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Nucleic acid nanomaterials with good biocompatibility, biodegradability, and programmability have important applications in biomedical field. Nucleic acid nanomaterials are usually combined with some inorganic nanomaterials to improve their biological stability. However, undefined toxic side effects of composite nanocarriers hamper their application in vivo. As a nanotool capable of avoiding potential biotoxicity, nanostructures composed entirely of DNA oligonucleotides have been rapidly developed in the field of biomedicine in recent years. Rolling circle amplification (RCA) is an isothermal enzymatic nucleic acid amplification technology for large-scale production of periodic DNA/RNA with pre-designed desirable structures and functions. RCA products with different functional parts can be customized by changing the sequence of the circular template, thereby generating complex multifunctional DNA nanostructures, such as DNA nanowire, nanoflower, origami, nanotube, nanoribbon, etc. More importantly, RCA products as nonnicked building blocks can enhance the biostability of DNA nanostructures, especially in vivo. These RCA products-based nucleic acid nanostructures can be used as scaffolds or nanocarriers to interact or load with metal nanoparticles, proteins, lipids, cationic polymers, therapeutic nucleic acids or drugs, etc. This paper reviews the assembly strategies of RCA based DNA nanostructures with different shape and their applications in biosensing, bioimaging and biomedicine. Finally, the development prospects of the nucleic acid nanomaterials in clinical diagnosis and treatment of diseases are described. As a nanotool capable of avoiding potential biotoxicity, nanostructures composed entirely of DNA oligonucleotides have been rapidly developed in the field of biomedicine in recent years. Rolling circle amplification (RCA) is an isothermal enzymatic nucleic acid amplification technology for large-scale production of periodic DNA/RNA with pre-designed desirable structures and functions. This paper reviews the construction of various shapes of pure nucleic acid nanomaterials based on RCA products and their applications in biosensing, bioimaging and biomedicine. This will promote the development of biocompatible DNA nanovehicles and their further application in living systems, including bioimaging, molecular detection, disease diagnosis and drug delivery, finally producing a significant impact in the field of nanotechnology and nanomedicine. [Display omitted] [ABSTRACT FROM AUTHOR]

The Ulva prolifera bloom is considered one of the most serious ecological disasters in the Yellow Sea in the past decade, forming a carbon sink in its source area within a short period but becoming a carbon source at its destination. To explore the effects of different environmental changes on seawater dissolved carbon pools faced by living U. prolifera in its originating area, U. prolifera were cultured in three sets with different light intensity (54, 108, and 162 μmol m−2 s−1), temperature (12, 20, and 28 °C) and nitrate concentration gradients (25, 50, and 100 μmol L−1). The results showed that moderate light (108 μmol m−2 s−1), temperature (20 °C), and continuous addition of exogenous nitrate significantly enhanced the absorption of dissolved inorganic carbon (DIC) in seawater by U. prolifera and most promoted its growth. Under the most suitable environment, the changes in the seawater carbonate system were mainly dominated by biological production and denitrification, with less influence from aerobic respiration. Facing different environmental changes, U. prolifera continuously changed its carbon fixation mode according to tissue δ13C results, with the changes in the concentrations of various components of DIC in seawater, especially the fluctuation of HCO 3 − and CO 2 concentrations. Enhanced light intensity of 108 μmol m−2 s−1 could shift the carbon fixation pathway of U. prolifera towards the C 4 pathway compared to temperature and nitrate stimulation. Environmental conditions at the origin determined the amount of dissolved carbon fixed by U. prolifera. Therefore, more attention should be paid to the changes in marine environmental conditions at the origin of U. prolifera , providing a basis for scientific management of U. prolifera. [Display omitted] • Moderate light, temperature and nitrate addition boost U. prolifera DIC absorption. • U. prolifera adapts carbon fixation modes to environmental changes. • Origin environmental conditions determine U. prolifera's carbon sink contribution. [ABSTRACT FROM AUTHOR]

