Section Summary: Noninvasive Evaluation of Structural Abnormalities of The Thyroid

1989 ◽  
pp. 197-201
Author(s):  
Joel I. Hamburger
Keyword(s):  
Noninvasive Evaluation ◽  
Structural Abnormalities

Ultrastructure of Giant Mitochondria and Their Inclusions in Schwann Cells of Bovine Splenic Nerve

1974 ◽  
Vol 32 ◽  
pp. 194-195
Author(s):  
Å. Thureson-Klein
Keyword(s):  
Schwann Cells ◽  
Cell Organelles ◽  
Giant Mitochondria ◽  
Matrix Density ◽  
Physiological Conditions ◽  
Unmyelinated Axons ◽  
Internal Structures ◽  
Structural Abnormalities ◽  
Cytotoxic Compounds ◽  
Cell Components

Giant mitochondria of various shapes and with different internal structures and matrix density have been observed in a great number of tissues including nerves. In most instances, the presence of giant mitochondria has been associated with a known disease or with abnormal physiological conditions such as anoxia or exposure to cytotoxic compounds. In these cases degenerative changes occurred in other cell organelles and, therefore the giant mitochondria also were believed to be induced structural abnormalities.Schwann cells ensheating unmyelinated axons of bovine splenic nerve regularly contain giant mitochondria in addition to the conventional smaller type (Fig. 1). These nerves come from healthy inspected animals presumed not to have been exposed to noxious agents. As there are no drastic changes in the small mitochondria and because other cell components also appear reasonably well preserved, it is believed that the giant mitochondria are normally present jin vivo and have not formed as a post-mortem artifact.

Mitochondrial Changes in Choline-Deficient Rat Myocardium

1968 ◽  
Vol 26 ◽  
pp. 112-113
Author(s):  
F. G. Zaki
Keyword(s):  
Muscle Fibers ◽  
Liver Mitochondria ◽  
Ultrastructural Changes ◽  
Choline Deficiency ◽  
Nutritional Disorder ◽  
Low Protein ◽  
Structural Abnormalities ◽  
Cross Striation ◽  
Pericardial Edema ◽  
Myocardial Lesions

Choline-deficiency was induced in Holtzman young rats of both sexes by feeding them a high fat - low protein diet.Preliminary studies of the ultrastructural changes in the myocardium of these animals have been recently reported from this laboratory. Myocardial lesions first appeared in the form of intraventricular mural thrombi, loss of cross striation of muscle fibers and focal necrosis of muscle cells associated with interstitial myocarditis. Prolonged choline-deficiency induced cardiomegaly associated with pericardial edema.During the early phase of this nutritional disorder, heart mitochondria - despite of not showing any swelling similar to that usually encountered in liver mitochondria of the same animal - ware the most ubiquitous site of marked structural abnormalities. Early changes in mitochondria appeared as vacuolation, disorganization, disruption and loss of cristae. Degenerating mitochondria were often seen quite enlarged and their matrix was replaced by whorls of myelin figures resembling lysosomal structures especially where muscle fibers were undergoing necrosis. In some areas, mitochondria appeared to be unusually clumped together where some contained membranelined vacuoles and others enclosed dense bodies and granular inclusions.

Bipolar Brains Exhibit Structural Abnormalities

2005 ◽  
Vol 33 (1) ◽  
pp. 64
Author(s):  
MICHELE G. SULLIVAN
Keyword(s):  
Structural Abnormalities

Starving the brain: Structural abnormalities and cognitive impairment in adolescents with anorexia nervosa

2001 ◽  
Vol 6 (2) ◽  
pp. 146-152 ◽  
Author(s):  
Debra K. Katzman ◽  
Bruce Christensen ◽  
Arlene R. Young ◽  
Robert B. Zipursky
Keyword(s):  
Anorexia Nervosa ◽  
Cognitive Impairment ◽  
Structural Abnormalities ◽  
The Brain

Lasertechniques treatment of vascular malformations

Phlebologie ◽  
2010 ◽  
Vol 39 (03) ◽  
pp. 167-175
Author(s):  
M. Poetke ◽  
P. Urban ◽  
H.-P. Berlien
Keyword(s):  
Endothelial Cells ◽  
Spontaneous Regression ◽  
Vascular System ◽  
Vascular Malformations ◽  
Clinical Importance ◽  
Vascular Structure ◽  
Laser Application ◽  
Vascular Morphogenesis ◽  
Structural Abnormalities

SummaryVascular malformations are structural abnormalities, errors of vascular morphogenesis, which can be localized in all parts of the vascular system. All vascular malformations by definition, are present at birth and grow proportionately with the child; their volume can change. In contrast to the haemangiomas, which only proliferate from the endothelial cells the division in stages is of clinical importance. Vascular malformations are divided from the part of vascular system, which is affected.In principle the techniques of laser application in congenital vascular tumours like haemangiomas and in vascular malformations are similar, but the aim is different. In tumours the aim is to induce regression, in vascular malformations the aim is to destroy the pathologic vascular structure because there is no spontaneous regression. This means that the parameters for treatment of vascular malformations must be more aggressive than for vascular tumours.

