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The advanced geosynchronous radiation imager (AGRI) is a geostationary sensor whose reflective solar band is calibrated by a solar diffuser (SD). The SD bidirectional reflectance distribution function (BRDF) degrades over time in the space environment. This degradation can be measured through the SD reflectance degradation monitor (SDRDM). The SDRDM calibration data are normally collected by three filtered detectors, covering wavelengths from 0.45μm to 0.90μm. The SD reflectance degradation can be derived by trending the ratio of the background-subtracted solar-angle corrected SDRDM sun and SD view responses. The conventional monitoring methods rely on geometry factors of the sun view port and the relative BRDF of the SD, and these parameters can cause uncertainties. Aiming at these uncertain factors, the present study collects calibration data at the same solar angle. This method compares the detector digital counts obtained at different times but with the same solar angle. Consequently, it cancels out the angle-dependent parameter to obtain the ratio of the BRDF degradation factors. The obtained results show that monitoring uncertainty of the proposed method is less than 0.18%, while the corresponding monitoring error is less than 0.66%. This method can be applicated in SD's BRDF monitoring.

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As the reference radiometric calibration standard of sensors on the Haiyang-1C (HY-1C) satellite platform, the satellite calibration spectrometer (SCS) is equipped with an onboard calibration system composed of double solar diffusers and an erbium-doped diffuser to monitor the postlaunch radiometric response change. Herein, through onboard calibration data analysis, the calibration diffuser performance remains stable without degradation, and the Moderate Resolution Imaging Spectroradiometer (MODIS) on Terra is adopted as a reference to repeatedly verify onboard radiometric calibration results by selecting different dates and reflectance scenes. The SCS equivalent reflectance is obtained by combining the mean digital number (DN) of the SCS crossing area image with the radiometric calibration coefficient. The spectral reflectance is obtained via interpolation and iteration, which is adopted as the actual MODIS incident pupil spectral reflectance because the small imaging time interval can be ignored and almost vertically observed, and it is convoluted with the MODIS spectral response function to obtain the predicted equivalent reflectance. Validation is completed by comparing the predicted MODIS equivalent reflectance to the measured value based on the onboard calibration coefficient. The results show that (1) the difference between the measured and predicted MODIS band equivalent reflectance is between -0.00466 and 0.0039, and (2) the percentage difference between the measured and predicted MODIS band equivalent reflectance ranges from 4.17% and 1.24%, indicating that the calibration system carried on HY-1C can perform high-precision SCS radiometric calibration, meeting the cross-calibration accuracy requirements of other loads on the same platform.

As one of the most important ways of improving the calibration accuracy at present, the calibration method based on a solar diffuser(SD) is an independent calibration way with advantages of high accuracy, high frequency and high efficiency . The principles, methods and implementation process of on-orbit calibration based on the SD is described in this thesis. The radiance reference for calibration in space is found and the physical model of the on-orbit reflectance calibration is provided. The main factor which affects the calibration uncertainty is the determination of the SD bidirectional reflectance distribution function (BRDF) value by analyzing the physical models of on-orbit calibration. Thus, the timing selection of the on-orbit calibration is introduced and the BRDF in the range of angles variety within the calibration timing is tested in the lab. During the on-orbit calibration time, the high accuracy on-orbit calibration in the remote sensors’ whole life is achieved by the accurate radiance input which is ensured by monitoring and correcting the SD BRDF value from its fabrication to its life end. Finally, the on-orbit calibration uncertainty is estimated based on the measurement levels of the parameters in the physical model. And the uncertainties of on-orbit reflectance calibration and method of radiance calibration are better than 2.03% and 2.04% by type B standard uncertainty evaluation method.

To solve the problem of harmonic pollution in distributed power system, a new type of grid-connected inverter with harmonic compensation is studied in this paper. This system adopts a unified control strategy with decoupled active and reactive power based on grid voltage orientation. Both the grid connection and harmonic compensation are realized together in one inverter, which improves the inverter’s utilization efficiency and protects the power grid from harmonic pollution. The simulation and experimental results are shown to prove the correctness of the control strategy.

