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Members of the genus Bougainvillea are rich sources of natural dyes, pigments, and traditional medicines. They are also commonly used as ornamentals in roadside landscape construction. However, the horticultural development of Bougainvillea flowers with extended growth periods and coloration is not always feasible. One reason is limited molecular knowledge and no genomic information for Bougainvillea. Here, we compiled an integrative transcriptome of all expressed transcripts for Bougainvillea × buttiana Miss Manila by integrating 20 Illumina-sequencing RNA transcriptomes. The integrative transcriptome consisted of 97,623 distinct transcripts. Of these, 47,006 were protein-coding, 31,109 were non-coding, and 19,508 were unannotated. In addition, we affirmed that the integrative transcriptome could serve as a surrogate reference to the genome in aiding accurate transcriptome assembly. For convenience, we curated the integrative transcriptome database for Bougainvillea, namely InTransBo, which can be freely accessed at http://www.bio-add.org/InTransBo/index.jsp. To the best of our knowledge, the present study is the most comprehensive genomic resource for Bougainvillea up-to-date. The integrative transcriptome helps fill the genomic gap and elucidate the transcriptional nature of Bougainvillea. It may also advance progress in the precise regulation of flowering in horticulture. The same strategy can be readily applied toward the systematic exploration of other plant species lacking complete genomic information.

A ternary hardening-accelerating admixture for Portland cement, comprising calcium fluoroaluminate (11CaO.7Al2O3.CaF2), calcium thiocyanate (Ca(SCN)2) and triethanolamine (C6H15NO3), was studied. The cement paste was investigated using compressive strength tests, X-ray diffraction, thermogravimetric analysis, scanning electron microscopy and porous medium surface area analysis. The results showed that the setting time of the cement had been shortened using the ternary admixture; the fluidity and early strength were improved compared with traditional admixtures cured at ambient temperature (20°C). The compressive strength reached 14·5 MPa at 1 d, which was twice that of cement without admixtures and 0·35 times higher than cement with a sodium chloride (NaCl) triethanolamine admixture. Moreover, the total pore volume in the cement with the ternary admixture was much less than the cement with the sodium chloride–triethanolamine admixture. When the ternary admixture was included, not only was the concentration of calcium ions (Ca2+) in the liquid phase increased, but there was also a complexation reaction between the ternary admixture and clinker, which accelerated the cement hydration reaction, and the concentrations of calcium silicate hydrates and ettringite were increased at an early age. The new admixture is a promising non-chloride accelerator and offers more options in hardening-accelerating admixtures for Portland cement systems.

Background Multiple sclerosis (MS) is an immune-mediated demyelinated disease of the central nervous system. Activation of microglia is involved in the pathogenesis of myelin loss. Objective This study is focused on the role of Hv1 in regulating demyelination and microglial activation through reactive oxygen species (ROS) production after lysophosphatidylcholine (LPC)-mediated demyelination. We also explored autophagy in this process. Methods A model of demyelination using two-point LPC injection into the corpus callosum was established. LFB staining, immunofluorescence, Western blot, and electron microscopy were used to study the severity of demyelination. Microglial phenotype and autophagy were detected by immunofluorescence and Western blot. Morris water maze was used to test spatial learning and memory ability. Results We have identified that LPC-mediated myelin damage was reduced by Hv1 deficiency. Furthermore, we found that ROS and autophagy of microglia increased in the demyelination region, which was also inhibited by Hv1 knockout. Conclusion These results suggested that microglial Hv1 deficiency ameliorates demyelination through inhibition of ROS-mediated autophagy and microglial phenotypic transformation.

