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M Pauwels

Publications and source records attributed to M Pauwels.

At least 37 records · Page 2Linked to original sources
PubMed1998

Repeat mediastinoscopy in the staging of lung cancer.

OBJECTIVE: Despite technical difficulties due to mediastinal fibrosis, repeat mediastinoscopy can be a valuable tool in the restaging of lung cancer. It provides essential pathological information on mediastinal invasion when selecting patients for surgical resection after induction chemotherapy in stage IIIa disease. The aim of our study was to evaluate the feasibility, sensitivity and accuracy of repeat mediastinoscopy. METHODS: From 1994 to 1997 we performed a repeat mediastinoscopy in 15 patients (13 men, two women) with bronchogenic carcinoma. Their age ranged from 49 to 75 years. (mean 64.7). Seven patients had induction chemotherapy for a non-small cell bronchogenic carcinoma with positive N2 nodes on mediastinoscopy. Four patients had a second primary contralateral lung cancer, one had a locoregional recurrence of bronchogenic carcinoma. The other three had a first mediastinoscopy for other reasons than lung cancer, repeat mediastinoscopy being performed for staging of malignant disease. RESULTS: In all 15 patients it was possible to perform a complete repeat mediastinoscopy. In one patient repeat mediastinoscopy turned out to be false negative, so, in our series, sensitivity was 87.5%, specificity 100% and accuracy 93.7%. CONCLUSION: Previous mediastinoscopy is no contraindication for a repeat one. Repeat mediastinoscopy offers valuable pathological information in restaging of lung cancer.

Aged↗
PubMed1998

Morphological adaptations of human liver peroxisomes in cholestasis.

Part of the bile acid synthesis takes place in peroxisomes. An altered enterohepatic circulation of bile acids might influence peroxisomal beta-oxidation enzymes and peroxisomal morphology. We performed a morphological and morphometric investigation of peroxisomes in liver biopsy samples of eight patients with cholestasis of different origin: graft versus host reaction (n = 1), obstruction of the bile flow (n = 3), and drug-induced cholestatic hepatitis (n = 4). Peroxisomes were identified using catalase cytochemistry. They were regularly shaped and showed individual differences in electron density. A perinuclear distribution was observed in a variable number of hepatocytes in each sample. Morphometric analysis of peroxisomes revealed an increase in numerical density and surface density in all, and a decreased mean diameter in four liver samples. Based on previously obtained data in experimental animals, we hypothesize that the observed alterations in peroxisomal morphology indicate an enhanced metabolic activity of the enzymes in the peroxisomal matrix. Among them are enzymes involved in bile acid synthesis.

Adult↗
PubMed1998

Peroxisome-proliferating effects of fenoprofen in mice.

We report on hepatic effects obtained in vivo by treating mice with different doses of fenoprofen, an arylpropionic acid previously shown to inhibit in vitro peroxisomal very long chain fatty acid oxidation. A strong and dose-related induction of peroxisomal palmitoyl-CoA oxidase, and of carnitine acyltransferase and acyl-CoA hydrolase activities was recorded in liver homogenates of mice fed diets supplemented with different contents [0.01, 0.05, 0.1, or 1% (w/w)] of fenoprofen for 6 d. Peroxisomal glycolate oxidase and mitochondrial butyryl-CoA, octanoyl-CoA, and palmitoyl-CoA dehydrogenases were unaffected or increased. Hepatic catalase activity was significantly increased in mice fed the diet with 0.05 and 0.1% fenoprofen but, surprisingly, was not stimulated in mice fed the 1% fenoprofen-containing diet. A time-related but unequal induction of acyl-CoA oxidases and catalase was observed with the 0.1% fenoprofen diet: at 21 d of treatment, the induction of lignoceroyl-CoA and palmitoyl-CoA oxidase activities were five-fold stronger than that of catalase activity. In mice treated with 1% fenoprofen for up to 6 d, only acyl-CoA oxidase activities were found to be significantly increased. Morphometric analysis of the liver peroxisomes in mice treated with 0.1% fenoprofen evidenced an increase in size, volume density, and surface density along with a reduced ratio between perimeter and area of the peroxisomal profiles. No morphological marker for very long chain fatty acid deposition could be detected in livers from fenoprofen-treated animals. Our findings clearly demonstrate that fenoprofen acts as a peroxisome proliferator in the liver of mice and do not support the occurrence of in vivo reduction of very long chain fatty acid oxidation in liver from treated animals.

