Tissue schematic representation

Fig. 2.—Schematic Representation of the Heparin Proteoglycan. [The polysaccharide chains, bound to the polypeptide matrix through a linkage region," are cleaved by tissue endoglycosidases (arrows) after the transformations illustrated in Scheme 1.]...

Fig. S. Schematic representation of coagulation pathway as currently understood. TF, tissue factor PPL, platelet phospholipid.

Figure 8.1 Body iron stores and daily iron exchange. The figure shows a schematic representation of the routes of iron movement in normal adult male subjects. The plasma iron pool is about 4 mg (transferrin-bound iron and non-transferrin-bound iron), although the daily turnover is over 30 mg. The iron in parenchymal tissues is largely haem (in muscle) and ferritin/haemosiderin (in hepatic parenchymal cells). Dotted arrows represent iron loss through loss of epithelial cells in the gut or through blood loss. Numbers are in mg/day. Transferrin-Tf haemosiderin - hs MPS - mononuclear phagocytic system, including macrophages in spleen and Kupffer cells in liver.

Figure 5 Schematic representation of absorbance of porphyrin compounds in relation to tissue transmittance at various wavelengths (see text). The lowest energy band (Band I) is shown in each case, apart from the porphyrin spectrum (etio type shown) on the left. The transmittance curve refers to a fold of human scrotal sac 0.7 cm thick (Wan, S. Parrish, J. A. Anderson, R. R. Madden, M. Photochem. Photobiol. 1981, 34, 679-681). The broad feature at ca. 500-600 nm is ascribed to haemoglobin (reproduced by permission of the Royal Society of Chemistry from Chem. Soc. Rev. 1995, 24, 19-33).

Figure 8.1 (A) Cross-sectional view of the organization of the small intestine, illustrating the serosa, the longitudinal and circular muscle layers (=muscularis externa), the submucosa, and the intestinal mucosa. The intestinal mucosa consists of four layers, the inner surface cell monolayer of enterocytes, the basal membrane, the lamina propria (connective tissue, blood capillaries), and the muscularis mucosae, (B) Schematic representation of an enterocyte (small intestinal epithehal cell) (according to Tso and Crissinger [151], with permission).

Figure 9.4. Schematic representation of the mechanism of action of the coaguligand approach. Cross linking of truncated Tissue Factor to tumour endothelial cells leads to local blood coagulation via the tTF/fVIIa complex. tTF, truncated Tissue Factor fVIIa, factor Vila fX (A), factor X (A).

Schematic representation of the fibrinolytic system. Plasmin is the active fibrinolytic enzyme. Several clinically useful activators are shown on the left in bold. Anistreplase is a combination of streptokinase and the proactivator plasminogen. Aminocaproic acid (right) inhibits the activation of plasminogen to plasmin and is useful in some bleeding disorders. t-PA, tissue plasminogen activator.

Figure 22.2 shows a schematic representation of the enzymatic process between paracetamol and peroxidase catalyzed by the zucchini tissue powder incorporated into the Nujol/graphite electrode and also the electrochemical reduction of V-acetyl-p-benzoquinoneimine to paracetamol at a potential of —0.12 V. 

Figure 6.4. Schematic representation of DNA isolation process. After tissue homogenization and cell lysis, the sample is extracted with phenol and the DNA remains in the aqueous phase. DNA is recovered from the aqueous phase by ethanol precipitation.

Fig. 17.5 Schematic representation of a physiological based model. Left figure shows the physiological structure, upper right figure shows a model for a perfusion rate limited tissue, and lower right figure shows a model for a permeability rate-limited tissue. Q denotes the blood flow, CL the excretion rate, KP the tissuerplasma distribution coefficient, and PS the permeability surface area coefficient.

Figure 14.7 Schematic representation of the process of gene delivery and expression. Extacellular environment —> tissue targetability —> cellular uptake —> intracellular trafficking —> nuclear entry —> gene expression...

Figure 32-1. (A) Schematic representation of the nonenzymatic glycation of proteins, including hemoglobin, resulting in glycated HbAlc. (B) Chemical structure of advanced glycation end products in tissues exposed to chronic hyperglycemia.The R groups designate tissue proteins that have become cross-linked and frequently become dysfunctional as a result of this process. Adapted from Brownlee (1992).

Figure 32-3. Schematic representation of fuel mobilization during fasting. Catabolism of muscle proteins provides alanine for gluconeogenesis and glutamine for utilization by the gut and kidney, while branched chain amino acids are primarily oxidized within the muscle. Breakdown of adipocyte triacylglycerols provides glycerol and free fatty acids (not shown) the free fatty acids provide fuel for liver, muscle and most other peripheral tissues. The liver utilizes both alanine and glycerol to synthesize glucose which is required for the brain and for red blood cells (not shown). Adapted from Besser and Thirner (2002).

Fig. 6.6. Schematic representation of a general approach that can be used to interpret the results of an in-vitro bioassay sample. The radionuclide quantities in (a) the whole body or (b) tissues or organs are expressed in logarithms because the retention curves, when expressed in such a manner, are often straight...