Revascularization and angiogenesis, as substrates of sustained collateral circulation, play a crucial role in determining the severity and clinical outcome of acute ischemic stroke (AIS) due to large vessel occlusion (LVO). Developing an adjunct biomarker to help identify and monitor collateral status would aid stroke diagnosis and prognosis. To screen the potential biomarkers, proteomic analysis was performed in this study to identify those distinct plasma protein profiles in AIS due to LVO with different collateral status. Interestingly, we found that levels of Plasma Factor VII Activating Protease (FSAP) significantly increased in those AIS patients with poor collaterals, and were correlated with worse neurological outcome. Furtherly, both in vitro and in vivo models of ischemic stroke were used to explore pathological mechanisms of FSAP in endothelial dysfunction. We demonstrated that the FSAP inhibitor, high-molecular-weight hyaluronan (HMW-HA), enhanced the pro-angiogenic vascular factors, improved the integrity of brain blood barrier, and promoted newly formed cerebral microvessels in the ischemic penumbra, consequently improving neurological function. To elucidate the pathways that might contribute to revascularization during LVO, we applied transcriptomic analysis via unbiased RNA sequencing and showed that Wnt signaling was highly involved in FSAP mediated endothelial dysfunction. Notably, inhibition of Wnt5a largely reversed the protective effects from HMW-HA treatment, implying that FSAP might aggravate endothelial dysfunction and neurological deficits by regulating Wnt5a signaling. Therefore, FSAP may represent a potential biomarker for collateral status after LVO and a promising therapeutic target to be explored in the treatment of stroke.

Sphingosine-1-phosphate (S1P) signaling is being increasingly recognized as a strong modulator of immune cell migration and endothelial function. Fingolimod and other S1P modulators in ischemic stroke treatment have shown promise in emerging experimental models and small-scale clinical trials. In this article, we will review the current knowledge of the role of S1P signaling in brain ischemia from the aspects of inflammation and immune interventions, sustaining endothelial functions, regulation of blood-brain barrier integrity, and functional recovery. We will then discuss the current and future therapeutic perspectives of targeting S1P for the treatment of ischemic stroke. Mechanism studies would help to bridge the gap between preclinical studies and clinical practice. Future success of bench-to-bedside translation shall be based on in depth understanding of S1P signaling during stroke and on the ability to have a fine temporal and spatial regulation of the signal pathway.

Ischemic stroke is a leading cause of morbidity and mortality worldwide. Resident microglia are the principal immune cells of the brain, and the first to respond to the pathophysiological changes induced by ischemic stroke. Traditionally, it has been thought that microglial activation is deleterious in ischemic stroke, and therapies to suppress it have been intensively explored. However, increasing evidence suggests that microglial activation is also critical for neurogenesis, angiogenesis, and synaptic remodeling, thereby promoting functional recovery after cerebral ischemia. Here, we comprehensively review the dual role of microglia during the different phases of ischemic stroke, and the possible mechanisms controlling the post-ischemic activity of microglia. In addition, we discuss the dynamic interactions between microglia and other cells, such as neurons, astrocytes, oligodendrocytes, and endothelial cells within the brain parenchyma and the neurovascular unit.

To determine the role of vaginal microbiota in the efficacy of cervical cerclage in obstetric outcomes of twin pregnancies.This retrospective study enrolled 68 twin pregnant women diagnosed with cervical incompetence (CIC) and 68 twin pregnancies without CIC. The CIC group was further divided into two subgroups: cerclage group (n = 51) and non-cerclage group (n = 17), according to whether cervical cerclage was performed in the second trimester. Data of vaginal microbiota and obstetric outcomes were collected and compared.Cervical incompetence had harmful effect on both pregnancy outcomes and vaginal microecology, characterized by earlier gestational week at delivery (30.3 ± 5.6 vs 35.6 ± 1.1, P 0.001), a lower birth weight of newborns (OR 0.40; 95% CI 0.22-0.74), a higher vaginal pH value (OR 0.11; 95% CI 0.04-0.30) and a lower abundance of Lactobacillus (OR 0.34; 95% CI 0.17-0.70). In addition, compared with the vaginal microbiota after cerclage, less normal diversity of bacterial flora (OR 0.35; 95% CI 0.12-1.01), less Lactobacillus (OR 0.40; 95% CI 0.18-0.91) and more Gardnerella vaginalis (OR 18.92; 95% CI 2.38-150.35) appeared before cerclage. Besides, the unhealthy vaginal environment also had an unfavorable influence on the neonatal outcomes, increased neonatal mortality rate was observed in the group of vaginal pH 4.5 (P 0.05). Fortunately, compared with the non-cerclage group, the cerclage group had a longer interval from diagnosis to delivery (≥ 8 weeks) and more of the newborns' birth weight were not less than 1500 g (P 0.05).A healthy vaginal environment is essential to improve the obstetric outcome for twin pregnancies with cervical cerclage.

