35 cm; 95% Cl: -0.65, -0.05 cm) and possibly in body weight (-280 g; 95% Cl: -620,5 g). Most importantly, these effects were sustained (although not significantly) in the consecutive 5 y for WC (-0.56 cm; 95% Cl: -108, 0.04 cm) and for body weight (-590 g; 95% Cl: -1005, -130 g), which indicated that physical activity was truly a determinant of body size changes.

Conclusions: An increase in physical activity was associated with a statistically significant lower gain in body weight and in WC, which was maintained during the following 5 y. These findings

support the need for public health programs that promote physical activity. Am J Clin Nutr 2010;92:491-9.”
“Background: Plasmodium vivax is the most widespread malaria parasite. It has a dormant stage in the human liver, LDN-193189 TGF-beta/Smad inhibitor which makes it difficult to eradicate. It is proposed

that a relapse of vivax malaria, besides being genetically determined by the specific strain, is induced by the bites of uninfected vectors.

Presentation of the hypothesis: The dormant stage maximizes the possibility for the parasite to reach the vector for sexual reproduction. The advantage would increase if the parasite was able to detect the presence of a new generation Z-VAD-FMK cost of vectors. The sporozoites function both in the vector and in the human hosts. They invade the cells of the salivary gland in the vector Cyclosporin A cost and the hepatocytes in the human. Some of the sporozoites develop into hypnozoites in the human liver. It is suggested that the hypnozoite activates when it recognizes the same Anopheles specific protein, which it had previously recognized as a sporozoite to invade the salivary gland in the vector. Another possibility is that the hypnozoite activates upon the bodily reaction by the human on a bite by an Anopheles female.

Testing the hypothesis: The

connection between the relapse and a new generation of vectors can be documented by simultaneous monitoring of both parasitaemia in humans and the presence of uninfective/infective vectors in the same area with seasonal malaria transmission. Experimental studies are needed to find the saliva components, which trigger the relapse. Although P. cynomolgi in monkeys also has hypnozoites and relapses, testing with monkeys might be problematical. These live in a reasonably stable tropical environment where relapses cannot easily be linked to vectors. The importance of the trigger increases in unpredictable variations in the vector season.

Implications of the hypothesis: Artificial triggering of hypnozoites would make the medication more effective and resistance against a protein that the parasite itself uses during its life cycle would not develop. In areas with seasonal vivax malaria it could be used locally for eradication.