query: the parietal cells of the gastric mucosa secrete

pos: Gastric mucosa produce pepsinogen (an inactive precursor of the pepsin enzyme). Parietal cells, which secrete hydrochloric acid (HCl) are scattered in the glands, with most of them in the middle part. The upper part of the glands consist of mucous neck cells; in this part the dividing cells are seen. The pyloric glands contain mucus-secreting cells. Several types of endocrine cells are found in throughout the gastric mucosa. The pyloric glands contain gastrin-producing cells (G cells); this hormone stimulates acid production from the parietal cells. Enterochromaffin-like cells (ECLs), found in the oxyntic glands release histamine, which also is a powerful stimulant of

pos: Gastric glands neck cells" that produce mucus. This is thought to be different from the mucus produced by the gastric mucosa. Fundic glands found in the fundus and also in the body have another two cell types–gastric chief cells and parietal cells (oxyntic)). The chief cells are found in the basal regions of the gland and release a zymogen – pepsinogen, a precursor to pepsin. The parietal cells ("parietal" means "relating to a wall") are found in the walls of the tubes. The parietal cells secrete hydrochloric acid–the main component of gastric acid. This needs to be readily available for the stomach

pos: Alkaline tide calcium oxalate urinary stones in cats, and potentially in other species. A more pronounced alkaline tide results from vomiting, which stimulates hyperactivity of gastric parietal cells to replace lost stomach acid. Thus, protracted vomiting can result in metabolic alkalosis. Alkaline tide Alkaline tide refers to a condition, normally encountered after eating a meal, where during the production of hydrochloric acid by parietal cells in the stomach, the parietal cells secrete bicarbonate ions across their basolateral membranes and into the blood, causing a temporary increase in pH. During hydrochloric acid secretion in the stomach, the gastric parietal cells extract chloride anions,

pos: Gastrin Gastrin is released in response to certain stimuli. These include: Gastrin release is inhibited by: The presence of gastrin stimulates parietal cells of the stomach to secrete hydrochloric acid (HCl)/gastric acid. This is done both directly on the parietal cell and indirectly via binding onto CCK2/gastrin receptors on ECL cells in the stomach, which then responds by releasing histamine, which in turn acts in a paracrine manner on parietal cells stimulating them to secrete H+ ions. This is the major stimulus for acid secretion by parietal cells. Along with the above-mentioned function, gastrin has been shown to have additional functions

pos: Regulation of gastric function fall excessively low. Gastric secretion is stimulated chiefly by three chemicals: acetylcholine (ACh), histamine, and gastrin. ACh is secreted by parasympathetic nerve fibers of both the short and long reflex .ml; pathways. Histamine is a paracrine secretion from the enteroendocrine cells in the gastric glands. Gastrin is a hormone produced by enteroendocrine G cells in the pyloric glands. All three of these stimulate parietal cells to secrete hydrochloric acid and intrinsic factor. The chief cells secrete pepsinogen in response to gastrin and especially Ach, and ACh also stimulates mucus secretion. Low intragastric pH stimulates antral D cells to release somatostatin.

pos: Gastric glands the fundus and body of the stomach. They are simple almost straight tubes, two or more of which open into a single duct. "Oxyntic" means acid-secreting and they secrete hydrochloric acid (HCl) and intrinsic factor. The pyloric glands are located in the antrum of the pylorus. They secrete gastrin produced by their G cells. There are millions of gastric pits in the gastric mucosa and their necessary narrowness determines the tubular form of the gastric gland. More than one tube allows for the accommodation of more than one cell type. The form of each gastric gland is similar; they are

pos: Parietal cell Parietal cell Parietal cells (also known as oxyntic or delomorphous cells) are the epithelial cells that secrete hydrochloric acid (HCl) and intrinsic factor. These cells are located in the gastric glands found in the lining of the fundus and in the cardia of the stomach. They contain an extensive secretory network (called canaliculi) from which the HCl is secreted by active transport into the stomach. The enzyme hydrogen potassium ATPase (H/K ATPase) is unique to the parietal cells and transports the H against a concentration gradient of about 3 million to 1, which is the steepest ion gradient formed in

pos: Parietal cell Pernicious anemia also leads to megaloblastic anemia. Atrophic gastritis, particularly in the elderly, will cause an inability to absorb B and can lead to deficiencies such as decreased DNA synthesis and nucleotide metabolism in the bone marrow. Parietal cell Parietal cells (also known as oxyntic or delomorphous cells) are the epithelial cells that secrete hydrochloric acid (HCl) and intrinsic factor. These cells are located in the gastric glands found in the lining of the fundus and in the cardia of the stomach. They contain an extensive secretory network (called canaliculi) from which the HCl is secreted by active transport into

pos: Alkaline tide Alkaline tide Alkaline tide refers to a condition, normally encountered after eating a meal, where during the production of hydrochloric acid by parietal cells in the stomach, the parietal cells secrete bicarbonate ions across their basolateral membranes and into the blood, causing a temporary increase in pH. During hydrochloric acid secretion in the stomach, the gastric parietal cells extract chloride anions, carbon dioxide, water and sodium cations from the blood plasma and in turn release bicarbonate back into the plasma after forming it from carbon dioxide and water constituents. This is to maintain the plasma's electrical balance, as the chloride

pos: Gastric glands Gastric glands The gastric glands are located in different regions of the stomach. These are the fundic glands, the cardiac glands, and the pyloric glands. The glands and gastric pits are located in the stomach lining. The glands themselves are in the lamina propria of the mucous membrane and they open into the bases of the gastric pits formed by the epithelium. The various cells of the glands secrete mucus, pepsinogen, hydrochloric acid, intrinsic factor, gastrin, and bicarbonate. The three types of gland are all located beneath the gastric pits within the gastric mucosa–the mucous membrane of the stomach. The

pos: Gastric acid enzymes for protein breakdown (inactive pepsinogen, and in infancy rennin). Hydrochloric acid activates pepsinogen into the enzyme pepsin, which then helps digestion by breaking the bonds linking amino acids, a process known as proteolysis. In addition, many microorganisms have their growth inhibited by such an acidic environment, which is helpful to prevent infection. A typical adult human stomach will secrete about 1.5 liters of gastric acid daily. Gastric acid secretion happens in several steps. Chloride and hydrogen ions are secreted separately from the cytoplasm of parietal cells and mixed in the canaliculi. Gastric acid is then secreted into the lumen

pos: Gastric acid network (called canaliculi) from which the hydrochloric acid is secreted into the lumen of the stomach. The pH of gastric acid is 1.5 to 3.5 in the human stomach lumen, the acidity being maintained by the proton pump H/K ATPase. The parietal cell releases bicarbonate into the bloodstream in the process, which causes a temporary rise of pH in the blood, known as an alkaline tide. The highly acidic environment in the stomach lumen causes proteins from food to lose their characteristic folded structure (or denature). This exposes the protein's peptide bonds. The gastric chief cells of the stomach secrete

pos: Gastric acid that it does not become too acidic. These cells also produce mucus, which forms a viscous physical barrier to prevent gastric acid from damaging the stomach. The pancreas further produces large amounts of bicarbonate and secretes bicarbonate through the pancreatic duct to the duodenum to completely neutralize any gastric acid that passes further down into the digestive tract. The main constituent of gastric acid is hydrochloric acid which is produced by parietal cells (also called oxyntic cells) in the gastric glands in the stomach. Its secretion is a complex and relatively energetically expensive process. Parietal cells contain an extensive secretory

