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Weekly Reports ㄗ103ㄘon International Trends of Cutting 每edge Life Science Development
Add Timeㄩ2013/12/16 16:18:24
1.      Caffeine energy drinks 'intensify heart contractions'
Caffeine energy drinks 'intensify heart contractions'
Energy drinks packed with caffeine can change the way the heart beats, researchers warn. The team from the University of Bonn in Germany imaged the hearts of 17 people an hour after they had an energy drink.
The study showed contractions were more forceful after the drink. The team told the annual meeting of the Radiological Society of North America that children and people with some health conditions should avoid the drinks.
Researcher Dr Jonas Dorner said: "Until now, we haven't known exactly what effect these energy drinks have on the function of the heart.
"The amount of caffeine is up to three times higher than in other caffeinated beverages like coffee or cola.
"There are many side effects known to be associated with a high intake of caffeine, including rapid heart rate, palpitations, rise in blood pressure and, in the most severe cases, seizures or sudden death."
The researchers gave the participants a drink containing 32mg per 100ml of caffeine and 400mg per 100ml of another chemical, taurine.
Short-term impact
They showed the chamber of the heart that pumps blood around the body, the left ventricle, was contracting harder an hour after the energy drink was taken than at the start of the study.
Dr Dorner added: "We've shown that energy drink consumption has a short-term impact on cardiac contractility.
"We don't know exactly how or if this greater contractility of the heart impacts daily activities or athletic performance."
The impact on people with heart disease is also unknown.
However, the research team advises that children and people with an irregular heartbeat should avoid the drinks.
2.      Control of the timing and dosage of IGF-I delivery from encapsulated cells
▽Text abstracts▼Journal of Tissue Engineering and Regenerative Medicine
Volume 7, Issue 6, pages 470每478, June 2013
Control of the timing and dosage of IGF-I delivery from encapsulated cells
Roshni S. Patel*, Amy Chang, Michael J. Lysaght, Jeffrey R. Morgan
We report here on the development and characterization of a cell-based system for the regulated delivery of bioactive insulin-like growth factor I (IGF-I). A stable mammalian cell line, CHO-K1 Tet-IGFI, was genetically modified to have tetracycline-induced transcription of the human IGF-I gene. Cells were activated to express IGF-I in the presence of doxycycline (DOX), a tetracycline derivative, while expression was inactivated in the absence of DOX. Temporal, or on-off, release of IGF-I from cells encapsulated within Ca2+-alginate hydrogels was demonstrated in a pilot study over the course of 10 days in culture. Released growth factor was bioactive, exhibiting a proliferative effect comparable to recombinant purified IGF-I protein. The dosage levels and temporal control of IGF-I release from encapsulated cells meet the requirements of orthopedic wound repair, making this approach an attractive means for the controlled synthesis and delivery of growth factors in situ for wound healing.
3.      Effect of chondroitin sulphate C on the in vitro and in vivo chondrogenesis of mesenchymal stem cells in crosslinked type II collagen scaffolds
▽Text abstracts▼Journal of Tissue Engineering and Regenerative Medicine, Volume 7, Issue 8, pages 665每672, August 2013
Effect of chondroitin sulphate C on the in vitro and in vivo chondrogenesis of mesenchymal stem cells in crosslinked type II collagen scaffolds
Wei-Chuan Chen1, Yu-Hong Wei2, I-Ming Chu1, Chao-Ling Yao3,
This study evaluates the crosslinkage effect of chondroitin sulphate C (CSC) and type II collagen (COL II) on chondrogenesis of mesenchymal stem cells (MSCs) in vitro and in vivo. In the in vitro studies, our results show that the weight ratio CSC:COL II that reaches 1.2:100 (CSC1.2/100每COL II scaffold) can provide an optimal microenvironment for MSC chondrogenesis. When MSCs are cultured in this CSC1.2/100每COL II scaffold, the chondrogenic gene expression of cultured cells is upregulated, while the osteogenic gene expression of these is downregulated. In addition, MSCs cultivated in the CSC1.2/100每COL II scaffold are found to express the highest glycosaminoglycans: DNA ratio as compared to those in scaffolds of other CSC:COL II ratios. Histological and immunohistological evidence also supports the result. In the in vivo study, our results show that MSCs cultivated in the CSC1.2/100每COL II scaffold demonstrate a better repair ability on cartilage lesions than does the COL II scaffold. After 1 month in vivo, the injected MSCs in the CSC1.2/100每COL II scaffold show lacuna structures and stimulate the formation of type II collagen at the defective sites. Six months after transplantation, the generated cells in the CSC1.2/100每COL II group show higher gene expressions of type II collagen and aggrecan but lower gene expression of type I collagen at the defective sites than those in the COL II group. The results strongly suggest that CSC1.2/100每COL II scaffold can serve as a potential candidate for cartilage repair and improve the chondrogenesis of MSCs in general.
4.      Programmed Cell Senescence during Mammalian Embryonic Development
▽Text abstracts▼Cell, Volume 155, Issue 5, 1104-1118, 14 November 2013
Programmed Cell Senescence during Mammalian Embryonic Development
Daniel Muñoz-Esp赤n, Marta Cañamero, Antonio Maraver
Cellular senescence disables proliferation in damaged cells, and it is relevant for cancer and aging. Here, we show that senescence occurs during mammalian embryonic development at multiple locations, including the mesonephros and the endolymphatic sac of the inner ear, which we have analyzed in detail. Mechanistically, senescence in both structures is strictly dependent on p21, but independent of DNA damage, p53, or other cell-cycle inhibitors, and it is regulated by the TGF-汕/SMAD and PI3K/FOXO pathways. Developmentally programmed senescence is followed by macrophage infiltration, clearance of senescent cells, and tissue remodeling. Loss of senescence due to the absence of p21 is partially compensated by apoptosis but still results in detectable developmental abnormalities. Importantly, the mesonephros and endolymphatic sac of human embryos also show evidence of senescence. We conclude that the role of developmentally programmed senescence is to promote tissue remodeling and propose that this is the evolutionary origin of damage-induced senescence.
5. Lysine Methylation Promotes VEGFR-2 Activation and Angiogenesis
▽Text abstracts▼Cell Stem Cell, Volume 13, Issue 5, 602-616, 12 September 2013
Lysine Methylation Promotes VEGFR-2 Activation and Angiogenesis
Activation of vascular endothelial growth factor receptor-2 (VEGFR-2), an endothelial cell receptor tyrosine kinase, promotes tumor angiogenesis and ocular neovascularization. We report the methylation of VEGFR-2 at multiple Lys and Arg residues, including Lys1041, a residue that is proximal to the activation loop of the kinase domain. Methylation of VEGFR-2 was independent of ligand binding and was not regulated by ligand stimulation. Methylation of Lys1041 enhanced tyrosine phosphorylation and kinase activity in response to ligands. Additionally, interfering with the methylation of VEGFR-2 by pharmacological inhibition or by site-directed mutagenesis revealed that methylation of Lys1041 was required for VEGFR-2每mediated angiogenesis in zebrafish and tumor growth in mice. We propose that methylation of Lys1041 promotes the activation of VEGFR-2 and that similar posttranslational modification could also regulate the activity of other receptor tyrosine kinases.

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