scholarly journals Thiocyanate Induces Cell Necrosis and Fibrosis in Selenium- and Iodine-Deficient Rat Thyroids: A Potential Experimental Model for Myxedematous Endemic Cretinism in Central Africa

Endocrinology ◽  
2004 ◽  
Vol 145 (2) ◽  
pp. 994-1002 ◽  
Author(s):  
Bernard Contempré ◽  
Gabriella Morreale de Escobar ◽  
Jean-François Denef ◽  
Jacques Emile Dumont ◽  
Marie-Christine Many
Keyword(s):  
Experimental Model ◽  
Central Africa ◽  
Cell Necrosis ◽  
Endemic Cretinism

scholarly journals Hormones of thyroid gland in sera of rats treated with different dose of concentrated potassium iodine solutions

2010 ◽  
Vol 138 (5-6) ◽  
pp. 323-327 ◽  
Author(s):  
Ljiljana Markovic ◽  
Violeta Mihailovic-Vucinic ◽  
Jelena Aritonovic
Keyword(s):  
Thyroid Gland ◽  
Genetic Susceptibility ◽  
Experimental Model ◽  
Wistar Rats ◽  
Morphological Changes ◽  
Cell Necrosis ◽  
High Iodine ◽  
Hormone Status ◽  
Potassium Iodine ◽  
Iodine Dose

Introduction Potassium iodine (KI) is used as a drug therapy for treating numerous diseases such as small-vessel vasculitis, erythema nodosum, vasculitis nodularis, Sweet's syndrome, tuberculosis and granulomatosis, and for iodized salt. At the same time, KI can be harmful. Iodine intake may increase the frequency of thyroiditis in humans, and may induce the occurrence of experimental thyroiditis (ET) in animals. Investigations on an experimental model for the examination of thyroiditis in Wistar rats have clearly showed morphological changes in the rat thyroid evoked by KI administration. Objective The purpose of this study was to compare the effects of low and high doses of KI on the thyroid gland of Wistar rats and determine the effect on hormone status (T4, T3 and TSH) in this rat strain. Methods Two groups of rats from the Wistar strain were treated with a low iodine dose (225 ?g/g BW) and with a high iodine dose (675 ?g/g BW) of KI solutions. Untreated nonimmunized animals served as controls. The solution was administrated daily intraperitoneally during the period of 26 consecutive days. Results Monitoring hormone status (TSH, T3 and T4) and morphological changes it was found that therapeutic doses of KI applied in treatment induced the occurrence of experimental thyroiditis (chronic destructive Hashimoto's thyroiditis in humans) and cell necrosis in animals not carrying a genetic susceptibility. Significant inflammatory changes were observed in rats treated with a high iodine dose. Conclusion The early iodine induced cell necrosis and inflammation in the nonimmunized animals without genetic susceptibility is a new experimental model of thyroiditis. .

scholarly journals Fulminant hepatitis with microvesicular steatosis (a histologic comparison of cases occurring in Brazil - Labrea hepatitis - and in central Africa - Bangui hepatitis)

1992 ◽  
Vol 25 (3) ◽  
pp. 155-160 ◽  
Author(s):  
Zilton A. Andrade ◽  
Jean L. Lesbordes ◽  
Paul Ravisse ◽  
Raimundo Paraná ◽  
Aluízio Prata ◽  
...  
Keyword(s):  
Single Cell ◽  
Fulminant Hepatitis ◽  
Central African Republic ◽  
Central Africa ◽  
Cell Necrosis ◽  
Microvesicular Steatosis ◽  
Unknown Factor ◽  
Equatorial Forest ◽  
Histopathologic Findings

A similar histopathologic picture of fatal hepatitis associated with widespread acute fatty changes in hepatocytes and single-cell necrosis was seen in epidemic cases occurring in two distinct equatorial areas having high prevalences of HBV and HDV infections. The cases were previously considered to be two different entities; Labrea hepatitis in Brazil, and Bangui hepatitis in the Central African Republic. However, the histopathologic findings suggest that they are pathogenetically and etiologically related to HBVand HDV infections, probably modified by some as yet unknown factor (s) present in equatorial forest zones.

