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Optical emission from a kilonova following a gravitational-wave-detected neutron-star merger

Nature's Advance Online Publication - Mon, 2017-10-16 07:00

Nature advance online publication 16 October 2017. doi:10.1038/nature24291

Authors: Iair Arcavi, Griffin Hosseinzadeh, D. Andrew Howell, Curtis McCully, Dovi Poznanski, Daniel Kasen, Jennifer Barnes, Michael Zaltzman, Sergiy Vasylyev, Dan Maoz & Stefano Valenti

The merger of two neutron stars has been predicted to produce an optical–infrared transient (lasting a few days) known as a ‘kilonova’, powered by the radioactive decay of neutron-rich species synthesized in the merger. Evidence that short ?-ray bursts also arise from neutron-star mergers has been accumulating. In models of such mergers, a small amount of mass (10?4–10?2 solar masses) with a low electron fraction is ejected at high velocities (0.1–0.3 times light speed) or carried out by winds from an accretion disk formed around the newly merged object. This mass is expected to undergo rapid neutron capture (r-process) nucleosynthesis, leading to the formation of radioactive elements that release energy as they decay, powering an electromagnetic transient. A large uncertainty in the composition of the newly synthesized material leads to various expected colours, durations and luminosities for such transients. Observational evidence for kilonovae has so far been inconclusive because it was based on cases of moderate excess emission detected in the afterglows of ?-ray bursts. Here we report optical to near-infrared observations of a transient coincident with the detection of the gravitational-wave signature of a binary neutron-star merger and with a low-luminosity short-duration ?-ray burst. Our observations, taken roughly every eight hours over a few days following the gravitational-wave trigger, reveal an initial blue excess, with fast optical fading and reddening. Using numerical models, we conclude that our data are broadly consistent with a light curve powered by a few hundredths of a solar mass of low-opacity material corresponding to lanthanide-poor (a fraction of 10?4.5 by mass) ejecta.

Categories: Topical E-Journals

The X-ray counterpart to the gravitational-wave event GW170817

Nature's Advance Online Publication - Mon, 2017-10-16 07:00

Nature advance online publication 16 October 2017. doi:10.1038/nature24290

Authors: E. Troja, L. Piro, H. van Eerten, R. T. Wollaeger, M. Im, O. D. Fox, N. R. Butler, S. B. Cenko, T. Sakamoto, C. L. Fryer, R. Ricci, A. Lien, R. E. Ryan, O. Korobkin, S.-K. Lee, J. M. Burgess, W. H. Lee, A. M. Watson, C. Choi, S. Covino, P. D’Avanzo, C. J. Fontes, J. Becerra González, H. G. Khandrika, J. Kim, S.-L. Kim, C.-U. Lee, H. M. Lee, A. Kutyrev, G. Lim, R. Sánchez-Ramírez, S. Veilleux, M. H. Wieringa & Y. Yoon

A long-standing paradigm in astrophysics is that collisions—or mergers—of two neutron stars form highly relativistic and collimated outflows (jets) that power ?-ray bursts of short (less than two seconds) duration. The observational support for this model, however, is only indirect. A hitherto outstanding prediction is that gravitational-wave events from such mergers should be associated with ?-ray bursts, and that a majority of these bursts should be seen off-axis, that is, they should point away from Earth. Here we report the discovery observations of the X-ray counterpart associated with the gravitational-wave event GW170817. Although the electromagnetic counterpart at optical and infrared frequencies is dominated by the radioactive glow (known as a ‘kilonova’) from freshly synthesized rapid neutron capture (r-process) material in the merger ejecta, observations at X-ray and, later, radio frequencies are consistent with a short ?-ray burst viewed off-axis. Our detection of X-ray emission at a location coincident with the kilonova transient provides the missing observational link between short ?-ray bursts and gravitational waves from neutron-star mergers, and gives independent confirmation of the collimated nature of the ?-ray-burst emission.

