Characterization of the complete chloroplast genome of Platycodon grandifloras (Campanulaceae: Platycodon), the herbal medicine in China

Platycodon grandiflorus is the single genus plant in family Campanulaceae, which is distributed in areas of China, Japan, Korea, and Russia. In this study, we assembled and annotated the complete chloroplast genome of P. grandiflorus. The chloroplast genome of P. grandiflorus is 171,624 bp long, containing a shorter small single-copy region (SSC) of 7,962 bp, a normal large single-copy region (LSC) of 79,690 bp and a longer pair of inverted repeat regions (IRs) of 41,986 bp. The whole chloroplast genome of P. grandiflorus has 146 genes, including 102 protein-coding genes (PCGs), 36 transfer RNA genes (tRNAs), and 8 ribosome RNA genes (rRNAs). The overall nucleotide composition is: A of 30.9%, T of 30.9%, C of 19.3%, and G of 18.9%, with a total G + C content of the chloroplast genome 38.2%. The phylogenetic and genetic analysis showed a close relationship between Platycodon grandiflorus and Codonopsis lanceolata

Precise Fabrication of Porous Microspheres by Iso-Density Emulsion Combined with Microfluidics

Polymer porous microspheres with large specific surface areas and good fluidity have promising important applications in the biomedical field. However, controllable fabrication of porous microspheres with precise size, morphology, and pore structure is still a challenge, and phase separation caused by the instability of the emulsion is the main factor affecting the precise preparation of porous microspheres. Herein, a method combining the iso-density emulsion (IDE) template and microfluidics was proposed to realize the controllable preparation of polymer porous microspheres. The IDE exhibited excellent stability with minimal phase separation within 4 h, thus showing potential advantages in the large-scale preparation of porous microspheres. With the IDE template combined microfluidics technique and the use of a customized amphoteric copolymer, PEG-b-polycaprolactone, polycaprolactone (PCL) porous microspheres with porosity higher than 90% were successfully prepared. Afterwards, the main factors, including polymer concentration, water–oil ratio and homogenization time were investigated to regulate the pore structure of microspheres, and microspheres with different pore sizes (1–30 μm) were obtained. PCL porous microspheres exhibited comparable cell viability relative to the control group and good potential as cell microcarriers after surface modification with polydopamine. The modified PCL porous microspheres implanted subcutaneously in rats underwent rapid in vivo degradation and tissue ingrowth. Overall, this study demonstrated an efficient strategy for the precise preparation of porous microspheres and investigated the potential of the as-prepared PCL porous microspheres as cell microcarriers and micro-scaffolds

M1 muscarinic acetylcholine receptor interacts with BACE1 and regulates its proteosomal degradation

A prime culprit in the pathogenesis of Alzheimer's disease (AD) is overproduction/aggregation of beta-amyloid (A beta), which is derived from beta-Amyloid Precursor Protein through sequential cleavages by beta-site APP cleaving protein 1 (BACE1) and gamma-secretase. The level/activity of BACE1 is elevated in sporadic AD and identification of proteins that affect BACE1 is important in AD research. Here we found that M1 Muscarinic acetylcholine receptor (M1 mAChR), an important G protein-coupled receptor involved in cholinergic neuronal activity, can interact with BACE1 and mediate its proteosomal degradation. Moreover, overexpression and downregulation of M1 mAChR can decrease and increase the levels of BACE1, as well as the generation of A beta, respectively. These findings point to a novel coupling of BACE1 and M1 mAChR in AD and possibly schizophrenia. (C) 2012 Elsevier Ireland Ltd. All rights reserved.Alzheimer's Association; National Natural Science Foundation of China [30973150, 81161120496, 81000540]; 973 Prophase Project [2010CB535004]; Natural Science Foundation of Fujian Province of China [2009J06022, 2010J01235]; Program for New Century Excellent Talents in Universities (NCET); Fundamental Research Funds for the Central Universities; Fok Ying Tung Education Foundatio

Trafficking regulation of proteins in Alzheimer's disease

National Institutes of Health [R01AG038710, R01AG021173, R01AG044420, R01NS046673]; Alzheimer's Association; National Natural Science Foundation of China [81225008, 81000540, 81161120496, 91332112, 91332114]; Fundamental Research Funds for the Central Universities of China; Fok Ying Tung Education FoundationThe beta-amyloid (A beta) peptide has been postulated to be a key determinant in the pathogenesis of Alzheimer's disease (AD). A beta is produced through sequential cleavage of the beta-amyloid precursor protein (APP) by beta-and gamma-secretases. APP and relevant secretases are transmembrane proteins and traffic through the secretory pathway in a highly regulated fashion. Perturbation of their intracellular trafficking may affect dynamic interactions among these proteins, thus altering A beta generation and accelerating disease pathogenesis. Herein, we review recent progress elucidating the regulation of intracellular trafficking of these essential protein components in AD

M1 muscarinic acetylcholine receptor in Alzheimer's disease

National Institutes of Health, USA [R01AG038710, R01AG021173, R01AG044420, R01NS046673]; Alzheimer's Association; National Natural Science Foundation of China [91332112, 81225008, 81161120496]; Fundamental Research Funds for the Central Universities of China; Fok Ying Tung Education FoundationThe degeneration of cholinergic neurons and cholinergic hypofunction are pathologies associated with Alzheimer's disease (AD). Muscarinic acetylcholine receptors (mAChRs) mediate acetylcholine-induced neurotransmission and five mAChR subtypes (M1-M5) have been identified. Among them, M1 mAChR is widely expressed in the central nervous system and has been implicated in many physiological and pathological brain functions. In addition, M1 mAChR is postulated to be an important therapeutic target for AD and several other neurodegenerative diseases. In this article, we review recent progress in understanding the functional involvement of M1 mAChR in AD pathology and in developing M1 mAChR agonists for AD treatment