Study of effects of environmental factors on biochemical compositions of four species of marine single-celled algae

Photosynthetic rates (PR ) of four species of marine single- celled algae were determined by means of 14C-tracer method under the experimental modelling conditions. The effects of environmental factors, such as light, temperature and nutrients, on the biochemical compositions of the algae were studied. The results indicate that the suitable light intensities for the growth of Phaeodactylum tricorntum, Dunaliella spp, Skeletonema costatum and Isochrysis galbana are in the range from 5. 8 X 103 to 15 x 103 lx, showing an increasing trend of photosynthetic rates with the heightened light intensities. The irradiance response of Dunaliella spp. and Isochrysis galbana is significant. The contents of carbohydrate increase, but those of protein decrease, and the contents of lipids change very little. The optimum temperatures for the growth of the four species of algae are 14, 26, 21 and 26t respectively, characterized by the maxima of PR and the contents of carbohydrate, protein and lipid as well as their variations. The apparent activation energies in the photosynthesis process of Phaeodactylum tricornutum, Dunaliella spp., Skeletonema costatum and Isochrysis galbana are 23. 2, 38. 5, 22. 4 and 61. 7 kJ/mol respectively, and the temperature coefficients for the four algae are 1. 74, 1. 74, 1. 38 and 1. 69 respectively. The peaks of PR appeared in some culture media (N/P = 16 ) of Phaeodactylum tricornutum and Skeletonema costatum, and in other media (N/P = 28) of Dunaliella spp. and Isochurysis galbana. The contents and their variations of carbohydrate, protein and lipid of the four species of algae are all maximum when N/P is equal to 16 in culture media.

Targeting STAT3 with SH-4-54 suppresses stemness and chemoresistance in cancer stem-like cells derived from colorectal cancer

BACKGROUND Over the years,the numbers of treatment options for colorectal cancer(CRC)have increased,leading to notable improvements in the overall survival of CRC patients.Although therapy may initially yield positive results,the development of drug resistance can result in treatment failure and cancer recurrence.This resistance is often attributed to the presence of cancer stem cells(CSCs).These CSCs not only contribute to therapeutic resistance but also play crucial roles in the initiation and development of tumor metastasis.AIM To investigate the antitumor effects of SH-4-54,which are mediated by targeting CSCs relative to treatment outcomes.METHODS CSCs were enriched by culturing CRC cells in serum-free medium.Hallmarks of stemness and IL-6/JAK2/STAT3 signaling were detected by Western blotting.Indicators of CSC malignancy,including proliferation,invasion,and tumor formation,were measured.RESULTS In this study,we employed SH-4-54,which exhibits anticancer activity in solid tumors through targeting the SH2 domain of both the signal transducer and activator of transcription(STAT)3 and the STAT5,and evaluated its effects on stemness and chemoresistance in colorectal CSCs.As expected,SH-4-54 treatment inhibited the phosphorylation of STAT3(p-STAT3)and decreased the percentage of ALDH1A1-positive CRC cells.The addition of SH-4-54 dissociated colorectal spheroids and decreased the expression of stemness markers,including ALDH1A1,CD44 and Nanog.SH-4-54 treatment decreased IL-6/JAK2/STAT3 signaling by inhibiting p-STAT3 and thus inhibited spheroid formation by SW480 and LoVo cells.Moreover,SH-4-54 treatment inhibited indicators of malignancy,including cell proliferation,invasion,and tumor formation,in CSCs in vitro and in vivo.Notably,SH-4-54 treatment significantly increased chemosensitivity to oxaplatin.CONCLUSION Taken together,these results indicate that SH-4-54 is a promising molecule that exerts antitumor effects on colorectal CSCs by inhibiting STAT3 signaling.

