Modeling and measurement of electrostatic spray behavior in a rectangular throat of Pease-Anthony venturi scrubber.

This paper presents the simulation and experimental results of the distribution of droplets produced by electrostatic nozzles inside a venturi scrubber. The simulation model takes into account initial liquid momentum, hydrodynamic, gravitational and electric forces, and eddy diffusion. The velocity and concentration profile of charged droplets injected from an electrostatic nozzle in the scrubber under the combined influence of hydrodynamic and electric fields were simulated. The effects of operating parameters, such as gas velocity, diameter of the scrubbing droplets, charge-to-mass ratio, and liquid-to-gas ratio on the distribution of the water droplets within the scrubber, were also investigated. The flux distribution of scrubbing liquid in the presence of electric field is improved considerably over a conventional venturi scrubber, and the effect increases with the increase in charge-to-mass ratio. Improved flux distribution using charged droplets increases the calculated overall collection efficiency of the submicron particles. However, the effect of an electric field on the droplet distribution pattern for small drop sizes in strong hydrodynamic field conditions is negligible. Simulated results are in good agreement with the experimental data obtained in the laboratory.

Comparison of methylene blue-directed biopsies and conventional biopsies in the detection of intestinal metaplasia and dysplasia in Barrett's esophagus: a preliminary study.

BACKGROUND: The diagnostic advantage of methylene blue (MB) chromoendoscopy in Barrett's esophagus is unclear. METHODS: Patients with columnar-lined esophagus (CLE) were enrolled into a prospective, randomized crossover trial of MB-directed biopsy versus conventional biopsy. RESULTS: Forty-seven patients (19 long-segment CLE; 28 short-segment CLE) were enrolled and underwent MB-directed biopsy. Sensitivity and specificity of MB for specialized intestinal metaplasia were 53% and 51%, respectively. Sensitivity and specificity of MB for dysplasia were 51% and 48%, respectively. Thirty-five patients (15 long-segment CLE; 20 short-segment CLE) completed the crossover trial. Relative frequencies for specialized intestinal metaplasia were 73% and 71% from MB-directed and conventional biopsy specimens, respectively (p = 0.73). Relative frequencies for dysplasia were 20% and 18% from MB-directed and conventional biopsy specimens, respectively (p = 0.65). In patients with long-segment CLE, dysplasia was diagnosed in 10 patients with MB and 7 patients with conventional biopsy methods (p = 0.25). The number of biopsy specimens per EGD was greater with MB, which may have influenced the diagnosis. Histologically, the grade of dysplasia was indefinite/low in nearly all of the dysplastic specimens. CONCLUSIONS: Results of MB-directed biopsy were similar to conventional biopsy in detecting specialized intestinal metaplasia and indefinite/low-grade dysplasia. MB was not useful in short-segment Barrett's esophagus.

Modeling and Monte Carlo simulation of TCDD transport in a river.

A one-dimensional water quality model to assess the long-term fate of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in three compartments (water, sediment, fish) of a river has been developed using the literature data on various model parameters. The transient deterministic model with constant or nonrandom parameters is solved numerically by the method of orthogonal collocation, while an analytical solution is developed for the steady-state model. The impact of uncertainty in several model parameters has been studied by means of Monte Carlo simulations assuming that the uncertain parameters are uncorrelated and can be modeled by three probability distributions (uniform, normal and lognormal). For the case of a high TCDD discharge into a small, shallow river, we find that the maximum TCDD contents of water and fish are well below the prescribed safe limits. We also find that the effects of uncertainty on water quality metrics are quite complex or nonintuitive and can be substantial. This is especially true for TCDD in fish, which can be higher by as much as 50-70% than the deterministic predictions, if the parameter uncertainties follow uniform distributions.

Prevention of acetaminophen-induced liver toxicity by 2(R,S)-n-propylthiazolidine-4(R)-carboxylic acid in mice.

