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Biomedical subjects

G Lemaigre

Publications and source records attributed to G Lemaigre.

At least 37 records · Page 2Linked to original sources
PubMed1992

[Experimental sclerosing cholangitis following intrabiliary injection of formol in the rat].

Our study was aimed at assessing the effect on the biliary epithelium of formol and hypertonic salt serum solutions used as parasiticide for hydatid cysts of the liver in rats. One hundred and forty six rats were administrated an intrabiliary injection of isotonic salt serum (control group), of 20% hypertonic salt serum and of 0.5% and 2% formol solutions. A histological study performed 3 months later did not show any abnormality in the rat control group (n = 11). In the hypertonic salt serum group (n = 14) and 0.5% formol group (n = 12), moderate lesions of biliary epithelium were observed. After a 2% formol injection, a periductal sclerosis was observed in 11 cases out of 16, associated with pseudocirrhosis lesions in 4 cases. A sequential histo-immunochemical study did not show any histological abnormalities in the rat control group (n = 24). In rats which were administrated a 2% formol solution (n = 36), first abnormalities were observed as soon as the 7th day with a IA antigen expression at the biliary epithelium level. Fibrosis lesions were observed after 2 months. After 9 months, the infiltration included only T lymphocytes in direct contact with biliary tracts. A cholangiographic study showed a normal aspect in the rat control group (n = 11) or in rats having received hypertonic salt serum (n = 11), and stenoses of biliary tracts, mainly intrahepatic, in 10 rats out of the 11 of the 2% formol group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Efficacy of long term recombinant interferon-alfa in patients with chronic hepatitis C. A clinical, biological, histological and immunohistological study.

A prospective, non randomized trial was conducted in 22 patients with chronic hepatitis C treated for 6 months with interferon-alfa at the dose of 3 million units three times a week followed by decreasing doses for the following 6 months. Transaminase activity measurements were taken at 2, 6, 12, 18, and 24 months and a liver biopsy was performed at zero and 6 months to assess efficacy. Immunohistochemical study of HLA class I and lymphocyte subsets was performed on the biopsy specimen before and after 6 months of treatment. A complete biological response was observed in 82, 82, 60, 64 and 70 percent of patients at 2, 6, 12, 24 and 36 months, respectively. Four patients relapsed including 2 patients who suddenly stopped taking interferon-alfa. An improvement of histological features was observed in 90 percent of patients for necrosis and in 80 percent of patients for inflammation, with an overall improvement in Knodell's score reaching 85 percent. Immunohistochemical studies showed CD8+ cell infiltration already present in the area of necrosis before treatment. These tests also showed that HLA class I expression by the hepatocyte membranes was increased at 6 months and was identical in patients with or without histological improvement.

Adult↗
PubMed1991

[Adenocarcinoma in heterotopic gastric pancreas].

The development of an adenocarcinoma in heterotopic pancreas of the stomach is uncommon and its diagnosis is difficult. We report the case of a 42 year-old man who was admitted for gastric stasis, related to an antral tumour. He had been treated for Hodgkin's disease by radiation therapy. 16 years ago. Gastrectomy was performed. On light microscopy, the gastric wall was infiltrated by pancreatic ectopic tissue, normal in the submucosa, but dedifferentiated with cytological and architectural criteria of malignancy in the muscular and the serous layers. Malignant transformation of an ectopic pancreas is theoretically possible but is very uncommon. In our case, the role of previous radiation therapy as a promoting factor is discussed.

Adenocarcinoma↗
PubMed1990

Deposition and remodelling of elastic fibres in chronic hepatitis.

A longitudinal study of elastic fibres was conducted in liver biopsies from 21 patients with chronic viral hepatitis. Biopsies were taken at the start of treatment with alpha-interferon, and after 6 months or 1 year of treatment. No elastic fibres could be detected in portal tracts or fibrous septa when inflammation and necrosis were present, whatever the duration of the disease. Once the liver lesions had healed, elastic fibres were synthesized. Fibres were of two types and patterns: at first, they were thin, long and parallel to each other. Later, they were thicker, shorter and tortuous and were closely wrapped around thick bundles of collagen fibres. These findings suggest that the deposition of elastic fibres acts as a marker of healing in chronic active hepatitis and that their remodelling occurs concomitantly with the deposit of large bundles of collagen fibres.

