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1.
The EPR spectrum of tooth enamel caused by 13C hyperfine interactions of the CO2 radical were studied on γ-irradiated powdered samples annealed for 40 min at different temperatures up to 250°C. The lineshape and hyperfine splitting of the spectra were found to depend on the annealing temperature. Experimental spectra were compared with calculated ones assuming that EPR spectra are formed by two CO2 species—axial (rotating) and orthorhombic (braked) radicals. We assumed that the axial CO2 radicals are centers located in perfect areas of the hydroxyapatite crystals of tooth enamel whereas the orthorhombic CO2 radicals are rotating centers which are braked by defects. The thermal treatment of enamel samples leads to defective annealing and transformation of the orthorhombic centers into axial ones. This results in an increasing axial CO2 radical contribution to the EPR spectrum with increase of annealing temperature.  相似文献   

2.
对辐照牙釉质EPR谱数学模拟的研究   总被引:2,自引:2,他引:0       下载免费PDF全文
目的 建立辐照牙釉质EPR谱数学模拟方法。方法 采用高斯函数一阶微商作为基本的模型函数 ,编写基于Marquardt Levenberg非线性最小二乘法曲线拟合算法的计算程序模拟辐照牙釉质EPR谱 ,并检验拟合精度。结果 对 2 70和 84 0mGy辐照的牙釉质样品的EPR复合谱 ,拟合后的残谱分别为 - 1 6 1± 2 3 5 9和 - 3 77± 2 4 94 ,残谱均值和标准差分别占各自峰高的 0 3%、3 8%和 0 4 %、3%。结论 这种算法和模型函数能很好地模拟辐照牙釉质EPR复合谱。  相似文献   

3.
The role of nitric oxide (NO) in epileptogenesis was studied in pentylenetetrazole (PTZ)-treated animals using in vivo and ex vivo EPR spectroscopy. NO generation was measured directly in the brain of a PTZ-induced mouse in vivo by an L-band EPR spectrometer. An elevation in NO production in the brain was observed during convulsions, and more NO was generated in the tonic seizure vs. the clonic seizure. NO content in several brain tissues (including the cerebral cortex (CR), cerebellum (CL), olfactory bulb (OB), hippocampus (HI), and hypothalamus (HT)) of PTZ-doped rats was analyzed quantitatively ex vivo by X-band EPR. To test the involvement of NO in seizure development, pharmacological analyses were performed using the NO synthase (NOS) inhibitors N(G)-nitro-L-arginine (L-NNA), N(G)-monomethyl-L-arginine (L-NMMA), and 3-bromo-7-nitroindazole (3Br-7NI). All of these inhibitors suppressed the convulsions, holding them at the clonic level, and prevented development of a tonic convulsion in rats doped with up to 80 mg/kg PTZ. 3Br-7NI completely inhibited NO production, but L-NNA and L-NMMA showed only 70% inhibition of NO production in PTZ-doped rats. In order to examine the contributions of NO in convulsions, rats were treated with anticonvulsants (phenytoin and diazepam) before PTZ treatment. Both drugs completely suppressed tonic convulsion in PTZ-doped rats at doses up to 80 mg/kg, but NO levels were similar to those detected in a clonic convulsion. These results support the notion that NO does not directly induce a clonic convulsion, but may be generated as a consequence of onset of seizure.  相似文献   

