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Biomedical subjects

H Dubner

Publications and source records attributed to H Dubner.

6 recordsLinked to original sources
PubMed1996

Infected pancreatic necrosis and peripancreatic fluid collections: serendipitous response to antibiotics and medical therapy in three patients.

Three patients with clinical and radiologic evidence of pancreatic necrosis or peripancreatic fluid collections/inflammatory masses who were advised to have surgery on the basis of bacterial infection on skinny-needle aspiration of the pancreas but were deemed medically unstable or refused operative intervention were treated with intensive antibiotic therapy. All three patients survived the attack of acute pancreatitis with infection on medical therapy alone. This suggests that occasional patients with infected necrosis and/or peripancreatic collections/inflammatory masses may respond to antibiotics, especially those antibiotics that have recently been shown to have a high penetration into pancreatic tissue.

Acute Disease↗
PubMed1995

Ursodeoxycholic acid inhibits glucagon-induced cAMP formation in hamster hepatocytes: a role for PKC.

The effect of bile acids on adenosine 3',5'-cyclic monophosphate (cAMP) synthesis was investigated in isolated hamster hepatocytes. Bile acids had no direct effect on cAMP production. However, ursodeoxycholic acid (UDCA) and tauroursodeoxycholic acid inhibited, by approximately 45%, cAMP formation induced by concentrations of glucagon greater than 1 nM, with a respective half-maximum inhibitory effect observed at 4 +/- 2 microM. Similar inhibition was observed with phorbol 12-myristate 13-acetate (PMA). Chenodeoxycholic, murocholic, and taurodeoxycholic acids were the next most potent bile acids. Taurolithocholic acid was 100-fold less potent than UDCA, whereas both ursocholic and taurocholic acids had no effect at concentrations up to 0.5 mM. Neither bile acids nor PMA affected either the binding of glucagon to its receptor, the cAMP-dependent phosphodiesterase, adenylate cyclase, or the inhibitory and stimulatory (Gs) GTP-binding proteins. The inhibitory effect of PMA and UDCA on glucagon-induced cAMP synthesis was abolished in the presence of the protein kinase C (PKC) inhibitor, staurosporine. Furthermore, UDCA induced PKC translocation from cytosol to membrane and stimulated phosphorylation of an 80-kDa protein substrate for PKC. In conclusion, mediated by PKC activation, bile acids inhibit glucagon-induced cAMP synthesis by uncoupling the glucagon receptor and Gs.

Angiotensin II↗
PubMed1995

The role of sodium in the uptake of ursodeoxycholic acid in isolated hamster hepatocytes.

The uptake of ursodeoxycholic acid (UDCA) was studied in isolated hamster hepatocytes. The uptake was rapid and linear up to 60 seconds for each concentration studied. When the uptake rate was plotted against UDCA concentration, the curve was nonlinear, indicating both saturable and nonsaturable uptake mechanisms. The nonsaturable process had a diffusion constant of 0.01 nmol.s-1.g of cell.mumol/L-1. The saturable component was characterized by a maximum rate of uptake (Vmax) of 5.68 nmol.s-1.g of cell-1 and a Michaelis constant (Km) of 224 mumol/L. In the presence of monensin, ouabain, and amiloride, the uptake of UDCA was significantly decreased by 35% to 55%, whereas the sodium-independent uptake of UDCA was not affected by either monensin or amiloride, thereby confirming sodium dependence of UDCA uptake. The sodium-dependent uptake of UDCA was characterized by a Vmax and a Km of 1.57 nmol.s-1.g of cell-1 and 46 mumol/L, respectively. The rate of uptake of UDCA was maximal at extracellular sodium concentrations > or = 20 mmol/L. Furthermore, the uptake of UDCA was competitively inhibited by both taurocholic acid and cholic acid with an inhibitory constant (Ki) of 60 mumol/L and 48 mumol/L, respectively. Finally, 1 mmol/L of 4,4'-diisothiocyano-2,2'-disulfonic stilbene (DIDS) inhibited solely the sodium-dependent uptake of cholic acid and UDCA. These findings confirm that the hepatocellular uptake of UDCA involves, at least in part, a sodium-dependent, ouabain, amiloride, and DIDS-sensitive transporter.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1994

Predicting gallstone pancreatitis with laboratory parameters: a meta-analysis.

OBJECTIVES: In order to define the usefulness of biochemical laboratory values in distinguishing gallstone from non-gallstone acute pancreatitis, we performed a meta-analysis. METHODS: Studies that utilized the bilirubin, alkaline phosphatase, alanine aminotransferase (ALT), and aspartate transaminase in the evaluation of the gallstone pancreatitis were included. RESULTS: Using receiver operating characteristic curves for each of these four parameters, we determined that the ALT level was the most clinically useful parameter. The higher the serum level of ALT, the greater its specificity and positive predictive value in diagnosing gallstone pancreatitis. At ALT levels greater than or equal to 150 IU/L (approximately a 3-fold elevation), the probability of gallstone pancreatitis is 95%. Our analyses of total bilirubin and alkaline phosphatase serum levels indicate that these tests are not useful in the diagnosis of gallstone pancreatitis. Aspartate transaminase levels are nearly as useful as ALT. CONCLUSIONS: A > or = 3-fold elevation of ALT in the presence of acute pancreatitis has a positive predictive value of 95% in diagnosing acute gallstone pancreatitis.

Acute Disease↗