Modeling Hidden Nodes Collisions in Wireless Sensor Networks: Analysis Approach

This paper studied both types of collisions. In this paper, we show that advocated solutions for coping with hidden node collisions are unsuitable for sensor networks. We model both types of collisions and derive closed-form formula giving the probability of hidden and visible node collisions. To reduce these collisions, we propose two solutions. The first one based on tuning the carrier sense threshold saves a substantial amount of collisions by reducing the number of hidden nodes. The second one based on adjusting the contention window size is complementary to the first one. It reduces the probability of overlapping transmissions, which reduces both collisions due to hidden and visible nodes. We validate and evaluate the performance of these solutions through simulations

MEK1/2-ERK1/2 signaling pathway is essential for S1P-induced MMP-2 upregulation and invasion of HTR8/SVneo cells.

<p>(A) Cells were treated with 10 nM S1P for the indicated time. The level of phosphorylated MEK1/2, ERK1/2 were determined by western blot using phospho-specific antibodies (p-MEK1/2, pERK1/2 respectively). (B), Pretreatment of cells with 10 µM U0126, an inhibitor of MEK1/2, for 60 minutes resulted in significantly less of ERK1/2 phosphorylation (B), which downregulated level of MMP-2 (C). The invasion of MEK1/2 induced by S1P was also inhibited(D). N = 3 performed in triplicate and values were expressed as mean ±SEM with <i>p</i><0.05 considered as significant.</p

S1P promotes invasion in HTR8/SVneo Cells.

<p>The transwell insert invasion assay was performed on HTR8/SVneo cells treated with the indicated concentrations of S1P for 24 hours. Invasion index was expressed as the percentage of invaded cell number compared with the corresponding control. N = 4 performed in triplicate, values were presented as mean ±SEM with <i>p</i><0.05 considered as significant.</p

S1P induces MMP-2 expression.

<p>Gelatin zymography (A) and western blot (B) that performed on cells treated with S1P for 48 hours demonstrated that MMP-2 expression was induced by S1P. Real-time PCR revealed that expression of MMP-2 (C), but not MMP-9 (D), was induced by S1P treatment for 48 hours in HTR8/SVneo cells. Cells were transfected with control siRNA or siRNA targeting MMP-2. Knockdown expression of MMP-2 was confirmed by Real-time PCR (E). Invasion index was expressed as the percentage of invaded cell number compared with the corresponding control (F). N = 3 performed in triplicate and values were presented as mean ±SEM with <i>p</i><0.05 considered as significant.</p

S1P-induced MMP-2 upregulation and signaling pathways is mediated through S1PR1 receptor.

<p>(A) HTR8/SVneo cells were pretreated for 30 minutes with the S1PR1 and S1PR3 receptor antagonist VPC23019 (1 µM) before stimulation with S1P (10 nM). (B) HTR8/SVneo were pretreated for 30 minutes with the selective S1PR3 receptor antagonist CAY10444 (1 µM) before stimulation with S1P. (C) HTR8/SVneo were pretreated for 30 minutes with VPC23019 (1 µM) before stimulation with the selective S1PR1 receptor agonist SEW2871 (1 µM). (D) Cells were transfected with control siRNA or siRNAs targeting S1PR1 (50 pmol). Knockdown of S1P1 was confirmed by Real-time PCR. (E) Induction of MMP-2 by S1P was disrupted in siRNA transfected cells. (F) The levels of activated MEK1/2, ERK1/2 were determined by western blot using phospho-specific antibodies (p-MEK1/2, p-ERK1/2, respectively). N = 3 performed in triplicate and values were expressed as mean ±SEM with <i>p</i><0.05 considered as significant.</p

Primer sequences for Real-time qPCR.

<p>Primer sequences for Real-time qPCR.</p

A proposed model of mechanisms involving in S1P-induced invasion of HTR8/SVneo human EVT cells.