Long non-coding RNA H19 regulates neurogenesis of induced neural stem cells in a mouse model of closed head injury

Stem cell-based therapies have been proposed as a potential treatment for neural regeneration following closed head injury.We previously reported that induced neural stem cells exert beneficial effects on neural regeneration via cell replacement.However,the neural regeneration efficiency of induced neural stem cells remains limited.In this study,we explored differentially expressed genes and long non-coding RNAs to clarify the mechanism underlying the neurogenesis of induced neural stem cells.We found that H19 was the most downregulated neurogenesis-associated lnc RNA in induced neural stem cells compared with induced pluripotent stem cells.Additionally,we demonstrated that H19 levels in induced neural stem cells were markedly lower than those in induced pluripotent stem cells and were substantially higher than those in induced neural stem cell-derived neurons.We predicted the target genes of H19 and discovered that H19 directly interacts with mi R-325-3p,which directly interacts with Ctbp2 in induced pluripotent stem cells and induced neural stem cells.Silencing H19 or Ctbp2 impaired induced neural stem cell proliferation,and mi R-325-3p suppression restored the effect of H19 inhibition but not the effect of Ctbp2 inhibition.Furthermore,H19 silencing substantially promoted the neural differentiation of induced neural stem cells and did not induce apoptosis of induced neural stem cells.Notably,silencing H19 in induced neural stem cell grafts markedly accelerated the neurological recovery of closed head injury mice.Our results reveal that H19 regulates the neurogenesis of induced neural stem cells.H19 inhibition may promote the neural differentiation of induced neural stem cells,which is closely associated with neurological recovery following closed head injury.

Bone marrow-derived mesenchymal stem cell-derived exosomeloaded miR-129-5p targets high-mobility group box 1 attenuates neurological-impairment after diabetic cerebral hemorrhage

BACKGROUND Diabetic intracerebral hemorrhage(ICH)is a serious complication of diabetes.The role and mechanism of bone marrow mesenchymal stem cell(BMSC)-derived exosomes(BMSC-exo)in neuroinflammation post-ICH in patients with diabetes are unknown.In this study,we investigated the regulation of BMSC-exo on hyperglycemia-induced neuroinflammation.AIM To study the mechanism of BMSC-exo on nerve function damage after diabetes complicated with cerebral hemorrhage.METHODS BMSC-exo were isolated from mouse BMSC media.This was followed by transfection with microRNA-129-5p(miR-129-5p).BMSC-exo or miR-129-5poverexpressing BMSC-exo were intravitreally injected into a diabetes mouse model with ICH for in vivo analyses and were cocultured with high glucoseaffected BV2 cells for in vitro analyses.The dual luciferase test and RNA immunoprecipitation test verified the targeted binding relationship between miR-129-5p and high-mobility group box 1(HMGB1).Quantitative polymerase chain reaction,western blotting,and enzyme-linked immunosorbent assay were conducted to assess the levels of some inflammation factors,such as HMGB1,interleukin 6,interleukin 1β,toll-like receptor 4,and tumor necrosis factorα.Brain water content,neural function deficit score,and Evans blue were used to measure the neural function of mice.RESULTS Our findings indicated that BMSC-exo can promote neuroinflammation and functional recovery.MicroRNA chip analysis of BMSC-exo identified miR-129-5p as the specific microRNA with a protective role in neuroinflammation.Overexpression of miR-129-5p in BMSC-exo reduced the inflammatory response and neurological impairment in comorbid diabetes and ICH cases.Furthermore,we found that miR-129-5p had a targeted binding relationship with HMGB1 mRNA.CONCLUSION We demonstrated that BMSC-exo can reduce the inflammatory response after ICH with diabetes,thereby improving the neurological function of the brain.

miR-24-3p promotes proliferation and inhibits apoptosis of porcine granulosa cells by targeting P27

Ovarian follicle development is associated with the physiological functions of granulosa cells(GCs),including proliferation and apoptosis.The level of miR-24-3p in ovarian tissue of high-yielding Yorkshire×Landrace sows was significantly higher than that of low-yielding sows.However,the functions of miR-24-3p on GCs are unclear.In this study,using flow cytometry,5-ethynyl-2′-de-oxyuridine(EdU)staining,and cell count,we showed that miR-24-3p promoted the proliferation of GCs increasing the proportion of cells in the S phase and upregulating the expression of cell cycle genes,moreover,miR-24-3p inhibited GC apoptosis.Mechanistically,on-line prediction,bioinformatics analysis,a luciferase reporter assay,RT-qPCR,and Western blot results showed that the target gene of miR-24-3p in proliferation and apoptosis is cyclin-dependent kinase inhibitor 1B(P27/CDKN1B).Furthermore,the effect of miR-24-3p on GC proliferation and apoptosis was attenuated by P27 overexpression.These findings suggest that miR-24-3p regulates the physiological functions of GCs.

