It is well established that Rab5 mainly localizes on early endosomes and regulates the homotypic fusion of early endosomes by interacting with EEA1. Furthermore, Rab5 is known to have GSI-IX several regulators and effectors such as Rabex-5, Rabaptin-5, Rabenosyn-5 and Rabankyrin-5, although little is known about those of Rab21. The present study revealed that Rab21 and Rab5 showed similar but not identical spatiotemporal dynamics in RAW264 macrophages during macropinocytosis. Recently, Porat-Shiliom et al. have shown that Rab5 is recruited to macropinosomes after the loss of PIP2 in HeLa cells over-expressing the active mutant of H-Ras which induces membrane ruffling and macropinocytosis. In our study, it was found that Rab21 was largely colocalized with Rab5 on macropinosomes before the accumulation of Lamp1. Moreover, we observed that the loss of PIP2 from the membrane was followed by the recruitment of Rab21 as well as Rab5. These facts imply that Rab21, like its close homologue Rab5, may play a role in regulating macropinocytosis at an early stage. Overall we have demonstrated very high levels of target organ damage among workers with hypertension in urban Ghana associated with poor control of hypertension. Our findings strongly suggest a substantial future burden of both morbidity and mortality from uncontrolled hypertension in Africa. Affordable measures to improve the detection, treatment and control of high blood pressure, and public health measures aimed at reducing blood pressure and cardiovascular risk in the population as a whole are urgently needed. Diseases associated with the accumulation of fibrillar forms of aSyn are commonly known as synucleinopathies. The preferential vulnerability of dopaminergic neurons in PD is unclear, but a link between dopamine biology and aSyn as been hypothesized, since dopamine was shown to form adducts with aSyn in the test tube, appears to stabilize protofibrillar forms of aSyn, and inhibits aSyn fibril formation in vitro. In contrast to habituation, associative learning increase synaptic sensitivity and cause a dynamic remodeling of synapses. In our work we demonstrate that complete loss of both isoforms of MAGI-1 impairs mechanosensation through the command interneurons, demonstrated by the lack of response to nose touch in magi-1 mutant worms. Furthermore, loss of MAGI-1 has additional effect on neuronal plasticity besides the demonstrated role in non-associative learning. Large sets of novel genes that mediate resistance to a variety of DNA damaging agents have been identified using the isogenic yeast deletion strain collections. Surprisingly, screens previously considered near saturation by classical mutagenesis screening methods, including those for ionizing radiation sensitivity, have uncovered a large number of previously uncharacterized radiation resistance genes.