An integrated observation of NO x that included coastal cities and oceanic cruises covering the Qingdao coastal waters sites (QDCW) and the Yellow Sea and East China Sea sites (YECS) was conducted in spring. The average concentrations of the coastal cities, the QDCW, and the YECS were 5.4 ± 4.1, 4.2 ± 3.5, and 2.9 ± 6.8 ppb for NO while 18.5 ± 7.2, 9.4 ± 5.2, and 4.9 ± 6.4 ppb for NO 2 , depicting lowest levels in the open seas. Atmospheric NO and NO 2 showed similar spatial variations over the seas, the stations where the air masses originated from land or nearshore regions showed higher levels, but the decisive influencing factors were not the same in the different study areas. The calculated NO x flux value in the YECS (−8.7 × 10−17 mol N cm−2) indicated that the sea surface was a net sink of atmospheric NO x. The sea was an important sink of the atmospheric NO x. NO x showed a decreasing trend from the coastal cities to the open seas. Light and wind speed were decisive factors influencing atmospheric NO x distributions. [ABSTRACT FROM AUTHOR]

Production of dimethylsulfoniopropionate (DMSP), dimethylsulfide (DMS), and acrylic acid (AA) from 22 marine microalgae representing six phyla were examined at different growth stages. The concentrations of DMSP, DMS, and AA per cell in the media showed significant changes during the whole growth period, and the highest concentrations were found at the stationary growth phase or the senescent phase. Different species had different concentration levels of DMSP, DMS, and AA, among which Pyrrhophyta, Bacillariophyte, and Chrysophyta had relatively large release. The highest concentrations of DMSP, DMS, and AA were 56.70, 0.86, and 44.60 fmol cell−1 in Scrippsiella trochoidea , Prymnesiacee , and Karenia mikimotoi , respectively. The ratios of DMS/DMSP and AA/(DMSP+AA) in the 22 marine microalgae differed dramatically over the growth cycle. The DMS/DMSP ratios were <25%, indicating that only a small fraction of DMSP was converted to DMS by enzymatic cleavage. Moreover, there was a higher ratio of enzymatic degradation of DMSP in the senescent growth stage. The AA/(DMSP+AA) ratio, representing the degradation ratio of DMSP, increased significantly at the beginning of growth period and then decreased. Hence, the changes in these ratios could approximately illustrate the degradation mechanism of DMSP among diverse species at different growth phases. • High DMSP, DMS and AA concentrations were detected in Pyrrophyta and Bacillariophyta. • The maximum concentrations of DMSP and DMS appeared in the stationary growth stage. • The highest release of AA was observed in the early exponential growth period. • The maximum value of DMSP enzymatic degradation appeared in late growth phase. [ABSTRACT FROM AUTHOR]

To examine the sulfate assimilation and reduction process and the regulation of illumination, diatom Phaeodactylum tricornutum and dinoflagellate Amphidinium carterae were selected for continuous simulation incubation under different photon flux densities (PFDs) (54, 108 and 162 μmol photons m−2 s−1), and concentration variations of related sulfur compounds sulfate, dimethylsulfoniopropionate (DMSP), dimethylsulfide (DMS) and acrylic acid (AA) in the culture system were observed. The optimal PFD for the growth of two microalgae was 108 μmol photons m−2 s−1. However, the maximum sulfate absorption occurred at 162 μmol photons m−2 s−1 for P. tricornutum and at 54 μmol photons m−2 s−1 for A. carterae. With the increase of PFD, the release of DMSP by P. tricornutum decreased while A. carterae increased. The largest release amount of DMS was 0.59 ± 0.05 fmol cells−1 for P. tricornutum and 2.61 ± 0.89 fmol cells−1 for A. carterae under their optimum growth light condition. The sulfate uptake of P. tricornutum was inhibited by the addition of amino acids, cysteine had a greater inhibitory effect than methionine, and the absorption process was controlled by light. The intermediate products of sulfur metabolism had an up–control effect on the sulfate uptake process of P. tricornutum. However, the addition of amino acids had no obvious effect on the sulfate absorption of A. carterae. • Illumination regulated sulfate assimilation of P. tricornutum and A. carterae. • 108 μmol photons m−2 s−1 was the optimum light condition for the algal growth. • Related sulfur compounds concentrations varied under different illumination. • Sulfur metabolic intermediates inhibited the sulfate uptake of P. tricornutum. • Sulfur metabolic intermediates had no obvious regulative law on A. carterae. [ABSTRACT FROM AUTHOR]

