Relevant bibliographies by topics / Hepatic and Periportal fibrosis

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  2. Dissertations / Theses
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Academic literature on the topic 'Hepatic and Periportal fibrosis'

Author: Grafiati
Published: 19 February 2023

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Journal articles on the topic "Hepatic and Periportal fibrosis"

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Ferraz, Álvaro Antônio Bandeira, Pedro Cavalcanti de Albuquerque, Edmundo Pessoa de Almeida Lopes, José Guido Corrêa de Araújo Jr., Anderson Henrique Ferreira Carvalho, and Edmundo Machado Ferraz. "The influence of periportal (pipestem) fibrosis on long term results of surgical treatment for schistosomotic portal hypertension." Arquivos de Gastroenterologia 40, no. 1 (March 2003): 4–10. http://dx.doi.org/10.1590/s0004-28032003000100002.

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AIM: To evaluate the degree of influence that periportal fibrosis has on clinical development and the long term results of surgical treatment on patients with hepatic-splenic schistosomiasis with previous gastrointestinal hemorrhages. METHODS: During the period of 1992-1998, 111 patients underwent surgical treatment for the treatment of hepatic-splenic schistosomiasis with previous gastrointestinal hemorrhages. The degree of fibrosis was classified as: degree I - the portal spaces show a rich increase of young connective cells, a slight collagen production and a varying presence of inflammatory infiltrate. The periportal blade unchangeable (29/111); degree II - there is an expansion of the connective tissue with the emission of radial collagen septa, producing a star shaped aspect (38/111); degree III - the connective septa form bridges with other portal spaces or with the vein, with evident angiomatoid neo-formation (44/111). CONCLUSION: The patients with periportal fibrosis degree I present recurrent hemorrhages statistically less than patients with periportal fibrosis degrees II and III, and that the intensity of the periportal fibrosis is not the only pathophysiological factor of the esophageal varices, gastric varices, prevalence of post-operative portal vein thrombosis and hematological and biochemical alterations of the patients with pure mansoni schistosomiasis.
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Bindseil, Erling, Tine Iburg, Maria H. Hurst, and Maria V. Johansen. "Distinguishing periportal fibrosis from portal fibrosis in hepatic schistosomiasis." Trends in Parasitology 20, no. 8 (August 2004): 361–62. http://dx.doi.org/10.1016/j.pt.2004.05.009.

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Ruiz-Guevara, Raiza, Belkisyolé Alarcón de Noya, Sharon Kay Valero, Pablo Lecuna, Miguel Garassini, and Oscar Noya. "Clinical and ultrasound findings before and after praziquantel treatment among Venezuelan schistosomiasis patients." Revista da Sociedade Brasileira de Medicina Tropical 40, no. 5 (October 2007): 505–11. http://dx.doi.org/10.1590/s0037-86822007000500003.

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Abdominal ultrasound can be a useful tool for diagnosing periportal fibrosis related to Schistosoma mansoni infection, and also for planning and monitoring the evolution of hepatic morbidity following control measures. We evaluated the standardized ultrasound methodology proposed by the World Health Organization for detecting periportal fibrosis and portal hypertension, among patients from an endemic area in Venezuela, and the impact of praziquantel treatment 3-5 years later. After chemotherapy, complete reversal of periportal lesions was observed in 28.2% of the cases and progression of the disease in 5.1%. Improvement in the hepatic disease started with a reduction in the periportal thickening followed by a decrease in the size of the left hepatic lobe, spleen and mesenteric and spleen veins. Ultrasound confirmed the clinical findings after chemotherapy among the patients with reversal of the disease. However, in patients with more advanced disease, these findings were contradictory. There was no correlation between evolution of the disease seen on ultrasound and age, intensity of infection or serological findings.
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Christen, Urs, Edith Hintermann, Selina Christen, and Monika Bayer. "Activation of hepatic stellate cells during fibrosis: Comparison of the CYP2D6 model for autoimmune hepatits and CCl4 injection (130.2)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S227. http://dx.doi.org/10.4049/jimmunol.178.supp.130.2.