<p>A proposed model of mechanisms involving in S1P-induced invasion of HTR8/SVneo human EVT cells.</p

A new liquid chromatography–fluorescence method for determination of perfluorooctanesulphonyl fluoride upon derivatisation with 1-naphthol

<div><p>Perfluorooctanesulphonyl fluoride (PFOSF), as a main precursor of perfluorooctanesulphonate (PFOS) that is ubiquitous in the environment, has been released to the environment with substantial quantity. Determination of PFOSF presents significant analytical challenges for using liquid chromatography with UV (LC–UV) and fluorescence detection (LC–FLD) due to the lack of chromophore in the molecular structure. In this study, a new method was developed by derivatising PFOSF with 1-naphthol to form 1-naphthylperfluorooctanesulphonate (NPFOS), which allowed rapid qualitative and quantitative analysis using LC–UV and LC–FLD. The derivatising product was confirmed from the analyses by proton nuclear magnetic resonance and quadrupole–time of flight mass spectrometry. The LC–FLD method demonstrated good linearity in the NPFOS concentration range from 20 pg µL⁻¹ to 20 ng µL⁻¹ with a correlation coefficient better than 0.999, with the instrument detection limit of 1.5 pg µL⁻¹.</p></div

Image_4_Inactivation of photosynthetic cyclic electron transports upregulates photorespiration for compensation of efficient photosynthesis in Arabidopsis.tif

Plants have multiple mechanisms to maintain efficient photosynthesis. Photosynthetic cyclic electron transports around photosystem I (CET), which includes the PGR5/PGRL1 and NDH pathways, and photorespiration play a crucial role in photosynthetic efficiency. However, how these two mechanisms are functionally linked is not clear. In this study, we revealed that photorespiration could compensate for the function of CET in efficient photosynthesis by comparison of the growth phenotypes, photosynthetic properties monitored with chlorophyll fluorescence parameters and photosynthetic oxygen evolution in leaves and photorespiratory activity monitored with the difference of photosynthetic oxygen evolution rate under high and low concentration of oxygen conditions between the deleted mutant PGR5 or PGRL1 under NDH defective background (pgr5 crr2 or pgrl1a1b crr2). Both CET mutants pgr5 crr2 and pgrl1a1b crr2 displayed similar suppression effects on photosynthetic capacities of light reaction and growth phenotypes under low light conditions. However, the total CET activity and photosynthetic oxygen evolution of pgr5 crr2 were evidently lower than those of pgrl1a1b crr2, accompanied by the upregulation of photorespiratory activity under low light conditions, resulting in severe suppression of photosynthetic capacities of light reaction and finally photodamaged phenotype under high light or fluctuating light conditions. Based on these findings, we suggest that photorespiration compensates for the loss of CET functions in the regulation of photosynthesis and that coordination of both mechanisms is essential for maintaining the efficient operation of photosynthesis, especially under stressed conditions.</p

Image_2_Inactivation of photosynthetic cyclic electron transports upregulates photorespiration for compensation of efficient photosynthesis in Arabidopsis.tif

Plants have multiple mechanisms to maintain efficient photosynthesis. Photosynthetic cyclic electron transports around photosystem I (CET), which includes the PGR5/PGRL1 and NDH pathways, and photorespiration play a crucial role in photosynthetic efficiency. However, how these two mechanisms are functionally linked is not clear. In this study, we revealed that photorespiration could compensate for the function of CET in efficient photosynthesis by comparison of the growth phenotypes, photosynthetic properties monitored with chlorophyll fluorescence parameters and photosynthetic oxygen evolution in leaves and photorespiratory activity monitored with the difference of photosynthetic oxygen evolution rate under high and low concentration of oxygen conditions between the deleted mutant PGR5 or PGRL1 under NDH defective background (pgr5 crr2 or pgrl1a1b crr2). Both CET mutants pgr5 crr2 and pgrl1a1b crr2 displayed similar suppression effects on photosynthetic capacities of light reaction and growth phenotypes under low light conditions. However, the total CET activity and photosynthetic oxygen evolution of pgr5 crr2 were evidently lower than those of pgrl1a1b crr2, accompanied by the upregulation of photorespiratory activity under low light conditions, resulting in severe suppression of photosynthetic capacities of light reaction and finally photodamaged phenotype under high light or fluctuating light conditions. Based on these findings, we suggest that photorespiration compensates for the loss of CET functions in the regulation of photosynthesis and that coordination of both mechanisms is essential for maintaining the efficient operation of photosynthesis, especially under stressed conditions.</p