The Rh factor genetic information is also inherited from our parents, but it is inherited independently of the ABO blood type alleles. There are 2. The Rh factor is an antigen capable of inducing the strongest known immune reaction .. 39 The relationship of traffic accident risk and the titer of Toxo- specific .. Our results showed that in blood donors, Dominance (factor E) significantly. Individuals who are homozygous dominant (DD) or heterozygous (Dd) are Rh+. Those Clinically, the Rh factor, like ABO factors, can lead to serious medical.
The set-up we used with the military drivers is called a prospective cohort study. This study did not have the ambiguity of the case-control study, because it was carried out only on the drivers who were willing to participate in it. Such a hypothesis would have to be fairly complicated, and include additional assumptions: A simpler and more reasonable explanation would be that toxoplasmosis increases the risk of driving accidents in Rh negative people — especially when we consider that in independent studies we already proved that toxoplasmosis worsens reaction time in Rh negatives.
We started our study before knowing about the possible role of the Rh factor. The study ran around five years, and at first it seemed that it would bring negative results. Simple tests showed no statistically significant difference between Toxo positives and negatives in the risk of car accidents.
But as soon as we included the variable of the Rh factor in our analysis, we got data which agreed with results from our previous performance testing of Rh positive Toxo positive people. In Rh positives, infection by Toxoplasma had practically no effect on the probability of driving accidents, whereas in Rh negative subjects it greatly increased this risk. In Rh negatives, the risk of a driving accident decreased with lower Toxoplasma antibody levels.
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That corresponded with the results of the previous study, because even among Prague inhabitants the highest risk of driving accidents was among people with relatively high antibody levels. Once more we found that although reaction time worsens with time after infection, the infected drivers are gradually able to adapt to their worsened abilities. Our study brought another Fig.
The uninfected drivers have a similar risk of a driving accident, regardless their Rh factor, but Toxo positive Rh negatives have a higher risk, which further increases with increasing levels of Toxoplasma antibodies.
The antibodies were determined using complement-fixation test. Rh negative drivers with a titer of 1: The numbers indicate the ratio of Rh positive to Rh negative drivers with a given titer of antibodies.
A suspiciously large number of the drivers who had a driving accident had not participated in our study. This indicates that the drivers with the greatest risk of driving accidents refused to participate in our testing.
Such as his willingness to cooperate. The case of the Rh factor and toxoplasmosis can be used as an example of an often-recounted mistake of scientists. In other words, a study should supposedly be set-up so that each experiment analyzes the effect of one factor. But if we had followed taken this approach, we never would have discovered the interaction between the Rh factor and toxoplasmosis.
When we studied the effect of the Rh factor on reaction times for a group of Toxo positive and negative people, as undoubtedly many scientists had done before us, we found no difference in reaction time between Rh positive and negative people. But when we included both the factors in our analysis toxoplasmosis and the Rh factorwe suddenly discovered that uninfected Rh negative subjects have better reaction times than do uninfected Rh positives — but infected Rh negatives have much worse reaction times do Rh positives.
In my experience, any study requires one to look for and then simultaneously analyze as many factors as possible. To this end, I always tried to track several variables and run the same people through the maximum number of tests.
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Then I could analyze a large number of relationships and interactions between the studied variables. Of course, this approach also has its bad parts.
As we study more relationships, there is a greater risk of Type I errors — there is a greater probability that some of the relationships we observe between the variables will happenstance. As I like to stress, the p-value given by a statistical significance test which helps us to estimate the probability that an observed phenomenon is the result of chancecan only be applied to a single statistical test. But you have to know how to deal with the results of such experiments.
I teach my students to treat them like the results of an exploratory study see Box 10 Statistical evaluation of data. You always have to meticulously explore the data from all possible angles and find as many potentially interesting phenomena as possible.
In a way, each of my studies is both confirmatory and exploratory. They are also exploratory because I always look for other possible phenomena in the new data, whether they relate to the original direction of our study, or are just relationships between variables that we happened to include. Like I said, we usually test a large number of variables — both to statistically filter out their confounding effects on the target variable, and to discover any possible relationship between the confounding variables see also Box 20 Dependent, independent, and confounding variables; fixed and random factors.