In response to various types of environmental and cellular stress, microglia rapidly activate and exhibit either pro- or anti-inflammatory phenotypes to maintain tissue homeostasis. Activation of microglia can result in changes in morphology, phagocytosis capacity, and secretion of cytokines. Furthermore, microglial activation also induces changes to cellular energy demand, which is dependent on the metabolism of various metabolic substrates including glucose, fatty acids, and amino acids. Accumulating evidence demonstrates metabolic reprogramming acts as a key driver of microglial immune response. For instance, microglia in pro-inflammatory states preferentially use glycolysis for energy production, whereas, cells in anti-inflammatory states are mainly powered by oxidative phosphorylation and fatty acid oxidation. In this review, we summarize recent findings regarding microglial metabolic pathways under physiological and pathological circumtances. We will then discuss how metabolic reprogramming can orchestrate microglial response to a variety of central nervous system pathologies. Finally, we highlight how manipulating metabolic pathways can reprogram microglia towards beneficial functions, and illustrate the therapeutic potential for inflammation-related neurological diseases.

Rationale: Ischemic white matter damage frequently results in myelin loss, accompanied with microglial activation. We previously found that directing microglia towards an anti-inflammatory phenotype provided a beneficial microenvironment and helped maintain white matter integrity during chronic cerebral hypoperfusion. However, the molecular mechanisms underlying microglial polarization remain elusive. Methods: Hypoperfusion induced white matter damage mice model and lipopolysaccharide (LPS) induced primary cultured microglia were established. Autophagy activation in microglia was detected both in vivo and in vitro by immunofluorescence, Western blot and electron microscopy. Autophagy inhibitors/agonist were administrated to investigate the role of autophagic process in modulating microglial phenotypes. Quantitative real time-polymerase chain reaction and Western blot were carried out to investigate the possible pathway. Results: We identified rapid accumulation of autophagosomes in primary cultured microglia exposed to LPS and within activated microglia during white matter ischemic damage. Autophagy inhibitors switched microglial function from pro-inflammatory to anti-inflammatory phenotype. Furthermore, we found TLR4, one of the major receptors binding LPS, was most highly expressed on microglia in corpus callosum during white matter ischemic damage, and TLR4 deficiency could mimic the phenomenon in microglial functional transformation, and exhibit a protective activity in chronic cerebral hypoperfusion. Whereas, the anti-inflammatory phenotype of microglia in TLR4 deficiency group was largely abolished by the activation of autophagic process. Finally, our transcriptional analysis confirmed that the up-regulation of STAT1 and down-regulation of STAT6 in microglia exposure to LPS could be reversed by autophagy inhibition. Conclusion: These results indicated that TLR4-dependent autophagy regulates microglial polarization and induces ischemic white matter damage via STAT1/6 pathway.

BACKGROUND Iron deficiency anemia (IDA) has been a major public health problem all over the world. Developing new iron (Fe) fortificants with both high bioavailability and negligible food sensory changes for IDA is in urgent demand. MATERIAL AND METHODS The Fe nanoparticles were fabricated through a one-pot reduction process under the protection of bovine serum albumin (BSA). The BSA-Fe nanoparticles were characterized systematically. The comparisons between BSA-Fe nanoparticles and FeSO4 in bioavailability were carried out through hemoglobin (Hb) repletion method. The biocompatibility of BSA-Fe nanoparticles was also investigated through in vitro and in vivo assays. RESULTS BSA-Fe nanoparticles have super-small size and good water solubility as well as water stability. The Hb repletion assay demonstrated that BSA-Fe nanoparticles have comparative bioavailability with FeSO4. The in vitro cell viability assay, in vivo histological analysis, and biochemical measurements proved the remarkable biocompatibility of BSA-Fe nanoparticles. CONCLUSIONS The BSA-Fe nanoparticles fabricated through a one-pot facile method have good water solubility, comparative bioavailability with FeSO4, and acceptable biocompatibility, exhibiting good potential for further clinical translations.

