What's new for 'JKB_daily1' in PubMed

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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Tuesday, 2014 December 16
Search: (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))

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PubMed Results

Items 1 - 10 of 10

1.	Science. 2014 Nov 14;346(6211):1256272. doi: 10.1126/science.1256272. Synthetic biology. Genomically encoded analog memory with precise in vivo DNA writing in living cell populations. Farzadfard F1, Lu TK2. Comment in Synthetic biology. Dynamic genome engineering in living cells. [Science. 2014] Synthetic biology. Dynamic genome engineering in living cells.Ausländer S, Fussenegger M. Science. 2014 Nov 14; 346(6211):813-4. Abstract Cellular memory is crucial to many natural biological processes and sophisticated synthetic biology applications. Existing cellular memories rely on epigenetic switches or recombinases, which are limited in scalability and recording capacity. In this work, we use the DNA of living cell populations as genomic "tape recorders" for the analog and distributed recording of long-term event histories. We describe a platform for generating single-stranded DNA (ssDNA) in vivo in response to arbitrary transcriptional signals. When coexpressed with a recombinase, these intracellularly expressed ssDNAs target specific genomic DNA addresses, resulting in precise mutations that accumulate in cell populations as a function of the magnitude and duration of the inputs. This platform could enable long-term cellular recorders for environmental and biomedical applications, biological state machines, and enhanced genome engineering strategies. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25395541 [PubMed - indexed for MEDLINE]
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2.	Science. 2014 Nov 7;346(6210):763-7. doi: 10.1126/science.1257570. Epub 2014 Nov 6. Phylogenomics resolves the timing and pattern of insect evolution. Misof B1, Liu S2, Meusemann K3, Peters RS4, Donath A5, Mayer C5, Frandsen PB6, Ware J7, Flouri T8, Beutel RG9, Niehuis O5, Petersen M5, Izquierdo-Carrasco F8, Wappler T10, Rust J10, Aberer AJ8, Aspöck U11, Aspöck H12, Bartel D13, Blanke A14, Berger S8, Böhm A13, Buckley TR15, Calcott B16, Chen J17, Friedrich F18, Fukui M19, Fujita M20, Greve C5, Grobe P5, Gu S17, Huang Y2, Jermiin LS21, Kawahara AY22, Krogmann L23, Kubiak M18, Lanfear R24, Letsch H25, Li Y2, Li Z17, Li J17, Lu H17, Machida R20, Mashimo Y20, Kapli P26, McKenna DD27, Meng G2, Nakagaki Y20, Navarrete-Heredia JL28, Ott M29, Ou Y17, Pass G13, Podsiadlowski L30, Pohl H9, von Reumont BM31, Schütte K32, Sekiya K20, Shimizu S20, Slipinski A33, Stamatakis A34, Song W2, Su X2, Szucsich NU13, Tan M2, Tan X17, Tang M2, Tang J17, Timelthaler G13, Tomizuka S20, Trautwein M35, Tong X36, Uchifune T37, Walzl MG13, Wiegmann BM38, Wilbrandt J5, Wipfler B9, Wong TK21, Wu Q2, Wu G17, Xie Y17, Yang S2, Yang Q2, Yeates DK33, Yoshizawa K39, Zhang Q2, Zhang R2, Zhang W17, Zhang Y17, Zhao J2, Zhou C2, Zhou L2, Ziesmann T5, Zou S17, Li Y17, Xu X17, Zhang Y2, Yang H17, Wang J17, Wang J40, Kjer KM41, Zhou X42. Abstract Insects are the most speciose group of animals, but the phylogenetic relationships of many major lineages remain unresolved. We inferred the phylogeny of insects from 1478 protein-coding genes. Phylogenomic analyses of nucleotide and amino acid sequences, with site-specific nucleotide or domain-specific amino acid substitution models, produced statistically robust and congruent results resolving previously controversial phylogenetic relations hips. We dated the origin of insects to the Early Ordovician [~479 million years ago (Ma)], of insect flight to the Early Devonian (~406 Ma), of major extant lineages to the Mississippian (~345 Ma), and the major diversification of holometabolous insects to the Early Cretaceous. Our phylogenomic study provides a comprehensive reliable scaffold for future comparative analyses of evolutionary innovations among insects. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25378627 [PubMed - indexed for MEDLINE]
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3.	Science. 2014 Nov 7;346(6210):698-9. doi: 10.1126/science.1258871. Evolution. Searching for new branches on the tree of life. Woyke T1, Rubin EM2.
