Abdominal mass in a 19-year-old with neurofibromatosis.
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Adult↗
Biomedical subjects
I Samuel
Publications and source records attributed to I Samuel.
Ligation-induced acute pancreatitis increases pancreatic circulating trypsinogen activation peptides.
Ligation of the common bile-pancreatic duct induces hyperamylasemia and acute pancreatitis in rats. Pancreatic morphologic changes include edema, acinar cell damage, and mild inflammation. The pathogenesis of acute pancreatitis in this model is not understood, but may involve altered secretion and intrapancreatic activation of acinar proteases. We hypothesized that trypsinogen activation, measured by the production of plasma and pancreatic trypsinogen activation peptides (TAP), occurs early in this model. We performed the following experiments: rats were prepared with (1) bile-pancreatic ducts ligated and (2) ducts dissected but not ligated (sham). Rats were killed after 6, 24, and 48 hr. Serum amylase was measured and histologic sections were analyzed for morphologic changes. TAP was measured in both serum and pancreatic tissue homogenates using a specific polyclonal. anti-TAP antibody in an enzyme-linked immunosorbant assay. After 6, 24, and 48 hr of bile-pancreatic duct ligation, hyperamylasemia and acute morphologic changes of acute pancreatitis were observed. Evidence of acinar cell destruction was not evident until 48 hr after ligation. Levels of serum and pancreatic tissue TAP were significantly elevated at both 24 and 48 hr after ligation compared to those of sham. We conclude that increased intrapancreatic trypsinogen activation occurs early in this form of experimental acute pancreatitis and that it occurs prior to evidence of acinar cell destruction. These data and observations support the possibility that intrapancreatic protease activation contributes to the pathogenesis of ligation-induced acute pancreatitis.
Acute Disease↗
Bile-pancreatic juice replacement not cholinergic- and cholecystokinin-receptor blockade reverses acinar cell hyperstimulation after bile-pancreatic duct ligation.
BACKGROUND: Acinar cell inhibitors (eg, atropine) fail to ameliorate clinical and experimental acute pancreatitis. We hypothesized that amelioration of pancreatic acinar cell hyperstimulation after bile and pancreatic duct ligation is better with gut replacement of bile and pancreatic juice than with cholinergic- and cholecystokinin (CCK)-receptor blockade. METHODS: Using acinar cell amylase activity as an index of hyperstimulation, we studied 63 rats in two sets of experiments. Bile-pancreatic juice exclusion from gut--without (set one) and with (set two) bile and pancreatic duct obstruction--was treated with atropine and CCK-receptor antagonist L-364,718, or with enteral replacement of bile-pancreatic juice. RESULTS: In the set one experiment, acinar cell hyperstimulation after bile-pancreatic juice exclusion was reversed by combined L-364,718 and atropine pretreatment. In set two, acinar cell hyperstimulation after bile and pancreatic duct ligation was reversed by enteral bile and pancreatic juice replacement, but not by combined L-364,718 and atropine pretreatment. CONCLUSIONS: According to this experimental corollary of early gallstone impaction, prevention of acinar cell hyperstimulation after duct occlusion should be aimed at the source of the response to bile-pancreatic juice exclusion, namely, the gut, rather than at the target of the response, the pancreatic acinar cell.
Amylases↗
Ligation-induced acute pancreatitis in opossums: acinar cell necrosis in the absence of colocalization.