The cysteine (Cys) precursor 2(R,S)-n-propylthiazolidine-4(R)-carboxylic acid (PTCA) was shown previously to maintain near normal levels of hepatic GSH and GSSG at 24 hr and to protect against hepatic necrosis and mortality at 48 hr after toxic doses of acetaminophen (APAP) in mice. Studies were performed in C57BL/6 mice to determine: (a) the time course of APAP-induced hepatic sulfhydryl depletion, and (b) the effectiveness of PTCA in preventing APAP-induced decreases in sulfhydryl concentrations at the time of maximal depletion. APAP (400-800 mg/kg in 50% propylene glycol; 2.65-5.29 mmol/kg) and PTCA (1-5 mmol/kg 30 min after APAP) were administered i.p. Hepatic GSH, GSSG, and Cys concentrations were determined by HPLC. Hepatocellular damage was assessed by elevations in serum glutamate-pyruvate transaminase (SGPT) activity and histopathologic examination. APAP and PTCA produced dose-dependent effects. At 4 hr after the highest dose of APAP, hepatic GSH and Cys concentrations were reduced to 5 and 14%, respectively, of values in vehicle-treated controls, and the GSSG concentration was below the sensitivity of the analytical method. At 24 hr, recovery of hepatic sulfhydryls was incomplete, and there was hepatic necrosis with an approximately 100-fold increase in SGPT activity. At the highest dose of PTCA, the concentrations of GSH, Cys, and GSSG at 4 hr after APAP (800 mg/kg) were 66, 116, and 111%, respectively, of vehicle controls. PTCA in doses of 1.75 to 5 mmol/kg attenuated the APAP-induced increases in SGPT activity. It was concluded that the protective effect of PTCA is most likely related to prevention of hepatic sulfhydryl depletion.

The role of alphabeta- and gammadelta-T cells in allogenic donor marrow on engraftment, chimerism, and graft-versus-host disease.

BACKGROUND: We previously characterized a facilitating cell (FC) in mouse marrow that enables engraftment of allogeneic hematopoietic stem cells (HSCs) without causing graft-versus-host disease (GVHD). The FC shares some cell surface molecules with T cells (Thy1+, CD3epsilon+, CD8+, CD5+, and CD2+) but is T-cell receptor (TCR) negative. Historically, depletion of CD3+ or CD8+ cells from rat marrow was associated with an increased rate of failure of engraftment. In this study, we evaluated whether depletion of alphabeta- and gammadelta-TCR(+) T cells from donor marrow would retain engraftment potential yet avoid GVHD. METHODS: Wistar-Furth rats were conditioned with 950 cGy of total body irradiation and transplanted with ACI bone marrow processed to remove either alphabeta-TCR(+), gammadelta-TCR(+), or alphabeta- plus gammadelta-TCR(+) T cells. Recipients were typed for chimerism at 28 days and monthly thereafter. RESULTS: Recipients of marrow depleted of alphabeta- (group A), gammadelta- (group B), or alphabeta- and gammadelta-TCR(+) T cells (group C) engrafted and had an average chimerism level of 73.0+/-8.3%, 92.3+/-9.2%, and 46.3+/-32.8%, respectively. Aggressive T-cell depletion did not remove the FC population (CD8+/CD3+/TCR(-)). Group A and group B both developed GVHD, with a higher incidence of GVHD in group B compared to group A. None of the recipients in group C developed GVHD. CONCLUSIONS: These data demonstrate that depletion of T cells from rat marrow does not impair engraftment of HSCs, indirectly supporting the existence of FCs in rat marrow. Moreover, donor alphabeta- and gammadelta-TCR(+) T cells contribute to GVHD in a nonredundant fashion, although alphabeta-TCR(+) T cells are more potent as the effector cells. Finally, the level of donor chimerism is influenced by the composition of the graft, because recipients of marrow that contain alphabeta-TCR(+) T cells exhibited significantly higher donor chimerism compared to recipients of marrow depleted of both alphabeta- and gammadelta-TCR(+) T cells.

Increased expression of proliferating cell nuclear antigen in liver allograft rejection.

Detection of proliferating cell nuclear antigen is useful for the study of proliferative activity of neoplastic and non-neoplastic lymphoid, parenchymal, and mesenchymal cells. Allograft rejection is associated with the recruitment of circulating cells and their proliferation in the graft. The intrahepatic expression of proliferating cell nuclear antigen on paraffin-embedded liver biopsy specimens (n = 110 from 32 patients) was examined by an avidin-biotin peroxidase method using a monoclonal antibody to proliferating cell nuclear antigen. The percentage of positive nuclei was determined in hepatocytes, biliary epithelium, and lymphocytes. There were four histologic groups: 1, moderate-to-severe rejection (n = 19); 2, mild rejection (n = 28); 3, nonspecific inflammation (n = 45); and 4, donor livers (n = 18). The percentage of positive nuclei was higher in group 1 compared to group 2 (hepatocytes p = 0.01; biliary epithelium p = 0.0007; lymphocytes p = 0.0001), to group 3 (hepatocytes p = 0.0002; biliary epithelium p = 0.0001; lymphocytes p = 0.0001), and to group 4 (for all three locations p < 0.0001). When group 2 was compared to group 3 the results were significant for biliary epithelium (p = 0.0001) and lymphocytes (p = 0.0001), but not for hepatocytes (p = 0.07). We conclude that proliferating cell nuclear antigen expression, especially in lymphocytes, correlates with the severity of histologic rejection. Proliferating cell nuclear antigen expression may be useful in predicting the progression and response to different antirejection therapies.

