Stem cells observational studies

Some reports showed that pure CNTs can cross cell membrane with high efficiency (Kam et al., 2005 Pantarotto et al., 2004). Some reports showed that CNTs could not be found in cells by HR-TEM (Carrero-Sanchez et al., 2006 Stone and Donaldson, 2006). In our previous studies, we also found that pure CNTs were very difficult to enter into cells such as human fibroblast cells (Tian et al., 2006) and HEK293 cells (Cui et al., 2005), and stem cells, we spent almost 6 months on sectioning these cells and looking for CNTs within cells by HR-TEM, finally we could not find CNTs within cells, we only observed that a lot of CNTs attached to the surface of cells (Fig. 9.10a), and some tubers appeared on the surface of CNTs (Fig. 9.10c). That is to say, non-modified CNTs enter into cells via low-efficient means. However, biomolecules-modified CNTs can efficiently enter into almost all... 

The most extensive formal validation study in this area addressed whole embryo culmre (WEC), micromass (MM), and the embryonic stem cell test (EST) (26). This validation study proved a great learning experience in view of understanding the value of a study with a limited amount of diverse compounds in terms of extrapolation to the universe of chemicals. Subsequent application of the validated EST taught us that the 80% predictability was not reproduced with additional compounds (27). One of the issues underlying this discrepancy was in the mathematical prediction model used, which did not always appear to match the biology of the assay in terms of observed differentiation inhibition. 

The best demonstration that the loss of active normal p53 explains the oncogenic behavior of mutant p53 comes from studies in which a null mutation was introduced into the gene by homologous recombination in murine embryonic stem cells. Mice homozygous for the null allele appear to be normal but are prone to the development of a variety of neoplasms by 6 months of age. These observations suggest that a normal p53 gene is dispensable for embryonic development but that its absence predisposes the animal to neoplastic disease. 

In conclusion, the origin of TH ve neurons observed in the SNpc must remain a matter of speculation. They are likely to be a fruitful area for further study, providing insights into the process of neuronal repair in the brain, as well as for the deployment of stem cells for the repair of the nigra. 

More animal than human data are available from which to determine LOAEL or NOAEL values of benzene hematotoxicity. The data show that animal responses to benzene exposure are variable and may depend on factors such as species, strain, duration of exposure, and whether exposure is intermittent or continuous. Wide variations have also been observed in normal hematological parameters, complicating statistical evaluation. The studies show that benzene exerts toxic effects at all phases of the hematological system, from stem cell depression in the bone marrow, to pancytopenia, to histopathological changes in the bone marrow. The following studies demonstrate these adverse hematological effects in animals. Effects on leukocytes, lymphocytes, and bone marrow are also discussed in Section 2.2.1.3. 

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