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Abstract Only little is known about the mechanisms of periportal fibrosis in the pathogenesis of human autoimmune hepatitis. We used the virus induced CYP2D6 model system to investigate the activation of hepatic stellate cells (HSC) and the kinetics of fibrosis in comparison with the CCl4-induced fibrosis model. CYP2D6 transgenic mice express the human Cytochrome P450 in the liver and develop liver damage upon Adenovirus-CYP2D6 infection. In the CYP2D6 model we found mostly subcapsular fibrosis resulting in the fusion of individual lobules (Sirius Red, Collagen I). At 10–12 weeks post-infection, weak periportal fibrosis became apparent. In contrast, in CCl4-treated mice the kinetic of extracellular matrix deposition was accelerated resulting in periportal fibrosis after 3–4 week of CCl4 administration. At later times, fibrosis was much more pronounced in CCl4-treated mice compared to virus-infected CYP2D6 mice but subcapsular fibrosis was not as dominat. Activation of HSCs could be detected by staining for α-smooth muscle actin (αSMA) in liver sections of both CCl4-treated mice and virus-infected CYP2D6 mice. In addition, isolation of HSCs revealed an enhanced activation status (decreased amount of oil droplets, de novo αSMA expression) in CCl4-treated mice and virus-infected CYP2D6 mice. Our data indicate that virus-infected CYP2D6 mice display subcapsular and periportal fibrosis that correlates with an activation of HSCs similar to CCl4-induced fibrosis. Thus, the CYP2D6 mouse is a good model system to further investigate the molecular mechanisms involved in fibrotic events during autoimmune hepatitis.
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Thompson, Michael D., Alaina Derse, Jeremie LA Ferey, Michaela Reid, Yan Xie, Miranda Christ, Deyali Chatterjee, et al. "Transgenerational impact of maternal obesogenic diet on offspring bile acid homeostasis and nonalcoholic fatty liver disease." American Journal of Physiology-Endocrinology and Metabolism 316, no. 4 (April 1, 2019): E674—E686. http://dx.doi.org/10.1152/ajpendo.00474.2018.

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Studies show maternal obesity is a risk factor for metabolic syndrome and nonalcoholic fatty liver disease (NAFLD) in offspring. Here we evaluated potential mechanisms underlying these phenotypes. Female C57Bl6 mice were fed chow or an obesogenic high-fat/high-sucrose (HF/HS) diet with subsequent mating of F1 and F2 female offspring to lean males to develop F2 and F3 generations, respectively. Offspring were fed chow or fibrogenic (high transfat, cholesterol, fructose) diets, and histopathological, metabolic changes, and bile acid (BA) homeostasis was evaluated. Chow-fed F1 offspring from maternal HF/HS lineages (HF/HS) developed periportal fibrosis and inflammation with aging, without differences in hepatic steatosis but increased BA pool size and shifts in BA composition. F1, but not F2 or F3, offspring from HF/HS showed increased steatosis on a fibrogenic diet, yet inflammation and fibrosis were paradoxically decreased in F1 offspring, a trend continued in F2 and F3 offspring. HF/HS feeding leads to increased periportal fibrosis and inflammation in chow-fed offspring without increased hepatic steatosis. By contrast, fibrogenic diet-fed F1 offspring from HF/HS dams exhibited worse hepatic steatosis but decreased inflammation and fibrosis. These findings highlight complex adaptations in NAFLD phenotypes with maternal diet.
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Andrade, Zilton A., and Ediriomar Peixoto. "Pathology of periportal fibrosis involution in human schistosomiasis." Revista do Instituto de Medicina Tropical de São Paulo 34, no. 4 (August 1992): 263–72. http://dx.doi.org/10.1590/s0036-46651992000400001.

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Optical and electron microscopical evidences of focal matrix degradation were frequently seen in liver sections of periportal fibrosis caused by schistosomiasis mansoni in man. The material came from 14 wedge hepatic biopsies taken from patients with chronic advanced hepatosplenic disease and undergoing operations for the relief of portal hypertension. Besides the presence of focal areas of rarefaction, fragmentation and dispersion of collagen fibers, the enlarged portal spaces also showed hyperplasia of elastic tissue and disarray of smooth muscle fibers following destruction of portal vein branches. Eggs were scanty in the tissue sections, and matrix degradation probably represented involuting changes related to the progressive diminution of parasite-related aggression, which occurs spontaneously with age or after cure by chemotherapy. The changes indicative of matrix degradation now described are probably the basic morphological counterpart of periportal fibrosis involution currently being documented by ultrasonography in hepatosplenic patients submitted to curative chemotherapy.
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Abou Basha, L. M. "Hepatic fibrosis due to fascioliasis and/or schistosomiasis in Abis 1 village, Egypt." Eastern Mediterranean Health Journal 6, no. 5-6 (December 15, 2000): 870–78. http://dx.doi.org/10.26719/2000.6.5-6.870.

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An epidemiological study of fascioliasis and/or schistosomiasis was conducted in Abis 1 village. Stool specimens were collected from 2492 individuals and examined. Fascioliasis, alone or combined with schistosomiasis, was more prevalent among children aged between 5 years and 15 years than in adults. Serum procollagen III peptide [PIIIP]levels were determined as an indicator of active fibrosis, and liver histopathology and ultrasonography used as indicators of established fibrosis. PIIIP levels were significantly higher in children than in adults, and in mixed infections than in fascioliasis alone. In adults, fibrosis around granulomata detected by histopathology and grade 3 periportal fibrosis detected by sonography were encountered more frequently in dual than in single infections.
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Sebastian, Kimberley, Rebecca C. Smedley, Alexander Bartel, and Matti Kiupel. "Patterns of Lymphocytic Infiltrates Can Differentiate Feline Hepatic Lymphoma from Lymphocytic Portal Hepatitis." Veterinary Sciences 10, no. 2 (February 7, 2023): 127. http://dx.doi.org/10.3390/vetsci10020127.