Nitric oxide (NO) has been identified as a key physiological modulator and signaling molecule in animals and plants. However, due to its high reactivity, our knowledge of its production and consumption pathways in the ocean remain limited. Laboratory experiments showed that Ulva prolifera can produce NO, producing as much as 0.44 ± 0.04 nmol h−1 g−1. During the growth period, U. prolifera released NO, but during the decay period NO was absorbed by U. prolifera and bacteria. Furthermore, field investigations examined NO concentrations in the coastal waters of the Yellow Sea off Qingdao, where the U. prolifera green tide occurred in summer 2018. The average concentrations of NO in the surface seawater were 70.2 ± 38.2 pmol L−1 and 18.9 ± 10.3 pmol L−1 in the late- and after-bloom periods, respectively. NO release by U. prolifera was the primary contributor to the high NO concentrations during the late-bloom period. The study area was a net source of NO to the atmosphere during the study period, with average NO sea-air fluxes from the Qingdao coastal waters being 1.5 × 10−12 mol m−2 s−1 and 0.4 × 10−12 mol m−2 s−1 in the late- and after-bloom periods, respectively. This study concluded that the coastal waters of the Yellow Sea off Qingdao contributed more NO to the atmosphere during the bloom of U. prolifera than afterward. Image 1 • The growing U. prolifera could produce NO with the maximum rate of 0.44 nmol h−1 g−1. • The rate of NO release by U. prolifera was lower than the photoproduction rate. • NO concentration during the late-bloom was 2.7 times higher than after the bloom. • The study area acted as a source of NO to the air with a higher flux during a bloom. [ABSTRACT FROM AUTHOR]

Brain-derived neurotrophic factor (BDNF)/tropomyosin-related kinase B (TrkB) pathway is associated with ischemic heart diseases (IHD). 7,8-dihydroxyflavone (7,8-DHF), BDNF mimetic, is a potent agonist of TrkB. We aimed to investigate the effects and the underlying mechanisms of 7,8-DHF on cardiac ischemia. Myocardial ischemic mouse model was induced by ligation of left anterior descending coronary artery. 7,8-DHF (5 mg/kg) was administered intraperitoneally two days after ischemia for four weeks. Echocardiography, HE staining and transmission electron microscope were used to examine the function, histology and ultrastructure of the heart. H9c2 cells were treated with hydrogen peroxide (H 2 O 2), 7,8-DHF or TrkB inhibitor ANA-12. The effects of 7,8-DHF on cell viability, mitochondrial membrane potential (MMP) and mitochondrial superoxide generation were examined. Furthermore, mitochondrial fission and protein expression of mitochondrial dynamics (Mfn2 [mitofusin 2], OPA1 [optic atrophy 1], Drp1 [dynamin-related protein 1] and Fis-1 [fission 1]) was detected by mitotracker green staining and western blot, respectively. 7,8-DHF attenuated cardiac dysfunction and cardiomyocyte abnormality of myocardial ischemic mice. Moreover, 7,8-DHF increased cell viability and reduced cell death accompanied by improving MMP, inhibiting mitochondrial superoxide and preventing excessive mitochondrial fission of H 2 O 2 -treated H9c2 cells. The cytoprotective effects of 7,8-DHF were antagonized by ANA-12. Mechanistically, 7,8-DHF repressed OMA1-dependent conversion of L-OPA1 into S-OPA1, which was abolished by Akt inhibitor. In conclusion, 7,8-DHF protects against cardiac ischemic injury by inhibiting the proteolytic cleavage of OPA1. These findings provide a novel pharmacological effect of 7,8-DHF on mitochondrial dynamics and a new potential target for IHD. Image 1 • 7,8-DHF attenuates ischemia/H 2 O 2 -induced cardiomyocyte injury. • 7,8-DHF inhibits excessive mitochondrial fission in ischemic heart. • 7,8-DHF inhibits OMA1-dependent conversion of L-OPA1 into S-OPA1. • Akt inhibitor abolished the effects of 7,8-DHF on mitochondrial dynamics. [ABSTRACT FROM AUTHOR]