Animals↗
PubMed1996

The influence of a pneumoperitoneum on the peritoneal implantation of free intraperitoneal colon cancer cells.

BACKGROUND: In order to test the influence of a pneumoperitoneum on the peritoneal implantation of free intraperitoneal colon cancer cells, 40 male syngeneic WAG rats were at random divided into four groups. METHODS: Group 1 (n = 10) animals underwent a midline laparotomy and 10(4) CC531 colon cancer cells were injected intraperitoneally (IP); in group 2 (n = 10) 10(4) CC531 cells were injected IP without further manipulation; in group 3 (n = 10) a pneumoperitoneum up to 10 mmHg was created after the IP injection of the same amount of CC531 cells. The pneumoperitoneum was maintained for 15 min. Finally in group 4 (n = 10) after the IP injection of 10(4) CC531 cells and after the creation of a pneumoperitoneum, two 14-G IV catheters simulating trocars were introduced in each flank. A follow-up period of 8 weeks was used. Tumor implantation was scored according to the peritoneal cancer index of Eggermont and the index of Chauffert. RESULTS: Tumor nodules were found varying from 60% in groups 1-3 to 50% in group 4. There was no statistical difference between the implantation rate in the four groups. A port-site recurrence was seen in group 4; all the other tumor implants were located in the mesenterium, omentum, internal genitals, or parietal peritoneum. CONCLUSIONS: The presence of a pneumoperitoneum does not enhance the implantation of free intraperitoneal malignant colon cancer cells in the rat, but the presence of a "port" may lead to abdominal-wall metastases.

Adenocarcinoma↗
PubMed1996

Dietary docosahexaenoic acid has little effect on peroxisomes in healthy mice.

NMRI mice were fed diets supplemented with 0.05, 0.2, or 2% (w/w) docosahexaenoic acid (DHA), a polyunsaturated fatty acid present in fish oil, for 3 d, 3 wk, or 3 mon. The doses of DHA were chosen to supply the mice with concentrations of DHA which approximate those that have been reported to be beneficial to patients with peroxisomal disease. Diets containing 0.05 or 0.2% DHA did not change hepatic, myocardial, and renal catalase (EC 1.11.1.6) activity except for a slight but significant increase (to 120%) in myocardial catalase activity in mice treated with the 0.05% DHA diet for 3 mon. A diet with 2% DHA induced myocardial catalase activity to 150% after both 3 d and 3 wk of administration. In the liver of mice fed this diet for 3 wk, hepatic catalase activity was increased to 140% while no induction of palmitoyl-CoA oxidase (EC 1.3.99.3), urate oxidase (EC 1.7.3.3), and L-alpha-hydroxyisovalerate oxidase (EC 1.1.3.a) was observed. With the light microscope, no changes in peroxisomal morphology were visually evaluated in catalase stained sections of liver, myocardium, and kidney of mice fed either diet. Our results show that in healthy mice a low dietary DHA dose (< 0.2%; this corresponds to a dose prescribed to peroxisomal patients) has no effect on several hepatic peroxisomal H2O2-producing enzymes, including the rate-limiting enzyme of the peroxisomal fatty acid beta-oxidation. This may indicate that such a DHA dose will not add a strong load on the often disturbed fatty acid metabolism in the liver of patients with peroxisomal disorders.

Acyl-CoA Oxidase↗
PubMed1996

Morphometric characteristics of human hepatocellular peroxisomes in alcoholic liver disease.