Acute necrotizing pancreatitis in opossums after bile and pancreatic duct ligation (BPDL) is a useful experimental corollary of gallstone-induced acute pancreatitis in humans. In experimental and human acute pancreatitis, a loss of segregation of the lysosomal enzyme cathepsin B and the zymogen proenzyme trypsinogen (colocalization) is implicated as the triggering event of disease pathogenesis, as cathepsin B can activate trypsinogen. The object of this study was to quantitate acinar cell necrosis and to study subcellular distribution of cathepsin B in BPDL-induced acute necrotizing pancreatitis in opossums. Bile and pancreatic ducts were ligated separately (no bile reflux) in four opossums while ducts were dissected in four sham controls. Opossums were killed 24 hr after operation. Three equidistant cross-sectional portions of each opossum pancreas were submitted to histologic examination. In blinded fashion, each focus of acinar cell necrosis was photographed and quantitated with digitizing morphometry. Numerical density (foci/cm2) and areal density (x10(3) micron 2/cm2) of focal acinar cell necrosis were determined. Differentially centrifuged pancreatic homogenates were assayed for cathepsin B, the lysosomal marker enzyme N-acetylglucosaminidase, and amylase. Morphometric quantitation of acinar cell necrosis confirmed development of acute necrotizing pancreatitis after 24 hr of BPDL in opossums. However, colocalization was not observed after BPDL, as evidenced by an absence of subcellular shift of cathepsin B activity (and N-acetyl-glucosaminidase activity) from the lysosome-enriched to the zymogen-enriched subcellular fraction. Amylase activity was increased in subcellular fractions after BPDL.(ABSTRACT TRUNCATED AT 250 WORDS)
Acetylglucosaminidase↗
Bile and pancreatic juice replacement ameliorates early ligation-induced acute pancreatitis in rats.
BACKGROUND: In healthy rats, combined bile and pancreatic juice diversion from gut has a synergistic rather than additive effect on stimulation of exocrine pancreatic protein secretion. We hypothesized that exclusion of combined bile and pancreatic juice from gut exacerbates bile and pancreatic-duct ligation-induced acute pancreatitis in rats to a greater extent than exclusion of either bile or pancreatic juice alone. METHODS: Bile and pancreatic juice (obtained fresh from donor rats) were replaced, separately or together, via a duodenal fistula beginning immediately before 6 hours of duct ligation. Pancreatic morphologic changes were evaluated with an acute pancreatitis histology score and morphometric quantitation of acinar-cell necrosis. Plasma amylase and cholecystokinin concentrations and pancreatic subcellular distribution of cathepsin B activity were determined. Characteristics of bile and pancreatic juice obtained from donor rats were also studied. RESULTS: Combined bile and pancreatic juice replacement limited the increase in acute pancreatitis histology score by 77%, acinar cell necrosis by 95%, hyperamylasemia by 77%, and hypercholecystokininemia by 99%, while preventing subcellular redistribution of cathepsin B. Amelioration of pancreatic morphologic changes was significantly greater with combined bile and pancreatic juice replacement than with replacement of either bile or pancreatic juice alone. CONCLUSION: In this experimental corollary of early gallstone-induced acute pancreatitis, combined bile and pancreatic juice exclusion from gut contributes to disease pathogenesis to a greater extent than exclusion of either bile or pancreatic juice alone.
Acute Disease↗
Ligation-induced acute pancreatitis in rats and opossums: a comparative morphologic study of the early phase.
Bile and pancreatic duct ligation (BPDL) in rats does not induce severe acute pancreatitis but only mild inflammation, which is self-limiting and eventually leads to pancreatic atrophy. However, BPDL in opossums induces severe acute necrotizing pancreatitis which uniformly leads to death within 14 days. We compared pancreatic morphologic changes after 24 hr of BPDL in rats and opossums. Pancreatitis histology score and acinar cell ultrastructural changes were evaluated. In both species, BPDL was associated with significant increases in histology score compared to sham controls (5.0 +/- 0.3 vs 1.5 +/- 0.3 in rats, 5.3 +/- 0.4 vs 1.1 +/- 0.1 in opossums; mean +/- SEM, ANOVA, P < 0.05). However, there was no significant difference in histology score between rats and opossums following BPDL; histologic changes, such as white blood cell infiltration, acinar cell vacuolation, and focal acinar cell necrosis, were similar. Acinar cell ultrastructural changes after BPDL in both species included dilated endoplasmic reticulum and autophagic vacuole formation. These findings indicate that the early morphologic changes after BPDL in rats are quite similar to those seen early in the course of BPDL-induced acute necrotizing pancreatitis in opossums. As the rat is a more economical and convenient model to study than the opossum, this study supports the use of the rat model to conduct pilot studies of early events in the development of BPDL-induced acute pancreatitis. This study also suggests the potential for investigating mechanisms that may be present in the rat which protect against progressive and fatal acute necrotizing pancreatitis as observed in opossums after longer periods of BPDL.
