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Rh incompatibility

Rh incompatibility may occur when an Rh negative mother carries an Rh-positive fetus. At the time of delivery, a small amount of the baby s Rh-positive blood may gain access to the maternal circulation. In response, the immune system of the mother produces anti-Rh antibodies. During the subsequent pregnancy, the fetus is exposed to these antibodies as they cross the placenta. If this fetus is also Rh-positive, then the anti-Rh antibodies attack the fetal erythrocytes and cause hemolytic disease of the newborn (erythroblastosis fetalis). This may occur in about 3% of second Rh-positive babies and about 10% of third Rh-positive babies. The incidence continues to increase with subsequent pregnancies. [Pg.230]

Besides the simple effects of mesophase stabilization by increased polar-apolar incompatibility and modification of mesophase morphology due to size effects, there are additional specific effects based on the lipophobicity (R[ -RH incompatibility) and rigidity of perfluorinated segments. In this respect it is important to... [Pg.31]

EN57 Miller, J.J. and Valdes, R. (1991). Discrepant bilirubin fractionation in a newborn with Rh incompatibility and hyperbilirubinemia. Clin. Chem. 37, 987, Abstr. 368. [Pg.314]

A major complicating factor can be hemolytic anemia such as that of erythroblastosis fetalis caused by Rh incompatibility between mother and child. The hemolysis increases the rate of bilimbin formation, which soon overwhelms the liver and produces severe jaundice and ker-nicterus. Sickle cell anemia has a similar effect. Congenital absence of bilimbin UDP-glucuronyltransferase (Crigler-Najjar syndrome type 1) usually causes a kemictems that is fatal shortly afterbirth. Inhibition of glucuronyltransferase... [Pg.696]

The medical name of this condition is actually a description of the effects of the Rh incompatibility on the fetus. During pregnancy, a mother whose blood is Rh negative (from 12 to 15% of Americans have this type of blood) may develop antibodies against a fetus that is Rh positive. Some of the maternal antibodies may cross the placenta into the fetus, where they may destroy some of the red blood cells (this effect is called erythroblastosis). Pigment released from the blood cells may poison the infant s brain before or after birth. It is noteworthy that this condition was the cause of death in 1 of every 400 births at the Chicago Lying-In... [Pg.891]

It was pointed out in my 1949 paper (5) that resonance of electron-pair bonds among the bond positions gives energy bands similar to those obtained in the usual band theory by formation of Bloch functions of the atomic orbitals. There is no incompatibility between the two descriptions, which may be described as complementary. It is accordingly to be expected that the 0.72 metallic orbital per atom would make itself clearly visible in the band-theory calculations for the metals from Co to Ge, Rh to Sn, and Pt to Pb for example, the decrease in the number of bonding electrons from 4 for gray tin to 2.56 for white tin should result from these calculations. So far as I know, however, no such interpretation of the band-theory calculations has been reported. [Pg.405]

II cytolytic Cell-associated Clonal expansion B cells IgM, IgG generated. Ig binds to cell bound antigen in the presence of complement and/or activated macrophages cell lysis occurs Rh factor incompatability, hemolytic anemeia in reaction to drugs... [Pg.546]

A consequent 5-dimensional treatment would require Unified Theory of Quantum Mechanics and General Relativity. This unified theory is not available now, and we know evidences that present QM is incompatible with present GR. The well-known demonstrative examples are generally between QFT and GR (e.g. the notion of Quantum Field Theory vacua is only Lorentz-invariant and hence come ambiguities about the existence of cosmological Hawking radiations [19]). But also, it is a fundamental problem that the lhs of Einstein equation is c-number, while the rhs should be a quantum object. [Pg.305]

Following are some properties of AECP explosion /emp(PA method) 305—10°(5 sec) impact test with 2kg wt—detonated at 12" bygroscopicity(% gain in wt at RT and 77% RH) 23% after 6 days and 22.3% after 13 days thermal stability—relatively stable at 85° for long periods of time but decomp extensively at 125° within a week tensile strength—decreases with increase in perchlorate content solubility—insol in common solvents, sometimes dissolved at elevated temps with decompn, swelled in some polar liquids dissociated to some extent in HaO compatibility with NC—incompatible... [Pg.204]

