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Organic carbon (OC) plays a pivotal role in earth surface systems. However, current three-dimensional (3D) mapping studies usually focus on a soil depth of 1 m rather than the depth to the bedrock. A top-down method using piecewise depth functions was proposed to fit the OC vertical decline patterns in a subtropical catchment in southern China. The vertical variation in OC was greatly affected by the heterogeneous topsoil due to natural processes and anthropogenic disturbances. Thus, topsoil OC maps were produced and utilized as covariates to indicate the OC decline rates and to benefit the 3D OC simulation. A distribution map of the underground critical zone thickness (UCZT) was applied as a lower boundary for the 3D simulation. Six widely used mapping techniques were performed to predict the spatial distribution of topsoil OC and depth function parameters. The overall cross-validation results showed a root mean squared error (RMSE) of 1.7 g kg–1 and a ratio of performance to deviation (RPD) of 1.82. Given limited boreholes, validation showed that the depth function performed better in the lower part (>1 m) than in the upper part (<1 m). The proposed framework could holistically employ sufficient topsoil samples and limited boreholes and provides a promising solution to simulate the 3D information of subsurface systems. We anticipate that continuous 3D OC maps can be integrated with other critical zone information to elucidate the complex interactions of various processes and to support potential service management decisions. [ABSTRACT FROM AUTHOR]

Shen Q, Xu H, Cao Q, Zhou L-J, Xu J, Fang X-Y, Ge J. Long-term remission of recurrent severe anemia as a result of parvovirus B19 infection in a pediatric renal transplant recipient. Pediatr Transplantation 2011: 15: E76-E79. © 2010 John Wiley & Sons A/S. We studied a case of recurrent PV-B19-associated anemia in a renal transplant child with long-term remission induced by baseline immunosuppression adjusted and intensive IVIG therapy. This was a 15-yr-old boy. Seven wk after transplantation, he experienced acute rejection, which was treated with high-dose steroids, ATG, and plasmapheresis. Ten wk after transplantation (three wk after rejection), his hemoglobin dropped to 54 g/L and serum PV-B19 PCR was positive. After therapy with IVIG and conversion from mycophenolate mofetil to rapamycin, anemia resolved. But the patient had fever on the fourth day of IVIG with mild pulmonary edema and rise in serum creatinine. Two months after the first course of IVIG, anemia recurred and a second course of IVIG (preadministration methylprednisolone) was given, which was followed by the resolution of anemia without side effect and recurrence two months later again. Baseline immunosuppression was adjusted with dual immunosuppression and low doses including prednisolone and tacrolimus. At the same time, monthly course of IVIG was repeated four times. Within the next 23 months, anemia did not recur and renal function remained stable. In conclusion, PV-B19-associated anemia can be recurrent in immunocompromised children and baseline immunosuppression should be carefully adjusted to control PV-B19 infection. [ABSTRACT FROM AUTHOR]

The article presents a study that examines the immunoglobulin G (IgG ) expression in 80 soft tissue lesions through immunohistochemistry (IHC), polymerase chain reaction (PCR), and in situ hybridization. The immunohistochemical and statistical analyses were used to assess the correlation between Ig expression and proliferation markers in sarcomas. Its results show that Igκ was found in 97.4% of sarcomas and in 31.7% of benign lesions and that the difference was statistically significant.

Aim: To investigate the effects of hematoporphyrin derivative-mediated photodynamic therapy (HPD-PDT) on cell growth in human cholangiocarcinoma in vitro and in vivo, as well as the underlying mechanisms of these effects. Methods: 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was used to evaluate growth status of human cholangiocarcinoma cell line (QBC939). Hoechst 33258 staining and flow cytometry assays were applied to determine cell apoptosis. Western blotting analysis was performed to detect the release of cytochrome c in QBC939 cells, and caspases enzymatic assay was used to investigate the activation of caspase-3, -8, and -9. Further, tumor growth after subcutaneous implantation of QBC939 cells in nude mice was monitored. Results: HPD-PDT inhibits QBC939 cell growth via cell apoptosis in vitro, and initiates cell mitochondria apoptosis pathway by the release of cytochrome c and the activation of caspase-9 and -3. Moreover, HPD-PDT also inhibits subcutaneous tumor growth of QBC939 cells and reduces tumor cell mitosis in nude mice. Conclusion: HPD-PDT inhibits tumor growth of human cholangiocarcinoma, suggesting that HPD-PDT is useful in cholangiocarcinoma therapy. [ABSTRACT FROM AUTHOR]

The article presents a study on the role of Cyr61, an extracellular matrix protein, in the fibroblast-like synoviocytes (FLS) proliferation regulation from rheumatoid arthritis (RA) patients. It is stated that cell adhesion, proliferation and differentiation involve Cyr61. It notes that the study analyzed its expression in synovial tissue (ST) and FLS proliferation. It also mentions that the study found Cyr61 overexpression in ST and FLS, indicating that its critical role in the proliferation.

