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The rafting of the microstructure of Ni-based superalloys significantly deteriorates the mechanical properties. According to the plastic rafting model based on the dislocation mechanism, the directional atomic diffusion induced by the interaction between the alloying atom and the interfacial dislocation is critical to the evolution of the rafting microstructure. In the present work, the interactions between the alloying atom and dislocation core in both matrix γ phase and the precipitate γ′ phase are investigated by using a first principles method in combination with the semi-discrete variational Peierls-Nabarro dislocation model. We show that the alloying atoms Al, Cr, Co, Mo, Ru, Ta, W, Re lower the (edge for Cr and Co) dislocation core energy in the γ phase, indicating that the alloying atoms are attractive to the dislocation core. For the γ′ phase, Cr, Mo, Ta, W, Re raise whereas Co and Ru lower the dislocation core energy, i.e., Cr, Mo, Ta, W, Re are repulsive but Co and Ru are attractive to the dislocation core. With the calculated interaction between the alloying atoms and the dislocation core, the influence of these alloying elements on the rafting of the superalloy is discussed.

High alkaline environment can lead to respiratory alkalosis and ammonia toxification to freshwater fish. However, the Amur ide (Leuciscus waleckii), which inhabits an extremely alkaline lake in China with titratable alkalinity up to 53.57 mM (pH 9.6) has developed special physiological and molecular mechanisms to adapt to such an environment. Nevertheless, how the Amur ide can maintain acid-base balance and perform ammonia detoxification effectively remains unclear. Therefore, this study was designed to study the ammonia excretion rate (Tamm), total nitrogen accumulation in blood and tissues, including identification, expression, and localization of ammonia-related transporters in gills of both the alkali and freshwater forms of the Amur ide. The results showed that the freshwater form Amur ide does not have a perfect ammonia excretion mechanism exposed to high-alkaline condition. Nevertheless, the alkali form of Amur ide was able to excrete ammonia better than freshwater from Amur ide, which was facilitated by the ionocytes transporters (Rhbg, Rhcg1, Na+/H+ exchanger 2 (NHE2), and V-type H+ ATPase (VHA)) in the gills. Converting ammonia into urea served as an ammonia detoxication strategy to reduced endogenous ammonia accumulation under high-alkaline environment.

Abstract Background Perioperative neurocognitive disorders (PND), such as delirium and cognitive impairment, are commonly encountered complications in aged patients. The inhibitory neurotransmitter γ-aminobutyric acid (GABA) is aberrantly synthesized from reactive astrocytes following inflammatory stimulation and is implicated in the pathophysiology of neurodegenerative diseases. Additionally, the activation of NOD-like receptor protein 3 (NLRP3) inflammasome is involved in PND. Herein, we aimed to investigate whether the NLRP3–GABA signaling pathway contributes to the pathogenesis of aging mice’s PND. Methods 24-month-old C57BL/6 and astrocyte-specific NLRP3 knockout male mice were used to establish a PND model via tibial fracture surgery. The monoamine oxidase-B (MAOB) inhibitor selegiline (1 mg/kg) was intraperitoneally administered once a day for 7 days after the surgery. PND, including impulsive-like behaviors and cognitive impairment, was evaluated by open field test, elevated plus maze, and fear conditioning. Thereafter, pathological changes of neurodegeneration were explored by western blot and immunofluorescence assays. Results Selegiline administration significantly ameliorated TF-induced impulsive-like behaviors and reduced excessive GABA production in reactive hippocampal astrocytes. Moreover, astrocyte-specific NLRP3 knockout mice reversed TF-induced impulsive-like and cognitive impairment behaviors, decreased GABA levels in reactive astrocytes, ameliorated NLRP3-associated inflammatory responses during the early stage, and restored neuronal degeneration in the hippocampus. Conclusions Our findings suggest that anesthesia and surgical procedures trigger neuroinflammation and cognitive deficits, which may be due to NLRP3–GABA activation in the hippocampus of aged mice.

Context Ursolic acid (UA) and acteoside (ATS) are important active components that have been used to treat Alzheimer’s disease (AD) because of their neuroprotective effects, but the exact mechanism is still unclear.Objective Network pharmacology was used to explore the mechanism of UA + ATS in treating AD, and cell experiments were used to verify the mechanism.Materials and methods UA + ATS targets and AD-related genes were retrieved from TCMSP, STITCH, SwissTargetPrediction, GeneCards, DisGeNET and GEO. Key targets were obtained by constructing protein interaction network through STRING. The neuroprotective effects of UA + ATS were verified in H2O2-treated PC12 cells. The subsequent experiments were divided into Normal, Model (H2O2 pre-treatment for 4 h), Control (H2O2+ solvent pre-treatment), UA (5 μM), ATS (40 μM), UA (5 μM) + ATS (40 μM). Then apoptosis, mitochondrial membrane potential, caspase-3 activity, ATG5, Beclin-1 protein expression and Akt, mTOR phosphorylation levels were detected.Results The key targets of UA + ATS-AD network were mainly enriched in Akt/mTOR pathway. Cell experiments showed that UA (ED50: 5 μM) + ATS (ED50: 40 μM) could protect H2O2-induced (IC50: 250 μM) nerve damage by enhancing cells viability, combating apoptosis, restoring MMP, reducing the activation of caspase-3, lessening the phosphorylation of Akt and mTOR, and increasing the expression of ATG5 and Beclin-1.Conclusions ATS and UA regulates multiple targets, bioprocesses and signal pathways against AD pathogenesis. ATS and UA synergistically protects H2O2-induced neurotrosis by regulation of AKT/mTOR signalling.

