Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The blebbed surface morphology produced by trypsinisation of Chinese hamster ovary cells is subsequently reorganized to a microvillous topography, even in the continued presence of trypsin. Scanning and transmission electron microscope (SEM and TEM) observations of this transition showed the initial formation of a "crown' of densely clustered microvilli at one pole of the cell. At the periphery of this region the blebs coalesced to form ridges which subsequently extended over the entire cell surface. Long, and occasionally branched microvilli were generated from the ridges. Large numbers of membrane associated vesicles were also characteristic of these areas of surface reorganisation.
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PMID:Conversion of blebs to microvilli: cell surface reorganisation after trypsin. 732 17

It was the purpose of this study to define whether trypsin inhibitors impair protein digestibility via enhanced loss of exogenous or endogenous protein by quantifying those losses using the homoarginine technique, recently developed in this laboratory. Pigs fitted with permanent ileal T-cannulas were fed test meals containing homoarginine-labeled protein. The meals contained casein and increasing doses of trypsin inhibitors (Experiment 1) or alternatively either heat-treated or raw ground soybeans (Experiment 2). Following a casein meal (425 mmol nitrogen, no trypsin inhibitors), ileal protein was predominantly of endogenous rather than of exogenous origin (105 vs. 9 mmol nitrogen). Addition of isolated trypsin inhibitors (3000 mg) enhanced appearance of both endogenous and exogenous protein at the ileum (by 73 and 9 mmol nitrogen, respectively). Feeding raw instead of heat-treated soybeans in one single test meal caused a significant increase of endogenous protein from 217 +/- 42 to 263 +/- 47 mmol (mean +/- SEM) and of exogenous protein from 16 +/- 3 to 48 +/- 14 mmol. If fed continuously for 1 wk, a raw soybean diet caused endogenous protein loss to rise significantly from 221 +/- 26 to 432 +/- 85 mmol. We conclude that ingestion of food containing trypsin inhibitor affects nitrogen balance more by losses of amino acids of endogenous secreta than by losses of dietary amino acids.
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PMID:Soybean trypsin inhibitor(s) reduce absorption of exogenous and increase loss of endogenous protein in miniature pigs. 750 18

Trypsinogen activation peptide (TAP) concentration and alpha 2-macroglobulin-trypsin complex (alpha 2M-T) activity were measured in two experimental models of acute pancreatitis in rats to evaluate the significance of activation of trypsinogen in acute pancreatitis. TAP concentration and alpha 2M-T activity in serum rose significantly in trypsin-taurocholate-induced hemorrhagic acute pancreatitis, while in cerulein-induced edematous acute pancreatitis they did not rise in spite of a similar increase in immunoreactive trypsin. When rats in trypsin-taurocholate-induced pancreatitis were treated by protease inhibitor (FUT-175; nafamostat mesilate; FUT group), alpha 2M-T activity in serum was significantly lower than that in nontreated controls (mean +/- SEM, 20.8 +/- 1.43 U/L in the FUT group vs 79.1 +/- 24.5 in controls; p < 0.01). The survival rate at 24 h was significantly improved in the FUT group compared with the controls (70 vs 43%; p < 0.05). The increase in TAP concentration in the FUT group was similar to that in controls. The TAP concentration in pancreatic tissue at 24 h was significantly (p < 0.01) lower in the survival group (7.8 +/- 0.8 ng/ml) than in the lethal group (25.9 +/- 3.7 ng/ml). Activation of trypsinogen and its subsequent enzyme activity play an important role in the evolution of severe acute pancreatitis.
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PMID:Activation of trypsinogen in experimental models of acute pancreatitis in rats. 754 73

Activation of the contact phase of coagulation has been implicated in the pathogenesis of septic shock. We wanted to determine if inhibition of plasma kallikrein can prevent arterial hypotension and liberation of kinins from kininogen, induced by an infusion of bacterial lipopolysaccharide (LPS) in anesthetized, ventilated 20-kg pigs. The LPS was given IV in a dose of 5 micrograms/kg/h for 8 hours. The plasma kallikrein inhibitor aprotinin, 537 mumol, was given IV during 8 hours, resulting in plasma levels above 10 mumol/L. Ten animals (SA) received LPS and aprotinin and ten randomized controls (SC) received LPS and saline. Kinin-containing kininogen was determined on the basis of the amount of kinin releasable in plasma samples by incubation with trypsin. Kininogen decreased to 58% +/- 4% of the baseline value without any difference between groups. This may indicate participation of other processes than degradation by plasma kallikrein in the decrease of kininogen. Arterial blood pressure was higher at 7 hours in the SA animals than in the SC group (101% +/- 11% vs. 68% +/- 8%; mean +/- SEM; p = 0.026). Fibrin monomer and C3adesArg plasma levels were attenuated by aprotinin treatment. These findings underscore the important role of the contact system in LPS shock.
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PMID:Inhibition of plasma kallikrein with aprotinin in porcine endotoxin shock. 768 84

