Amylase, isoamylase, and lipase activities in cyclosporine-treated rats.
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Biomedical subjects
Publications and source records attributed to M Fabre.
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Radiologic patterns of the liver in nodular regenerative hyperplasia are poorly known. The authors describe the features of the liver observed during ultrasonography, angiography, computed tomography and magnetic resonance imaging in 9 patients with nodular regenerative hyperplasia. Generally the liver appeared normal, occasionally with signs of portal hypertension. However, a pseudotumoral pattern was observed in 2 patients: they had well limited hypoechoic lesions on ultrasonography, and in one patient angiography showed hypervascularity.
This short review deals with the role of the pathologist in a liver transplant program and summarizes the main histopathologic features of liver graft injury. The role of the pathologist is pivotal, first, during diagnostic work-up of patients prior to liver transplantation and then after transplantation in the differential diagnosis of liver graft dysfunction. The histologic features of early graft dysfunction, acute and chronic rejection, viral and bacterial infection and toxic injury are briefly described. The frequency of simultaneous pathologic processes in the transplant patient is emphasized in regard to the need of information exchange between the physician and the pathologist.
We report three cases of nodular regenerative hyperplasia of the liver: the clinical onset of hepatic disease occurred between 24 and 30 months after renal transplantation. Nodular regenerative hyperplasia was associated with peliosis hepatitis in two cases, and with veno-occlusive disease in one case. Two patients developed portal hypertension, but are doing well. The third patient developed jaundice and died of septic shock. We discuss the aetiological role of renal transplantation, cytomegalovirus infection, and azathioprine in the development of nodular regenerative hyperplasia of the liver.
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The aim of this study was to specify the signs and course of patients with a dilated common bile duct without obstruction. We included patients with a dilated common bile duct of more than 12 mm on endoscopic retrograde cholangiography, and we excluded patients with stones, tumor or other visible obstruction. Two hundred and seven patients (8.4 p. 100 of endoscopic retrograde cholangiography) were included. One hundred and nineteen (57.5 p. 100) had undergone cholecystectomy. Sixty-five p. 100 of patients had signs suggesting biliary tract disease, and 78 p. 100 had biological signs of cholestasis. The size of the common bile duct was not different whether the patient had been cholecystectomized (16.2 +/- 0.3 mm.M +/- SEM) or not (16.2 +/- 0.4 mm). Forty-one patients in the non cholecystectomized group had gallbladder stones. Thus, 47 of our 207 patients (23 p. 100) had neither gallbladder stones nor previous cholecystectomy. Endoscopic retrograde cholangiography was completed by endoscopic sphincterotomy in 130 patients, either in the intent of not missing obstruction, or for therapeutic purposes. Follow-up more than one month after endoscopic retrograde cholangiography was available for 159 patients (77 p. 100). The median survival was 73 months. One hundred and ten patients (69 p. 100) were asymptomatic, 36 (23 p. 100) had atypical abdominal pain while 13 (8 p. 100) patients had episodes of biliary colic and/or fever and/or jaundice. During follow-up, an initially unrecognized obstacle was discovered in 8 patients: 5 common bile duct stones, 2 ampullary tumors and one pancreatic tumor.(ABSTRACT TRUNCATED AT 250 WORDS)
HLA-DR and T6 surface antigens are expressed only by Langerhans cells and indeterminate cells in normal human epidermis. We have previously demonstrated that T6 antigens are internalized in Langerhans cells and indeterminate cells by receptor-mediated endocytosis. This process is induced by the binding of BL6, a monoclonal antibody directed against T6 antigens. In the present study, using a monoclonal antibody directed against HLA-DR antigens, on human epidermal cells in suspension, we show that the surface HLA-DR antigens are also internalized by receptor-mediated endocytosis in Langerhans and indeterminate cells. Moreover, using immunogold double labeling, we demonstrate that T6 and HLA-DR antigens are internalized through common coated regions of the membrane of Langerhans or indeterminate cells. The receptor-mediated endocytosis that is induced involves coated pits and vesicles, receptosomes, lysosomes, and also, in Langerhans cells, the Birbeck granules. Thus, T6 antigens, which are considered to be "unusual" or "nonclassical" major histocompatibility complex class I molecules, and the major histocompatibility complex class II molecules, HLA-DR, are internalized in Langerhans and indeterminate cells through common receptor-mediated endocytosis organelles.
