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pancreatitis/phosphatase
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 415 tuloksia
Cross-talk between oxidative stress and pro-inflammatory cytokines in acute pancreatitis: a key role for protein phosphatases.
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Acute pancreatitis is an acute inflammatory process localized in the pancreatic gland that frequently involves peripancreatic tissues. It is still under investigation why an episode of acute pancreatitis remains mild affecting only the pancreas or progresses to a severe form leading to multiple
Map kinase phosphatases (MKP's) are early responsive genes during induction of cerulein hyperstimulation pancreatitis.
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Mitogen-activated protein kinase (MAPK) family members such as c-jun N-terminal kinase (JNK) may act as signal transducers early during pancreatitis development and evidence indicates that MAPK phosphatases (MKP) downregulate MAPK. We therefore investigated expression and regulation of pancreatic
[Isoenzyme profile of alkaline phosphatase in patients with pancreatitis].
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In patients with pancreatitis an increase of the total amount of alkaline phosphatase (ALP; EC 3.1.3.1) and the appearance of its macro isoenzyme which parallels the decrease of bone isoenzyme was found. This isoenzymatic profile suggests that the increase of ALP in pancreatitis is due to the
Alkaline phosphatase and acid lysosomal hydrolases in pancreatic juice and fibroblast cell cultures of patients with chronic calcifying pancreatitis.
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Nine lysosomal enzymes and alkaline phosphatase have been assayed in human pancreatic juice from controls and patients with chronic calcifying pancreatitis. Specific activities were evaluated by a nonparametric test (Wilcoxon) with a probability of 2 P less than or equal to 0.5. The values of acid
Pentoxifylline prevents loss of PP2A phosphatase activity and recruitment of histone acetyltransferases to proinflammatory genes in acute pancreatitis.
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Mitogen-activated protein kinases (MAPKs) are considered major signal transducers early during the development of acute pancreatitis. Pentoxifylline is a phosphodiesterase inhibitor with marked anti-inflammatory properties through blockade of extracellular signal regulated kinase (ERK)
Marked alkaline phosphatase elevation with partial common bile duct obstruction due to calcific pancreatitis.
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This study characterizes a syndrome of partial common bile duct obstruction and marked elevation in serum alkaline phosphatase in 6 male alcoholic patients with calcific pancreatitis. In each patient, a marked elevation in serum alkaline phosphatase was associated with minimal, if any, elevation in
Factors predictive of liver histopathological appearance in chronic alcoholic pancreatitis with common bile duct stenosis and increased serum alkaline phosphatase.
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In the course of alcoholic chronic pancreatitis, increased serum alkaline phosphatase level is usually caused by common bile duct stenosis but may also be due to alcoholic liver disease. The aims of this prospective study were to investigate whether clinical, biochemical and radiological factors
Acid phosphatase activity in different organs as a marker of acute pancreatitis.
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The aim of the experiment was to establish and quantify the changes in the activity of acid phosphatase in the pancreas, liver, spleen and kidneys during the course of experimental pancreatitis. The experiment was carried out on 65 male rats of Wistar strain, whose weight varied from 250 to 350 g.
Elevated serum alkaline phosphatase level may aid in the diagnosis of pancreatitis.
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Ten cases of pancreatitis with elevated serum alkaline phosphatase (SAP) levels are reported. Patients with chronic or relapsing pancreatitis may at times develop increased SAP levels, either with or without definitive biochemical evidence of pancreatic disease. SAP estimation may assist in
Pancreatic Protein Tyrosine Phosphatase 1B Deficiency Exacerbates Acute Pancreatitis in Mice.
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Acute pancreatitis (AP) is a common and devastating gastrointestinal disorder that causes significant morbidity. The disease starts as local inflammation in the pancreas that may progress to systemic inflammation and complications. Protein tyrosine phosphatase 1B (PTP1B) is implicated in
Pancreatic T cell protein-tyrosine phosphatase deficiency ameliorates cerulein-induced acute pancreatitis.
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BACKGROUND
Acute pancreatitis (AP) is a common clinical problem whose incidence has been progressively increasing in recent years. Onset of the disease is trigged by intra-acinar cell activation of digestive enzyme zymogens that induce autodigestion, release of pro-inflammatory cytokines and acinar
Effect of caerulein on gamma-glutamyl transpeptidase and alkaline phosphatase in the duodenal juice in chronic pancreatitis.
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During infusion of caerulein, the output of gamma-glutamyl transpeptidase and biliary alkaline phosphatase is significantly more increased in chronic pancreatitis patients than in normal subjects. The presence of the gall-bladder is necessary to observe this effect of caerulein. It is not related to
PAR2 exerts local protection against acute pancreatitis via modulation of MAP kinase and MAP kinase phosphatase signaling.
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During acute pancreatitis, protease-activated receptor 2 (PAR2) can be activated by interstitially released trypsin. In the mild form of pancreatitis, PAR2 activation exerts local protection against intrapancreatic damage, whereas, in the severe form of pancreatitis, PAR2 activation mediates some
Role of redox signaling, protein phosphatases and histone acetylation in the inflammatory cascade in acute pancreatitis. Therapeutic implications.
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Acute pancreatitis starts as a local inflammation of the pancreatic tissue but often leads to the systemic inflammatory response syndrome and death by multiple organ failure. Pro-inflammatory cytokines, particularly TNF-alpha and Il-1beta, play a pivotal role together with oxidative stress and
Protein phosphatases and chromatin modifying complexes in the inflammatory cascade in acute pancreatitis.
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Acute pancreatitis is an inflammation of the pancreas that may lead to systemic inflammatory response syndrome and death due to multiple organ failure. Acinar cells, together with leukocytes, trigger the inflammatory cascade in response to local damage of the pancreas. Amplification of the
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