Experimental allergic neuritis (EAN) is a T cell-mediated animal model of Guillain-Barré syndrome characterized by inflammation and demyelination of peripheral nerves. EAN can be induced by immunization of rats with bovine peripheral nerve myelin (BPM) or the myelin proteins P2 or P0, but the extent of T cell responses over the course of EAN is incompletely defined. We studied the T cell responses to these proteins and the glycolipid GM1 by enumerating T helper type 1 (Th1)-like cells secreting interferon-gamma (IFN-gamma) after short-term culture of mononuclear cells (MNC) in presence of antigen. Already 7 days post immunization (p.i.) with BPM and before onset of clinical EAN, lymph nodes contained elevated levels of P2 responsive T cells. At the height of EAN on day 14 p.i. and during recovery, T cell levels responding to BPM, P0 and GM1 were also elevated. The same temporal profiles and specificities were registered for antigen reactive spleen MNC. The results implicate that Th1-like cells with multiple specificities including the glycolipid GM1 occur at increased levels in lymphoid organs in EAN rats, and that IFN-gamma may be an important effector molecule in the induction of nerve damage.

The aim of our study is to evaluate computed tomography (CT) coronary angiography in patients with a high heart rate using 16-slice spiral CT with 0.37-s gantry rotation time. We compare the image quality of patients whose heart rates were over 70 beats per minute (bpm) with that of patients whose heart rates were 70 bpm or less. Sixty patients with various heart rates underwent retrospectively ECG-gated multislice spiral CT (MSCT) coronary angiography. Two experienced observers who were blind to the heart rates of the patients evaluated all the MSCT coronary angiographic images and calculated the assessable segments. A total of 620 out of 891 (69.6%) segments were satisfactorily visualized. On average, 10.3 coronary artery segments per patient could be evaluated. In 36 patients whose heart rates were below 70 bpm [mean 62.2 bpm+/-5.32 (standard deviation, SD)], the number of assessable segments was 10.72+/-2.02 (SD). In the other 24 patients whose heart rates were above 70 bpm [mean 78.6 bpm+/-8.24 (SD)], the corresponding number was 9.75+/-1.74 (SD). No statistically significant difference was found in these two subgroups' t test, P0.05. The new generation of 16-slice spiral CT with 0.37-s rotation time can satisfactorily evaluate the coronary arteries of patients with high heart rates (above 70 bpm, up to 102 bpm).

NKX3.1 is a prostate-specific homeoprotein and tumor suppressor that is affected by the loss of 8p21 in prostate cancer. In mice, Nkx3.1 haploinsufficiency results in prostatic dysplasia and complements cancer formation induced by loss of other suppressor genes. However, NKX3.1 expression can be immunohistochemically detected in most primary prostate cancers. We examined the relationship between suppressor gene haploinsufficiency, methylation, and quantitative NKX3.1 expression levels in primary prostate cancer. NKX3.1 gene copy number was assessed by microsatellite analysis, fluorescence in situ hybridization, and quantitative PCR. NKX3.1 gene methylation was determined in prostate cancer cell lines and we thereby identified potential CpG methylation sites for methylation-specific PCR analysis in tissues. We validated and then applied an internally controlled fluorescence immunomicroscopic assay for NKX3.1 protein expression in 48 primary prostate cancer specimens from radical prostatectomies. NKX3.1 loss of heterozygosity was found in 27 of 43 tissues tested. Classic CpG island methylation of the NKX3.1 gene was not found in either prostate cancer cell lines or tissues. However, in 33 of 40 samples tested, CpG sites at −921, −903, and −47 were methylated to a greater degree in malignant than in adjacent normal cells. In 43 of 48 samples, NKX3.1 protein expression was reduced from 0.34 to 0.90 compared with adjacent normal luminal epithelium (mean of all samples, 0.68; 95% confidence interval, 0.05). In 12 cases that also had high-grade prostatic intraepithelial neoplasia, NKX3.1 expression levels were similar in preinvasive and invasive cancer cells and significantly lower than adjacent normal cells. Even in the presence of allelic loss, NKX3.1 expression is reduced over a wide range in prostate cancer at the time of prostatectomy, suggesting that diverse factors influence expression. Samples with protein expression below the median level in cancer cells had both NKX3.1 deletion and selective CpG methylation.

In recent years, numerous reports have described the diverse roles of the CD40-CD40 ligand receptor-ligand pair. The interaction of these two cell-surface molecules regulates both humoral and cell-mediated immune functions. Because the CD40 ligand is known to be highly expressed on the peripheral blood mononuclear cells (PBMC) of multiple sclerosis (MS) patients, and because activated helper T cells expressing CD40 ligand have been found in the brain sections of MS patients, but not in those of normal controls, the protein is believed to be involved in MS development. We studied the influence of a polymorphic dinucleotide-repeat marker located in the 3' untranslated region of the X-linked gene encoding CD40 ligand (CD40LG) on susceptibility to and disease severity in MS. From a total cohort of 771 Nordic definite-MS patients, the most (n = 92) and least (n = 90) disabled octiles, as well as random samples of intermediately disabled males (n = 119) and females (n = 121), were genotyped; 135 ethnically matched healthy subjects were used as controls. In addition, the effect of the polymorphism on CD40 ligand mRNA expression was assessed using PBMC from 54 MS patients and 22 controls. The phenotype frequencies for the CD40LG marker did not differ significantly between gender-conditioned intermediate-MS subgroups and controls, or between gender-conditioned disability octiles. Nor did the polymorphism appear to exert any significant effect on mRNA expression in either patients or controls.