Using immunogold staining of a suspension of living human epidermal cells to identify the Langerhans cell membrane-associated antigen T6 (revealed by the monoclonal antibody BL6), we have observed internalization of T6 antigen in Langerhans cells. This phenomenon is at least partly due to receptor-mediated endocytosis involving coated pits, coated vesicles, endosomes, the smooth endoplasmic reticulum, and lysosomes. These ultrastructural results suggest that T6 antigen may be part of a receptor site. Following receptor-mediated endocytosis, the appearance in the cell center of the first labeled Birbeck granules suggests that Birbeck granules could represent T6 intracellular transport organelles carrying T6 from the central part of the cell to an unknown destination.
A minor (non-H-2) graft-vs.-host reaction (GVHR) was induced in adult irradiated (DBA/2 X B10.D2)F1 mice by hematopoietic parental B10.D2 cell grafts. Syngeneic (F1) cell transplantation was performed as control. In one set of experiments T4 plasma level (enzyme linked immunosorbent assay) was systematically followed up in individual GVHR and control mice. Compared to the control, GVHR triggered off a significant and sustained decrease of T4 plasma level. In another set of experiments, TSH plasma levels (RIA) were measured in killed animals. GVHR induced an early elevation of plasma TSH. In a third set of experiments, mice undergoing GVHR received daily injections of L-T4 (0.03, 0.15, or 0.3 microgram/mouse). Compared to the control (saline injected) GVHR mice, T4 supply did not improve GVHR state. No positive effect of the high dose and rather a negative effect of both lower doses especially on glucose plasma concentration, were observed. All these data suggest that thyroid gland is primarily and very early involved in the onset of the GVH disease.
A subset of T6 positive cells was recently separated from normal human cord blood mononuclear cells. It was shown to coexpress HLA-DR and myeloid differentiation antigens (Mo1, MY4). The phenotype and ultrastructure of the cells suggested that these T6 positive cells might be the precursors of the Langerhans cells of the skin. We have previously demonstrated by immunogold labeling techniques that the T6 surface antigen of human Langerhans cells of the skin is internalized in unfixed Langerhans cells or indeterminate cells by a process of receptor-mediated endocytosis. This process involved the formation of coated pits, coated vesicles, endosomes and lysosomes. Following this process, in Langerhans cells, gold labeled Birbeck granules appeared in the cell center often in continuity with endosomes. In the present study, we used an indirect immunogold labeling technique to reveal the T6 antigen present on the surface of living T6 positive cord blood mononuclear cells. We observed the internalization of the T6 surface antigen by a process of receptor-mediated endocytosis similar to that described in Langerhans cells of the skin. This process, however, was not followed by the appearance of intracytoplasmic Birbeck granules.
In earlier papers, we reported that the activity of prolidase (EC 3.4.13.9) increased in the plasma of patients with cirrhosis, while that of serum prolinase (EC 3.4.13.8) was normal and was affected only by necrosis. In this work, we investigated prolinase and prolidase activity during short and long-term CCL4 administration in the rat. After a single dose, prolinase activity increased in serum faster than did prolidase activity and it also decreased more slowly. Within the liver, no significant change in these two enzyme activities was observed during the acute phase of necrosis. During chronic CCl4 intoxication, the rises in prolidase and prolinase activity in rat serum were difficult to interpret, because of the liver necrosis present throughout the experiment. However, within the liver, prolinase activity was not affected, unlike that of prolidase which rose at week 3, reached a maximum value at week 6 (reversible fibrosis) and remained elevated at weeks 10 and 12 (irreversible fibrosis). The increase in prolidase activity was specific for liver and was not observed in other tissues. These results are in agreement with those obtained in humans; they highlight the possible physiological significance of enhanced liver prolidase activity during the fibrotic process.