Objective To investigate the expression of and interleukin-12 (IL-12) and interferon-γ (IFN-γ) in relation to the pathology of damp-heat of spleen-stomach syndrome (DHSS) induced by Helicobacter pylori (H. pylori) infection. Methods In total, 114 individual gastric mucosal specimens including 83 DHSS, 19 spleen-qi deficiency syndrome (SQD) and 12 from healthy volunteers (CON) were collected by gastroscopy. To explore the relationship between the two syndromes and H. pylori infection, individual samples were tested using rapid urease and methylene blue tests. Hematoxylin and eosin stained sections were examined to grade for the degree of inflammation and inflammatory activity, and expression of IL-12 and IFN-γ was investigated by immunohistochemistry. Results Statistically significant differences in the degree of inflammation and inflammatory activity were observed between the groups of specimens: DHSS, SQD and CON ( P 0.05) groups. Intriguingly, in gastric specimens exhibiting IM and dysplasia, IL-12 translocated from the nucleus into the cytoplasm. Conclusion Our findings suggest that IL-12 and IFN-γ are involved in DHSS pathology, but not in SQD, acting as healthy- Qi . DHSS is not just the consequence of those two cytokines but results from the cross-talk between a number of cytokines and/or other proteins, which may warrant further investigation in DHSS patients infected with H. pylori.

Background Acute ischemic stroke (AIS) due to large vessel occlusion (LVO) is a devastating cerebrovascular disorder, which could benefit from collateral circulation. Proteins associated with acute LVO pathogenesis and endothelial function may appear in blood samples of AIS patients due to LVO, thus permitting development of blood-based biomarkers for its diagnosis and prognosis. Methods This study is a single-center, retrospective, observational case–control trial. Consecutive patients who presented at the Department of Neurology of Tongji Hospital were recruited from July 2016 to April 2018. In the discovery phase, a proteomic approach with iTRAQ-based LC–MS/MS was used to investigate the altered proteomic pattern in plasma from patients with AIS due to LVO. In the validation study, Western blots was used to identify biomarkers associated with stroke diagnosis as well as their prognostic value associated with different collateral statuses. Results For this exploratory study, the proteomic analysis of plasma from 40 patients with AIS due to LVO and 20 healthy controls revealed seven differentially expressed proteins with a 1.2/0.83-fold or greater difference between groups. The four elevated proteins, PPBP (1.58 ± 0.78 vs 0.98 ± 0.37; P Conclusions The identified 4-biomarker panel could provide diagnostic aid to the existing imaging modalities for AIS due to LVO, and the prognostic value of IGF2, LYVE1, and THBS1 was proved in predicting functional outcomes related to collateral status. Trial registration ClinicalTrials.gov NCT 03122002. Retrospectively registered April 20, 2017. URL of trial registry record: https://www.clinicaltrials.gov/ct2/show/NCT03122002?term=NCT+03122002&rank=1

