A novel triple secured technique for pancreatic reconstruction following pancreaticoduodenectomy for a soft pancreas.

BACKGROUND/AIMS: Soft pancreases are susceptible to developing pancreatic fistula following pancreaticoduodenectomy. To reduce the incidence of pancreatic fistula after pancreaticoduodenectomy in patients with a soft pancreas, we developed a triple secured technique. In this study, we describe the details of this technique and also report on the postoperative outcomes. METHODOLOGY: The triple secured technique employed an ultrasonic dissector for pancreatic transection with skeletonizing and ligating of the small pancreatic branch ducts, duct-invagination or duct-to-mucosa anastomosis for main pancreatic duct management, and, finally, four large stitches between the pancreatic stump parenchyma and the jejunal seromuscular layer to prevent minor pancreatic leakage. A total of 28 consecutive patients with a soft pancreas who underwent pancreaticoduodenectomy using our technique were included in this study. RESULTS: Postopetrative complications occurred in 16 patients. Grade B pancreatic fistula developed in 6 patients. However, no grade C pancreatic fistula occurred in this series. Neither any reoperation nor in-hospital mortality was observed in this series. CONCLUSIONS: Our triple secured technique after pancreaticoduodenectomy was feasible and safe, with an acceptable rate of grade B pancreatic fistula and no grade C pancreatic fistula for patients with a soft pancreas.

Quantitative analysis of double-stranded DNA amplified by a polymerase chain reaction employing surface-enhanced Raman spectroscopy.

Surface-enhanced Raman spectroscopy (SERS) was utilized for the quantitative analysis of double-stranded (ds) DNA amplified by a polymerase chain reaction (PCR). 4?, 6-Diamidino-2-phenylindole dihydrochloride (DAPI), which intercalates into ds-DNA but does not form a complex with single-stranded (ss) DNA, was added to a DNA solution after amplification by PCR. When the solution was mixed, including ds-DNA-DAPI complexes and free DAPI with silver colloid sol, only free DAPI was adsorbed on the colloid surface. The dye on the colloid gave very intense SERS signals with excitation at 514.5 nm, whereas DAPI engaging in the intercalation with ds-DNA did not show any SERS signal. The SERS spectrum of DAPI on the colloid showed a strong band at 1610 cm(-1) due to the C?N stretching mode, and a linear relationship was observed between the peak intensity of the C?N stretching band and the concentration of free DAPI. Therefore one can determine the concentration of free DAPI by the SERS measurement. The more ds-DNA there is in the solution, the less free DAPI there is. Thus it is possible to quantitatively analyze the ds-DNA amplified by PCR indirectly by using SERS. The correlation coefficient between the peak intensity of the C?N stretching band and the concentration of ds-DNA amplified by PCR was calculated to be 0.988 for a concentration range from 0.1 to 1.3 mg/ml.

MRI of the TMJ disc with intravenous administration of gadopentetate dimeglumine.

PURPOSE: The purpose of this study was to ascertain whether MR imaging with intravenous administration of gadopenetate dimeglumine (Gd-DTPA) is useful in the demonstration of the temporomandibular joint (TMJ) disc. METHOD: Sagittal T1-weighted MR images of 50 TMJs (25 patients) were obtained using a 0.5-T system both before and after intravenous injection of Gd-DTPA. The authors depicted the TMJ in which intravenous injection of Gd-DTPA improved visulization of the disc. RESULTS: Intravenous injection of Gd-DTPA increased intensity in the retrodiscal space, the pterygoid venous plexus, as well as joint effusion by diffused Gd-DTPA. The technique improved visualization of 10 (50%) of 20 normal discs and 20 (67%) of 30 anterior disc displacements in closed-mouth position, and also 23 (74%) of 31 normal discs and 12 (63%) of 19 anterior disc displacements in open-mouth position. There were 12 TMJs (24% of the 50 TMJs) in which equivocal findings became highly diagnostic. The incidence in marked contrast effect was higher in TMJs with severe internal derangement than in those with normal or mild internal derangement (p < 0.005). CONCLUSION: Using a 0.5-T MR imager, T1-weighted imaging with intravenous injection of Gd-DTPA showed more anatomic details than imaging without the contrast agent.

Development of a fistula between an internal mammary artery graft and the pulmonary vasculature following coronary artery bypass grafting: report of a case.

We report herein the rare case of a 56-year-old man who gradually developed congestive cardiac failure 6 months after undergoing coronary artery bypass grafting and was found to have a fistula between the internal mammary artery and the pulmonary artery of the upper lobe diagnosed by selective left internal mammary arteriogram. A second sternotomy was performed and demonstrated dense adhesion between the fissure surrounding the internal mammary artery and the upper lobe, and the fistula was resected. We believe that the patient's increasing cardiac failure was almost certainly caused by coronary seal.

