Browsing by Subject "Cysts"

Now showing 1 - 8 of 8
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    Central nervous system cryptococcosis: parenchymal calcification and large gelatinous pseudocysts
    (American Society of Neuroradiology, 1997-01) Caldemeyer, Karen S.; Mathews, Vincent P.; Edwards-Brown, Mary K.; Smith, Richard R.; Radiology and Imaging Sciences, School of Medicine
    In an 11-year-old immunocompetent girl with protracted cryptococcal infection of the central nervous system, CT showed multiple areas of parenchymal calcification. MR imaging showed large gelatinous pseudocysts around the brain stem. These imaging features and the child's age are unusual for intracranial cryptococcosis.
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    Healthy Peribiliary Glands are Necessary for Successful Liver Transplantation
    (Wolters Kluwer, 2022) Francis, Heather; Kundu, Debjyoti; Baiocchi, Leonardo; Medicine, School of Medicine
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    Histone-Modifying Complexes Regulate Gene Expression Pertinent to the Differentiation of the Protozoan Parasite Toxoplasma gondii
    (Taylor & Francis, 2005) Saksouk, Nehmé; Bhatti, Micah M.; Kieffer, Sylvie; Smith, Aaron T.; Musset, Karine; Garin, Jérôme; Sullivan, William J., Jr.; Cesbron-Delauw, Marie-France; Hakimi, Mohamed-Ali; Pharmacology and Toxicology, School of Medicine
    Pathogenic apicomplexan parasites like Toxoplasma and Plasmodium (malaria) have complex life cycles consisting of multiple stages. The ability to differentiate from one stage to another requires dramatic transcriptional changes, yet there is a paucity of transcription factors in these protozoa. In contrast, we show here that Toxoplasma possesses extensive chromatin remodeling machinery that modulates gene expression relevant to differentiation. We find that, as in other eukaryotes, histone acetylation and arginine methylation are marks of gene activation in Toxoplasma. We have identified mediators of these histone modifications, as well as a histone deacetylase (HDAC), and correlate their presence at target promoters in a stage-specific manner. We purified the first HDAC complex from apicomplexans, which contains novel components in addition to others previously reported in eukaryotes. A Toxoplasma orthologue of the arginine methyltransferase CARM1 appears to work in concert with the acetylase TgGCN5, which exhibits an unusual bias for H3 [K18] in vitro. Inhibition of TgCARM1 induces differentiation, showing that the parasite life cycle can be manipulated by interfering with epigenetic machinery. This may lead to new approaches for therapy against protozoal diseases and highlights Toxoplasma as an informative model to study the evolution of epigenetics in eukaryotic cells.
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    Mucinous cystic neoplasms of the liver: presence of biliary communication
    (Oxford University Press, 2019-12) Rodriguez, Robert M.; Barrio, Martin; Parker, Mitch L.; Saeed, Omer; Sherman, Stuart; Ceppa, Eugene P.; Surgery, School of Medicine
    A 35-year-old woman was referred for a symptomatic liver mass. Diagnostic workup detected a septated cyst located centrally in the liver measuring 10 × 7 cm. The cyst had gradually increased in size from previous studies with new intrahepatic biliary dilation. Due to concern for malignancy and symptomatic presentation of the patient, a partial central hepatectomy was performed. Pathology revealed a smooth-walled, multiloculated cyst lined with mucinous epithelium and ovarian-type stroma. The diagnosis of low-grade mucinous cystic neoplasm of the liver (MCN-L) was made. Characteristics of MCN-L have not been elucidated due to its rarity.
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    Pioglitazone Attenuates Cystic Burden in the PCK Rodent Model of Polycystic Kidney Disease
    (2010) Blazer-Yost, Bonnie; Haydon, Julie; Eggleston-Gulyas, Tracy; Chen, Jey-Hsin; Wang, Xiaofang; Gattone, Vincent; Torres, Vicente E.
