PubMed Health⌕ Search

Biomedical subjects

I Sandovici

Publications and source records attributed to I Sandovici.

4 recordsLinked to original sources

Regulation of placental efficiency for nutrient transport by imprinted genes.

Intrauterine growth and development can impact upon the long-term health of an individual. The fetus is dependent upon the placenta for its supply of nutrients and oxygen from the mother. In turn, the functional capacity of the placenta to supply that demand is under the control of the fetal and maternal genomes. Recent evidence suggests that imprinted genes, a class of genes found in placental mammals whose expression depends on their parental origin, have multiple roles in the placenta. The imprinted genes regulate the growth and transport capacity of the placenta, thereby controlling the supply of nutrients. They may also regulate the growth rate of fetal tissues directly, thereby controlling nutrient demand by the fetus. Recent studies using mice with deletions or disruption of imprinted genes with an altered balance between placental and fetal growth and changes in placental efficiency are indicative of feto-placental signalling of fetal nutrient demand. We propose that signalling mechanisms involving growth demand signals and nutrient transporters are likely to occur and are important for fine tuning normal fetal growth.

Animals↗

[Chaperone proteins--essential proteins for cellular activity].

Molecular chaperones are an ubiquitous, abundant and highly conserved group of proteins which bind and stabilize proteins at intermediate stages of folding, assembly, translocation across membranes and degradation. They first came to attention because of their specific induction during the cellular response of all organisms to heat shock, but are now known to be constitutively and abundantly expressed in the absence of any stress. Despite the obvious importance of stress responses, only recently has scrutiny focused on the role of heat shock proteins in the control of disease pathology. Knowledge about Hsp functions in bacteria is much further advanced than in eukaryotes, but already some hints of Hsp involvement in mammalian diseases have emerged.

Animals↗

[Genetic susceptibility to cancer].

Hereditary predisposition is a common trait of many cancers. 15 to 20 percent of all cancers occur in individuals who have inherited a single gene alteration being members of families where multiple persons carry a high risk of developing cancer. Other than these so-called high penetrance genes which confer elevated risks of cancer development, there are many other genes that generate less dramatic but clinically important risks of cancer, often only if associated to specific exposures.

Gene Expression Regulation, Neoplastic↗

[DNA repair pathways and their involvement in human diseases].

Integrity maintenance of the genome is crucial. Human DNA is vulnerable to damage arising from both endogenous and exogenous sources. Different DNA repair pathways counteract these potentially mutagenic accidents: damage reversal by methylguanine methyl transferase (MGMT), base nucleotide repair (BER), nucleotide excision repair (NER), mismatch repair (MMR) and repair of strand breaks. In some cases, DNA damage is not repaired but is instead bypassed by specialized DNA polymerases. The existence of human diseases associated with defects in DNA repair illustrates the importance of this process of quality control. Many of these human diseases have an increased susceptibility to cancer.

DNA Damage↗