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Supplementary Material 7

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Supplementary Material 6

Supplementary Material 4

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Supplementary Material 8

A prompt gamma ray neutron activation analysis detection system was developed to detect the heavy metals in sediments by using an 241Am-Be neutron source and BGO detector. The samples containing cadmium and mercury were used to test the performance of setup. The linear relationship between prompt gamma ray counts and the concentrations was studied. The results showed the counts of the prompt gamma rays from cadmium do not increase linearly with its concentrations, while the prompt gamma ray counts from Hg vary nearly linearly with the concentrations, due to the neutron self-shielding. Then a method was used to correct the effect and the non-linearly response was restored after the correction. And the minimum detectable concentration of Cd and Hg were 52.8 (at 8.484 MeV) and 81.6 (at 5.967 MeV) ppm, respectively.

To address the simultaneous AUV localization under the condition of single sonar beacon, we propose a bearing only measurements based approach for real-time AUV localization applications, assuming the depth of beacon is known as a prior. A state-space model considering AUV motion with 2-DOF attitude is derived using coordinates transformation, which bases the localization solution using an extended Kalman filter (EKF). The principle of filter selection for this application is analyzed in the prospective of real-world implementation and parameter tuning. The efficiency of proposed method is tested by simulations. The results suggest that our method is more robust and favorable in terms of filtering accuracy and convergence in comparison with distance measurements based methods.

A laboratory investigation of the radiation-induced degradation of aniline by gamma irradiation is the subject of this paper. During the inquiry, several aqueous samples with aniline concentrations of 25, 50, 75, 100 and 200 mg/L were irradiated for 5, 10, 15, 20, 25 and 30 h, respectively, by a

Effects of GTP-binding proteins on the activation of secretory phospholipase A2 (sPLA2) and cytosolic phospholipase A2 (cPLA2) in rat liver during two different phases of sepsis were studied. Sepsis was induced by cecal ligation and puncture (CLP). Experiments were divided into three groups: control, early sepsis, and late sepsis. Early and late sepsis refers to those animals sacrificed at 9 and 18 h, respectively, after CLP. The results show that in the absence of G-protein modulator, hepatic sPLA2 and cPLA2 activities were activated by 40.8-46 and 91.6-105.8%, respectively, during early and late phases of sepsis. GTPγS and fluoroaluminate (A1F4-) stimulated sPLA2 and cPLA2 activities within each experimental group, i.e., control, early sepsis, and late sepsis. The GTPγS and A1F4--stimulated sPLA2 and cPLA2 activities remained significantly elevated during early phase (22.3-65.6% increase) and late phase (32.5-109.1% increase) of sepsis. Further analyses demonstrate that cholera toxin significantly stimulated sPLA2 and cPLA2 activities within each experimental group, and that the cholera toxin stimulated sPLA2 and cPLA2 activities remained significantly higher during early phase (23.5-37%increase) and late phase (56.7-70% increase) of sepsis. In contrast, pertussis toxin significantly inhibited sPLA2 and cPLA2 activities within each experimental group, and that the pertussis toxin-inhibited sPLA2 and cPLA2 activities remained significantly higher in early septic (57-68.5% increase) and late septic (34.6-45.5% increase) experiments. These data demonstrate that cholera toxin-sensitive Gαs and pertussis toxin-sensitive Gαi were both involved in the activation of sPLA2 and cPLA2 activities in rat liver during the progression of sepsis.

To investigate the role of mitogen-activated protein kinase phosphatase-1 (MKP-1) in the regulation of cells proliferation, the expression of MKP-1 and extracellular signal-regulated kinase-1 (ERK-1) in heart and aorta of spontaneous hypertensive rat (SHR) and WKY were studied. We also investigated the effect of MKP-1 genes,which were transfected into vascular smooth muscle cells (VSMC) using the classical calcium phosphate coprecipitation technique, on the incorporation of 3H-TdR in VSMC stimulated by angiotensin II (Ang II).(1) Compared with that of WKY, MKP-1 expression in heart and aorta were significantly decreased by 53% (P0.01) and 45% (P0.01) in SHR, respectively. While the expression of ERK-1 in heart and aorta of SHR were higher than that of WKY (P0.01). The ratio of ERK-1/MKP-1 in heart and aorta of SHR were significantly higher than that of WKY. (2) 3H-TdR incorporation in VSMC stimulated by Ang II (10(-7) mol/L) was increased by 207% (P0.01), compared with control group. In the transfected cells with wild MKP-1 gene, Ang II-induced incorporation of 3H-TdR lowered 63%, compared with untransfected cells (P0.05). There were no marked inhibitive role between mutant MKP-1-transfected cells and blank vector-transfected cells in response to Ang II, compared with Ang II group (P0.05).These results showed that the expression of ERK-1 in heart and aorta isolated from SHR, which stimulated proliferation and hypertrophy of cells, is higher than that of MKP-1 which dephosphorylates and inactivated ERK-1. In addition, MKP-1 significantly inhibits Ang II-stimulated proliferation of VSMC.

Changes of activity and content of myocardial group II phospholipase A(2) and its mRNA transcription and stability during rat sepsis were investigated. Results showed that, compared with control group,myocardial group II phospholipase A(2) activity in early and late sepsis decreased by 25.0%(P0.05) and increased by 47.6%(P0.01),respectively group II phospholipase A(2) protein concentration reduced by 27.0% and augmented by 48.0%(P0.01),respectively. Myocardial group II phospholipase A(2) mRNA transcription rate and content showed similar two-phases changes. The mRNA transcription rate during early and late sepsis decreased by 45.0% and increased by 70.0%(P0.01),respectively. The mRNA content decreased by 34.1% in early sepsis and increased by 157.0% in late sepsis(P0.01), respectively. The half-life of group II phospholipase A(2) mRNA remained unchanged notably during early and late stage of sepsis. These data suggest that myocardial group II phospholipase A(2) activity decreased in early stage of sepsis and increased in its late stage, and these changes were regulated transcriptionally.

Changes in alpha1-adrenoceptor (alpha1AR) gene expression in the rat liver during different phases of sepsis were studied. Sepsis was induced by cecal ligation and puncture (CLP). Septic rats exhibit two metabolically distinct phases: an initial hyperglycemic phase (9 h after CLP, early sepsis) followed by a hypoglycemic phase (18 h after CLP; late sepsis). The [3H]prazosin binding studies show that the density of alpha1AR was increased by 30% during the early phase while it was decreased by 24% during the late phase of sepsis. Western blot analyses reveal that alpha1AR protein level was elevated by 48% during early sepsis but was decreased by 55% during late sepsis. Northern blot analyses depict that the steady-state level of alpha1bAR mRNA was enhanced by 21% during the early phase but was declined by 29% during the late phase of sepsis. Nuclear run-off assays show that the transcription rate of alpha1bAR gene transcript was increased by 76% during early sepsis while it was decreased by 29% during late sepsis. The actinomycin D pulse-chase studies indicate that the half-life of alpha1bAR mRNA remained unaffected during the early and the late phases of sepsis. These findings demonstrate that during the early phase of sepsis, the increase in the rate of transcription of alpha1bAR gene paralleled with the elevations in the alpha1bAR mRNA abundance and alpha1AR protein level, while during the late phase of sepsis, the decrease in the rate of transcription of alpha1bAR gene coincided with the declines in the alpha1bAR mRNA abundance and the alpha1AR protein level in the rat liver. These observations indicate that the altered expression of alpha1AR genes in the rat liver during the progression of sepsis was regulated transcriptionally.