Far-infrared therapy promotes exercise capacity and glucose metabolism in mice by modulating microbiota homeostasis and activating AMPK.

The benefits of physical exercise on human health make it desirable to identify new approaches that would mimic or potentiate the effects of exercise to treat metabolic diseases. However, whether far-infrared (FIR) hyperthermia therapy could be used as exercise mimetic to realize wide-ranging metabolic regulation, and its underling mechanisms remain unclear. Here, a specific far-infrared (FIR) rays generated from graphene-based hyperthermia devices might promote exercise capacity and metabolisms. The material characterization showed that the graphene synthesized by chemical vapour deposition (CVD) was different from carbon fiber, with single-layer structure and high electrothermal transform efficiency. The emission spectra generated by graphene-FIR device would maximize matching those adsorbed by tissues. Graphene-FIR enhanced both core and epidermal temperatures, leading to increased blood flow in the femoral muscle and the abdominal region. The combination of microbiomic and metabolomic analysis revealed that graphene-FIR modulates the metabolism of the gut-muscle axis. This modulation was characterized by an increased abundance of short-chain fatty acids (SCFA)-producing bacteria and AMP, while lactic acid levels decreased. Furthermore, the principal routes involved in glucose metabolism, such as glycolysis and gluconeogenesis, were found to be altered. Graphene-FIR managed to stimulate AMPK activity by activating GPR43, thus enhancing muscle glucose uptake. Furthermore, a microbiota disorder model also demonstrated that the graphene-FIR effectively restore the exercise endurance with enhanced p-AMPK and GLUT4. Our results provided convincing evidence that graphene-based FIR therapy promoted exercise capacity and glucose metabolism via AMPK in gut-muscle axis. These novel findings regarding the therapeutic effects of graphene-FIR suggested its potential utility as a mimetic agent in clinical management of metabolic disorders.

Study of Molecular Dimer Morphology Based on Organic Spin Centers: Nitronyl Nitroxide Radicals.

In this work, in order to investigate the short-range interactions between molecules, the spin-magnetic unit nitronyl nitroxide (NN) was introduced to synthesize self-assembly single radical molecules with hydrogen bond donors and acceptors. The structures and magnetic properties were extensively investigated and characterized by UV-Vis absorption spectroscopy, electron paramagnetic resonance (EPR), and superconducting quantum interference devices (SQUIDs). Interestingly, it was observed that the single molecules can form two different dimers (ring-closed dimer and "L"-type dimer) in different solvents, due to hydrogen bonding, when using EPR to track the molecular spin interactions. Both dimers exhibit ferromagnetic properties (for ring-closed dimer, J/kB = 0.18 K and ΔES-T = 0.0071 kcal/mol; for "L"-type dimer, the values were J/kB = 9.26 K and ΔES-T = 0.037 kcal/mol). In addition, the morphologies of the fibers formed by the two dimers were characterized by transmission electron microscopy (TEM) and atomic force microscopy (AFM).

VENOARTERIAL EXTRACORPOREAL MEMBRANE OXYGENATION REDUCES MYOCARDIAL AND MITOCHONDRIAL DAMAGE IN ACUTE MYOCARDIAL INFARCTION.

ABSTRACT: Background: Myocardial infarction (MI) is a common cardiovascular disease with a high fatality rate once accompanied by cardiogenic shock. The efficacy of extracorporeal membrane oxygenation (ECMO) in treating MI is controversial. Methods: MI was induced by ligating the left anterior descending artery (LAD) in adult male rats. Groups were defined as follows: MI group, reperfusion for 90 min after 30 min of LAD occlusion; MI + ECMO group, reperfusion and ECMO were performed for 90 min immediately after 30 min of LAD occlusion; prolonged MI + ECMO group, ECMO was used immediately after 30 min of occlusion with persistent occlusion of the LAD for an additional 30 min, followed by 90 min of reperfusion. The myocardial infarct size and mitochondrial morphology and function data were collected and compared of each group. Results: The ECMO groups had a smaller myocardial infarct size and larger percentage ejection fraction. Compared with the prolonged MI + ECMO group, the immediate reperfusion group had a lower percentage of infarct size (63.28% vs. 17.97% vs. 31.22%, MI vs. MI + ECMO vs. prolonged MI + ECMO). Mitochondria isolated from the ischemic zone showed an intact mitochondrial structure, including fewer voids and broken cristae, and preserved activity of mitochondrial complex II and complex IV in ECMO groups. Conclusions: ECMO support in MI can reduce myocardial injury despite delayed coronary reperfusion.

