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Weekly Reports ㄗ109ㄘon International Trends of Cutting 每edge Life Science Development
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Add Timeㄩ2014/2/12 17:21:04
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1.      Birth order link to being overweight
 
Birth order link to being overweight
Helen Briggs
 
First-born children may be more likely than second-borns to be overweight in later life.
A small study of middle-aged men living in New Zealand found children born first into their family were about one stone (7kg) heavier and had a bigger BMI than second-borns.
They also had more insulin resistance, which can lead to health problems.
Birth order may affect the risk of cardiovascular disease and type 2 diabetes, say researchers.
Larger studies are needed to fully evaluate this link, they add.
There is some evidence to suggest birth order may influence the body's fat make-up and metabolism, from infancy to the teenage years.
However, the potential impact in mid-life is unknown.
"Being first born is one such risk factor, it does not mean first-borns will become overweight or diabetic, being first-born simply increases the risk."
The researchers say the study needs to be repeated in pairs of siblings and with more subjects.
Christopher Allen, senior cardiac nurse at the British Heart Foundation, said carrying extra weight can not only increase the risk of cardiovascular disease, but also affect how sensitive the body is to insulin.
"By having lower insulin sensitivity, this increases your risk of developing type 2 diabetes.
"It's also important to note where you carry your weight.
"People who carry more fat around their middle are more likely to be resistant to the insulin their body is producing."
 
 
2.      Alveolar progenitor and stem cells in lung development, renewal and cancer
▽Text abstracts▼Nature (2014) doi:10.1038/nature12930
 
Alveolar progenitor and stem cells in lung development, renewal and cancer
Tushar J. Desai, Douglas G. Brownfield & Mark A. Krasnow
Alveoli are gas-exchange sacs lined by squamous alveolar type (AT) 1 cells and cuboidal, surfactant-secreting AT2 cells. Classical studies suggested that AT1 arise from AT2 cells, but recent studies propose other sources. Here we use molecular markers, lineage tracing and clonal analysis to map alveolar progenitors throughout the mouse lifespan. We show that, during development, AT1 and AT2 cells arise directly from a bipotent progenitor, whereas after birth new AT1 cells derive from rare, self-renewing, long-lived, mature AT2 cells that produce slowly expanding clonal foci of alveolar renewal. This stem-cell function is broadly activated by AT1 injury, and AT2 self-renewal is selectively induced by EGFR (epidermal growth factor receptor) ligands in vitro and oncogenic Kras(G12D) in vivo, efficiently generating multifocal, clonal adenomas. Thus, there is a switch after birth, when AT2 cells function as stem cells that contribute to alveolar renewal, repair and cancer. We propose that local signals regulate AT2 stem-cell activity: a signal transduced by EGFR-KRAS controls self-renewal and is hijacked during oncogenesis, whereas another signal controls reprogramming to AT1 fate.
 
3.      High-Dose Parenteral Ascorbate Enhanced Chemosensitivity of Ovarian Cancer and Reduced Toxicity of Chemotherapy
▽Text abstracts▼Sci Transl Med 5 February 2014: Vol. 6, Issue 222, p. 222ra18
 
High-Dose Parenteral Ascorbate Enhanced Chemosensitivity of Ovarian Cancer and Reduced Toxicity of Chemotherapy
Yan Ma, Julia Chapman, Mark Levine, et al.
 
Ascorbate (vitamin C) was an early, unorthodox therapy for cancer, with an outstanding safety profile and anecdotal clinical benefit. Because oral ascorbate was ineffective in two cancer clinical trials, ascorbate was abandoned by conventional oncology but continued to be used in complementary and alternative medicine. Recent studies provide rationale for reexamining ascorbate treatment. Because of marked pharmacokinetic differences, intravenous, but not oral, ascorbate produces millimolar concentrations both in blood and in tissues, killing cancer cells without harming normal tissues. In the interstitial fluid surrounding tumor cells, millimolar concentrations of ascorbate exert local pro-oxidant effects by mediating hydrogen peroxide (H2O2) formation, which kills cancer cells. We investigated downstream mechanisms of ascorbate-induced cell death. Data show that millimolar ascorbate, acting as a pro-oxidant, induced DNA damage and depleted cellular adenosine triphosphate (ATP), activated the ataxia telangiectasia mutated (ATM)/adenosine monophosphate每activated protein kinase (AMPK) pathway, and resulted in mammalian target of rapamycin (mTOR) inhibition and death in ovarian cancer cells. The combination of parenteral ascorbate with the conventional chemotherapeutic agents carboplatin and paclitaxel synergistically inhibited ovarian cancer in mouse models and reduced chemotherapy-associated toxicity in patients with ovarian cancer. On the basis of its potential benefit and minimal toxicity, examination of intravenous ascorbate in combination with standard chemotherapy is justified in larger clinical trials.
 
4. In Vivo Direct Reprogramming of Reactive Glial Cells into Functional Neurons after Brain Injury and in an Alzheimer*s Disease Model
▽Text abstracts▼Cell Stem Cell, Volume 14, Issue 2, 188-202, 19 December 2013
 
In Vivo Direct Reprogramming of Reactive Glial Cells into Functional Neurons after Brain Injury and in an Alzheimer*s Disease Model
Ziyuan Guo, Lei Zhang, Zheng Wu, et al.
 
Loss of neurons after brain injury and in neurodegenerative disease is often accompanied by reactive gliosis and scarring, which are difficult to reverse with existing treatment approaches. Here, we show that reactive glial cells in the cortex of stab-injured or Alzheimer*s disease (AD) model mice can be directly reprogrammed into functional neurons in vivo using retroviral expression of a single neural transcription factor, NeuroD1. Following expression of NeuroD1, astrocytes were reprogrammed into glutamatergic neurons, while NG2 cells were reprogrammed into glutamatergic and GABAergic neurons. Cortical slice recordings revealed both spontaneous and evoked synaptic responses in NeuroD1-converted neurons, suggesting that they integrated into local neural circuits. NeuroD1 expression was also able to reprogram cultured human cortical astrocytes into functional neurons. Our studies therefore suggest that direct reprogramming of reactive glial cells into functional neurons in vivo could provide an alternative approach for repair of injured or diseased brain.
 
5.      Fundamental Differences in Dedifferentiation and Stem Cell Recruitment during Skeletal Muscle Regeneration in Two Salamander Species
▽Text abstracts▼Cell Stem Cell, Volume 14, Issue 2, 174-187, 21 November 2013
 
Fundamental Differences in Dedifferentiation and Stem Cell Recruitment during Skeletal Muscle Regeneration in Two Salamander Species
Tatiana Sandoval-Guzm芍n, Heng Wang, Shahryar Khattak, et al.
 
Salamanders regenerate appendages via a progenitor pool called the blastema. The cellular mechanisms underlying regeneration of muscle have been much debated but have remained unclear. Here we applied Cre-loxP genetic fate mapping to skeletal muscle during limb regeneration in two salamander species, Notophthalmus viridescens (newt) and Ambystoma mexicanum (axolotl). Remarkably, we found that myofiber dedifferentiation is an integral part of limb regeneration in the newt, but not in axolotl. In the newt, myofiber fragmentation results in proliferating, PAX7mononuclear cells in the blastema that give rise to the skeletal muscle in the new limb. In contrast, myofibers in axolotl do not generate proliferating cells, and do not contribute to newly regenerated muscle; instead, resident PAX7+ cells provide the regeneration activity. Our results therefore show significant diversity in limb muscle regeneration mechanisms among salamanders and suggest that multiple strategies may be feasible for inducing regeneration in other species, including mammals.
 

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