Aim: Recent studies have underlined causative links between microRNA (miRNA) deregulation and cancer development. However, the relevance of abnormally expressed miRNA to tumor biology has not been well understood in hepatocellular carcinoma (HCC). Methods: A bead-based miRNA expression profiling method was performed on 20 pairs of surgically removed HCC and adjacent non-tumorous tissue (NT). Special miR-338 downregulations and miR-338 associated with clinical characteristics was validated in an extended samples set of 36 paired HCC and adjacent non-tumorous liver tissues by real-time reverse transcription polymerase chain reaction (RT-PCR) analysis. Results: Out of our bead-based microarray data, 12 upregulated and 19 downregulated miRNA were found to be associated with HCC. Further characterization of miRNA-338, in which 20 pairs of the samples were clustered clearly into two groups according to expression of miR-338, revealed that the level of miR-338 expression can be associated with clinical aggressiveness, such as, tumor size, tumor–node–metastasis stage, vascular invasion and intrahepatic metastasis. These results were validated by real-time RT-PCR analysis. Conclusion: Our study suggests that miRNA expression could have relevance to the clinical behavior of HCC and that the bead-based miRNA expression profiling method might be a suitable system to assay miRNA expression in large-scale diagnostic trails. [ABSTRACT FROM AUTHOR]

Aim: To investigate the status of Phosphatidylinositol 3-kinase (PI3K)/PTEN/AKT/mammalian target of rapamycin (mTOR) pathway and its correlation with clinicopathological features and matrix metalloproteinase-2, -9 (MMP-2, 9) in human hepatocellular carcinoma (HCC). Methods: PTEN, Phosphorylated AKT (p-AKT), Phosphorylated mTOR (p-mTOR), MMP-2, MMP-9 and Ki-67 expression levels were evaluated by immunohistochemistry on tissue microarrays containing 200 HCCs with paired adjacent non-cancerous liver tissues. PTEN, MMP-2 and MMP-9 mRNA levels were determined by real-time RT-PCR in 36 HCCs. The relationships between PI3K/PTEN/AKT/mTOR pathway and clinicopathological factors and MMP-2, 9 were analyzed in HCC. Results: In HCC, PTEN loss and overexpression of p-AKT and p-mTOR were associated with tumor grade, intrahepatic metastasis, vascular invasion, TNM stage and high Ki-67 labeling index ( P < 0.05). PTEN loss was correlated with p-AKT, p-mTOR and MMP-9 overexpression. Furthermore, PTEN and MMP-2, 9 mRNA levels were down-regulated and up-regulated in HCC compared with paired non-cancerous liver tissues, respectively ( P < 0.01). PTEN, MMP-2 and MMP-9 mRNA levels were correlated with tumor stage and metastasis. There was an inverse correlation between PTEN and MMP-9 mRNA expression. However, PI3K/PTEN/AKT/mTOR pathway was not correlated with MMP-2. Conclusions: PI3K/PTEN/AKT/mTOR pathway, which is activated in HCC, is involved in invasion and metastasis through up-regulating MMP-9 in HCC. [ABSTRACT FROM AUTHOR]

