Zinc-doped hydroxyapatite and poly(propylene fumarate) nanocomposite scaffold for bone tissue engineering

Hydroxyapatite (HA) is a bioceramic material that shares similar crystal and chemical structures with inorganic components of the bone. However, HA lacks osteoinductive activity and has a brittle nature, making it challenging to apply for direct load-bearing bone applications. In this study, we used a wet chemical method to synthesize zinc-doped hydroxyapatite powders with different Zn/(Zn+Ca) molar ratios of 0, 0.025, 0.05, and 0.1. The corresponding Zn-HA was designated as HA, Zn2.5-HA, Zn5-HA, and Zn10-HA. The Zn-HA powders at 30 wt% were used to fabricate poly(propylene fumarate) (PPF)-based nanocomposite scaffolds (HA/PPF, Zn2.5-HA/PPF, Zn5-HA/PPF, and Zn10-HA/PPF). The physical properties of obtained scaffolds were examined by scanning electron microscopy, energy-dispersive X-ray spectroscopy (EDS), transmission electron microscopy (TEM), and atomic force microscopy (AFM). Live/dead cell viability assay showed that these scaffolds were biocompatible and supported excellent adhesion of MC3T3-E1 preosteoblast cells. Additionally, the proliferation of cells was detected at 1, 4, and 7 days on these scaffolds. Alkaline phosphatase (ALP) activity measurement and alizarin red staining showed good osteogenic differentiation and matrix mineralization for MC3T3-E1 cells growing on these scaffolds. Taken together, the results here indicate that Zn5-HA/PPF nanocomposite scaffolds are promising scaffold material for bone tissue engineering.

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Role of α2-Adrenoceptor Subtypes in Suppression of L-Type Ca2+ Current in Mouse Cardiac Myocytes

Sarcolemmal α2 adrenoceptors (α2-AR), represented by α2A, α2B and α2C isoforms, can safeguard cardiac muscle under sympathoadrenergic surge by governing Ca²⁺ handling and contractility of cardiomyocytes. Cardiomyocyte-specific targeting of α2-AR would provide cardiac muscle-delimited stress control and enhance the efficacy of cardiac malfunction treatments. However, little is known about the specific contribution of the α2-AR subtypes in modulating cardiomyocyte functions. Herein, we analyzed the expression profile of α2A, α2B and α2C subtypes in mouse ventricle and conducted electrophysiological antagonist assay evaluating the contribution of these isoforms to the suppression of L-type Ca²⁺ current (I_CaL). Patch-clamp electro-pharmacological studies revealed that the α2-agonist-induced suppression of I_CaL involves mainly the α2C, to a lesser extent the α2B, and not the α2A isoforms. RT-qPCR evaluation revealed the presence of adra2b and adra2c (α2B and α2C isoform genes, respectively), but was unable to identify the expression of adra2a (α2A isoform gene) in the mouse left ventricle. Immunoblotting confirmed the presence only of the α2B and the α2C proteins in this tissue. The identified α2-AR isoform-linked regulation of I_CaL in the mouse ventricle provides an important molecular substrate for the cardioprotective targeting.     

The Derivation of a New Blind Equalization Algorithm

Blind equalization is a technique for adaptive equalization of a communication channel without the aid of training sequences. This paper proposes a new blind equalization algorithm. The advantage of the new algorithm is that it has the lower residual error than the GA (proposed by Godard) and Sign_GA (proposed by Weerackody et al.). The superior performance of the proposed algorithm is illustrated for the 16-QAM signal constellation. A Rummler channel model is assumed as a transmission medium. The performance of the proposed algorithm is compared to the GA, Sign_GA and Stop & Go Algorithm (SGA). The simulation results demonstrate that an improvement in performance is achieved with the proposed equalization algorithm.