Acute Disease↗
A new model for study of pancreatic exocrine secretion: the tethered pancreatic fistula rat.
Diversion and recirculation of bile and pancreatic juice in rats are done in studies of pancreatic exocrine secretion. Previously, the modified Bollman cage was used to restrain rats with bile and pancreatic fistulas. To mimic physiologic conditions as closely as possible and to develop a more humane model, we designed a partial-restraint tethering system to study pancreatic exocrine secretion. Eight rats were prepared with biliary pancreatic, and duodenal fistulas, of which five were given enteral supplements via a gastric fistula and three were given saline supplements via a jugular venous line. Catheters exited at the nape of the neck and passed through the hollow of a cable coil that tethered the rat. On the fourth postoperative day pancreatic juice flow and protein output were studied. The tethering system allowed grooming, feeding, and ample mobility. This model of the tethered pancreatic fistula rat is a more human model for studies of pancreatic exocrine secretion in conscious rats, compared with the Bollman cage system of near total restraint.
Animals↗
Increased circulating cholecystokinin in obstruction-induced acute pancreatitis. I. Bile duct obstruction with and without pancreatic duct obstruction.
Bile exclusion from the gut exacerbates pancreatic duct obstruction-induced acute pancreatitis. We hypothesized that obstruction-induced acute pancreatitis involves an increase in circulating cholecystokinin (CCK), as bile and pancreatic juice exclusion from the gut stimulates duodenal CCK release. We studied 54 rats after the following operations: (1) sham operation (n = 18), (2) hepatic bile duct obstruction alone (n = 18), (3) hepatic bile duct and common bile-pancreatic duct obstruction (n = 18). Rats recovered and were killed in subgroups of six rats each at 3, 6, and 18 hr after operation; blood was collected for measurement of plasma CCK and amylase concentrations. Each pancreas was excised, weighed, and processed for histological examination; an acute pancreatitis score was determined. Combined bile and pancreatic duct obstruction induced acute pancreatitis and was associated with a marked increase of circulating CCK concentration. Bile duct obstruction alone did not induce acute pancreatitis but was associated with an increase of circulating CCK of lower magnitude. The time course of circulating CCK increase showed an early peak. These findings support our hypothesis and suggest that CCK plays a role in the pathogenesis of obstruction-induced acute pancreatitis.
Amylases↗
Increased circulating cholecystokinin in obstruction-induced acute pancreatitis. II. Pancreatic duct obstruction with and without bile duct obstruction.
Pancreatic exocrine stimulation by cholecystokinin (CCK) has been implicated in the pathogenesis of experimental acute pancreatitis. Bile exclusion from the gut stimulates duodenal CCK release and exacerbates obstruction-induced acute pancreatitis. Pancreatic and bile duct obstruction increases circulating CCK concentration. We hypothesized that acute pancreatitis induced by pancreatic and bile duct obstruction would be ameliorated when bile was returned to the duodenum. As many small pancreatic ducts drain into the bile duct in rats, preservation of bile flow required the use of a bile shunt. We studied acute pancreatitis and the time course of circulating CCK increase in three groups of rats after: (1) sham operation (dissection, no obstruction), (2) bile and pancreatic duct obstruction, and (3) bile and pancreatic duct obstruction with bile shunt. The rats were killed at 3-, 6-, and 18-hr intervals after operation. Their blood was collected for measurement of CCK, amylase, and bilirubin concentrations. The pancreata were excised, weighed, and processed for histological examination. The shunting of bile back to the duodenum ameliorated the acute pancreatitis along with a simultaneous limitation of the rise in CCK concentration. This suggests that bile duct obstruction, another form of bile exclusion, exacerbates pancreatic duct obstruction-induced acute pancreatitis. The elevation in CCK concentration showed an early peak indicating that the potential role of CCK in the pathogenesis of obstruction-induced acute pancreatitis is predominantly in the early phase of its development.