Bile duct changes in alcoholic liver disease. The Veterans Administration Cooperative Study Group.

The histologic significance of various changes in the bile ductal structures as observed by cytokeratin immunoperoxidase assay was studied in 122 patients with alcoholic liver disease (ALD) as a part of a large Veterans Administration Cooperative Study on alcoholic hepatitis. Four types of morphologic changes in the biliary structures were observed: 1) proliferation of interlobular bile ducts in the portal tracts; 2) marginal bile ductular proliferation at the periphery of the portal tracts; 3) appearance of bile duct type cells ("oval cells") in the liver parenchyma; and 4) metaplasia of bile duct epithelium to cells resembling hepatocytes. These bile ductal changes correlated strongly with liver fibrosis (p = 0.0003; 0.0003; 0.05; 0.0035, for 1, 2, 3, and 4, respectively), cirrhosis (p < 0.0001 for all four parameters), portal inflammation (p < 0.0001 for 1, 2, and 4; p = 0.0024 for "oval cells"), and with overall histologic severity scores (p < 0.0001; p = 0.0001; p = 0.0017; p = 0.0005, respectively). However, these changes did not correlate significantly with fatty change, parenchymal degeneration and necrosis, cellular infiltrate or Kupffer cell hyperplasia, suggesting that they are probably not the direct consequences of liver cell necrosis. Periportal piecemeal necrosis correlated significantly with both portal bile duct (p = 0.0041) and marginal (p = 0.0078) bile ductular proliferation. Among all these changes, only marginal bile ductular proliferation correlated significantly with Mallory bodies present both in the hepatocytes (p = 0.05) and the bile ducts (p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Tumor necrosis factor in alcohol enhanced endotoxin liver injury.

Endotoxin administration causes liver injury. Patients with alcoholic liver disease frequently have portal vein and systemic endotoxemia, and some investigators have suggested that endotoxin plays an etiologic role in alcoholic liver injury. Many of the metabolic effects of endotoxin are mediated by the cytokine tumor necrosis factor (TNF). It was the purpose of this study to determine whether TNF plays a role in ethanol-enhanced endotoxin liver injury. Rats were fed either a diet in which 36% of the calories were from ethanol or an isocaloric control diet. After 6 weeks, groups of 10 rats were intravenously injected with either saline, 1 mg/kg endotoxin, or 30 micrograms/kg of a prostaglandin E1 (PGE1) analogue + 1 mg/kg endotoxin 24 hr prior to sacrifice. Ethanol/endotoxin-treated rats had significantly higher liver enzyme levels (ALT: 1064 +/- 355 IU/liter, AST: 2024 +/- 515 IU/liter) compared with isocaloric/endotoxin controls (ALT: 237 +/- 54 IU/liter, AST: 602 +/- 80 IU/liter). Ethanol/endotoxin rats also had significantly higher peak serum TNF concentrations (992 +/- 200 units/ml) compared with isocaloric/endotoxin controls (344 +/- 96 units/ml). Pretreatment of ethanol/endotoxin rats with PGE1 caused significant attenuation of liver injury (ALT: 267 +/- 64 IU/liter, AST: 612 +/- 77 IU/liter) and a diminished serum TNF response. In contrast to chronic ethanol administration, acute gavage with 2 mg/kg ethanol (30% w/v) followed by intravenous injection of 2 mg/kg endotoxin produced significantly lower peak serum TNF concentrations (401 +/- 76 units/ml) than gavage with distilled water (1152 +/- 208 units/ml).(ABSTRACT TRUNCATED AT 250 WORDS)

Expression of carcinoembryonic antigen in ulcerative colitis, tubular adenomas and hyperplastic polyps: correlations with the degree of dysplasia.