pos: Foveolar cell amounts of rough endoplasmic reticulum. Mucous neck cells are located within gastric glands, interspersed between parietal cells. These are shorter than their surface counterpart and contain lesser quantities of mucin granules in their apical surface. The mucus produced by these cells is extremely important, as it prevents the stomach digesting itself. Parietal cells produce potent hydrochloric acid, which damages cells. Gastric chief cells produce pepsinogen, which is activated by the acid to form pepsin. Pepsin is a protease that can digest and damage stomach cells. To prevent these disastrous effects, mucus and bicarbonate ions (HCO) are secreted by the foveolar

pos: Gastric pits mucus in a healthy adult. Hydrochloric acid is secreted by parietal cells, pepsinogen is secreted by gastric chief cells and mucus is secreted by mucus neck cells. Gastric pits Gastric pits are indentations in the stomach which denote entrances to 3-5 tubular shaped gastric glands. They are deeper in the pylorus than they are in the other parts of the stomach. The human stomach has several million of these pits which dot the surface of the lining epithelium. Surface mucous cells line the pits themselves but give way to a series of other types of cells which then line the

pos: Parietal cell the human body. Parietal cells are primarily regulated via histamine, acetylcholine and gastrin signaling from both central and local modulators ("see 'Regulation')". A canaliculus is an adaptation found on gastric parietal cells. It is a deep infolding, or little channel, which serves to increase the surface area, e.g. for secretion. The parietal cell membrane is dynamic; the numbers of canaliculi rise and fall according to secretory need. This is accomplished by the fusion of canalicular precursors, or "tubulovesicles", with the membrane to increase surface area, and the reciprocal endocytosis of the canaliculi (reforming the tubulovesicles) to decrease it. Hydrochloric acid

neg: Enterochromaffin-like cell Enterochromaffin-like cell Enterochromaffin-like cells or ECL cells are a type of neuroendocrine cell found in the gastric glands of the gastric mucosa beneath the epithelium, in particular in the vicinity of parietal cells, that aid in the production of gastric acid via the release of histamine. They are also considered a type of enteroendocrine cell. ECL cells synthesize and secrete histamine. These cells are stimulated by the hormones gastrin (not depicted in the adjacent diagram) and pituitary adenylyl cyclase-activating peptide. G cells are stimulated by vagal stimulation through the neurotransmitter gastrin-releasing peptide; this causes the G cells to secrete gastrin,

neg: Troxipide oxygen radicals in gastric mucosa. Experimental studies have demonstrated that troxipide restrains NSAID-induced generation of porphyrins, tissue peroxidation and gastric lesion formation. Gastric parietal cells are rich in mitochondria which provide energy in the form of ATP for cells by oxidative phosphorylation, critical to maintain the proper morphology and function of gastric mucosa. The mitochondrion is the major target of intracellular oxidative stress associated with aggressive factors like "H. pylori", alcohol and NSAIDs, which disturb the energy metabolism of mitochondria. Troxipide accelerates oxygen intake of marginal gastric mucosa and glycogen consumptive stimulation of the gastric mucosa of the corpus, thereby

neg: Fundic gland polyposis the polyposis. These symptoms include: The polyps on endoscopy are usually tiny, numerous and sessile, and usually scattered throughout the fundus of the stomach, where parietal cells are more numerous. They have the same colour as the gastric mucosa, and never have a stalk. When the polyps are biopsied, the pathology typically shows shortened gastric pits, and both superficial and deep cystic lesions in the fundic glands, lined by all three types of cells of acid-producing mucosa: mucous, parietal and chief cells. As sometimes parietal cell hyperplasia may develop deep dilations of gland, one should be really strict in the

neg: Regulation of gastric function neurons and other enteric nervous system neurons release GRP which stimulates antral G cells to produce and release gastrin. Gastrin stimulates acid secretion by directly stimulating parietal cells as well as by promoting histamine secretion by ECL cells. 4.)In both the antrum and corpus, the vagus nerve inhibits D cells, thus reducing their release of somatostatin and reducing background inhibition of gastrin release. Gastric chief cells are primarily activated by ACh. However the decrease in pH caused by activation of parietal cells further activates gastric chief cells. Alternatively, acid in the duodenum can stimulate S cells to secrete secretin which

neg: Gastric acid secrete two stimulatory neurotransmitters: acetylcholine and gastrin-releasing peptide. Their action is both direct on parietal cells and mediated through the secretion of gastrin from G cells and histamine from enterochromaffine-like cells. Gastrin acts on parietal cells directly and indirectly too, by stimulating the release of histamine. The release of histamine is the most important positive regulation mechanism of the secretion of gastric acid in the stomach. Its release is stimulated by gastrin and acetylcholine and inhibited by somatostatin. In the duodenum, gastric acid is neutralized by sodium bicarbonate. This also blocks gastric enzymes that have their optima in the acid

neg: Regulation of gastric function the dorsal nucleus of the vagus nerve. Stimulation of acid secretion occurs as it does in the cephalic phase. 2.) Local ENS Pathway Activated ENS releases ACh stimulating parietal cells to secrete acid. As dietary protein is digested, it breaks down into smaller peptides and amino acids, which directly stimulate the G cells to secrete even more gastrin – a positive feedback loop that accelerates protein digestion. As discussed earlier gastrin stimulates by activating parietal cells and stimulating ECL to produce histamine (histamine stimulates parietal cells to produce acid). Small peptides also buffer stomach acid so the pH does not

neg: Hydrogen potassium ATPase Hydrogen potassium ATPase Gastric hydrogen potassium ATPase, also known as H/K ATPase, is an enzyme which functions to acidify the stomach. The gastric hydrogen potassium ATPase or H/K ATPase is the proton pump of the stomach. It exchanges potassium from the intestinal lumen with cytoplasmic hydronium and is the enzyme primarily responsible for the acidification of the stomach contents and the activation of the digestive enzyme pepsin (see gastric acid). The H/K ATPase is found in parietal cells, which are highly specialized epithelial cells located in the inner cell lining of the stomach called the gastric mucosa. Parietal cells possess

neg: Vitamin B12 deficiency anemia is localised to the body of the stomach, where parietal cells are located. Antibodies to intrinsic factor and parietal cells cause the destruction of the oxyntic gastric mucosa, in which the parietal cells are located, leading to the subsequent loss of intrinsic factor synthesis. Without intrinsic factor, the ileum can no longer absorb the B. Although the exact role of "Helicobacter pylori" infection in PA remains controversial, evidence indicates "H. pylori" is involved in the pathogenesis of the disease. A long-standing "H. pylori" infection may cause gastric autoimmunity by a mechanism known as molecular mimicry. Antibodies produced by the immune

neg: Foveolar cell Foveolar cell Foveolar cells or surface mucous cells are mucus-producing cells which cover the inside of the stomach, protecting it from the corrosive nature of gastric acid. These cells line the gastric mucosa (mucous neck cells are found in the necks of the gastric pits). The mucus-secreting cells of the stomach can be distinguished histologically from the intestinal goblet cells, another type of mucus-secreting cell. The mucous membrane that lines the inner wall of the stomach has a set of microscopic features called gastric glands which, depending on the location within the stomach, secrete different substances into the lumen of