Abstract Metal nanoclusters (NCs) are ultrasmall molecular aggregates consisting of dozens to hundreds of metal atoms consolidated by organic ligands, which represent an emerging area of nanoscience. Amide a myriad of metal NCs, copper NCs (CuNCs) comprise a low‐cost, high‐value subclass that has attracted great attention. The variable copper cores and diversity of protecting ligands have rendered CuNCs interesting molecular aggregates featuring structural and compositional versatility, hence showing distinctive properties and potential applications. In the present review, we have summarized the progress on atomically precise CuNCs that exhibit a range of appealing properties and applications in different fields. This review is expected to provide not only an overview of the current development on atomically precise CuNCs, but also possible directions for the future design of novel CuNCs for fundamental studies and practical applications.

Summary: Time-restricted eating (TRE) is known to improve metabolic health, whereas very few studies have compared the effects of early and late TRE (eTRE and lTRE) on metabolic health. Overweight and obese young adults were randomized to 6-h eTRE (eating from 7 a.m. to 1 p.m.) (n = 21), 6-h lTRE (eating from 12 p.m. to 6 p.m.) (n = 20), or a control group (ad libitum intake in a day) (n = 19). After 8 weeks, 6-h eTRE and lTRE produced comparable body weight loss compared with controls. Compared with control, 6-h eTRE reduced systolic blood pressure, mean glucose, fasting insulin, insulin resistance, leptin, and thyroid axis activity, whereas lTRE only reduced leptin. These findings shed light on the promise of 6-h eTRE and lTRE for weight loss. Larger studies are needed to assess the promise of eTRE to yield better thyroid axis modulation and overall cardiometabolic health improvement.

Parental effects can influence offspring fitness, which may further impact interspecific competition. However, few studies have tested the role of clonal parental effects in regulating interspecific interactions and examined the underlying mechanisms. We conducted two consecutive experiments with two clonal plants (Pistia stratiotes and Eichhornia crassipes). In the first experiment, the mother ramet of P. stratiotes and E. crassipes were grown in two nutrient levels and treated with a DNA demethylation reagent (5-azacytidine) or not. In the second experiment, the offspring ramets from each of the four treatments in the first experiment were grown alone (no competition) or with a heterospecific neighbor (with interspecific competition). We found no parental nutrient effect on the competitive ability of E. crassipes, but a significant parental nutrient effect of both E. crassipes and P. stratiotes on the competitive ability of P. stratiotes. Furthermore, the parental nutrient effect of P. stratiotes on the competitive ability of P. stratiotes varied depending on the DNA methylation status of both P. stratiotes and E. crassipes. These clonal parental effects were related to resource provisioning and/or DNA methylation. We conclude that clonal parental nutrient effects can regulate interspecific competition between P. stratiotes and E. crassipes by altering the competitive ability of P. stratiotes. Both resource provisioning and epigenetic mechanisms can be involved in these clonal parental effects. By regulating interspecific competition, clonal parental effects may further influence species coexistence, community structure, and ecosystem functioning.

Parental (environmental) effects can modify the growth of offspring, which may play an essential role in their adaptation to environmental variation. While numerous studies have tested parental effects on offspring growth, most have considered offspring growth of only one generation and very few have considered offspring growth of different generations. We conducted a greenhouse experiment with an aquatic clonal plant Pistia stratiotes. We grew a single ramet of P. stratiotes under low or high nutrients, the initial (parent) ramets produced three different generations of offspring ramets, and these offspring ramets were also subjected to the same two nutrient levels. High nutrients currently experienced by the offspring increased biomass accumulation and ramet number of all three offspring generations of P. stratiotes. However, these positive effects on biomass were greater when the offspring ramets originated from the parent ramets grown under low nutrients than when they were produced by the parent ramets grown under high nutrients. These results suggest that parental effects can impact the performance of different offspring generations of clonal plants. However, heavier offspring ramets produced under high nutrients in parental conditions did not increase the subsequent growth of the offspring generations. This finding indicates that parental provisioning in favorable conditions may not always increase offspring growth, partly depending on root allocation but not ramet size such as ramet biomass.

Nutrients are often released heterogeneously over time (e.g., in pulses) in natural habitats. Different genotypes of the same plant species may vary in their responses to temporal nutrient heterogeneity so that temporal nutrient heterogeneity may influence intraspecific interactions. To test effects of temporal nutrient heterogeneity on intra-genet (competition between ramets of the same genotype) and inter-genet competition (competition between ramets of different genotypes), we conducted a greenhouse experiment with five genotypes of the clonal herb Hydrocotyle vulgaris. We grew one ramet (no competition), two ramets of the same genotype or two ramets of different genotypes in a pot and supplied the pot with the same total amount of nutrients either homogeneously or heterogeneously. Results showed that temporal nutrient heterogeneity affected the growth and biomass allocation of some genotypes, but had no impact on those of other genotypes of H. vulgaris. These suggested that responses to temporal nutrient heterogeneity were different between genotypes of H. vulgaris. Temporal nutrient heterogeneity had little effect on intra-genet competition of H. vulgaris likely because ramets of the same genotype did not differ in their responses to temporal nutrient heterogeneity. However, temporal nutrient heterogeneity increased the competitive ability of the genotype of H. vulgaris with higher plant productivity. We conclude that temporal nutrient heterogeneity can influence intraspecific interactions of the clonal plant H. vulgaris by altering inter-genet competition, and this effect may further change population dynamics of the plant.