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Hepatic lymphoma is poorly characterized in cats and differentiating between inflammation and lymphomas is often difficult. The diagnosis of hepatic lymphoma in humans relies on recognition of specific patterns of lymphocytic infiltrates and clonality testing of antigen receptors. Herein, we defined similar patterns of lymphocytic infiltrates in hepatic biopsies of cats and correlated them with clonality to determine which patterns are predictive of lymphoma. A retrospective study was performed on surgical biopsies from 44 cats. The immunophenotype was characterized using CD3 and CD20 on all 44 samples. All 44 samples were tested using PCR for T-cell receptor gamma-gene rearrangements. PCR for immunoglobulin heavy chain gene rearrangements was performed on 24 of these cats. Four patterns of lymphocytic infiltrates were characterized: (1) tightly periportal, (2) periportal and centrilobular, (3) nodular, and (4) periportal with sinusoidal extension. Other histomorphologic features (fibrosis, biliary hyperplasia, bile ductopenia, bile duct targeting, hepatic hematopoiesis, lipogranulomas, lymphonodular aggregates, other inflammatory cells) were also evaluated. The sensitivity and specificity of the lymphocytic patterns to diagnose lymphomas were determined using Bayesian Hui–Walter analysis (BLCM) against clonality results. Lymphocytic patterns 2, 3, and 4 accurately diagnosed hepatic lymphomas with a sensitivity and specificity of 82% (CI 95%: 0.65, 0.96) and 77% (CI 95%: 0.54, 1.00), respectively. None of the other microscopic features evaluated were predictive of a lymphoma or inflammation. Our study identified specific patterns of lymphocytic infiltration that differentiate feline hepatic lymphoma from inflammation while other histologic features were not associated with an accurate diagnosis.
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Andrade, Zilton A., Ana Paula Baptista, and Thaynã Souto Santana. "Remodeling of hepatic vascular changes after specific chemotherapy of schistosomal periportal fibrosis." Memórias do Instituto Oswaldo Cruz 101, suppl 1 (October 2006): 267–72. http://dx.doi.org/10.1590/s0074-02762006000900041.

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Lee, Myung Hwan, Hyun Joo Shin, Haesung Yoon, Seok Joo Han, Hong Koh, and Mi-Jung Lee. "Periportal thickening on magnetic resonance imaging for hepatic fibrosis in infantile cholestasis." World Journal of Gastroenterology 26, no. 21 (June 7, 2020): 2821–30. http://dx.doi.org/10.3748/wjg.v26.i21.2821.

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Dissertations / Theses on the topic "Hepatic and Periportal fibrosis"

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Probert, Philip Michael Evan. "Refining and replacing models of hepatocytes and periportal fibrosis." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2700.

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The liver plays an important role in drug toxicity, in part through its significant expression of drug-metabolising enzymes. For this reason, liver cells are often used in toxicity screening. Chronic liver injury is also a growing health concern, but its study in-vivo is limited by the severity of the bile duct ligation (BDL) animal model. In investigating ways to replace animals as a source of liver cells for toxicity screening and reduce and refine the BDL model, rat AR42J-B-13 (B-13) cells have been examined as an alternative to primary hepatocytes and chemical alternatives to BDL have been examined respectively. B-13 cells were readily converted by glucocorticoid treatment to hepatocyte-like (B-13/H) cells, which expressed functional CYP1A and CYP3A sub-families whose expression could be induced in response to prototypical inducers. CYP2B1 could be induced at mRNA but not protein level. The CYP1A2 gene in B-13 cells was disrupted/non-functional, however stable introduction of human CYP1A2 showed B-13 cells could be humanised and used for assessment of bioactivation-dependent genotoxins. Drug transporter mRNA expression was low in B-13 and B-13/H cells, but HNF4α overexpression enhanced transporter mRNA expression and function in B-13/H cells. The chronic administration of methapyrilene and α-naphthylisothiocyanate in rats and mice respectively, caused liver injury qualitatively equivalent to that seen after BDL but without the associated mortality or severity seen with BDL. These data suggest that B-13/H cells could be used as an alternative to primary hepatocytes for drug toxicity screening. Chronic administration of methapyrilene and α-naphthylisothiocyanate could be used as alternative less severe models of periportal fibrosis in rats and mice respectively. Use of B-13/H cells would reduce the number of animals required for hepatocyte derivation and through refinement of the BDL model of periportal fibrosis, fewer rodents would be subject to the associated complications and high mortality rate of BDL.
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Vyas, Samir Kumar. "Stromelysin-1 and hepatic stellate cells." Thesis, University of Southampton, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.242487.

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Kawser, Choudhury Ali. "Regulation of secretion of #alpha#-2 macroglobulin by hepatic lipocytes in relation to hepatic fibrosis." Thesis, University of Southampton, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.240644.

