Response: New neurons from old beliefs in the adult piriform cortex? A Commentary on: 'Occurrence of new neurons in the piriform cortex'

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Specialized Vasculature in the Rostral Migratory Stream as a Neurogenic Niche and Scaffold for Neuroblast Migration

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Image processing methods to elucidate spatial characteristics of retinal microglia after optic nerve transection

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Local proliferation is the main source of rod microglia after optic nerve transection

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MS4a4B, a CD20 Homologue in T Cells, Inhibits T Cell Propagation by Modulation of Cell Cycle

MS4a4B, a CD20 homologue in T cells, is a novel member of the MS4A gene family in mice. The MS4A family includes CD20, FcεRIβ, HTm4 and at least 26 novel members that are characterized by their structural features: with four membrane-spanning domains, two extracellular domains and two cytoplasmic regions. CD20, FcεRIβ and HTm4 have been found to function in B cells, mast cells and hematopoietic cells respectively. However, little is known about the function of MS4a4B in T cell regulation. We demonstrate here that MS4a4B negatively regulates mouse T cell proliferation. MS4a4B is highly expressed in primary T cells, natural killer cells (NK) and some T cell lines. But its expression in all malignant T cells, including thymoma and T hybridoma tested, was silenced. Interestingly, its expression was regulated during T cell activation. Viral vector-driven overexpression of MS4a4B in primary T cells and EL4 thymoma cells reduced cell proliferation. In contrast, knockdown of MS4a4B accelerated T cell proliferation. Cell cycle analysis showed that MS4a4B regulated T cell proliferation by inhibiting entry of the cells into S-G2/M phase. MS4a4B-mediated inhibition of cell cycle was correlated with upregulation of Cdk inhibitory proteins and decreased levels of Cdk2 activity, subsequently leading to inhibition of cell cycle progression. Our data indicate that MS4a4B negatively regulates T cell proliferation. MS4a4B, therefore, may serve as a modulator in the negative-feedback regulatory loop of activated T cell

Proteomics: in pursuit of effective traumatic brain injury therapeutics

Effective traumatic brain injury (TBI) therapeutics remain stubbornly elusive. Efforts in the field have been challenged by the heterogeneity of clinical TBI, with greater complexity among underlying molecular phenotypes than initially conceived. Future research must confront the multitude of factors comprising this heterogeneity, representing a big data challenge befitting the coming informatics age. Proteomics is poised to serve a central role in prescriptive therapeutic development, as it offers an efficient endpoint within which to assess post-TBI biochemistry. We examine rationale for multifactor TBI proteomic studies and the particular importance of temporal profiling in defining biochemical sequences and guiding therapeutic development. Lastly, we offer perspective on repurposing biofluid proteomics to develop theragnostic assays with which to prescribe, monitor and assess pharmaceutics for improved translation and outcome for TBI patients

Identifying the structure of Zn-N-2 active sites and structural activation

Identification of active sites is one of the main obstacles to rational design of catalysts for diverse applications. Fundamental insight into the identification of the structure of active sites and structural contributions for catalytic performance are still lacking. Recently, X-ray absorption spectroscopy (XAS) and density functional theory (DFT) provide important tools to disclose the electronic, geometric and catalytic natures of active sites. Herein, we demonstrate the structural identification of Zn-N-2 active sites with both experimental/theoretical X-ray absorption near edge structure (XANES) and extended X-ray absorption fine structure (EXAFS) spectra. Further DFT calculations reveal that the oxygen species activation on Zn-N-2 active sites is significantly enhanced, which can accelerate the reduction of oxygen with high selectivity, according well with the experimental results. This work highlights the identification and investigation of Zn-N-2 active sites, providing a regular principle to obtain deep insight into the nature of catalysts for various catalytic applications

Serum amyloid A primes microglia for ATP-dependent interleukin-1\u3b2 release

Acute-phase response is a systemic reaction to environmental/inflammatory insults and involves production of acute-phase proteins, including serum amyloid A (SAA). Interleukin-1\u3b2 (IL-1\u3b2), a master regulator of neuroinflammation produced by activated inflammatory cells of the myeloid lineage, in particular microglia, plays a key role in the pathogenesis of acute and chronic diseases of the peripheral nervous system and CNS. IL-1\u3b2 release is promoted by ATP acting at the purinergic P2X7 receptor (P2X7R) in cells primed with toll-like receptor (TLR) ligands

Apparent temperature and acute myocardial infarction hospital admissions in Copenhagen, Denmark: a case-crossover study

<p>Abstract</p> <p>Background</p> <p>The influence of temperature on acute myocardial infarction (AMI) has not been investigated as extensively as the effects of broader outcomes of morbidity and mortality. Sixteen studies reported inconsistent results and two considered confounding by air pollution. We addressed some of the methodological limitations of the previous studies in this study.</p> <p>Methods</p> <p>This is the first study of the association between the daily 3-hour maximum apparent temperature (Tapp_max) and AMI hospital admissions in Copenhagen. The study period covered 1 January 1999-31 December 2006, stratified in warm (April - September) and cold (October - March) periods. A case-crossover epidemiology study design was applied. Models were adjusted for public holidays and influenza, confounding by PM₁₀, NO₂and CO was investigated, the lag and non-linear effects of Tapp_maxwas examined, effect modification by age, sex and SES was explored, and the results of the case-crossover models were compared to those of the generalised additive Poisson time-series and generalised estimating equation models.</p> <p>Results</p> <p>14 456 AMI hospital admissions (12 995 people) occurred during the study period. For an inter-quartile range (6 or 7°C) increase in the 5-day cumulative average of Tapp_max, a 4% (95% CI:-2%; 10%) and 9% (95% CI: 3%; 14%) decrease in the AMI admission rate was observed in the warm and cold periods, respectively. The 19-65 year old group, men and highest SES group seemed to be more susceptible in the cold period.</p> <p>Conclusion</p> <p>An increase in Tapp_maxis associated with a decrease in AMI admissions during the colder months.</p