	PMID: 25378606 [PubMed - indexed for MEDLINE]
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4.	Science. 2014 Nov 7;346(6210):684-5. doi: 10.1126/science.346.6210.684. Infectious Diseases. Delays hinder Ebola genomics. Vogel G.
	PMID: 25378599 [PubMed - indexed for MEDLINE]
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5.	Nature. 2014 Oct 30;514(7524):548. doi: 10.1038/514548a. Geneticists tap human knockouts. Callaway E.
	PMID: 25355341 [PubMed - indexed for MEDLINE]
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6.	Nature. 2014 Oct 23;514(7523):438-40. doi: 10.1038/nature13758. Epub 2014 Oct 1. Lung disease: Treatment by cell transplant. Thomassen MJ1, Kavuru MS2. Comment on Pulmonary macrophage transplantation therapy. [Nature. 2014] Pulmonary macrophage transplantation therapy.Suzuki T, Arumugam P, Sakagami T, Lachmann N, Chalk C, Sallese A, Abe S, Trapnell C, Carey B, Moritz T, et al. Nature. 2014 Oct 23; 514(7523):450-4. Epub 2014 Oct 1.
	PMID: 25274303 [PubMed - indexed for MEDLINE]
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7.	Nature. 2014 Oct 23;514(7523):450-4. doi: 10.1038/nature13807. Epub 2014 Oct 1. Pulmonary macrophage transplantation therapy. Suzuki T1, Arumugam P2, Sakagami T1, Lachmann N3, Chalk C1, Sallese A1, Abe S1, Trapnell C4, Carey B1, Moritz T3, Malik P2, Lutzko C2, Wood RE5, Trapnell BC6. Comment in Lung disease: Treatment by cell transplant. [Nature. 2014] Lung disease: Treatment by cell transplant.Thomassen MJ, Kavuru MS. Nature. 2014 Oct 23; 514(7523):438-40. Epub 2014 Oct 1. Abstract Bone-marrow transplantation is an effective cell therapy but requires myeloablation, which increases infection risk and mortality. Recent lineage-tracing studies documenting that resident macrophage populations self-maintain independently of haematological progenitors prompted us to consider organ-targeted, cell-specific therapy. Here, using granulocyte-macrophage colony-stimulating factor (GM-CSF) receptor-β-deficient (Csf2rb(-/-)) mice that develop a myeloid cell disorder identical to hereditary pulmonary alveolar proteinosis (hPAP) in children with CSF2RA or CSF2RB mutations, we show that pulmonary macrophage transplantation (PMT) of either wild-type or Csf2rb-gene-corrected macrophages without myeloablation was safe and well-tolerated and that one administration corrected the lung disease, secondary systemic manifestations and normalized disease-related biomarkers, and prevented disease-specific mortality. PMT-derived alveolar macrophages persisted for at least one year as did therapeutic effects. Our findings identify mechanisms regulating alveolar macrophage population size in health and disease, indicate that GM-CSF is required for phenotypic determination of alveolar macrophages, and support translation of PMT as the first specific therapy for children with hPAP. PMCID: PMC4236859 [Available on 2015/4/23]
	PMID: 25274301 [PubMed - indexed for MEDLINE]
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8.	Science. 2014 Nov 7;346(6210):751-5. doi: 10.1126/science.1255638. Epub 2014 Sep 18. Quality control of inner nuclear membrane proteins by the Asi complex. Foresti O1, Rodriguez-Vaello V1, Funaya C2, Carvalho P3. Comment in Cell Biology. Local synthesis and disposal. [Science. 2014] Cell Biology. Local synthesis and disposal.Shao S, Hegde RS. Science. 2014 Nov 7; 346(6210):701-2. Protein quality control: Nuclear membrane proteins in check. [Nat Rev Mol Cell Biol. 2014] Protein quality control: Nuclear membrane proteins in check.Baumann K. Nat Rev Mol Cell Biol. 2014 Nov; 15(11):700-1. Epub 2014 Oct 15. Abstract Misfolded proteins in the endoplasmic reticulum (ER) are eliminated by a quality control system called ER-associated protein degradation (ERAD). However, it is unknown how misfolded proteins in the inner nuclear membrane (INM), a specialized ER subdomain, are degraded. We used a quantitative proteomics approach to reveal an ERAD branch required for INM protein quality control in yeast. This branch involved the integral membrane proteins Asi1, Asi2, and Asi3, which assembled into an Asi complex. Besides INM misfolded proteins, the Asi complex promoted the degradation of functional regulators of sterol biosynthesis. Asi-mediated ERAD was required for ER homeostasis, which suggests that spatial segregation of protein quality control systems contributes to ER function. Copyright © 2014, American Association for the Advancement of Science.