Biopsy↗
PubMed1990

Expression of histocompatibility antigens and characterization of the lymphocyte infiltrate in hyperplastic polyps of the large bowel.

HLA-DR expression, lymphocyte subsets, and the distribution of proliferating cells were studied in hyperplastic polyps from the colorectum. The density of T-cells (CD5+) (mean of cells/mm2 of tissue +/- SEM) was higher in the lamina propria of hyperplastic polyps (64.2 +/- 4.2) than in normal colonic mucosa (36.7 +/- 2.6, P less than .001). The CD4/CD8 ratio was higher in hyperplastic polyps (6.3 +/- 0.9, P less than .0001) and in colonic adenomas (5.9 +/- 0.9, P less than .001) compared with normal mucosa (2.3 +/- 0.2). Lymphocytes of the lamina propria were never Ki-67 positive either in normal mucosa or in hyperplastic polyps or adenomas. The epithelial layer of hyperplastic polyps and of normal mucosa did not express the HLA-DR antigen, whereas pericryptal fibroblasts and most of the leukocytes of the lamina propria were strongly positive for this antigen. In the epithelial layer proliferating cells were localized exclusively in the lower part of epithelial crypts, as was the case in normal mucosa, whereas in adenomas Ki-67-positive cells were present throughout the entire height of the mucosa. Thus, in hyperplastic polyps lymphocytes are increased in the lamina propria, with a predominance of the CD4 subset in close contact with HLA-DR positive pericryptal fibroblasts.

Adenoma↗
PubMed1990

Lymphocyte subsets and HLA-DR expression in normal pancreas and chronic pancreatitis.

In an attempt to study the mechanisms leading to fibrosis in chronic pancreatitis, an in situ immunohistochemical investigation of lymphocytes and of class II major histocompatibility complex expression (HLA-DR) by epithelial cells has been designed. Samples of normal pancreas (n = 8), chronic calcifying pancreatitis (n = 4), chronic obstructive pancreatitis (n = 6), and diffuse fibrosing pancreatitis (n = 6) have been studied. In normal pancreas, T-lymphocytes were rare and were located in the epithelial layer of pancreatic ducts and in the periductal connective tissue. Duct cells were constantly HLA-DR negative. In chronic calcifying pancreatitis and chronic obstructive pancreatitis, T cells were numerous and were located around ducts and in the spreading areas of fibrous septa. In chronic obstructive pancreatitis, the duct cells strongly expressed the HLA-DR antigen. In diffuse fibrosing pancreatitis, fibrous tissue was devoid of lymphocytes and duct cells never expressed the HLA class II antigen. These results suggest that lymphocytes are involved in the fibrosing process occurring in chronic calcifying pancreatitis and chronic obstructive pancreatitis but not in diffuse fibrosing pancreatitis. The significance of de novo expression of HLA-DR antigen by duct cells is discussed.

Adult↗
PubMed1990

Serum apolipoprotein A-I in alcoholic patients with chronic calcifying pancreatitis.

Serum apolipoprotein A-I measurement was compared in alcoholic patients according to presence or absence of chronic pancreatitis and liver fibrosis. Among alcoholic patients without liver disease, apolipoprotein A-I was significantly lower in patients with chronic pancreatitis (157 +/- 70 mg/dl) than in patients without pancreatitis (209 +/- 74 mg/dl, p less than 0.001). In cirrhotic patients, apolipoprotein A-I was lower in patients with chronic pancreatitis (82 +/- 35 mg/dl) than in patients without pancreatitis (102 +/- 45 mg/dl), but this difference was not significant. The decrease of serum apolipoprotein A-I was independent of nutritional parameters whether or not there was cirrhosis. Immunohistochemical study of pancreatic samples with chronic pancreatitis showed that apolipoprotein A-I was located in the pancreatic fibrosis whereas lobules were unstained. This study suggests that apolipoprotein A-I is trapped by the pancreatic extracellular matrix and that this sequestration might explain, in part, the decrease of the serum apolipoprotein A-I.

