1 nt to the chronic injury of aging-associated testicular atrophy.

2 viable, but sterile flies, exhibiting severe testicular atrophy.

3  counts, abnormal sperm morphology, and mild testicular atrophy.

4 tin mice aged 19 to 22 months showed greater testicular atrophy and decreased average seminiferous tu

5 of partial androgen insensitivity, including testicular atrophy and decreased fertility, are common i

6 E2F-1 are viable and fertile, yet experience testicular atrophy and exocrine gland dysplasia.

7 mbryonic Sertoli cells (SCs) leads to severe testicular atrophy and male sterility owing to rapid dep

8 o the developmental arrest of spermatocytes, testicular atrophy, and infertility.

9                       Males exhibited marked testicular atrophy associated with increased apoptosis o

10 in the absence of liver dysfunction produces testicular atrophy by reduction in mitosis, maturation a

11 e a knock-in mouse model that reproduces the testicular atrophy, diminished fertility, and systemic s

12 der increased gonadotrophin drive because of testicular atrophy inducing events.

13 ing cell-type-specific markers, we find that testicular atrophy is due to severe loss of germ cells,

14 pecia, skin atrophy, kyphosis, osteoporosis, testicular atrophy, lipofuscin accumulation in renal pro

15 ad unilateral obstruction with contralateral testicular atrophy or epididymal obstruction.

16  However, PRL1(-/-)/PRL2(+/-) male mice show testicular atrophy phenotype similar to PRL2(-/-) mice.

17 ands attributed to androgen effects, such as testicular atrophy, seminiferous tubule diameter reducti

18  At post-natal day 200, random appearance of testicular atrophy was noted in exposed offspring, and l