Sun, Sun Microsystems, the Sun Logo, Solstice, Java, JavaBeans, JDK, and Solaris are trademarks or registered trademarks of Sun Microsystems, Inc. in the . SLSE6 REV G.2 General programming concepts – Covered in SL SL Fundamentals of the Java™ Programming Language, or have. Course Java Programming Language (SLSE6). Overview The Java Programming Language course provides students with information about the syntax of.
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It provides you with clear technical vocabulary and accurate search terms which enable you to quickly deep-dive into a new API. Also, the certificate looks great on your resume. As your applications grow a point where you can save months in developing time by investing one week in training.
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What Class Should I Take? The most important step before deciding on a class is determining your entry-level. A good advanced class teaches one technology in depth; a good beginner's class gives you a wide overview of all the language features and technical terms. When look for a solid and comprehensive introduction to platform-independent software development, SL The Java Programming Language is for you: This class covers object-oriented programming concepts in general, and the Java environment and syntax in particular.
If you have no prior experience with general programming concepts, consider taking the SL Fundamentals of the Java Programming Language class first. SL assumes that you already have fundamental programming experience. You should be familiar with terms like variable or operator, and with using a text editor and a web browser.
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Compte Twitter. Is your machine ready for Second Life. Injury to sinusoidal endothelial cells stimulates production of a splice variant of cellular fibronectin EIIIA isoform , which has an activating effect on stellate cells Molecular approaches to explore stellate cell gene regulation during early activation have identified differentially up-regulated genes These efforts have yielded a transcription factor 13 , an adhesion molecule ICAM-1 14 , and interestingly, the prion protein 15 , among others.
At least two other KLF proteins also regulate stellate cell activation. Sp1, the first member of the KLF family, binds more actively to its consensus motif in activated versus quiescent stellate cells 17 , Basic transcription element binding protein 1 BTEB1 mediates the increase in collagen gene expression, which occurs in response to UV radiation or expression of the transcription factor Jun Enhanced cytokine responses occurs through multiple mechanisms 12 ; among these, increased expression of cell membrane receptors and enhanced signaling are especially important see Ref.
In particular, receptor tyrosine kinases RTKs , which mediate many of the stellate cell's responses to cytokines, are broadly up-regulated during liver injury Continued ECM remodeling during this phase underlies virtually all cellular responses characterizing progressive liver injury. The low density subendothelial matrix is progressively replaced by one rich in fibril-forming collagen.
This fundamental shift in ECM composition affects the behavior of hepatocytes, sinusoidal endothelium, and stellate cells Fig. Fibril-forming ECM also accelerates stellate cell activation. These effects are mediated not only through interactions with integrins, the classic ECM receptors, but also through binding to at least one RTK.
Recently, a subfamily of receptor tyrosine kinases, discoidin domain receptors DDRs , has been characterized, which unlike other RTKs signal in response to fibrillar collagens rather than growth factors 22 , With the identification of discoidin domain receptor-2 DDR2 mRNA in stellate cells 21 , a mode of matrix-cell interaction in liver has emerged that may explain why fibril-forming matrix especially collagen type I provokes activation of stellate cells during sinusoidal fibrosis.
Thus, as the subendothelial basement membrane is replaced by fibrillar collagen stellate cell activation may be perpetuated via binding of collagen to the DDR2 receptor 21 , Phenotypic Responses of Activated Stellate Cells Discrete phenotype responses of stellate cells can be identified as their activation in response to liver injury is perpetuated.
These include: a proliferation; b contractility; c fibrogenesis; d matrix degradation; e chemotaxis; f retinoid loss; and g cytokine release and white blood cell chemoattraction. Proliferation Increased numbers of stellate cells in injured liver arise in part from local proliferation in response to polypeptide growth factors, most of which signal through receptor tyrosine kinases. Platelet-derived growth factor PDGF is the best characterized and most potent among these proliferative factors in hepatic fibrosis.
Additionally, activation of phosphoinositol 3-kinase is necessary for both mitogenesis and chemotaxis by pathways largely independent of ERK activation Contractility Contractility by activated stellate cells represents an important mechanism underlying increased portal resistance during liver injury.
The key contractile stimulus toward stellate cells is endothelin-1 ET-1 , which in part is autocrine-derived 27 , Up-regulation of ET-1 production is accompanied by increased endothelin-converting enzyme-1, which activates the latent ET-1 ET-1, in addition to its potent contractile effect, also regulates stellate cell proliferation 28 , At least two G-protein-coupled receptors mediate the effects of ET Unlike receptor tyrosine kinases, which are generally induced during activation, ET receptor types A and B are expressed on both quiescent and activated stellate cells