The activation of the kallikrein-kinin system is thought to be one of the pathophysiological factors in acute pancreatitis. A radioimmunoassay for porcine, pancreatic tissue kallikrein was developed and used to measure levels in normal plasma and peritoneal fluid and in experimental, bile-induced (group A) and bile trypsin-induced (group B) acute pancreatitis in the pig. Normal porcine plasma and peritoneal fluid contained about 2.17 +/- 0.11 and 1.91 +/- 0.19 microgram/l (SEM) tissue kallikrein, respectively. In experimental, acute pancreatitis there was a rapid rise in the plasma level of tissue kallikrein, followed by a slow increase to a final value of about 150% of the normal plasma level in both groups. In the peritoneal exudate a large increase (200-fold in group A and 2,000-fold in group B) in tissue kallikrein was seen, with a maximum within about 1/3 of the survival time, followed by a slow decrease until death in group B. In group A a smaller second peak was seen at about 2/3 of the survival time. Gelfiltration of peritoneal exudates showed complexes with alpha 1-, alpha 2-macroglobulin (alpha 1 alpha 2-M), and alpha 1-proteinase inhibitor (alpha 1-PI) and a large portion of free tissue kallikrein. The complexes with alpha 1 alpha 2-M and the free tissue kallikrein were found to be enzymatically active when tested on chromogenic tripeptide substrate. The presence of large amounts of free and active tissue kallikrein in the peritoneal exudate leads us to the conclusion that tissue kallikrein may be a major cause of local release of kinins in acute pancreatitis.
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PMID:Studies on the release of tissue kallikrein in experimental pancreatitis in the pig. 800 67

Hepatocyte growth factor is a recently cloned potent mitogen to hepatocytes, but its extrahepatic roles are not completely defined. It causes proliferation of endothelial and epithelial cells implicating potential action in the glomerulus. We aimed to determine whether cultured human mesangial cells secrete hepatocyte growth factor and the effect of high glucose conditions. Mesangial cells were isolated from the normal cortex of a child's kidney. After differential glomerular sieving and trypsin digestion of glomeruli, mesangial cells were cultured in 20% fetal calf serum/RPMI. Glucose concentration in the medium was adjusted to 5 mmol/l, 11 mmol/l, 25 mmol/l or 5 mmol/l/20 mmol/l mannitol to correct for osmolality. After 0, 24, 48, 72 h incubation, hepatocyte growth factor was measured in the supernatant by enzyme immuno assay using recombinant hepatocyte growth factor and monoclonal antibodies to human hepatocyte growth factor. Hepatocyte growth factor was secreted by cultured mesangial cells. High glucose and hyperosmolar conditions caused a 100-200% increase in hepatocyte growth factor secretion at 48-72 h (p = 0.001). Hepatocyte growth factor secretion at 48 h in 5 mmol/l glucose was 16.46 +/- 1.09 ng/ml (mean +/- SEM), 11 mmol/l glucose: 32.98 +/- 4.54, 25 mmol/l glucose: 33.32 +/- 7.89, 5 mmol/l glucose/20 mmol/l mannitol: 34.05 +/- 3.64; at 72 h in 5 mmol/l glucose: 23.92 +/- 2.85 ng/ml, 11 mmol/l glucose: 28.26 +/- 2.03, 25 mmol/l glucose: 62.04 +/- 12.2, 5 mmol/l glucose/20 mmol/l mannitol: 45.76 +/- 6.25. Trypan blue exclusion demonstrated membrane integrity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:High glucose and hyperosmolality stimulate hepatocyte growth factor secretion from cultured human mesangial cells. 805 93