The proinflammatory cytokine interferon (IFN)-gamma has been shown to influence the course of multiple sclerosis (MS). The IFN-gamma (IFNG) contains a multiallelic dinucleotide repeat in intron 1. To investigate whether alleles at this locus influence susceptibility to MS, we performed linkage and familial association analyses on 100 sibling pairs from four Nordic countries, and case-control association analysis on 220 intermediately disabled sporadic MS patients and 266 controls. To determine the effect of the polymorphism on disease outcome, we compared genotype frequencies in the most and least disabled octiles of a total cohort of 913 cases. We also measured IFN-gamma mRNA levels in unstimulated peripheral blood mononuclear cells from 46 MS patients and 27 controls grouped according to IFNG intron 1 genotype. Both nonparametric linkage analysis and transmission disequilibrium testing of the 100 sibling pairs produced negative results. Genotype frequencies for intermediate-MS patients did not differ significantly from those for controls; nor did genotype frequencies in the benign-MS octile differ significantly from those in the severe-MS octle. Comparison of IFN-gamma mRNA levels in genotype-conditioned subgroups revealed no significant differences. Thus, alleles at the IFNG intron 1 dinucleotide repeat appear to affect neither MS susceptibility and severity nor IFN-gamma mRNA expression in vivo.

Dendritic cells (DC) are important antigen presenting cells (APC) and play a major role in initiating and orchestrating immune responses by priming T cells. Little is known about involvement of DC in multiple sclerosis (MS), where auto-aggressive T cells against myelin autoantigens are considered to contribute to inflammation and demyelination in the central nervous system. In this study, we compared phenotype and cytokine secretion of DC from patients with MS, other neurological diseases (OND) and healthy subjects. DC were generated from blood adherent mononuclear cells (MNC) by culture for 7 days with granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4). The yield and morphology of DC were similar in MS patients and controls. In both, the DC phenotype was that of immature myeloid lineage, comprising CD1a+ and CD11c+. The proportion of CD1a+ DC, being important for presentation of lipid antigens to T cells, was higher in MS patients compared to controls. The proportion of CD86+ DC, a co-stimulatory molecule that is assumed to promote Th2 differentiation, was low in MS. Low proportions of CD86+ DC were only observed in untreated MS patients but not in patients treated with IFN-b. Production of IL-10 and IL-12 p40 by DC did not differ in MS patients and controls. These findings indicate that alterations of functionally important surface molecules on DC are associated with MS.

Interleukin-18 is a proinflammatory cytokine, which strongly induces IFN-gamma production. We have cloned the human IL-18 promoter and screened for possible polymorphisms. Three single nucleotide polymorphisms were detected in the promoter and two polymorphisms in the 5'-nontranslated region of the gene. Three combinations of these polymorphisms were observed in the Swedish population. All IL-18 promoter alleles were found to have clear promoter activity when inserted into a luciferase reporter vector. There were no significant differences in promoter activity between alleles without stimulation, but after stimulation with PMA/ionomicin one of the alleles had clearly lower activity than the other (P

Multiple sclerosis (MS) is an inflammatory, demyelinating disease that is specific to the central nervous system. Cytokines are thought to be key mediators of the autoimmune attack against central nervous system myelin in MS. To investigate the involvement of cytokines in MS, the mRNA levels of interferon gamma (IFN-g), tumor necrosis factor alpha (TNF-a), interleukin-4 (IL-4) and interleukin-10 (IL-10) in peripheral blood mononuclear cells without stimulation in vitro were quantified by a competitive reverse transcription polymerase chain reaction technique. The level of IL-10 specific mRNA was significantly decreased in 47 MS patients compared with 42 healthy controls (P50.0001). TNF-a was significantly increased in MS patients compared with healthy controls (P=0.014), especially in the patients with chronic progressive MS (P=0.0003). Thus we conclude that there are significant in vivo alterations in cytokine gene expression in the periphery in MS.