Acute Disease↗
Accidental intra-arterial drug injection successfully treated with Iloprost.
A 35-year-old drug abuser inadvertently injected adulterated heroin into her left femoral artery and presented with critical ischaemia of her left leg. Treatment with intravenous Iloprost, a stable prostacyclin analogue, combined with Heparin, produced a dramatic improvement in her circulation within 4 h.
Adult↗
Octreotide and cholecystokinin antagonist reduce edema in obstruction-induced acute pancreatitis.
Obstruction-induced acute pancreatitis in rats is associated with increased plasma cholecystokinin (CCK) levels. Duodenal replacement of bile reduces severity of pancreatitis and limits CCK increase. We investigated the role of CCK in the pathogenesis of obstruction-induced acute pancreatitis by pretreating rats with the somatostatin analog octreotide and the CCK antagonist L-364,718. Octreotide inhibits duodenal CCK release, and L-364,718 competitively blocks CCK receptors. We studied 31 rats after (1) sham operation (n = 7), (2) bile and pancreatic duct obstruction (BPDO) (n = 12), (3) BPDO plus octreotide (20 micrograms/kg IP and then 5 micrograms/kg/hr IV) (n = 6), and (4) BPDO plus L-364,718 (1 mg/kg IP and then 0.25 mg/kg/hr IV) (n = 6). Rats were killed after 18 hours. Pancreas weight, acute pancreatitis histology score, and plasma amylase and CCK levels were determined. Octreotide and L-364,718 limited the increase in pancreas weight. Octreotide also limited the rise in plasma CCK levels. These findings suggest that CCK may play a role in the pathogenesis of obstruction-induced acute pancreatitis.
Acute Disease↗
Actinomycosis complicating chronic diverticulitis of the sigmoid colon: a missed association?
The diagnosis and treatment of abdominal actinomycosis is difficult. We report a case of chronic diverticulitis of the sigmoid colon with stricture formation and obstruction, which was complicated by intramural actinomycosis. We suggest that diverticular strictures and actinomycosis may coexist more often than the literature suggests.
Actinomycosis↗
Initial experience of laparoscopic cholecystectomy in a district hospital.
Fifty-five consecutive unselected patients were submitted for laparoscopic cholecystectomy, and the procedure completed laparoscopically in fifty cases. The outcome is presented with particular reference to the duration of surgery, postoperative pain and nausea, the length of hospital stay and the time taken to recover normal activities. This technique is shown to have major advantages over conventional gallbladder surgery for the majority of patients.
Adult↗
A pseudoisochromosome 18q and an isodicentric chromosome 18.
A case of pseudoisochromosome 18q of prezygotic origin and a case of isodicentric chromosome 18 of postzygotic origin are presented to validate the differentiation between a true isochromosome and a pseudoisochromosome. This differentiation may be useful in elucidating the mechanism of the origin of an isochromosome.
Abnormalities, Multiple↗
Phonon characterization of YBa2(Cu1-xAlx)3O7- delta by Raman spectroscopy.
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Journal Article↗
Kartagener's syndrome with normal spermatozoa.
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Adult↗
Double supernumerary isochromosome 9p in myeloproliferative syndrome.
The presence of supernumerary isochromosome 9p in duplicate in about 50% of bone marrow cells of an elderly female patient with myeloproliferative syndrome is reported.
Aged↗
Ameloblastic sarcoma of the mandible: report of case.
A case of ameloblastic sarcoma of the mandible in a 19-year-old man is presented. Pain, paresthesia, and rapidity of growth were features of the lesion. Successful excision was followed by death from secondary hemorrhage.
Adult↗