Recurrent Cushing's disease associated with nephrotic syndrome.

A case of recurrent Cushing's disease with nephrotic syndrome due to membranoproliferative glomerulonephritis (MPGN) is presented. Functional pituitary adenoma recurred 6 years after transsphenoidal pituitary adenomectomy. Due to infiltration into the surrounding tissues, transcranial surgery was performed. However, this failed to induce a remission and thus gamma knife therapy was applied. Histopathological evaluation revealed that the glomerular lesions had progressed to a rather advanced stage of MPGN. Although this association could be coincidental, the recurrence of pituitary macroadenoma might be induced by the cessation of steroid treatment for the nephrotic syndrome.

Endothelin-1 stimulates prostaglandin E2 production in an extracellular calcium-independent manner in cultured rat mesangial cells.

To study a possible role of endothelin-1 (ET-1) in the regulation of glomerular function, we examined the presence of receptors for, and the biological action of, ET-1 in cultured rat mesangial (M) cells. The first-subcultured M cells prepared from isolated glomeruli of Sprague-Dawley rats were used. ET-1 binding was assayed by using 125I-ET-1. Inositol 1,4,5-trisphosphate (IP3) was determined by IP3-specific binding assay. Intracellular calcium (iCa2+) was measured in fura-2 loaded cells. Prostaglandin E2 (PGE2) was measured by radioimmunoassay. In M cells there existed two classes of binding sites specific for ET-1 (Kd was 0.24 and 4.4 nmol/L, Bmax was 130 and 1070 fmol/mg, respectively). ET-1 (10(-7) mol/L) induced a rapid and transient increase in IP3, followed by transient and sustained increases in iCa2+. Nicardipine (10(-6) mol/L) inhibited only the sustained increase in iCa2+. ET-1 (10(-9) mol/L to 10(-7) mol/L) significantly stimulated PGE2 production with the concentration dependency. Nicardipine (10(-6) mol/L) and diltiazem (10(-6) mol/L) did not inhibit the PGE2 production. We conclude that M cells have specific ET-1 receptors linked to phosphoinositide turnover and PGE2 production, and PGE2 production by ET-1 may be through an extra-cellular calcium-independent mechanism. Our results suggest that ET-1 plays an important role in the regulation of glomerular functions by modulating PGE2 production in M cells.

A case of polycystic kidney disease with nephrotic syndrome.

Nephrotic syndrome developed in a patient with autosomal-dominant polycystic kidney disease. Renal biopsy revealed minor glomerular abnormalities. This type of nephrotic syndrome complication in an autosomal-dominant polycystic kidney disease has only rarely been reported.

Relationship between hypertriglyceridemia and uric acid production in primary gout.

The relationship between uric acid metabolism and lipid levels was analyzed in 148 male subjects with primary gout. The subjects were divided into three groups according to their alcohol consumption: heavy drinkers, moderate drinkers, and nondrinkers or mild drinkers. There was no correlation between urinary uric acid excretion and serum triglyceride (TG) levels in the heavy group, but a marginally significant correlation was shown in the moderate group (P less than .05), and a significant correlation was observed in the nondrinker or mild group (P less than .001). This relationship in the nondrinker or mild group was also found to be significant after adjustment for BMI and age by multiple regression analysis. Serum lipoproteins were analyzed by sequential preparative ultracentrifugation in 21 patients with primary gout who neither drank alcohol nor were obese; VLDL-TG level, but not the VLDL cholesterol level, was found to be significantly correlated with 24-hour urinary uric acid excretion. These results indicate that there is a close correlation between the degree of uric acid production, as judged by 24-hour urinary uric acid excretion, and lipoprotein TG metabolism when the influence of alcohol intake is excluded.

Trial of IgG therapy for lupus nephritis--report of two cases with a successful response.

Two cases with systemic lupus erythematosus (SLE) were treated with high-dose intravenous IgG. In patient 1, the IgG therapy dramatically improved both the lupus nephritis and serological titers for SLE. In patient 2, intravenous IgG yielded a partial remission in the lupus nephritis as well as a satisfactory decrease in proteinuria and disappearance of the skin rash characteristic of SLE. IgG therapy is suggested as possibly beneficial for the treatment of SLE based on different mechanisms from those of corticosteroid action. Further studies are needed to determine the detailed efficacy of IgG therapy for SLE.

Endothelin-1 receptors in rat renal glomeruli.

Renal glomeruli form a dynamic structure capable of regulating the glomerular filtration rate (GFR). To explore possible regulating effects of endothelin-1 (ET-1) upon glomerular functions, the presence of specific ET-1 receptors and the biological actions of ET-1 were studied in isolated rat renal glomeruli. The specific binding of [125I]ET-1 to glomeruli was time and temperature dependent. Scatchard analysis of the binding data indicated the presence of a single class of high-affinity binding sites with the apparent dissociation constant of 8.3 nM and the maximal binding capacity of 1.5 pmol/mg protein. ET-1 stimulated prostaglandin (PG) E2 production in glomeruli with the time course and the concentration dependency similar to those found in [125I]ET-1 binding to glomeruli. These results indicate the presence of high-affinity binding sites for ET-1 linked to PGE2 production in glomeruli, suggesting a possible role of ET-1 in the regulation of glomerular function.

