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C26H26N6O5, monoclinic, P21/c (no. 14), a = 10.9393(1) Å, b = 16.8724(2) Å, c = 13.5836(2) Å, β = 102.843(1)°, V = 2444.43(5) Å3, Z = 4, R gt(F) = 0.0318, wRref (F 2) = 0.0827, T = 173 K.

C54H48N4O2, triclinic, P1‾$P\overline{1}$ (no. 2), a = 11.1883(5) Å, b = 13.5364(5) Å, c = 14.3412(5) Å, α = 105.885(3)°, β = 97.710(3)°, γ = 94.126(3)°, Z = 2, V = 2056.64(14) Å3, Rgt(F) = 0.0685, wRref(F2) = 0.1606, T = 293(2) K.

C44H45N5O2, triclinic P1‾ $P\overline{1}$ (no. 2), a = 11.2140(4) Å, b = 11.9932(5) Å, c = 14.2703(5) Å, α = 98.879(3)°, β = 102.025(3)°, γ = 91.122(3)°, Z = 2, V = 1851.98(12) Å3, R gt(F) = 0.0549, wR ref(F 2) = 0.1616, T = 293(2) K.

In this study, we investigated the effects of different Ca2+ and Mg2+ concentrations in the water column on the growth and molting of Macrobrachium rosenbergii. We used three concentrations of both Ca2+ and Mg2+ and tested these in culture experiments over a period of four complete molting cycles. Analyses revealed that increasing concentrations of Ca2+ in the water led to a gradual reduction in the expression levels of MIH and a gradual increase in the expression levels of EcR and chitinase, thus accelerating molting frequency and shortening the molting cycle. However, high concentrations of Ca2+ significantly reduced the survival rate of M. rosenbergii. Increasing concentrations of Mg2+ in the water column led to a significant increase in heart beat count (P < 0.05); in addition, malate dehydrogenase activity during postmolt A and intermolt C tended to increase, and energy metabolism was accelerated. Furthermore, increased Ca2+ concentrations in the water column promoted an increase in the Ca2+ content of muscles and shells. In contrast, as the Mg2+ concentration in the water column increased, the Mg2+ content in the muscles and shells showed different patterns of change. Too low or too high Ca2+ and Mg2+ concentrations in the external environment had differing degrees of negative effects on the gill tissue such as edema and necrosis. In summary, low levels of Ca2+ and Mg2+ in the external environment reduced ion levels in the muscle and shell; inhibited growth, molting, and survival; and exerted negative effects on the gill tissue. Furthermore, high concentrations of Ca2+ and Mg2+ may accelerate molting rate and energy metabolism, but can cause more serious damage to gill tissue and reduce the survival rate. [ABSTRACT FROM AUTHOR]

C26H26N6O5, monoclinic, P21/c (no. 14), a = 10.9393(1) Å, b = 16.8724(2) Å, c = 13.5836(2) Å, β = 102.843(1)°, V = 2444.43(5) Å3, Z = 4, Rgt(F) = 0.0318, wRref(F2) = 0.0827, T = 173 K. [ABSTRACT FROM AUTHOR]

In the present paper, on the basis of molecular hybridization, a series of 4,6-dihydrazone pyrimidine derivatives containing the pyridine moiety were synthesized, structurally characterized, and evaluated in vitro for their antitumor activity. According to the results, all the tested compounds demonstrated broad-spectrum antitumor activity against selected tumor cell lines (MCF-7, BGC-823, A549, and BEL-7402) and no obvious toxicity toward normal cells HL-7702. In particular, compounds 10a and 10f were found to be the most promising antitumor agents among the tested compounds against BGC-823 cells (IC50 = 9.00 μM and 7.89 μM) and BEL-7402 cells (IC50 = 6.70 μM and 7.66 μM), respectively. Compounds 10a and 10f exhibited higher potency against BGC-823 and BEL-7402 than the positive control 5-FU (IC50 = 15.18 μM and 15.81 μM). Further mechanism investigations demonstrated that compounds 10a and 10f could significantly increase the level of cellular ROS and induce early apoptosis of BGC-823 cells in a dose-dependent manner. Moreover, the DNA binding results from UV/Vis, CD spectroscopy, and molecular docking studies indicated that 10a and 10f bind with DNA via groove binding and partial intercalation. These results demonstrated that 10a and 10f may serve as novel lead compounds for the discovery of more dihydrazone pyrimidine derivatives with improved antitumor potency and selectivity. [ABSTRACT FROM AUTHOR]

C26H26N6O5, monoclinic, P21/c (no. 14), a = 10.9393(1) Å, b = 16.8724(2) Å, c = 13.5836(2) Å, β = 102.843(1)°, V = 2444.43(5) Å3, Z = 4, Rgt(F) = 0.0318, wRref(F2) = 0.0827, T = 173 K. [ABSTRACT FROM AUTHOR]

C44H45N5O2, triclinic P 1 ‾ $P\bar{1}$ (no. 2), a = 11.2140(4) Å, b = 11.9932(5) Å, c = 14.2703(5) Å, α = 98.879(3)°, β = 102.025(3)°, γ = 91.122(3)°, Z = 2, V = 1851.98(12) Å3, R gt (F) = 0.0549, wR ref(F 2) = 0.1616, T = 293(2) K. [ABSTRACT FROM AUTHOR]