Sarcoidosis affecting the lungs may cause obstructive and/or restrictive lung function impairment. The bronchial reactivity is related to the release of histamine from the mast cells. Upon activation mast cells also release tryptase. This enzyme may activate latent collagenase and thus possibly contribute to the fibrosis formation observed in sarcoidosis. We analyzed the bronchoalveolar lavage fluid (BALF) from 13 nonsmoking and untreated patients with sarcoidosis and from 30 healthy volunteers (18 smokers) with regard to the number of mast cells and the tryptase concentration. Concomitantly albumin, fibronectin and hyaluronan were measured as markers of the inflammatory reaction in the alveoli and interstitium. The number of mast cells was higher (p < 0.001) in patients with sarcoidosis than in controls. Also, the concentration of tryptase was significantly higher in patients (225.3 +/- 83.9 [SEM] mU/L) compared to nonsmoking and smoking controls (34.7 +/- 7.8 and 44.7 +/- 13.0 mU/L, respectively; p < 0.01 for both). In addition, the concentrations of albumin, fibronectin and hyaluronan were higher in patients with sarcoidosis compared to the nonsmoking controls (p < 0.001 for all). However, there was no relationship between either the mast cell number or the tryptase concentration and the lung function parameters (VC, TLC, FEV1, FEV%, DLCO). As our patients did not show any functional signs of bronchial obstruction (FEV1 91.7% +/- 13.3 [SD] and FEV% 99.5% +/- 6.4 of predicted) the lack of correlation is not surprising. The high concentrations observed in the BALF of the noncellular components may just reflect an ongoing inflammatory process that may resolve or, if exaggerated, lead to fibrosis.
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PMID:Elevated levels of tryptase in bronchoalveolar lavage fluid from patients with sarcoidosis. 813 9

Uterine homogenates of cycling and early pregnant Sprague Dawley rats and purified rat urinary kallikrein showed similar curves of displacement of 125I-kallikrein binding to a polyclonal antibody. Uterine kallikrein concentration measured by RIA was 8.7 +/- 2 SEM ng/g wet weight during the cycle (n = 6 in diestrus and metestrus) and 20.8 +/- 2 SEM (n = 7) ng/g wet weight on Day 7 of pregnancy (P7) (p < 0.001). On P7, kallikrein concentration was increased 12.4-fold in the implantation nodes, as compared to the interimplantation segments. Uterine homogenates of rats on P7, submitted to DEAE-cellulose chromatography and Sephadex gel filtration, yielded two fractions containing kallikrein immunoreactivity and kininogenase activity, with molecular masses that ranged from 120-125 kDa and 39-43 kDa, respectively. In the RIA, both fractions displayed parallelism with purified kallikrein. Enzymatic activity was expressed after activation by trypsin. It was inhibited by aprotinin, PMSF, p-amino-benzamidine, and leupeptin, but not by soybean or ovomucoid trypsin inhibitors. Kallikrein mRNA was demonstrated by reverse transcriptase/polymerase chain reaction in uteri of nonpregnant and P7 rats. These results show that rat uterus synthesizes one or more serine proteases that are immunologically and enzymatically related to tissue kallikrein in the implantation node on P7--determined both by an increment of whole uterus kallikrein content and a depletion of the interimplantation segments--suggests that kallikrein may play a role in the vasoactive changes of implantation.
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PMID:Uterine kallikrein in the early pregnant rat. 821 45

This study assessed the effect of profound inhibition of gastric secretion by an H2 antagonist on postprandial gastric emptying of acid and chyme, and on bile acid and pancreatic enzyme secretion under physiological conditions in humans. Six subjects were studied before and while they were given famotidine (40 mg). This study combined a continuous intestinal perfusion technique using 14C-polyethylene glycol (14C-PEG) as duodenal recovery marker, with intermittent sampling of gastric content using PEG 4000 as meal marker. During the three hour study, the area under the curve for gastric acid output decreased from mean (SEM) 88.9 (7.6) mmol for those not receiving treatment, to 21.2 (2.7) mmol for subjects receiving famotidine (p < 0.01). The corresponding values for the rate of acid delivery into the duodenum decreased from 65.2 (11.9) to 16.6 (2.9) mmol (p < 0.05), and those for the rate of gastric emptying of chyme remained unchanged for the group receiving no treatment and during famotidine (1040 (200) v 985 (160) ml respectively, NS). Duodenal bile acid and trypsin output remained unchanged (area under the curve, 457 (128) v 373 (86) umol/kg and 5022 (565) v 5058 (400) IU/kg respectively, NS) receiving no treatment and during famotidine. It is concluded that profound inhibition of postprandial gastric acid secretion by anti-secretory drugs is not accompanied by changes in biliary and pancreatic secretion, mainly because the gastric emptying of chyme is unaffected.
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PMID:Postprandial biliary and pancreatic secretion during profound inhibition of gastric secretion in humans. 824 51

The collagen fibres of rabbit and human ureter were exposed by digestion with trypsin and hyaluronidase. The fibre structure was examined using an SEM and examples of the inner and outer fibre structures are shown together with the effects of different types of mechanical strain. An interesting difference between the arrangements of the inner fibres of human and rabbit was seen where the human ureter had a cross-ply structure while in the rabbit it was helical.
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PMID:Collagen arrangements in ureter. 827 87


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