Adult↗
PubMed1990

Stable circadian mechanisms of toxicity of two platinum analogs (cisplatin and carboplatin) despite repeated dosages in mice.

The toxicities and tissue uptake of cisplatin (CDDP) and carboplatin (CBDCA) vary largely according to the time of injection of a single dose. Repeated dosages may alter the mechanisms involved with such circadian-dependent toxicity. Weekly i.v. injections of CDDP (5 mg/kg) or CBDCA (50 mg/kg) were given over 2 months to 288 male B6D2F1 mice standardized by an alternation of 12 hr of light and 12 hr of darkness at any one of three circadian dosing times (0, 8 or 16 hr after light onset--HALO). Survival; body weight; complete blood cell counts; histologic lesions in kidney, liver, spleen, bone marrow and intestinal tract; platinum concentration in kidney, spleen and colon were determined every 2 weeks throughout treatment. Thrombocytopenia was 10-fold larger following CBDCA as compared with CDDP. Severe bone marrow necrosis was cumulative following CDDP, but reversible following CBDCA. Leukopenia and bone marrow lesions were, respectively, half as severe following the dosing of either drug at 16 HALO compared with 0 or 8 HALO. Cortical tubular necrosis was observed in CDDP-treated mice. It was cumulative and half as extensive after drug dosing at 16 HALO, as compared with 0 or 8 HALO (P less than or equal to .05). Total Pt accumulation in all three tissues was 3- to 4-fold higher following repeated dosages of CDDP as compared with CBDCA. Tissue Pt uptake was halved after CDDP or CBDCA dosing at 16 HALO as compared with 8 HALO (P less than or equal to .01). Dosing either Pt complex at the appropriate time is even more critical if administrations are to be repeated. Mechanisms appear to involve the circadian rhythm-dependent ability of target tissues to take up the drug.

Animals↗
PubMed1990

IL-2 mRNA expression in Tac-positive malignant lymphomas.

Expression of the IL-2 receptor (Tac antigen/CD25) is documented in malignant lymphomas. Because IL-2 is a major lymphocyte growth factor, an IL-2-dependent growth could be involved in the proliferation of Tac-positive lymphomas. Indeed such a mechanism has been demonstrated experimentally for the growth of T-cell lines. To investigate this point in human lymphomas, we used in situ hybridization to analyze the expression of the IL-2 gene in 20 non-Hodgkin's lymphomas, among which 12 expressed the IL-2 receptor. Nine of these were anaplastic large cell lymphomas expressing the Ki-1-related antigen. We here show that IL-2-producing cells are present in all the lymphomas we analyzed. As a mean, there is no significant difference in the percentage of IL-2-producing cells between Tac-positive and -negative lymphomas. However, the level of IL-2 production is highly heterogeneous in both groups, and the highest density of IL-2-producing cells was observed in 2 Tac-positive lymphomas. Simultaneous detection of cellular antigens and of IL-2 mRNA demonstrates that IL-2 is produced by reactive T cells rather than by tumor cells. These results suggest that if IL-2 is involved in the growth of Tac-positive lymphomas, it acts as a paracrine, rather than an autocrine, factor.

Adolescent↗
PubMed1989

Circadian rhythm in toxicities and tissue uptake of 1,2-diamminocyclohexane(trans-1)oxalatoplatinum(II) in mice.

