Association of antibodies to Plasmodium falciparum reticulocyte binding protein homolog 5 with protection from clinical malaria.

Emerging evidence suggests that antibodies against merozoite proteins involved in Plasmodium falciparum invasion into the red blood cell (RBC) play an important role in clinical immunity to malaria. The protein family of parasite antigens known as P. falciparum reticulocyte binding protein-like homolog (PfRh) is required for RBC invasion. PfRh5 is the only member within the PfRh family that cannot be genetically deleted, suggesting it plays an essential role in parasite survival. This antigen forms a complex with the cysteine-rich P. falciparum Rh5 interacting protein (PfRipr), on the merozoite surface during RBC invasion. The PfRh5 ectodomain sequence and a C-terminal fragment of PfRipr were cloned and expressed in Escherichia coli and baculovirus-infected cells, respectively. Immunization of rabbits with these recombinant proteins induced antibodies able to inhibit growth of various P. falciparum strains. Antibody responses to these proteins were investigated in a treatment-re-infection study conducted in an endemic area of Papua New Guinea (PNG) to determine their contribution to naturally acquired immunity. Antibody titers to PfRh5 but not PfRipr showed strong association with protection against P. falciparum clinical episodes. When associations with time-to-first infection were analyzed, high antibody levels against PfRh5 were also found to be associated with protection from high-density infections but not from re-infection. Together these results indicate that PfRh5 is an important target of protective immunity and constitutes a promising vaccine candidate.

Erythrocytic adenosine deaminase in post myocardial infarction angina patients.

A comparative study on the levels of erythrocyte adenosine deaminase and lipid peroxidation has been undertaken in post myocardial infarction angina patients along with age and sex matched healthy individuals serving as control. Present findings show that levels of adenosine deaminase is highly elevated in post myocardial infarction angina patients compared to healthy persons. Malondialdehyde levels are also significantly increased in post myocardial infarction angina patients. The study shows that adenosine deaminase has an important implication in ischemic myocardial syndrome.

Xanthine oxidase as a marker of myocardial infarction.

In the present communication, we report remarkably elevated levels of xanthine oxidase activity in the blood of the patients with myocardial infarction when compared to age and sex matched healthy persons. Highly significant increase of malondialdehyde, serving as an index of lipid peroxidation and thus free radical mediated damage, has also been found in the patients. We propose the measurement of the blood levels of xanthine oxidase, a very simple, reliable and less time consuming method as an indicator of myocardial infarction.

Adenosine deaminase in ischemia reperfusion injury in patients with myocardial infarction.

A comparative study on the levels of erythrocyte adenosine deaminase and lipid peroxidation has been undertaken in patients with myocardial infarction before and after thrombolysis along with matched healthy individuals. Our findings show that adenosine deaminase activity is highly elevated in post-reperfused patients when compared to pre- thrombolysed and healthy persons. Malondialdehyde(MDA) levels are also significantly increased in post-thrombolysed patients. The study reveals an important role of adenosine deaminase in reperfusion injury in patients with myocardial infarction.