Vacuolar hepatopathies in dogs

Vacuolar hepatopathies include a heterogeneous group of so-called overloading hepatopathies. Their diagnosis is based on histological criteria, such as hepatocyte swelling resulting in cytomegaly with vacuolated and reticulated cytoplasm. Vacuolar hepatopathy is often idiopathic. Its development can be secondary to a simple reactive hepatopathy, and include numerous associated conditions. Endogenous or exogenous hypercorticism is the most common cause of vacuolar hepatopathy in dogs. The frequency and complications of idiopathic vacuolar hepatopathy in Scottish terriers suggest a breed and familial predisposition.Les hépatopathies vacuolaires désignent un groupe assez hétérogène d'hépatopathies dites de surcharge, dont le diagnostic repose sur des critères histologiques comme la ballonisation des hépatocytes, qui entraîne une cytomégalie, la vacuolisation et la réticulation de leur cytoplasme. Les hépatopathies vacuolaires sont souvent idiopathiques. Elles peuvent être le prolongement d'une simple hépatopathie réactive et de nombreuses affections peuvent s'associer à leur développement. Un hypercorticisme endogène ou exogène est la cause la plus fréquente d'hépatopathie vacuolaire chez le chien. Il existe chez le chien de race Scottish terrier une hépatopathie vacuolaire idiopathique dont la fréquence et les complications permettent d'envisager une prédisposition raciale et familiale

Myofibroblasts in Schistosomal Portal Fibrosis of Man

Myofibroblasts, cells with intermediate features between smooth muscle cells and fibroblasts, have been described as an important cellular component of schistosomal portal fibrosis. The origin, distribution and fate of myofibroblasts were investigated by means of light, fluorescent, immunoenzymatic and ultrastructural techniques in wedge liver biopsies from 68 patients with the hepatosplenic form of schistosomiasis. Results demonstrated that the presence of myofibroblasts varied considerably from case to case and was always related to smooth muscle cell dispersion, which occurred around medium-sized damaged portal vein branches. By sequential observation of several cases, it was evident that myofibroblasts derived by differentiation of vascular smooth muscle and gradually tended to disappear, some of them further differentiating into fibroblasts. Thus, in schistosomal pipestem fibrosis myofibroblasts appear as transient cells, focally accumulated around damaged portal vein branches, and do not seem to have by themselves any important participation in the pathogenesis of hepatosplenic schistosomiasis

Hepatic Connective Tissue Changes in Hepatosplenic Schistosomiasis

Submitted by Ana Maria Fiscina Sampaio ([email protected]) on 2016-06-28T16:32:17Z No. of bitstreams: 1 Andrade ZA Hepatic connective....pdf: 7948561 bytes, checksum: 3b24d3ddbb617efb6ac86109b90a3a94 (MD5)Approved for entry into archive by Ana Maria Fiscina Sampaio ([email protected]) on 2016-06-28T16:45:40Z (GMT) No. of bitstreams: 1 Andrade ZA Hepatic connective....pdf: 7948561 bytes, checksum: 3b24d3ddbb617efb6ac86109b90a3a94 (MD5)Made available in DSpace on 2016-06-28T16:45:40Z (GMT). No. of bitstreams: 1 Andrade ZA Hepatic connective....pdf: 7948561 bytes, checksum: 3b24d3ddbb617efb6ac86109b90a3a94 (MD5) Previous issue date: 1992Made available in DSpace on 2016-07-07T11:39:45Z (GMT). No. of bitstreams: 3 Andrade ZA Hepatic connective....pdf.txt: 27976 bytes, checksum: 8f44ee0f0bbedabeccdda3c11ac8809f (MD5) Andrade ZA Hepatic connective....pdf: 7948561 bytes, checksum: 3b24d3ddbb617efb6ac86109b90a3a94 (MD5) license.txt: 2991 bytes, checksum: 5a560609d32a3863062d77ff32785d58 (MD5) Previous issue date: 1992Fundação Gonçalo Moniz, Centro de Pesquisas Gonçalo Moniz. Salvador, BA, BrasilRoberto Santos Central Hospital. Salvador, BA, BrasilInstitut Pasteur. Lyon, FranceInstitut Pasteur. Lyon, FranceDestruction of intrahepatic portal vein branches with dispersion of smooth muscle cells into the periportal fibrosis and preservation of arterial and ductal structures were the main characteristic findings seen in 66 surgical liver biopsies from patients with the hepatosplenic form of schistosomiasis. Besides these diagnostic features, the present histologic, immunocytochemical, and ultrastructural study revealed the presence of a complex matrix forming the portal and septal fibrosis in advanced schistosomiasis. There was marked hyperplasia of elastic tissue, presence of several collagen isotypes (I, III, procollagen III, IV, and V), actin. desmin, fibronectin, and laminin in a richly vascularized connective tissue. Signs of multifocal matrix (collagen) degradation were observed both at light and electron microscopic levels, suggesting a predominance of a fibrolytic process, at the time parasite-related lesions had almost disappeared. The latter findings are related to the involution of periportal fibrosis now being observed in patients who have undergone antischistosomal chemotherapy. They exemplify morphologic changes connected with chronic collagen degradation in human schistosomiasis that are similar to those first seen in experimental material. Evidence of either persistent or active chronic hepatitis was seen in several cases but its etiology could not be determined