Furosemide accelerates gentamicin accumulation in cultured renal cells (LLC-PK1 cells).

Furosemide is known to potentiate gentamicin nephrotoxicity. The mechanism of potentiation is unclear. In our previous studies, we demonstrated that furosemide enhanced gentamicin accumulation in rabbit renal tissues when injected as a bolus [Kidney int. 33:363, 1988] or repeatedly subcutaneously [Diuretics II, Elsevier, New York 1987, pp.693]. In this study, we evaluated the effects of furosemide on gentamicin accumulation in cultured renal cells (LLC-PK1) and hepatoma cells (H4IIE). Thus, we excluded effects secondary to furosemide-elicited hemodynamic changes. Seven days after seeding, the culture medium was exchanged for medium containing 1 mM gentamicin alone [G] or 1 mM gentamicin +1 mM furosemide [GF]. In LLC-PK1 cells, gentamicin concentration in [GF] was significantly higher than that in [G], while gentamicin was not detected in H4IIE cells with or without furosemide. We conclude that furosemide can accelerate gentamicin accumulation in renal tissues and potentiate gentamicin nephrotoxicity.

Cholesterol-lowering effect of N-(alpha-methylbenzyl)linoleamide (melinamide) in cholesterol-fed diabetic rats.

Cholesterol loading of diabetic rats is known to induce marked hyperlipoproteinaemia, and we have reported that enhancement of the activity of intestinal acyl-CoA:cholesterol acyltransferase (ACAT), one of the key enzymes involved in cholesterol absorption, might play an important role in the development of hypercholesterolaemia in these animals. In the present study, we have shown that treatment with N-(alpha-methylbenzyl)linoleamide (melinamide), a new hypocholesterolaemic drug, caused a substantial decrease of the enhanced intestinal ACAT activity in diabetic rats, but did not affect intestinal cholesterol esterase activity. Furthermore, marked improvement of hypercholesterolaemia in cholesterol-fed diabetic rats occurred concomitantly with the drug treatment. These results suggest that intestinal ACAT activity is closely related to the serum cholesterol level in diabetic rats, and show that melinamide lowers intestinal ACAT activity.

Angiotensin II-induced increase in inositol 1,4,5-trisphosphate in cultured rat mesangial cells: evidence by refined high performance liquid chromatography.

Angiotensin II-induced change in inositol phosphates were studied in cultured rat mesangial cells prelabeled with [3H]myo-inositol. By using anion-exchange high performance liquid chromatography, we could analyzed the change in inositol mono-, bis-, and tris-phosphate more rapidly and easily with higher resolution than the previously reported methods. Angiotensin II rapidly increased inositol 1,4,5-trisphosphate and inositol 1,4-bisphosphate within 15 sec, followed by an increase in inositol 1-monophosphate at 30 sec. Angiotensin II-induced increases in inositol phosphates were dose-dependent and completely blocked by saralasin. These results indicate that angiotensin II induces the production of inositol phosphates including inositol 1,4,5-trisphosphate, an intracellular Ca2+-releasing factor, in cultured rat mesangial cells.

Phosphoinositide turnover enhanced by angiotensin II in isolated rat glomeruli.

To clarify the signal transduction mechanism of angiotensin II in renal glomeruli, we studied the effect of the hormone on phospholipid metabolism using isolated rat glomeruli. Stimulation of the glomeruli pulse-chase labeled with [3H]glycerol by angiotensin II caused a rapid (within 15 s) breakdown of phosphatidylinositol 4,5-bisphosphate (PIP2) with a concurrent production of 1,2-diacylglycerol. This effect of angiotensin II was in a dose-dependent manner within the range from 10(-12) M to 10(-6) M, and was inhibited by saralasin. Angiotensin II also decreased the 3H radioactivity of PIP slightly only at 15 s and increased that of phosphatidic acid after 15 s, with no significant effect upon the labelings of phosphatidylinositol (PI), phosphatidylcholine (PC) and phosphatidylethanolamine (PE) within 1 min. The change in phospholipid metabolism by angiotensin II was similar when the glomeruli were labeled with [32P]orthophosphate: the decrease in the labeling of PIP2 and the increase in the labeling of phosphatidic acid after 15 s. In addition, 32P labeling of PI increased after 2 min. These results suggest that angiotensin II, after binding to glomerular receptors, induces initial PIP2 hydrolysis to diacylglycerol and subsequent resynthesis of PIP2 through phosphoinositide turnover.