Hepatocellular peroxisomes harbor one of the metabolic pathways for ethanol metabolism (i.e., catalase in the presence of H2O2-generating enzymes). We studied the morphometric characteristics of these organelles in 26 biopsy samples of patients with different alcohol-induced lesions (12 with steatosis, 5 with hepatitis, and 9 with cirrhosis) and compared the findings with those obtained in seven control livers. All 33 human liver biopsy samples were stained for catalase activity to facilitate peroxisomal identification. Morphometric analysis of the peroxisomes was performed on calibrated electron micrographs. The numerical density of the peroxisomes was significantly increased to 183%, whereas the mean peroxisomal diameter (dcircle) revealed a significant decrease to 89%. This resulted in a normal volume density of the peroxisomal compartment, whereas the surface density was significantly induced. Peroxisomal shape was not different between alcoholic and control livers. When alcoholic livers were divided into three subgroups according to histopathological findings, similar morphometric results were obtained when compared with control livers, although significantly was sometimes lost. No differences in peroxisomal characteristics were found among alcoholic subgroups. The mean peroxisomal diameter per human liver (alcoholic and control) was inversely correlated to the numerical density. It is concluded that the peroxisomal adaptation in human alcoholic liver is such as to create an efficient environment for a presumably increased peroxisomal metabolism.

Adult↗
PubMed1996

Female urethral diverticula: a report of 5 cases.

During the last 3 years we treated 5 women with an important urethral diverticulum. In this paper we present their case studies and a literature review. Four patients were treated by vaginal resection of the diverticulum, and in one patient, that underwent periurethral surgery earlier on, the diverticle was approached by a laparotomy. In all these patients the complaints disappeared postoperatively.

Adult↗
PubMed1995

Alterations of peroxisomes in steatosis of the human liver: a quantitative study.

We investigated the hepatocellular peroxisomes in 27 patients with steatosis of the liver by means of catalase cytochemistry, light and electron microscopic study, and morphometry. Seven normal human livers were used as controls. In our patients, fatty liver was mainly associated with alcohol abuse or obesity. Indications for a slight decrease in catalase activity and for a proliferation were found in visual evaluation of the peroxisomes. Morphometric analysis showed a significant decrease in mean peroxisomal diameter (to 87%) and a simultaneous significant elevation to numerical density of the peroxisomes (to 188%); this resulted in a normal volume density and a significant increase to (133%) in surface density. However, individual differences were found. No differences in peroxisomal characteristics were found between fatty livers of different causes. A significant inverse linear correlation between mean peroxisomal diameter and numerical density was found in patients with fatty livers. Because a similar correlation was also found when control data were added to the fatty liver data, we hypothesize that the peroxisomal compartment in human fatty livers is adapted in such a way to permit the same metabolic efficiency as in control livers.

Adult↗
PubMed1995

Peroxisomes in mice fed a diet supplemented with low doses of fish oil.

The influence of low dietary doses (0.1 and 0.8% w/w) of a commercial fish oil preparation on peroxisomes in normal mice was studied and compared to the known strong inductive effects of high (10%) fish oil diets. Low fish oil doses were chosen to supply the mice with a concentration of docosahexaenoic acid, which was beneficial to patients with a peroxisomal disease. Peroxisomes were evaluated by cytochemical, morphometric, and enzymological techniques. The 0.1% fish oil diet had no effect on peroxisomes in liver, heart, and kidney even after prolonged treatment. The 0.8% diet did not change the peroxisomal number nor the catalase (EC 1.11.1.6) activity in the liver. Hepatic peroxisomal beta-oxidation, however, was increased by 50% after 14 d. This was accompanied by reduced peroxisomal size. The 0.8% diet also caused a small increase (+25%) in myocardial catalase activity. No effect was observed in kidneys. Our results indicate that in mice a low (< 0.8%) dietary fish oil dose has no or only a slight effect on hepatic peroxisomal beta-oxidation. This may be of particular interest to patients with a peroxisomal fatty acid beta-oxidation defect and who display a severe deficiency of docosahexaenoic acid--diets supplemented with low fish oil doses will improve the docosahexaenoic acid level without adding a strong load to the disturbed fatty acid metabolism.

Animals↗
PubMed1994

Induction by zinc of specific metallothionein isoforms in human monocytes.

A low-molecular-mass zinc-containing protein was isolated by gel permeation and anion-exchange chromatography of lysates of human monocytes induced with zinc acetate. Characterization by sodium dodecyl sulphate/polyacrylamide gel electrophoresis and amino acid sequencing identified the two major charge-separable fractions and an occasionally occurring third fraction as metallothionein-1, metallothionein-2 and metallothionein-0, respectively. Metallothionein-1 was shown to consist of a mixture of isoforms, confirmed as metallothionein-1e, metallothionein-1g and metallothionein-1l by comparison with cDNA sequences obtained by screening a human monocyte cDNA library. We can find no previous observation in the literature of metallothionein-1g at both the protein and RNA level in a non-tumour cell, and of metallothionein-0 in a non-fetal cell or tissue. Since isoform-specific polymerase-chain-reaction amplification showed the presence of metallothionein-0 mRNA in zinc-induced but not in untreated monocytes, these cells can be used as an in vitro system to investigate the expression of this previously considered fetal isoform.