Background: Adipose differentiation-related protein (ADRP) is a lipid droplet-associated protein that coats cytoplasmic lipid droplets. The present study evaluated whether alcohol feeding enhances ADRP expression and whether ADRP is a lipid droplet marker in alcoholic fatty liver of rats. Because medium-chain triglycerides (MCT) reduce alcoholic hepatosteatosis, their effects on ADRP were also evaluated. Methods: Fatty liver was induced in rats by the consumption of the Lieber-DeCarli alcohol liquid diet with or without replacement of long-chain triglycerides (LCT) by MCT (32% of calories). Immunohistochemical staining for ADRP was performed in formalin-fixed, paraffin-embedded liver sections. ADRP immunostaining was quantified by image analysis. Triacylglycerol was measured chemically. ADRP mRNA and protein were analyzed by real-time polymerase chain reaction and western blot, respectively. Double staining technique was performed to distinguish ADRP from glycogen in hepatocytes. Results: Alcohol feeding for 21 days increased ADRP staining in the centrilobular and mid zonal regions of the liver lobules coincident with fat deposition in the liver. Replacing LCT in the alcohol diet with MCT diminished ADRP immunostaining in parallel with reduced steatosis. MCT also attenuated the up-regulation of ADRP mRNA and protein after alcohol. In steatotic hepatocytes ADRP selectively stained the surface of macrovesicular and microvesicular lipid droplets. ADRP immunostaining quantitatively correlated with hepatic triacylglycerol levels, validating ADRP as a reliable lipid droplet marker. Compared with hematoxylin and eosin stains, ADRP was more sensitive in detecting microvesicular lipid droplets. ADRP immunostaining also distinguished lipid droplets from glycogen, as demonstrated by double staining for ADRP and glycogen. Conclusions: Alcohol induction of fatty liver enhances ADRP expression and MCT oppose the alcohol effects. ADRP is a reliable and sensitive marker for lipid droplets in alcoholic fatty liver. ADRP immunostaining permits quantification of fatty change in hepatocytes and can be used as an ancillary technique in assessing the efficacy of diets or drugs against hepatosteatosis. [ABSTRACT FROM AUTHOR]

Background/Aims: Leptin has been recognized as a profibrogenic hormone in the liver and is involved in collagen type I formation by activated hepatic stellate cells (HSCs) in response to fibrogenic substances, but the molecular signal mechanisms by which leptin promotes liver fibrogenesis through upregulation of collagen type I expression is not clear. We investigated whether leptin-induced collagen type I is mediated by the Janus kinase–phosphatidylinositol 3-kinase–Akt (JAKs–PI3K–Akt) pathway in a human HSC cell line, LX-2. Methods: LX-2 cells were treated with or without various inhibitors in the presence of leptin. Results: Leptin increased α1(I) collagen mRNA and protein. JAK1, PI3K and Akt were activated after leptin stimulation. AG490, a JAK inhibitor, blocked JAK1 phosphorylation accompanied by inhibition of PI3K and Akt activation as well as α1(I) collagen mRNA expression, indicating a JAK1-dependent mechanism. Wortmannin, a PI3K inhibitor, prevented PI3K and Akt activation and resulted in suppression of α1(I) collagen mRNA expression, suggesting a PI3K-mediated process. These changes were reproduced by overexpression of the dominant-negative p85α mutant. A443654.3, an Akt inhibitor, opposed Akt activation, leading to downregulation of α1(I) collagen mRNA. Overexpression of the dominant-negative Akt mutant led to similar alterations. Conclusion: Leptin has a direct action on liver fibrogenesis by stimulating α1(I) collagen production in activated HSC. The process appears to be mediated by the PI3K/Akt pathway through activated JAK1. [ABSTRACT FROM AUTHOR]

A series of liquefied‐MDI‐based polyurethanes having shape memory behavior, with various soft segments, chain extenders, and micro‐phase separation promoters were synthesized. Their morphology and properties were investigated in terms of thermal properties, dynamic mechanical properties, and shape recovery behavior. The results indicate that the soft segment formed with longer chain segment incline to crystallize during the cooling scans and the resulting SMPU have the higher crystallinity. Meanwhile, the chain extenders, which can enhance the polarity of hard segment, incline to have excellent shape memory properties with bigger storage modulus in rubbery state too. It was also found that the micro‐phase separation promoters have great influence on the shape memory behavior due to the enhancement of micro‐phase separation of SMPU. Furthermore, it was proved again that SMPU with longer soft segment and lower hard segment contents usually showed good shape memory behavior. © 2007 Wiley Periodicals, Inc. J Appl Polym Sci, 2007 [ABSTRACT FROM AUTHOR]