Many plant species forage for nutrients by accumulating more biomass or ramets where soil nutrient availability is high. Nutrient foraging ability differs between species and between genotypes within species, can increase plant performance when nutrients are patchy, and may lead to differences in competitive ability and have community-level effects. Effects of intraspecific variation in nutrient foraging ability could be particularly strong in clonal species, in which individual genotypes can form large clones and persist for long times. We tested the hypotheses that clones with greater foraging ability (1) have greater ability to compete with other clones of the same species but (2) experience greater competition within a clone. Sets of clonal fragments of five clones of the perennial, creeping herb Hydrocotyle vulgaris were grown alone, with a fragment of a different clone, or with a second fragment of the same clone in pots with a uniform or patchy distribution of soil nutrients. Consistent with the first hypothesis, foraging ability and between-clone competitiveness as measured by less negative competitive response were positively related when nutrients were patchy but not when they were uniform. Contrary to the second hypothesis, foraging and within-clone competitiveness were negatively related. Intraspecific competition both between and within clones could thus select for greater foraging ability. If this in turn increases ability to compete with other species, it may help explain the dominance of some clonal species.

PurposePost hemorrhagic shock mesenteric lymph (PHSML) return contributes to CD4+ T cell dysfunction, which leads to immune dysfunction and uncontrolled inflammatory response. Tumor necrosis factor α induced protein 8 like-2 (TIPE2) is one of the essential proteins to maintain the immune homeostasis. This study investigated the role of TIPE2 in regulation of CD4+ T lymphocyte function in interaction of PHSML and TLR2/TLR4.MethodsThe splenic CD4+ T cells were isolated from various mice (WT, TLR2-/-, TLR4-/-) by immunomagnetic beads, and stimulated with PHSML, normal lymphatic fluid (NML), respectively. Application of TIPE2-carrying interfering fragments of lentivirus were transfected to WT, TLR4-/-, and TLR2-/- CD4+ T cells, respectively. After interference of TIPE2, they were stimulated with PHSML and NML for the examinations of TIPE2, TLR2, and TLR4 mRNA expressions, proliferation, activation molecules on surface, and cytokine secretion function.ResultsPHSML stimulation significantly upregulated TIPE2, TLR2, and TLR4 mRNA expressions, decreased proliferation, CD25 expression, and IFN-γ secretion, and increased the secretion ability of IL-4 in WT CD4+ T cells. TIPE2 silencing enhanced proliferative capacity, upregulated CD25 expression, and increased IFNγ secretion in CD4+ T cells. PHSML stimulated TLR2-/-CD4+ T or TLR4-/-CD4+ T cells of which TIPE2 were silenced. TLR2 or TLR4 knockout attenuated PHSML-induced CD4+ T cells dysfunction; PHSML stimulation of silent TIPE2-expressing TLR2-/-CD4+ T or TLR4-/-CD4+ T revealed that the coexistence of low TIPE2 expression with lack of TLR2 or TLR4 eliminated this beneficial effect.ConclusionTIPE2 improves the PHSML-mediated CD4+T cells dysfunction by regulating TLR2/TLR4 pathway, providing a new intervention target following hemorrhagic shock-induced immune dysfunction.

AIM: To observe the application of light emitting diode(LED)irradiation in rat retinal vascular endothelial cells with high glucose and its effect and mechanism on photobioregulation. METHODS:Rat retinal vascular endothelial cells were randomly divided into three groups: normal control group, high glucose model group, high glucose model light emitting diode irradiation group, and cells in the high glucose model light emitting diode group began to use light emitting diodes in the incubator 48h after modeling. The cells are irradiated. MTT cell apoptosis experiment was used to detect the apoptosis rate of each group; laser confocal microscope was used to observe the changes of intracellular calcium in retinal vascular endothelial cells; Western blot was used to detect the phosphorylated serine-threonine kinase(P-AKT)protein in each group expression.RESULTS: The apoptosis rates of normal control group, high glucose model group, and high glucose model light emitting diode irradiation group were 7.54%±2.67%, 31.69%±5.74%, and 21.65%±3.52%, respectively(P2+ fluorescence showed green fluorescence with a pixel value of 192.65±50.54. In the high-sugar model group, the cytoplasm showed a stronger green fluorescence with a fluorescent pixel value of 710.69±100.38. The green fluorescent pixel value was 430.47±80.67, which was significantly higher than the normal control group, but significantly lower than the high-sugar model group. The intra-Ca2+ fluorescence pixel values in the three groups were statistically significant(PPCONCLUSION: High-glucose environment inhibits the activity of threonine kinase pathway, which has an effect on calcium homeostasis of rat retinal vascular endothelial cells and promotes apoptosis. Low-intensity led irradiation can activate threonine kinase pathway and reduce the apoptosis rate caused by high glucose, which is of great application value.