Rab5a, a key member of the Rab family of GTPases, was determined to be a regulator of vascular smooth muscle cell (VSMC) proliferation and migration. However, the exact regulatory mechanism remains unclear. As Rab5a has been shown to be associated with autophagy, which is essential for the conversion of VSMCs from a contractile to a synthetic phenotype in order to prevent cell death due to oxidative stress. The present study hypothesized that autophagy may be responsible for the proliferation and migration of VSMCs via the Rab5a protein. The aim of the present study was to evaluate the effect of Rab5a on autophagy in VSMCs. The human aorta vascular smooth muscle cell line, T/G HA‑VSMCs, was treated with small interfering (si)RNA against Rab5a and/or platelet‑derived growth factor (PDGF). Following treatment, the phenotype transition of the VSMCs was evaluated by detecting the mRNA and protien expression levels of VSMC molecular markers using reverse transcription‑quantitative polymerase chain reaction and western blotting, respectively. In addition, autophagy in VSMCs was evaluated by western blotting for autophagy‑associated proteins, flow cytometry of acidic vesicular organelles, punctate fluorescence of microtubule associated protein light chain 3 and transmission electron microscopy of typical scattered double‑membrane vacuolar structures. Additionally, the proliferation, migration, cell cycle and apoptotic response of VSMCs were detected by sulforhodamine B assay, transwell assay and flow cytometry, respectively. The results revealed that transfection with siRNA against Rab5a led to a significant decrease in Rab5a protein expression, while the reduced expression trend of Rab5a was rescued by intervention with PDGF. Furthermore, cells transfected with siRNA against Rab5a inhibited the autophagy of VSMCs. Downregulated Rab5a inhibited the phenotype transition of VSMCs. Additionally, downregulated Rab5a led to slowed cell growth, decreased numbers of migrated cells, decreased numbers of cells at the G0‑G1 phase and a higher apoptosis rate. However, PDGF significantly rescued these phenomena caused by siRNA against Rab5a. These results indicated that Rab5a‑mediated autophagy may regulate the phenotype transition and cell behavior of VSMCs through the activation of the extracellular‑regulated kinase 1/2 signaling pathway.

Introduction Microglial activation plays a crucial role in the pathology of ischemic stroke. Recently, we demonstrated that fingolimod (FTY720) exerted neuroprotective effects via immunomodulation in ischemic white matter damage induced by chronic cerebral hypoperfusion, which was accompanied by robust microglial activation. In this study, we assessed the pro-angiogenic potential of FTY720 in a murine model of acute cortical ischemic stroke. Methods The photothrombotic (PT) method was used to induce cortical ischemic stroke in mice. We evaluated cortical damage, behavioral deficits, microglial polarization, and angiogenesis to identify the neuroprotective effects and possible molecular mechanisms of FTY720 in acute ischemic stroke. Results In vivo, a reduction in neuronal loss and improved motor function were observed in FTY720-treated mice after PT stroke. Immunofluorescence staining revealed that robust microglial activation and the associated neuroinflammatory response in the peri-infarct area were ameliorated by FTY720 via its ability to polarize microglia toward the M2 phenotype. Furthermore, both in vivo and in vitro, angiogenesis was enhanced in the microglial M2 phenotype state. Behaviorally, a significant improvement in the FTY720-treated group compared to the control group was evident from days 7 to 14. Conclusions Our research indicated that FTY720 treatment promoted angiogenesis via microglial M2 polarization and exerted neuroprotection in PT ischemic stroke.

With the development of high-speed and heavy-haul railway in China, problems like insufficient thickness of ballast bed and overlarge track stiffness are obvious. Ballast may break into small particles and their contact status will deteriorate under cyclic loading, resulting in ballast degradation. Discrete element method (DEM) was used to research improved performance of ballast bed using elastic sleeper. Clusters were generated by bonding spheres to model real ballasts, while broken bonds were utilized to distinguish breakage. Two kinds of ballast beds with elastic sleeper and conventional sleeper were established, respectively. After applying cyclic loading to the models, differences of mechanical properties between two models were analyzed by contrasting their dynamic behavior indexes, such as particle contact force, sleeper settlement, vibration velocity and acceleration, breakage characteristic. The results illustrate that compared with conventional sleeper, elastic sleeper increases sleeper settlement, while reduces ballast vibration and contact force between particles, which could depress ballast breakage.