A novel mouse model of calcific aortic valve stenosis.

BACKGROUND: Calcific aortic valve stenosis (CAVS) is one of the most challenging heart diseases in clinical with rapidly increasing prevalence. However, study of the mechanism and treatment of CAVS is hampered by the lack of suitable, robust and efficient models that develop hemodynamically significant stenosis and typical calcium deposition. Here, we aim to establish a mouse model to mimic the development and features of CAVS. METHODS: The model was established via aortic valve wire injury (AVWI) combined with vitamin D subcutaneous injected in wild type C57/BL6 mice. Serial transthoracic echocardiography was applied to evaluate aortic jet peak velocity and mean gradient. Histopathological specimens were collected and examined in respect of valve thickening, calcium deposition, collagen accumulation, osteogenic differentiation and inflammation. RESULTS: Serial transthoracic echocardiography revealed that aortic jet peak velocity and mean gradient increased from 7 days post model establishment in a time dependent manner and tended to be stable at 28 days. Compared with the sham group, simple AVWI or the vitamin D group, the hybrid model group showed typical pathological features of CAVS, including hemodynamic alterations, increased aortic valve thickening, calcium deposition, collagen accumulation at 28 days. In addition, osteogenic differentiation, fibrosis and inflammation, which play critical roles in the development of CAVS, were observed in the hybrid model. CONCLUSIONS: We established a novel mouse model of CAVS that could be induced efficiently, robustly and economically, and without genetic intervention. It provides a fast track to explore the underlying mechanisms of CAVS and to identify more effective pharmacological targets.

Bi-ligand-fabricated CdS quantum dots to photo-induce aqueous-phase aldol condensation for biomass-derived carbonyl compounds.

CdS QDs were fabricated using bi-ligands 11-sulfanylundecanoic acid and proline for photo-induced aqueous-phase aldol condensation of biomass-derived furfural compounds and ketones, and they displayed acceptable selectivity, activity and recycling properties for generation of a wide range of products with diverse applications. This work facilitates understanding the molecular-level design concepts of semiconductor photocatalysts.

Phenotypic characteristics and immune response of Procypris merus following challenge with aquatic isolate of Klebsiella pneumoniae.

Currently, aquaculture is a relatively mature industry; however, disease problems are continuously threatening the industry and hindering its development to a certain extent. Klebsiella pneumoniae is one of the zoonotic bacteria widely present in different hosts and has caused some degree of harm to the aquaculture industry, posing a potential threat to the water environment and indirectly also affecting human food safety issues. In this study, K. pneumoniae was isolated from the aquaculture environment, named as ELD, and subjected to pathogenic and immunological related studies. The results of the study showed that the strain carries at least four virulence-related genes, magA, wabG, ureA and uge, and has developed resistance to at least seven antibacterial drugs, such as amoxicillin, doxycycline, rifampicin, and so on. Moreover, the strain is highly pathogenic and is capable of causing systemic clinical foci in Procypris merus. In addition, after infection with K. pneumoniae, the expression of IL-1ß, IL-8, HSP70 and C2 was upregulated in P. merus as a whole, whereas the expression of TNF-α did not change significantly in any of the tissues, which might be a kind of immune response of P. merus against K. pneumoniae infection. This study provides an important theoretical basis for the in-depth exploration of the pathogenic mechanism of K. pneumoniae in fish and the immune response that occurs after the disease is contracted in fish, as well as theoretical support for the development of effective preventive and therapeutic strategies against K. pneumoniae-infected aquatic animals in the future.

Enhanced glycolysis-mediated energy production in alveolar stem cells is required for alveolar regeneration.

