A novel herpes-like virus inducing branchial lesions in a tiger shark (Galeocerdo cuvier)

A juvenile, male tiger shark ( Galeocerdo cuvier) developed illness after capture in Florida waters and was euthanized. Gross lesions included mild skin abrasions, hepatic atrophy, and coelomic fluid. Histologically, gills contained multifocal lamellar epithelial cell necrosis and thromboses. Scattered gill and esophageal epithelial cells had large, basophilic, intracytoplasmic, and intranuclear inclusions. Ultrastructurally, lamellar epithelial cells contained arrays of intracytoplasmic viral particles and scattered intranuclear nucleocapsids. Capsulated virions were 148 ± 11 nm with an 84 ± 8 nm icosahedral nucleocapsid and an electron-dense core. Next-generation sequencing, quantitative polymerase chain reaction, and in situ hybridization performed on formalin-fixed tissue confirmed a herpes-like viral infection. The viral polymerase shared 24% to 31% protein homology with other alloherpesviruses of fish, indicating a divergent virus. This report documents the pathologic findings associated with a molecularly confirmed novel herpes-like virus in an elasmobranch.

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Effect of Calcium on the Growth and Differentiation of Cultured Rat Esophageal Epithelial Cells

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100053383 ◽

1982 ◽

Vol 40 ◽

pp. 132-133

Author(s):

W.T. Gunning ◽

M.R. Marino ◽

M.S. Babcock ◽

G.D. Stoner

Keyword(s):

Epithelial Cells ◽

Cell Types ◽

Replication Rate ◽

Enzymatic Dissociation ◽

Growth Assay ◽

Epidermal Growth ◽

Fetal Bovine ◽

Esophageal Epithelial Cells ◽

Cellular Replication

The role of calcium in modulating cellular replication and differentiation has been described for various cell types. In the present study, the effects of Ca++ on the growth and differentiation of cultured rat esophageal epithelial cells was investigated.Epithelial cells were isolated from esophagi taken from 8 week-old male CDF rats by the enzymatic dissociation method of Kaighn. The cells were cultured in PFMR-4 medium supplemented with 0.25 mg/ml dialyzed fetal bovine serum, 5 ng/ml epidermal growth factor, 10-6 M hydrocortisone 10-6 M phosphoethanolamine, 10-6 M ethanolamine, 5 pg/ml insulin, 5 ng/ml transferrin, 10 ng/ml cholera toxin and 50 ng/ml garamycin at 36.5°C in a humidified atmosphere of 3% CO2 in air. At weekly intervals, the cells were subcultured with a solution containing 1% polyvinylpyrrolidone, 0.01% EGTA, and 0.05% trypsin. After various passages, the replication rate of the cells in PFMR-4 medium containing from 10-6 M to 10-3 M Ca++ was determined using a clonal growth assay.

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Severe Antithrombin III Deficiency in an Infant Associated with Multiple Arterial and Venous Thromboses

Thrombosis and Haemostasis ◽

10.1055/s-0038-1648068 ◽

1976 ◽

Vol 36 (03) ◽

pp. 495-502 ◽

Cited By ~ 14

Author(s):

Geoffrey Mendelsohn ◽

Edward D. Gomperts ◽

Dennis Gurwitz

Keyword(s):

Antithrombin Iii ◽

Adult Life ◽

Rare Condition ◽

Male Infant ◽

Liver Cells ◽

Liver Pathology ◽

Fixed Tissue ◽

Formalin Fixed Tissue ◽

First Case ◽

At Iii

SummaryInherited antithrombin III (AT-II, heparin cofactor) deficiency is a rare condition, presenting with thrombotic disease in adult life. This paper reports an 8 months old South African Black male infant with multiple large vessel venous and arterial thromboses, and E. coli septicaemia. This was associated with an extremely low plasma AT-II level. Micronodular cirrhosis and intracytoplasmic hyaline globules in the liver cells were present. These globules were eosinophilic, and PAS-positive after diastase. They measured approximately 5 μ to 30 μ in diameter, occurred singly in the liver cells and were located mainly in the periportal areas. The histological findings in the liver are similar to those observed in α1-antitrypsin (AAT) deficiency in which the intracytoplasmic globules represent accumulation of altered AAT. Immunochemical studies carried out on formalin fixed tissue failed to detect cross reaction material with anti-α1 antitrypsin or anti-AT III antiserum. This is the first case report of AT-III deficiency presenting in infancy. It is also the first case associated with distinctive liver pathology.The available data presented are insufficient to distinguish between an inborn defect and acquired causes of the severely depressed AT-III plasma level and the distinctive liver pathology.