For polycatenar hydrogen bonded complexes with fluorinated chains at both ends (e.g., 138,139, see Fig. 36) formation of columnar phases was observed [246]. However, compound 137, having a branched Rp-chain at one end and three RH-chains at the other has a sequence of three distinct phases in the unusual sequence Cub-Col-SmA-Iso. For the SmA phase of compound 137 a structure with intercalated aromatic cores and RF-chains and separated layers of the hydrocarbon chains was proposed. At lower temperature, when incompatibility rises and the aromatics and Rp-chains disintegrate, all three components form their own layers. However, this produces interface curvature and a columnar phase with square lattice is formed. On further cooling a transition to a cubic phase with Im3m lattice takes place which is most likely of the bicontinuous type [262]. This leads to the unusual phase sequence Cubv-Col-SmA where the positions of the Cubv and Col phases are exchanged with respect to the usually observed phase sequences. The Col-Cub transition at lower temperature could be the result of the decreased conformational disorder of the terminal chains which reduces the steric frustration and hence reduces the interface curvature. [Pg.52]

Rh = 3 1, because the molecules between adjacent squares have to give their Rsi-chains into one of the adjacent RF filled squares [42], Note that in this structure the number of distinct columns is larger than the number of incompatible chains attached to the rod-like core. This means that mixing of the distinct chains gives rise to additional colors which further enhances the complexity of LC self-assembly. [Pg.79]

The gestational age of the infant is a major factor in the development of neonatal hyperbilirubinemia. The more premature the infant is, the lower the level of expression of the enzymes necessary for synthesis of conjugated bilirubin (discussed in the section on Hepatic Metabolism of Bilirubin) and the more likely the child is to develop jaundice. Babies are not routinely screened for the cause of jaundice until the condition manifests itself. Testing would be instituted early if there were a sibling who had experienced prolonged jaundice, or if the mother is blood type O or is Rh negative. All mothers who have good prenatal care are tested for blood type and Rh antibodies. This alerts the physician to potential problems and allows the physician to anticipate the most common forms of jaundice, namely, ABO incompatibilities. [Pg.235]

Although ABO incompatibility and Rh-anti-body formation are the most common causes of hemolysis, other causes need to be considered, such as cephalohematoma formation during delivery with resultant increase in bilirubin production as the hematoma is resorbed hereditary spherocytosis, which is a red cell membrane defect that results in premature breakdown of the red cells and glucose 6-phosphate dehydrogenase deficiency, which is involved in maintaining adequate reduced glutathione levels in the red cell. Infection in the neonatal period is uncommon but still must be considered as a cause of jaundice. In particular, infections of the urinary tract lead frequently to jaundice as a preliminary symptom. The increase in infection associated with instrumentation in the premature infant is always a concern. [Pg.235]

OSHA PEL TWA 0.001 mg(Rh)/m3 ACGIH TLV TWA 1 mg(Rh)/m3 SAFETY PROFILE Poison by ingestion, intraperitoneal, and intravenous routes. Experimental reproductive effects. Questionable carcinogen with experimental carcinogenic data. Mutation data reported. Incompatible with pentacarbonyl iron + zinc. When heated to decomposition it emits toxic fumes of CT. See also RHODIUM and CHLORIDES. [Pg.1211]


See other pages where Rh incompatibility is mentioned: [Pg.661]    [Pg.1263]    [Pg.15]    [Pg.17]    [Pg.2]    [Pg.185]    [Pg.1416]    [Pg.541]    [Pg.322]    [Pg.618]    [Pg.619]    [Pg.619]    [Pg.923]    [Pg.661]    [Pg.1263]    [Pg.15]    [Pg.17]    [Pg.2]    [Pg.185]    [Pg.1416]    [Pg.541]    [Pg.322]    [Pg.618]    [Pg.619]    [Pg.619]    [Pg.923]    [Pg.161]    [Pg.544]    [Pg.301]    [Pg.15]    [Pg.13]    [Pg.15]    [Pg.17]    [Pg.33]    [Pg.36]    [Pg.41]    [Pg.46]    [Pg.62]    [Pg.89]    [Pg.97]    [Pg.336]    [Pg.344]    [Pg.440]    [Pg.176]    [Pg.789]    [Pg.204]    [Pg.4106]    [Pg.135]   
See also in sourсe #XX -- [ Pg.230 ]




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Incompatibility Incompatible

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Rh factor incompatibility

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