Direct Abortion or Legitimate Medical Procedure Double Effect?

The distinction between direct abortion and legitimate medical procedures deemed necessary to save the life of the mother but resulting in the death of the unborn child challenge all clinicians and persons of faith. A careful analysis of the principle of double effect and a recent statement by the Committee on Doctrine of the United States Conference of Catholic Bishops offer some clarity to this difficult conflict. Two case examples offer illustration for the analysis.

Pathophysiologically relevant levels of hydrogen peroxide induce glutamate-independent neurodegeneration that involves activation of transient receptor potential melastatin 7 channels.

Stroke/brain ischemia is a leading cause of death and long-term disabilities. Increased oxidative stress plays an important role in the pathology of brain ischemia. Hydrogen peroxide (H(2)O(2)) is a major oxidant known to cause neuronal injury; however, the detailed mechanism remains unclear.

Transient receptor potential melastatin 7-like current in human head and neck carcinoma cells: role in cell proliferation.

Ion channels are involved in normal physiologic processes and in the pathology of various diseases. In this study, we investigated the presence and potential function of transient receptor potential melastatin 7 (TRPM7) channels in the growth and proliferation of FaDu and SCC25 cells, two common human head and neck squamous carcinoma cell lines, using a combination of patch-clamp recording, Western blotting, immunocytochemistry, small interfering RNA (siRNA), fluorescent Ca(2+) imaging, and cell counting techniques. Although voltage-gated K(+) currents were recorded in all cells, none of FaDu cells express voltage-gated Na(+) or Ca(2+) currents.

Extracellular zinc protects against acidosis-induced injury of cells expressing Ca2+-permeable acid-sensing ion channels.

Acidosis is a common feature of neurological conditions including brain ischemia, epileptic seizures, and neurotrauma. Activation of Ca(2+)-permeable acid-sensing ion channels (ASIC1a) is involved in acidosis-mediated ischemic brain injury. Zn(2+) is a divalent cation concentrated in nerve terminals in various brain regions, and is released into the extracellular space during excitatory stimulation.

Modulation of acid-sensing ion channel currents, acid-induced increase of intracellular Ca2+, and acidosis-mediated neuronal injury by intracellular pH.

Acid-sensing ion channels (ASICs), activated by lowering extracellular pH (pH(o)), play an important role in normal synaptic transmission in brain and in the pathology of brain ischemia. Like pH(o), intracellular pH (pH(i)) changes dramatically in both physiological and pathological conditions. Although it is known that a drop in pH(o) activates the ASICs, it is not clear whether alterations of pH(i) have an effect on these channels.