MiR-150-5p inhibits cell proliferation and metastasis by targeting FTO in osteosarcoma

Background:Osteosarcoma(OS),recognized as the predominant malignant tumor originating from bones,necessitates an in-depth comprehension of its intrinsic mechanisms to pinpoint novel therapeutic targets and enhance treatment methodologies.The role of fat mass and obesity-associated(FTO)in OS,particularly its correlation with malignant traits,and the fundamental mechanism,remains to be elucidated.Materials and Methods:1.The FTO expression and survival rate in tumors were analyzed.2.FTO in OS cell lines was quantified utilizing western blot and PCR.3.FTO was upregulated and downregulated separately in MG63.4.The impact of FTO on the proliferation and migration of OS cells was evaluated using CCK-8,colony formation,wound healing,and Transwell assays.5.The expression of miR-150-5p in OS cells-derived exosomes was identified.6.The binding of miR-150-5p to FTO was predicted by TargetScan and confirmed by luciferase reporter assay.7.The impact of exosome miR-150-5p on the proliferation and migration of OS cells was investigated.Results:The expression of FTO was higher in OS tissues compared to normal tissues correlating with a worse survival rate.Furthermore,the downregulation of FTO significantly impeded the growth and metastasis of OS cells.Additionally,miR-150-5p,which was downregulated in both OS cells and their derived exosomes,was found to bind to the 3′-UTR of FTO through dual luciferase experiments.Exosomal miR-150-5p was found to decrease the expression of FTO and inhibit cell viability.Conclusions:We identified elevated levels of FTO in OS,which may be attributed to insufficient miR-150-5p levels in both the cells and exosomes.It suggests that the dysregulation of miR-150-5p and its interaction with FTO could potentially promote the development of OS.

Exosome-Transmitted miR-224-5p Promotes Colorectal Cancer Cell Proliferation via Targeting ULK2 in p53-Dependent Manner

Objective To investigate the role and molecular mechanism of exosomal miR-224-5p in colorectal cancer(CRC).Methods The miR-224-5p expression in CRC patient tissues and cell-derived exosomes was measured by laser capture microdissection and qRT-PCR,respectively.Dual-luciferase reporter gene assay was used to determine the target gene of miR-224-5p.The protein expressions of p53 and unc-51 like kinase 2(ULK2)in CRC cells were detected by western blot.Flow cytometry was used to detect cell cycle and apoptosis.Cell proliferation was measured by CCK8 and EdU assay.Results The miR-224-5p expression was upregulated in CRC tissues and increased progressively with the rise of CRC stage.CRC cells secreted extracellular miR-224-5p mainly in an exosome-dependent manner,and then miR-224-5p could be transferred to surrounding tumor cells to regulate cell proliferation in the form of autocrine or paracrine.Moreover,ULK2 was characterized as a direct target of miR-224-5p and was downregulated in CRC tissues.Interestingly,ULK2 inhibited CRC cell proliferation in a p53-dependent manner.Furthermore,exosome-derived miR-224-5p partially reversed the proliferation regulation of ULK2 on CRC cells.Conclusion Our findings demonstrate that exosome-transmitted miR-224-5p promotes p53-dependent cell proliferation by targeting ULK2 in CRC,which may offer promising targets for CRC prevention and therapy.