neg: G cell stomach, stimulates the release of gastrin from the G cells. Gastrin stimulates enterochromaffin-like cells to secrete histamine. Gastrin also targets parietal cells by increasing the amount of histamine and the direct stimulation by gastrin, causing the parietal cells to increase HCl secretion in the stomach. G cells have a distinctive microscopic appearance that allows one to separate them from other cells in the gastric antrum; their nuclei are centrally located in the cell. They are found in the middle portion of the gastric glands. G cell In anatomy, the G cell (or γ-cell) is a type of cell in the

neg: Gastritis typically begins in response to chronic mucosal injury in the antrum, and may extend to the body. Gastric mucosa cells change to resemble intestinal mucosa and may even assume absorptive characteristics. Intestinal metaplasia is classified histologically as complete or incomplete. With complete metaplasia, gastric mucosa is completely transformed into small-bowel mucosa, both histologically and functionally, with the ability to absorb nutrients and secrete peptides. In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibits dysplasia. Often, a diagnosis can be made based on the patient's description of their symptoms, but other

neg: Chief cell associated with protein synthesis. As in many endocrine organs, with age, more oxyphil cells appear in the parathyroid gland. In gastric tissue, a loss of parietal cells due to chronic inflammation has been shown to affect chief cell differentiation and can induce chief cells to transdifferentiate back into neck cells and can lead to the formation of mucus cell metaplasia known as spasmolytic polypeptide expressing metaplasia (SPEM) that could be precancerous. If parietal cells are lost, mature chief cells do not form. Parietal cells may secrete factors that lead to transdifferentiation of chief cells, so if lost, chief cells do

neg: Gastric glands all said to have a neck region that is closest to the pit entrance and basal regions on the lower parts of the tubes. The epithelium from the gastric mucosa travels into the pit and at the neck the epithelial cells change to short columnar granular cells. These cells almost fill the tube and the remaining lumen is continued as a very fine channel. Cells found in the gastric glands include foveolar cells, chief cells, parietal cells, G cells and enterochromaffin-like cells (ECLs). The first cells of all of the glands are foveolar cells in the neck region–also called "mucous

neg: Cephalic phase gastrin circulation. It will also stimulate Chief cells to release Pepsinogen. Thinking of food (i.e. smell, sight) – Stimulates cerebral cortex – Sends messages to hypothalamus – to the medulla oblongata – to parasympathetic nervous system by the vagus nerve – to stomach (Gastric Glands in walls of fundus and body of stomach) – to secrete gastric juice. a. Food enters stomach – stomach stretches and activates stretch Receptors – sends message to the medulla oblongata (vagus nerve) and then back – to stomach by the vagus nerve — Result: parietal cell secrete gastric juice. b. Chemical Stimuli (i.e. partially

neg: Enterochromaffin-like cell secretion, however there is no data to support this conclusion and proton pump inhibitors are not thought to contribute to gastric cancer. The name is derived from their location in the enteric system and their chromaffin-like staining pattern in histologic sections, which is characterized by silver staining. Enterochromaffin-like cell Enterochromaffin-like cells or ECL cells are a type of neuroendocrine cell found in the gastric glands of the gastric mucosa beneath the epithelium, in particular in the vicinity of parietal cells, that aid in the production of gastric acid via the release of histamine. They are also considered a type of

neg: Digestion gastrin) activity via D cell secretion of somatostatin. The gastric phase takes 3 to 4 hours. It is stimulated by distension of the stomach, presence of food in stomach and decrease in pH. Distention activates long and myenteric reflexes. This activates the release of acetylcholine, which stimulates the release of more gastric juices. As protein enters the stomach, it binds to hydrogen ions, which raises the pH of the stomach. Inhibition of gastrin and gastric acid secretion is lifted. This triggers G cells to release gastrin, which in turn stimulates parietal cells to secrete gastric acid. Gastric acid is about

neg: Zollinger–Ellison syndrome tumors as part of a condition called multiple endocrine neoplasia type 1 (MEN 1). MEN I patients have tumors in their pituitary gland and parathyroid glands, in addition to tumors of the pancreas. Gastrin works on the parietal cells of the gastric glands, causing them to secrete more hydrogen ions into the stomach lumen. In addition, gastrin acts as a trophic factor for parietal cells, causing parietal cell hyperplasia. Thus, there is an increase in the number of acid-secreting cells, and each of these cells produces acid at a higher rate. The increase in acidity contributes to the development of

neg: Gastric glands release of histamine is stimulated by the secretion of gastrin from the G cells. Histamine promotes the production and release of bicarbonate ions from the parietal cells to the blood and protons to the stomach lumen. When the stomach pH decreases(becomes more acidic), the ECLs stop releasing histamine. The G cells are mostly found in pyloric glands in the antrum of the pylorus; some are found in the duodenum and other tissues. The G cells secrete gastrin. The gastric pits of these glands are much deeper than the others and here the gastrin is secreted into the bloodstream not the

neg: Stomach of the gastric glands. The three types of gland are all located beneath the gastric pits within the gastric mucosa–the mucous membrane of the stomach. The gastric mucosa is pitted with innumerable gastric pits which house the gastric glands. The "cardiac glands" are found in the cardia of the stomach, enclosing the opening where the esophagus joins to the stomach. Only cardiac glands are found here and they primarily secrete mucus. They are fewer in number than the other gastric glands and are more shallowly positioned in the mucosa. There are two kinds - either simple tubular with short ducts

neg: Parietal cell is formed in the following manner: As a result of the cellular export of hydrogen ions, the gastric lumen is maintained as a highly-acidic environment. The acidity aids in digestion of food by promoting the unfolding (or denaturing) of ingested proteins. As proteins unfold, the peptide bonds linking component amino acids are exposed. Gastric HCl simultaneously cleaves pepsinogen, a zymogen, into active pepsin, an endopeptidase that advances the digestive process by breaking the now-exposed peptide bonds, a process known as proteolysis. Parietal cells secrete acid in response to three types of stimuli: Activation of histamine through H receptor causes increases

neg: Vitamin B12 deficiency anemia (ileum) after binding to a protein known as intrinsic factor. Intrinsic factor is produced by parietal cells of the gastric mucosa (stomach lining) and the intrinsic factor-B complex is absorbed by cubilin receptors on the ileum epithelial cells. PA is characterised by B deficiency caused by the absence of intrinsic factor. PA may be considered as an end stage of immune gastritis, a disease characterised by stomach atrophy and the presence of antibodies to parietal cells and intrinsic factor. A specific form of chronic gastritis, type A gastritis or atrophic body gastritis, is highly associated with PA. This autoimmune disorder

neg: Ostertagia ostertagi abomasal mucosa. In severe cases, edema may extend over the abomasum and into the small intestine and omentum. When examined histologically, abomasal gastric glands contain larvae in varying stages of development, which results in hyperplasia and distention of the glands, and flattening of the glandular epithelium. Affected glands lack differentiated acid-producing parietal and pepsinogen producing chief cells. Type I and type II disease is often differentiated by the presence of increased numbers of globule leucocytes, eosinophils and focal aggregates of lymphoplasmocytic cells in animals with type II disease. Consequences of the damage done to the gastric gland by "O. ostertagi"

neg: Stomach to other organs, with only some 20 genes being highly specific. The corresponding specific proteins expressed in stomach are mainly involved in creating a suitable environment for handling the digestion of food for uptake of nutrients. Highly stomach-specific proteins include GKN1, expressed in the mucosa; pepsinogen PGC and the lipase LIPF, expressed in chief cells; and gastric ATPase ATP4A and gastric intrinsic factor GIF, expressed in parietal cells. In early human embryogenesis, the ventral part of the embryo abuts the yolk sac. During the second week of development, as the embryo grows, it begins to surround parts of the sac.