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Thompson, Kerry C. "The expression and function of interleukin-10 in liver injury." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285873.

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Ramachandran, Prakash. "Identification and characterisation of the restorative hepatic macrophage." Thesis, University of Edinburgh, 2014. http://hdl.handle.net/1842/9555.

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Long thought to be irreversible, it is now clear that liver fibrogenesis is a dynamic process, with scar tissue capable of being remodelled as well as deposited. Macrophages have been shown to have a critical role in both liver fibrogenesis and fibrosis resolution. Whilst previous work has identified a Ly-6Chi hepatic macrophage population, derived from recruitment of inflammatory monocytes, as being the main pro-fibrogenic population, the nature and phenotype of the pro-resolution macrophage subset is unknown. In this thesis, I sought to identify and characterise this restorative hepatic macrophage. I established a reversible murine model of liver fibrosis using CCl4. At the time of initiation of fibrosis regression, Ly-6Clo CD11bhi F4/80int hepatic macrophages represented the most numerous macrophage population and the principal expresser of matrix degrading MMP enzymes. Depletion of this population in CD11b-diphtheria toxin (DTR) mice prevented fibrosis resolution. Subsequent, adoptive transfer and in situ labelling experiments, demonstrated that this restorative macrophage population derives from inflammatory monocytes, a common origin to the pro-fibrotic Ly-6Chi hepatic macrophage subset, indicating a switch in macrophage phenotype in situ to form the restorative phenotype. Characterisation of FACS-sorted restorative and pro-fibrogenic liver macrophage subsets using gene expression profiling demonstrated higher expression of pro-resolution genes and lower expression of pro-fibrotic genes in restorative macrophages, which also upregulated a number of genes involved in phagocytosis. Confocal microscopy confirmed that restorative macrophages showed evidence of prior phagocytosis. This could be replicated in vitro, where feeding macrophages with cellular debris resulted in matrix-degrading properties analogous to those seen in vivo, which was dependent on activation of the ERK signalling cascade. This effect was also demonstrated with the phagocytosis of liposomes in vitro. Finally, the administration of liposomes to CCl4-injured mice in vivo induced phagocytosis, causing an increase in hepatic restorative macrophage number and accelerating fibrosis regression. Hence, I have been able to identify and characterise the restorative hepatic macrophage and have utilised these data to develop a novel method to alter macrophage phenotype in vivo and accelerate the resolution of liver fibrosis and restoration of normal tissue architecture.
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Maltby, Julia. "The T-lymphocyte/hepatic stellate cell axis in liver fibrosis." Thesis, University of Southampton, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418619.

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Chang, Ping. "Quantitative evaluation of hepatic morphological alterations and pharmacokinetic changes of cationic drugs in fibrosis-inducing hepatic diseases /." St. Lucia, Qld, 2001. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16767.pdf.

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Pickering, Judith Ann. "Function of tissue inhibitor of metalloproteinase-1 in liver fibrosis." Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244995.

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Reichenbach, Marinkovic Vedrana. "Hepatic remodeling, serum biomarkers and prevention of fibrosis progression in liver disease." Doctoral thesis, Universitat de Barcelona, 2012. http://hdl.handle.net/10803/107757.