Categories: Topical E-Journals

Erratum: Strains, functions and dynamics in the expanded Human Microbiome Project

Nature's Advance Online Publication - Thu, 2017-10-12 07:00

Nature advance online publication 12 October 2017. doi:10.1038/nature24485

Author: Jason Lloyd-Price, Anup Mahurkar, Gholamali Rahnavard, Jonathan Crabtree, Joshua Orvis, A. Brantley Hall, Arthur Brady, Heather H. Creasy, Carrie McCracken, Michelle G. Giglio, Daniel McDonald, Eric A. Franzosa, Rob Knight, Owen White & Curtis Huttenhower

Categories: Topical E-Journals

Gravitational waves: A golden binary

Nature's Advance Online Publication - Wed, 2017-10-11 07:00

Nature advance online publication 16 October 2017. doi:10.1038/nature24153

Author: M. Coleman Miller

The discovery of gravitational waves from a neutron-star merger and the detection of the event across the electromagnetic spectrum give insight into many aspects of gravity and astrophysics.

Categories: Topical E-Journals

Neurobiology: Domains to the rescue for Rett syndrome

Nature's Advance Online Publication - Wed, 2017-10-11 07:00

Nature advance online publication 11 October 2017. doi:10.1038/nature24151

Author: Anne E. West

Rett syndrome is a brain disorder caused by disrupted forms of the protein MECP2, but how MECP2 loss affects the brain is unknown. A mouse study now implicates key domains of the protein and offers therapeutic insights.

Categories: Topical E-Journals

Cancer development: Origins in the oesophagus

Nature's Advance Online Publication - Wed, 2017-10-11 07:00

Nature advance online publication 11 October 2017. doi:10.1038/nature24150

Authors: Lizhe Zhuang & Rebecca C. Fitzgerald

The cellular origins of a precancerous condition called Barrett's oesophagus have been unclear. Tracking and analysis of epithelial cells at the affected site could shed light on the problem.

Categories: Topical E-Journals

DNA sequencing at 40: past, present and future

Nature's Advance Online Publication - Wed, 2017-10-11 07:00

Nature advance online publication 11 October 2017. doi:10.1038/nature24286

Authors: Jay Shendure, Shankar Balasubramanian, George M. Church, Walter Gilbert, Jane Rogers, Jeffery A. Schloss & Robert H. Waterston

Categories: Topical E-Journals

Human TRPML1 channel structures in open and closed conformations

Nature's Advance Online Publication - Wed, 2017-10-11 07:00

Nature advance online publication 11 October 2017. doi:10.1038/nature24036

Authors: Philip Schmiege, Michael Fine, Günter Blobel & Xiaochun Li

Categories: Topical E-Journals

Structure of mammalian endolysosomal TRPML1 channel in nanodiscs

Nature's Advance Online Publication - Wed, 2017-10-11 07:00

Nature advance online publication 11 October 2017. doi:10.1038/nature24035

Authors: Qingfeng Chen, Ji She, Weizhong Zeng, Jiangtao Guo, Haoxing Xu, Xiao-chen Bai & Youxing Jiang

Transient receptor potential mucolipin 1 (TRPML1) is a cation channel located within endosomal and lysosomal membranes. Ubiquitously expressed in mammalian cells, its loss-of-function mutations are the direct cause of type IV mucolipidosis, an autosomal recessive lysosomal storage disease. Here we present the single-particle electron cryo-microscopy structure of the mouse TRPML1 channel embedded in nanodiscs. Combined with mutagenesis analysis, the TRPML1 structure reveals that phosphatidylinositol-3,5-bisphosphate (PtdIns(3,5)P2) binds to the N terminus of the channel—distal from the pore—and the helix–turn–helix extension between segments S2 and S3 probably couples ligand binding to pore opening. The tightly packed selectivity filter contains multiple ion-binding sites, and the conserved acidic residues form the luminal Ca2+-blocking site that confers luminal pH and Ca2+ modulation on channel conductance. A luminal linker domain forms a fenestrated canopy atop the channel, providing several luminal ion passages to the pore and creating a negative electrostatic trap, with a preference for divalent cations, at the luminal entrance. The structure also reveals two equally distributed S4–S5 linker conformations in the closed channel, suggesting an S4–S5 linker-mediated PtdInsP2 gating mechanism among TRPML channels.

