Objective: This study was aimed to investigate the effects of pre-pubertal exposure of Ara-C on testesticular development

in juvenile SD rats and their function at puberty. Materials and methods: Ara-C was injected at the doses of 50, 100 and 200 mg/kg/day from postnatal AZD6738 day (PND) 29-42 (14 days) by intraperitoneal (i.p.) route. Half of the animals were sacrificed on PND 43 and remaining on PND 70. End points of the evaluation included gross pathological examination, histomorphometric analysis, sperm count and sperm head morphology, cell proliferation and DNA damage as well as apoptosis analysis. Results: Ara-C treatment significantly decreased food and water intake, weight gain, testes and epididymis weight and increased histological alterations in the seminiferous tubule. Furthermore, Ara-C treatment significantly decreased the PCNA-positive cells and sperm count in a dose-dependent manner. Ara-C treatment also increased the DNA damage and apoptosis in testes and sperm as evident from the comet and TUNEL assays results. Discussion: The present study results

clearly indicated that Bucladesine Ara-C treatment impaired spermatogenesis and adversely affects the testicular development and its function in rats by reducing the germ cell proliferation and the inducing DNA damage and apoptosis.”
“Cognitive decline presents a therapeutic selleck products challenge for patients with multiple sclerosis (MS), a disease characterized by recurrent autoimmune demyelination and by progressive CNS degeneration. Glatiramer acetate

(GA, also known as Copolymer 1, Cop-1, or Copaxone), commonly used to treat MS, reduces the frequency of relapses; it has both anti-inflammatory and neuroprotective properties. However, clinical trials have not definitively shown that GA improves cognitive impairment during MS. Using an in vivo animal model of autoimmune demyelination, i.e., relapsing-remitting experimental autoimmune encephalomyelitis (EAE), we tested short-term memory in EAE mice (EAE), in EAE mice treated with GA for 10 days starting at the time of immunization (EAE + GA), and in age-matched healthy, na smaller than ve mice (Na smaller than ve). Short-term memory was assessed using the cross-maze test at 10, 20, and 30 days post-immunization (d.p.i.); data were analyzed at each time point and over time. At 10 d.p.i., EAE and EAE + GA mice had better memory function than Na smaller than ve mice. However, at the later time points, EAE mice had a steep negative slope of memory function (indicating decline), whereas EAE + GA mice had a flatter, less-negative slope of memory function. Notably, the memory function of EAE mice significantly decreased over time compared with that of Na smaller than ve mice, indicating that EAE had a negative impact on cognitive ability.