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Segment, colon

AM Metcalf, SF Phillips, AR Zinsmeister, RL Mac-Carty, RW Beart, BG Wolff. Simplified assessment of segmental colonic transit. Gastroenterology 92 40-47, 1987. [Pg.74]

Ishizawa, M. and Miyaraki, E. (1975) Effect of prostaglandin Fj. on propulsive activity of the isolated segmental colon of the guinea-pig. Prostaglandins 10 759-768. [Pg.416]

An already published sequential 3D thinning algorithm (Palagyi et al. 2001) is applied to extract the medial lines from the segmented colon. [Pg.260]

In the case of cadaverous phantoms, a total of 13 artificial polyps were created using fat tissues. Figure 18.9a exhibits the surface-rendered 3D reconstruction of the segmented colon, and Figure 18.9b presents the same binary object with its central path as a transparent 3D model. In Figure 18.10 the appearance of the created polyps on axial and virtual endoscopic views can be seen. [Pg.264]

Fig. 18.9a,b. The cadaverous phantom, a Surface-rendered image of the segmented colon, b Transparent 3D model showing the central path obtained by skeletonization... [Pg.264]

In this patient population with history of colitis and possible prior segmental colonic resections, fistulas and strictures often develop at the anastomosis and make passage of the colonoscopy device impossible. Scarring of the mesentery may also cause rigidity and may lead to failed colonoscopies. Historically, patients would then go on to double contrast barium enema for complete evaluation of the colon. [Pg.20]

The most common pitfalls are inflammatory stenosis and the segmental colonic spasm. Inflammatory and post-inflammatory stenosis more often show cone-shapedmildwall thickening with involvement of a long segment (>10 cm) and pericolonic fat stranding. Sometimes fluid is present at the root of the mesentery (Chintapalli et al. 1999) (compare Figs. 13.10b and 13.11a, vs Fig. 13.14 and 13.15). [Pg.169]

Fig. 13.16a-d. Segmental colonic spasm in the descending colon (arrow) focal, irregular circular wall thickening with shoulder formation in the supine position (a-c). The lesion shows soft tissue attenuation and CM enhancement (a). Normal colon wall without wall thickening or stenosis in the prone position (d). It is important to identify the same segment as in the supine position... [Pg.169]

The physiological role of the ICOR is not clear and may be heterogeneous in the various tissues. In the thick ascending limb of the loop of Henle this channel appears to serve as the exit for CP at the basal cell pole [16,65,66], This conductive mechanism, therefore, is required for the reabsorption of Na and CP by this segment of the nephron [16]. In the rectal gland of Squalus acanthias a very similar channel is utilized for Na" and CP secretion. In these latter cells the CP-channel is present in the luminal membrane and is controlled by cytosolic cAMP [15,56,71]. It has been claimed that this kind of channel is also responsible for the secretion of CP in the colonic crypt cell, in colonic carcinoma cells and in respiratory epithelial cells [17,19,20,22]. Recent data have cast some doubt on this concept ... [Pg.280]

I have noted that NPPB is structurally related to loop diuretics of the furosemide (Fig. 2) type. These latter compounds bind to the Na 2CNK -cotransporter [16] and inhibit NaCl reabsorption in the TAL segment and NaCl secretion in epithelia such as the colonic crypt cell and rectal gland of Squalus acanthias [15]. We were able to show that only minor modification of the NPPB molecule on one side and of furosemide on the other led to compounds with altered selectivities [70,91-93]. One prototype of an intermediate blocker, i.e., a substance blocking both Na 2Cl K -cotransport and CP-channels, is torasemide (Fig. 2). Hence we have performed a systematic study in order to define the constraints defining the effectiveness of this class of substances [91]. [Pg.286]

The large intestine consists of the cecum the ascending, transverse, descending, and sigmoid colon segments and the... [Pg.1342]

Drugs may also undergo hydrolysis by intestinal esterases (hydrolases), more specifically carboxylesterases (EC 3.1.1.1) in the intestinal lumen and at the brush border membrane [58, 59]. It has been shown that intestinal hydrolase activity in humans was closer to that of the rat than the dog or Caco-2 cells [60]. In these studies, six propranolol ester prodrugs and p-nitrophenylacetate were used as substrates, and the hydrolase activity found was ranked in the order human > rat Caco-2 cells > dog for intestinal microsomes. The rank order in hydrolase activity for the intestinal cytosolic fraction was rat > Caco-2 cells = human > dog. The hydrolase activity towards p-nitrophenylacetate and tenofovir disoproxil has also been reported in various intestinal segments from rats, pigs and humans. The enzyme activity in intestinal homogenates was found to be both site-specific (duodenum > jejunum > ileum > colon) and species-dependent (rat > man > Pig)-... [Pg.512]

The results showed there to be an asymmetry in colonic distribution among healthy subjects, with two-thirds of the administered dose in the proximal colon and one-third in the distal colon. In the patients, this difference was even more pronounced, with only one-tenth of the administered dose in the distal segment. [Pg.561]

There is also a segmental distribution of the types of bacteria. Strict anaerobic species are normally confined to the oral cavity and the colon, habitats they densely colonize and predominate [1-5] (fig. 1). Bacteria indigenous to the upper respiratory tract (URT flora) and anaerobic bacteria of oral origin are swallowed with saliva and recovered from the upper gut at densities below 105 CFU/ ml. Under physiological conditions, they are considered transitory rather than indigenous to the upper gut. Facultative anaerobic bacteria are usually confined to the distal small bowel and colon, but transient species entering the gut with nutrients are occasionally recovered from the healthy upper gut at low counts. [Pg.2]

When the mechanisms restricting bacterial colonization in the upper gut fail, due to disease or dysfunction, bacterial overgrowth develops. The segmental distribution may be gastric, intestinal or both depending on the type of failure. The consequences for the host vary from none to life-threatening complications, caused by severe water and electrolyte deficiencies and septic manifestations. [Pg.2]

Location and extent Gastric stomach Similar flora present in duodenum and proximal jejunum Small intestine, segmental or global Backwards colonization of the stomach in severe forms... [Pg.3]

Intubation techniques have been used extensively to appraise the absorption rate in the stomach, duodenum, jejunum, ileum, and colon (23). These methods can be adapted to provide direct evaluation of the dissolution rate in different segments of the GI tract. [Pg.343]

Raab Y, Hallgren R, Knutson L, Krog M and Gerdin B (1992) A Technique for Segmental Rectal and Colonic Perfusion in Humans. Am J Gastroenterol 10 pp 1453-1459. [Pg.74]


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See also in sourсe #XX -- [ Pg.155 ]




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