Categories: Topical E-Journals

Nucleosome–Chd1 structure and implications for chromatin remodelling

Nature's Advance Online Publication - Wed, 2017-10-11 07:00

Nature advance online publication 11 October 2017. doi:10.1038/nature24046

Authors: Lucas Farnung, Seychelle M. Vos, Christoph Wigge & Patrick Cramer

Chromatin-remodelling factors change nucleosome positioning and facilitate DNA transcription, replication, and repair. The conserved remodelling factor chromodomain-helicase-DNA binding protein 1(Chd1) can shift nucleosomes and induce regular nucleosome spacing. Chd1 is required for the passage of RNA polymerase IIthrough nucleosomes and for cellular pluripotency. Chd1 contains the DNA-binding domains SANT and SLIDE, a bilobal motor domain that hydrolyses ATP, and a regulatory double chromodomain. Here we report the cryo-electron microscopy structure of Chd1 from the yeast Saccharomyces cerevisiae bound to a nucleosome at a resolution of 4.8?Å. Chd1 detaches two turns of DNA from the histone octamer and binds between the two DNA gyres in a state poised for catalysis. The SANT and SLIDE domains contact detached DNA around superhelical location (SHL) ?7 of the first DNA gyre. The ATPase motor binds the second DNA gyre at SHL +2 and is anchored to the N-terminal tail of histone H4, as seen in a recent nucleosome–Snf2 ATPase structure. Comparisons with published results reveal that the double chromodomain swings towards nucleosomal DNA at SHL +1, resulting in ATPase closure. The ATPase can then promote translocation of DNA towards the nucleosome dyad, thereby loosening the first DNA gyre and remodelling the nucleosome. Translocation may involve ratcheting of the two lobes of the ATPase, which is trapped in a pre- or post-translocation state in the absence or presence, respectively, of transition state-mimicking compounds.

Categories: Topical E-Journals

Cryo-electron microscopy structure of the lysosomal calcium-permeable channel TRPML3

Nature's Advance Online Publication - Wed, 2017-10-11 07:00

Nature advance online publication 11 October 2017. doi:10.1038/nature24055

Authors: Marscha Hirschi, Mark A. Herzik Jr, Jinhong Wie, Yang Suo, William F. Borschel, Dejian Ren, Gabriel C. Lander & Seok-Yong Lee

The modulation of ion channel activity by lipids is increasingly recognized as a fundamental component of cellular signalling. The transient receptor potential mucolipin (TRPML) channel family belongs to the TRP superfamily and is composed of three members: TRPML1–TRPML3. TRPMLs are the major Ca2+-permeable channels on late endosomes and lysosomes (LEL). They regulate the release of Ca2+ from organelles, which is important for various physiological processes, including organelle trafficking and fusion. Loss-of-function mutations in the MCOLN1 gene, which encodes TRPML1, cause the neurodegenerative lysosomal storage disorder mucolipidosis type IV, and a gain-of-function mutation (Ala419Pro) in TRPML3 gives rise to the varitint–waddler (Va) mouse phenotype. Notably, TRPML channels are activated by the low-abundance and LEL-enriched signalling lipid phosphatidylinositol-3,5-bisphosphate (PtdIns(3,5)P2), whereas other phosphoinositides such as PtdIns(4,5)P2, which is enriched in plasma membranes, inhibit TRPMLs. Conserved basic residues at the N terminus of the channel are important for activation by PtdIns(3,5)P2 and inhibition by PtdIns(4,5)P2. However, owing to a lack of structural information, the mechanism by which TRPML channels recognize PtdIns(3,5)P2 and increase their Ca2+ conductance remains unclear. Here we present the cryo-electron microscopy (cryo-EM) structure of a full-length TRPML3 channel from the common marmoset (Callithrix jacchus) at an overall resolution of 2.9?Å. Our structure reveals not only the molecular basis of ion conduction but also the unique architecture of TRPMLs, wherein the voltage sensor-like domain is linked to the pore via a cytosolic domain that we term the mucolipin domain. Combined with functional studies, these data suggest that the mucolipin domain is responsible for PtdIns(3,5)P2 binding and subsequent channel activation, and that it acts as a ‘gating pulley’ for lipid-dependent TRPML gating.