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Hepatic fibrosis is characterized by intense tissue remodeling. In this study, we assessed whether CO3-610, a new identified neoepitope, could be used as a surrogate biomarker of liver fibrosis and portal hypertension in CCl4-induced experimental fibrosis. Serum CO3-610 was measured by ELISA. Liver fibrosis was quantified by Sirius red staining. Serum hyaluronic acid (HA) was measured with a binding-protein assay. Gene expression of collagens I and III, MMP2 and MMP9, and tissue inhibitors of matrix metalloproteinase 1 and 2 was quantified by PCR. Hemodynamic measurements were taken in a subgroup of animals. A close direct relationship was found between serum CO3-610 and hepatic collagen content (r= 0.78; P<0.001), superior to that found for serum HA (r= 0.49; P<0.05). CO3-610 levels in rats with severe fibrosis (43.5±3.3 ng/mL, P<0.001) and cirrhosis (60.6±4.3 ng/mL, P<0.001) were significantly higher than those in control animals (26.6±1.3 ng/mL). Importantly, a highly significant relationship was found between serum CO3-610 and portal hypertension (r= 0.84; P<0.001). Liver MMP9 expression increased significantly in fibrotic animals but decreased to control levels in cirrhotic ones. Circulating CO3-610 behaves as a reliable indicator of hepatic remodeling and portal hypertension in experimental fibrosis. Therefore, this peptide could ultimately be a useful marker for the management of liver disease in patients. Endocannabinoids behave as antifibrogenic agents by interacting with cannabinoid CB2 receptors, whereas the apelin (AP) system acts as a proangiogenic and profibrogenic mediator in the liver. This study assessed the effect of long-term stimulation of CB2 receptors or AP receptor (APJ) blockade on fibrosis progression in rats under a non-discontinued fibrosis induction program. The study was performed in control and CCl4-treated rats for 13 weeks. Fibrosis-induced rats received a CB2 receptor agonist (AM1241) (1 mg/kg), an APJ antagonist (F13A) (75 μg/kg), or vehicle daily during the last 5 weeks of the CCl4 inhalation program. Mean arterial pressure (MAP), portal pressure (PP), hepatic collagen content, angiogenesis, cell infiltrate, and mRNA expression of a panel of fibrosis-related genes were measured in all animals. Fibrosis-induced rats showed increased hepatic collagen content, reduced MAP, PP, and increased expression of the assessed messengers in comparison with control rats. However, fibrotic rats treated with either AM1241 or F13A had reduced hepatic collagen content, improved MAP and PP, ameliorated cell viability, and reduced angiogenesis and cell infiltrate compared with untreated fibrotic rats. These results were associated with attenuated induction of PDGFRβ, α-SMA, MMPs, and TIMPs. CB2 receptor stimulation or APJ blockade prevents fibrosis progression in CCl4-treated rats. The mechanisms underlying these phenomena are coincident despite the marked dissimilarities between the CB2 and APJ signaling pathways, thus opening new avenues for preventing fibrosis progression in liver diseases. PDGF is the most potent stimulus for proliferation and migration of stellate cells. PDGF receptor β expression is an important phenotypic change in myofibroblastic cells that mediates proliferation and chemotaxis. Here we analyzed the relationship between PDGFRβ expression, hemodynamic deterioration, and fibrosis. Thereafter, we investigated the effects produced by an adenovirus encoding a dominant-negative soluble PDGFRβ (sPDGFRβ) on hemodynamic parameters, PDGFRβ signaling pathway, and fibrosis. Hemodynamics, PDGFRβ mRNA expression, and hepatic collagen were assessed in controls and fibrosic/cirrhotic rats. Next, 30 fibrotic rats were randomized into three groups receiving iv saline and an adenovirus encoding for sPDGFRβ or β-galactosidase. After 7days, hemodynamics, serum sPDGFRβ, and hepatic collagen were measured. CCl4-treated animals for 18weeks showed a significantly higher increase in PDGFRβ mRNA compared to those treated for 13weeks and control rats. In CCl4-treated rats, the fibrous tissue area ranged from moderate to severe fibrosis. A direct relationship between the degree of fibrosis, hemodynamic changes, and PDGFRβ expression was observed. Fibrotic rats transduced with the adenovirus encoding sPDGFRβ showed increased MAP, decreased PP, lower activation of the PDGFRβ signaling pathway, and reduced hepatic collagen than fibrotic rats receiving β-gal or saline. PDGFRβ activation closely correlates with hemodynamic disorders and increased fibrosis in CCl4-treated rats. Adenoviral dominant negative soluble PDGFRβ improved fibrosis. As a result, the hemodynamic abnormalities were ameliorated. Cirrhotic patients have altered host-defense response mechanisms. Here we assessed whether impaired expression of CB2 receptor in monocytic cells of cirrhotic patients could be involved in the pathogenesis of this phenomenon. CB2 mRNA and protein expression was assessed in a differentiated human monocytic cell line (U937) stimulated with endotoxin (LPS). A PCR array of 86 different genes was assessed in U937 cells treated with LPS. A migration assay towards endocannabinoids or the CB2 antagonist, SR144528, was performed in U937 cells exposed to LPS. Finally, CB1 and CB2 mRNA expression were measured in monocytes and macrophages of cirrhotic patients with or without spontaneous bacterial peritonitis. LPS reduced CB2 expression in human monocytes. Endocannabinoids increased the migratory activity of U937 cells, which was reverted when the experiments were performed in the presence of LPS. Transcriptional profiling showed marked upregulation of 9 genes related to proinflammatory signaling. However, only two genes encoding for CB1 and CB2 were reduced in LPS-treated cells. Circulating monocytes of cirrhotic patients showed a significantly diminished mRNA expression of CB1 and CB2. Markedly low CB1 and CB2 mRNA levels were found in peritoneal macrophages of cirrhotic patients with ascites, being almost suppressed when analyzed in patients with peritonitis. LPS reduces CB2 expression in human monocytes resulting in depressed chemotactic activity and therefore impaired host defense response of these cells.
La característica más destacable de la fibrosis es la desregulación de la ME. El equilibrio que existe entre la síntesis y la degradación de la ME en un hígado normal se pierde, y como consecuencia se favorece la síntesis y acumulación de fibras de colágeno, el cual provoca la distorsión de la arquitectura del parénquima y de la red vascular hepática. El CO3-610 es un producto de degradación del colágeno III que ha mostrado estar correlacionado significativamente con el aumento de la cantidad de colágeno y progresión de la fibrosis. Los valores máximos de CO3-610 se han encontrado ratas cirróticas. El resultado más importante es que el CO3-610 ha mostrado tener una estrecha correlación con los valores de presión portal. Existe un gran interés en investigar y desarrollar terapias dirigidas a la prevención de la progresión de la fibrosis. Los endocannabinoides son moléculas lipídicas que participan en un amplio rango de procesos fisiológicos. Los efectos son mediados por dos tipos de receptores, el CB1 y el CB2. El sistema de la apelina es otro sistema endógeno que ha despertado mucho interés en los últimos años. La apelina es el único ligando conocido para el receptor APJ. El tratamiento con AM1241, un agonista selectivo de CB2 y F13A, un antagonista de APJ mejoró la función hepática, la hemodinámica sistémica y portal, y provocó una reducción significativa del grado de fibrosis hepática. Ambos tratamientos produjeron una disminución del infiltrado inflamatorio, angiogénesis y del grado de apoptosis en el parénquima hepático. El análisis de la expresión del mRNA de varios genes importantes implicados en el proceso fibrogénico, reveló que el tratamiento tanto con AM1241 como con F13A, producían una disminución de la expresión del PDGFRβ, del αSMA y de genes de remodelado tisular. La inhibición parcial de la vía de PDGF mediante la administración de un dominante negativo para la fracción soluble del receptor β de PDGF, ha demostrado que mejora la hemodinámica sistémica y la presión portal además de mejorar el grado de fibrosis. Por último, los pacientes cirróticos con ascitis tienen una mayor probabilidad de sufrir infecciones (peritonitis bacteriana espontánea, PBE). Se ha observado que estos pacientes tienen una menor expresión de CB2. In vitro se han realizado experimentos con células monocíticas (U937) y se ha observado que el LPS disminuye drásticamente la expresión de CB2 al igual que afecta a la capacidad de migración de estas células. En conjunto, se puede concluir que la evaluación de la fibrosis hepática es una herramienta muy importante para el diagnostico de la enfermedad hepática y que éste puede mejorarse a través del uso de biomarcadores no invasivos que correlacionen con la hemodinámica y el grado de fibrosis hepática. La prevención de la progresión de la fibrosis a través de fármacos o bien actuando sobre genes clave involucrados en la fibrogénesis son posibles dianas terapéuticas. Finalmente, es posible mejorar la calidad de vida de los pacientes cirróticos con ascitis con infección por PBE mediante terapias que involucren los receptores de cannabinoides CB2.
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MacFarlane, David Peter. "Factors determining the progression of nonalcoholic fatty liver disease : the role of abnormal fatty acid and glucocorticoid metabolism." Thesis, University of Edinburgh, 2011. http://hdl.handle.net/1842/5914.