neg: Glossitis of the tongue in iron deficiency anemia has been described as diffuse or patchy atrophy with tenderness or burning. One cause of iron deficiency anemia is sideropenic dysphagia (Plummer–Vinson or Paterson–Brown–Kelly syndrome) which is also characterized by esophageal webbing and dysphagia. Pernicious anemia is usually caused by autoimmune destruction of gastric parietal cells. Parietal cells secrete intrinsic factor which is required for the absorption of vitamin B12. Vitamin B12 deficiency results in megaloblastic anemia and may present as glossitis. The appearance of the tongue in vitamin B12 deficiency is described as "beefy" or "fiery red and sore". There may be

neg: Intestinal gland duodenum, jejunum, and ileum, and in the large intestine (colon), where they are sometimes called "colonic crypts". Intestinal glands of the small intestine contain a base of replicating stem cells, Paneth cells of the innate immune system, and goblet cells, which produce mucus. In the colon, crypts do not have Paneth cells. The enterocytes in the small intestinal mucosa contain digestive enzymes that digest specific foods while they are being absorbed through the epithelium. These enzymes include peptidase, sucrase, maltase, lactase and intestinal lipase. This is in contrast to the gastric glands of the stomach where chief cells secrete pepsinogen.

neg: Gastric glands gastric mucosa is pitted with innumerable gastric pits which each house 3-5 gastric glands. The cardiac glands are found in the cardia of the stomach which is the part nearest to the heart, enclosing the opening where the esophagus joins to the stomach. Only cardiac glands are found here and they primarily secrete mucus. They are fewer in number than the other gastric glands and are more shallowly positioned in the mucosa. There are two kinds - either simple tubular with short ducts or compound racemose resembling the duodenal Brunner's glands The fundic glands (or "oxyntic glands"), are found in

neg: Vagovagal reflex of vomiting due to the inability of the proximal stomach smooth muscle to undergo receptive relaxation. The vagal afferents are activated during the gastric phase of digestion when the corpus and fundus of the stomach are distended secondary to the entry of a food bolus. The stimulation of the mechanical receptors located in the gastric mucosa stimulates the vagus afferents. The completion of the reflex circuit by vagus efferents leads to the stimulation of postganglionic muscarinic nerves. These nerves release acetylcholine to stimulate two end effects. One, the parietal cells in the body of the stomach are stimulated to release

neg: Omeprazole increase the plasma concentrations of methotrexate. Omeprazole is a selective and irreversible proton pump inhibitor. It suppresses stomach acid secretion by specific inhibition of the H/K-ATPase system found at the secretory surface of gastric parietal cells. Because this enzyme system is regarded as the acid (proton, or H) pump within the gastric mucosa, omeprazole inhibits the final step of acid production. Omeprazole also inhibits both basal and stimulated acid secretion irrespective of the stimulus. The inhibitory effect of omeprazole occurs within 1 hour after oral administration. The maximum effect occurs within 2 hours. The duration of inhibition is up to

neg: Hydrochloric acid and acidifies the stomach content to a pH of 1 to 2. Chloride (Cl) and hydrogen (H) ions are secreted separately in the stomach fundus region at the top of the stomach by parietal cells of the gastric mucosa into a secretory network called canaliculi before it enters the stomach lumen. Gastric acid acts as a barrier against microorganisms to prevent infections and is important for the digestion of food. Its low pH denatures proteins and thereby makes them susceptible to degradation by digestive enzymes such as pepsin. The low pH also activates the enzyme precursor pepsinogen into the active

neg: Gastrointestinal tract gastric ATPase ATP4A and gastric intrinsic factor GIF, expressed in parietal cells of the stomach mucosa. Specific proteins expressed in the stomach and duodenum involved in defence include mucin proteins, such as mucin 6 and intelectin-1. The time taken for food or other ingested objects to transit through the gastrointestinal tract varies depending on many factors, but roughly, it takes less than an hour after a meal for 50% of stomach contents to empty into the intestines while total emptying takes around 2 hours. Subsequently, 50% emptying of the small intestine takes between 1 and 2 hours. Finally, transit through

neg: Intestinal mucosal barrier influence barrier function both directly, by stimulating epithelial cell proliferation and secretion of IL-8, and indirectly by producing short-chain fatty acids, which are an important energy source for colonic epithelial cells. The bile produced by the liver to aid in the digestion of lipids has bactericidal properties. The gastric acid produced by the stomach can also kill microorganisms. Both contribute to intestinal barrier function although they are not produced by the intestinal mucosa. Specialised secretory epithelial cells called Paneth cells secrete abundant quantities human α-defensins into the intestinal lumen of healthy individuals. Lysozyme is another defensive molecule secreted by Paneth

neg: Zollinger–Ellison syndrome Association meeting in Philadelphia in April 1955 heard the first public description of the syndrome, and Zollinger and Ellison subsequently published their findings in "Annals of Surgery". Zollinger–Ellison syndrome Zollinger–Ellison syndrome (ZES) is a disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers. Symptoms include abdominal pain and diarrhea. The syndrome is caused by a gastrinoma, a neuroendocrine tumor that secretes a hormone called gastrin. The tumor causes excessive production of gastric acid, which leads to the growth of gastric mucosa and proliferation of parietal and ECL cells. ZES may occur on its

neg: Zollinger–Ellison syndrome Zollinger–Ellison syndrome Zollinger–Ellison syndrome (ZES) is a disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers. Symptoms include abdominal pain and diarrhea. The syndrome is caused by a gastrinoma, a neuroendocrine tumor that secretes a hormone called gastrin. The tumor causes excessive production of gastric acid, which leads to the growth of gastric mucosa and proliferation of parietal and ECL cells. ZES may occur on its own or as part of an autosomal dominant syndrome called multiple endocrine neoplasia type 1 (MEN 1). The primary tumor is usually located in the pancreas, duodenum

neg: Ménétrier's disease gastric folds in the fundus and body, with the antrum generally spared, giving the mucosa a cobblestone or cerebriform (brain-like) appearance. Histologically, the most characteristic feature is massive foveolar hyperplasia (hyperplasia of surface and glandular mucous cells). The glands are elongated with a corkscrew-like appearance and cystic dilation is common. Inflammation is usually only modest, although some cases show marked intraepithelial lymphocytosis. Diffuse or patchy glandular atrophy, evident as hypoplasia of parietal and chief cells, is typical. Although ICD-10 classifies it under "Other gastritis" (K29.6), and the lamina propria may contain mild chronic inflammatory infiltrate, Ménétrier disease is not considered

neg: Gastric mucosa and at the bottom of each may be seen one or more minute orifices, the openings of the gland tubes. Gastric glands are simple or branched tubular glands that emerge on the deeper part of the gastric foveola, inside the gastric areas and outlined by the folds of the mucosa. There are three types of glands: cardiac glands (in the proximal part of the stomach), fundic (oxyntic) glands (the dominating type of gland), and pyloric glands. The cardiac glands mainly contain mucus-producing cells called foveolar cells. The bottom part of the oxyntic glands is dominated by zymogenic (chief) cells that