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The hereditary, hypertrophic interstitial neuropathy which afflicts the trembler mouse manifests itself about two weeks after birth. Consequently, the identification of these mutant mice was not possible before this age, except when double mutants were available. We show that the trembler mice can be easily distinguished from their normal littermates before the clinical symptoms appear by using an HPTLC/densitometry technique that allows the simple and rapid analysis of the polar lipids extracted from one sciatic nerve. The results presented in this paper demonstrate important differences between the polar lipid compositions of sciatic nerves from 8-day-old normal and trembler littermates, whose phenotypes were confirmed by the morphological analysis of the contralateral sciatic nerves. The small amount of material that is needed for this identification makes it possible to use the remaining nerve material for other studies. Furthermore, important differences between the sciatic nerve protein compositions of normal and trembler mice, identified according to their polar lipid composition, were also observed and these differences can, therefore, also be employed for the identification of the mutants before the manifestation of the clinical symptoms of the trembler neuropathy.
The quantitative evolution of 10 polar lipids was examined in the sciatic nerves of normal and trembler mice between the ages of 3 days and 60 days. In normal nerves, the polar lipids accumulated slowly until the age of 9 days. A period of rapid accumulation then took place until 18 days of age, after which the phospholipids plateaued, while the glycolipid content continued to increase at a slower rate. The results obtained for the sciatic nerves of trembler mice show that the accumulation of all the polar lipids studied, except phosphatidylcholine and hydroxysulfatides, is abnormal from the earliest stages of postnatal development, and strongly support the view that the primary disorder in the trembler peripheral nervous system is one of dysmyelination. With the exception of cardiolipin, all the lipids in the trembler nerves stopped accumulating at the age of 18 days. The cerebrosides were the lipids the most affected severely at all ages.
Laser recanalization of occluded femoral or popliteal arteries was performed in 12 patients using a continuous wave neodymium yttrium aluminum garnet (Nd-YAG) laser. The histologic findings of the laser-irradiated arterial segments in two of these patients are reported. The specimens were obtained 2 and 4 weeks after the laser procedure. The laser-irradiated vessel in Patient 1 had been partially recanalized with reduction of the atherosclerotic occlusion from 3 to 1 cm. The lased arterial lumen manifested thermal injury to the inner quarter of the arterial wall with vacuolization and a rim of carbonization occupying 10% of the width of the arterial wall, but without thrombus formation. Histologic examination in Patient 2 revealed no fibrin deposits, atherosclerotic debris or thrombi at the intimal arterial edge. At the crater site, thermal injury was apparent with vacuolization of the intimal fibrous tissue. The histologic sections obtained 4 weeks after the procedure revealed new fibrous intimal tissue without endothelialization in some of the heavily calcified tissue sections. Where the plaques were noncalcified, reendothelialization was noted with only minimal damage to the surrounding tissue. No medial or elastic fiber disruption was seen, and no aneurysmal dilation had occurred. Intimal splitting with a cleft between the tunica media and the intima was noted at the site of previous balloon angioplasty. In conclusion, the follow-up histologic findings 2 and 4 weeks after laser angioplasty in two patients using a specially designed catheter delivery system and cooling blood perfusate revealed thermal injury to the inner quarter of the arterial vessel wall and no evidence of thrombus formation.
A technique which enables good visualization of the membranous ATPase activity of epidermal Langerhans cells is described. The method has the advantage of keeping intact most of the ultrastructural details. It may allow the observation, under pathologic conditions, of ultrastructural modifications in ATPase-negative Langerhans cells still recognizable by their Langerhans cell granules.
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