	PMID: 25236469 [PubMed - indexed for MEDLINE]
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9.	Nature. 2014 Oct 23;514(7523):494-7. doi: 10.1038/nature13591. Epub 2014 Aug 20. Pre-Columbian mycobacterial genomes reveal seals as a source of New World human tuberculosis. Bos KI1, Harkins KM2, Herbig A3, Coscolla M4, Weber N5, Comas I6, Forrest SA7, Bryant JM8, Harris SR8, Schuenemann VJ7, Campbell TJ9, Majander K7, Wilbur AK10, Guichon RA11, Wolfe Steadman DL12, Cook DC13, Niemann S14, Behr MA15, Zumarraga M16, Bastida R17, Huson D5, Nieselt K5, Young D18, Parkhill J8, Buikstra JE10, Gagneux S19, Stone AC10, Krause J20. Abstract Modern strains of Mycobacterium tuberculosis from the Americas are closely related to those from Europe, supporting the assumption that human tuberculosis was introduced post-contact. This notion, however, is incompatible with archaeological evidence of pre-contact tuberculosis in the New World. Comparative genomics of modern isolates suggests that M. tuberculosis attained its worldwide distribution following human dispersals out of Africa during the Pleistocene epoch, although this has yet to be confirmed with ancient calibration points. Here we present three 1,000-year-old mycobacterial genomes from Peruvian human skeletons, revealing that a member of the M. tuberculosis complex caused human disease before contact. The ancient strains are distinct from known human-adapted forms and are most closely related to those adapted to seals and sea lions. Two independent dating approaches suggest a most recent common ancestor for the M. tuberculosis complex less than 6,000 years ago, which supports a Holocene dispersal of the disease. Our results implicate sea mammals as having played a role in transmitting the disease to humans across the ocean.
	PMID: 25141181 [PubMed - indexed for MEDLINE]
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10.	PLoS One. 2014 Jan 22;9(1):e81229. doi: 10.1371/journal.pone.0081229. eCollection 2014. Network analysis reveals distinct clinical syndromes underlying acute mountain sickness. Hall DP1, MacCormick IJ2, Phythian-Adams AT2, Rzechorzek NM3, Hope-Jones D2, Cosens S2, Jackson S2, Bates MG4, Collier DJ5, Hume DA6, Freeman T6, Thompson AA7, Baillie JK8. Abstract Acute mountain sickness (AMS) is a common problem among visitors at high altitude, and may progress to life-threatening pulmonary and cerebral oedema in a minority of cases. International consensus defines AMS as a constellation of subjective, non-specific symptoms. Specifically, headache, sleep disturbance, fatigue and dizziness are given equal diagnostic weighting. Different pathophysiological mechanisms are now thought to underlie headache and sleep disturbance during acute exposure to high altitude. Hence, these symptoms may not belong together as a single syndrome. Using a novel visual analogue scale (VAS), we sought to undertake a systematic exploration of the symptomatology of AMS using an unbiased, data-driven approach originally designed for analysis of gene expression. Symptom scores were collected from 292 subjects during 1110 subject-days at altitudes between 3650 m and 5200 m on Apex expeditions to Bolivia and Kilimanjaro. Three distinct patterns of symptoms were consistently identified. Although fatigue is a ubiquitous finding, sleep disturbance and headache are each commonly reported without the other. The commonest pattern of symptoms was sleep disturbance and fatigue, with little or no headache. In subjects reporting severe headache, 40% did not report sleep disturbance. Sleep disturbance correlates poorly with other symptoms of AMS (Mean Spearman correlation 0.25). These results challenge the accepted paradigm that AMS is a single disease process and describe at least two distinct syndromes following acute ascent to high altitude. This approach to analysing symptom patterns has potential utility in other clinical syndromes. PMCID: PMC3898916 Free PMC Article
	PMID: 24465370 [PubMed - indexed for MEDLINE]
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