When CR is initiated regardless of initiation time the maternal protein restriction in our rodent models can increase or decrease lifespan depending on whether the restriction is imposed during pregnancy or during lactation. As maternal protein restricted offspring were weaned onto the same lab chow it is hypothesized that permanent changes in organ structure and/or function occur during this early time period and these changes can assert long term effects on the regulation of lifespan. Maternal protein restriction applied during suckling to pups born to normally fed mothers significantly retarded their growth. Conversely, pups of low birth weight due to protein restriction during pregnancy underwent rapid catch-up growth when they were suckled by normally fed mothers. We reported previously that growth retardation during lactation was associated with extended lifespan whereas in utero growth restriction followed by catch-up growth was associated with shorter lifespan. These associations may be in line with the observation that small body weight in early life is a significant predictor of lifespan with a strong inverse correlation between growth retardation early in life and longevity in a genetically heterogeneous mouse population. Such inverse correlation was found to be strongest for body weights Foretinib measured early in adult life. In our maternally protein restricted mice we reported previously that PLP mice remained smaller throughout life whereas recuperated mice remained heavier than control animals throughout most of the adult life. Furthermore, genetic mutations in mouse models that lead to increase in lifespan are often associated with dwarfism or reduced body weight. Vertebrate lamins are of two types; A-type lamins are expressed in differentiating cells, while B-type lamins are expressed ubiquitously. Drosophila has two lamin genes; lamC and lamDm0 that are expressed in A- and B-type patterns respectively. Schistosomes have haploid genomes estimated to be approximately 270 MB, arrayed on seven pairs of autosomes and one pair of sex chromosomes. Although a schistosome genome has yet not been sequenced in its entirety, several hundred thousand schistosome expressed sequence tags and genome survey sequences are represented in GenBank, Sanger center, Shanghai LSBI, and some private databases. A unique repertoire of genes whose expression differs with life cycle stage and sex indicates that schistosomes have a complex gene regulation pattern. Genomics and transcriptomics studies have revealed several ESTs in schistosomes with homology to Dicer and Argonaut, protein components of the miRNA silencing pathway. Recently, the structure and expression of the Dicer gene of S. mansoni was characterized. Furthermore, several studies have shown that schistosomes possess RNA interference molecular machinery, and that the addition of exogenous double-stranded RNAs can suppress target gene expression. Four putative miRNA candidates were predicted by bioinformatics methods.