Impaired differentiation of alveolar stem cells has been identified in a variety of acute and chronic lung diseases. In this study, we investigate the mechanisms that modulate alveolar regeneration and understand how aging impacts this process. We have discovered that the process of alveolar type II (AT2) cells differentiating into AT1 cells is an energetically costly process. During alveolar regeneration, activated AMPK-PFKFB2 signaling upregulates glycolysis, which is essential to support the intracellular energy expenditure that is required for cytoskeletal remodeling during AT2 cell differentiation. AT2 cells in aged lungs exhibit reduced AMPK-PFKFB2 signaling and ATP production, resulting in impaired alveolar regeneration. Activating AMPK-PFKFB2 signaling in aged AT2 cells can rescue defective alveolar regeneration in aged mice. Thus, beyond demonstrating that cellular energy metabolism orchestrates with stem cell differentiation during alveolar regeneration, our study suggests that modulating AMPK-PFKFB2 signaling promotes alveolar repair in aged lungs.

Natural occurrences and characterization of Elizabethkingia miricola infection in cultured bullfrogs (Rana catesbeiana).

Introduction: The bacterium Elizabethkingia miricola is a multispecies pathogen associated with meningitis-like disease that has been isolated from several amphibian species, including the bullfrog, but this is the first isolation in Guangxi. In the present study, the dominant bacteria were isolated from the brains of five bullfrogs with meningitis-like disease on a South China farm in Guangxi. Methods: The NFEM01 isolate was identified by Gram staining; morphological observations; 16S rRNA, rpoB, and mutT-based phylogenetic tree analysis; and physiochemical characterization and was subjected to drug sensitivity and artificial infection testing. Results and discussion: As a result of identification, the NFEM01 strain was found to be E. miricola. An artificial infection experiment revealed that NFEM01 infected bullfrogs and could cause symptoms of typical meningitis-like disease. As a result of the bacterial drug sensitivity test, NFEM01 is highly sensitive to mequindox, rifampicin, enrofloxacin, nitrofural, and oxytetracycline and there was strong resistance to gentamicin, florfenicol, neomycin, penicillin, amoxicillin, doxycycline, and sulfamonomethoxine. This study provides a reference to further study the pathogenesis mechanism of E. miricola-induced bullfrog meningitislike disease and its prevention and treatment.

Enterobacter asburiae E7, a Novel Potential Probiotic, Enhances Resistance to Aeromonas veronii Infection via Stimulating the Immune Response in Common Carp (Cyprinus carpio).

Probiotics are an alternative strategy for antibiotics, but most probiotics are Gram-positive bacteria suitable for terrestrial animals. Therefore, it is imperative to develop dedicated probiotics for the common carp industry to be ecologically efficient and environmentally friendly. A novel Enterobacter asburiae named E7 was isolated from the intestine of healthy common carp and displayed an extensive antibacterial spectrum against Aeromonas hydrophila, A. veronii, A. caviae, A. media, A. jandaei, A. enteropelogenes, A. schubertii, A. salmonicida, Pseudomonas aeruginosa, Ps. putida, Plesiomonas shigelloides, and Shewanella. E7 was nonpathogenic to the host and susceptible to the majority of antibiotics used in human clinical practice. E7 could grow between 10 and 45°C and between pH 4 and 7 and was extremely resistant to 4% (wt/vol) bile salts. Diets were supplemented with 1 × 107 CFU/g E. asburiae E7 for 28 days. No significant difference in the growth of fish was observed. Expression of immune-related genes IL-10, IL-8, and lysozyme in common carp kidney was significantly upregulated at weeks 1, 2, and 4 (P < 0.01). A significant upregulation of IL-1ß, IFN, and TNF-α expression was observed after week 4 (P < 0.01). There was a significant increase in mRNA expression of TGF-ß at week 3 (P < 0.01). Following challenge by Aeromonas veronii, the survival rate (91.05%) was significantly higher than observed in the controls (54%; P < 0.01). Collectively, E. asburiae E7 is a promising new Gram-negative probiotic that can enhance health and bacterial resistance of aquatic animals and could thus be developed as an exclusive aquatic probiotic. IMPORTANCE In the present study, we evaluated for the first time the efficiency of Enterobacter asburiae as a prospective probiotic for aquaculture applications. The E7 strain showed extensive resistance to Aeromonas, no pathogenicity to the host, and stronger environmental tolerance. We observed that the resistance of common carp to A. veronii was enhanced by feeding a diet containing 1 × 107 CFU/g E. asburiae E7 for 28 days, but growth was not improved. Strain E7 can act as an immunostimulant to induce the upregulation of some innate cellular and humoral immune responses, resulting in enhanced resistance to A. veronii. Hence, the continuous activation of immune cells can be maintained by adding suitable fresh probiotics to the diet. E7 has the potential to act as a probiotic agent for green, sustainable aquaculture and aquatic product safety.

