Discrepancies between Reasons of Palliative Care Team Consultation and Palliative Care Team Activities.

Background: Palliative care team (PCT) is a common type of palliative care services. However, distress in cancer patients may be underestimated by hospital staff. Reasons for PCT consultation may be inconsistent with patients' actual needs.

[A search for the risk factors for hiccups and evaluation of antiemetic therapy in CDDP-based chemotherapy, using cluster analysis].

Hiccups are often observed in patients treated with cisplatin(CDDP)-based chemotherapy. It has been reported that gender and specific dosages of CDDP and antiemetic drugs(e.g.

[A survey of the dosage of zoledronic acid and investigation of the relationship between renal function and adverse events].

Zoledronic acid(ZA)dosage should be adjusted according to the risk it poses for renal impairment. The recommended dosage for patients with creatinine clearance(Ccr)of less than 60mL/min was established on the basis of an area under the curve analysis, but is doubted because it was calculated without performing a clinical trial. Creatinine secretion from the renal tubule affects Ccr; therefore, using Ccr as the basis for dosage adjustment may be inappropriate since this can cause an overestimation of the glomerular filtration rate(GFR).

Characteristics for enhanced response of serotonin-evoked ion dynamics in differentiated NG108-15 cells.

Characteristics for the up-regulated response in the concentration of intracellular calcium ion ([Ca(2+)]( i )) and in the sodium ion (Na(+)) current by serotonin (5-HT) were investigated in differentiated neuroblastoma x glioma hybrid NG108-15 (NG) cells. The results for the changes in [Ca(2+)]( i ) by 5-HT were as follows, (1) The 5-HT-induced Ca(2+) response was inhibited by 3 x 10(-9) M tropisetron (a 5-HT(3) receptor blocker), but not by other types of 5-HT receptor blockers; (2) The 5-HT-induced Ca(2+) response was mainly inhibited by calciseptine (a L-type Ca(2+) blocker), but not by other types of Ca(2+) channel blockers or 10(-7) M TTX (a voltage-sensitive Na(+) channel blocker); (3) When the extracellular Na(+) was removed by exchange with choline chloride or N-methyl-D-glucamine, the 5-HT-induced Ca(2+) response was extremely inhibited. The results for the 5-HT-induced Na(+) current by the whole cell patch-clamp technique were as follows, (1) The 5-HT-induced Na(+) current in differentiated cells was significantly larger than that in undifferentiated cells; (2) The ED(50) value for 5-HT-induced Na(+) current in undifferentiated and differentiated cells was almost the same, about 4 x 10(-6) M each other; (3) The 5-HT-induced Na(+) current was completely blocked by 3 x 10(-9) M tropisetron, but not by other 5-HT receptor antagonists and 10(-7) M TTX.

Enhancement of sodium current in NG108-15 cells during neural differentiation is mainly due to an increase in NaV1.7 expression.

It is well known that morphological and functional changes during neural differentiation sometimes accompany the expression of various voltage-gated ion channels. In this work, we investigated whether the enhancement of sodium current in differentiated neuroblastoma x glioma NG108-15 cells treated with dibutyryl cAMP is related to the expression of voltage-gated sodium channels. The results were as follows.

Enhancement of serotonin- and bradykinin-evoked calcium ion dynamics in differentiated NG108-15 cells.

Dynamic changes in the concentration of intracellular free-calcium ion ([Ca(2+)](i)) by carbachol (CCh) and neurotransmitter candidates was investigated in undifferentiated and differentiated neuroblastomaxglioma hybrid NG108-15 (NG) cells. [Ca(2+)](i) was increased in a dose-dependent manner by bradykinin (BK) and serotonin (5-HT) in differentiated NG cells, and the response to BK and 5-HT was significantly greater than that in undifferentiated NG cells. The EC(50) value of BK was approximately 1.

Enhancement of veratridine-induced sodium dynamics in NG108-15 cells during differentiation.

Developmental changes in dynamics of Na+ were studied in neuroblastomaxglioma hybrid NG108-15 cells during differentiation which was induced by dibutyryl cAMP (Bt2cAMP). Ratiometric Na+ imaging with a Na+-sensitive fluorescent dye SBFI (sodium-binding benzofuran isophthalate) revealed that the intracellular Na+ concentration ([Na+]i) was not affected by the application of high K+ (60 mM) solution to either control or differentiated cells. When cells were exposed to 50 microM veratridine (Vtd), an agonist of voltage-sensitive sodium channels (VSSCs), a significant increase in [Na+]i was observed in differentiated but not in undifferentiated cells.

Increased response to high KCl-induced elevation in the intracellular-Ca(2+) concentration in differentiated NG108-15 cell and the inhibitory effect of the L-type Ca(2+) channel blocker, calciseptine.

Characteristics of the increasing effect for the concentration of intracellular calcium ions ([Ca(2+)](i)) by high-KCl application were investigated in the neuroblastomaxglioma hybrid NG108-15 cell line (NG108-15 cells). The present study confirmed that the increasing effect of [Ca(2+)](i) by high-KCl application in single NG108-15 cells, differentiated with dibutyryl cAMP (Bt(2)cAMP), was significantly enhanced, compared to undifferentiated cells. The following observations were made at first: (1) The response to high-KCl application, in both undifferentiated and differentiated cells, was significantly inhibited by calciseptine (CaS), an L-type Ca(2+) channel blocker, but not by N-, P- and R-type Ca(2+) channel blockers.

Effects of calmodulin and Ca2+ channel blockers on omega-conotoxin GVIA binding to crude membranes from alpha1B subunit (Cav2.2) expressed BHK cells and mice brain lacking the alpha1B subunits.

Characteristics for the specific binding of 125I-omega-CTX GVIA and 125I-omega-CTX MVIIC to crude membranes from BHKN101 cells expressing the alpha1B subunits of Cav2.2 channels and from mice brain lacking the alpha1B subunits of Cav2.2 channels, particularly, the effects of CaM and various Ca2+ channel blockers on these specific bindings were investigated.