Effects of miR-214-5p and miR-21-5p in hypoxic endometrial epithelial-cell-derived exosomes on human umbilical cord mesenchymal stem cells

BACKGROUND Thin endometrium seriously affects endometrial receptivity,resulting in a significant reduction in embryo implantation,and clinical pregnancy and live birth rates,and there is no gold standard for treatment.The main pathophysiological characteristics of thin endometrium are increased uterine arterial blood flow resistance,angiodysplasia,slow growth of the glandular epithelium,and low expression of vascular endothelial growth factor,resulting in endometrial epithelial cell(EEC)hypoxia and endometrial tissue aplasia.Human umbilical cord mesenchymal stem cells(HucMSCs)promote repair and regeneration of damaged endometrium by secreting microRNA(miRNA)-carrying exosomes.However,the initiation mechanism of HucMSCs to repair thin endometrium has not yet been clarified.AIM To determine the role of hypoxic-EEC-derived exosomes in function of HucMSCs and explore the potential mechanism.METHODS Exosomes were isolated from normal EECs(EEC-exs)and hypoxia-damaged EECs(EECD-exs),before characterization using Western blotting,nanoparticletracking analysis,and transmission electron microscopy.HucMSCs were cocultured with EEC-exs or EECD-exs and differentially expressed miRNAs were determined using sequencing.MiR-21-5p or miR-214-5p inhibitors or miR-21-3p or miR-214-5p mimics were transfected into HucMSCs and treated with a signal transducer and activator of transcription 3(STAT3)activator or STAT3 inhibitor.HucMSC migration was assessed by Transwell and wound healing assays.Differentiation of HucMSCs into EECs was assessed by detecting markers of stromal lineage(Vimentin and CD13)and epithelial cell lineage(CK19 and CD9)using Western blotting and immunofluorescence.The binding of the miRNAs to potential targets was validated by dual-luciferase reporter assay.RESULTS MiR-21-5p and miR-214-5p were lowly expressed in EECD-ex-pretreated HucMSCs.MiR-214-5p and miR-21-5p inhibitors facilitated the migratory and differentiative potentials of HucMSCs.MiR-21-5p and miR-214-5p targeted STAT3 and protein inhibitor of activated STAT3,respectively,and negatively regulated phospho-STAT3.MiR-21-5p-and miR-214-5p-inhibitor-induced promotive effects on HucMSC function were reversed by STAT3 inhibition.MiR-21-5p and miR-214-5p overexpression repressed HucMSC migration and differentiation,while STAT3 activation reversed these effects.CONCLUSION Low expression of miR-21-5p/miR-214-5p in hypoxic-EEC-derived exosomes promotes migration and differentiation of HucMSCs into EECs via STAT3 signaling.Exosomal miR-214-5p/miR-21-5p may function as valuable targets for thin endometrium.

Insight into Function and Subcellular Localization of a Type III-Secreted Effector in Pseudomonas syringae pv. tomato DC3000

Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) is a bacterial pathogen of tomato and of the model plants Arabidopsis and Nicotiana benthamiana (N. benthamiana). Like numerous Gram-negative bacterial pathogens of animals and plants, Pst DC3000 exploits the conserved type III secretion system (TTSS) to deliver multiple virulence effectors directly into the host cells. Type III effectors (T3Es) collectively participate in causing disease, by mechanisms that are not well clarity. Elucidating the virulence function of individual effector is fundamental for understanding bacterial infection of plants. Here, we focused on studying one of these effectors, HopAA1-1, and analyzed its potential function and subcellular localization in N. benthamiana. Using an Agrobacterium-mediated transient expression system, we found that HopAA1-1 can trigger domain-dependent cell death in N. benthamiana. The observation using confocal microscopy showed that the YFP-tagged HopAA1-1 localizes to diverse cellular components containing nucleus, cytoplasm and cell membrane, which was demonstrated through immunoblot analysis of membrane fractionation and nuclear separation. Enforced HopAA1-1 subcellular localization, by tagging with a nuclear localization sequence (NLS) or a nuclear export sequence (NES), shows that HopAA1-1-induced cell death in N. benthamiana is suppressed in the nucleus but enhanced in the cytoplasm. Our research is lay a foundation for revealed the molecular pathogenesis of Pseudomonas syringae pv. tomato.