High responsivity of VIS-NIR photodetector based on Ag2S/P3HT heterojunction.

Ag2S quantum dot (QD) photodetectors (PDs) have attracted a lot of attention in the field of imaging system and optical communication. However, the current Ag2S PDs mainly works in the near-infrared band, and its detection ability in the visible band remains to be strengthened. In this paper, we used poly(3-hexylthiophene) (P3HT) with high carrier mobility and Ag2S QDs to construct heterojunction PD. Stronger absorption in blends with polymer P3HT compared to single Ag2S QDs. The optical absorption spectra show that the Ag2S/P3HT has strong light absorption peak at 394 and 598 nm. The results show that P3HT significantly enhances the absorption of Ag2S QDs from the visible to near-infrared band. The output characteristics, transfer characteristics and fast switching capability of the device at 405 nm, 532 nm and 808 nm were tested. The device has the responsivity of 6.05 A W-1, 83.72 A W-1and 37.31 A W-1under 405 nm, 532 nm and 808 nm laser irradiation. This work plays an important role in improving the detection performance of Ag2S QDs and broadening its applications in photoelectric devices for weak light and wide spectrum detection.

Causal relationship between tea intake and cardiovascular diseases: A Mendelian randomization study.

Background: Although studies suggest that tea consumption is associated with a reduced risk of cardiovascular disease (CVD). There is no unified conclusion about the potential relationship between tea drinking and CVD. We used a two-sample Mendelian randomized (MR) analysis to systematically explore the causal relationship between tea intake and CVD subtypes for the first time. Furthermore the mediating effect of hypertension was also explored by a two-step MR. Methods: Genetic instruments for tea intake were identified from a genome-wide association studies (GWAS) involving 447,485 people. Summary data on cardio-vascular disease came from different GWAS meta-analysis studies. In the first step we explored the causal effect of tea intake and CVD. In the second step, we examined the association of hypertension with heart failure and ischemic stroke and estimated the mediating effect of hypertension. Inverse variance weighted MR analysis was used as the primary method for causal analysis. A further sensitivity analysis was performed to ensure robustness of the results. Results: One standard deviation increase in tea intake was associated with a 25% (OR = 0.75, 95%CI = 0.61-0.91, p = 0.003) lower risk of hypertension, a 28% (OR = 0.72, 95%CI = 0.58-0.89, p = 0.002) lower risk of heart failure, and a 29% (OR = 0.71, 95%CI = 0.55-0.92, p = 0.008) lower risk of ischemic stroke, respectively. And the association between tea drinking and the risk of heart failure and ischemic stroke may be mediated by hypertension. Sensitivity analyses found little evidence of pleiotropy. Conclusion: Our two-sample MR analysis provided genetic evidence that tea intake was significantly associated with a reduced risk of hypertension, heart failure, and ischemic stroke, and that hypertension may be a potential mediator. Further large randomized controlled trials should be conducted to confirm the causal effect of tea consumption on cardiovascular disease risk.

[Retracted] Downregulation of microRNA­198 suppresses cell proliferation and invasion in retinoblastoma by directly targeting PTEN.

Following the publication of this paper, it was drawn to the Editors' attention by a concerned reader that certain of the data shown for the cell invasion assays in Figs. 2C and 4C were strikingly similar to data appearing in different form in other articles by different authors. Owing to the fact that the contentious data in the above article had already been published elsewhere, or were already under consideration for publication, prior to its submission to Molecular Medicine Reports, the Editor has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [Molecular Medicine Reports 18: 595­602, 2018; DOI: 10.3892/mmr.2018.8979].

