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B. Eskenazi

Researcher at University of California, Berkeley

Publications -  9
Citations -  2047

B. Eskenazi is an academic researcher from University of California, Berkeley. The author has contributed to research in topics: Sperm & Sperm motility. The author has an hindex of 9, co-authored 9 publications receiving 1927 citations.

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Effects of male age on semen quality and fertility: a review of the literature

TL;DR: The weight of the evidence suggests that increased male age is associated with a decline in semen volume, sperm motility, and sperm morphology but not with sperm concentration.
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Advancing age has differential effects on DNA damage, chromatin integrity, gene mutations, and aneuploidies in sperm

TL;DR: There are multiple spermatogenic targets for genomically defective sperm with substantially variable susceptibilities to age, and it is predicted that as healthy males age, they have decreased pregnancy success with trends beginning in their early reproductive years, increased risk for producing offspring with achondroplasia mutations, and risk of fathering offspring with Apert syndrome.
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The association of age and semen quality in healthy men

TL;DR: In a convenience sample of healthy men from a non-clinical setting, semen volume and sperm motility decreased continuously between 22-80 years of age, with no evidence of a threshold.
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The effects of male age on sperm DNA damage in healthy non-smokers

TL;DR: Investigation of the associations between male age and sperm DNA damage and the influence of several lifestyle factors in a healthy non-clinical group of 80 non-smokers with no known fertility problems indicates that older men have increased sperm DNADamage associated with alkali-labile sites or single-strand DNA breaks and independent of age, men with substantial daily caffeine consumption have increased DNA damage associated with double-stranded DNA breaks.
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The Paternal-Age Effect in Apert Syndrome Is Due, in Part, to the Increased Frequency of Mutations in Sperm

TL;DR: It was shown that the number of sperm with mutations increased in the oldest age groups among men who did not have a child with AS, and contributing factors to the paternal-age effect may include selection and a higher number of mutant sperm in a subset of men ascertained because they had a children with AS.