The medicinal fungus Ganoderma lucidum is used as a dietary supplement and health tonic, but whether it affects longevity remains unclear. We show here that a water extract of G. lucidum mycelium extends lifespan of the nematode Caenorhabditis elegans . The G. lucidum extract reduces the level of fibrillarin (FIB-1), a nucleolar protein that correlates inversely with longevity in various organisms. Furthermore, G. lucidum treatment increases expression of the autophagosomal protein marker LGG-1, and lifespan extension is abrogated in mutant C. elegans strains that lack atg-18 , daf-16 , or sir-2.1 , indicating that autophagy and stress resistance pathways are required to extend lifespan. In cultured human cells, G. lucidum increases concentrations of the LGG-1 ortholog LC3 and reduces levels of phosphorylated mTOR, a known inhibitor of autophagy. Notably, low molecular weight compounds (<10 kDa) isolated from the G. lucidum water extract prolong lifespan of C. elegans and the same compounds induce autophagy in human cells. These results suggest that G. lucidum can increase longevity by inducing autophagy and stress resistance.

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An automated system is constructed to record the complete course of erythrocyte sedimentation process. In this system a light source and a paired photodetector are employed to monitor the change of light transmittance at the junction of plasma and the sedimenting red blood cell column, thus providing a continuous record of erythrocyte sedimentation as a function of time. Differentiation of this sedimentation--time curve yields a velocity--time curve of erythrocyte sedimentation. Frequently recorded "spikes" on top of the velocity--time curve imply the episodes of very rapid fall of erythrocytes in the sedimentation tube that cannot be explained by the currently accepted theory of erythrocyte sedimentation based mainly on Stokes' law, and a new mechanism of rouleau coalescing and fracturing is proposed to account for them.