The Association Between Psoriasis and Risk of Cardiovascular Disease: A Mendelian Randomization Analysis.

Background: A large number of observational studies showed that patients with psoriasis have a higher risk of cardiovascular disease (CVD), but most studies did not fully adjust for confounding factors, so it is not clear whether the risk of CVD is directly attributed to psoriasis. We used Mendelian randomization (MR) to evaluate the potential causal relationship between psoriasis and CVD. Methods: We used genetic instruments from the genome-wide association study (GWAS) of European descent for psoriasis to investigate its relationship with CVD. Inverse variance-weighted (IVW) MR analyses were used for the primary analysis. In addition, a variety of other methods were used to replicate the analysis. Results: The fixed-effects IVW method indicated that genetic susceptibility to psoriasis was associated with a higher risk of heart failure (HF) [odds ratio (OR) = 1.04; 95% CI, 1.01-1.06, P = 2.72E-03], atrial fibrillation (AF) (OR = 1.04; 95% CI, 1.02-1.07, P = 3.27E-04), myocardial infarction (MI) (OR = 1.07; 95% CI, 1.01-1.12, P = 0.01), valvular heart disease (VHD) (OR = 1.001; 95% CI, 1.000-1.002, P = 1.85E-03), and large artery stroke (LAS) (OR = 1.11; 95% CI, 1.05-1.18, P = 5.37E-04) but not with the other two subtypes of ischemic stroke (IS) [cardioembolic stroke (CES) (OR = 1.03; 95% CI, 0.98-1.07, P = 0.27) and small vessel stroke (SVS) (OR = 1.00; 95% CI, 0.95-1.07), P = 0.88)]. Sensitivity analysis found weak evidence of horizontal diversity and heterogeneity to ensure the stability of the results. Conclusion: Our study provided evidence for a potential causal link between psoriasis and CVD. These findings partly suggest that early monitoring of cardiovascular risk in patients with psoriasis is intentional.

Associations Between Vitamin D Levels and Risk of Heart Failure: A Bidirectional Mendelian Randomization Study.

Background: Although studies suggest that concentrations of serum 25-hydroxyvitamin D (25(OH)D) are lower in individuals with Heart Failure (HF), the beneficial effects of vitamin D supplementation are controversial. Therefore, in this study, we aimed to determine whether there is a causal relationship between serum Vitamin D (VD) levels and HF. Methods: We obtained genetic instruments from the largest available genome-wide association study (GWAS) of European descent for 25(OH)D (443, 734 individuals) to investigate the association with HF (47,309 cases, 930,014 controls), and vice versa. Two-sample bidirectional Mendelian Randomization (MR) analysis was performed to infer the causality. In addition to the primary analysis using inverse variance-weighted (IVW) MR, we applied five additional methods to control for pleiotropy [MR-Egger, weighted median, Maximum-likelihood, MR-robust adjusted profile score (MR-RAPS) and MR-pleiotropy residual sum and outlier (MR-PRESSO)] and compared their respective MR estimates. We also performed a sensitivity analysis to ensure that our results were robust. Results: Mendelian randomized analysis showed that increased serum 25(OH)D was associated with a lower risk of HF in the IVW method (odds ratio [OR] = 0. 81;95%CI, 0.70-0.94, P = 0.006). In the reverse MR analyses, the genetic predisposition to HF was negatively correlated with serum 25(OH)D level (OR = 0. 89;95%CI, (0.82-0.97), P = 0.009). Conclusion: Our study revealed the possible causal role of 25(OH)D on decreasing the risk for HF. Meanwhile, reverse MR analysis suggested that HF may be associated with lower vitamin D levels, it could be the potential implications for dietary recommendations.

Review of Medicinal Plants and Active Pharmaceutical Ingredients against Aquatic Pathogenic Viruses.