Exosomes derived from microRNA-540-3p overexpressing mesenchymal stem cells promote immune tolerance via the CD74/nuclear factor-kappaB pathway in cardiac allograft

BACKGROUND Heart transplantation is a crucial intervention for severe heart failure,yet the challenge of organ rejection is significant.Bone marrow mesenchymal stem cells(BMSCs)and their exosomes have demonstrated potential in modulating T cells,dendtitic cells(DCs),and cytokines to achieve immunomodulatory effects.DCs,as key antigen-presenting cells,play a critical role in shaping immune responses by influencing T-cell activation and cytokine production.Through this modulation,BMSCs and their exosomes enhance graft tolerance and prolonging survival.AIM To explore the immunomodulatory effects of exosomes derived from BMSCs overexpressing microRNA-540-3p(miR-540-3p)on cardiac allograft tolerance,focusing on how these exosomes modulating DCs and T cells activity through the CD74/nuclear factor-kappaB(NF-κB)pathway.METHODS Rat models were used to assess the impact of miR-540-3p-enhanced exosomes on immune tolerance in cardiac allografts.MiR-540-3p expression was manipulated in BMSCs,and derived exosomes were collected and administered to the rat models post-heart transplantation.The study monitored expression levels of major histocompatibility complex II,CD80,CD86,and CD274 in DCs,and quantified CD4^(+)and CD8^(+)T cells,T regulatory cells,and cytokine profiles.RESULTS Exosomes from miR-540-3p-overexpressing BMSCs lead to reduced expression of immune activation markers CD74 and NF-κB p65 in DCs and T cells.Rats treated with these exosomes showed decreased inflammation and improved cardiac function,indicated by lower levels of pro-inflammatory cytokines(interleukin-1β,interferon-γ)and higher levels of anti-inflammatory cytokines(interleukin-10,transforming growth factorβ1).Additionally,miR-540-3p skewed the profiles of DCs and T cells towards immune tolerance,increasing the ratio of T regulatory cells and shifting cytokine secretion to favor graft acceptance.CONCLUSION Exosomes derived from BMSCs overexpressing miR-540-3p significantly enhance immune tolerance and prolong cardiac allograft survival by modulating the CD74/NF-κB pathway,which regulates activities of DCs and T cells.These findings highlight a promising therapeutic strategy to improve heart transplantation outcomes and potentially reduce the need for prolonged immunosuppression.

Ghrelin regulates insulin resistance by targeting insulin-like growth factor-1 receptor via miR-455-5p in hepatic cells

Objective: To explore the mechanism by which ghrelin regulates insulin sensitivity through modulation of miR-455-5p in hepatic cells. Methods: HepG2 cells were treated with or without DAG (1 μM). Glucose consumption, intracellular glycogen content, phosphorylation of PI3K and Akt stimulated by insulin, expression of miR-455-5p, as well as IGF-1R protein level were analyzed. In addition, bioinformatic analysis, dual luciferase reporter assay, miR- 455-5p mimic or inhibitor treatment was conducted to investigate the molecular mechanisms. Results: High glucose treatment upregulated miR-455-5p expression but reduced glucose consumption and glycogen content. DAG reversed the effect of high glucose on glucose metabolism, increased protein level of IGF-1R and phosphorylation of PI3K/Akt stimulated by insulin, as well as downregulated miR-455-5p expression. Bioinformatic analysis indicated IGF-1R was the target of miR-455-5p. Dual luciferase reporter assay, as well as transfection with miR-455-5p mimic/inhibitor confirmed that DAG activated IGF-1R/PI3K/Akt signaling via inhibiting miR-455-5p. Conclusion: DAG improves insulin resistance via miR-455-5p- mediated activation of IGF-1R/PI3K/Akt system, suggesting that suppression of miR-455-5p or activation of DAG may be potential targets for T2DM therapy.