To optimize the formulation of Eisemia foetida protein (EFP) burn spray.A five-factor, three-level response surface method was employed; The response variable was the proliferation effect of EFP on NIH3T3 cells.The optimization formulation was as follows: the proportion of EFP, glycerol and mannitol was 0.91%, 1.42% and 5%, respectively; 0.02 mol/L Na2 HPO4 and 0.01 mol/L citric acid buffer system corresponding pH value was 7.0.The response surface method is reliable, efficient and suitable for optimizing the formulation of EFP burn spray.

Gold nanoparticles about 10 nm in size were prepared by improved trisodium citrate reduction procedure, and were used to label goat anti-human C3 to obtain a sensitive spectral probe for complement 3 (C3) in the condition of pH 7.5. The immune reaction between nanogold-labeled C3 antibody (anti-C3) and the antigen C3 took place to form the nanogold immune complex in pH 5.6 Na2 HPO4-C6H8O7 buffer solution and in the presence of polyethylene (PEG). The optimal immunoreaction conditions were pH 5.6-9.7 microg x mL(-1) nanogold-labeled anti-C3, 6.0% PEG 6000 and incubation time 15 min under ultrasonic irradiation. After centrifuging for 10 min at 12 000 r x min(-1), the excess nanogold-labeled anti-C3 in the upper solutions was obtained, and was used to catalyze the colored particle reaction between HAuCl4 and NH2 OH x HCl to produce gold particles with bigger size. The influence on the immunonanogold catalytic reaction was considered spectrophotometrically. A pH 2.97 Na3C6H5O7-HCl buffer solution, 53.33 microg x mL(-1) HAuCl4, 74.13 microg x mL(-1) NH2OH x HCl, and reaction time of 3 min at 37 degrees C water bath were chosen for use. Results demonstrated that with increasing C3, the concentration of gold labeled anti-C3 in the upper solution decreased, and the absorbance decreased linearly. Linear relationships between the decreased absorbance and the C3 concentration in the range of 0.025-0.60 ng x mL(-1) were obtained by spectrophotometry at 760 nm. The regress equation was deltaA760 nm = 0.276c+0.025 4, the correlation coefficient was 0.990 3, and the detection limit reached 0.007 2 ng x mL(-1) of C3. The influence of foreign substances such as HAS, BSA, and ammonia acid on the determination of 0.2 ng x mL(-1) of C3was examined. Results showed that this assay has high selectivity. The sensitive, rapid and highly specific assay was applied to the quantification of C3 in human sera, with satisfactory results.

To explore the characters of coronary calcified plaques by using 16-slice spiral CT and determine their stenosis degree according to the results of catheter coronary angiography.Twenty patients who had received 16-slice spiral CT coronary angiography and conventional coronary angiography (CAG) were found to be with calcified plaques. The characters of these plaques, including the diameter of calcified plaques and lumen diameter of the exact artery segment, were retrospectively analyzed. The stenosis degree of the corresponding segment was judged in accordance with the results of CAG.Totally 84 calcified plaques were observed in 16-slice spiral CT images in these 20 patients. Among them there were 16 small nodules (diameter:0.15 cm), 56 purely calcified plaques (diameter:or = 0. 15 cm), and 12 complex plaques with calcify component. There was no obvious stenosis in artery segments with little calcified nodules. The stenosis degree of most segments with purely calcified plaques (75%) was less than 50%. The stenosis degree had no significant correlation with the size of plaques (P0.05). However, the stenosis degree of complex plaques had much closer relationship with the characters of mixed plaques.Most coronary segments with calcified plaques have slight stenosis. Their stenosis degree is not related with the size of plaques. The stenosis degree of complex plaques has a closer relationship with the characters of mixed plaques.

T cell-mediated cancer immunotherapy is dose dependent and optimally requires participation of antigen-specific CD4+ and CD8+ T cells. Here, we isolated tumor-sensitized T cells and activated them in vitro using conditions that led to greater than 108-fold numerical hyperexpansion of either the CD4+ or CD8+ subset while retaining their capacity for in vivo therapeutic efficacy. Murine tumor-draining lymph node (TDLN) cells were segregated to purify the CD62Llow subset, or the CD4+ subset thereof. Cells were then propagated through multiple cycles of anti-CD3 activation with IL-2 + IL-7 for the CD8+ subset, or IL-7 + IL-23 for the CD4+ subset. A broad repertoire of TCR Vβ families was maintained throughout hyperexpansion, which was similar to the starting population. Adoptive transfer of hyper-expanded CD8+ T cells eliminated established pulmonary metastases, in an immunologically specific fashion without the requirement for adjunct IL-2. Hyper-expanded CD4+ T cells cured established tumors in intracranial or subcutaneous sites that were not susceptible to CD8+ T cells alone. Because accessibility and antigen presentation within metastases varies according to anatomic site, maintenance of a broad repertoire of both CD4+ and CD8+ T effector cells will augment the overall systemic efficacy of adoptive immunotherapy.

