Some Molecular Aspects of Antibody Formation

2015 ◽  
pp. 64-81 ◽  
Author(s):  
Brigitte A. Askonas ◽  
A.R. Williamson
Keyword(s):  
Antibody Formation ◽  
Molecular Aspects

Relationship of Major Histocompatibility Complex Class II Genes to Inhibitor Antibody Formation in Hemophilia A

1990 ◽  
Vol 64 (04) ◽  
pp. 564-568 ◽  
Author(s):  
Lloyd E Lippert ◽  
Lyman Mc A Fisher ◽  
Lawrence B Schook
Keyword(s):  
Major Histocompatibility Complex ◽  
Factor Viii ◽  
Antibody Formation ◽  
Rflp Analysis ◽  
Class Ii ◽  
Major Histocompatibility ◽  
Odds Ratios ◽  
Inhibitory Antibody ◽  
Histocompatibility Complex ◽  
Hla Dr

SummaryApproximately 14% of transfused hemophiliacs develop an anti-factor VIII inhibitory antibody which specifically neutralizes factor VIII procoagulant activity. In this study an association of the major histocompatibility complex (MHC) with inhibitor antibody formation was evaluated by restriction fragment length polymorphism (RFLP) analysis using BamHI, EcoRI, HindII, PstI, PvuII and TaqI digested genomic DNA probed with DP beta, DQ alpha, DQ beta and DR beta class II MHC gene probes. The RFLP patterns for 16 non-inhibitor and 11 inhibitor hemophiliac patients were analyzed. These 24 enzyme:probe combinations generated 231 fragments. Fifteen (15) fragments associated with the inhibitor phenotype; odds ratios ranged from 5.1 to 45 and lower bounds of 95% confidence intervals were > 1.000 for all 15 fragments. Five (5) fragments associated with non-inhibitors, with odds ratios ranging from 6.4 to 51.7. This report establishes a MHC related genetic basis for the inhibitor phenotype. No statistically significant differences in the distribution of serologically defined HLA-DR phenotypes were observed between the inhibitor and non-inhibitor groups.

Molecular Aspects of Defibrination in a Case of Amniotic Fluid Embolism

1977 ◽  
Vol 38 (03) ◽  
pp. 0724-0727 ◽  
Author(s):  
H Graeff ◽  
R Hafter ◽  
R von Hugo
Keyword(s):  
Amniotic Fluid ◽  
Amniotic Fluid Embolism ◽  
Molecular Aspects

THE HEXOSAMINE CONTENT OF THE ORBIT IN RELATION TO ANTI-THYROTROPHIN ANTIBODY TITRES IN SERA OF THYROTROPHIN-TREATED RABBITS WITH AND WITHOUT CORTISONE ADMINISTRATION

1962 ◽  
Vol 41 (3) ◽  
pp. 474-480 ◽  
Author(s):  
Otto Wegelius ◽  
E. J. Jokinen
Keyword(s):  
Connective Tissue ◽  
Guinea Pigs ◽  
Antibody Formation ◽  
Direct Proof ◽  
Significant Rise ◽  
Extraocular Muscles ◽  
Concomitant Treatment ◽  
Antibody Titres ◽  
Hexosamine Content ◽  
Synergetic Action

ABSTRACT In all previous investigations on experimental exophthalmos, heterologous thyrotrophic pituitary extracts have been used. These protein hormones stimulate antihormone formation in the test animals. Cortisone has been reported to effectively block antibody formation. In addition, it has been shown to potentiate TSH-induced exophthalmos in guinea-pigs. With rabbits as test animals, the hexosamine content of the orbital tissues was determined and used as an index of exophthalmos development and at the same time the antibody titres in the sera were followed. TSH injections for six weeks led to a highly significant accumulation of hexosamine in the retrobulbar connective tissue and in the extraocular muscles, i. e. an increase of up to 400% as compared with the control animals. At the same time a significant rise in antihormonal titres was detectable in the sera. Concomitant treatment with cortisone brought about an equal or higher accumulation of hexosamine but significantly lower antibody titres. The known opposite peripheral actions of TSH and cortisone can be reconciled with the synergy in producing experimental exophthalmos by attributing the synergetic action of cortisone to the blocking of antihormone formation. If less antihormones are produced, the effect of TSH is enhanced. Our experiments do not provide direct proof for this hypothesis. High hexosamine values in the orbit and low antihormone titres in the serum are, however, concomitant phenomena.

MOLECULAR ASPECTS OF SARCOPENIA PATHOGENESIS IN CHRONOC KIDNEY DISEASE: INTEGRATED ROLE OF mTOR

2018 ◽  
Vol 22 (5) ◽  
pp. 9-16 ◽  
Author(s):  
M. Z. Gasanov
Keyword(s):  
Kidney Disease ◽  
Muscle Mass ◽  
Protein Metabolism ◽  
Mammalian Target Of Rapamycin ◽  
Healthy Person ◽  
Scientific Review ◽  
Cytoskeleton Organization ◽  
Molecular Aspects ◽  
End Stage

In recent decades, the main pathogenetic mechanisms for maintaining muscle mass and strength have been discovered. Most of the scientific papers on the molecular aspects of the  pathogenesis of sarcopenia were focused on the Akt-signaling  pathway. The subject of the study were people of elderly and senile  age, immobilized patients, patients with CKD 1-4 stages, animals. However, recently more attention has been paid to the role  of protein – the mammalian target of rapamycin mTOR. It seems to be a key link in the control of muscle mass and is a promising  marker in understanding the mechanisms of the pathogenesis of  sarcopenia. Its importance in protein metabolism in patients with  end stage kidney disease is not studied and requires further research. The presented scientific review contains  information on the role of mTOR and its components – mTORC1 and mTORC2 in maintaining muscle mass and strength in a healthy  person and in the formation of sarcopenia in patients with CKD. The  general aid of mTORC1 complex is regulation of protein production  which is necessary for cell growth and differentiation. mTORC2  complex functions are not enough studied. It is established that it  plays important role in such biological processes as cytoskeleton  organization, intracellular homeostasis maintaining, so it provides  cell resistance and cell survivability in negative external and internal  impulses. mTOR protein can be considered as promising molecular  marker in diagnostics of protein metabolism early disturbances in  patients with CKD and also as additory factor of sarcopenia severity assessment.

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