Activity of IgG and IgM ABO Antibodies against Some Weak A (A3, Ax, Aend) and Weak B (B3, Bx) Red Cells

The IgG and IgM anti-A and anti-B activities from several immune and non-immune O, A and B sera were tested against a panel of weak (A (A3, AX, AND Aend) and weak B (B3 and Bx) red cells. In all cases it is the IgM which agglutinated optimally Ax (or Bx) cells, while IgG and IgM anti-A (or anti-B) reacted similarly with A3 and Aend (or B3) cells. The agglutinating activity of all these ABO antibodies was found straightly related to their association constant for the A (or the B) receptor.     

OKT4/OKT8 Ratio in Asymptomatic Heroin Addicts

The OKT₄ (helper) and OKT₈ (suppressor) lymphocytic subpopulations were enumerated in a sample of 60 asymptomatic drug addicts and in 17 controls. No significant differences in the ratio could be found that could not be explained by the action of HIV. It can be concluded that heroin itself was not responsible for any alteration in the T₄/T₈ ratio in the population considered.     

Dose-Dependent Destruction of A1 Cells by Anti-A1

Abstract. In a patient of subgroup A₂ the serum contained an unusually potent anti-A₁, giving the following reactions with A₁ red cells in vitro: agglutination of saline-suspended cells up to a temperature of 32°C; a positive indirect antiglobulin test (complement only) at 37°C and lysis of enzyme-treated cells at 37°C. A series of tests was carried out to estimate the ability of the antibody to destroy varying amounts of A₁ red cells in vivo . When about 0.55 ml of red cells was injected, about 65% of the cells were destroyed within 30 min; 2 days later when 18.9 ml of cells were injected, only about 45% were destroyed within 30 min; 5 days after this when a whole unit of A₁ red cells was transfused, survival at 24 h was about 90%. This last figure may indicate that destruction of red cells by anti-A₁ was negligible since at the time of the transfusion of the whole unit the patient was bleeding into her gastrointestinal tract. On the other hand, the titre of anti-A₁ appeared to be declining spontaneously during the period in which tests were carried out so that, if the whole unit of A₁ blood had been transfused at the beginning of this period, survival might have been less good. Nevertheless, from the observed difference in survival between the 0.55 ml and 18.9 ml doses it seems safe to conclude that, even if the unit had been transfused at the time when the antibody concentration was maximal, the percentage of cells destroyed would have been small.     

BHm a Weak B Antigen Variant

Abstract. A weak B antigen has been found on the red cells of a healthy blood donor. His saliva contains B blood group substance. The mother is group A₂B and a sibling is group B, both with strongly reactive B antigens, while the father is group O. The weak B phenotype has been named B^H_m.     

Ethanol-Induced Changes in Chloride Flux are Mediated by Both GABAA and GABAB Receptors

Low concentrations of ethanol (10-30 mM) in the presence of a GABAB receptor agonist, baclofen, promoted 36Cl- uptake into membrane vesicles (microsacs) prepared from mouse cortex. Neither ethanol nor baclofen alone altered chloride influx. The GABAB antagonists, phaclofen and 2-hydroxy-saclofen, completely blocked the increase in chloride flux produced by ethanol in the presence of either baclofen or GABA. Ethanol increased the chloride conductance produced by the GABAA agonists muscimol, isoguvacine, imidazolacetic acid and amino-propane sulfonic acid and this action of ethanol was blocked by phaclofen. The specific GABAA antagonist, bicuculline, blocked ethanol-induced increase in chloride flux in the presence of either baclofen or GABA. GABA-activated chloride channels were also studied in Xenopus oocytes expressing mouse brain mRNA. In this preparation, GABA action was enhanced by ethanol, pentobarbital, and diazepam, and 2-hydroxy-saclofen partially antagonized the action of ethanol without altering the effects of pentobarbital or diazepam. These results suggest that ethanol enhancement of GABAA receptor-chloride channel function also requires activation of GABAB receptors.     

T4 Thyrotoxicosis with Normal or Low Serum T3 Concentration

Summary: : T₄ thyrotoxicosis with normal or low serum T₃ concentration. A. Joasoo, Aust. N.Z. J. Med , 1975, 5, pp. 432–434.     

Four Examples of Bhm Blood in One Family

Abstract. During routine blood grouping, the patient's (L.S.) red cells typed as group O, but the serum lacked anti-B agglutinins. Further investigation revealed that the red cells had no H antigen but did have a weak expression of B. The saliva contained both B and H in amounts comparable to normal B. Family studies provided evidence that this rare phenotype, designated B^h_m, is recessive, dependent on a genetic locus possibly independent of, but linked to, the ABO locus.     