Sections of tubular adenomas (n = 40), ulcertive colitis (n = 97) and hyperplastic polyps (n = 31) were examined by immunoperoxidase staining to carcinoembryonic antigen (CEA) in order to assess its potential diagnostic value in predicting malignant potential of these lesions. We compared the degree of epithelial abnormality in these mucosal specimens with the extent of immunoperoxidase staining for CEA. We found that CEA staining correlated with the degree of epithelial alteration in tubular adenoma and ulcerative colitis groups. Scattered weakly positive staining was found in eight of 31 hyperplastic polyps. High tissue expression of CEA, when combined with histologic dysplasia, may prove to be an additional factor in the evaluation of malignant potential in ulcerative colitis specimens and adenomas.

Alcoholic liver disease: pathologic, pathogenetic and clinical aspects.

Alcoholic liver disease includes steatosis, alcoholic hepatitis and cirrhosis. Other liver diseases of genetic origin, but with a curious association with alcohol intake, are hemochromatosis and porphyria cutanea tarda. The attribution of chronic hepatitis to alcohol intake remains speculative, and the association may reflect hepatitis C infection. Hepatic injury attributed to alcohol includes the changes reported in the fetal alcohol syndrome. Steatosis, the characteristic consequence of excess alcohol intake, is usually macrovesicular and rarely microvesicular. Acute intrahepatic cholestasis, which in rare instances accompanies steatosis, must be distinguished from other causes of intrahepatic cholestasis (e.g., drug-induced) and from mechanical obstruction of the intrahepatic bile ducts (e.g., pancreatitis, choledocholithiasis) before being accepted. Alcoholic hepatitis (steatonecrosis) is characterized by a constellation of lesions: steatosis, Mallory bodies (with or without a neutrophilic inflammatory response), megamitochondria, occlusive lesions of terminal hepatic venules, and a lattice-like pattern of pericellular fibrosis. All these lesions mainly affect zone 3 of the hepatic acinus. Other changes, observed at the ultrastructural level, are of importance in progression of the disease. They include widespread cytoplasmic shedding, and capillarization and defenestration of sinusoids. Progressive fibrosis complicating alcoholic hepatitis eventually leads to cirrhosis that is typically micronodular but can evolve to a mixed or macronodular pattern. Hepatocellular carcinoma occurs in 5 to 15% of patients with alcoholic liver disease. The clinical syndrome of alcoholic liver disease is the result of three factors--parenchymal insufficiency, portal hypertension and the clinical consequences of extrahepatic damage produced by alcohol. At the several phases of the life history of alcoholic liver disease, the individual factors play a different role. The clinical manifestations of alcoholic steatosis are mainly extrahepatic in origin. Those of alcoholic hepatitis reflect mainly parenchymal insufficiency and those of cirrhosis are mainly those of portal hypertension. Alcoholic liver injury appears to be generated by the effects of ethanol metabolism and the toxic effects of acetaldehyde, perhaps the immune responses to alcohol- or acetaldehyde-altered proteins, and questionably enhanced by viral hepatitis. Alcoholic hepatitis may be mimicked histologically, and to a varying degree clinically, by a number of conditions (obesity, diabetes, several drug-induced injuries, jejunoileal bypass, and related "shortcircuiting" of the bowel). Perhaps the most important facet of the hepatotoxicity of alcohol is its enhancement of the effects of a number of other hepatotoxic agents, among which acetaminophen is the prime example.

Carcinoembryonic antigen, alpha 1-antitrypsin, and alpha-fetoprotein in the pancreas of patients with cystic fibrosis.

The ductular accumulation of "abnormal mucus" is the key histologic feature in cystic fibrosis. This material is periodic acid-Schiff positive and diastase resistant, suggesting that it is glycoprotein in nature. We used the avidin-biotin-peroxidase method to identify this material using antibodies to the serum glycoproteins carcinoembryonic antigen, alpha 1-antitrypsin, and alpha-fetoprotein on paraffin sections of pancreas obtained from a total of 21 patients: 9 with cystic fibrosis, 5 with chronic pancreatitis, and 7 controls. The control patients had normal pancreatic histologic findings, no alpha 1-antitrypsin or alpha-fetoprotein was demonstrated, and only the ductular epithelium reacted weakly for carcinoembryonic antigen. The pancreas in pancreatitis showed fibrosis, acinar atrophy, and ectasia of the ducts that contained only a small amount of periodic acid-Schiff-positive material. This material reacted weakly for carcinoembryonic antigen and alpha 1-antitrypsin. The appearance of the pancreas in cystic fibrosis was similar to that in chronic pancreatitis. However, the ducts contained a greater amount of periodic acid-Schiff-positive material, mostly in the form of globules that reacted strongly for carcinoembryonic antigen and alpha 1-antitrypsin and weakly for alpha-fetoprotein, as did the ductular epithelium. This study shows that the periodic acid-Schiff-positive material in cystic fibrosis contains at least the three serum glycoproteins and that the accumulation may represent a possible defect in cellular synthesis, assembly, or transport of glycoproteins in the ducts.