The smaller our data sample, the more false positive results we usually obtain. But if we confirm them on other groups, we do try to publish the results, whether they relate to toxoplasmosis, or the relationship between sexual preference and the length ratio of fingers on the left hand Box 73 Do homosexuals have a longer pointer finger than ring finger? As a result, a person not familiar with our work might look at our published articles and be hard-pressed to determine our field of study.
Box 73 Do homosexuals have a longer pointer finger than ring finger? All relationships between the length ratio of these fingers and psychical or biological traits are purely statistical. Among women, the difference between homosexuals and heterosexuals generally does not correlate with the finger length ratio.
On the other hand, a difference in the length ratio for homosexual versus heterosexual men is usually observed in both Americans and Europeans 81 82 The problem is, whereas among Europeans homosexual men have a lower length ratio than heterosexual men and men identifying themselves as bisexual have an even lower length ratioamong Americans it is the other way around.
We have not yet found an explanation. In one study conducted on visitors of the Municipal Library of Prague, we measured the length of each finger, and administered an anonymous survey to determine sexual preference and behavior. The group had about people, but only between and roughly same amount of men as women answered the questions regarding sexuality.
Our results showed no difference in finger length ratio between homosexuals versus heterosexuals, neither among men, nor among women. Surprisingly, we found a significantly higher length ratio a relatively longer pointer finger among women who answered that they were sexually aroused by tying hands whether their partner tied their hands, or they did so their partneri.
After we started including the effect of the Rh factor in our models, we saw that the effect of Toxoplasma, or rather the interaction of Toxoplasma and Rh factor, showed up not just in the results of simple reaction time tests, but also in those of more complex performance tests.
Usually the interaction manifested similarly as it did in the simpler tests. Rh negatives performed better than did Rh positives, but only among Toxo negatives. When the people were infected by Toxoplasma, then the Rh negatives performed significantly worse.
For example, we found that Rh negative Toxo positive men performed better in intelligence tests and have higher IQ values, than did uninfected Rh negatives. But among Rh positive men, we saw no such difference.
In this case, infection by Toxoplasma might have an effect opposite to what we observed for simple reaction times. Our next results, obtained as a side-product of a primarily Toxoplasma study, indirectly supported this possibility.
When we graphed reaction time versus intelligence for a group of soldiers, we found that the shorter the reaction time, the worse the result of the IQ test.
But this was only true for tests which measure nonverbal intelligence. Tests which targeted verbal intelligences did not show such a relationship. In our first studies, it seemed that the intelligence of infected men was lower than that of uninfected men. In some groups, the difference between the average intelligence of infected vs. For women, some groups showed an opposite relationship — that intelligence of infected women was higher than that of uninfected women.
As I mentioned, infected women have a higher superego and are also more sociable Cattell's factors G and Awhich are certainly personality factors which can make someone try harder on the test. Furthermore, the intelligence of Toxo positive versus Toxo negative people can be different without toxoplasmosis having any effect — direct or indirect — on intelligence.
First off, the cause-effect relationship may be the other way around. And secondly, there may exist an unknown, third factor which influences both intelligence and the risk of Toxoplasma-infection.
But when we examined the same thing for verbal intelligence measured using the Otis questionnairewe discovered that people from larger towns tested as more intelligent. When we included the factor of residence settlement population in our models studying the relationship of toxoplasmosis and verbal intelligence — or when we looked at the relationship separately for people from villages, towns and cities — the correlation between Toxo-positivity and verbal intelligence was no longer statistically significant Fig.
Currently, we are starting on a project in which we will meticulously study the relationship between latent Fig. Over the course of 5 years, we examined 42 groups with of soldiers in each group. Only in four groups were the differences between infected and uninfected soldiers in verbal intelligence, as determined by Otis test, statistically significant after filtering out the size of their settlement.
