Energy-Efficient Non-Orthogonal Transmission under Reliability and Finite Blocklength Constraints

This paper investigates an energy-efficient non-orthogonal transmission design problem for two downlink receivers that have strict reliability and finite blocklength (latency) constraints. The Shannon capacity formula widely used in traditional designs needs the assumption of infinite blocklength and thus is no longer appropriate. We adopt the newly finite blocklength coding capacity formula for explicitly specifying the trade-off between reliability and code blocklength. However, conventional successive interference cancellation (SIC) may become infeasible due to heterogeneous blocklengths. We thus consider several scenarios with different channel conditions and with/without SIC. By carefully examining the problem structure, we present in closed-form the optimal power and code blocklength for energy-efficient transmissions. Simulation results provide interesting insights into conditions for which non-orthogonal transmission is more energy efficient than the orthogonal transmission such as TDMA.Comment: accepted by IEEE GlobeCom workshop on URLLC, 201

Ursolic Acid Florotriazole Treatment Causes Inhibition of Squamous Cell Carcinoma through Fas Signaling Pathway

Purpose: To investigate the effect of ursolic acid florotriazole (UFT), on SCC-15 oral squamous cancer cells.Methods: Confocal laser microscope with a 490 nm argon laser was used to record the fluorescence of the cells and capture the images. Flow cytometry and Cell Quest program were used to analyze the DNA content of the stained cells. Apoptosis was characterized by YO-PRO-1 staining.Results: Treatment of SCC-15 cells with UFT for 48 h significantly reduced cell viability in a dosedependent manner. At 20 μg/mL concentration of UFT, SCC-15, cell viability was reduced to 19 % compared to 100 % in the untreated cells (p = 0.0002). UFT treatment enhanced the proportion of apoptotic cells which was evident from YO-PRO-1 staining. In UFT-treated cultures, the population of cells in sub-G1 phase increased to 38.54 % compared to 7.32 % for control after 48 h. Expression of Fas in UFT-treated cells was also higher (p = 0.0002) than in untreated cells. In C3H/HeJ mice, administration of UFT daily for 14 days caused a significant (p = 0.0002) reduction in tumor volume and weight after 30 days of SCC-15 carcinoma cell administration.Conclusion: UFT treatment inhibits viability and induces apoptosis in squamous cell carcinoma cells through suppression of Fas expression. Therefore, UFT may be useful for the treatment of squamous cell cancer.Keywords: Ursolic acid florotriazole, Squamous cell cancer, Fas expression, Tumor volume, Cell viability, Apoptosi

{4-Bromo-2-[3-(diethyl­ammonio)propyl­imino­meth­yl]phenolato}diiodidozinc(II) methanol solvate

In the title complex, [ZnI2(C14H21BrN2O)]·CH3OH, the asymmetric unit consists of a mononuclear zinc(II) complex mol­ecule and a methanol solvent mol­ecule. The compound was derived from the zwitterionic form of the Schiff base 4-bromo-2-[3-(diethyl­amino)propyl­imino­meth­yl]phenol. The ZnII atom is four-coordinated by the imine N and phenolate O atoms of the Schiff base ligand and by two iodide ions in a distorted tetra­hedral coordination. In the crystal structure, the methanol mol­ecules are linked to the Schiff base mol­ecules through N—H⋯O and O—H⋯O hydrogen bonds. One I atom is disordered over two positions in a 0.702 (19):0.298 (19) ratio

{4-Bromo-2-[2-(piperidin-1-ium-1yl)ethyl­iminometh­yl]phenolato}diiodido­zinc(II)

In the title complex, [ZnI2(C14H19BrN2O)], the ZnII atom is four-coordinated by the imine N and phenolate O atoms of the Schiff base ligand and by two iodide ions in a distorted tetra­hedral coordination. In the crystal structure, mol­ecules are linked through inter­molecular N—H⋯O hydrogen bonds, forming chains running along the b axis

Diiodido[N′-(2-methoxy­benzyl­idene)-N,N-dimethyl­ethane-1,2-diamine]zinc(II)

In the title complex, [Zn(C12H18N2O)I2], the ZnII ion is four-coordinated by the imine N and amine N atoms of the Schiff base ligand and by two iodide ions in a distorted tetra­hedral coordination

Inhibition of Caspase-3, -6, -8 and -9 Expression in Rats with Acute Spinal Cord Injury by Cantharidin Treatment

Purpose: To demonstrate the anti-apoptotic effects of cantharidin in mice with acute spinal cord injury (ASCI).Methods: In total, 30 male Sprague-Dawley mice were divided into three groups of 10 animals each. ASCI was induced in two of the groups using a modified Allen's method, consisting of treatment with 10 mg/kg body weight cantharidin after injury, and sacrifice on days 2, 5, 10, 20 and 30 to extract the spinal cord. The activity levels of caspase-3, -6, -8, and -9 were determined spectrophotometrically at 455 nm with a microplate reader.Results: The results showed that cantharidin treatment caused a significant reduction in the expression levels of all four caspases – caspase-3, -6, -8, and -9 – compared with the untreated groups. Two hours after ASCI, caspase levels in the cantharidin-treated group increased, reaching maximum after day 5, but were significantly lower than in the untreated group. The expression levels of caspases in the cantharidin-treated group were similar to those in the control group on days 20 and 30 following ASCI (p> 0.05).Conclusion: Cantharidin treatment exerts an anti-apoptotic effect against secondary spinal cord injury (SCI) by suppressing caspase activity. Thus, cantharidin may be suitable for the treatment of secondary SCI.Keywords: Cantharidin, Caspase, Anti-apoptotic, Inhibition, Regeneratio

Diiodido{4-nitro-2-[2-(piperidin-1-yl)ethyl­imino­meth­yl]phenolato}zinc(II)

In the title complex, [ZnI2(C14H19N3O3)], the ZnII atom is four-coordinated by the imine N and phenolate O atoms of the Schiff base ligand, and by two iodide ions in a distorted tetra­hedral coordination. In the crystal structure, mol­ecules are linked through inter­molecular N—H⋯O hydrogen bonds, forming dimers