Endothelial cells (ECs) are critical for angiogenesis and microRNA plays important roles in this process. In this study, we investigated the function and mechanism of miR-302c in the process of endothelial-mesenchymal transition (EndMT) in ECs. When miR-302c was overexpressed in HUVECs, the motility of the HUVECs was weakened; the expression levels of EndMT markers were also changed: vascular endothelial (VE)-cadherin was up-regulated, whereas β-catenin, FSP1 and α-SMA were down-regulated. Further in vivo and in vitro experiments showed that the growth of HCC was inhibited when co-cultured or co-injected with HUVECs overexpressing miR-302c. On the contrary, when miR-302c was suppressed in HUVECs, the opposite results were observed. Reporter assays showed that miR-302c inhibited metadherin (MTDH) expression through directly binding to its 3′UTR. In addition, compared to ECs isolated from normal liver tissues of HCC patients, ECs isolated from tumor tissues expressed markedly low levels of miR-302c but high levels of MTDH. These results suggest that EC-specific miR-302c suppresses tumor growth in HCC through MTDH-mediated inhibition of EndMT. MTDH and miR-302c might provide a new strategy for anti-angiogenic therapy in HCC.

Background There are different reports about operative methods for the treatment of hypertensive intracerebral hematomas. Our experience of transsylvian-transinsular microsurgical approach to hypertensive putaminal hematomas was analyzed. Methods A retrospective analysis was performed on 28 consecutive patients with hypertensive intracerebral hematomas who underwent surgical treatment at the Department of Neurosurgery, Renji Hospital, from January 2004 to December 2007. Results The transsylvian-transinsular approach to evacuate the hypertensive putaminal hematoma gains a good result. We believe it allows decompression of important deep-seated neurostructures with a more suitable angle and shorter distance from the cortex to the hematoma; allows easier access to vessels responsible for the bleeding, reducing the rate of rebleeding postoperatively; and avoids damage to the temporal or frontal cortex. Conclusions Transsylvian-transinsular approach for hypertensive putaminal hematoma is advocated.

Purpose: The aim of this article was to assess whether and to what extent pulmonary function recovered to normal degree postoperatively and to investigate the changes in pulmonary function after surgical correction and the value of surgical correction. Methods: A total of 27 patients who could be questioned and examined in person at the outpatient department of our hospital were included in this study. Of these patents, 24 were boys and 3 were girls. Their ages ranged from 3 to 16 years (mean, 8.67) at follow-up. The mean age at surgery was 4 years, and mean years of follow-up was 6.8. Pulmonary functional measurements included in vital capacity (VC), total lung capacity (TLC), residual volume (RV), functional residual capacity (FRC), RV-TLC ratio, maximal voluntary ventilation (MVV), force ventilatory capacity (FVC), forced expiratory volume in one second (FEV 1 ), maximal midexpiratory flow curve (MMEF), maximal expiratory flow in 75% vital capacity (V 75 ), maximal expiratory flow in 50% vital capacity (V 50 ), maximal expiratory flow in 25% vital capacity (V 25 ), and breathing reserve ratio (BR). Results: TLC, FRC, MVV, MMEF, V 75 , and V 50 values were not different from the normal values. IVC, FVC, FEV 1 , and V 25 values were decreased significantly compared with the normal values. The RV and RV-TLC were high in 87.5% cases. Conclusions: Preoperative symptoms obviously improved after operation. There was little airway obstruction in the patients postoperatively. The patients with pectus excavatum should be operated on as soon as possible.

In moyamoya disease (MMD), subsequent aneurysm in the proximal part of the posterior communicating artery (PcomA) is extremely rare. We report the case of a middle-aged female patient with MMD, who presented with a ruptured wide-necked aneurysm at the proximal part of the developed PcomA that converged with the posterior cerebral artery (PCA) and supplied the distal area. Endovascular treatment was performed, but the stent-assisted coil embolization resulted in occlusion of the internal carotid artery (ICA) above the ophthalmic artery and PcomA. Due to good compensatory collateral circulation, the patient was improved after surgery and had no complications. One-year followup DSA did not show recurrence of the aneurysm. The right ICA was still embolized, but with good compensatory collateral circulation. We conclude that, for an MMD patient with an aneurysm at the proximal part of the developed PcomA, if the ICA and PcomA are accidentally occluded, then the patient may still have a good prognosis due to sufficient collateral blood circulation.