The Effect of Dimethyl Sulfoxide on In Vitro Platelet Function

1976 ◽  
Vol 36 (01) ◽  
pp. 221-229 ◽  
Author(s):  
Charles A. Schiffer ◽  
Caroline L. Whitaker ◽  
Morton Schmukler ◽  
Joseph Aisner ◽  
Steven L. Hilbert
Keyword(s):  
Platelet Count ◽  
Platelet Aggregation ◽  
Dimethyl Sulfoxide ◽  
Platelet Function ◽  
Platelet Volume ◽  
Short Term ◽  
Platelet Factor ◽  
Short Term Exposure ◽  
Structural Abnormalities

SummaryAlthough dimethyl sulfoxide (DMSO) has been used extensively as a cryopreservative for platelets there are few studies dealing with the effect of DMSO on platelet function. Using techniques similar to those employed in platelet cryopreservation platelets were incubated with final concentrations of 2-10% DMSO at 25° C. After exposure to 5 and 10% DMSO platelets remained discoid and electron micrographs revealed no structural abnormalities. There was no significant change in platelet count. In terms of injury to platelet membranes, there was no increased availability of platelet factor-3 or leakage of nucleotides, 5 hydroxytryptamine (5HT) or glycosidases with final DMSO concentrations of 2.5, 5 and 10% DMSO. Thrombin stimulated nucleotide and 5HT release was reduced by 10% DMSO. Impairment of thrombin induced glycosidase release was noted at lower DMSO concentrations and was dose related. Similarly, aggregation to ADP was progressively impaired at DMSO concentrations from 1-5% and was dose related. After the platelets exposed to DMSO were washed, however, aggregation and release returned to control values. Platelet aggregation by epinephrine was also inhibited by DMSO and this could not be corrected by washing the platelets. DMSO-plasma solutions are hypertonic but only minimal increases in platelet volume (at 10% DMSO) could be detected. Shrinkage of platelets was seen with hypertonic solutions of sodium chloride or sucrose suggesting that the rapid transmembrane passage of DMSO prevented significant shifts of water. These studies demonstrate that there are minimal irreversible alterations in in vitro platelet function after short-term exposure to DMSO.

An Immunoradiometric Assay for Factor VIII Related Antigen (VIIIRAg) Using Two Monoclonal Antibodies-Comparison with Polyclonal Rabbit Antibodies for Use in von Willebrand’s Disease Diagnosis

1984 ◽  
Vol 52 (03) ◽  
pp. 250-252 ◽  
Author(s):  
Y Sultan ◽  
Ph Avner ◽  
P Maisonneuve ◽  
D Arnaud ◽  
Ch Jeanneau
Keyword(s):  
Monoclonal Antibodies ◽  
Structural Changes ◽  
Polyclonal Antibodies ◽  
Disease Diagnosis ◽  
Immunoradiometric Assay ◽  
Von Willebrand's Disease ◽  
Von Willebrand’S Disease ◽  
Structural Abnormalities ◽  
Antigenic Material ◽  
Von Willebrand

SummaryTwo monoclonal antibodies raised against FVIII/von Willebrand protein were used in an immunoradiometric assay (IRMA) to measure this antigen in normal plasma and plasma of patients with different forms of von Willebrand’s disease. The first antibody, an IgG1 was used to coat polystyrene tubes, the second one, an IgG2a, iodinated and used in the second step. Both antibodies inhibit ristocetin induced platelet agglutination and react strongly with platelets, megacaryocytes and endothelial cells. The IRMA test using these antibodies showed greater sensitivity than that using rabbit polyclonal anti VIIIRAg antibodies. A good correlation between the two tests was nevertheless found when VIIIRAg was measured in the majority of patient’s plasma. However 5 patients from 3 different families showed more antigenic material in the rabbit antibody IRMA than in the monoclonal antibody IRMA. It is suggested therefore that the monoclonal antibodies identify part of the VIIIR:Ag molecule showing structural abnormalities in these vWd patients, these structural changes remaining undetected by the polyclonal antibodies.

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