Aquaculture offers a promising source of economic and healthy protein for human consumption, which can improve wellbeing. Viral diseases are the most serious type of diseases affecting aquatic animals and a major obstacle to the development of the aquaculture industry. In the background of antibiotic-free farming, the development and application of antibiotic alternatives has become one of the most important issues in aquaculture. In recent years, many medicinal plants and their active pharmaceutical ingredients have been found to be effective in the treatment and prevention of viral diseases in aquatic animals. Compared with chemical drugs and antibiotics, medicinal plants have fewer side-effects, produce little drug resistance, and exhibit low toxicity to the water environment. Most medicinal plants can effectively improve the growth performance of aquatic animals; thus, they are becoming increasingly valued and widely used in aquaculture. The present review summarizes the promising antiviral activities of medicinal plants and their active pharmaceutical ingredients against aquatic viruses. Furthermore, it also explains their possible mechanisms of action and possible implications in the prevention or treatment of viral diseases in aquaculture. This article could lay the foundation for the future development of harmless drugs for the prevention and control of viral disease outbreaks in aquaculture.

Systemic Lupus Erythematosus and Cardiovascular Disease: A Mendelian Randomization Study.

Background: Previous studies have shown that patients with systemic lupus erythematosus (SLE) tend to have a higher risk of cardiovascular disease (CVD), but the potential causal relationship between genetic susceptibility to SLE and CVD risk is not clear. This study systematically investigated the potential association between genetically determined SLE and the risk of CVD. Methods: The genetic tools were obtained from genome-wide association studies of SLE and CVD, with no overlap between their participating populations. Mendelian randomization (MR) analysis was performed using inverse variance weighting as the primary method. Simultaneously, a series of repeated analyses, sensitivity analyses, and instrumental variable strength evaluations were performed to verify the reliability of our results. Results: MR analysis showed that genetic susceptibility to SLE was associated with a higher risk of heart failure (OR=1.025, 95% CI [1.009-1.041], P=0.002), ischemic stroke (OR=1.020, 95% CI [1.005-1.034], P=0.009), and venous thromboembolism (OR=1.001, 95% CI [1.000-1.002], P=0.014). However, genetic susceptibility to SLE was negatively correlated with the risk of type 2 diabetes (OR=0.968, 95% CI [0.947-0.990], P=0.004). Sensitivity analysis found no evidence of horizontal pleiotropy or heterogeneity. Conclusion: Our MR study explored the causal role of SLE in the etiology of CVD, which would help improve our understanding of the basic disease mechanisms of SLE and provide comprehensive CVD assessment and treatment for SLE patients.

Oncogenic magnesium transporter 1 upregulates programmed death-1-ligand 1 expression and contributes to growth and radioresistance of glioma cells through the ERK/MAPK signaling pathway.

Radiotherapy has been established as a major therapeutic modality for glioma, whereas new therapeutic targets are needed to prevent tumor recurrence. This study intends to explore the regulatory role of magnesium transporter 1 (MAGT1) in radiotherapy resistance of glioma through modulating ERK and programmed death-1-ligand 1 (PD-L1). Our bioinformatics analysis identified differentially expressed MAGT1 in glioma, expression of which was subsequently determined in cohort data of TCGA database and microarray dataset as well as glioma cell lines. Artificial modulation of MAGT1, ERK, and PD-L1 expression was performed to examine their effects on glioma cell proliferation and radioresistance, as reflected by MTT and colony formation assays under irradiation. Mouse glioma cells with manipulated MAGT1 and ERK inhibitors were further injected into mice to assess the in vivo tumor formation ability of glioma cells. It was noted that MAGT1 expression was highly expressed in glioma tissues of TCGA data and microarray dataset, which was then validated in glioma cell lines. Ectopic expression of MAGT1 was revealed to promote the proliferation and radioresistance of glioma cells, which was attributed to the MAGT1-mediated activation of the ERK/MAPK signaling pathway. It was illuminated that MAGT1 stimulated PD-L1 expression through the ERK/MAPK pathway and thus facilitated glioma cell growth. Additionally, MAGT1 overexpression accelerated the in vivo tumor formation of glioma cells, while the ERK inhibitor negated its effect. In conclusion, MAGT1 enhances the growth and radioresistance of glioma cells through the ERK/MAPK signaling pathway-mediated upregulation of PD-L1 expression.

A Hybrid Assembly with Nickel Poly-Pyridine Polymer on CdS Quantum Dots for Photo-Reducing CO2 into Syngas with Controlled H2 /CO Ratios.

