A Houdini act: Transient loss of Jka resulting in anti‐Jk3 antibody formation

2021 ◽  
Author(s):  
Philip Wong ◽  
Ritesh Chatrapati ◽  
Sue Williams ◽  
Kelli McGrath ◽  
Glenda Millard ◽  
...  
Keyword(s):  
Antibody Formation ◽  
Transient Loss

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.

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.

Can conversation analytic findings help with differential diagnosis in routine seizure clinic interactions?

2016 ◽  
Vol 12 (1) ◽  
pp. 13-24 ◽  
Author(s):  
Katie Ekberg ◽  
Markus Reuber
Keyword(s):  
Differential Diagnosis ◽  
Correct Diagnosis ◽  
Diagnostic Errors ◽  
Epileptic Seizures ◽  
Routine Clinical Setting ◽  
Choice Of Treatment ◽  
Transient Loss ◽  
Factual Content ◽  
Patient’S History ◽  
Linguistic Methods

There are many areas in medicine in which the diagnosis poses significant difficulties and depends essentially on the clinician’s ability to take and interpret the patient’s history. The differential diagnosis of transient loss of consciousness (TLOC) is one such example, in particular the distinction between epilepsy and ‘psychogenic’ non-epileptic seizures (NES) is often difficult. A correct diagnosis is crucial because it determines the choice of treatment. Diagnosis is typically reliant on patients’ (and witnesses’) descriptions; however, conventional methods of history-taking focusing on the factual content of these descriptions are associated with relatively high rates of diagnostic errors. The use of linguistic methods (particularly conversation analysis) in research settings has demonstrated that these approaches can provide hints likely to be useful in the differentiation of epileptic and non-epileptic seizures. This paper explores to what extent (and under which conditions) the findings of these previous studies could be transposed from a research into a routine clinical setting.

Pentoxifylline and Oxypurinol: Potential Drugs to Prevent the “Cytokine Release (Storm) Syndrome” Caused by SARS-CoV-2?

2020 ◽  
Vol 26 (35) ◽  
pp. 4515-4521
Author(s):  
Francisco J. López-Iranzo ◽  
Ana M. López-Rodas ◽  
Luis Franco ◽  
Gerardo López-Rodas
Keyword(s):  
Lung Parenchyma ◽  
Interstitial Tissue ◽  
Cytokine Release ◽  
Phase I Clinical Trials ◽  
Infected People ◽  
Tnf Α ◽  
Transient Loss ◽  
Anti Inflammatory ◽  
And Control ◽  
Inflammatory Action

Background: COVID-19, caused by SARS-CoV-2, is a potentially lethal, rapidly-expanding pandemic and many efforts are being carried out worldwide to understand and control the disease. COVID-19 patients may display a cytokine release syndrome, which causes severe lung inflammation, leading, in many instances, to death. Objective: This paper is intended to explore the possibilities of controlling the COVID-19-associated hyperinflammation by using licensed drugs with anti-inflammatory effects. Hypothesis: We have previously described that pentoxifylline alone, or in combination with oxypurinol, reduces the systemic inflammation caused by experimentally-induced pancreatitis in rats. Pentoxifylline is an inhibitor of TNF-α production and oxypurinol inhibits xanthine oxidase. TNF-α, in turn, activates other inflammatory genes such as Nos2, Icam or IL-6, which regulate migration and infiltration of neutrophils into the pulmonary interstitial tissue, causing injury to the lung parenchyma. In acute pancreatitis, the anti-inflammatory action of pentoxifylline seems to be mediated by the prevention of the rapid and presumably transient loss of PP2A activity. This may also occur in the hyperinflammatory -cytokine releasing phase- of SARS-CoV-2 infection. Therefore, it may be hypothesized that early treatment of COVID-19 patients with pentoxifylline, alone or in combination with oxypurinol, would prevent the potentially lethal acute respiratory distress syndrome. Conclusion: Pentoxifylline and oxypurinol are licensed drugs used for diseases other than COVID-19 and, therefore, phase I clinical trials would not be necessary for the administration to SARS-CoV-2- infected people. It would be worth investigating their potential effects against the hyperinflammatory response to SARS-CoV-2 infection.

scholarly journals Genetic Control of the Radiosensitivity of Lymphoid Cells for Antibody Formation Ability in Mice.

1994 ◽  
Vol 35 (3) ◽  
pp. 179-185
Author(s):  
MASAAKI OKUMOTO ◽  
NOBUKO MORI ◽  
SHUNSUKE IMAI ◽  
SATOMI HAGA ◽  
JO HILGERS ◽  
...  
Keyword(s):  
Genetic Control ◽  
Antibody Formation ◽  
Lymphoid Cells

scholarly journals P19 Efficacy of thiopurines in preventing infliximab antibody formation when used in dual therapy: experience from a single tertiary paediatric gastroenterology department

2021 ◽  
Author(s):  
Muhamad Azim Muhamad Amin ◽  
Varsha Datta ◽  
Danica Hapuarachchi ◽  
Loveday Jago ◽  
Andrew Fagbemi ◽  
...  
Keyword(s):  
Antibody Formation ◽  
Dual Therapy

scholarly journals Implementation of Adenovirus-Mediated Pulmonary Expression of Human ACE2 in HLA Transgenic Mice Enables Establishment of a COVID-19 Murine Model for Assessment of Immune Responses to SARS-CoV-2 Infection

Pathogens ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 940
Author(s):  
Theodor Chitlaru ◽  
Erez Bar-Haim ◽  
Liat Bar-On ◽  
Shahar Rotem ◽  
Hila Cohen ◽  
...  
Keyword(s):  
Transgenic Mice ◽  
Immune Responses ◽  
Post Infection ◽  
High Reproducibility ◽  
Cellular Immune Responses ◽  
Loss Of Weight ◽  
Transient Loss ◽  
Different Strains ◽  
Cellular Immune ◽  
Human Specific

HLA transgenic mice are instrumental for evaluation of human-specific immune responses to viral infection. Mice do not develop COVID-19 upon infection with SARS-CoV-2 due to the strict tropism of the virus to the human ACE2 receptor. The aim of the current study was the implementation of an adenovirus-mediated infection protocol for human ACE2 expression in HLA transgenic mice. Transient pulmonary expression of the human ACE2 receptor in these mice results in their sensitisation to SARS-CoV-2 infection, consequently providing a valuable animal model for COVID-19. Infection results in a transient loss in body weight starting 3 days post-infection, reaching 20–30% loss of weight at day 7 and full recovery at days 11–13 post-infection. The evolution of the disease revealed high reproducibility and very low variability among individual mice. The method was implemented in two different strains of HLA immunized mice. Infected animals developed strong protective humoral and cellular immune responses specific to the viral spike-protein, strictly depending on the adenovirus-mediated human ACE2 expression. Convalescent animals were protected against a subsequent re-infection with SARS-CoV-2, demonstrating that the model may be applied for assessment of efficacy of anti-viral immune responses.

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