Reversibility of cardiac fibrosis in mice chronically infected with Trypanosoma cruzi, under specific chemotherapy

This investigation was performed to verify the effect of specific chemotherapy (Benznidazole or MK-346) on the inflammatory and fibrotic cardiac alterations in mice chronically infected with the strains 21 SF (Type II) and Colombian (Type III) of Trypanosoma cruzi. To obtain chronically infected mice, two groups of 100 Swiss mice each, were infected with either the 21 SF or the Colombian strain (2x 10 [raised to the power of] 4 and 5x 10 [raised to the power of] 4 blood forms respectively). The rate of morality in the acute phase was of 80% for both groups. Twenty surviving mice chronically infected with the 21 SF strain and 20 with the Colombian strain were then divided in treated and untreated groups. Excluding those that died during the course of treatment, 14 mice chronically infected with the 21 SF strain and 15 with the Colombian strain were evaluated in the present study. Chemotherapy was performed with Benznidazole (N-benzil-2-nitro-1-imidazolacetamide) in the dose of 100mg/k.b.w/day, for 60 days, or with the MK-436(3(1-methyl-5 nitroimidazol-2-yl) in two daily doses of 250 mg/k.b.w, for 20 days. Parasitological cure tests were performed (xenodiagnosis, haemoculture, subinovulation of the blood into newborn mice), and serological indirect immunofluorescence test. The treated and untreated mice as well as intact controls were killed at different periods after treatment and the heart were submitted to histopathological study with hematoxilineosin and picrosirius staining; ultrastructural study; collagen immunotyping, fibronectin and laminin identification by immunofluorescence tests. Results: the untreated controls either infected with 21 SF or Colombian strain, showed inflammatory and fibrotic alterations that were mild to moderate with the 21 SF strain and intense with the Colombian strain. Redpicrosirius staining showed bundles of collagen in the interstitial space and around cardiac fibers. Increased deposits of mitritial components and collagen fibers, macrophages and fibroblasts appeared at the ultra structural examination. Deposits of fibronectin, laminin, pro-III and IV collagens were seen, most intense in those infected with the Colombian strain. Treated nice, parasitologically cured, presented clear-cut regression of the inflammatory lesions and of the interstitial matrix thickening. Mice infected with the Colombian strain and treated with MK-436, was parasitologically cured in 5/6 cases and showed mild inflammatory infiltration and fibrosis. The mice treated with Benznidazole (Colombian strain) did not cure and showed moderate fibrosis and inflammation. Treatment of the nice infected with the 21 SF with Benznidazole determined parasitological cure of all animals, that showed mild inflammation and fibrosis of the myocardium. The cured mice of all groups and treated but uncured showed collagen degradation at electronmicroscopy and decrease of immunofluorescence pattern of the matrix

Nucleic acid polymer REP 2139 and nucleos(T)ide analogues act synergistically against chronic hepadnaviral infection in vivo in Pekin ducks

International audienc

Action of colchicine on hepatic schistosomal granuloma.