Blood group A1 and A2 revisited: an immunochemical analysis

Background and Objective  The basis of blood group A₁ and A₂ phenotypes has been debated for many decades, and still the chemical basis is unresolved. The literature generally identifies the glycolipid chemical differences between blood group A₁ and A₂ phenotypes as being poor or no expression of A type 3 and A type 4 structures on A₂ red cells, although this assertion is not unanimous.
Materials and Methods  Using purified glycolipids and specific monoclonal antibodies, we revisited the glycolipid basis of the A₁ and A₂ phenotypes. Purified glycolipids were extracted from four individual A₁ and four individual A₂ blood units. One blood unit from an A weak subgroup was also included. Monoclonal anti-A reagents including those originally used to define the basis of A₁ and A₂ phenotypes were used in a thin layer chromatography – enzyme immunoassay to identify the presence of specific glycolipids.
Results  A type 3 glycolipid structures were found to be present in large amounts in all phenotypes. In contrast, the A type 4 glycolipid structure was virtually undetectable in the A₂ phenotype, but was present in the A₁ and A subgroup samples.
Conclusion  The major glycolipid difference between the A₁ and A₂ phenotypes is the dominance of A type 4 glycolipids in the A₁ phenotype.     

New Variants in the ABOH Blood Group System due to Interaction of Recessive Genes Controlling the Formation of H Antigen in Erythrocytes: the ''Bombay''-Like Phenotypes OHm, OBHm and OABHm

Abstract. New variants of the ABOH blood group system are described which are similar to the 'Bombay' phenotype, but differ from it by Le(a-b+) erythrocytes and secretion of ABH and Le^a and Le^b antigens. The erythrocytes of the proposita and members of her family are group O, negative with anti-H; agglutinins if the 'Bombay' type, active also at 37°C, but weakened owing to interference by the secreted antigens, were found in the sera. The genetic background of the observed phenotypes is discussed. It appears likely that the atypical blood groups are due to a pair of recessive genes at a locus designated as Z/z and responsible for biosynthesis of H antigen in erythrocytes. The Z/z locus very probably belongs to the operator/regulator gene complex for the structural gene H , and has a position similar that of the Y/y pair in relation to A gene. The homozygous combination zz causes suppression (modification) of the H phenotype in erythrocytes. As a result, the expression of the blood groups, as determined by the structural gene A or B , is also suppressed. It is suggested that these variants (phenotypes) be given the symbols O_Hm, O^A_Hm, O^B_Hm and O^AB_Hm if the genetic information O, A, B or AB can be demonstrated only indirectly, and symbols A_Hm and B_Hm if the phenotype can be demonstrated by specific agglutination reactions.     

Two Siblings with Rhnull Disease

Abstract. Two siblings with the rare phenotype Rh_null are described; the parents are related to each other. Serologic investigation of the family gives indirect support for the action of an amorphous gene. As demonstrated in the propositus, the splenectomy resulted in health improvement. Titration tests in 1,803 unrelated blood donors revealed 4 heterozygous — types. On the basis of this calculation one can assume one Rh_null patient among 6 million inhabitants.     

Rhnull Red Cells and Pregnancy

Abstract. The haemoglobin, haematocrit and osmotic fragility red cell values in a South African white woman with Rh_null cells and the corresponding haematological syndrome were shown to vary only minimally during her third pregnancy. This occurred in spite of the precautionary donation by her of two units of her blood at 20 and at 27 weeks of pregnancy for storage in liquid nitrogen. Although there was fear to the contrary, the woman's infant was found at birth to be suffering only mildly from haemolytic disease of the newborn due to the anti-Rh29 antibodies present in her plasma.     

Cellular Basis for Complex T Waves and Arrhythmic Activity Following Combined IKr and IKs Block

INTRODUCTION: A growing number of cardiomyopathies have been shown to result in a reduction in both I(Kr) and I(Ks) yet little is known about the electrophysiologic and ECG characteristics of combined I(Kr) and I(Ks) block. METHODS AND RESULTS: To address this gap in our knowledge, transmembrane action potentials (APs) from epicardial, M, and endocardial cells were recorded simultaneously, together with a transmural ECG from arterially perfused canine left ventricular wedge preparations exposed to combined I(Kr) (d-sotalol; 100 micromol/L) and I(Ks) (chromanol 293B; 30 to 60 micromol/L) block. Under baseline conditions, the T wave was typically upright; epicardium repolarized first, coinciding with the peak of the T wave, and the M cells repolarized last, coinciding with the end of the T wave (T(end)). Complex (inverted, biphasic, and triphasic) T waves developed following combined I(Kr) and I(Ks) block. M and epicardial APs prolonged dramatically, so that the endocardial AP was now the earliest to repolarize, coinciding with the first nadir of the complex T wave. In the case of biphasic/triphasic or inverted T waves, Tend coincided with repolarization of either M or epicardial cells, whichever was the last to repolarize. QT intervals prolonged from 286+/-13 msec up to 744+/-148 msec and transmural dispersion of repolarization (TDR) increased from 33+/-10 msec up to 244+/-71 msec. Early afterdepolarizations (EADs) developed in M and epicardial cells, evoking extrasystoles that precipitated polymorphic ventricular tachycardia. Acceleration-induced EADs and T wave alternans also were observed. CONCLUSION: Combined I(Kr) and I(Ks) block gives rise to inverted, biphasic, and triphasic T wave morphologies, a dramatic increase in TDR, and a high incidence of EADs. The diversity of T wave morphologies derives from a preferential AP prolongation of different transmural layers leading to variation in the predominance of voltage gradients on either side of the M cell region. Our study provides direct evidence linking EADs that arise in ventricular epicardial and M cells to the triggered beats that precipitate polymorphic ventricular tachycardia. Our results also suggest possible guidelines for the estimation of TDR from complex T waves appearing in the precordial leads of the surface ECG.