A hybrid photocatalytic assembly with Ni poly-pyridine polymers binding on CdS quantum dots was developed via thiophene immobilization. The fabricated hybrid assembly facilitated efficient charge separation, and each component endowed great synergy. As a result, a high syngas production rate was achieved over 5500 µmol gcat -1 h-1 from photocatalytic CO2 reduction under visible-light irradiation, accompanied by an adjustable H2 /CO ratio ranging from 4 : 1 to 1 : 3. A novel hybrid assembly was described for syngas synthesis with boosted activity and controlled selectivity, which provides a profile to ingeniously understand molecular-level design for photocatalysts.

Sedimentary Nitrogen and Sulfur Reduction Functional-Couplings Interplay With the Microbial Community of Anthropogenic Shrimp Culture Pond Ecosystem.

Sediment nitrogen and sulfur cycles are essential biogeochemical processes that regulate the microbial communities of environmental ecosystems, which have closely linked to environment ecological health. However, their functional couplings in anthropogenic aquaculture sedimentary ecosystems remain poorly understood. Here, we explored the sediment functional genes in shrimp culture pond ecosystems (SCPEs) at different culture stages using the GeoChip gene array approach with 16S amplicon sequencing. Dissimilarity analysis showed that the compositions of both functional genes and bacterial communities differed at different phases of shrimp culture with the appearance of temporal distance decay (p < 0.05). During shrimp culture, the abundances of nitrite and sulfite reduction functional genes decreased (p < 0.05), while those of nitrate and sulfate reduction genes were enriched (p < 0.05) in sediments, implying the enrichment of nitrites and sulfites from microbial metabolism. Meanwhile, nitrogen and sulfur reduction genes were found to be linked with carbon degradation and phosphorous metabolism (p < 0.05). The influence pathways of nutrients were demonstrated by structural equation modeling through environmental factors and the bacterial community on the nitrogen and sulfur reduction functions, indicating that the bacterial community response to environmental factors was facilitated by nutrients, and led to the shifts of functional genes (p < 0.05). These results indicate that sediment nitrogen and sulfur reduction functions in SCPEs were coupled, which are interconnected with the SCPEs bacterial community. Our findings will be helpful for understanding biogeochemical cycles in anthropogenic aquaculture ecosystems and promoting sustainable management of sediment environments through the framework of an ecological perspective.

The dynamic changes in autophagy activity and its role in lung injury after deep hypothermic circulatory arrest.

Deep hypothermic circulatory arrest (DHCA) can cause acute lung injury (ALI), and its pathogenesis mimics ischaemia/reperfusion (I/R) injury. Autophagy is also involved in lung I/R injury. The present study aimed to elucidate whether DHCA induces natural autophagy activation and its role in DHCA-mediated lung injury. Here, rats were randomly assigned to the Sham or DHCA group. The sham group (n = 5) only received anaesthesia and air intubation. DHCA group rats underwent cardiopulmonary bypass (CPB) followed by the DHCA procedure. The rats were then sacrificed at 3, 6 and 24 h after the DHCA procedure (n = 5) to measure lung injury and autophagy activity. Chloroquine (CQ) was delivered to evaluate autophagic flux. DHCA caused lung injury, which was prominent 3-6 h after DHCA, as confirmed by histological examination and inflammatory cytokine quantification. Lung injury subsided at 24 h. Autophagy was suppressed 3 h but was exaggerated at 6 h. At both time points, autophagic flux appeared uninterrupted. To further assess the role of autophagy in DHCA-mediated lung injury, the autophagy inducer rapamycin and its inhibitor 3-methyladenine (3-MA) were applied, and lung injury was reassessed. When rapamycin was administered at an early time point, lung injury worsened, whereas administration of 3-MA at a late time point ameliorated lung injury, indicating that autophagy contributed to lung injury after DHCA. Our study presents a time course of lung injury following DHCA. Autophagy showed adaptive yet protective suppression 3 h after DHCA, as induction of autophagy caused worsening of lung tissue. In contrast, autophagy was exaggerated 6 h after DHCA, and autophagy inhibition attenuated DHCA-mediated lung injury.