Categories: Topical E-Journals

Transitional basal cells at the squamous–columnar junction generate Barrett’s oesophagus

Nature's Advance Online Publication - Wed, 2017-10-11 07:00

Nature advance online publication 12 October 2017. doi:10.1038/nature24269

Authors: Ming Jiang, Haiyan Li, Yongchun Zhang, Ying Yang, Rong Lu, Kuancan Liu, Sijie Lin, Xiaopeng Lan, Haikun Wang, Han Wu, Jian Zhu, Zhongren Zhou, Jianming Xu, Dong-Kee Lee, Lanjing Zhang, Yuan-Cho Lee, Jingsong Yuan, Julian A. Abrams, Timothy C. Wang, Antonia R. Sepulveda, Qi Wu, Huaiyong Chen, Xin Sun, Junjun She, Xiaoxin Chen & Jianwen Que

In several organ systems, the transitional zone between different types of epithelium is a hotspot for pre-neoplastic metaplasia and malignancy, but the cells of origin for these metaplastic epithelia and subsequent malignancies remain unknown. In the case of Barrett’s oesophagus, intestinal metaplasia occurs at the gastro-oesophageal junction, where stratified squamous epithelium transitions into simple columnar cells. On the basis of a number of experimental models, several alternative cell types have been proposed as the source of this metaplasia but in all cases the evidence is inconclusive: no model completely mimics Barrett’s oesophagus in terms of the presence of intestinal goblet cells. Here we describe a transitional columnar epithelium with distinct basal progenitor cells (p63+KRT5+KRT7+) at the squamous–columnar junction of the upper gastrointestinal tract in a mouse model. We use multiple models and lineage tracing strategies to show that this squamous–columnar junction basal cell population serves as a source of progenitors for the transitional epithelium. On ectopic expression of CDX2, these transitional basal progenitors differentiate into intestinal-like epithelium (including goblet cells) and thereby reproduce Barrett’s metaplasia. A similar transitional columnar epithelium is present at the transitional zones of other mouse tissues (including the anorectal junction) as well as in the gastro-oesophageal junction in the human gut. Acid reflux-induced oesophagitis and the multilayered epithelium (believed to be a precursor of Barrett’s oesophagus) are both characterized by the expansion of the transitional basal progenitor cells. Our findings reveal a previously unidentified transitional zone in the epithelium of the upper gastrointestinal tract and provide evidence that the p63+KRT5+KRT7+ basal cells in this zone are the cells of origin for multi-layered epithelium and Barrett’s oesophagus.

Categories: Topical E-Journals

The prevalence of Plasmodium falciparum in sub-Saharan Africa since 1900

Nature's Advance Online Publication - Wed, 2017-10-11 07:00

Nature advance online publication 11 October 2017. doi:10.1038/nature24059

Authors: Robert W. Snow, Benn Sartorius, David Kyalo, Joseph Maina, Punam Amratia, Clara W. Mundia, Philip Bejon & Abdisalan M. Noor

Malaria transmission is influenced by climate, land use and deliberate interventions. Recent declines have been observed in malaria transmission. Here we show that the African continent has witnessed a long-term decline in the prevalence of Plasmodium falciparum from 40% prevalence in the period 1900–1929 to 24% prevalence in the period 2010–2015, a trend that has been interrupted by periods of rapidly increasing or decreasing transmission. The cycles and trend over the past 115 years are inconsistent with explanations in terms of climate or deliberate intervention alone. Previous global initiatives have had minor impacts on malaria transmission, and a historically unprecedented decline has been observed since 2000. However, there has been little change in the high transmission belt that covers large parts of West and Central Africa. Previous efforts to model the changing patterns of P. falciparum transmission intensity in Africa have been limited to the past 15 years or have used maps drawn from historical expert opinions. We provide quantitative data, from 50,424 surveys at 36,966 geocoded locations, that covers 115 years of malaria history in sub-Saharan Africa; inferring from these data to future trends, we would expect continued reductions in malaria transmission, punctuated with resurgences.

Categories: Topical E-Journals

Radically truncated MeCP2 rescues Rett syndrome-like neurological defects

Nature's Advance Online Publication - Wed, 2017-10-11 07:00

Nature advance online publication 11 October 2017. doi:10.1038/nature24058

Authors: Rebekah Tillotson, Jim Selfridge, Martha V. Koerner, Kamal K. E. Gadalla, Jacky Guy, Dina De Sousa, Ralph D. Hector, Stuart R. Cobb & Adrian Bird