• NOx in wetlands was mainly generated from vegetation-covered sediments. • Denitrifiers dominated NO production, showing sensitivity to environmental gradients. • NO emissions would be underestimated without considering tidal pulses. Intertidal wetland sediments are an important source of atmospheric nitrogen oxides (NO x), but their contribution to the global NO x budget remains unclear. In this work, we conducted year-round and diurnal observations in the intertidal wetland of Jiaozhou Bay to explore their regional source-sink patterns and influence factors on NO x emissions (initially in the form of nitric oxide) and used a dynamic soil reactor to further extend the mechanisms underlying the tidal pulse of nitric oxide (NO) observed in our investigations. The annual fluxes of NO x in the vegetated wetland were significantly higher than those in the wetland without vegetation. Their annual variations could be attributed to changes in temperature and the amount of organic carbon in the sediment, which was derived from vegetated plants and promoted the carbon-nitrogen cycle. Anaerobic denitrifiers had advantages in the intertidal wetland sediment and accounted for the major NO production (63.8 %) but were still limited by nitrite and nitrate concentrations in the sediment. Moreover, the tidal pulse was likely a primary driver of NO x emissions from intertidal wetlands over short periods, which was not considered in previous investigations. The annual NO exchange flux considering the tide pulse contribution (8.93 ± 1.72 × 10–2 kg N ha–1 yr–1) was significantly higher than that of the non-pulse period (4.14 ± 1.13 × 10–2 kg N ha–1 yr–1) in our modeling result for the fluxes over the last decade. Therefore, the current measurement of NO x fluxes underestimated the actual gas emission without considering the tidal pulse. [Display omitted] [ABSTRACT FROM AUTHOR]

PIWI proteins and piRNAs primarily functions as a safeguard of germline cells by activating epigenetic regulations, silencing transposons and maintaining chromatin structure. Increasing evidences reveal that PIWI proteins and piRNAs have broader functions in many vital biological processes including cell proliferation, differentiation and survival. They have been recognized as a crucial factor in the cellular events due their role in controlling mRNA expression, turnover and translation. PIWIs, with or without its partner non-coding RNA (piRNA), govern the expression and activity of many transcription factors and signaling molecules by mastering their expression and/or post-translational modifications by directly interacting with them. In this review, we focus on the functional role of PIWI family of proteins and piRNA in physiological and pathological conditions. We compile the current knowledge about the impact of alterations of PIWI and/or piRNA on expression and activities of signaling mediators and transcriptional networks associated with cell differentiation, proliferation and survival. [ABSTRACT FROM AUTHOR]

Brain-derived neurotrophic factor (BDNF)/tyrosine kinase receptor B (TrkB) pathway is a therapeutic target in cardiac diseases. A BDNF mimetic, 7,8-dihydroxyflavone (7,8-DHF), is emerging as a protective agent in cardiomyocytes; however, its potential role in cardiac fibroblasts (CFs) and fibrosis remains unknown. Thus, we aimed to explore the effects of 7,8-DHF on cardiac fibrosis and the possible mechanisms. Myocardial ischemia (MI) and transforming growth factor-β1 (TGF-β1) were used to establish models of cardiac fibrosis. Hematoxylin & eosin and Masson's trichrome stains were used for histological analysis and determination of collagen content in mouse myocardium. Cell viability kit, EdU (5-ethynyl-2′-deoxyuridine) assay and immunofluorescent stain were employed to examine the effects of 7,8-DHF on the proliferation and collagen production of CFs. The levels of collagen I, α-smooth muscle actin (α-SMA), TGF-β1, Smad2/3, and Akt as well as circadian rhythm-related signals including brain and muscle Arnt-like protein 1 (Bmal1), period 2 (Per2), and cryptochrome 2 (Cry2) were analyzed. Treatment with 7,8-DHF markedly alleviated cardiac fibrosis in MI mice. It inhibited the activity of CFs accompanied by decreasing number of EdU-positive cells and downregulation of collagen I, α-SMA, TGF-β1, and phosphorylation of Smad2/3. 7,8-DHF significantly restored the dysregulation of Bmal1, Per2, and Cry2, but inhibited the overactive Akt. Further, inhibition of Bmal1 by SR9009 effectively attenuated CFs proliferation and collagen production of CFs. In summary, these findings indicate that 7,8-DHF attenuates cardiac fibrosis and regulates circadian rhythmic signals, at least partly, by inhibiting Bmal1/Akt pathway, which may provide new insights into therapeutic cardiac remodeling. [Display omitted] • 7,8-DHF alleviates ischemia-induced cardiac fibrosis. • 7,8-DHF inhibits the proliferation and differentiation of cardiac fibroblasts. • 7,8-DHF restores circadian rhythm and Akt signals in cardiac fibrosis. • Inhibition of Bmal1 by SR9009 inhibits the activity of cardiac fibroblasts. [ABSTRACT FROM AUTHOR]