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Obesity and insulin resistance are associated with a constellation of features including hypertension, dyslipidaemia, type 2 diabetes, and premature cardiovascular disease, collectively termed the metabolic syndrome. Non-alcoholic fatty liver disease (NAFLD) represents the hepatic component of this syndrome, incorporating a spectrum of liver disease with increasing morbidity and mortality, from simple steatosis, to non-alcoholic steatohepatitis (or NASH), fibrosis, cirrhosis and ultimately hepatocellular carcinoma. However, factors influencing this progression are incompletely understood. In this thesis I sought to investigate pathways which promote hepatic inflammation and fibrosis by studying two contrasting dietary models of NAFLD in mice in which the risk of hepatic inflammation, insulin resistance and fibrosis differ; namely the methionine and choline deficient diet (MCDD) which induces steatohepatitis, hepatic insulin resistance, and weight loss, and the choline deficient diet (CDD) which may be protected from insulin resistance, and leads to steatosis without inflammation or weight loss. I investigated the possible molecular mechanisms underlying these differences, and whether they influenced progression to hepatic fibrosis induced by carbon tetrachloride (CCl4).
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Books on the topic "Hepatic and Periportal fibrosis"

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Cheng, Ming-liang. The basic study and clinical research on hepatic fibrosis. Los Angeles: First Jumbo Publishing Co., 2002.

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Chisato, Hirayama, and Kivirikko K. I, eds. Pathobiology of hepatic fibrosis: Proceedings of the International Symposium on Pathobiology of Hepatic Fibrosis, Matsue, Japan, 16-17 Japan [i.e. June] 1985. Amsterdam: Excerpta Medica, 1985.

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Hepatic Fibrosis. Elsevier, 2022. http://dx.doi.org/10.1016/c2021-0-02535-9.

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PhD, Pablo Muriel. Hepatic Fibrosis: Mechanisms and Targets. Academic Press, 2022.

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Muriel, Pablo. Hepatic Fibrosis: Mechanisms and Targets. Elsevier Science & Technology Books, 2022.

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Hirayama. Pathobiology Hepatic Fibrosis: (International Congress Series). Excerpta Medica, 1985.

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Cellular and Molecular Mechanisms Underlying the Pathogenesis of Hepatic Fibrosis. MDPI, 2020. http://dx.doi.org/10.3390/books978-3-03936-189-2.