Importance of diabetes in inhibition of pancreatic cancer by streptozotocin.

Previous studies in our laboratory have demonstrated that the beta-cell toxin streptozotocin (STZ) inhibits the development of exocrine pancreatic cancer in the hamster when STZ is administered prior to treatment with the pancreatic carcinogen N-nitrosobis(2-oxopropyl)amine (BOP). Because the administration of STZ leads to diabetes, we wished to determine whether the presence of diabetes was important in the inhibitory effect of STZ on pancreatic carcinogenesis or whether STZ acted through a mechanism unrelated to diabetes, perhaps by a direct toxic effect on tumor precursor cells. Whole pancreas transplantation was used to create a two-pancreas hamster model to test this hypothesis. The study demonstrated that (1) STZ inhibits the induction of pancreatic cancer in the hamster when given prior to BOP and (2) the inhibitory effect of STZ was demonstrable only when diabetes was present. The inhibitory effect of STZ appears to be systemic, related to diabetes, and not a direct effect on the pancreas.

Hemodynamic and electrocardiographic effects of ioversol during cardiac angiography. Comparison with iopamidol and diatrizoate.

We studied the hemodynamic and electrocardiographic responses to left ventriculography and coronary arteriography with three angiographic contrast agents. Two were nonionic agents (ioversol 32% iodine, 60 patients, and iopamidol 37% iodine, 30 patients). The third was a conventional ionic agent (diatrizoate 37% iodine, 30 patients). Cardiovascular hemodynamics and the electrocardiogram were recorded for 5 minutes after left ventricular injection and for 2 minutes after coronary injections. Following left ventriculography, diatrizoate caused a greater increase in cardiac output, left ventricular end diastolic pressure, and corrected QT interval while causing a greater decrease in arterial pressure than did either ioversol or iopamidol, which were indistinguishable from each other. Following left coronary arteriography, diatrizoate caused a significant decrease in heart rate, prolongation of the corrected QT interval, and increase in T wave amplitude. In contrast, neither ioversol nor iopamidol caused significant changes in any electrocardiographic parameters. Adverse reactions were more common with diatrizoate than with either ioversol or iopamidol. There were no recognizable differences in angiographic image quality among the three agents. We conclude that the angiographic performance of ioversol is equivalent to that of iopamidol and that both cause less hemodynamic and electrocardiographic disturbance than diatrizoate.

The interactions of insulin-like growth factor I(IGF-I) with protein-calorie malnutrition in patients with alcoholic liver disease: V.A. Cooperative Study on Alcoholic Hepatitis VI.

Plasma concentrations of insulin-like growth factor I (IGF-I) were measured in 95 alcoholic men with a spectrum of alcoholic liver injury and protein-calorie malnutrition (PCM). Circulating levels of IGF-I were depressed in the alcoholic patients (0.23 +/- 0.02 U/ml; mean +/- S.E.M.) compared to controls (1.0 +/- 0.07, P less than 0.0001). Plasma IGF-I levels declined progressively with falling indices of PCM (P less than 0.001) and correlated especially with the parameters relating to protein deficiency. While the severity of liver dysfunction and histopathologic alterations in the liver also related to plasma IGF-I concentration, partial correlation analysis showed that only PCM correlated significantly with IGF-I levels independent of the other factors. These findings indicate that IGF-I levels reflect nutritional status even in the presence of alcoholic liver disease.

Serum vitamin A deficiency and increased intrahepatic expression of cytokeratin antigen in alcoholic liver disease.