The funnel plot wide end to left in which the size of observed effect is plotted against the number of individuals in the study demonstrates that the effect of Toxoplasma was significant only in small or medium size studies, and that all individual points representing the effect are located symmetrically around the null line. If this were a real meta-analysis which funnel plots are commonly used forand the individual points indicated the results of already published studies, then the symmetry of graph would testify that there is not a substantial publication bias in the specific research field.
You may need the following tests to check for Rh disease: Testing for Rh positive antibodies in your blood. This test can show enlarged organs or fluid buildup in your baby. This test checks the amount of bilirubin in the amniotic fluid. In this test, a needle is inserted into your abdominal and uterine wall. It goes through to the amniotic sac.
The needle takes a sample of amniotic fluid. Percutaneous umbilical cord blood sampling or fetal blood sampling. How is Rh disease treated? Treatment will depend on your pregnancy and general health. It will also depend on how severe the condition is. Intrauterine blood transfusion This test puts red blood cells into your baby's circulation. In this test, a needle is placed through your uterus. Your baby may need sedative medicine to keep him or her from moving. You may need to have more than one transfusion.
Early delivery If your baby gets certain complications, he or she may need to be born early. Your healthcare provider may induce labor once your baby has mature lungs.
What are the complications of RH disease? Abstract Background Rhesus-positive and rhesus-negative persons differ in the presence-absence of highly immunogenic RhD protein on the erythrocyte membrane. This protein is a component of NH3 or CO2 pump whose physiological role is unknown.
Several recent studies have shown that RhD positivity protects against effects of latent toxoplasmosis on motor performance and personality. It is not known, however, whether the RhD phenotype modifies exclusively the response of the body to toxoplasmosis or whether it also influences effects of other factors.
We found that the positive effect of age on performance and intelligence was stronger in RhD-positive soldiers, while the negative effect of smoking on performance and intelligence was of similar size regardless of the RhD phenotype. The effect of age on four Cattell's personality factors, i. Conclusions RhD phenotype modulates the influence not only of latent toxoplasmosis, but also of at least two other potentially detrimental factors, age and smoking, on human behavior and physiology.
The negative effect of smoking on health estimated on the basis of the self-rated number of common viral and bacterial diseases in the past year was much stronger in RhD-negative than RhD-positive subjects.
It is critically needed to confirm the differences in health response to smoking between RhD-positive and RhD-negative subjects by objective medical examination in future studies. Introduction About sixteen percent of the population of the Czech Republic express the RhD- negative phenotype, i.
Rh Disease - Health Encyclopedia - University of Rochester Medical Center
The biological function of the RhD molecule is unknown. Its structure suggests that the molecular complex with RhD protein transports NH3 or CO2 molecules across the erythrocyte cell membrane  — .
In the RhD negative rhesus minus subjects, the product of the particular protein is not synthesized due to a large deletion in the RHD gene. This results in the absence of the D-antigen, probably the most immunogenic epitope on the human red cell membrane . Blood cells of rhesus-positive subjects are therefore a strong antigen for rhesus-negative subjects.
Under normal conditions, there are no anti-D antibodies in the serum of RhD-negative subjects. However, after immunization either by transfusion or by delivery of an RhD positive child by an RhD negative mother, large amounts of anti-D antibodies are synthesized by RhD-negative subjects.
The presence of these antibodies not only complicates future transfusions and transplantations, but it also represents a strong health risk for delivery of future RhD-positive children. The existence of genetic polymorphism is an evolutionary enigma since its discovery in the forties of the last century. Theoretically, neither the RhD-negative allele can successfully spread in the RhD positive population nor the RhD-positive allele can spread in the RhD negative population . Before the advent of modern medicine, a positive frequency dependent selection systematically penalized the less abundant allele because lots of children of RhD-negative women in the mostly RhD-positive population as well as children of RhD- positive men in the mostly RhD-positive population were dying of hemolytic anemia.
In the past sixty years, several mechanisms explaining the origin and stable existence of RhD polymorphism were suggested and the evidences for them were nonsystematically searched for.