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Friedman, Scott. Hepatic Fibrosis: Pathogenesis, Diagnosis and Emerging Therapies - Clinics in Liver Disease. Elsevier - Health Sciences Division, 2008.

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Plebani, Mario, Monica Maria Mion, and Martina Zaninotto. Biomarkers of renal and hepatic failure. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0039.

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In the last few years, major advances have been achieved in the understanding of the molecular and pathophysiological mechanisms which underlie the complex interactions between the heart and the kidney, as well as between the heart and the liver. According to these new insights, new biomarkers have been proposed for better evaluating and monitoring patients affected by cardiovascular diseases. In addition, some biomarkers should be used as risk factors and for an early identification and treatment of these severe diseases. This chapter reviews the most important biomarkers for evaluating the ‘cardiorenal syndrome’, in particular, the measurement of serum creatinine and its use for calculating the glomerular filtration rate which, with the new and more efficient equation, namely Chronic Kidney Disease Epidemiology Collaboration, still remains the most widely used biomarker. The role of newer biomarkers will be explored. The measurement of cystatin C, representing additional information, particularly in paediatric age groups and in the early phase of kidney disease, plays an increasing role. Neutrophil gelatinase-associated lipocalin is a recently developed and very promising new biomarker for the diagnosis of acute kidney injury, while the well-known albumin/creatinine ratio has been re-evaluated as a simple and useful tool for an early identification of kidney disease. Regarding liver diseases, a growing body of evidence demonstrates the usefulness of non-invasive makers of hepatic fibrosis that may avoid the need for a liver biopsy in most patients. A promising field of research is represented by the role of non-alcoholic fatty liver disease in the pathogenesis of cardiovascular disease.
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Keshav, Satish, and Palak Trivedi. Chronic liver failure. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0210.

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Chronic liver failure is the functional syndrome resulting from cirrhosis. Clinical features of chronic hepatic decompensation include encephalopathy, coagulopathy, and hepatocellular jaundice. Cirrhosis is the final common pathway for a variety of chronic liver diseases and is characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules. There often exists a poor correlation between biopsy findings and the clinical presentation. Some individuals with cirrhosis are asymptomatic and have a reasonably good life expectancy, while others have severe symptoms of chronic liver failure and limited life expectancy.
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Book chapters on the topic "Hepatic and Periportal fibrosis"

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Friedman, Scott L. "Hepatic Fibrosis." In Schiff's Diseases of the Liver, 269–89. Oxford, UK: John Wiley & Sons, Ltd, 2017. http://dx.doi.org/10.1002/9781119251316.ch10.

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Rockey, Don C. "Hepatic Fibrosis." In Yamada's Atlas of Gastroenterology, 436–46. Oxford, UK: John Wiley & Sons, Ltd, 2016. http://dx.doi.org/10.1002/9781118512104.ch54.

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Friedman, Scott L. "Hepatic Fibrosis." In Schiff's Diseases of the Liver, 295–315. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781119950509.ch12.

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Metze, Dieter, Vanessa F. Cury, Ricardo S. Gomez, Luiz Marco, Dror Robinson, Eitan Melamed, Alexander K. C. Leung, et al. "Hepatic Fibrosis." In Encyclopedia of Molecular Mechanisms of Disease, 810. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_6116.

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Nazer, Dena, and Hisham M. Nazer. "Congenital Hepatic Fibrosis." In Textbook of Clinical Pediatrics, 2013–16. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-02202-9_208.

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Reynolds, Telfer B. "Congenital Hepatic Fibrosis." In Portal Hypertension, 319–23. Tokyo: Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68361-2_25.

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Pavelka, Margit, and Jürgen Roth. "Congenital Hepatic Fibrosis." In Functional Ultrastructure, 220–21. Vienna: Springer Vienna, 2010. http://dx.doi.org/10.1007/978-3-211-99390-3_114.

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Peters, Nils, Martin Dichgans, Sankar Surendran, Josep M. Argilés, Francisco J. López-Soriano, Sílvia Busquets, Klaus Dittmann, et al. "Congestive Hepatic Fibrosis." In Encyclopedia of Molecular Mechanisms of Disease, 404. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_7405.

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Weiskirchen, Sabine, Carmen G. Tag, Sibille Sauer-Lehnen, Frank Tacke, and Ralf Weiskirchen. "Isolation and Culture of Primary Murine Hepatic Stellate Cells." In Fibrosis, 165–91. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7113-8_11.

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Devaraj, Ezhilarasan, and S. Rajeshkumar. "Nanomedicine for Hepatic Fibrosis." In Nanoparticles and their Biomedical Applications, 45–64. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-0391-7_2.

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Conference papers on the topic "Hepatic and Periportal fibrosis"

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Zhang, Xuejun, Chan Lian, Huan Lao, Binmei Liang, Dongbo Wu, Li Lin, and Yinghua Sun. "Online system for staging hepatic fibrosis." In International Forum on Medical Imaging in Asia 2021, edited by Ruey-Feng Chang. SPIE, 2021. http://dx.doi.org/10.1117/12.2590861.

