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Cells acinar

The word hormone is derived from the Greek hormaein, meaning to set in motion or to excite. It was used initially to define the activity of secretin [1393-25-5] (1), a gastrointestinal polypeptide released into the blood by the duodenal mucosa to stimulate pancreatic acinar cells to release bicarbonate and water. [Pg.169]

AQP10 has only been identified in the small intestine so far and is thought to play a role in hormonal secretion. AQP11 is expressed in kidney, liver, testis and brain, but no function has been found so far. AQP12 has been identified in pancreatic acinar cells, where it is thought to facilitate the release of digestive enzymes into the pancreatic duct. [Pg.217]

TRPV5 and TRPV6, also known as the epithelial Ca2+ channel or ECaC (TRPV5) and Ca2+transporter 1 or Ca2+ transporter-like (TRPV6), are the only two Ca2+-selective TRP channels identified so far. They may function in vitamin D-dependent transcellular transport of Ca2+in kidney, intestine and placenta. TRPV6 is also expressed in pancreatic acinar cells, and in prostate cancer, but not in healthy prostate or in benign prostate hyperplasia. [Pg.1246]

Amylase enters the blood largely via the lymphatics. An increase in hydrostatic pressure in the pancreatic ducts leads to a fairly prompt rise in the amylase concentration of the blood. Neither an increase in volume flow of pancreatic juice nor stimulation of pancreatic enzyme production will cause an increase in senm enzyme concentration. Elevation of intraductal pressure is the important determinant. Stimulation of flow in the face of obstruction can, however, augment the entry of amylase into the blood, as can disruption of acinar cells and ducts. A functional pancreas must be present for the serum amylase to rise. Serum amylase determination is indicated in acute pancreatitis in patients with acute abdominal pain where the clinical findings are not typical of other diseases such as appendicitis, cholecystitis, peptic ulcer, vascular disease or intestinal obstruction. In acute pancreatitis, the serum amylase starts to rise within a few hours simultaneously with the onset of symptoms and remains elevated for 2 to 3 days after which it returns to normal. The peak level is reached within 24 hours. Absence of increase in serum amylase in first 24 hours after the onset of symptoms is evidence against a diagnosis of acute pancreatitis (76). [Pg.211]

KATAOKA K, DiMAGNO E p (1998) Effect of chronic amylase inhibition on pancreatic growth and acinar cell secretory function in rats. Pancreas. 17 50-56. [Pg.179]

The pancreas is a gland in the abdomen lying in the curvature of the stomach as it empties into the duodenum. The pancreas functions primarily as an exocrine gland, although it also has endocrine function. The exocrine cells of the pancreas are called acinar cells. They produce an alkaline fluid known as pancreatic... [Pg.337]

S Muallem. (1989). Calcium transport pathways of pancreatic acinar cells. Annu Rev Physiol 51 83-105. [Pg.382]

H Sterb, RF Irvine, MJ Berridge, I Schulz. (1983). Release of Ca2+ from a nonmito-chondrial intracellular store in pancreatic acinar cells by inositol-4,5-triphosphate. Annu Rev Physiol 306 67-69. [Pg.382]

Progressive ultrastructural degeneration of pancreatic acinar cells evident as early as day 5 (Kazacos and Van Vleet 1989). [Pg.707]

AP is initiated by premature activation of pancreatic zymogens (inactive enzymes) within the acinar cells, pancreatic ischemia, or pancreatic duct obstruction. [Pg.318]

Release of cytokines injures acinar cells and enhances the inflammatory response. Injured acinar cells liberate chemoattractants that attract neutrophils, macrophages, and other cells to the area of inflammation, and increased vascular permeability promotes tissue edema. [Pg.318]

Eisner There are experiments in pancreatic acinar cells showing that Ca2+ can tunnel through the ER from one end of the cell to the other. [Pg.23]

Zhang X, Wen J, Bidasee KR, Besch HR Jr, Rubin RP 1997 Ryanodine receptor expression is associated with intracellular Ca2+ release in rat parotid acinar cells. Am T Physiol 273 0 306-0314... [Pg.173]