neg: Gastric acid cell to produce gastric acid, both directly acting on parietal cells and indirectly, through the stimulation of the secretion of the hormone histamine from enterochromaffine-like cells (ECL). Vasoactive intestinal peptide, cholecystokinin, and secretin all inhibit production. The production of gastric acid in the stomach is tightly regulated by positive regulators and negative feedback mechanisms. Four types of cells are involved in this process: parietal cells, G cells, D cells and enterochromaffine-like cells. Besides this, the endings of the vagus nerve (CN X) and the intramural nervous plexus in the digestive tract influence the secretion significantly. Nerve endings in the stomach

neg: Cephalic phase digested proteins, caffeine) – directly activates – G cells (Enteroendocrine Cells) located in the pyloric region of the stomach – to secrete gastrin – Gastrin stimulates – Gastric Glands to secrete gastric Juice. Cephalic phase The cephalic phase of digestion is the gastric secretion that occurs even before food enters the stomach, especially while it is being eaten. It results from the sight, smell, thought, or taste of food, and the greater the appetite, the more intense is the stimulation. Neurogenic signals that cause the cephalic phase of gastric secretion originate from the cerebral cortex and in the appetite centers

neg: Enteroendocrine cell somatostatin Gastric enteroendocrine cells are found in the gastric glands, mostly at their base. The G cells secrete gastrin, post-ganglionic fibers of the vagus nerve can release gastrin-releasing peptide during parasympathetic stimulation to stimulate secretion. Enterochromaffin-like cells are enteroendocrine and neuroendocrine cells also known for their similarity to chromaffin cells secreting histamine, which stimulates G cells to secrete gastrin. Other hormones produced include cholecystokinin, somatostatin, vasoactive intestinal peptide, substance P, alpha and gamma-endorphin. Pancreatic enteroendocrine cells are located in the islets of Langerhans and produce most importantly the hormones insulin and glucagon. The autonomous nervous system strongly regulates their secretion,

neg: Intrinsic factor usually an autoimmune disease, autoantibodies directed against intrinsic factor or parietal cells themselves lead to an intrinsic factor deficiency, malabsorption of vitamin B, and subsequent megaloblastic anemia. Atrophic gastritis can also cause intrinsic factor deficiency and anemia through damage to the parietal cells of the stomach wall. Pancreatic exocrine insufficiency can interfere with normal dissociation of vitamin B from its binding proteins in the small intestine, preventing its absorption via the intrinsic factor complex. Other risk factors contributing to pernicious anemia are anything that damages or removes a portion of the stomach's parietal cells, including bariatric surgery, gastric tumors, gastric

neg: KCNE2 KCNE2 is also highly expressed in parietal cells of the gastric epithelium, also at the apical side. In these cells, KCNQ1-KCNE2 K channels, which are constitutively active, provide a conduit to return K ions back to the stomach lumen. The K ions enter the parietal cell through the gastric H/K-ATPase, which swaps them for protons as it acidifies the stomach. While KCNQ1 channels are inhibited by low extracellular pH, KCNQ1-KCNE2 channels activity is augmented by extracellular protons, an ideal characteristic for their role in parietal cells. KCNE2 forms constitutively active K channels with KCNQ1 in the basolateral membrane of thyroid

neg: Antihistamine cross the blood–brain barrier to a much lower degree than the first-generation antihistamines. Their main benefit is they primarily affect peripheral histamine receptors and therefore are less sedating. However, high doses can still induce drowsiness through acting on the central nervous system. Some second-generation antihistamines, notably cetirizine, can interact with CNS psychoactive drugs such as bupropion and benzodiazepines. Examples of H antagonists include: The H receptor inverse agonists include: H-antihistamines, like H-antihistamines, occur as inverse agonists and neutral antagonists. They act on H histamine receptors found mainly in the parietal cells of the gastric mucosa, which are part of the

neg: Tumor of the stomach Tumor of the stomach A gastric tumor is a tumor of the stomach. It can be benign or malignant (gastric cancer). The gastric mucosa is composed of columnar epithelium arranged with pits known as crypts. There are several types of cells that make up gastric mucosa that give rise to gastric tumours: adenocarcinomas comprise 90% of these. Gastric tumours are mostly metastatic and are usually detected at a late stage. They occur more commonly in men than women in the 6th decade of life. Risk Factors 1. Smoking 2. Helicobacter pylori infection. 2. Diet low in fruits and vegetables. 3.

neg: Chronic gastritis in the loss of iron, calcium, magnesium and zinc absorption. The loss of mucous glands resulted in the growth of immature glandular and epithelial cells resembling the glands in the small bowel or colon (intestinal metaplasia) which can cause gastric adenocarcinoma through intraepithelial neoplasia. "H. pylori" infection is the most common form of chronic gastritis. In the beginning, the involvement tends to occur in either an gastric antrum, then progressive spreading to the gastric fundus, where the whole gastric mucosa is involved or with the sparing of certain parts of gastric mucosa. This resulted in the progressive reduced secretion of

neg: Chief cell that the gastric chief cell secretes leptin in response to the presence of food in the stomach. Leptin has been found in the pepsinogen granules of chief cells. Gastric pit cells are replaced every 2–4 days. This high rate of turnover is a protective mechanism designed to protect the epithelial lining of the stomach from both the proteolytic action of pepsin and the acid produced by parietal cells. Gastric chief cells are much longer lived and are believed to differentiate from stem cells located higher in the gastric unit in the isthmus. These stem cells differentiate into mucous neck cells

neg: Enteroendocrine cell in the duodenum and jejunum. I cells secrete cholecystokinin (CCK), and are located in the duodenum and jejunum. They modulate bile secretion, exocrine pancreas secretion, and satiety. Stomach enteroendocrine cells, which release gastrin, and stimulate gastric acid secretion. Enterochromaffin cells are enteroendocrine and neuroendocrine cells with a close similarity to adrenomedullary chromaffin cells secreting serotonin. Enterochromaffin-like cells or ECL cells are a type of neuroendocrine cell secreting histamine. Located in the jejunum, N cells release neurotensin, and control smooth muscle contraction. S cells secrete secretin from the duodenum and jejunum, and stimulate exocrine pancreatic secretion. also called Delta cells, secrete

neg: Gastrin Gastrin Gastrin is a peptide hormone that stimulates secretion of gastric acid (HCl) by the parietal cells of the stomach and aids in gastric motility. It is released by G cells in the pyloric antrum of the stomach, duodenum, and the pancreas. Gastrin binds to cholecystokinin B receptors to stimulate the release of histamines in enterochromaffin-like cells, and it induces the insertion of K/H ATPase pumps into the apical membrane of parietal cells (which in turn increases H release into the stomach cavity). Its release is stimulated by peptides in the lumen of the stomach. In humans, the "GAS" gene

neg: Gastric chief cell stomach. Gastrin and secretin may also act as secretagogues. It works in conjunction with the parietal cell, which releases gastric acid, converting the pepsinogen into pepsin. The terms "chief cell" and "zymogenic cell" are often used without the word "gastric" to name this type of cell. However those terms can also be used to describe other cell types (for example, parathyroid chief cells). Chief cells are also known as peptic cells. Gastric chief cell A gastric chief cell (or peptic cell, or gastric zymogenic cell) is a type of cell in the stomach that releases pepsinogen and gastric lipase and

neg: Parietal cell on the maximum histamine-stimulated gastric acid secretion. The effect of histamine, acetylcholine and gastrin is synergistic, that is, effect of two simultaneously is more than additive of effect of the two individually. It helps in non-linear increase of secretion with stimuli physiologically. Parietal cells also produce intrinsic factor. Intrinsic factor is required for the absorption of vitamin B in the diet. A long-term deficiency in vitamin B can lead to megaloblastic anemia, characterized by large fragile erythrocytes. Pernicious anaemia results from autoimmune destruction of gastric parietal cells, precluding the synthesis of intrinsic factor and, by extension, absorption of Vitamin B.