Multiple sclerosis (MS) is supposedly a T-cell mediated autoimmune disorder of the central nervous system. Cytokines and other molecules involved in the regulation of apoptosis are thought to be of importance for the pathogenesis of MS. In this study, the mRNA levels of interleukin 18 (IL-18), IL-1b and their processing enzyme caspase-1 were quantified by a competitive RT-PCR method in unstimulated peripheral blood mononuclear cells (PBMCs) in MS patients never treated with disease modifying drugs. Western blot was used to support the expression pattern at the protein level. We found that the expression of caspase-1 and IL-18 was significantly increased in MS patients compared with healthy controls. Analysis of clinical subgroups revealed that caspase-1 was increased in all subgroups, whereas IL-18 was upregulated in chronic progression (P-0.001) and relapsing MS patients in remission (P-0.002) but not significantly during relapses (P-0.12). mRNA levels of IL-1b were not significantly altered in MS except for a possible decrease in chronic progression (P-0.03). An increased IL-18 expression, potentially augmented at the mature protein level, may indicate a pathway worth considering in future therapeutic strategies in MS.

It is increasingly clear that the CD40 and CD40 ligand (CD40L) receptor-ligand pair mediates a crucial activation signal in both cell-mediated and humoral immune responses. Here, we detected mRNA levels of CD40 and CD40L in non-stimulated peripheral blood mononuclear cells in 46 patients with multiple sclerosis (MS) and 46 healthy controls by a competitive RT-PCR procedure allowing quantification without previous culture or antigenic stimulation. The levels of CD40 and CD40L mRNA were markedly increased in MS patients (P

Experimental autoimmune myasthenia gravis (EAMG) is induced by a single injection of acetylcholine receptor (AChR) with complete Freund's adjuvant and represents a useful animal model for studying the mechanisms by which autoimmune responses to AChR and its subunits are coupled to the development of human myasthenia gravis. Using an immunospot assay, we enumerated cells secreting IgG antibodies against Torpedo AChR and the alpha-, beta-, gamma- and delta-subunits of Torpedo AChR in lymph nodes, spleen and thymus from Lewis rats over the course of EAMG. Cells secreting IgG antibodies to AChR and to all four subunits were detected at higher numbers in the three immune organs in EAMG compared to controls. Numbers were highest in lymph nodes followed by spleen and thymus. Cells secreting IgG antibodies against native AChR were always higher than those against individual subunits. The immunogenicity between the four subunits did not differ, with the exception that the alpha-subunit induced a slightly higher B cell response in thymus and lymph nodes. The patterns of B cell responses were similar when analyzed over the course of EAMG from week 2 to week 5, and there was no restriction of the B cell repertoire early in EAMG. Anti-AChR and anti-subunit antibody-secreting cells were also detected in control animals immunized with adjuvant only, but at numbers which were much lower, and which were within the same level as numbers of cells secreting IgG antibodies to the control antigen myelin basic protein, probably reflecting naturally occurring autoimmune B cells.

T cell-mediated cancer immunotherapy is dose dependent and optimally requires participation of antigen-specific CD4+ and CD8+ T cells. Here, we isolated tumor-sensitized T cells and activated them in vitro using conditions that led to greater than 108-fold numerical hyperexpansion of either the CD4+ or CD8+ subset while retaining their capacity for in vivo therapeutic efficacy. Murine tumor-draining lymph node (TDLN) cells were segregated to purify the CD62Llow subset, or the CD4+ subset thereof. Cells were then propagated through multiple cycles of anti-CD3 activation with IL-2 + IL-7 for the CD8+ subset, or IL-7 + IL-23 for the CD4+ subset. A broad repertoire of TCR Vβ families was maintained throughout hyperexpansion, which was similar to the starting population. Adoptive transfer of hyper-expanded CD8+ T cells eliminated established pulmonary metastases, in an immunologically specific fashion without the requirement for adjunct IL-2. Hyper-expanded CD4+ T cells cured established tumors in intracranial or subcutaneous sites that were not susceptible to CD8+ T cells alone. Because accessibility and antigen presentation within metastases varies according to anatomic site, maintenance of a broad repertoire of both CD4+ and CD8+ T effector cells will augment the overall systemic efficacy of adoptive immunotherapy.