Heterozygous mutations in the X-linked MECP2 gene cause the neurological disorder Rett syndrome. The methyl-CpG-binding protein 2 (MeCP2) protein is an epigenetic reader whose binding to chromatin primarily depends on 5-methylcytosine. Functionally, MeCP2 has been implicated in several cellular processes on the basis of its reported interaction with more than 40 binding partners, including transcriptional co-repressors (for example, the NCoR/SMRT complex), transcriptional activators, RNA, chromatin remodellers, microRNA-processing proteins and splicing factors. Accordingly, MeCP2 has been cast as a multi-functional hub that integrates diverse processes that are essential in mature neurons. At odds with the concept of broad functionality, missense mutations that cause Rett syndrome are concentrated in two discrete clusters coinciding with interaction sites for partner macromolecules: the methyl-CpG binding domain and the NCoR/SMRT interaction domain. Here we test the hypothesis that the single dominant function of MeCP2 is to physically connect DNA with the NCoR/SMRT complex, by removing almost all amino-acid sequences except the methyl-CpG binding and NCoR/SMRT interaction domains. We find that mice expressing truncated MeCP2 lacking both the N- and C-terminal regions (approximately half of the native protein) are phenotypically near-normal; and those expressing a minimal MeCP2 additionally lacking a central domain survive for over one year with only mild symptoms. This minimal protein is able to prevent or reverse neurological symptoms when introduced into MeCP2-deficient mice by genetic activation or virus-mediated delivery to the brain. Thus, despite evolutionary conservation of the entire MeCP2 protein sequence, the DNA and co-repressor binding domains alone are sufficient to avoid Rett syndrome-like defects and may therefore have therapeutic utility.

Categories: Topical E-Journals

Structural phase transition in monolayer MoTe2 driven by electrostatic doping

Nature's Advance Online Publication - Wed, 2017-10-11 07:00

Nature advance online publication 11 October 2017. doi:10.1038/nature24043

Authors: Ying Wang, Jun Xiao, Hanyu Zhu, Yao Li, Yousif Alsaid, King Yan Fong, Yao Zhou, Siqi Wang, Wu Shi, Yuan Wang, Alex Zettl, Evan J. Reed & Xiang Zhang

Monolayers of transition-metal dichalcogenides (TMDs) exhibit numerous crystal phases with distinct structures, symmetries and physical properties. Exploring the physics of transitions between these different structural phases in two dimensions may provide a means of switching material properties, with implications for potential applications. Structural phase transitions in TMDs have so far been induced by thermal or chemical means; purely electrostatic control over crystal phases through electrostatic doping was recently proposed as a theoretical possibility, but has not yet been realized. Here we report the experimental demonstration of an electrostatic-doping-driven phase transition between the hexagonal and monoclinic phases of monolayer molybdenum ditelluride (MoTe2). We find that the phase transition shows a hysteretic loop in Raman spectra, and can be reversed by increasing or decreasing the gate voltage. We also combine second-harmonic generation spectroscopy with polarization-resolved Raman spectroscopy to show that the induced monoclinic phase preserves the crystal orientation of the original hexagonal phase. Moreover, this structural phase transition occurs simultaneously across the whole sample. This electrostatic-doping control of structural phase transition opens up new possibilities for developing phase-change devices based on atomically thin membranes.

Categories: Topical E-Journals

Establishment of mouse expanded potential stem cells

Nature's Advance Online Publication - Wed, 2017-10-11 07:00

Nature advance online publication 11 October 2017. doi:10.1038/nature24052

Authors: Jian Yang, David J. Ryan, Wei Wang, Jason Cheuk-Ho Tsang, Guocheng Lan, Hideki Masaki, Xuefei Gao, Liliana Antunes, Yong Yu, Zhexin Zhu, Juexuan Wang, Aleksandra A. Kolodziejczyk, Lia S. Campos, Cui Wang, Fengtang Yang, Zhen Zhong, Beiyuan Fu, Melanie A. Eckersley-Maslin, Michael Woods, Yosuke Tanaka, Xi Chen, Adam C. Wilkinson, James Bussell, Jacqui White, Ramiro Ramirez-Solis, Wolf Reik, Berthold Göttgens, Sarah A. Teichmann, Patrick P. L. Tam, Hiromitsu Nakauchi, Xiangang Zou, Liming Lu & Pentao Liu

