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At least 937 records · Page 52Linked to original sources
PubMed2002

The effects of aging and radiation exposure on blood pressure levels of atomic bomb survivors.

The Adult Health Study (AHS) is a longitudinal study that has included biennial blood pressure measurements since 1958. In the present study, we applied the mixed effects model for serially measured data on the AHS population to (1) examine age-related changes in blood pressure and (2) detect possible radiation effects. The estimated longitudinal model of systolic blood pressure (SBP) depicted a linear increase from 30 to 80 years of age for both sexes. The diastolic blood pressure (DBP) rose linearly to about 65 years of age and then leveled off. There were marked differences in the longitudinal trends of DBP among birth cohorts, particularly for men, with higher DBP levels in the younger cohort. The present analysis demonstrated a small but statistically significant effect of ionizing radiation on the longitudinal trends of both SBP and DBP. This phenomenon is compatible with the degenerative effect of ionizing radiation on blood vessels.

Adult↗
PubMed2003

Nuclear war: the granzyme A-bomb.

Granzyme A, a serine protease in the cytotoxic granules of natural killer cells and cytotoxic T lymphocytes, induces caspase-independent cell death when introduced into target cells by perforin. Granzyme A induces single-stranded DNA damage as well as rapid loss of cell membrane integrity and mitochondrial transmembrane potential through unknown mechanisms. Granzyme A destroys the nuclear envelope by targeting lamins and opens up DNA for degradation by targeting histones. A special target of the granzyme A cell death pathway is an endoplasmic reticulum-associated complex, called the SET complex, which contains three granzyme A substrates, the nucleosome assembly protein SET, the DNA bending protein HMG-2, and the base excision repair endonuclease Ape1. The SET complex also contains the tumor suppressor protein pp32 and the granzyme A-activated DNase NM23-H1, which is inhibited by SET. Granzyme A cleavage of SET releases the inhibition and unleashes NM23-H1. Cleavage of Ape1 by granzyme A interferes with the ability of the target cell to repair itself. The novel cell death pathway initiated by granzyme A provides a parallel pathway for apoptosis, important in destroying targets that overexpress bcl-2 or are otherwise invulnerable to the caspases.

Animals↗