Abstract Background Catechins, caffeine, and theanine as three important metabolites in the tea leaves play essential roles in the formation of specific taste and shows potential health benefits to humans. However, the knowledge on the dynamic changes of these metabolites content over seasons, as well as the candidate regulatory factors, remains largely undetermined. Results An integrated transcriptomic and metabolomic approach was used to analyze the dynamic changes of three mainly metabolites including catechins, caffeine, and theanine, and to explore the potential influencing factors associated with these dynamic changes over the course of seasons. We found that the catechins abundance was higher in Summer than that in Spring and Autumn, and the theanine abundance was significantly higher in Spring than that in Summer and Autumn, whereas caffeine exhibited no significant changes over three seasons. Transcriptomics analysis suggested that genes in photosynthesis pathway were significantly down-regulated which might in linkage to the formation of different phenotypes and metabolites content in the tea leaves of varied seasons. Fifty-six copies of nine genes in catechins biosynthesis, 30 copies of 10 genes in caffeine biosynthesis, and 12 copies of six genes in theanine biosynthesis were detected. The correlative analysis further presented that eight genes can be regulated by transcription factors, and highly correlated with the changes of metabolites abundance in tea-leaves. Conclusion Sunshine intensity as a key factor can affect photosynthesis of tea plants, further affect the expression of major Transcription factors (TFs) and structural genes in, and finally resulted in the various amounts of catechins, caffeine and theaine in tea-leaves over three seasons. These findings provide new insights into abundance and influencing factors of metabolites of tea in different seasons, and further our understanding in the formation of flavor, nutrition and medicinal function.

Abstract Background Shanzhuyu (the dried mature sarcocarp of Cornus officinalis Sieb. et Zucc., DMSCO) is a Chinese herb that can be used for the treatment of Alzheimer’s disease (AD), but its mechanism remains unknown. The present study aimed to investigate the active ingredients and effective mechanisms of DMSCO for the treatment of AD based on a network pharmacology approach. Methods The active components of DMSCO were collected from the TCMSP and ETCM databases and the target proteins of these compounds were predicted using TCMSP, SwissTargetPrediction and the STITCH database. The AD-related target proteins were identified from the OMIM, DisGeNet, GEO and GeneCards databases. The network interaction model of the compound-target-disease was established and was used to obtain the key targets of DMSCO on AD through network topology analysis. Subsequently, gene enrichment in Gene Ontology (GO) and KEGG pathways were conducted using the David 6.8 online tool. Results A total of 30 DMSCO effective compounds and 209 effective drug targets were obtained. A total of 172 AD-related genes and 37 shared targets of DMSCO and AD were identified. A total of 43 key targets for the treatment of AD were obtained from the topological analysis of the DMSCO-AD target network. These key targets were involved in a variety of biological processes, including amyloid deposition, apoptosis, autophagy, inflammatory response and oxidative stress and pathways, such as the PI3K-AKT, MAPK and TNF pathways. Three key compounds, namely ursolic acid, anethole and β-sitosterol were obtained from the analysis of the key targets. Conclusions Ursolic acid, anethole and β-sitosterol may be the main active components of DMSCO in the treatment of AD. DMSCO can treat AD by regulating amyloid deposition, apoptosis, autophagy, inflammatory response and oxidative stress via the PI3K-AKT, MAPK and other signaling pathways.

Abstract Background Oxidative stress mediates the nerve injury during the pathogenesis of Alzheimer’s disease (AD). Protecting against oxidative stress damage is an important strategy to prevent and treat AD. Di-Huang-Yi-Zhi (DHYZ) is a Chinese medicine used for the treatment of AD, but its mechanism remains unknown. This study is aimed to investigate the effect of DHYZ on H2O2 induced oxidative damage in PC12 cells. Methods PC12 cells were treated with H2O2 and DHYZ. Cell proliferation was detected by Cell counting kit-8 (CCK-8) assay. Cytotoxicity of H2O2 was measured by lactate dehydrogenase (LDH) release assay. Apoptosis were identified by Annexin V-FITC/PI staining. Caspase 3 activity was detected by commercial kit. Mitochondrial membrane potential (MMP) was detected by JC-1 staining. Reactive oxygen species (ROS) was 2′, 7′-Dichlorodihydrofluorescein diacetate (DCFH-DA) staining. Protein expression and phosphorylation was identified by western blot. Results The results showed that DHYZ antagonized H2O2-mediated cytotoxicity and proliferation inhibition. DHYZ reduced ROS production, stabilize mitochondrial membrane potential, inhibit Caspase-3 activity and apoptosis induced by H2O2. In addition, DHYZ inhibited the phosphorylation of ASK1, JNK1/2/3 and p38 MAPK which were up-regulated by H2O2. Conclusions The present study suggested that DHYZ protected PC12 cells from H2O2-induced oxidative stress damage and was related to inhibition of ROS production and ASK1-JNK/p38 MAPK signaling. The present study provides experimental evidence for the application of DHYZ for the management of oxidative stress damage and AD.

The potato tuber moth (PTM), Phthorimaea operculella (Zeller), is one of the most economically significant insect pests for potato in both field and storage worldwide. To evaluate the infestation, reduction of potato yield and the control efficacy for PTM, field tests were conducted in two seasons by intercropping of potato as the host plant with maize as a non-host plant of PTM. Three intercropping patterns were tested, which were 2 rows of potatoes with either 2, 3, or 4 rows of maize (abbreviated 2P:2M, 2P:3M, and 2P:4M), and the monocropped potato as the control, 2 rows of potatoes, without maize, (abbreviated 2P:0M). Results showed that the population and infestation of PTM in the 2P:3M intercropping pattern was significantly lower than those in 2P:2M, 2P:4M and the monocropping pattern of 2P:0M, due to the enhancement of natural enemies. Cumulative mines and tunneling in potato leaves in 2P:3M intercropping were significantly lower than those in 2P:2M and 2P:4M patterns. The population of parasitoids and the parasitism rate of PTM in intercropping pattern of 2P:3M were significantly higher than that in intercropping pattern of 2P:2M, 2P:4M and monocropping pattern of 2P:0M. We conclude that the potato intercropped with maize reduced the adult and larva populations, and reduced the damage from PTM by enhancing the number of parasitoids and the level of parasitism. The greatest population density of parasitoids and parasitism rate were in the intercropping pattern of 2 rows of potatoes with 3 rows of maize. These data indicate that the host/non-host intercropping patterns can be used as a biological control tactic against PTM by enhancing the density of natural enemies in the agro-ecosystems.