neg: Tumor of the stomach Diet high in salt and nitrates. 4. Polyps 5. Genetic alterations - p53 mutation, microsatellite instability, E-cadherin gene 6. Previous radiation 7. Pernicious anaemia Signs and Symptoms Dysphagia, indigestion, feeling full after eating very little, loss of appetite, nausea, abdominal pain, loss of weight, vomitting blood and passing black stool. Investigations Upper Gastointestinal Endoscopy. Tumor of the stomach A gastric tumor is a tumor of the stomach. It can be benign or malignant (gastric cancer). The gastric mucosa is composed of columnar epithelium arranged with pits known as crypts. There are several types of cells that make up gastric mucosa

neg: Atrophic gastritis system attacking the parietal cells. "Environmental Metaplastic Atrophic Gastritis" (EMAG) is due to environmental factors, such as diet and "H. pylori" infection. EMAG is typically confined to the body of the stomach. Patients with EMAG are also at increased risk of gastric carcinoma. "Autoimmune metaplastic atrophic gastritis" (AMAG) is an inherited form of atrophic gastritis characterized by an immune response directed toward parietal cells and intrinsic factor. The presence of serum antibodies to parietal cells and to intrinsic factor are characteristic findings. The autoimmune response subsequently leads to the destruction of parietal cells, which leads to profound Achlorhydria (and elevated

neg: Gastric glands in a plentiful supply, and so from their positions in the walls, their secretory networks of fine channels called canaliculi can project and ingress into all the regions of the gastric-pit lumen. Another important secretion of the parietal cells is intrinsic factor. Intrinsic factor is a glycoprotein essential for the absorption of vitamin B12. The parietal cells also produce and release bicarbonate ions in response to histamine release from the nearby ECLs, and so serve a crucial role in the pH buffering system. The enterochromaffin-like cells store and release histamine when the pH of the stomach becomes too high. The

neg: Chief cell not normally develop. Chief cell In human anatomy, there are three types of chief cells, the gastric chief cell, the parathyroid chief cell, and the type 1 chief cells found in the carotid body. The gastric chief cell (also known as a zymogenic cell or peptic cell) is a cell in the stomach that releases pepsinogen and chymosin. Pepsinogen is activated into the digestive enzyme pepsin when it comes in contact with acid produced by gastric parietal cells. This type of cell also secretes gastric lipase enzymes, which help digest triglycerides into free fatty acids and di- and mono-glycerides. There

neg: Chief cell Chief cell In human anatomy, there are three types of chief cells, the gastric chief cell, the parathyroid chief cell, and the type 1 chief cells found in the carotid body. The gastric chief cell (also known as a zymogenic cell or peptic cell) is a cell in the stomach that releases pepsinogen and chymosin. Pepsinogen is activated into the digestive enzyme pepsin when it comes in contact with acid produced by gastric parietal cells. This type of cell also secretes gastric lipase enzymes, which help digest triglycerides into free fatty acids and di- and mono-glycerides. There is also evidence

neg: Peptic ulcer disease itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 ("COX-1"), which is essential for the production of these prostaglandins. Besides, NSAIDs also inhibits stomach mucosa cells proliferation and mucosal blood flow, reducing bicarbonate and mucus secretion, which reduces the integrity of the mucosa. Another type of NSAIDs, called COX-2 selective anti-inflammatory drugs (such as celecoxib), preferentially inhibit "COX-2", which is less essential in the gastric mucosa. This reduces the probability of getting peptic ulcers; however, it can still delay ulcer healing for those who

neg: Foveolar cell cells. The mucus allows the acid at pH above 4 to penetrate lining, but below pH 4 (i.e. when acid is more concentrated) the acid cannot penetrate the mucus. This is called viscous fingering. Thus the foveolar cells can pump out a lot of acid, but acid once in the lumen of the stomach is prevented from returning. Foveolar cell Foveolar cells or surface mucous cells are mucus-producing cells which cover the inside of the stomach, protecting it from the corrosive nature of gastric acid. These cells line the gastric mucosa (mucous neck cells are found in the necks of

neg: KCNE2 to the parietal cell apical membrane but the gastric phenotype is even worse than for "Kcne2"-/- mice, emphasizing that KCNQ1 requires KCNE2 co-assembly for functional attributes other than targeting in parietal cells. "Kcne2"-/- mice also develop gastritis cystica profunda and gastric neoplasia. Human KCNE2 downregulation is also observed in sites of gastritis cystica profunda and gastric adenocarcinoma. Positron emission tomography data show that with KCNE2, 124I uptake by the thyroid is impaired. "Kcne2" deletion does not impair organification of iodide once it has been taken up by NIS. Pups raised by "Kcne2"-/- dams are particularly severely affected because rhey receive

neg: Enterochromaffin cell parietal cells to stimulate the release of gastric acid. The presence of ECL cells is critical in regulation of endocrine-induced gastric acid secretion. ECL cells histologically appear similar to EC cells and are hence named as such. They are however a different cell type and do not possess any serotonin synthesizing mechanisms. In developing chick embryos, EC cells have been found in biopsies of developing GIT tissue before the migration of neural crest cells. Whilst EC cells have neuroendocrine properties and are similar chemically and histologically to cells of the adrenal medulla they are not derivatives of the neural crest

neg: Equine gastric ulcer syndrome throughout the day. Unlike carnivores, who produce stomach acid during meals, horses constantly secrete acid to help digest this source of grass, leading up to 9 gallons produced per day. Unchecked, the stomach acid can lower the pH to levels that will damage the gastric mucosa, leading to ulcers. The stomach is divided into 2 main sections: a squamous region at the upper 1/3 of the stomach near the cardiac sphincter, and a lower glandular region. These 2 regions are separated by a band of tissue called the margo plicatus. The pH of the stomach contents varies by location. The

neg: Human digestive system the colon or large intestine. Water is absorbed here and the remaining waste matter is stored prior to defecation. Most of the digestion of food takes place in the small intestine. A major digestive organ is the stomach. Within its mucosa are millions of embedded gastric glands. Their secretions are vital to the functioning of the organ. There are many specialised cells of the GI tract. These include the various cells of the gastric glands, taste cells, pancreatic duct cells, enterocytes and microfold cells. Some parts of the digestive system are also part of the excretory system, including the large

