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Weekly Reports ㄗ92ㄘon International Trends of Cutting 每edge Life Science Development
Add Timeㄩ2013/5/6 17:07:06
1. Histone Demethylases Set the Stage for Cancer Metastasis
▽Text abstracts▼Sci. Signal, Vol. 6, Issue 273, p. pe15
Histone Demethylases Set the Stage for Cancer Metastasis
Jian Cao & Qin Yan
Metastasis is the major cause of cancer-related mortality. It is increasingly evident that epigenetic alterations in tumor cells enable them to overcome various barriers in this multistage process of cell spreading, and insight into the molecular roles of epigenetic regulators in tumor metastasis are just beginning to emerge. Histone demethylases appear to have critical roles in creating suitable epigenetic states for tumor cells to gain metastatic potential. These studies shed light on the roles of histone demethylases in tumor metastasis and highlight the importance of targeting these enzymes to suppress metastatic disease.
2. Translating Memories
▽Text abstracts▼Sci. Signal.,Vol. 6, Issue 273, p. ec94
Translating Memories
Nancy R. Gough
The cellular model of memory is a synaptic plasticity event called long-term potentiation (LTP). LTP can be divided into two phases: The early phase (E-LTP) lasts less than 2 hours and does not require new protein synthesis, and the late phase (L-LTP) can last many hours and requires new protein synthesis. Translation of mRNAs is regulated through various mechanisms, one of which is the binding of poly(A)-binding protein (PABP) to the poly(A) tail of the target mRNA. PAIP2A and PAIP2B (PAIP-interacting protein 2A and 2B) inhibit translation by interfering with PABP function. Khoutorsky et al. found that degradation of PAIP2A, which is the form that is abundant in the brain, linked synaptic activity to enhanced translation and contributed to learning and memory in mice. Hippocampal slices from Paip2a每/每 mice showed L-LTP in response to a stimulus that only triggered E-LTP in slices from wild-type mice and showed impaired L-LTP in response to a stimulus that triggered L-LTP in slices from wild-type mice. Consistent with these electrophysiological studies, behavorial memory tests indicated that Paip2a每/每 mice showed faster learning in spatial long-term memory tests in response to weak training but showed impaired learning in response to a long-term contextual fear conditioning test that used a strong training paradigm. Experiments with cultured neurons and hippocampal slices showed an activity-dependent decrease in the abundance of PAIP2A that could be prevented by pharmacological inhibition of the calcium-dependent proteases calpains. The calpain-dependent reduction in PAIP2A was also detected in mice subjected to the contextual fear conditioning paradigm, and infusion of calpain inhibitors impaired long-term contextual fear memory. Increased production of calcium-calmodulin kinase II汐 (CaMKII汐) occurs in response to synaptic activity and is necessary for learning. The abundance of CaMKII汐 in the hippocampus was increased in Paip2a每/每 mice trained in a contextual fear conditioning paradigm compared with untrained mice or wild-type trained mice. This increase in CaMKII汐 resulted from increased translation because CaMKII汐 mRNA was shifted to heavy polysome fractions in the brains of Paip2a每/每 trained mice and the association of PABP with this mRNA was greatest in the Paip2a每/每 trained mice. Thus, activity-dependent degradation of a translation inhibitor contributes to the enhanced translation needed for learning and memory.
3. Turn Off Youth
▽Text abstracts▼Sci. Signal., Vol. 6, Issue 272, p. ec91
Turn Off Youth
Pamela J. Hines
Our neurons regenerate better when we are young than when we are more mature. Studying the mechanosensory anterior ventral microtubule (AVM) neuron of the nematode Caenorhabditis elegans, Zou et al. (see the Perspective by Nix and Bastiani) found that worms lacking microRNA machinery had unusually robust axon regeneration and youthful-looking growth cones. Under- and overexpression of let-7 microRNA confirmed its involvement in depressing axon regeneration.
