The effect of a pathology clinic on the mental state and adjustment of patients with breast cancer.

OBJECTIVE: In this study, we examine whether a pathology clinic, conducted by pathologists, a novel medical tool that provides an explanation for the diagnosis of a cancer, can influence the mental state and adjustment of breast cancer patients. METHOD: We created a paper-based questionnaire and interviewed targeted breast cancer patients, who had undergone radical surgery, before and after they visited the clinic. RESULTS: We found that there may be increased motivation for treatment, a greater sense of reassurance, and reduced anxiety (as indicated by the Hospital Anxiety and Depression Scale (HADS)) in the group that attended the clinic. SIGNIFICANCE OF RESULTS: Our results suggest that visiting the pathology clinic may reduce anxiety over the short term. On the other hand, Mental Adjustment to Cancer (MAC) Anxious Preoccupation scores were significantly higher in this group as well, both before and after attendance, compared to the group that did not attend. The attending group may have reduced anxiety by such actions as collecting medical data on the cause of their anxiety and adopting healthier behaviors. Our findings suggest that appropriate emotional support and provision of medical information are very important in dealing with patient anxiety.

Intracellular calcium level is an important factor influencing ion channel modulations by PLC-coupled metabotropic receptors in hippocampal neurons.

Signaling pathways involving phospholipase C (PLC) are involved in various neural functions. Understanding how these pathways are regulated will lead to a better understanding of their roles in neural functions. Previous studies demonstrated that receptor-driven PLCß activation depends on intracellular Ca(2+) concentration ([Ca(2+)]i), suggesting the possibility that PLCß-dependent cellular responses are basically Ca(2+) dependent. To test this possibility, we examined whether modulations of ion channels driven by PLC-coupled metabotropic receptors are sensitive to [Ca(2+)]i using cultured hippocampal neurons. Muscarinic activation triggered an inward current at -100 mV (the equilibrium potential for K(+)) in a subpopulation of neurons. This current response was suppressed by pirenzepine (an M1-preferring antagonist), PLC inhibitor, non-selective cation channel blocker, and lowering [Ca(2+)]i. Using the neurons showing no response at -100 mV, effects of muscarinic activation on K(+) channels were examined at -40 mV. Muscarinic activation induced a transient decrease of the holding outward current. This current response was mimicked and occluded by XE991, an M-current K(+) channel blocker, suppressed by pirenzepine, PLC inhibitor and lowering [Ca(2+)]i, and enhanced by elevating [Ca(2+)]i. Similar results were obtained when group I metabotropic glutamate receptors were activated instead of muscarinic receptors. These results clearly show that ion channel modulations driven by PLC-coupled metabotropic receptors are dependent on [Ca(2+)]i, supporting the hypothesis that cellular responses induced by receptor-driven PLCß activation are basically Ca(2+) dependent.