neg: Regulation of gastric function Somatostatin inhibits gastrin release from G cells. Reduced gastrin secretion reduces acid secretion. 5-10% of gastric secretion occurs during this phase. The intestinal phase is a stage in which the duodenum responds to arriving chyme and moderates gastric activity through hormones and nervous reflexes. The duodenum initially enhances gastric secretion, but soon inhibits it. Presence of partially digested proteins and amino acids in the duodenum stimulates acid secretion in the stomach by three methods: 1.) Peptones stimulate duodenal G Cells to secrete gastrin. 2.) Peptones stimulate an unknown endocrine cell to release an additional humoral signal, "enterooxytonin". 3.) Amino Acids

neg: Misoprostol the prevention of NSAID-induced gastric ulcers. It acts upon gastric parietal cells, inhibiting the secretion of gastric acid by G-protein coupled receptor-mediated inhibition of adenylate cyclase, which leads to decreased intracellular cyclic AMP levels and decreased proton pump activity at the apical surface of the parietal cell. Because other classes of drugs, especially H2-receptor antagonists and proton pump inhibitors, are more effective for the treatment of acute peptic ulcers, misoprostol is only indicated for use by people who are both taking NSAIDs and are at high risk for NSAID-induced ulcers, including the elderly and people with ulcer complications. Misoprostol is

neg: Gastric lipase Gastric lipase Gastric lipase, also known as LIPF, is an enzymatic protein that, in humans, is encoded by the "LIPF" gene. Gastric lipase is an acidic lipase secreted by the gastric chief cells in the fundic mucosa in the stomach. It has a pH optimum of 3–6. Gastric lipase, together with lingual lipase, comprise the two acidic lipases. These lipases, unlike alkaline lipases (such as pancreatic lipase), do not require bile acid or colipase for optimal enzymatic activity. Acidic lipases make up 30% of lipid hydrolysis occurring during digestion in the human adult, with gastric lipase contributing the most of

neg: Enteroendocrine cell act as chemoreceptors, initiating digestive actions and detecting harmful substances and initiating protective responses. Enteroendocrine cells are located in the stomach, in the intestine and in the pancreas. Intestinal enteroendocrine cells are not clustered together but spread as single cells throughout the intestinal tract. Hormones secreted include somatostatin, motilin, cholecystokinin, neurotensin, vasoactive intestinal peptide, and enteroglucagon. K cells secrete gastric inhibitory peptide, an incretin, which also promotes triglyceride storage. L cells secrete glucagon-like peptide-1, an incretin, pancreatic peptide YY, oxyntomodulin and glucagon-like peptide-2. L cells are primarily found in the ileum and large intestine (colon), but some are also found

neg: Regulation of gastric function secretion (via parietal and G cells). Sensory stimuli from food activate dorsal motor nucleus of vagus nerve in the medulla (activating the parasympathetic nervous system). Insulin induced hypoglycemia also stimulates the vagus nerve. This results in four distinct physiological events. 1.) In the body of the stomach, the vagal postganglionic muscarinic nerves release acetylcholine(ACh) which stimulates parietal cell H+ secretion. 2.) In the lamina propria of the body of the stomach the ACh released from the vagal endings triggers histamine secretion from ECL cells. Histamine also stimulates H+ secretion from parietal cells. 3.) In the antrum, peptidergic postganglionic parasympathetic vagal

neg: Peptic ulcer disease in the chronic form. In the ulcerative form of gastric cancer the borders are irregular. Surrounding mucosa may present radial folds, as a consequence of the parietal scarring. A gastric peptic ulcer is a mucosal perforation which penetrates the muscularis mucosae and lamina propria, usually produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows 4 zones: fibrinoid necrosis, inflammatory exudate, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis. Conditions that may appear similar include: Prevention

neg: Meckel's diverticulum obstruction, ischemia, and necrosis. A technetium-99m (99mTc) pertechnetate scan, also called Meckel scan, is the investigation of choice to diagnose Meckel's diverticula in children. This scan detects gastric mucosa; since approximately 50% of symptomatic Meckel's diverticula have ectopic gastric or pancreatic cells contained within them, this is displayed as a spot on the scan distant from the stomach itself. In children, this scan is highly accurate and noninvasive, with 95% specificity and 85% sensitivity; however, in adults the test is only 9% specific and 62% sensitive. Patients with these misplaced gastric cells may experience peptic ulcers as a consequence. Therefore,

neg: Cathepsin E Cathepsin D. Cathepsin E associates with the membrane tissue in the intracellular canaliculi of gastric parietal cells, bile canaliculi of hepatic cells, cells of the rinal proximal tubule in the kidney, epithelial cells in the intestine, trachea and bronchi, osteoclasts and even in erythrocytes. Its localization in the endosome structures can be seen in many different cell types such as antigen-presenting B cell lymphoblasts, gastric cells and microglia. Its presence is also detected in the cisternae of the cell’s endoplasmic reticulum. Cathepsin E plays a vital role in protein degradation, antigen processing via the MHC class II pathway and bioactive

neg: Cephalic phase of the gastric secretion associated with eating a meal. Gastric secretion in response to sensory stimuli prepares the gastrointestinal tract for food processing. These cephalic phase responses are both innate and acquired. This enhanced secretory activity brought on by the thought or sight of food is a conditioned reflex. It only occurs when we like or want food. When appetite is depressed this part of the cephalic reflex is inhibited. The cephalic phase induces ECL cells in the gastric glands to secrete histamine and increase HCl in the stomach. There will also be an influence on G cells to increase

neg: Indometacin ionised form, leaving very little unionised form of indometacin to cross a cell membrane. If the pH gradient across a cell membrane is high, most of the indometacin molecules will be trapped in one side of the membrane with higher pH. This phenomenon is called "ion trapping". The phenomenon of ion trapping is particularly prominent in the stomach as pH at the stomach mucosa layer is extremely acidic, while the parietal cells are more alkaline. Therefore, indometacin are trapped inside the parietal cells in ionised form, damaging the stomach cells, causing stomach irritation. This stomach irritation can reduce if the

neg: Tumour heterogeneity the heterogeneity of hypoxia in solid tumors is due to the mechanochemical reactions with oxygen nanobubbles. The biological phenomena of mechanochemical heterogeneity maybe used for differential gastric cancer diagnostics against patients with inflammation of gastric mucosa and for increasing antimetastatic activity of dendritic cells based on vaccines when mechanically heterogenized microparticles of tumor cells are used for their loading. There is also a possible methodical approach based on the simultaneous ultrasound imaging diagnostic techniques and therapy, regarding the mechanochemical effect on nanobubles conglomerates with drugs in the tumour. Heterogeneity between tumour cells can be further increased due to heterogeneity in

neg: Pertechnetate used historically to evaluate for testicular torsion, although ultrasound is more commonly used in current practice, as it does not deliver a radiation dose to the testes. It is also used in labeling of autologus red blood cells for MUGA scans to evaluate left ventricular cardiac function, localization of gastrointestinal bleeding prior to embolization or surgical management, and in damaged red blood cells to detect ectopic splenic tissue. It is actively accumulated and secreted by the mucoid cells of the gastric mucosa, and therefore, technetate(VII) radiolabeled with Tc99m is injected into the body when looking for ectopic gastric tissue as

neg: Helicobacter pylori the location of the ulcer, depends on the acidity of the stomach. In people producing large amounts of acid, "H. pylori" colonizes near the pyloric antrum (exit to the duodenum) to avoid the acid-secreting parietal cells at the fundus (near the entrance to the stomach). In people producing normal or reduced amounts of acid, "H. pylori" can also colonize the rest of the stomach. The inflammatory response caused by bacteria colonizing near the pyloric antrum induces G cells in the antrum to secrete the hormone gastrin, which travels through the bloodstream to parietal cells in the fundus. Gastrin stimulates the