Mouse embryonic stem cells derived from the epiblast contribute to the somatic lineages and the germline but are excluded from the extra-embryonic tissues that are derived from the trophectoderm and the primitive endoderm upon reintroduction to the blastocyst. Here we report that cultures of expanded potential stem cells can be established from individual eight-cell blastomeres, and by direct conversion of mouse embryonic stem cells and induced pluripotent stem cells. Remarkably, a single expanded potential stem cell can contribute both to the embryo proper and to the trophectoderm lineages in a chimaera assay. Bona fide trophoblast stem cell lines and extra-embryonic endoderm stem cells can be directly derived from expanded potential stem cells in vitro. Molecular analyses of the epigenome and single-cell transcriptome reveal enrichment for blastomere-specific signature and a dynamic DNA methylome in expanded potential stem cells. The generation of mouse expanded potential stem cells highlights the feasibility of establishing expanded potential stem cells for other mammalian species.

Categories: Topical E-Journals

Ion sieving in graphene oxide membranes via cationic control of interlayer spacing

Nature's Advance Online Publication - Mon, 2017-10-09 07:00

Nature advance online publication 09 October 2017. doi:10.1038/nature24044

Authors: Liang Chen, Guosheng Shi, Jie Shen, Bingquan Peng, Bowu Zhang, Yuzhu Wang, Fenggang Bian, Jiajun Wang, Deyuan Li, Zhe Qian, Gang Xu, Gongping Liu, Jianrong Zeng, Lijuan Zhang, Yizhou Yang, Guoquan Zhou, Minghong Wu, Wanqin Jin, Jingye Li & Haiping Fang

Graphene oxide membranes—partially oxidized, stacked sheets of graphene—can provide ultrathin, high-flux and energy-efficient membranes for precise ionic and molecular sieving in aqueous solution. These materials have shown potential in a variety of applications, including water desalination and purification, gas and ion separation, biosensors, proton conductors, lithium-based batteries and super-capacitors. Unlike the pores of carbon nanotube membranes, which have fixed sizes, the pores of graphene oxide membranes—that is, the interlayer spacing between graphene oxide sheets (a sheet is a single flake inside the membrane)—are of variable size. Furthermore, it is difficult to reduce the interlayer spacing sufficiently to exclude small ions and to maintain this spacing against the tendency of graphene oxide membranes to swell when immersed in aqueous solution. These challenges hinder the potential ion filtration applications of graphene oxide membranes. Here we demonstrate cationic control of the interlayer spacing of graphene oxide membranes with ångström precision using K+, Na+, Ca2+, Li+ or Mg2+ ions. Moreover, membrane spacings controlled by one type of cation can efficiently and selectively exclude other cations that have larger hydrated volumes. First-principles calculations and ultraviolet absorption spectroscopy reveal that the location of the most stable cation adsorption is where oxide groups and aromatic rings coexist. Previous density functional theory computations show that other cations (Fe2+, Co2+, Cu2+, Cd2+, Cr2+ and Pb2+) should have a much stronger cation–? interaction with the graphene sheet than Na+ has, suggesting that other ions could be used to produce a wider range of interlayer spacings.

Categories: Topical E-Journals

Biochemistry: Complex assistance for DNA invasion

Nature's Advance Online Publication - Wed, 2017-10-04 07:00

Nature advance online publication 04 October 2017. doi:10.1038/nature24149

Author: Petr Cejka

Repair of broken DNA is vital for genome stability and to prevent the development of cancer. Research shows how the tumour-suppressor protein BRCA1 promotes a DNA-repair pathway called homologous recombination.

Categories: Topical E-Journals

Mathematics: A pariah finds a home

Nature's Advance Online Publication - Wed, 2017-10-04 07:00

Nature advance online publication 04 October 2017. doi:10.1038/nature24147

Author: Terry Gannon

Pariahs are fundamental building blocks in a branch of mathematics called group theory, but seem to be unconnected from both physics and other areas of mathematics. Such a connection has now been identified.

Categories: Topical E-Journals

Cancer: Tumours addicted to drugs are vulnerable

Nature's Advance Online Publication - Wed, 2017-10-04 07:00

Nature advance online publication 04 October 2017. doi:10.1038/nature24148

Authors: Rebecca J. Lee & Richard Marais

Cancer cells can develop an 'addiction' to the drugs they are treated with, so that they need the drugs to survive. Analysis of the underlying mechanism reveals a potential clinical strategy for harnessing this phenomenon.

Categories: Topical E-Journals
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