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Complex Expression (complex + expression)
Selected AbstractsSkin Repair Using a Porcine Collagen I/III Membrane,Vascularization and Epithelization PropertiesDERMATOLOGIC SURGERY, Issue 6 2010FALK WEHRHAN MD BACKGROUND Collagen membranes have been developed to overcome the problem of limited availability of skin grafts. Vascularization and restricted functional epithelization limit the success of bioartificial constructs. OBJECTIVE To compare the vascularization, epithelization, and integration of a porcine collagen I/III membrane with that of split-thickness skin grafts on skin wounds. MATERIALS AND METHODS In 21 adult pigs, full-thickness skin defects on the rear side of the ear healed by split-thickness skin grafting, by covering with the membrane, or by free granulation. Skin samples on postoperative days 1, 3, 7, 14, 21, and 28 were evaluated histologically (hematoxylin-eosin, Sirius Red) and using immunohistochemistry (cytokeratin 5/6, transforming growth factor beta receptor (TGF,R-III) and immunoblot (TGF,1,3, Smad2/3). Epithelial thickness and TGF,R-III-positive capillary area were quantitatively assessed. RESULTS Epithelization and vascularization in the membrane group were not significantly different from in the group treated with a split-thickness skin graft. Free granulation showed significantly slower epithelization and vascularization (p<.05). TGF,1 and Smad2/3 complex expression were high during free granulation. Matrix was distinguishable until day 7. CONCLUSIONS This membrane serves as a suitable full-thickness dermal substitute, because the membrane is vascularized faster than free granulation tissue and enables early epithelization. Geistlich Biomaterials (Wolhusen, Switzerland) provided the collagen membrane used in this study [source] Can We Derive the Principle of Compositionality (if We Deflate Understanding)?DIALECTICA, Issue 2 2009Antonio Rauti Paul Horwich has claimed that we can derive a certain form of the principle of compositionality from a deflationary account of what it is to understand a complex expression. If this were the case, we would realize a surprising theoretical economy, and if the derivation involved basic ideas from a use theory of meaning, we would have a novel argument for use theories of meaning. Horwich does not offer a detailed derivation. In this paper I reconstruct a possible derivation and show that it begs the question. I then extend my discussion to explain why it is unlikely that alternative arguments can fare better. [source] Deregulation of E-cadherin,catenin complex in precancerous lesions of gastric adenocarcinomaJOURNAL OF GASTROENTEROLOGY AND HEPATOLOGY, Issue 5 2003ANNIE ON-ON CHAN Abstract Background and Aim: Decrease in expression of the E-cadherin,catenin complex is an important element in gastric carcinogenesis. However, the expression of the complex in gastric precancerous lesions has not been well studied. The present study aimed to examine the serial change in expression of E-cadherin,catenin complex in the precancerous lesions of gastric cancer patients. Methods: Gastrectomy specimens of 40 patients with gastric cancer were retrieved. Areas with chronic gastritis, atrophic gastritis, intestinal metaplasia and adenocarcinoma were identified and immunostained for ,-catenin, ,-catenin and E-cadherin. The results were scored semiquantitatively by two independent pathologists using a validated scoring system. Results: A significant decrease in score was observed in 5% (1/22) of ,-catenin, 0% (0/22) of ,-catenin and 9% (2/22) of E-cadherin in chronic atrophic gastritis patients, and in 28% (5/18) of ,-catenin, 67% (10/15) of ,-catenin and 57% (8/14) of E-cadherin in intestinal metaplasia patients. The scoring of ,-catenin, ,-catenin and E-cadherin correlated with each other. Forty-three percent of patients had concordant changes of scores along the gastritis,adenocarcinoma sequence. There was no association between Helicobacter pylori status and E-cadherin,catenin complex expression. Conclusion: Deregulation of the E-cadherin,catenin complex was observed in the majority of precancerous lesions in patients with gastric adenocarcinoma, which has potential diagnostic and therapeutic implications. © 2003 Blackwell Publishing Asia Pty Ltd [source] Role of the transmembrane domain of glycoprotein IX in assembly of the glycoprotein Ib,IX complexJOURNAL OF THROMBOSIS AND HAEMOSTASIS, Issue 12 2007S.-Z. LUO Summary.,Background:,The glycoprotein (GP) Ib,IX complex is critically involved in platelet adhesion to von Willebrand factor and in the initial step of platelet activation. How this complex is assembled is not clear. We previously showed that the transmembrane (TM) domains of the GPIb, and GPIb, subunits interact and participate in complex assembly. Objectives and methods:,Here, we have investigated the role of the TM and cytoplasmic domains of GPIX in assembly of the GPIb,IX complex, by analyzing the mutational effects on complex expression and assembly in transiently transfected Chinese hamster ovary cells. Results:,Replacing the cytoplasmic domain of GPIX with a poly-alanine sequence had little effect on surface expression and structural integrity of the GPIb,IX complex. In contrast, replacing the GPIX TM domain (residues 132,153) with