    Polycystic kidney disease (PKD) is a genetic disorder characterized by growth of fluid-filled cysts predominately in kidney tubules and liver bile ducts. Currently, the clinical management of PKD is limited to cyst aspiration, surgical resection or organ transplantation. Based on an observation that PPARγ agonists such as pioglitazone and rosiglitazone decrease mRNA levels of a Cl(-) transport protein, CFTR (cystic fibrosis transmembrane conductance regulator), and the Cl(-) secretory response to vasopressin in cultured renal cells, it is hypothesized that PPARγ agonists will inhibit cyst growth. The current studies show that a 7- or 14-week pioglitazone feeding regimen inhibits renal and hepatic bile duct cyst growth in the PCK rat, a rodent model orthologous to human PKD. These studies provide proof of concept for the mechanism of action of the PPARγ agonists and suggest that this class of drugs may be effective in controlling both renal and hepatic cyst growth and fibrosis in PKD.
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    Structural and Functional Analyses of Liver Cysts from the BALB/c-cpk Mouse Model of Polycystic Kidney Disease
    (2009) Muchatuta, Monalisa N.; Gattone, Vincent H.; Witzmann, Frank A.; Blazer-Yost, Bonnie
    Liver cysts arising from hepatic bile ducts are a common extra-renal pathology associated with both autosomal dominant and recessive polycystic kidney disease in humans. To elucidate the functional and structural changes inherent in cyst formation and growth, hepatic bile duct epithelia were isolated from the BALB/ c-cpk mouse model of polycystic kidney disease. Light and transmission electron microscopy revealed substantial fibrosis in the basal lamina surrounding hepatic bile duct cysts isolated from heterozygous (BALB/c-cpk/+) and homozygous (BALB/c-cpk/cpk) animals. Scanning electron microscopy and length analysis of normal, precystic and cystic bile ducts provided the unique observation that primary cilia in cholangiocytes isolated from bile ducts and cysts of animals expressing the mutated cpk gene had lengths outside the minimal and maximal ranges of those in cells lining bile ducts of wild-type animals. Based on the hypothesis that PKD is one of several diseases characterized as ciliopathies, this abnormal variability in the length of the primary cilia may have functional implications. Electrophysiological analyses of freshly isolated cysts indicate that the amiloride-sensitive epithelial Na(+) channel (ENaC) is inactive/absent and cAMP-mediated anion secretion is the electrogenic transport process contributing to cyst fluid accumulation. Anion secretion can be stimulated by the luminal stimulation of adenylyl cyclase.
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    Virtual-tissue computer simulations define the roles of cell adhesion and proliferation in the onset of kidney cystic disease
    (The American Society for Cell Biology, 2016-11-07) Belmonte, Julio M.; Clendenon, Sherry G.; Oliveira, Guilherme M.; Swat, Maciej H.; Greene, Evan V.; Jeyaraman, Srividhya; Glazier, James A.; Bacallao, Robert L.; Department of Medicine, IU School of Medicine
    In autosomal dominant polycystic kidney disease (ADPKD), cysts accumulate and progressively impair renal function. Mutations in PKD1 and PKD2 genes are causally linked to ADPKD, but how these mutations drive cell behaviors that underlie ADPKD pathogenesis is unknown. Human ADPKD cysts frequently express cadherin-8 (cad8), and expression of cad8 ectopically in vitro suffices to initiate cystogenesis. To explore cell behavioral mechanisms of cad8-driven cyst initiation, we developed a virtual-tissue computer model. Our simulations predicted that either reduced cell-cell adhesion or reduced contact inhibition of proliferation triggers cyst induction. To reproduce the full range of cyst morphologies observed in vivo, changes in both cell adhesion and proliferation are required. However, only loss-of-adhesion simulations produced morphologies matching in vitro cad8-induced cysts. Conversely, the saccular cysts described by others arise predominantly by decreased contact inhibition, that is, increased proliferation. In vitro experiments confirmed that cell-cell adhesion was reduced and proliferation was increased by ectopic cad8 expression. We conclude that adhesion loss due to cadherin type switching in ADPKD suffices to drive cystogenesis. Thus, control of cadherin type switching provides a new target for therapeutic intervention.