese medicine that is widely used for treatment of respiratory systems disease. However, the molecular basis for the function of YFSJF has not been determined. Here we investigate the contribution of YFSJF in BLM-induced PF mice. Administration with YFSJF significantly alleviated the degree of BLM-induced collagen I and III deposition and the inflammatory injuring in the lungs and suppressed hydroxyproline release in PF animals. The active components of YFSJF are comprised with flavonoid, amino acids, saponins, oligosaccharide, organic acid, vitamin, esters, purine nucleosides. Additionally, there was a significant increase in autophagosomes, after treatment with YFSJF in PF animals. Interestingly, autophagy dysfunction by the blocker chloroquine (CQ) resulted in collagen deposition and inducing the expression of fibrosis-related genes. In addition, YFSJF-induced autophagy is mediated by the PI3K-AKT-mTOR pathway, and knockdown of PI3K by siRNA up-regulated the expression of autophagy-related genes and down-regulated the expression of collagen in human lung fibroblasts (HLF). Our findings provide a detailed understanding that YFSJF-antifibrotic effects are mainly mediated by triggering autophagy, and suppressing phosphorylation of the PI3K-AKT-mTOR pathway is required for YFSJF-curative effect.

Curcumin and Curcumol Inhibit NF-κB and TGF-ß 1/Smads Signaling Pathways in CSE-Treated RAW246.7 Cells.

E-Zhu (Curcuma zedoaria) is known as a classical traditional Chinese medicine and widely used in the treatment of cancers, cardiovascular disease, inflammation, and other diseases. Its main components include curcumol and curcumin, which have anti-inflammatory and antifibrosis effects. Here we established an in vitro inflammatory injury model by stimulating RAW246.7 cells with cigarette smoke extract (CSE) and detected the intervention effects of curcumin and curcumol on CSE-treated Raw246.7 macrophage cells to explore whether the two compounds inhibited the expression of inflammatory cytokines by inhibiting the NF-κB signaling pathway. We detected the antifibrosis effects of curcumin and curcumol via TGF-ß 1/Smads signaling pathways. The model of macrophage damage group was established by CSE stimulation. Curcumol and curcumin were administered to Raw246.7 macrophage cells. The efficacy of curcumol and curcumin was evaluated by comparing the activation of proinflammatory factors, profibrotic factors, and NF-κB and TGF-ß 1/Smads signaling pathway. In addition, CSE-treated group was employed to detect whether the efficacy of curcumol and curcumin was dependent on the NF-κB signaling via the pretreatment with the inhibitor of NF-κB. Our findings demonstrated that curcumol and curcumin could reduce the release of intracellular ROS from macrophages, inhibit the NF-κB signaling pathway, and downregulate the release of proinflammatory factor. Curcumol and curcumin inhibited the TGF-ß 1/Smads signaling pathway and downregulated the release of fibrotic factors. Curcumin showed no anti-inflammatory effect in CSE-treated cells after the inhibition of NF-κB. Curcumol and curcumin showed an anti-inflammatory effect by inhibiting the NF-κB signaling pathway.

Self-assembled reversed bilayers directed by pnictogen bonding to form vesicles in solution.

Artificial vesicles can aid in the study and understanding of biological cell membranes. This study employs pnictogen bonding to actively direct the self-assembly of a true reversed bilayer. Antimony(iii) alkoxide cages that self-assemble through multiple strong SbO interactions propagate in two dimensions to form a reverse bilayer structure in the solid state. Long alkyl tails allow these reverse bilayers to be processed into vesicles in solution that are a reverse of biological cell membranes.

Precise Steric Control over 2D versus 3D Self-Assembly of Antimony(III) Alkoxide Cages through Strong Secondary Bonding Interactions.

Antimony(III) alkoxide cages were designed as building blocks for predictable supramolecular self-assembly. Supramolecular synthons featuring two Sb···O secondary bonding interactions (SBIs), each SBI stronger than 30 kJ/mol, were used to drive the formation of the supramolecular architectures. Judicious choice of pendant groups provided predictable control over the formation of self-assembled 3D columnar helices, which crystallized with hollow morphologies, or a self-assembled 2D bilayer. The Sb-O stretching frequency provides a spectroscopic signature of Sb···O SBI formation.