a poly-leucine-alanine sequence markedly disrupted complex formation of GPIX with GPIb,, interfered with GPIb formation, and decreased surface expression of the host complex. We further analyzed the contributions of a number of GPIX TM residues to complex formation by mutagenesis and found significant roles for Asp135 and several Leu residues. Conclusions:,The TM domain, rather than the cytoplasmic domain, of GPIX plays an important role in expression and assembly of the GPIb,IX complex by interacting with its counterparts of GPIb. These TM domains may form a parallel four-helical bundle structure in the complex. [source] Dendritic cells from spondylarthritis-prone HLA,B27,transgenic rats display altered cytoskeletal dynamics, class II major histocompatibility complex expression, and viabilityARTHRITIS & RHEUMATISM, Issue 9 2009Maarten Dhaenens Objective Spondylarthritis (SpA) is characterized by spinal and peripheral joint inflammation, frequently combined with extraarticular manifestations. Despite the well-established association of SpA with the class I major histocompatibility complex (MHC) allele HLA,B27, there are still different, parallel hypotheses on the relationship between HLA,B27 and disease mechanisms. The present study was undertaken to investigate several characteristics of mature dendritic cells (DCs), which are believed to be essential for triggering disease in a model of SpA in HLA,B27,transgenic rats. Methods We combined different whole-proteome approaches (2-dimensional polyacrylamide gel electrophoresis and iTRAQ) to define the most aberrant molecular processes occurring in spleen DCs. Videomicroscopy and flow cytometry were used to confirm both cytoskeletal and class II MHC expression deficiencies. Results Our proteome studies provided evidence of up-regulation of proteins involved in class I MHC loading, and unfolded protein response, along with a striking down-regulation of several cytoskeleton-reorganizing proteins. The latter result was corroborated by findings of deficient motility, altered morphology, and decreased immunologic synapse formation. Furthermore, class II MHC surface expression was reduced in DCs from B27-transgenic rats, and this could be linked to differences in class II MHC,induced apoptotic sensitivity. Finally, we found reduced viability of the CD103+CD4, DC subpopulation, which likely exerts tolerogenic function. Conclusion Taken together, our findings have different important implications regarding the physiology of B27-transgenic rat DCs, which have a putative role in spontaneous disease in these rats. In particular, the reduced motility and viability of putatively tolerogenic CD4+ DCs could play an important role in initiating the inflammatory process, resulting in SpA. [source] HLA,B27 up-regulation causes accumulation of misfolded heavy chains and correlates with the magnitude of the unfolded protein response in transgenic rats: Implications for the pathogenesis of spondylarthritis-like diseaseARTHRITIS & RHEUMATISM, Issue 1 2007Matthew J. Turner Objective HLA,B27 is implicated in the pathogenesis of spondylarthritis (SpA), yet the molecular mechanisms are incompletely defined. HLA,B27 misfolding has been associated with endoplasmic reticulum stress and activation of the unfolded protein response (UPR) in macrophages from HLA,B27/human ,2 -microglobulin,transgenic (B27-transgenic) rats. This study was performed to assess the mechanisms that drive activation of the HLA,B27,induced UPR and to determine whether splenocytes respond in a similar manner. Methods Splenocytes were isolated and bone marrow macrophages were derived from B27-transgenic and wild-type rats. Cells were treated for up to 24 hours with cytokines that induce class I major histocompatibility complex expression. HLA,B27 expression and misfolding were assessed by real-time reverse transcription,polymerase chain reaction, flow cytometry, and immunoblotting. Activation of the UPR was measured by quantifying UPR target gene expression and X-box binding protein 1 messenger RNA (mRNA) splicing. Results HLA,B27 mRNA up-regulation was accompanied by a dramatic increase in the accumulation of misfolded heavy chains and preceded robust activation of the UPR in macrophages. When macrophages were treated with various cytokines, the magnitude of the UPR correlated strongly with the degree of HLA,B27 up-regulation. In contrast, B27-transgenic splenocytes exhibited only low-level differences in the expression of UPR target genes after exposure to interferon-, or concanavalin A, which resulted in minimal HLA,B27 up-regulation. Conclusion These results suggest that HLA,B27,associated activation of the UPR in macrophages is attributable to the accumulation of misfolded heavy chains, and that certain cell types may be more susceptible to the effects of HLA,B27 misfolding. Strategies that eliminate HLA,B27 up-regulation and/or the accumulation of misfolded heavy chains may be useful in evaluating the role of these events in the pathogenesis of SpA. [source] correspondence: Single novel mutation in transmembrane region of glycoprotein (GP) IX affects GP Ib- IX complex expression and causes Bernard,Soulier syndromeBRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2010Li-min Xu No abstract is available for this article. [source] | ||||||||||