Inhibitory Effect of Flavonoid Glycosides from Chlorophytum comosum on Nasopharyngeal Carcinoma 5-8F Cells and Its Mechanism

[Objectives]To study the inhibitory activity of two flavonoid glycosides isolated from Chlorophytum comosum Laxum R.Br on human nasopharyngeal carcinoma(NPC)cell line 5-8F in vitro and its mechanism.[Methods]The flavonoid glycosides were isolated and purified from the ethanol alcoholic extract of the roots of Liliaceae plant Chlorophytum comosum by silica gel column chromatography,macroporous resin column chromatography,Sephadex LH-20,and reverse column chromatography(ODS).The inhibitory activity of flavonoid glycosides on human nasopharyngeal carcinoma cells was analyzed by CCK-8 method,and the potential mechanism was preliminarily analyzed by molecular docking.[Results]Two flavonoid glycosides were identified as isovitexin 2″-0-rhamnoside and 7-2″-di-O-β-glucopyranosylisovitexin.Two flavonoid glycosides showed promising inhibitory effect on human nasopharyngeal carcinoma cell line 5-8F,with IC_(50) values of 24.8 and 27.5μmol/L,respectively.Molecular docking results showed that the potential targets of two flavonoid glycosides include CyclinD1,Bcl-2β-Catenin,ILK,TGF-β,in addition,two glycosides showed higher predicted binding affinity towards CyclinD1,which verifies the cytotoxicity of the two compounds on human nasopharyngeal carcinoma cell line 5-8F in vitro.[Conclusions]Two flavonoid glycosides are the active molecules in Chlorophytum comosum that can inhibit the proliferation of human nasopharyngeal carcinoma cells,and have the potential to be used in the research and development of anti nasopharyngeal carcinoma drugs.

Automatic cell object extraction of red tide algae in microscopic images

Extracting the cell objects of red tide algae is the most important step in the construction of an automatic microscopic image recognition system for harmful algal blooms.This paper describes a set of composite methods for the automatic segmentation of cells of red tide algae from microscopic images.Depending on the existence of setae,we classify the common marine red tide algae into non-setae algae species and Chaetoceros,and design segmentation strategies for these two categories according to their morphological characteristics.In view of the varied forms and fuzzy edges of non-setae algae,we propose a new multi-scale detection algorithm for algal cell regions based on border-correlation,and further combine this with morphological operations and an improved GrabCut algorithm to segment single-cell and multicell objects.In this process,similarity detection is introduced to eliminate the pseudo cellular regions.For Chaetoceros,owing to the weak grayscale information of their setae and the low contrast between the setae and background,we propose a cell extraction method based on a gray surface orientation angle model.This method constructs a gray surface vector model,and executes the gray mapping of the orientation angles.The obtained gray values are then reconstructed and linearly stretched.Finally,appropriate morphological processing is conducted to preserve the orientation information and tiny features of the setae.Experimental results demonstrate that the proposed methods can effectively remove noise and accurately extract both categories of algae cell objects possessing a complete shape,regular contour,and clear edge.Compared with other advanced segmentation techniques,our methods are more robust when considering images with different appearances and achieve more satisfactory segmentation effects.

Overexpression of 14-3-3 protein protects pheochromocytoma cells against 1-methyl-4-phenylpyridinium toxicity

Objective To investigate the effects of 14-3-3 protein overexpression on the 1-methyl-4-phenylpyridinium （MPP^＋） induced pheochromocytoma （PC12） cell death and the potential mechanisms. Methods pcDNA3.1（＋）-14-3-3 plasmids, which could be expressed in mammalian cell, were constructed and transfected into PC 12 cells with Lipofectamine 2000. The expression of 14-3-3 protein, Bcl-2 protein, and BAD protein were determined by western blot. 3-（4,5- dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay, microplate reader, and flow cytometric analysis were used to measure cell viability, the caspase activity, and apoptotic ratio respectively. Results （1） The expression of 14-3-3 protein increased significantly three weeks after pcDNA3.1（＋）-14-3-3 plasmids transfected into PC 12 cells. （2） MPP^＋ caused a decrease of cell viability in a dose-dependent manner. At 100μmol/L MPP^＋, cell viability reduced approximately 50%. （3） The caspase activity increased along with the MPP^＋ concentrations rising and reached its maximum value （0.34 μmol/mg protein） at 100 μmol/L MPP＊. However caspase activity decreased significantly when the MPP^＋ concentration exceeded 100 μmol/L. （4） Overexpression of 14-3-3 protein decreased the apoptosis ratio of PC 12 cells treated with 100μmol/L MPP^＋ from 26.5% to 8.6%. （5） Bcl-2 protein tended to decrease but BAD protein tended to increase after treatment of PC 12 cells with 100 μmol/L MPP^＋. Overexpression of 14-3-3 protein significantly increased the cellular level of Bcl-2 protein and decreased that of BAD protein. Conclusion Overexpression of 14-3-3 protein may reduce MPP^＋-induced apoptotic cell death in PC12 cells by up-regulating the Bcl-2 expression and down-regulating the BAD expression. These results may provide a promising target for treatment of Parkinson＇s disease.

