20 research outputs found

    Characterization of the promoter library.

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    <p>(A) Sequence analysis of the selected promoters. N = A, G, T or C. (B) Determination of promoter strength from the transcript quantification of the <i>gfp</i> gene (black) and dynamics of GFP production based on fluorescence intensity (gray). (C) Specific NoxE activity (black) under the control of eleven selected promoters (promoter activity is shown as gray). In panels (B) and (C) the values are means ± standard deviations of three independent experiments.</p

    Metabolite accumulation and cell survival of <i>L. lactis</i> DA and the recombinant strain.

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    <p>Lactate production (A) and diacetyl production (B) by strains <i>L. lactis</i> DA (▪) and <i>L. lactis</i> DA/pB6nox (•) in RSM added 1% (wt/vol) glucose. Cell survival (C) and H<sub>2</sub>O<sub>2</sub> accumulation (D) in <i>L. lactis</i> DA (▪) and <i>L. lactis</i> DA/pB6nox (•) after aerobic cultivation in GM 17 medium. In panels (A), (B), (C) and (D) the values are means ± standard deviations of three independent experiments.</p

    Promoter library for constitutive gene expression in <i>L. lactis</i>.

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    <p>The activity of the promoter is measured as RFU per OD600. The data are the means and standard deviations of results from five independent experiments. The arrowhead indicates the native promoter O159.</p

    Metabolic pathway of glycolysis and diacetyl biosynthesis in L. lactis.

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    <p>PEP, phosphoenolpyruvate; LDH, lactate dehydrogenase; ALS, α-acetolactate synthase; ALDB, acetolactate decarboxylase; PDH, pyruvate dehydrogenase; DR, diacetyl reductase; PFL, pyruvate formate lyase; NoxE, H<sub>2</sub>O-forming NADH oxidase.</p

    DataSheet_1_Genetic polymorphism in HTR2A rs6313 is associated with internet addiction disorder.docx

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    IntroductionInternet addiction disorder (IAD) has grown into public health concern of global proportions. Previous studies have indicated that individuals with IAD may exhibit altered levels of serotonin and dopamine, which are known to play crucial roles in depression, anxiety, impulsivity, and addiction. Therefore, polymorphisms in the receptors that mediate the effects of serotonin and dopamine and affect their functional states as well as their activities are suspect. In this study, we aimed to investigate the association between IAD and rs6313 (T102C) polymorphism in the serotonin 2A receptor (5-HT2A) gene, (HTR2A).MethodsTwenty patients with IAD and twenty healthy controls (HCs) were included in this study. Young’s Internet Addiction Test (IAT), Self-Rating Anxiety Scale, Self-Rating Depression Scale, Yale-Brown Obsessive-Compulsive Scale (Y-BOCS), Barratt Impulse Scale, Pittsburgh Sleep Quality Index (PSQI), and Social Support Rating Scale (SSRS) were used to assess the severity of internet addiction, mental status, impulsive traits, sleep quality, and social support. Genotyping was performed to identify rs6313 polymorphisms in the HTR2A gene of all participants.ResultsThe frequencies of the C and T alleles of HTR2A T102C were 28% and 72% in the IAD group and 53% and 47% in the HCs group, respectively, indicating that the differences between these two groups were significant. No significant difference was observed in the distribution of the CC, CT, and TT genotypes of HTR2A gene T102C between the IAD and the HCs groups. Additionally, there was no difference in the distribution of the frequencies of the HTR2A gene T102C CC and CT+TT genotypes between the two groups. However, the distribution between the TT and CC+CT genotypes showed an apparent statistical difference in the HTR2A gene T102C between the two groups. Correlation analysis indicated that the IAT score was positively correlated with the Y-BOCS and BIS scores for the CC+CT genotype in patients with IAD. Moreover, the IAT score was positively correlated with the PSQI score in patients with IAD carrying the TT genotype.ConclusionThe present study demonstrates that rs6313 in HTR2A is associated with IAD, and that the T allele of rs6313 in HTR2A may be a risk factor for IAD.</p

    Total Syntheses of β‑Carboline Alkaloids Manzamine C, Orthoscuticelline C, and Quassidine S

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    A regioselective olefin hydrofunctionalization reaction of pavettine (4) with various nucleophiles was developed and used as the key step in the total syntheses of β-carboline natural products manzamine C (3), orthoscuticelline C (5), and quassidine S (6). In the 6-step total synthesis of manzamine C (3), an efficient two-step procedure, comprising a Wittig olefination reaction and a Fukuyama–Mitsunobu reaction, was devised for the synthesis of the N-macrocycle with a Z-olefin

    Interactions of CuO nanoparticles with the algae <i>Chlorella pyrenoidosa</i>: adhesion, uptake, and toxicity

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    <p>The potential adverse effects of CuO nanoparticles (NPs) have increasingly attracted attention. Combining electron microscopic and toxicological investigations, we determined the adhesion, uptake, and toxicity of CuO NPs to eukaryotic alga <i>Chlorella pyrenoidosa</i>. CuO NPs were toxic to <i>C. pyrenoidosa</i>, with a 72 h EC<sub>50</sub> of 45.7 mg/L. Scanning electron microscopy showed that CuO NPs were attached onto the surface of the algal cells and interacted with extracellular polymeric substances (EPS) excreted by the organisms. Transmission electron microscopy (TEM) showed that EPS layer of algae was thickened by nearly 4-fold after CuO NPs exposure, suggesting a possible protective mechanism. In spite of the thickening of EPS layer, CuO NPs were still internalized by endocytosis and were stored in algal vacuoles. TEM and electron diffraction analysis confirmed that the internalized CuO NPs were transformed to Cu<sub>2</sub>O NPs (d-spacing, ∼0.213 nm) with an average size approximately 5 nm. The toxicity investigation demonstrated that severe membrane damage was observed after attachment of CuO NPs with algae. Reactive oxygen species generation and mitochondrial depolarization were also noted upon exposure to CuO NPs. This work provides useful information on understanding the role of NPs–algae physical interactions in nanotoxicity.</p
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