Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.

Input: Consider Input: Abstract: The short-term effects of incremental doses of procainamide (7.5, 15, 22.5, and 30 mg/kg) on right ventricular effective refractory period, intraventricular conduction, and induction of ventricular tachycardia were determined in 31 patients who had a history of sustained, unimorphic ventricular tachycardia. QRS duration during incremental ventricular pacing was used as an index of rate-dependent changes in intraventricular conduction. The mean plasma procainamide concentrations corresponding to the incremental doses were 5.5 +/- 1.2 (+/- SD), 9.0 +/- 1.6, 12.6 +/- 2.2, and 16.3 +/- 3.2 mg/liter. Each incremental dose of procainamide up to a dose of 30 mg/kg resulted in a significant increment in right ventricular effective refractory period and each dose up to 22.5 mg/kg potentiated a rate-dependent prolongation of QRS duration. After the 7.5 mg/kg dose of procainamide, induction of ventricular tachycardia was suppressed in eight of 31 patients. After higher doses of procainamide, induction of ventricular tachycardia was suppressed in two additional patients. In three of 10 patients in whom the induction of ventricular tachycardia was suppressed by 7.5, 15, or 22.5 mg/kg of procainamide, sustained unimorphic ventricular tachycardia was again inducible after a higher dose of procainamide. In three of 31 patients, only nonsustained ventricular tachycardia was inducible after a 7.5 to 22.5 mg/kg dose of procainamide; however, in two of these three patients, sustained ventricular tachycardia was again inducible after administration of a higher dose of procainamide. In conclusion, during electropharmacologic testing with procainamide, it is worthwhile to test a dose of 7.5 mg/kg, because this dose is often effective in patients who respond to this drug. However, the results of this study indicate that procainamide may be effective in suppressing the induction of sustained ventricular tachycardia at a relatively low plasma concentration, but not at a higher plasma concentration. Therefore, during long-term therapy with procainamide it may be important to avoid plasma procainamide concentrations not only lower, but also higher than the concentration that results in the suppression of induction of tachycardia.

Output: Effects of incremental doses of procainamide on ventricular refractoriness, intraventricular conduction, and induction of ventricular tachycardia.

Input: Consider Input: Abstract: When bovine parathyroid cells in culture are exposed to the active vitamin D metabolite 1,25(OH)2D3, a significant decrease in the steady-state levels of pre-proparathyroid hormone (pre-proPTH) mRNA occurs. The possibility that the fall in specific mRNA is due to a decrease in rate of transcription of the PTH gene was examined in this study. In the presence of 1,25(OH)2D3, there was a rapid and steady decline in PTH gene transcription rate which fell to a minimum of 10-15% of control at 24 h. The effect was observed at physiological levels (10(-11)M) and was also fully reversible.

Output: Suppression by 1,25(OH)2D3 of transcription of the pre-proparathyroid hormone gene.

Input: Consider Input: Abstract: The NK-1.1(-) mouse was constructed by weekly injections of monoclonal anti-NK-1.1 antibody from birth through adulthood. Spleen cells from these mice have decreased NK-1.1+ cells and null (Thy-1- and B220-) cells. Their splenic NK activity to YAC targets was low and was not enhanced by IFN-alpha or IFN-beta. Bone marrow (BM) of these NK-1.1(-) mice have normal precursors to NK cells: 1) NK activity could be generated from NK-1.1(-) BM cells cultured in rIL 2 for 5 to 6 days. These cultured BM cells expressed Qa-5, Thy-1, AsGm-1, and NK-1.1 antigens. The precursor cells of these BM cytotoxic cells are NK-1.1-; 2) transfer of BM cells from the NK-1.1(-) mice reconstituted the NK activity of irradiated, NK-depleted recipients. Lymphokine-activated killer cells could also be generated from spleens of these NK-1.1(-) mice. Therefore, the NK-1.1(-) mice were specifically depleted of mature cytotoxic NK cells, but not the NK-1.1- precursors of NK cells. This mouse model is valuable to study ontogeny and physiologic relevance of NK cells.
Output: The NK-1.1(-) mouse: a model to study differentiation of murine NK cells.