Involvement of ERK1/2 and p38 MAPK in up-regulation of 14-3-3 protein induced by hydrogen peroxide preconditioning in PC12 cells

Objective To investigate the protective effects of hydrogen peroxide preconditioning （HPP） on the pheochromocytoma （PC12） cells treated with 1-methyl-4-phenylpyridinium （MPP^＋） and to explore the potential mechanisms. Methods The viability and apoptosis of PC 12 cells were determinded by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide （MTT） assay and 4′,6′-diamidino-2-phenylindole （DAPI） staining, respectively. The expressions of 14-3-3 protein and phospholylated p38 mitogen-activated protein kinase （MAPK） were determined by Western blot. Enzyme-linked immunosorbent assay （ELISA） was used to measure the activity of extracellular signal-regulated protein kinase 1/2 （ERK1/2）. Results The cell viability decreased and the number of apoptotic cells increased dramatically in MPP^＋ group compared with that in Control group. HPP induced a significant increase in cell viability and a marked decrease in population of apoptotic cells of the MPP^＋- treated PC 12 cells, accompanied with up-regulation of 14-3-3 protein and increase of ERK 1/2 and p38 MAPK activities. The 14-3-3 protein expression was positively correlated with the phosphorylation of ERK1/2. Furthermore, inhibition of the ERK1/2 with PD98059 abolished the 14-3-3 protein up-regulation in PC 12 cells induced by HPP. Conclusion HPP protects PC 12 cells against MPP＋ toxicity by up-regulating 14-3-3 protein expression through the ERK1/2 and p38 MAPK signaling pathways.

Ionic Conduction and Fuel Cell Performance of Ba0.98Ce0.8Tm0.2O3-α Ceramic

The perovskite-type oxide solid solution Ba0.98Ce0.8Tm0.2O3-α was prepared by high temperature solid-state reaction and its single phase character was confirmed by X-ray diffraction. The conduction property of the sample was investigated by alternating current impedance spectroscopy and gas concentration cell methods under different gases atmospheres in the temperature range of 500-900 ℃. The performance of the hydrogen-air fuel cell using the sample as solid electrolyte was measured. In wet hydrogen, the sample is a pure protonic conductor with the protonic transport number of 1 in the range of 500-600 ℃, a mixed conductor of proton and electron with the protonic transport number of 0.945-0.933 above 600 ℃. In wet air, the sample is a mixed conductor of proton, oxide ion, and electronic hole. The protonic transport numbers are 0.010-0.021, and the oxide ionic transport numbers are 0.471-0.382. In hydrogen-air fuel cell, the sample is a mixed conductor of proton, oxide ion and electron, the ionic transport numbers are 0.942 0.885. The fuel cell using Ba0.98Ce0.8Tm0.2O3-α as solid electrolyte can work stably. At 900 ℃, the maximum power output density is 110,2 mW/cm2, which is higher than that of our previous cell using Ba0.98Ce0.8Tm0.2O3-α （x〈≤1, RE=Y, Eu, Ho） as solid electrolyte.

