"A number of researchers have noticed similarities between some of the mitochondrial depletion diseases in humans and some of the abnormalities seen in SCNT and hypothesize that aberrant nuclear-mitochondrial interactions in SCNTs could be responsible for some of these abnormalities. A research team in Germany found that “A survey of perinatal clinical data from human subjects with deficient mitochondrial respiratory chain activity has revealed a plethora of phenotypes that have striking similarities with abnormalities commonly encountered in SCNT fetuses and offspring. We discuss the limited experimental data on nuclear-mitochondrial interaction effects in SCNT and explore the potential effects in the context of new findings about the biology of mitochondria” (Hiendleder et al. 2005: 69). Researchers in the United Kingdom have suggested that potential overpopulation of mitochondria could lead to the large offspring syndrome often seen in SCNT cow clones and call for more work in this area: “a cytoplasm over-populated with mitochondria would lead to cellular expansion that might be indicative of the reported large-offspring syndromes. This under-researched area of investigation could provide clear answers to some of the developmental abnormalities witnessed in NT offspring and aborted feotuses, whether mediated through failure of somatic cell reprogramming or independently” (St John et al. 2004: 638-639)."