Bax redistributed from cytosol to mitochondria from 12 to 48 h after bufalin treatment in living cells expressed with green fluorescent protein Bax. Treatment with the antioxidant N-acetyl-cysteine (NAC), a ROS scavenger, inhibited ROS generation and selleck products Bax translocation and led to a significant protection against bufalin-induced apoptosis. Our results also revealed that bufalin induced
a prominent increase of caspase-3 activation blocked potently by NAC. Taken together, bufalin induced ROS-mediated Bax translocation, mitochondrial permeability transition and caspase-3 activation, implying that bufalin induced apoptosis via ROS-dependent mitochondrial death pathway in ASTC-a-1 cells.”
“Purpose: To report the histological and immunohistochemical findings in a cornea
removed from a patient who had undergone collagen cross-linking (CXL) with riboflavin and ultraviolet-A for progressive keratoconus. CXL was performed following the Siena protocol. Two years post-CXL, a visual acuity impairment in the treated eye secondary Salubrinal manufacturer to corneal stromal opacity had occurred, together with corneal thinning and flattening.\n\nMethods: The excised cornea was formalin-fixed, paraffin-embedded, and examined microscopically. Deparaffinized 4-mu m sections were stained with hematoxylin-eosin and Masson trichrome. Further tissue sections were subjected to immunohistochemical evaluation of CD34 and Ki-67 antigens.\n\nResults: Histologically, there was no scar tissue in the failed cornea. The biomicroscopic stromal opacity corresponded microscopically to an acellular area, devoid of keratocytes, and to compaction of the lamellar collagen. Amorphous, weakly eosinophilic interlamellar deposits, extending from the anterior to the posterior two thirds of the stroma, were noted.\n\nConclusions: CXL is a promising procedure for the treatment of progressive keratoconus with minimal reported side effects. In the present case,
we speculate that the short corneal soaking time (15 minutes according LSD1 inhibitor to the Siena protocol) may have resulted in inefficient ultraviolet-A blocking, thermal injury, and deeper keratocyte death. Inadequate keratocyte stem cells reservoir could also play a role in individual cases.”
“The robustness of commercial power metal-oxide semiconductor field-effect transistors to combined gamma-heavy ion irradiation has been investigated, evidence that the degradation of the gate oxide caused by the gamma irradiation can severely corrupt the robustness to single-event effects and drastically modify the physical behavior of the device under test after the impact of a heavy ion. A decrease of the critical voltages at which destructive burnouts and gate ruptures for heavy ion impact appear, has been detected in the devices under test, which were previously irradiated with gamma rays.