一种基于三苯胺-噻吩基团的新型荧光探针在藻细胞中检测CN‒的应用

氰根离子(CN‒)是最具毒性的阴离子之一,一些食用藻类可以从其生活环境中释放氰化物或吸收氰化物,这可能对人类健康造成危害。因此,设计并合成了一种新的荧光探针TI,可用于在活体藻类细胞中检测CN‒。探针TI由三苯胺-噻吩部分和吲哚部分组成,其分子结构中碳氮双键易与CN‒发生亲核加成反应,碳氮双键中共轭π键被打断,探针TI在473 nm处出现显著的蓝色荧光,从而可用来检测CN‒。探针TI可单一性识别CN‒,最低检测限可达95.7 nmol/L。最重要的是,探针TI可用于实时检测活藻类细胞和食用藻类中的CN‒。

Ni doped La_(0.6)Sr_(0.4)FeO_(3-δ) symmetrical electrode for solid oxide fuel cells

The conventional Ni cermet anode suffers from severe carbon deposition and sulfur poisoning when fossil fuels are used. Alternative anode materials are desired for high performance hydrocarbon fuel solid oxide fuel cells （SOFCs）. We report the rational design of a very active Ni doped La0.6Sr0.4FeO3‐δ（LSFN） electrode for hydrocarbon fuel SOFCs. Homogeneously dispersed Ni‐Fe alloy nanoparticles were in situ extruded onto the surface of the LSFN particles during the operation of the cell. Sym‐metric SOFC single cells were prepared by impregnating a LSFN precursor solution onto a YSZ （yt‐tria stabilized zirconia） monolithic cell with a subsequent heat treatment. The open circuit voltage of the LSFN symmetric cell reached 1.18 and 1.0 V in humidified C3H8 and CH4 at 750？？, respective‐ly. The peak power densities of the cells were 400 and 230 mW/cm2 in humidified C3H8 and CH4, respectively. The electrode showed good stability in long term testing, which revealed LSFN has good catalytic activity for hydrocarbon fuel oxidation.

Allelopathic effect of Acorus tatarinowii upon algae

Besides competing with algae for light and mineral nutrients (i. e. N, P, etc.), the root system of Acorus tatarinowii excretes some chemical substances, which injure and eliminate alga cells, to inhibit the growth of the algae. When the algae cells were treated in 'A. tatarinowii water', some of the chlorophyll a were destroyed and the photosynthetic rate of algae decreased markedly and the ability of alga cells to deoxidize triphenyltetrazolium chloride (TTC) reduced greatly. Then alga cells turned from bright red to bluish green under fluorescence microscope. These showed that the allelopathic effects of A. tatarinowii on algae were obvious and planting A. tatarinowii can control some green algae. The experiment on the extractions of the secretions of the root system showed that the inhibitory effect had a concentration effect. If the concentration of the root secretion was below 30 μl/disc, the inhibitory rate was negative; if it was over 45 μl/disc, the inhibitory rate was positive. This proved that the influence of the root secretion on the same acceptor was a kind of concentration effect. When the concentration of the root secretion was low, it promoted the growth of algae; when the concentration reached a definite threshold value, it restrained the growth of algae. In present case, the threshold value was between 30 μl/disc and 45 μl/disc.

Rice leaf inclination2, a VIN3-1ike protein, regulates leaf angle through modulating cell division of the collar

As an important agronomic trait, inclination of leaves is crucial Ior crop architecture and grain yields. 10 understand the molecular mechanism controlling rice leaf angles, one rice leaf inclination2 （1c2, three alleles） mutant was identified and functionally characterized. Compared to wild-type plants, lc2 mutants have enlarged leaf angles due to increased cell division in the adaxial epidermis of lamina joint. The LC2 gene was isolated through positional cloning, and encodes a vernalization insensitive 3-like protein. Complementary expression of LC2 reversed the enlarged leaf angles of lc2 plants, confirming its role in controlling leaf inclination. LC2 is mainly expressed in the lamina joint during leaf development, and particularly, is induced by the phytohormones abscisic acid, gibberellic acid, auxin, and brassinosteroids. LC2 is localized in the nucleus and defects of LC2 result in altered expression of cell division and hormone-responsive genes, indicating an important role of LC2 in regulating leaf inclination and mediating hormone effects.