Mechanisms involved in the circadian rhythm in murine tolerance for the new platinum analogue, 1,2-diamminocyclohexane(trans-1)oxalatoplatinum(II) (1-OHP) were sought in 404 male C57BL/6 x DBA/2 F1 mice standardized by 12 h light-12 h dark. A potentially lethal dose of 1-OHP (17 mg/kg i.v.) resulted in 76% long-term survival at 15 h after light onset (HALO) (activity span) as compared to 24% after treatment at 7 HALO (rest span) (chi 2 21.3; P less than 0.001). A total of 204 mice received the same dose of 1-OHP at one of three circadian stages (0, 8, or 16 HALO). No renal toxicity was encountered. Bone marrow and jejunal villi constituted the chief targets of 1-OHP toxicity at this dosage and schedule. Hematological tolerance as gauged by leukocyte counts was optimal when the drug was given at 16 HALO (P from analysis of variance, less than 0.001). Jejunal lesions were less severe after 1-OHP dosing at 16 HALO as compared to 8 HALO (P less than 0.001). Total platinum concentrations were determined in 18 tissues 24 h after 1-OHP dosing. The highest levels of platinum were found in the spleen on day 1 as well as on day 5 following 1-OHP treatment. Despite the fact that the highest platinum concentrations in tissues usually corresponded to drug dosing at 8 HALO, no correlation was documented between such variables and tissue toxicity. Tissue pharmacokinetics of 1-OHP contribute only in part if at all to the circadian rhythm in hematological and jejunal toxicity of this drug.

Animals↗
PubMed1989

Analysis of mucosal bladder leucocyte subpopulations in patients treated with intravesical Bacillus Calmette-Guerin.

Immunohistochemical techniques were used to investigate leucocyte subpopulations in the bladders of patients with superficial transitional cell carcinoma treated with BCG Pasteur. Leucocyte subsets were enumerated with a panel of monoclonal antibodies which included CD3, CD4, CD8, TQ1, Leu7, CD15, HLA-DR, CD25, CD22. We demonstrated in the bladders of patients treated with BCG a particular lymphocyte population; the major subset was an inducer (CD4+, TQ1-) which was activated (CD25+, HLA-DR+) and associated with polymorphonuclear eosinophils. There was neither inducer of suppression nor major cytotoxic/suppressive subsets. CD8+ and NK cells could not be the primary mediators of BCG activity. These data supported the hypothesis of a helper T lymphocyte activity associated with lymphokine production and activation of effector killer cells.

BCG Vaccine↗
PubMed1989

A longitudinal study of histologic and immunohistologic changes in an experimental model of sclerosing cholangitis.

A longitudinal study of intra and extrahepatic bile duct injuries was performed in an animal model of secondary sclerosing cholangitis induced by formalin injection into the common bile duct. Lymphocytic infiltration inside and around the bile ducts occurred seven days after injection. The disease later evolved to a fibrous cholangitis of the small bile ducts. Septal intrahepatic and extrahepatic bile duct involvement became evident three months after formalin injection. The ductular proliferation led to a progressive biliary cirrhosis with portal to portal fibrous septa. After formalin injection, bile duct cells expressed the Ia antigen in the cytoplasm and/or on the membrane of bile duct cells. The intensity of staining did not correlate with the duration or severity of the disease. Lymphocytes infiltrating into and around the bile duct were mainly T-cells. This study suggests that a local cell-mediated immune response to the injection of a toxic agent induces pathological features similar to those of sclerosing cholangitis in man.

Animals↗
PubMed1989

HIV-associated endometritis.

Using immunohistochemical staining, in situ hybridization and a combination of both, we demonstrate here the replication of HIV in the endometrial stroma. Infected cells do not belong to the T-lymphocyte lineage but rather to a monocyte-macrophage cell type. This report suggests a possible relationship between HIV infection and endometritis. Moreover, HIV replication in endometrial tissues could play a role in heterosexual and materno-fetal transmission.

Acquired Immunodeficiency Syndrome↗
PubMed1989

Apolipoprotein AI is a serum and tissue marker of liver fibrosis in alcoholic patients.