The clinical and histologic significance of cytokeratin antigen expression in various intrahepatic locations was assessed in 57 patients with alcoholic liver disease as part of a large Veterans Administration Cooperative Study of Alcoholic Hepatitis. Cytokeratin antigen was demonstrated in fixed, paraffin-embedded liver tissue by an avidin-biotin peroxidase method using a mixture of two different monoclonal antibodies, AE1 (acidic; 48, 50 and 56.5 kD) and AE3 (basic; 52, 56, 58 and 65 to 67 kD). In contrast to the normal liver, in which only bile duct epithelium was positive, this antibody mixture stained both bile ducts and hepatocytes in pathologic livers. Serum levels of vitamin A showed a significant inverse correlation with the amount of cytokeratin antigen (scale: 0 to 3) in hepatocytes without Mallory bodies (p = 0.001), in Mallory body-containing hepatocytes (p less than 0.0001) and in bile ducts (p = 0.0074). Increased amount of cytokeratin antigen in each of these locations, in turn, correlated directly with the histologic severity of the liver disease. Histologic severity (fibrosis, parenchymal degeneration/necrosis, hepatocyte regeneration and inflammation) was significantly higher in patients when either Mallory bodies (p less than 0.0001) or cytokeratin antigen (p = 0.0021) was present in hepatocytes. Demonstration of cytokeratin antigen in hepatocytes which contained Mallory bodies correlated positively (p = 0.03) with clinical severity of the liver disease as determined by high serum bilirubin and prolonged prothrombin time (Maddrey's discriminant function).(ABSTRACT TRUNCATED AT 250 WORDS)

Bile duct adenomas in heterozygous (MZ) deficiency of alpha 1-protease inhibitor.

A case of bile duct adenomas in association with heterozygous (MZ) deficiency of alpha 1-proteinase inhibitor (API) is presented. The salient features were the presence of large API-containing globules in the adenomatous tissue and only minimally, in granular form, in hepatocytes. alpha 1-Proteinase inhibitor was not demonstrated in portal bile ducts entrapped in the adenomatous tissue or in bile ducts present in the liver parenchyma. Bile duct markers such as cytokeratin and carcinoembryonic antigens were present in the adenomatous tissue and also in the normal bile ducts, but not in the hepatocytes, suggesting that the adenomatous structures are ductular in origin, and probably not from ductular metaplasia of liver cells. Accumulation of API is postulated to be a triggering factor in neoplastic transformation.

Diabetes enhances growth of pancreatic carcinoma cells.

Clinical studies suggest that carcinoma of the pancreas may be more common in patients with chronic diabetes mellitus. To examine the effect of diabetes on growth of pancreatic carcinoma, 5 X 10(5) cultured hamster H2T pancreatic carcinoma cells were implanted into the cheek pouches of streptozocin-diabetic and nondiabetic Syrian hamsters. Tumor size and weight and total tumor DNA content 22 days after implantation were significantly greater in animals with diabetes. Thus streptozocin diabetes appears to promote the growth of pancreatic carcinoma cells in the hamster.

Cytokeratin antigen in BOP-induced pancreatic tumors--implications for histogenesis.

Pancreatic carcinoma induced in the Syrian hamster by the carcinogen N-nitrosobis(2-oxopropyl)amine (BOP) is of interest because of the ductal/ductular morphology of the tumors, which resembles human pancreatic cancer. However, whether hamster tumors arise from pre-existing ductal epithelium or from acinar cells has not yet been determined. The present study shows that a monoclonal antiserum to cytokeratin (an epithelial marker), when applied to normal hamster pancreas sections, stained centroacinar, ductular and ductal epithelium but did not stain acinar cells. We therefore examined pancreatic tissue from hamsters with benign and malignant neoplasms induced by BOP. The antiserum strongly stained the cells of all BOP-induced lesions (cysts, pseudoductules, hyperplasia, dysplasia and carcinomas). No acinar cell staining was observed in BOP-treated pancreas. These findings support the hypothesis that BOP-induced neoplasms arise from ductal epithelium and not from acinar cells.

Immunohistochemical demonstration of alpha-1-proteinase inhibitor in brain tumors.

Using light microscopy and immunoperoxidase methods (PAP), the presence of alpha-1-proteinase inhibitor (API) was studied in seventeen brain tumors and four normal brain samples. The brain tumors included four glioblastomas, five low-grade gliomas, two metastatic lung carcinomas, two acoustic schwannomas, and four meningiomas. Normal brain displayed a finely granular intracytoplasmic staining confined to neuronal cells. Glial cells were negative for API. Fifteen of the 17 brain tumors were positive for API. Only two of five low-grade gliomas were negative for API. Glioblastoma and metastatic tumors exhibited the strongest positivity followed by acoustic neuroma, meningioma, and low-grade glioma. All positive samples exhibited finely granular intracytoplasmic API, and 50% exhibited extracellular API positivity. Metastatic and glioblastoma tumors demonstrated prominent extracellular API staining. Our results support the concept of a local production of API by brain tumors.