In this study, we design a homogeneous system consisting of Ag nanoprisms and glucose oxidase (GOx) for simple, sensitive, and low-cost colorimetric sensing of glucose in serum. The unmodified Ag nanoprisms and GOx are first mixed with each other. Glucose is then added in the homogeneous mixture. Finally, the nanoplates are etched from triangle to round by H2O2 produced by the enzymatic oxidation, which leads to a more than 120 nm blue shift of the surface plasmon resonance (SPR) absorption band of the Ag nanoplates. This large wavelength shift can be used not only for visual detection (from blue to mauve) of glucose by naked eyes but for reliable and convenient glucose quantification in the range from 2.0 × 10(-7) to 1.0 × 10(-4) M. The detection limit is as low as 2.0 × 10(-7) M, because the used Ag nanoprisms possess (1) highly reactive edges/tips and (2) strongly tip sharpness and aspect ratio dependent SPR absorption. Owing to ultrahigh sensitivity, only 10-20 μL of serum is enough for a one-time determination. The proposed glucose sensor has great potential in the applications of point-of-care diagnostics, especially for third-world countries where high-tech diagnostics aids are inaccessible to the bulk of the population.
The regulation of stomatal lineage cell development has been extensively investigated. However a comprehensive characterization of this biological process based on single-cell transcriptome analysis has not yet been reported. Here, we performed RNA-seq on over 12,844 individual cells from the cotyledons of five-day-old Arabidopsis seedlings. We identified 11 cell clusters corresponding mostly to cells at specific stomatal developmental stages with a series of new marker genes. Comparative analysis of genes with the highest variable expression in these cell clusters revealed three transcriptional networks that regulate the development of mesophyll and guard cells, as well as the differentiation from protodermal to guard mother cells. We investigated the developmental dynamics of marker genes via pseudo-time analysis which revealed potential interactions between them. The identification of several novel marker genes suggests new regulatory mechanisms during development of stomatal cell lineage. .
SummaryAccumulating data indicate that strigolactones (SLs) are implicated in the response to environmental stress, implying a potential effect of SLs on stomatal response and thus stress acclimatization. In this study, we investigated the molecular mechanism underlying the effect of SLs on stomatal response and their interrelation with abscisic acid (ABA) signaling.The impact of SLs on the stomatal response was investigated by conducting SL-feeding experiments and by analyzing SL-related mutants. The involvement of endogenous ABA and ABA-signaling components in SL-mediated stomatal closure was physiologically evaluated using genetic mutants. Pharmacological and genetic approaches were employed to examine hydrogen peroxide (H 2 O 2 ) and nitric oxide (NO) production.SL-related mutants exhibited larger stomatal apertures, while exogenous SLs were able to induce stomatal closure and rescue the more widely opening stomata of SL-deficient mutants. The SL-biosynthetic genes were induced by abiotic stress in shoot tissues. Disruption of ABA-biosynthetic genes, as well as genes that function in guard cell ABA signaling, resulted in no impairment in SL-mediated stomatal response. However, disruption of MORE AXILLARY GROWTH2 (MAX2), DWARF14 (D14), and the anion channel gene SLOW ANION CHANNEL-ASSOCIATED 1 (SLAC1) impaired SL-triggered stomatal closure. SLs stimulated a marked increase in H 2 O 2 and NO contents, which is required for stomatal closure.Our results suggest that SLs play a prominent role, together with H 2 O 2 /NO production and SLAC1 activation, in inducing stomatal closure in an ABA-independent mechanism.
NLR and PLR as novel inflammatory biomarkers are independent predictors of DCI development and functional outcome after acute aSAH. When combined together, they may help to identify high-risk patients more powerfully.
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