4. Evidence of a Role for Fibrocyte and Keratinocyte-like Cells in the Formation of Hypertrophic Scars
▽Text abstracts▼Journal of Burn Care & Research, March/April 2013 - Volume 34 - Issue 2 - p 227每231
Evidence of a Role for Fibrocyte and Keratinocyte-like Cells in the Formation of Hypertrophic Scars
Curran, Terry-Ann MB Bch BAO; Ghahary, Aziz PhD
Burn injuries affect millions of people every year, and dermal fibrosis is a common complication for the victims. This disfigurement has functional and cosmetic consequences and many research groups have made it the focus of their work to understand the mechanisms that underlie its development. Although significant progress has been made in wound-healing processes, the complexity of events involved makes it very difficult to come up with a single strategy to prevent this devastating fibrotic condition. Inflammation is considered one predisposing factor, although this phase is a necessary aspect of the wound-healing process. Inflammation, driven by infiltrated immune cells, begins minutes after the burn injury and is the prevalent phase of wound healing in the early stages. Accompanying the inflammatory infiltrate, there is evidence that subpopulations of bone marrow每derived cells are also present. These populations include fibrocytes and keratinocyte-like cells, derivatives of CD14+ monocytes, a component of the peripheral blood mononuclear cell infiltrate. There is evidence that these cells contribute to regeneration and repair of the wound site, but it is interesting to note that there are also reports that these cells can have adverse effects and may contribute to the development of dermal fibrosis. In this article, the authors present a review of the origin and transdifferentiation of these cells from bone marrow stem cells, the environments that direct this transdifferentiation, and evidence to support their role in fibrosis, as well as potential avenues for therapeutics to control their fibrotic effects.
5. Mitochondrial Activity on Aging
▽Text abstracts▼Trends in Endocrinology & Metabolism, Volume 24, Issue 5, 247-256,
Mitochondrial Activity on Aging
Matthew L. Johnson, Matthew M. Robinson, K. Sreekumaran NairSee
Decline in human muscle mass and strength (sarcopenia) is a hallmark of the aging process. A growing body of research in the areas of bioenergetics and protein turnover has placed the mitochondria at the center of this process. It is now clear that, unless an active lifestyle is rigorously followed, skeletal muscle mitochondrial decline occurs as humans age. Increasing research on mitochondrial biology has elucidated the regulatory pathways involved in mitochondrial biogenesis, many of which are potential therapeutic targets, and highlight the beneficial effects of vigorous physical activity on skeletal muscle health for an aging population.
6. Skin Cell Proliferation Stimulated by Microneedles
▽Text abstracts▼Journal of the American College of Clinical Wound Specialists
Volume 4, Issue 1
Skin Cell Proliferation Stimulated by Microneedles
A classical wound may be defined as a disruption of tissue integrity. Wounds, caused by trauma from accidents or surgery, that close via secondary intention rely on the biological phases of healing, i.e., hemostasis, inflammation, proliferation, and remodeling (HIPR). Depending on the wound type and severity, the inflammation phase begins immediately after injury and may last for an average of 7每14 days. Concurrent with the inflammation phase or slightly delayed, cell proliferation is stimulated followed by the activation of the remodeling (maturation) phase. The latter phase can last as long as 1 year or more, and the final healed state is represented by a scar tissue, a cross-linked collagen formation that usually aligns collagen fibers in a single direction. One may assume that skin microneedling that involves the use of dozens or as many as 200 needles that limit penetration to 1.5 mm over 1 cm2 of skin would cause trauma and bleeding followed by the classical HIPR. However, this is not the case or at least the HIPR phases are significantly curtailed and healing never ends in a scar formation. Conversely dermabrasion used in aesthetic medicine for improving skin quality is based on ※ablation§ (destruction or wounding of superficial skin layers), which requires several weeks for healing that involves formation of new skin layers. Such procedures provoke an acute inflammatory response. We believe that a less intense inflammatory response occurs following microneedle perforation of the skin. However, the mechanism of action of microneedling appears to be different. Here we review the potential mechanisms by which microneedling of the skin facilitates skin repair without scarring after the treatment of superficial burns, acne, hyperpigmentation, and the non-advancing periwound skin surrounding the chronic ulcerations of the integument.

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