Local variations in static slip, slip velocity, or rupture velocity contributes significantly to the information research on ground motions. Therefore, the characteristics of asperity and the position of the single asperity, are quantified to recognize its influence to the high-frequency radiation. In this paper a modified empirical Green's functions (EGF) method is suggested and used for ground motion simulation. The source parameters of asperity and rupture process are decided by the inhomogeneous fault. The synthesis of Tangshan earthquake in far field is used to study.

Oligosaccharides could induce some physiological responses in algae to defend attacks from pathogens. One of the earliest responses induced by oligosaccharides was so-called oxidative burst. This study has surveyed the recognition and oxidative burst response of Porphyra haitanenesis to agaro-oligosaccharide. Oxygen consumption was detected by an oxygen electrode. H2O2 concentrations in the medium were determined by measuring the dimerization of (p-hydroxyphenyl) acetic acid. The elicited oxidative burst was observed by loading the P. haitanenesis with redox-sensitive fluorescent probe dichlorohydrofluorescin (DCFH-DA). Gene expression level of NADPH oxidase (named Phrboh) was detected by real-time PCR. 2-AMAC labeled agaro-oligosaccharides were used to research the binding of agaro-oligosaccharide on algae. Results showed that two respiration peaks were observed after addition of 100 μg/mL agaro-oligosaccharide in P. haitanensis. Fourfold increase occurred in the first respiration peak 4 minutes after the addition, and fourteen times higher in the second response 10 minutes after the exposure to agaro-oligosaccharide. The accumulation of H2O2 in the culture medium was detected 5 minutes after challenged with agaro-oligosaccharide. The concentration of H2O2 reached its peak after 15 minutes, which was nearly ten times higher than control. The gene expression level of NADPH oxidase in P. haitanensis was up-regulated 3 minutes after the addition of agaro-oligosaccharide, suggesting that the synthesis of H2O2 was closely related to the activation of Phrboh. Based on the analyses of the fluorescence of redox-sensitive dye, activated oxygen species mainly accumulated around the plasma membrane. Under the fluorescent microscope, specific binding of 2-AMAC labeled agaro-oligosaccharide on cell plasma membrane was also observed, which indicated that there was recognition site of agaro-oligosaccharide on P. haitanensis plasma membrane. In summary, P. haitanensis could recognize agaro-oligosaccharide and respond with oxidative burst which was associated with the activation of NADPH oxidase.

The marine red algae Gracilaria/Gracilariopsis lemaneiformis were used as materials to study the effects of different concentration of salicylic acid on their growth and stress physiology under high temperature condition.The antioxidant enzyme activity,the osmotic regulation substances,phycobiliprotein,the features of chlorophyll fluorescence and HSP70 gene were studied when the algae grew in high temperature environment.Results showed that in the salicylic acid treatment group,the growth rate,enzymatic activity or membrane lipids damage degree were better than those of the control group at various degrees,and 5.0 and 10.0 μg/mL of salicylic acid treatment groups were obviously better than the other groups.The treatment with 10.0 μg/mL of salicylic acid showed the best effect with the daily relative growth rate increased 340% compared with the control group.When the treatment was on the 3rd day,each index of the 10.0 μg/mL group reached the maximum value,SOD increased 74%,POD increased 70%,CAT increased 40%,mannitol and proline increased 70% and 26% respectively.The content of phycoerythrin increased 46.2%,phycocyanin content increased 40%.Compared with the control group,the decrease of MDA content on the first day was the most obvious and decreased nearly 10%.The chlorophyll parameters of Fv/Fm,Fv/Fo,qP and ΦPSⅡ of G.lemaneiformis decreased under high temperature stress,and the variation tendency of NPQ increased first and then declined.It was found that 10.0 μg/mL of salicylic acid could increase the five kinds of chlorophyll fluorescence values compared with the control group.The expression level of HSP70 gene under high temperature was higher than those under normal conditions,while the expression level of high temperature group with salicylic acid treatment was lower than the control group.In conclusion,salicylic acid showed the effect of improving the high temperature resistance of G.lemaneiformis.