Interpretation (1953-1955) of the ultrastructures which, after cell disruption and differential centrifugation, gave rise to microsomes, proved quite difficult. Porter described a vacuolar system with canal-iculi and cistemae which was particularly evident in protein-secreting cells such as the acinar cells of the pancreas. The appearance was... [Pg.153]

Serum lipase is synthesized and stored in the granules of pancreatic acinar cells and is excreted from the apical poles of the acinar cells into the duct system of the gland. Lipases are produced not only in the pancreas but also at various sites in the human digestive tract [126][127]. Lipases are also found in leucocytes, adipose tissue, lung, and milk. [Pg.55]

In a transgenic mouse model of ductal pancreatic adenocarcinoma, the development of ductal carcinoma is preceded by trans-differentiation of acinar cells to ductal-like cells.The anti-apoptotic protein Bc1-Xl is highly expressed... [Pg.57]

Pancreatic secretions. In the acinar cells, the pancreas forms a secretion that is alkaline due to its HCOa content, the buffer capacity of which is suf cient to neutralize the stomach s hydrochloric acid. The pancreatic secretion also contains many enzymes that catalyze the hydrolysis of high-molecular-weight food components. All of these enzymes are hydrolases with pH optimums in the neutral or weakly alkaline range. Many of them are formed and secreted as proenzymes and are only activated in the bowel lumen (see p. 270). [Pg.268]

PANCREAS Membrane potential measurements in pancreatic /3 cells with intracellular microelectrodes, 192, 235 stimulation of secretion by secretagogues, 192, 247 pancreatic secretion in vivo, perfused gland, and isolated duct studies, 192, 256 dispersed pancreatic acinar cells and pancreatic acini, 192, 271 permeabilizing cells some methods and applications for the study... [Pg.451]

Rats fed diets containing 30 or 300ppm ammonium perfluorooctanoate for 2 years had increased liver weights with occasional necrosis and an apparent dose-dependent increase in Leydig cell adenomas, but there was no evidence of an increased incidence of hepatocellular carcinoma. In a follow-up study in male mice, 300ppm in the diet for 2 years caused increases in liver, Leydig cell, and pancreatic acinar cell tumors that may have been associated with the peroxisome-proliferating capabilities of the compound. Ammonium perfluorooctanoate also produced sustained increases in serum estradiol concentrations. ... [Pg.47]

Although several epidemiological studies have suggested a positive association between dichlorvos exposure and cancer, conclusions are limited because all have involved small study groups and exposure to several agents. In animal studies chronic gavage administration of dichlorvos caused a dose-related increase in papillomas of the forestomach in mice and a dose-related increase in mononuclear-cell leukemia and an increased incidence of pancreatic acinar cell adenomas in male rats. The lARC has determined that there is sufficient evidence for the carcinogenicity of DDVP in experimental animals and inadequate evidence in humans. ... [Pg.240]

De Castro CR, Bernacchi AS, De Ferreyra EC, et al. 1978. Carbon tetrachloride induced ultrastructural alterations in pancreatic acinar cells and in the hepatocytes. Similarities and differences. Toxicology 11 289- 296. [Pg.156]

Pancreatic effect. Cigarette smoke, administered to anesthetized rats alone or in combination with iv ethanol infusion, reduced pancreatic blood flow temporarily and increased leukocyte-endothelium interaction (roller p < 0.001, sticker p < 0.01 vs baseline). Cigarette smoke potentiated the impairment of pancreatic capillary perfusion caused by ethanol, and both the number of rolling leukocytes and myeloperoxidase activity levels were increased compared with ethanol or nicotine administration alone h Tobacco-specific nitrosamines, administered to rats, induced pancreatic acinar cell and ductal cell neoplasms. One of the tumors had a mixed ductal-squamous-islet cell components . [Pg.327]

Krane CM, Melvin JE, Nguyen HV, Richardson L, Towne JE, Doetschman T, Menon AG (2001) Salivary acinar cells from aquaporin 5-deficient mice have decreased membrane water permeability and altered cell volume regulation. J Biol Chem 276 23413-23420... [Pg.53]


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See also in sourсe #XX -- [ Pg.90 ]




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