Necrosis is programmed and is one of the main forms of cell death in the pathological process in cardiac diseases. MicroRNAs (miRNAs) have emerged as key gene regulators in many diseases. However, how miRNAs contribute to programmed necrosis is poorly defined. Here we report that miR-2861 and adenine nucleotide translocase 1 (ANT1) constitute an axis that regulates necrotic cell death in the heart. Our results show that ANT1 inhibits H 2 O 2 -induced cardiomyocytes necrosis. ANT1 also antagonizes myocardial necrosis in a mouse ischemia/reperfusion (I/R) model. We further demonstrate that miR-2861 directly binds to the coding sequence of ANT1 and suppresses the expression of ANT1 mRNA and protein. MiR-2861 induces necrotic cell death. In contrast, knockdown of miR-2861 attenuates H 2 O 2 -induced necrosis in cardiomyocytes. Also, miR-2861 knockdown protects heart from I/R injury and necrotic cell death in vivo. MiR-2861 regulates necrosis and myocardial infarction through targeting ANT1. Collectively, these data identify miR-2861 and ANT1 as two novel regulators of cardiomyocyte necrosis and myocardial infarction, and suggest potential therapeutic targets in treatment of cardiac diseases. [ABSTRACT FROM AUTHOR]

Abstract: Cardiac hypertrophic program is a chronic, complex process, and occurs in response to long-term increases of hemodynamic load related to a variety of pathophysiological conditions. Mitochondria, known as “the cellular power plants”, occupy about one‐third of cardiomyocyte volume and supply roughly 90% of the adenosine triphosphate (ATP). Impairment of energy metabolism has been regarded as one of the main pathogenesis of cardiac hypertrophy. Thus, we summarize here the molecular events of mitochondrial adaptations, including the mitochondrial genesis, ATP generation, ROS signaling and Ca2+ homeostasis in cardiac hypertrophy, expecting that this effort will shed new light on understanding the maladaptive cardiac remodeling. [Copyright &y& Elsevier]

Abstract: To assess the prevalence of antimicrobial resistance and three classes of integrons in Escherichia coli (E. coli) strains (n =57) isolated from bovine endometritis in Inner Mongolia of China, antimicrobial susceptibility and the presence of three types of integrons were characterized. Most isolates were susceptible to ceftiofur, furazolidone, ciprofloxacin and enrofloxacin, while 57 isolates were all resistant to sulfamethoxydiazine and trimethoprim. High resistant incidence rates were exhibited to sulfadiazine, tetracycline, oxytetracycline, cefazolin, chloramphenicol. Forty-six of 57 E. coli strains were resistant to above 10 antibiotics (80.70%). The integrase gene and gene cassettes of integrons were amplified by PCR. DNA sequencing and analysis were used to identify the genetic content of the integron-variable regions. Neither class II nor class III integron was detected, while 36.8% (n =21) of the isolates were positive for the presence of intI1 gene. Analysis of gene cassettes revealed that six gene cassettes were found, which encoded resistance to trimethoprim (dhfr, dhfrI, dfrA17) and aminoglycosides (aadA1, aadA2, aadA5). Among them, the gene cassette array dfrA17–aadA5 was found most prevalent (66.7%). The resistance profile of positive-integron isolates was relatively broad and they were resistant to more than eight antimicrobials (n ⩾ 8). The correlation analysis revealed the incidence of integrons among the isolates were related to the multiple antibiotic resistance profile, indicating integrons play an important role in the dissemination and spread of the antimicrobial resistant strains. [Copyright &y& Elsevier]