Abstract Background In sorghum (Sorghum bicolor), one paramount breeding objective is to increase grain quality. The nutritional quality and end use value of sorghum grains are primarily influenced by the proportions of tannins, starch and proteins, but the genetic basis of these grain quality traits remains largely unknown. This study aimed to dissect the natural variation of sorghum grain quality traits and identify the underpinning genetic loci by genome-wide association study. Results Levels of starch, tannins and 17 amino acids were quantified in 196 diverse sorghum inbred lines, and 44 traits based on known metabolic pathways and biochemical interactions amongst the 17 amino acids calculated. A Genome-wide association study (GWAS) with 3,512,517 SNPs from re-sequencing data identified 14, 15 and 711 significant SNPs which represented 14, 14, 492 genetic loci associated with levels of tannins, starch and amino acids in sorghum grains, respectively. Amongst these significant SNPs, two SNPs were associated with tannin content on chromosome 4 and colocalized with three previously identified loci for Tannin1, and orthologs of Zm1 and TT16 genes. One SNP associated with starch content colocalized with sucrose phosphate synthase gene. Furthermore, homologues of opaque1 and opaque2 genes associated with amino acid content were identified. Using the KEGG pathway database, six and three candidate genes of tannins and starch were mapped into 12 and 3 metabolism pathways, respectively. Thirty-four candidate genes were mapped into 16 biosynthetic and catabolic pathways of amino acids. We finally reconstructed the biosynthetic pathways for aspartate and branched-chain amino acids based on 15 candidate genes identified in this study. Conclusion Promising candidate genes associated with grain quality traits have been identified in the present study. Some of them colocalized with previously identified genetic regions, but novel candidate genes involved in various metabolic pathways which influence grain quality traits have been dissected. Our study acts as an entry point for further validation studies to elucidate the complex mechanisms controlling grain quality traits such as tannins, starch and amino acids in sorghum.

The functional role of procyanidins (PC) in PM2.5-induced cardiovascular diseases (CVD) is largely unexplored. This study aimed to explore the protective effect of PC against PM2.5-induced vascular smooth muscle cells (VSMCs) apoptosis and underlying mechanisms. Sprague Dawley rats were pretreated with three doses of PC (50, 100, and 200 mg/kg) and exposed to 10 mg/kg PM2.5 by intratracheal instillation three times a week. VSMCs were exposed to 5, 10, and 20 μM PC before the addition of 100 μg/mL PM2.5. In vivo, the PM2.5 exposure induced apoptosis in the thoracic aorta of rats. The PM2.5 exposure significantly elevated the reactive oxygen species (ROS) and malondialdehyde (MDA) levels and decreased the superoxide dismutase activity. Also, PC supplementation increased the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), and its downstream antioxidant genes, i.e., NAD(P)H dehydrogenase (quinine) 1 and heme oxygenase 1, attenuated oxidative stress and vascular apoptosis. In vitro, PM2.5 induced cytotoxicity in VSMCs in a dose-dependent manner. Besides, PC abolished the PM2.5-induced cytotoxicity by activating the Nrf2 signal pathway, alleviating oxidative stress, and decreasing apoptosis. In conclusion, this work is the first study to demonstrate that PC can suppress the PM2.5-induced VSMCs apoptosis via the activation of the Nrf2 signal pathway.

The Amur ide (Leuciscus waleckii) is a fish in the Cyprinidae family. Compared with other Amur ide living in freshwater ecosystems, the Amur ide population in Lake Dali Nor of China is famous for its high tolerance to the alkaline conditions of 54 mM (pH 9.6). Yet, surprisingly, the ionoregulatory mechanism responsible for this remarkable alkaline adaptation remains unclear. Therefore, this study sought to investigate how bicarbonate affects the acid-base balancing and ionoregulatory responses of this animal. Here, using a comparative approach, the alkali form of Amur ide and its ancestral freshwater form living in other freshwater basins were each exposed to 50 mM (pH 9.59 ± 0.09), a level close to the alkalinity of Lake Dali Nor, and their physiological (AE1) adjustment of ions and acid-base regulation were investigated. This study highlighted differences in blood pH and serum ions (e.g., Na+, K+, Cl−, and Ca2+), Na+/K+ ATPase (NKA) activity and its mRNA level, and mRNA expression of gill transporters (Na+/H+ exchanger member 2 and/or 3, Na+/HCO3- cotransporter (NBC1), Cl−/HCO3- exchanger, Na+/Cl− cotransporter (NCC), Na+/K+/2Cl− (NKCC1), SLC26A5, and SLC26A6) for alkalinity adaptation between the two forms of Amur ide differing in alkalinity tolerance. Specifically, close relationships among the serum Na+ and mRNA levels of NCC, NKCC1, and NHE, and also NKA and NBC1, in addition to serum Cl− and bicarbonate transporters (e.g., SLC26A5 and SLC26A6), characterized the alkali form of Amur ide. We propose that this ecotype can ensure its transepithelial Cl− and Na+ uptake/base secretions are highly functional, by its basolateral NKA with NBC1 and apical ionic transporters, and especially NCC incorporated with other transporters (e.g., SLC26). This suggests an evolved strong ability to maintain an ion osmotic and acid-base balance for more effectively facilitating its adaptability to the high alkaline environment. This study provides new insights into the physiological responses of the alkaline form of the Amur ide fish for adapting to extreme alkaline conditions. This information could be used as a reference to cultivating alkaline-tolerant fish species in abandoned alkaline waters.