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Inhibition of telomerase by mutant template telomerase RNA and anti-telomerase short interfering RNA induces ALT in immortalized human esophageal epithelial cells

Zeitschrift für Gastroenterologie ◽

10.1055/s-2006-950885 ◽

2006 ◽

Vol 44 (08) ◽

Cited By ~ 1

Author(s):

M Döbele ◽

A von Werder ◽

C Fulda ◽

S Heeg ◽

G Gössel ◽

...

Keyword(s):

Epithelial Cells ◽

Telomerase Rna ◽

Short Interfering Rna ◽

Esophageal Epithelial Cells ◽

Interfering Rna

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Evidence of predation by a tiger shark (Galeocerdo cuvier) on a spotted dolphin (Stenella attenuata) off O'ahu, Hawai'i

Aquatic Mammals ◽

10.1578/016754203101023915 ◽

2003 ◽

Vol 29 (1) ◽

pp. 84-87 ◽

Cited By ~ 11

Author(s):

Daniela Maldini

Keyword(s):

Tiger Shark ◽

Galeocerdo Cuvier ◽

Spotted Dolphin ◽

Stenella Attenuata

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Different macrophages equally induce EMT in endometria of adenomyosis and normal

Reproduction ◽

10.1530/rep-17-0174 ◽

2017 ◽

Vol 154 (1) ◽

pp. 79-92 ◽

Cited By ~ 7

Author(s):

Min An ◽

Dong Li ◽

Ming Yuan ◽

Qiuju Li ◽

Lu Zhang ◽

...

Keyword(s):

Epithelial Cells ◽

Transforming Growth Factor ◽

Epithelial Mesenchymal Transition ◽

Quantitative Polymerase Chain Reaction ◽

Immunohistochemical Analysis ◽

Secretory Phase ◽

Normal Endometrium ◽

Mesenchymal Transition ◽

Expression Levels ◽

Endometrial Cells

Endometrial cells and microenvironment are two important factors in the pathogenesis of adenomyosis. Our previous study demonstrated that macrophages can induce eutopic epithelial cells of adenomyosis to suffer from epithelial–mesenchymal transition (EMT). The aim of this study is to detect whether macrophages interacting with epithelial cells equally induce the EMT process in normal and eutopic endometria of healthy and adenomyotic patients; and whether macrophages parallelly polarize to M2. We investigated the expression levels of epithelial cadherin (E-cadherin), neural cadherin (N-cadherin), cytokeratin7 (CK7), vimentin, transforming growth factor-β1 (TGFB1), SMAD3 and pSMAD3 using immunohistochemistry and western blot, and then estimated the genetic levels of CD163, IL10 and MMP12 using real-time quantitative polymerase chain reaction (RT-PCR) in macrophages. Eutopic and normal endometrial tissues were obtained from 20 patients with adenomyosis and 11 control patients without adenomyosis, respectively. The immunohistochemical analysis shows distinct EMT in eutopic endometria in secretory phase; the expression levels of TGFB1, SMAD3 and pSMAD3 that indicate signal pathway of EMT were also higher in secretory phase. Macrophages can induce EMT process in primary endometrial epithelial cells derived from normal and eutopic endometria. After co-culturing, THP-1-derived macrophages polarized to M2. Compared with the eutopic endometrium group, further polarization to M2 was observed in the normal endometrium group. These results indicate that adenomyosis may be promoted by the pathologic EMT of epithelial cells, which is induced by macrophages that incapably polarize to M2.

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