The aim of this study was to assess the specific correlation of apolipoprotein-AI to hepatic fibrosis in alcoholic patients. Four hundred eighty two patients were prospectively included with serum measurement of apolipoprotein-AI within 10 days before liver biopsy. Pathologic features were semiquantitatively assessed by two observers. In 28 patients liver biopsy was used for histomorphometric assessment of fibrosis and immunohistochemical labeling of apolipoprotein-AI. Serum apolipoprotein-AI was negatively correlated to semiquantitative score of fibrosis (r = -0.50; p less than 0.001), independently of the scores of steatosis and alcoholic hepatitis (r = -0.44; p less than 0.001) and of the value of serum albumin, bilirubin, and prothrombin time (r = -0.22; p less than 0.001) and independently of the nutritional parameters (r = -0.29; p less than 0.009). The mean value of apolipoprotein-AI decreased according to the grade of fibrosis from 220 +/- 6 mg/dl (mean +/- SEM) to 110 +/- 8 mg/dl. Serum apolipoprotein-AI was negatively correlated to the percentage of fibrosis (r = -0.70; p less than 0.001) in the biopsies morphometrically assessed. The labeling was superimposed to the extracellular matrix. In conclusion, this study shows that decrease of apolipoprotein-AI is a serum and tissue marker of liver fibrosis independently of steatosis, alcoholic hepatitis, liver function tests, and nutritional parameters.

Apolipoprotein A-I↗
PubMed1989

Perisinusoidal cells (Ito-cells) enlargement in a family with myotonic dystrophy.

Two cases are reported, a daughter and her mother who both have myotonic dystrophy with abnormalities of liver function tests and an important perisinusoidal cell enlargement without other pathologic features. In both cases, the myotonic dystrophy was clinically obvious and confirmed by electromyography. No other causes of perisinusoidal cell enlargement were found including vitamin A intake, psoriasis, viral disease or alcoholism. These observations suggest a genetic linkage and that serum test abnormalities could be associated with a perisinusoidal cell change.

Adolescent↗
PubMed1989

Quantitative estimation of the collagen content in normal and pathologic pancreas tissue.

The aims of the study were to measure the collagen content in pancreas using a colorimetric method and to compare the amount of collagen in normal pancreas (11 cases), diffuse fibrosing pancreatitis (17 cases), and chronic calcifying pancreatitis (11 cases). The procedure of fibrosis measurement was based on the selective capacity of two dyes, Sirius red and fast green, to set on collagen and noncollagenous proteins, respectively. After staining of sections, colors were eluted from the sections and the specific absorbance of each eluted dye was read on a spectrophotometer. The collagen content in normal pancreata was 26.5 +/- 7.2 micrograms collagen/mg protein. The amount of collagen increased with the age of patients: the mean value of the patients under the age of 50 was 18.2 +/- 4 micrograms collagen/mg protein whereas the mean value in older patients was 31.9 +/- 8 micrograms collagen/mg protein (p less than 0.01). The value of collagen in pancreas with a diffuse fibrosing pancreatitis was 44.7 +/- 7.5 micrograms collagen/mg protein. This value was significantly different from the collagen content in normal pancreas (p less than 0.001) and in pancreas with a chronic calcifying pancreatitis (77.9 +/- 8 micrograms collagen/mg protein, p less than 0.001). This method permits discrimination between different chronic diseases that can also be differentiated on a histopathologic basis.

Adult↗
PubMed1989

Localization of apolipoprotein A-I and apolipoprotein A-II in human atherosclerotic arteries.

Apolipoprotein A-I and apolipoprotein A-II, the two major protein components of the high-density lipoproteins, were visualized in human arteries using an immunofluorescence technique. Apolipoprotein A-I and apolipoprotein A-II were codeposited into the intima and upper media of normal arteries of atherosclerotic patients. The amount of deposits increased in fatty streaks. In atherosclerotic plaques, apolipoproteins accumulated around the necrotic material. These two apoproteins were present in the extracellular matrix as well as in the foam cells surrounding the atherosclerotic lesions. The concomitant intracellular localization of apolipoprotein A-I and of apolipoprotein A-II in the cytoplasm of foam cells supports the hypothesis that extracellular high-density lipoprotein particles are internalized in the macrophages during the atheromatous process.

Aged↗