4.
T2 of articular cartilage in the presence of Gd-DTPA2-.   总被引:1,自引:0,他引:1  
T(2) information and delayed gadolinium-enhanced MRI of cartilage (dGEMRIC) are both used to characterize articular cartilage. They are currently obtained in separate studies because Gd-DTPA(2-) (which is needed for dGEMRIC) affects the inherent T(2) information. In this study, T(2) was simulated and then measured at 8.45 T in 20 sections from two human osteochondral samples equilibrated with and without Gd-DTPA(2-). Both the simulations and data demonstrated that Gd-DTPA(2-) provides a non-negligible mechanism for relaxation, especially with higher (1 mM) equilibrating Gd-DTPA(2-) concentrations, and in areas of tissue with high T(2) (due to weak inherent T(2) mechanisms) and high tissue Gd-DTPA(2-) (due to a low glycosaminoglycan concentration). Nonetheless, T(2)-weighted images of cartilage equilibrated in 1 mM Gd-DTPA(2-) showed similar T(2) contrast with and without Gd-DTPA(2-), demonstrating that the impact on T(2) was not great enough to affect identification of T(2) lesions. However, T(2) maps of the same samples showed loss of conspicuity of T(2) abnormalities. We back-calculated inherent T(2)'s (T(2,bc)) using a T(2)-relaxivity value from a 20% protein phantom (r(2) = 9.27 +/- 0.09 mM(-1)s(-1)) and the Gd-DTPA(2-) concentration calculated from T(1,Gd). The back-calculation restored the inherent T(2) conspicuity, and a correlation between T(2) and T(2,bc) of r = 0.934 (P < 0.0001) was found for 80 regions of interest (ROIs) in the sections. Back-calculation of T(2) is therefore a viable technique for obtaining T(2) maps at high equilibrating Gd-DTPA(2-) concentrations. With T(2)-weighted images and/or low equilibrating Gd-DTPA(2-) concentrations, it may be feasible to obtain both T(2) and dGEMRIC information in the presence of Gd-DTPA(2-) without such corrections. These conditions can be designed into ex vivo studies of cartilage. They appear to be applicable for clinical T(2) studies, since pilot clinical data at 1.5 T from three volunteers demonstrated that calculated T(2) maps are comparable before and after "double dose" Gd-DTPA(2-) (as utilized in clinical dGEMRIC studies). Therefore, it may be possible to perform a comprehensive clinical examination of dGEMRIC, T(2), and cartilage volume in one scanning session without T(2) data correction.  相似文献   

5.

Purpose:

To investigate the transport of Gd‐DTPA2? in different layers of femoral knee cartilage in vivo.

Materials and Methods:

T1 measurements (1.5 Tesla) were performed in femoral knee cartilage of 23 healthy volunteers. The weight‐bearing central cartilage was analyzed before contrast and at eight time points after an intravenous injection of Gd‐DTPA2?: 12–60 min (4 volunteers) and 1–4 h (19 volunteers). Three regions of interest were segmented manually: deep, middle, and superficial.

Results:

Before contrast injection, a depth‐wise variation of T1 was observed with 50% higher values in the superficial region compared with the deep region. In the deep region, the uptake of Gd‐DTPA2? was not detected until 36 min and the concentration increased until 240 min, whereas in the superficial region, the uptake was seen already at 12 min and the concentration decreased after 180 min (P < 0.01). There was a difference between medial and lateral compartment regarding bulk, but not superficial Gd‐DTPA2? concentration. The bulk gadolinium concentration was negatively related to the cartilage thickness (r = ?0.68; P < 0.01).

Conclusion:

The depth‐wise and thickness dependent variations in Gd‐DTPA2 transport influence the interpretation of bulk dGEMRIC analysis in vivo. In thick cartilage, incomplete penetration of Gd‐DTPA2 will yield a falsely too long T1. J. Magn. Reson. Imaging 2011;. © 2011 Wiley Periodicals, Inc.
  相似文献   

6.
Localized, water-suppressed (1)H-[(13)C]-NMR spectroscopy was used to detect (13)C-label accumulation in cerebral metabolites following the intravenous infusion of [1,6-(13)C(2)]-glucose (Glc). The (1)H-[(13)C]-NMR method, based on adiabatic RF pulses, 3D image-selected in vivo spectroscopy (ISIS) localization, and optimal shimming, yielded high-quality (1)H-[(13)C]-NMR spectra with optimal NMR sensitivity. As a result, the (13)C labeling of [4-(13)C]-glutamate (Glu) and [4-(13)C]-glutamine (Gln) could be detected from relatively small volumes (100 microL) with a high temporal resolution. The formation of [n-(13)C]-Glu, [n-(13)C]-Gln (n = 2 or 3), [2-(13)C]-aspartate (Asp), [3-(13)C]-Asp, [3-(13)C]-alanine (Ala), and [3-(13)C]-lactate (Lac) was also observed to be reproducible. The (13)C-label incorporation curves of [4-(13)C]-Glu and [4-(13)C]-Gln provided direct information on metabolic pathways. Using a two-compartment metabolic model, the tricarboxylic acid (TCA) cycle flux was determined as 0.52 +/- 0.04 micromol/min/g, while the glutamatergic neurotransmitter flux equaled 0.25 +/- 0.05 micromol/min/g, in good correspondence with previously determined values.  相似文献   

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