Submitted by Ana Maria Fiscina Sampaio ([email protected]) on 2012-10-23T16:45:45Z No. of bitstreams: 1 Andrade ZA Action of colchicine on ....pdf: 620251 bytes, checksum: e885f572b54948d6a57cd79816dd2716 (MD5)Made available in DSpace on 2012-10-23T16:45:45Z (GMT). No. of bitstreams: 1 Andrade ZA Action of colchicine on ....pdf: 620251 bytes, checksum: e885f572b54948d6a57cd79816dd2716 (MD5) Previous issue date: 1990Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, BrasilFundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, BrasilFundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, BrasilFundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, BA, BrasilAmorphous material and altered collagen fragments within dilated secretory vesicles and cisternae of fibroblast cytoplasm were the main ultrastructural changes seen in hepatic periovular granulomas formed in mice infected with Schistosoma mansoni and treated with colchicine. Despite promoting ultrastructural changes in the fibroblasts found in hepatic periovular granulomas, colchicine administration to infected mice did not significantly change the light microscopic appearance of the hepatic schistosomal lesions, did not diminish the amount of total hepatic collagen, and did not change the collagen isotypes in the granulomas, as observed after a comparative study with non-colchicine treated infected control mice. When administered to mice two weeks after curative treatment of schistosomiasis with praziquantel, colchicine did not seem to increase extracellular collagen degradation or to induce a more rapid resorption of hepatic periovular granulomas, although still promoting ultrastructural alterations in fibroblasts

Ischemia Induces Early Expression of a New Transcription Factor (6A3-5) in Kidney Vascular Smooth Muscle Cells: Studies in Rat and Human Renal Pathology

Acute renal failure, characterized by rapid decline in glomerular filtration rate, is a major cause of morbidity and mortality. During the evolution of renal diseases chronic ischemia develops. Indeed, acute or chronic renal failure may occur as a result of renal ischemia, which induces cells to dedifferentiate, proliferate, or become apoptotic. In this study, we have investigated the expression of a newly identified transcription factor, 6A3-5, under in vitro and in vivo conditions. Proliferating vascular smooth muscle were investigated in response to different mitogenic agents. The 6A3-5 expression was then studied in ischemic rat kidney, induced by renal pedicle clamping, followed, or not, by reperfusion. Subsequently human renal biopsies from early kidney grafts and chronic renal diseases were also investigated for 6A3-5 protein expression by immunohistochemistry. In vitro study shows an over-expression of 6A3-5 following 2 to 4 hours stimulation by serum or Angiotensin II, of rat proliferating aortic smooth muscle cell. Moreover, in vivo study shows that this new protein is over expressed in rat kidney submitted to 45 minutes ischemia. An anti-6A3-5 antibody shows the protein to be expressed in smooth muscle cells of the arterioles and intermediate size arteries, in mesangial cells and interstitial myofibroblasts. In human biopsies of early kidney grafts and renal disease, the same up-regulation of 6A3-5, as in acute ischemic situation, is observed. This 6A3-5 expression is intimately associated with α-smooth muscle cell actin expression in mesangial cells, arteriolar smooth muscle cells as well as interstitial myofibroblasts. Transcription factor 6A3-5 could potentially be a novel early vascular marker of acute and chronic renal ischemic stress implicated in tissue remodeling

Enhanced magnitude and breadth of neutralizing humoral response to a DNA vaccine targeting the DHBV envelope protein delivered by in vivo electroporation

AbstractWe explored in the duck hepatitis B virus (DHBV) model the impact of electroporation (EP)-mediated DNA vaccine delivery on the neutralizing humoral response to viral preS/S large envelope protein. EP enhanced the kinetics and magnitude of anti-preS response compared to the standard needle DNA injection (SI). Importantly, EP dramatically enhanced the neutralizing potency of the humoral response, since antibodies induced by low DNA dose (10μg) were able to highly neutralize DHBV and to recognize ten antigenic regions, including four neutralization epitopes. Whereas, SI-induced antibodies by the same low DNA dose were not neutralizing and the epitope pattern was extremely narrow, since it was limited to only one epitope. Thus, EP-based delivery was able to improve the dose efficiency of DNA vaccine and to maintain a highly neutralizing, multi-specific B-cell response, suggesting that it may be an effective approach for chronic hepatitis B therapy at clinically feasible DNA dose