Figure 31.5. Leukocyte migration into locally ischemic brain. Histologic and schematic representations of changes in leukocyte behavior in the brain microvessels after focal ischemia. Shortly (within 1-6 h) after experimental stroke, many of the leukocytes, primarily neutrophils, in the ischemic tissue vessels are adherent to the post-capillary venuole and capillary walls. This can modify and exacerbate the decreased blood flow occurring in the already ischemic brain. Then, these neutrophils can find their way outside the vascular walls into the focal ischemic cortex over the next 6-24h. Macrophages move into the brain later (i.e., over 1-5 days) and significantly accumulate in the infarcted brain. These changes in leukocyte behavior are mediated by increased brain inflammatory cytokine, adhesion molecule(s), and chemokine expression in the ischemic/injured brain. Reproduced from ref Barone FC, Feuerstein GZ. Inflammatory mediators and stroke new opportunities for novel therapeutics. J Cereb Blood Flow Metab 1999 19 819-834. With permission from Nature.

Fig. 3 Schematic representation of iontophoresis. Two electrode chambers, connected to a power source, are placed in contact with the skin. Upon application of the electric field, drug ions are repelled from the electrode of similar polarity (in this case, cations are repelled from the anode). This electrorepulsion (ER) also imposes inward motion on i) other cations present in the anode formulation, and ii) the outward transport of anions (e.g., CP) from within the skin. At the non-working electrode (in this case, the cathode), negative anions from the electrolyte are driven into and through the skin, while cations (e.g., Na ) are extracted from the tissue. The direction of the electroosmotic flow (EO) is also shown.

Figure 4 Schematic representation of a PBPK model with different routes of entry. RPT, richly perfused tissues (e.g., brain, kidneys, and spleen) PPT, poorly perfused tissues (e.g., muscles, skin, and bone GIT, gastrointestinal tract. Kn and V ax are constants that characterize metabolizing tissues like the liver.

Figure 1 Schematic representation of stimuiation of tissue repair. Chemicais and drugs are metabolized in the tissue to their reactive metaboiites, which initiate injury. An inflammatory response foiiows the injury stimuiating reiease of cytokines and chemokines, which prime the quiescent ceiis to enter ceii cycie. Additionai stimuiation to compiete ceii division comes from growth factors. As cell proliferation increases, the dead tissue is replaced by viable cells and injury regresses.

Figure 2 Schematic representation depicting that tissue repair follows dose response. Tissue repair (TR) increases as the dose of the offending chemical increases, until a threshold dose (high dose in this graph), where TR is inhibited resulting in progression of injury and animal death.

FIGURE 2-29 Schematic representation of a physiologically based kinetic model for bioaccumulation of a chemical that is absorbed through the gills, transported by blood flow, stored in various body tissues, and metabolized by the liver. Such a model requires much more detailed information on the fish than does a partitioning model however, it may be necessary to use this more complex approach for chemicals that are metabolized or excreted by the fish more rapidly than they are exchanged with the water [adapted from Barron (1990). Reprinted with permission. 1990 American Chemical Society]. 

Figure 31-18 Schematic representation of the subunit structure of ferritins from various tissues. (From Harrison PM, Arosh P. The ferritins molecular properties, iron storage function and cellular regulation. Biochim Biophys Acta 1996 12 75 161-203.)...

Figure 4 Schematic representation of diffusion cell preparation for isolated tissue experiments. In this figure, PD represents the electrical potential difference (in millivolts) across the membrane and ISC, represents the current flow transepithelial resistance is PD. (From Ref. 62.)...

Figure 4.1. Schematic representation of leukocyte transmigration induced by chemokines. The first step involves rolling attributed to interaction between the leukocyte and the endothelial cells. This process is mediated by selectins and selectin ligands expressed on the surface of both cell types. In the next step a chemokine interacts with its receptor, inducing leukocyte activation and conformational changes in the adhesion molecules (integrins) and resulting in firm adhesion to the endothelial surface. It is believed that the chemokine is immobilized on the endothelial surface by interactions with glycosaminoglycans. The leukocytes then transmigrate into the tissues.

This dilference between the in vitro situation, which has of course served as a very important research object to understand basic points about electroporation, and tissue response to electric fields is important to highlight because proper attention must be paid to consequences of these dilferences. Schematic representations of this more complex situation are attempted in Figures 8.2 and 8.3. 

Figure 1. Schematic representation of the complexity of the in vivo model veiisus the simplistic approach followed with in vitro models (membrane-, cell- and tissue-based systems).

Schematic representation of the transport of CO2 from the tissues to the blood. Note that the majority of CO2 is transported as HCO in the plasma and that the principal buffer in the red blood cell is hemoglobin. Solid lines refer to major pathways, and broken lines refer to minor pathways. Hb = hemoglobin.

Schematic representation of the transfer of CO2 from the alveolus (and its loss in the expired air in the lungs) and oxygenation of hemoglobin. Note that the sequence of events occurring in the pulmonary capillaries is the opposite of the process taking place in the tissue capillaries (Figure 1-5). Solid lines indicate major pathways and broken lines indicate minor pathways. Hb = hemoglobin.

Schematic representation of the major steps in the regulation of thyroid hormone secretions and metabolism at five levels, namely, brain, hypothalamus, pituitary thyrotropes, thyroid, and peripheral tissues.

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