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Allam, Dalia, Hala Abdalla, and Dalia Allam. "P61 Assessment of clinically significant portal hypertension among periportal fibrosis versus liver cirrhosis patients using fibroscan." In Abstracts of the BSG Annual Meeting, 20–23 June 2022. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2022. http://dx.doi.org/10.1136/gutjnl-2022-bsg.119.

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Seitz, T., K. Freese, WE Thasler, and C. Hellerbrand. "Expression of paracrine fibroblast growth factors in hepatic stellate cells and hepatic fibrosis." In 37. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0040-1721957.

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Zhou, Guohui, Yuanyuan Wang, and Weiqi Wang. "Diagnosis of Hepatic Fibrosis by Ultrasonic Image Analysis." In 2012 International Conference on Biomedical Engineering and Biotechnology (iCBEB). IEEE, 2012. http://dx.doi.org/10.1109/icbeb.2012.143.

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Meziri, Mahmoud, Razika Bouzitoune, Christiano Bittencourt Machado, Frederic Padilla, Pascal Laugier, Chistiano Bittencourt Machado, Wagner Coelho de A. Pereira, Frederic Padilla, and Naceur Tiah. "Multiparametric study to identify the hepatic fibrosis stages." In 2009 IEEE International Ultrasonics Symposium. IEEE, 2009. http://dx.doi.org/10.1109/ultsym.2009.5441625.

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Satyadi, Iswan Abbas Nusi, Poernomo Boedi Setiawan, Herry Purbayu, Titong Sugihartono, Ummi Maimunah, Ulfa Kholili, et al. "Transient Elastography as Non-Invasive Examination of Hepatic Fibrosis." In Surabaya International Physiology Seminar. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007340104260430.

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Farfan, Blanca, Ricardo Strausz, David Kershenobich, Gabriela Mercado, and Victor Hernandez-Urbina. "Applying DNA computing to diagnose-and-interfere hepatic fibrosis." In 2010 Sixth International Conference on Natural Computation (ICNC). IEEE, 2010. http://dx.doi.org/10.1109/icnc.2010.5582557.

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Brödel, Susan, Marcin Krawczyk, Frank Lammert, and SusanneN Weber. "C5aR deficiency rescues hepatic fibrosis but hampers fibrotic resolution." In 38. Jahrestagung der Deutsche Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag, 2022. http://dx.doi.org/10.1055/s-0041-1740668.

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Bai, Yang, Guanghong Han, and Ying Xu. "Application value of elastography in the diagnosis of hepatic fibrosis." In INTERNATIONAL SYMPOSIUM ON THE FRONTIERS OF BIOTECHNOLOGY AND BIOENGINEERING (FBB 2019). AIP Publishing, 2019. http://dx.doi.org/10.1063/1.5110838.

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Shao, Jinhua, Jinrui Wang, Ke Liu, Jing Bai, Xiangdong Hu, and Linxue Qian. "Maximal accumulative respiration strain for the assessment of hepatic fibrosis." In 2008 IEEE Ultrasonics Symposium (IUS). IEEE, 2008. http://dx.doi.org/10.1109/ultsym.2008.0500.

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Reports on the topic "Hepatic and Periportal fibrosis"

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Bi, Junying, Liangjin Liu, and Tao Qin. Comparison of magnetic resonance elastography and transient elastography in the diagnosis of hepatic fibrosis: a meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2021. http://dx.doi.org/10.37766/inplasy2021.6.0076.

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Ismaiel, Abdulrahman, Ayman Jaaouani, Daniel-Corneliu Leucuta, Stefan-Lucian Popa, and Dan-Lucian Dumitrascu. The Visceral Adiposity Index in Non-Alcoholic Fatty Liver Disease and Liver Fibrosis — Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, December 2021. http://dx.doi.org/10.37766/inplasy2021.12.0056.

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Review question / Objective: The objective of the study was to compare the mean difference and AUROC of Visceral Adiposity Index (VAI) in NAFLD/NASH/liver fibrosis patients and controls in observational studies. Condition being studied: Nonalcoholic fatty liver disease (NAFLD) is a multi-system disease, being mainly a liver pathology involving excessive hepatic fat accumulation unrelated to alcohol consumption or other secondary causes of hepatic steatosis. It is an emerging cause of concern and increasing clinical burden, imposing a public health challenge. NAFLD is the most common chronic liver disease and is predicted to be the most common indication for a liver transplant in Western countries by 2030, owing to a prevalence of 25% worldwide. The visceral adiposity index (VAI) is a scoring system based on body mass index, triglycerides, high-density lipoproteins (HDLs), and waist circumferences (WCs).
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Guo, menglan, Qianren Tan, and jingjing Li. Meta-analysis of the value of transient elastography in the diagnosis of hepatic fibrosis staging in fatty liver disease. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, October 2022. http://dx.doi.org/10.37766/inplasy2022.10.0030.

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