Objective: The aim of this study was to clarify the role of autophagy in stellate ganglion block (SGB) reversing posthemorrhagic shock mesenteric lymph (PHSML)-mediated vascular hyporeactivity.Methods: Hemorrhagic shock model in conscious rats was employed to observe the effects of SGB (0.2 ml of 0.25% ropivacaine hydrochloride hydrate) and autophagy inhibitor 3-methyladenine (3-MA; 30 mg/kg) on the vascular reactivity of second-order rat mesenteric arteries in vitro, while the effects of PHSML (1 ml/kg) and autophagy agonist rapamycin (Rapa, 10 mg/kg) on the beneficial effect of SGB were investigated. The cellular viability, contractility, and autophagy-related protein expressions in vascular smooth muscle cells (VSMCs) were detected following treatments of PHSML, PHSML obtained from the rats that underwent hemorrhagic shock plus SGB (PHSML-SGB), and PHSML plus 3-MA (5 mM), respectively.Results: Hemorrhagic shock significantly decreased the vascular reactivity to gradient norepinephrine (NE), which is reversed by the SGB treatment and 3-MA administration. On the contrary, PHSML intravenous infusion and Rapa administration inhibited the vascular contractile responses in rats that underwent hemorrhagic shock plus SGB treatment. PHSML treatment significantly inhibited the cellular viability and contractility in VSMCs, increased the expressions of LC3-II and Beclin 1, and decreased the expression of p62, along with opposite appearances in these indices following PHSML-SGB treatment. In addition, 3-MA counteracted the adverse roles of PHSML in these indices in VSMCs.Conclusion: SGB inhibits PHSML-mediated vascular hyporeactivity by reducing the excessive autophagy in VSMCs.

Wolbachia is a group of intracellular symbiotic bacteria that widely infect arthropods and nematodes. Wolbachia infection can regulate host reproduction with the most common phenotype in insects being cytoplasmic incompatibility (CI), which results in embryonic lethality when uninfected eggs fertilized with sperms from infected males. This suggests that CI-induced defects are mainly in paternal side. However, whether Wolbachia-induced metabolic changes play a role in the mechanism of paternal-linked defects in embryonic development is not known. In the current study, we first use untargeted metabolomics method with LC-MS to explore how Wolbachia infection influences the metabolite profiling of the insect hosts. The untargeted metabolomics revealed 414 potential differential metabolites between Wolbachia-infected and uninfected 1-day-old (1d) male flies. Most of the differential metabolites were significantly up-regulated due to Wolbachia infection. Thirty-four metabolic pathways such as carbohydrate, lipid and amino acid, and vitamin and cofactor metabolism were affected by Wolbachia infection. Then, we applied targeted metabolomics analysis with GC-MS and showed that Wolbachia infection resulted in an increased energy expenditure of the host by regulating glycometabolism and fatty acid catabolism, which was compensated by increased food uptake. Furthermore, overexpressing two acyl-CoA catabolism related genes, Dbi (coding for diazepam-binding inhibitor) or Mcad (coding for medium-chain acyl-CoA dehydrogenase), ubiquitously or specially in testes caused significantly decreased paternal-effect egg hatch rate. Oxidative stress and abnormal mitochondria induced by Wolbachia infection disrupted the formation of sperm nebenkern. These findings provide new insights into mechanisms of Wolbachia-induced paternal defects from metabolic phenotypes.

Leuciscus waleckii is a freshwater fish that is known to inhabit the Dali Nor Lake, Inner Mongolia, China. The water in this lake has an HCO3–/CO32– concentration of 54 mM (pH 9.6) and a salinity of 0.6‰. The physiological mechanisms that allow this fish to tolerate these saline/alkaline conditions have yet to be elucidated. Transcriptional component analysis has shown that the expression levels of a large number of genes involved in the pathways responsible for osmo-ionoregulation and arachidonic acid metabolism pathway expression change significantly (p < 0.05) during the regulation of acid–base balance under high alkaline stress. In this study, we investigated the role of long non-coding RNAs (lncRNAs) during adaptation to high alkaline conditions. Fish were challenged to an NaHCO3-adjusted alkalinity of 0 mM, 30 mM (pH 9.44 ± 0.08), and 50 mM (pH 9.55 ± 0.06) for 20 days in the laboratory. Gill and kidney tissues were then collected for high-throughput sequencing assays. A total of 159 million clean reads were obtained by high-throughput sequencing, and 41,248 lncRNA transcripts were identified. Of these, the mean number of exons and the mean length of the lncRNA transcripts were 4.8 and 2,079 bp, respectively. Based on the analysis of differential lncRNA transcript expression, a total of 5,244 and 6,571 lncRNA transcripts were found to be differentially expressed in the gills and kidneys, respectively. Results derived from Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of the coding genes were correlated with the lncRNA expression profiles. GO analysis showed that many lncRNAs were enriched in the following processes: “transporter activity,” “response to stimulus,” and “binding.” KEGG analysis further revealed that metabolic pathways were significantly enriched. A random selection of 16 lncRNA transcripts was tested by RT-qPCR; these results were consistent with our sequencing results. We found that a large number of genes, with the same expression profiles as those with differentially expressed lncRNAs, were associated with the regulation of acid–base balance, ion transport, and the excretion of ammonia and nitrogen. Collectively, our data indicate that lncRNA-regulated gene expression plays an important role in the process of adaptation to high alkaline conditions in L. waleckii.

