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The kinin-kallikrein system is a network of circulating proteins mainly known for its roles in inflammation, blood pressure control, coagulation, and pain Furthermore, several recent studies have concluded that this system plays broader roles than those classically described, for example, in rosacea, cancer, cardiovascular, renal, and central nervous system pathologies26 The system consists of proteins, polypeptides, and a group of enzymes that activate and deactivate the compounds Kinins (bradykinin [BK] and kallidin[KD]) are polypeptides produced from kininogen and broken down by kininases They are rapidly generated after tissue injury and play a pivotal function in the development and maintenance of the inflammatory process, in which they cause dilation of blood vessels and increased vascular permeability They act on PLA2 to increase AA release and thus eicosanoid production27 (Fig 35-1) Kinins act by binding to two receptor types, namely B1, and B2, which belong to the G-protein coupled receptor family B2 receptors are constitutively expressed in various cells under physiologic conditions On the contrary, B1 receptors express rapidly under mainly pathologic conditions26 Kinins (BK and KD) have a higher affinity to B2 receptors, the activation of which leads to the release of cytokines and other inflammatory mediators (eg, PG-E2) Since its discovery, BK has been demonstrated to induce the four classical signs of inflammation heat, redness, swelling, and pain28 described at the beginning of this chapter BK possesses vasoactive properties that enable it to induce vasodilation and increase vascular permeability Additionally, it causes smooth muscle contraction, induces pain, and has the ability to activate nuclear factor- B (NF- B), further contributing to the inflammatory response

This appendix starts with some commonly used data dictionary views, and then lists views organized by the four separate view categories, which you can recognize by their prefix: ALL views have information about all accessible data. Regular database users have access to these views. USER views have information about your own data. Regular database users have access to these views. DBA views have database-wide information. You need DBA privileges (or some specific system privileges) to access these views. V$ views are dynamic performance views. You need DBA privileges (or some specific system privileges) to access these views. The first three categories are commonly referred to as static to distinguish them from the fourth category, the dynamic performance views. This appendix lists the names of the data dictionary views, without any column descriptions. For column details, you can use the SQL*Plus DESCRIBE command or query the DICT_COLUMNS data dictionary view (see Listing 3-11 in 3 of this book). The view descriptions themselves are also very concise, and they may refer to concepts or terms not covered anywhere in this book. See Oracle Reference for further data dictionary details and explanations.

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FIGURE 9-5

Table B-1 lists some commonly used data dictionary views. Table B-1. Commonly Used Data Dictionary Views

which it is exposed are numerous and diverse29 The translation of such insults, which include different pathogens and contact-sensitizing antigens, into cutaneous inflammation requires a complex interaction among multiple inflammatory mediators Notably, NF- B-mediated inflammation appears to be the final common pathway for the translation of environmental insults into inflammation of the skin NF- B, a powerful cellular signaling pathway, can be activated by IL-1, TNF- ,30 and as mentioned earlier, BK26 Interestingly, the epidermis is a storehouse of IL-1 and can produce considerable amounts of IL-1 and TNF- 31,32 It is known that ultraviolet (UV) radiation from sunlight induces activation of IL-1 and TNF- ,33 leading to NF- B-mediated inflammation NF- B regulates many genes in skin cells; however, those that are essential to the initiation of cutaneous inflammation include genes for E-selectin, cytokines, defensins (antibacterial peptides), and cell adhesion molecules30 Of special importance for cutaneous immunity is a subgroup of memory T cells with the ability to circulate preferentially to the skin These memory T cells are identified by a marker known as cutaneous lymphocyte antigen (CLA),34 and are generated in the lymph nodes that drain the skin Then, they are specifically recruited back to the skin during inflammation These unique skin-associated lymphocytes may be positive for either CD4 or CD8, and once activated, may be able to produce either type 1 T-cell cytokines (ie, INF- , IL-2, and lymphotoxin) or type 2 T-cell cytokines (ie, IL-4, IL-5, IL-10 and IL-13)29 It is the activation of the T cells and the subsequent release of cytokines and other effector molecules that result in clinically apparent T-cell-mediated inflammatory skin diseases29

CHAPTER 9:

DICTIONARY (or DICT) DICT_COLUMNS DUAL FLASHBACK_TRANSACTION_QUERY NLS_DATABASE_PARAMETERS NLS_INSTANCE_PARAMETERS NLS_SESSION_PARAMETERS PUBLICSYN ROLE_ROLE_PRIVS ROLE_SYS_PRIVS ROLE_TAB_PRIVS SESSION_PRIVS SESSION_ROLES

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