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Introduction: Intrathecal immunoglobulin G (IgG) and oligoclonal bands (OCBs) are the most consistent and characteristic features of Multiple Sclerosis (MS). OCBs in MS are considered products of clonally expanded B cells in the cerebrospinal fluid (CSF), representing the sum of contributions from B cells in the brain. However, large amounts of IgG can be eluted from MS plaques in which lymphocytes are absent, and there is no correlation between levels of plaque-associated IgG and the presence of lymphocytes. It is calculated that it would take 3.2 billion lymphocytes to generate such large amounts of intrathecal IgG (30 mg in 500 ml CSF) in MS patients. Therefore, circulating lymphocytes in CSF could only account for <0.1% of the extra IgG in MS. Methods: We analyzed clinical laboratory parameters from sera and CSF of 115 patients including 91 patients with MS and 24 patients with other inflammatory central nervous system (CNS) disorders (IC). We investigated the relationship between oligoclonal bands, IgG antibodies, CSF cells, IgG Index, albumin, and total protein. Results: MS patients have significantly elevated serum concentrations of IgG antibodies, albumin, and total protein, lower levels of lymphocytes, albumin, and total protein in the cerebrospinal fluid, but no difference in CSF IgG concentration compared to those with other inflammatory neurological disorders. Furthermore, in MS there was no linear relationship between the numbers of OCBs, CSF lymphocytes, CSF IgG, and IgG Index, and between serum IgG and serum albumin, but significant correlation between IgG in CSF and serum, and between CSF IgG and CSF albumin. Conclusion: There are unique differences between MS and patients with other inflammatory neurological disorders. Our data suggest that in MS patient (a) B cells and their products in the CSF may not be the sole source of intrathecal IgG; (b) oligoclonal bands may not be the products of single B cell clones in the CSF; and (c) there is a strong connection between serum components in the peripheral circulation and the central nervous system. [ABSTRACT FROM AUTHOR]

For the critical engine parts such as the crankshaft, the fatigue limit load is one of the most important parameters involved the design and manufacture stage. In previous engineering applications, this parameter has always been obtained by experiment, which is expensive and time-consuming. This paper, based on the theory of critical distance (TCD), first analyzes the stress distribution of a crankshaft under its limit load. In this way, the length of the critical distance can be obtained. Then a certain load is applied to a new crankshaft made of the same material and the effective stress is calculated based on the critical distance above. Finally, the fatigue limit load of the new crankshaft can be obtained by comparing the effective stress and the fatigue limit of the material. Comparison between the prediction and the corresponding experimental data shows that the traditional TCD may result in bigger errors on some occasions, while the modified TCD proposed in this paper can provide a more satisfactory result in terms of the fatigue limit for a quick engineering prediction. [ABSTRACT FROM AUTHOR]

Dense genetic maps, along with quantitative trait loci (QTLs) detected on such maps, are powerful tools for genomics and molecular breeding studies. In the important woody genus Eucalyptus, the recent release of E. grandis genome sequence allows for sequence-based genomic comparison and searching for positional candidate genes within QTL regions. Here, dense genetic maps were constructed for E. urophylla and E. tereticornis using genomic simple sequence repeats (SSR), expressed sequence tag (EST) derived SSR, EST-derived cleaved amplified polymorphic sequence (EST-CAPS), and diversity arrays technology (DArT) markers. The E. urophylla and E. tereticornis maps comprised 700 and 585 markers across 11 linkage groups, totaling at 1,208.2 and 1,241.4 cM in length, respectively. Extensive synteny and colinearity were observed as compared to three earlier DArT-based eucalypt maps (two maps with E. grandis × E. urophylla and one map of E. globulus) and with the E. grandis genome sequence. Fifty-three QTLs for growth (10–56 months of age) and wood density (56 months) were identified in 22 discrete regions on both maps, in which only one colocalizaiton was found between growth and wood density. Novel QTLs were revealed as compared with those previously detected on DArT-based maps for similar ages in Eucalyptus. Eleven to 585 positional candidate genes were obained for a 56-month-old QTL through aligning QTL confidence interval with the E. grandis genome. These results will assist in comparative genomics studies, targeted gene characterization, and marker-assisted selection in Eucalyptus and the related taxa. [ABSTRACT FROM AUTHOR]

Thermal effects such as conduction, convection and viscous dissipation are important to lubrication performance, and they vary with the friction conditions. These variations have caused some inconsistencies in the conclusions of different researchers regarding the relative contributions of these thermal effects. To reveal the relationship between the contributions of the thermal effects and the friction conditions, a steady-state THD analysis model was presented. The results indicate that the contribution of each thermal effect sharply varies with the Reynolds number and temperature. Convective effect could be dominant under certain conditions. Additionally, the accuracy of some simplified methods of thermo-hydrodynamic analysis is further discussed. [ABSTRACT FROM AUTHOR]

Stanniocalcin (STC), a glycoprotein hormone, is expressed in a wide variety of tissues to regulate Ca2+ and PO4- homeostasis. STC2, a member of STC family, has been reported to be associated with tumor development. In this study, we investigated whether the expression of STC2 is associated with migration and invasion of breast cancer cells. We found that breast cancer cell line 231 HM transfected with STC2 shRNA displayed high motility, fibroblast morphology, and enhanced cell migration and invasion. Introduction of STC2 in 231 cells reduced cell migration and invasion. In response to irradiation, silencing of STC2 in 231 HM cells reduced apoptosis, whereas overexpression of STC2 in 231 cells promoted apoptosis, compared with in control cells. Mechanistic study showed that STC2 negatively regulated PKC to control the expression of Claudin-1, which subsequently induced the expressions of EMT-related factors including ZEB1, ZO-1, Slug, Twist, and MMP9. Suppression of PKC activity by using a PKC inhibitor (Go 6983) restored the normal motility of STC2-silenced cells. Furthermore, in vivo animal assay showed that STC2 inhibited tumorigenesis and metastasis of breast cancer cells. Collectively, these results indicate that STC2 may inhibit EMT at least partially through the PKC/Claudin-1-mediated signaling in human breast cancer cells. Thus, STC2 may be exploited as a biomarker for metastasis and targeted therapy in human breast cancer. [ABSTRACT FROM AUTHOR]

Background: The role of CTGF varies in different types of cancer. The purpose of this study is to investigate the involvement of CTGF in tumor progression and prognosis of human nasopharyngeal carcinoma (NPC). Experimental design: CTGF expression levels were examined in NPC tissues and cells, nasopharynx (NP) tissues, and NP69 cells. The effects and molecular mechanisms of CTGF expression on cell proliferation, migration, invasion, and cell cycle were also explored. Results: NPC cells exhibited decreased mRNA expression of CTGF compared to immortalized human nasopharyngeal epithelial cell line NP69. Similarly, CTGF was observed to be downregulated in NPC compared to normal tissues at mRNA and protein levels. Furthermore, reduced CTGF was negatively associated with the progression of NPC. Knocking down CTGF expression enhanced the colony formation, cell migration, invasion, and G1/S cell cycle transition. Mechanistic analysis revealed that CTGF suppression activated FAK/PI3K/AKT and its downstream signals regulating the cell cycle, epithelial-mesenchymal transition (EMT) and MMPs. Finally, DNA methylation microarray revealed a lack of hypermethylation at the CTGF promoter, suggesting other mechanisms are associated with suppression of CTGF in NPC. Conclusion: Our study demonstrates that reduced expression of CTGF promoted cell proliferation, migration, invasion and cell cycle progression through FAK/PI3K/AKT, EMT and MMP pathways in NPC. [ABSTRACT FROM AUTHOR]