This article has been retracted. Please see the Retraction Notice for more detail: https://doi.org/10.1186/s12906-020-2834-8.

Current knowledge on responses of aquatic clonal plants to resource availability is largely based on studies manipulating limited resource levels, which may have failed to capture the "big picture" for aquatic clonal plants in response to resource availability. In a greenhouse experiment, we grew the floating clonal plant Spirodela polyrhiza under ten nutrient levels (i.e., 1/64×, 1/32×, 1/16×, 1/8×, 1/4×, 1/2×, 1×, 2×, 4× and 8×full-strength Hoagland solution) and examined their responses in terms of clonal growth, morphology and biomass allocations. The responses of total biomass and number of ramets to nutrient availability were unimodal. A similar pattern was found for frond mass, frond length and frond width, even though area per frond and specific frond area fluctuated greatly in response to nutrient availability. In contrast, the responses of root mass and root length to nutrient availability were U-shaped. Moreover, S. polyrhiza invested more to roots under lower nutrient concentrations. These results suggest that nutrient availability may have distinct influences on roots and fronds of the aquatic clonal plant S. polyrhiza, resulting in a great influence on the whole S. polyrhiza population.

ObjectiveThe mechanisms by which exposure of the late-stage progenitor cells to the anesthesia sevoflurane alters their differentiation are not known. We seek to query whether the effects of sevoflurane on late-stage progenitor cells might be regulated by apoptosis and/or autophagy.MethodsTo address the short-term impact of sevoflurane exposure on granule cell differentiation, we used 5-bromo-2-deoxyuridine (BrdU) to identify the labeled late-stage progenitor granule cells. Male or female rats were exposed to 3% sevoflurane for 4 h when the labeled granule cells were 2 weeks old. Differentiation of the BrdU-labeled granule cells was quantified 4 and 7 days after exposure by double immunofluorescence. The expression of apoptosis and autophagy in hippocampal dentate gyrus (DG) was determined by western blot and immunofluorescence. Western blot for the expression of NF-κB was used to evaluate the mechanism. Morris water maze (MWM) test was performed to detect cognitive function in the rats on postnatal 28–33 days.ResultsExposure to sevoflurane decreased the differentiation of the BrdU-labeled late-stage progenitor granule cells, but increased the expression of caspase-3, autophagy, and phosphorylated-P65 in the hippocampus of juvenile rats and resulted in cognitive deficiency. These damaging effects of sevoflurane could be mitigated by inhibitors of autophagy, apoptosis, and NF-κB. The increased apoptosis could be alleviated by pretreatment with the autophagy inhibitor 3-MA, and the increased autophagy and apoptosis could be reduced by pretreatment with NF-κB inhibitor BAY 11-7085.ConclusionThese findings suggest that a single, prolonged sevoflurane exposure could impair the differentiation of late-stage progenitor granule cells in hippocampal DG and cause cognitive deficits possibly via apoptosis activated by autophagy through NF-κB signaling. Our results do not preclude the possibility that the affected differentiation and functional deficits may be caused by depletion of the progenitors pool.

Vascular endothelial injury caused by post-hemorrhagic shock mesenteric lymph (PHSML) return is an important manifestation during refractory hemorrhagic shock. Using human umbilical vein endothelial cells (HUVECs) and transcriptome analysis, this study sought to investigate the molecular mechanism underlying the adverse effect of PHSML on vascular endothelium. Post-hemorrhagic shock mesenteric lymph was collected from male rats after they underwent hemorrhagic shock and following resuscitation, while normal mesenteric lymph (NML) was harvested from sham rats. Human umbilical vein endothelial cells were incubated with the culture medium containing either 10% phosphate buffered saline (Control), NML, or PHSML for 3 h, and then were harvested for RNA sequencing. In comparison with NML treated cells, 37 genes were differentially expressed in PHSML-treated HUVECs, including 32 upregulated genes and five downregulated genes. These differentially expressed genes were mainly enriched in inflammatory pathways, including signaling pathways for activation of the NOD-like receptors, NF-κB, and TNF. Furthermore, we found that C–C motif chemokine ligand 2 (CCL2) was increased significantly after PHSML treatment, and Bindarit, a CCL2 production inhibitor, attenuated the damage of HUVECs induced by PHSML. The results provide molecular evidence on vascular endothelium damage caused by PHSML. C–C motif chemokine ligand 2 might represent a new target for reducing vascular injury after severe hemorrhagic shock.