Background: Chronic alcohol consumption is known to induce cytochrome P450 2E1 (CYP2E1) leading to lipid peroxidation, mitochondrial dysfunction and hepatotoxicity. We showed that replacement of dietary long-chain triglycerides (LCT) by medium-chain triglycerides (MCT) could be protective. We now wondered whether the induction of mitochondrial CYP2E1 plays a role and whether liver injury could be avoided through mitochondrial intervention. Methods: Rats were fed 4 different isocaloric liquid diets. The control group received our standard dextrin-maltose diet with intake limited to the average consumption of the 3 alcohol groups fed ad libitum the alcohol containing Lieber-DeCarli liquid diet. The fat was either 32% of calories as LCT (alcohol), or 16% as LCT + 16% as MCT (alcohol-MCT 16%), or 32% as MCT only (alcohol-MCT 32%). Results: After 21 days, compared to the controls, the alcohol and both alcohol-MCT groups had a significant increase in mitochondrial CYP2E1 ( p < 0.05 for both). As shown before, the same was found for the microsomal CYP2E1. When MCT replaced all the fat, like in the alcohol-MCT 32% group, CYP2E1 was significantly reduced by 40% in mitochondria ( p < 0.05) and 30% in microsomes ( p < 0.01). In mitochondria, 4-hydroxynonenal (4-HNE), a parameter of oxidative stress, paralleled CYP2E1. Compared to controls, alcohol and alcohol-MCT 16% significantly raised mitochondrial 4-HNE ( p < 0.001), whereas the alcohol-MCT 32% diet brought it down to control levels ( p < 0.001). Mitochondrial reduced glutathione (GSH) was also significantly lowered by alcohol consumption ( p < 0.05), and it increased to almost normal levels with alcohol-MCT 32% ( p = 0.006). These changes in the mitochondria reflected the reduction observed in total liver in which alcohol-MCT 32% decreased the alcohol-induced steatosis with a diminution of triglycerides ( p < 0.001) and of the pro-inflammatory cytokine tumor necrosis factor- α ( p < 0.001). Conclusion: Mitochondria participate in the induction of CYP2E1 by alcohol and contribute to lipid peroxidation and GSH depletion. Thus, lipid composition of the diet is an important determinant for the beneficial effect of MCT, with a diet containing a mixture of LCT/MCT being ineffective. [ABSTRACT FROM AUTHOR]

Wireless body area network (WBAN) has begun to receive attention recently. Ultra wideband (UWB) is a promising technology for WBAN applications. This article presents the results of UWB radio channel measurements performed on human bodies from 3.1 to 10.6 GHz in indoor environments. The measurements were devised to generate the radiographs of path loss and delay spread for the first time. The radiographs contain both qualitative and quantitative information on the channel. They clearly display the influence of the body on the channel and thus reveal where the network nodes should be strategically placed on the body in the design of the UWB WBAN systems. They directly give such channel parameters as path loss and delay spread. They also reflect variations of the channel on and in close proximity to the body. In addition, the measurements were made in an anechoic chamber to expose the impact of the body and to study the effect of different environments on the channel. It is shown that for the UWB channel on the body the path loss exponent n = 2.7 can be used, while for the UWB channel through the body the path loss exponent increases to n = 3.7. The maximum value of the rms delay spread is 12 ns. The rms delay spread values are less than 6 ns 50% of the time. The number of multipath components increases with the separation between transmit and receive antennas. Because of the nonreflecting mechanism, the path loss is larger and the delay spread is smaller in the anechoic chamber environment. © 2007 Wiley Periodicals, Inc. Microwave Opt Technol Lett 49: 1365–1371, 2007; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/mop.22411 [ABSTRACT FROM AUTHOR]

Both dilinoleoylphosphatidylcholine (DLPC) and S-adenosylmethionine (SAMe) have antioxidant properties and antifibrogenic actions. Because H2O2 mediates signal transduction-stimulating liver fibrogenesis, we investigated whether DLPC and SAMe attenuate the production of tissue inhibitor of metalloproteinase (TIMP)-1 by inhibiting H2O2 formation. Methods: LX-2 human hepatic stellate cells were treated with leptin with or without DLPC, SAMe or various inhibitors. Results: Leptin-stimulated TIMP-1 mRNA and its protein were diminished by DLPC or SAMe alone, and the response was fully prevented by the combination of DLPC and SAMe. H2O2 was increased while glutathione was decreased; these changes were prevented by AG490, suggesting a Janus kinases (JAK)-mediated process. Up-regulation of leptin receptor and activation of JAK1 and 2 were not affected by DLPC+SAMe, whereas phosphorylation of ERK1/2 and p38 was blocked by DLPC+SAMe or catalase, suggesting an H2O2-dependent mechanism. These treatments also suppressed leptin-stimulated TIMP-1 promoter activity and decreased TIMP-1 mRNA stability, contributing to TIMP-1 mRNA down-regulation. PD098059, an ERK1/2 inhibitor, suppressed TIMP-1 promoter activity, whereas SB203580, a p38 inhibitor, decreased TIMP-1 message stability; both resulted in a partial reduction of TIMP-1 mRNA. Conclusion: As decreased TIMP-1 production may enhance collagen deposition, the combined administration of DLPC+SAMe should be considered for the prevention of H2O2-mediated signaling and the resulting fibrosis. [ABSTRACT FROM AUTHOR]