Adult↗
PubMed1994

Peroxisomes in liver, heart, and kidney of mice fed a commercial fish oil preparation: original data and review on peroxisomal changes induced by high-fat diets.

Male NMRI mice were fed a diet with 10% w/w Beromegan for up to three weeks. Beromegan is a commercial fish (salmon) oil preparation rich in eicosapentaenoic acid and docosahexaenoic acid. Peroxisomal beta-oxidation capacity, catalase activity, and ultrastructural morphometry of the hepatic peroxisomes were investigated. In myocardium and kidney, catalase activity, peroxisomal staining after catalase cytochemistry, peroxisomal morphology, and morphometry (in myocardium) were evaluated. In liver, we found a significant increase in peroxisomal beta-oxidation, catalase activity, and peroxisomal number already after 3 days of dietary treatment. These changes were more pronounced after 3 weeks. Peroxisomal size was not changed. Positive correlations were found between peroxisomal enzyme activities and the number but not the size of the peroxisomes, and between catalase activity and beta-oxidation capacity. The mean peroxisomal diameter per animal was inversely proportional to catalase activity measured in homogenate. In myocardium, catalase activity was increased with duration of fish oil feeding. Peroxisomal staining, number, and size were also increased when compared to controls. In kidney, no alterations were observed. Our results indicate a beneficial effect of a diet supplemented with fish oil on the peroxisomal metabolism in liver and myocardium; it differs from the changes induced by xenobiotic peroxisome proliferation.

Animals↗
PubMed1993

Alterations of hepatocellular peroxisomes in patients with cancer. Catalase cytochemistry and morphometry.

BACKGROUND: Hepatic catalase activity is decreased in patients with malignant diseases, but little is known about the organelles that contain the bulk of catalase: the peroxisomes. METHODS: The authors studied the hepatocellular peroxisomes in patients with malignant diseases by means of catalase cytochemistry, light and electron microscopic study, and morphometry. RESULTS: Under the light microscope, a decrease in catalase staining was observed in 21 of 39 patients with extrahepatic tumors. A peculiar perinuclear concentration of peroxisomes was seen by light microscopic study in 15 of 39 patients and reflected an increase in number in most patients. In one of two hepatoma livers, peroxisomes also showed this perinuclear configuration. Ultrastructural and morphometric analysis of 20 livers of patients with extrahepatic tumors revealed a decreased mean peroxisomal diameter and an increase in number. Electron microscopic study also showed peroxisomes with transparent matrical spots, cytoplasmic invaginations, protrusions, and gastruloid cisternae. In each liver, at least one of these changes was observed. In hepatoma livers, one-third of the peroxisomes revealed empty matrical spots. In one patient, peroxisomes were smaller but more numerous. CONCLUSIONS: Alterations of the peroxisomal compartment are constant findings in the livers of patients with malignant diseases, but individual differences in peroxisomal alterations are frequent.

Adolescent↗
PubMed1993

Peroxisomes in liver, kidney and duodenum of nude mice bearing xenografts of human pancreatic adenocarcinomas.

In the liver, kidney and duodenum of nude mice with xenografts of two human pancreatic adenocarcinomas differing in growth rate, catalase activity was assayed and peroxisomes were studied using catalase cytochemistry and light and electron microscopy. Hepatic and duodenal catalase activity were significantly decreased in tumour-bearing mice. Renal catalase activity was unchanged. At light microscopic level, a decrease in peroxisomal staining was evident in all duodenums and most livers of tumour-bearing mice. Only minor changes were observed in the kidneys. Ultrastructural morphometry of the hepatocellular peroxisomes revealed a decrease in size, volume density and surface density only in mice with fast-growing xenografts. These observations indicate that the two pancreatic adenocarcinomas exerted a different effect on the hepatic peroxisomes, and that catalase activity and peroxisomes in liver and duodenum are more affected than in kidney.

Adenocarcinoma↗