Does calcium set the physiological value of the dominant time constant of saturated mouse rod photoresponse recovery?
We conclude that the increase in τ(D) during low Ca(2+) treatment is not due to increased [cGMP], increased [Na(+)] or decreased [ATP] in rod outer segment (ROS). Also it cannot be due to protein translocation mechanisms. We suggest that a Ca(2+)-dependent mechanism controls the life time of active PDE.
DSM-TACE seems to be a promising option for advanced HCC patients ineligible for Sorafenib administration or dismissing it due to progressive disease or unbearable side effects.