Histopathological studies of the intoxicated rat testes revealed variable degrees of degenerative changes in the seminiferous tubules up to total cellular destruction.
The detailed histological examination of P21, P44 and P111 hsp90αgt/gt mutant testes revealed that meiosis is impaired.
Detailed histological analysis of DAZL-deficient rat testes revealed an apparently intact spermatogonial stem cell compartment, but clear failure to produce mature haploid gametes resulting in infertility.
Examination of 6 week-old Inha−/− and Rb cKO testes revealed multiple tubules with full complements of germ cells, including elongating spermatids, and intact tubular widths and lumens (Figure 4, bottom row).
Microarray analyses of the global testicular transcriptome and quantitative RT-PCR of VRK1-deficient testes revealed significantly reduced expression levels of undifferentiated spermatogonial marker genes in early postnatal mice.
In confirmation of the findings described above, examination of the permeation of lanthanum in 10-day-old control (Figure 2A) and SCARKO (Figure 2B) testes revealed free permeation of the spaces between SC and between SC and GC, indicating absence of barrier formation.
Histological analyses of the adult miR-dKO testes revealed severely disrupted spermatogenesis (Fig. 2).
Immunohistologic analysis of human testes revealed a decrease of about 20% in the total number of germ cells per testis after exposure to 1 μM Cd.
However, while PINK1/parkin mutants exhibit distinct morphological defects during spermatogenesis, 21, 22, 27, 28 the ultrastructural analysis of HtrA2 Δ1 testes revealed no observable defects.
Serially reconstructed electron micrographs of wild-type testes revealed ∼13 somatic cells, presumed to be the CySCs, in contact with the hub in young adults (Hardy et al, 1979).
Light and electron microscopic observations of the irradiated p53-deficient medaka testes revealed that all testis ova start to proliferate synchronously in cysts filled with type A or early type B spermatogonia.