Further Studies on Endemic Cretinism in Central Africa

1971 ◽  
Vol 3 (06) ◽  
pp. 431-437 ◽  
Author(s):  
F. Delange ◽  
A. Ermans
Keyword(s):  
Central Africa ◽  
Endemic Cretinism

Ultrastructural Alterations in Sinusoidal Endothelial Fenestrae as a Result of Hypoxia

1976 ◽  
Vol 34 ◽  
pp. 168-169
Author(s):  
Waykin Nopanitaya ◽  
Raeford E. Brown ◽  
Joe W. Grisham ◽  
Johnny L. Carson
Keyword(s):  
Endothelial Cells ◽  
Experimental Model ◽  
Hepatic Lobule ◽  
Ultrastructural Alterations ◽  
Large Type ◽  
Sinusoidal Endothelial Fenestrae ◽  
General Size ◽  
Sem Studies

Mammalian endothelial cells lining hepatic sinusoids have been found to be widely fenestrated. Previous SEM studies (1,2) have noted two general size catagories of fenestrations; large fenestrae were distributed randomly while the small type occurred in groups. These investigations also reported that large fenestrae were more numerous and larger in the endothelial cells at the afferent ends of sinusoids or around the portal areas, whereas small fenestrae were more numerous around the centrilobular portion of the hepatic lobule. It has been further suggested that under some physiologic conditions small fenestrae could fuse and subsequently become the large type, but this is, as yet, unproven.We have used a reproducible experimental model of hypoxia to study the ultrastructural alterations in sinusoidal endothelial fenestrations in order to investigate the origin of occurrence of large fenestrae.

Studies of Vegetative Plant Tissue Compatibility/Incompatibility: The Role of Acid Phosphatase in Lethal Cell Senescence in an Incompatible Heterograft

1980 ◽  
Vol 38 ◽  
pp. 530-531
Author(s):  
Randy Moore
Keyword(s):  
Acid Phosphatase ◽  
Thick Layer ◽  
Cell Necrosis ◽  
Enzyme Localization ◽  
Vegetative Plant ◽  
Cell Autolysis ◽  
Graft Interface ◽  
System 1 ◽  
Thin Fibril

Previous work has indicated that the graft incompatihility between Sedrmi telephoides and Solanum pennellil involves cell necrosis that results In a thick layer of collapsed cells at the graft Interface. This necrotic layer insulates the stock from the scion, which results in abscission of the Sedum scion after 4-6 weeks due to desiccation and starvation. Thus, cell autolysis (which is restricted to Sedum) characterizes the Incompatibility response in this system (1). In order to elucidate the events that lead to cell autolysis, and thus better understand the cellular site and mode of action of cellular incompatibility, the appearance and fate of the hydrolytlc enzyme acid phosphatase (AP) was followed in both the compatible Sedum autograft and the incompatible Sedum/Solanum heterograft. Acid phosphatase was localized by a modified Gomori-type reaction; positive (i.e., including NaF inhibitor) and negative (lacking substrate) controls showed no enzymatic precipitate. Following an initial association with the endoplasmic reticulum (ER) and dictyosomes at 6-10 hours after grafting, AP activity in the compatible Sedum autograft is associated primarily with the plasmalemma (Fig. 1). By 18-24 hours after grafting, the AP activity is restricted to the tono-plast and vacuole (Fig. 2). This strict compartmentation and absence of enzyme from the cytosol is maintained throughout the development of the compatible graft. While AP activity in the incompatible Sedum/Solanum heterograft is Initially similar to the compatible Sedum autograft (i.e., initially found on the ER and dictyosomes), there is a marked difference in enzyme localization in the two graft partners as the incompatibility response develops. As in the compatible autograft, Solanum cells at the graft interface show an Increase in AP activity that Is restricted to the vacuole and tonoplast, with little or no enzyme activity in the cytosol (Fig. 3). In comparable Sedum cells, however, there is a dramatic Increase In AP activity in the cytosol (Fig. h); this cytosollc AP activity is associated with thin fibril-like structures (Fig. 5) measuring approximately 60 A in diameter. This high cytoplasmic AP activity In Sedum cells results in cell autolysis, death, and eventual cell collapse to form the characteristic necrotic layer separating the two graft partners.

174 Early beneficial effects of vasopeptidase inhibtion n an experimental model of heart failure

2003 ◽  
Vol 2 (1) ◽  
pp. 33-34
Author(s):  
B SHIVALKAR ◽  
B MEURIS ◽  
R VANBENEDEN ◽  
J KETESLEGERS ◽  
F BECKERS ◽  
...  
Keyword(s):  
Heart Failure ◽  
Experimental Model ◽  
Beneficial Effects
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