neg: Discovery and development of gastrointestinal lipase inhibitors length of long-chain triglycerides prevent their absorption through the intestinal mucosa. For that reason lipases in the gastrointestinal tract must hydrolyse it to smaller molecules, free fatty acids and monoglyceride, before absorption can occur. Gastric- and lingual lipases are the two acidic lipolytic enzymes that origin preduodenal but the gastric lipase is in much higher levels in humans. Gastric lipase is synthesized and secreted from gastric chief cells in the stomach and is stable at pH 1,5-8, but has maximum activity at pH 3-6. Fat digestion begins when gastric lipase hydrolyses dietary triglycerides, by cleaving only one long-, medium- or

neg: Gastrointestinal wall Gastrointestinal wall The gastrointestinal wall surrounding the lumen of the gastrointestinal tract is made up of four layers of specialised tissue – from the lumen outwards: The epithelium, the most exposed part of the mucosa, is a glandular epithelium with many goblet cells. Goblet cells secrete mucus, which lubricates the passage of food along and protects the intestinal wall from digestive enzymes. In the small intestine, villi are folds of the mucosa that increase the surface area of the intestine. The villi contain a lacteal, a vessel connected to the lymph system that aids in the removal of lipids and

neg: Mucous membrane and to prevent bodily tissues from becoming dehydrated. The mucosa of organs are composed of one or more layers of epithelial cells that secrete mucus, and an underlying lamina propria of loose connective tissue. The type of cells and type of mucus secreted vary from organ to organ and each can differ along a given tract. Mucous membranes line the digestive, respiratory, and reproductive tracts and are the primary barrier between the external world and the interior of the body; in an adult human the total surface area of the mucosa is about 400 square meters while the surface area

neg: Hydrogen potassium ATPase strong association with pre-senile dementia. Hydrogen potassium ATPase Gastric hydrogen potassium ATPase, also known as H/K ATPase, is an enzyme which functions to acidify the stomach. The gastric hydrogen potassium ATPase or H/K ATPase is the proton pump of the stomach. It exchanges potassium from the intestinal lumen with cytoplasmic hydronium and is the enzyme primarily responsible for the acidification of the stomach contents and the activation of the digestive enzyme pepsin (see gastric acid). The H/K ATPase is found in parietal cells, which are highly specialized epithelial cells located in the inner cell lining of the stomach called the

neg: Gastric inhibitory polypeptide Gastric inhibitory polypeptide Gastric inhibitory polypeptide (GIP) or gastroinhibitory peptide, also known as the glucose-dependent insulinotropic peptide, is an inhibiting hormone of the secretin family of hormones. While it is weak inhibitor of gastric acid secretion, its main role is to stimulate insulin secretion. GIP, along with glucagon-like peptide-1 (GLP-1), belongs to a class of molecules referred to as incretins. GIP is derived from a 153-amino acid proprotein encoded by the GIP gene and circulates as a biologically active 42-amino acid peptide. It is synthesized by K cells, which are found in the mucosa of the duodenum and the jejunum

neg: Vitamin B12 deficiency anemia system can be cross-reactive and may bind to both "H. pylori" antigens and those found in the gastric mucosa. The antibodies are produced by activated B cells that recognise both pathogen and self-derived peptides. The autoantigens believed to cause the autoreactivity are the alpha and beta subunits of the H/K-ATPase. Less commonly, "H. pylori" and Zollinger-Ellison syndrome may also cause a form of nonautoimmune gastritis that can lead to pernicious anemia. Impaired B absorption can also occur following gastric removal (gastrectomy) or gastric bypass surgery. In these surgeries, either the parts of the stomach that produce gastric secretions are removed

neg: Helicobacter pylori parietal cells to secrete more acid into the stomach lumen, and over time increases the number of parietal cells, as well. The increased acid load damages the duodenum, which may eventually result in ulcers forming in the duodenum. When "H. pylori" colonizes other areas of the stomach, the inflammatory response can result in atrophy of the stomach lining and eventually ulcers in the stomach. This also may increase the risk of stomach cancer. The pathogenicity of "H. pylori" may be increased by genes of the" cag" pathogenicity island; about 50–70% of "H. pylori" strains in Western countries carry it. Western

neg: Gastric glands lumen. Fundic gland polyposis is a medical syndrome where the fundus and the body of the stomach develops many polyps. Pernicious anemia is caused when damaged parietal cells fail to produce the intrinsic factor necessary for the absorption of vitamin B12. This can be one of the causes of vitamin B12 deficiency. Gastric glands The gastric glands are located in different regions of the stomach. These are the fundic glands, the cardiac glands, and the pyloric glands. The glands and gastric pits are located in the stomach lining. The glands themselves are in the lamina propria of the mucous membrane

neg: Prostaglandin-endoperoxide synthase 2 FA tone, is a key factor regulating the activity of PGHS-2 and its response to PTGS (COX) inhibitors. PTGS2 (COX-2) is unexpressed under normal conditions in most cells, but elevated levels are found during inflammation. PTGS1 (COX-1) is constitutively expressed in many tissues and is the predominant form in gastric mucosa and in the kidneys. Inhibition of PTGS1 (COX-1) reduces the basal production of cytoprotective PGE2 and PGI2 in the stomach, which may contribute to gastric ulceration. Since PTGS2 (COX-2) is generally expressed only in cells where prostaglandins are upregulated (e.g., during inflammation), drug-candidates that selectively inhibit PTGS2 (COX-2) were

neg: Human digestive system secreted by innumerable gastric glands in the stomach, to provide a slimy protective layer against the damaging effects of the chemicals on the inner layers of the stomach. At the same time that protein is being digested, mechanical churning occurs through the action of peristalsis, waves of muscular contractions that move along the stomach wall. This allows the mass of food to further mix with the digestive enzymes. Gastric lipase secreted by the chief cells in the fundic glands in the gastric mucosa of the stomach, is an acidic lipase, in contrast with the alkaline pancreatic lipase. This breaks down

neg: Proton-pump inhibitor studies, it remains uncertain whether such associations are causal relationships. Proton pump inhibitors act by irreversibly blocking the hydrogen/potassium adenosine triphosphatase enzyme system (the H/K ATPase, or, more commonly, the gastric proton pump) of the gastric parietal cells. The proton pump is the terminal stage in gastric acid secretion, being directly responsible for secreting H ions into the gastric lumen, making it an ideal target for inhibiting acid secretion. Targeting the terminal step in acid production, as well as the irreversible nature of the inhibition, results in a class of drugs that are significantly more effective than H antagonists and

neg: TLR5 that an unknown "H. pylori" factor is responsible for this response In addition to inflammation induction, TLR5 is also shown to enhance gastric cancer cell proliferation through a ERK-dependent pathway. This is supported by the increased level of TLR5 expression from normal gastric mucosa to gastric cancer cells. TLR5 is suggested to be possibly involved in HPV induced inflammation and subsequent cervical neoplasia formation. TLR5 is generally absent in normal cervical squamous epithelium. However, a gradually increased level of TLR5 expression has been detected in low-grade cervical intraepithelial neoplasia (CIN), high grade CIN, and invasive cervical cancer. However, the exact