Connected ramets of aquatic clonal plants are susceptible to fragmentation by disturbance. Such clonal fragmentation may interact with nutrient availability and individual density to affect growth and morphology of aquatic clonal plants. We grew the widespread floating clonal plant Spirodela polyrhiza (duckweed) under three levels of population density (low, medium, or high), two levels of nutrient availability (low or high), and two levels of clonal fragmentation (with or without). Clonal fragmentation and high nutrients increased biomass and ramet number, but decreased frond width, frond length, and specific frond area of S. polyrhiza. Increasing population density decreased growth (biomass and ramet number) and frond and root size, and increased frond thickness of individual ramets of S. polyrhiza. The negative effect of population density on growth of S. polyrhiza was greater under high than under low nutrient availability. Furthermore, the negative effect of population density on total mass and frond mass of S. polyrhiza was greater with fragmentation than without. These results suggest that clonal fragmentation, nutrient availability and population density can interact to affect growth and morphology of clonal floating plants. Competition for nutrients and space, rather than light, may be the mechanisms underlying reduced growth of clonal floating plants. As clonal fragmentation can increase biomass and ramet production of S. polyrhiza, disturbance that potentially causes clonal fragmentation cannot be recommended as a measure to limit the spread of clonal floating plants.

Historical geology, climatic oscillations, and seed dispersal capabilities are thought to influence the population dynamics and genetics of plants, especially for distribution-restricted and threatened species. Investigating the genetic resources within and among taxa is a prerequisite for conservation management. The Cycas taiwaniana complex consists of six endangered species that are endemic to South China. In this study, we investigated the relationship between phylogeographic history and the genetic structure of the C. taiwaniana complex. To estimate the phylogeographic history of the complex, we assessed the genetic structure and divergence time, and performed phylogenetic and demographic historical analyses. Two chloroplast DNA intergenic regions (cpDNA), two single-copy nuclear genes (SCNGs), and six microsatellite loci (SSR) were sequenced for 18 populations. The SCNG data indicated a high genetic diversity within populations, a low genetic diversity among populations, and significant genetic differentiation among populations. Significant phylogeographical structure was detected. Structure and phylogenetic analyses both revealed that the 18 populations of the C. taiwaniana complex have two main lineages, which were estimated to diverge in the Middle Pleistocene. We propose that Cycas fairylakea was incorporated into Cycas szechuanensis and that the other populations, which are mainly located on Hainan Island, merged into one lineage. Bayesian skyline plot analyses revealed that the C. taiwaniana complex experienced a recent decline, suggesting that the complex probably experienced a bottleneck event. We infer that the genetic structure of the C. taiwaniana complex has been affected by Pleistocene climate shifts, sea-level oscillations, and human activities. In addition to providing new insights into the evolutionary legacy of the genus, the genetic characterizations will be useful for the conservation of Cycas species.

Abstract Background Abnormal expression of major histocompatibility complex class I (MHC-I) is increased in dopaminergic (DA) neurons in the substantia nigra (SN) in Parkinson’s disease (PD). Low-molecular-mass protein 7 (β5i) is a proteolytic subunit of the immunoproteasome that regulates protein degradation and the MHC pathway in immune cells. Methods In this study, we investigated the role of β5i in DA neurons using a 6-hydroxydopamine (6-OHDA) model in vitro and vivo. Results We showed that 6-OHDA upregulated β5i expression in DA neurons in a concentration- and time-dependent manner. Inhibition and downregulation of β5i induced the expression of glucose-regulated protein (Bip) and exacerbated 6-OHDA neurotoxicity in DA neurons. The inhibition of β5i further promoted the activation of Caspase 3-related pathways induced by 6-OHDA. β5i also activated transporter associated with antigen processing 1 (TAP1) and promoted MHC-I expression on DA neurons. Conclusion Taken together, our data suggest that β5i is activated in DA neurons under 6-OHDA treatment and may play a neuroprotective role in PD.

Abstract Purpose: To investigate the effect of mesenteric lymph drainage on the spleen injury and the expressions of inflammatory cytokines in splenic tissue in mice following hemorrhagic shock. Methods: Male C57 mice were randomly divided into the sham shock, shock and shock+drainage groups. The mice in both shock and shock+drainage groups suffered femoral artery bleeding, maintained mean arterial pressure (MAP) of 40±2 mmHg for 90 min, and were resuscitated. And mesenteric lymph drainage was performed in the shock+drainage group at the time of resuscitation. After three hours of resuscitation, the splenic tissues were harvested for the histological observation and protein and mRNA expression analysis of cytokines. Results: The spleen in the shock group revealed a significantly structural damage and increased mRNA expressions of MyD88 and TRAF6 and protein expressions of TIPE2, MyD88, TRIF and TRAF3 compared to the sham group. By contrast, the splenic pathological injury in the shock+drainage group was alleviated significantly, and the mRNA and protein expressions of TIPE2, MyD88, TRIF, TRAF3 and TRAF6 were significantly lower than those in the shock group. Conclusion: These results indicate that post-hemorrhagic shock mesenteric lymph drainage alleviates hemorrhagic shock-induced spleen injury and the expressions of inflammatory cytokines.

We successfully employed bisphenol A and several different formyl-containing monomers as useful building blocks to construct a series of hydroxy-group-containing porous organic polymers in a sealed tube at high temperature. Fourier transform infrared and solid-state 13C CP/MAS NMR spectroscopy are utilized to characterize the possible structure of the obtained polymers. The highest Brunauer–Emmet–Teller specific surface area of the phenolic-resin porous organic polymers (PPOPs) is estimated to be 920 m2 g–1. The PPOPs exhibit a highest carbon dioxide uptake (up to 15.0 wt % (273 K) and 8.8 wt % (298 K) at 1.0 bar), and possess moderate hydrogen storage capacities ranging from 1.28 to 1.04 wt % (77 K) at 1.0 bar. Moreover, the highest uptake of methane for the PPOPs is measured as 4.3 wt % (273 K) at 1.0 bar.