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Proceedings of the National Academy of Sciences of the United States of America (often abbreviated PNAS or PNAS USA) is a peer-reviewedmultidisciplinaryscientific journal. It is the official journal of the National Academy of Sciences, published since 1915, and publishes original research, scientific reviews, commentaries, and letters. According to Journal Citation Reports, the journal has a 2019 impact factor of 9.412.^[1]PNAS is the second most cited scientific journal, with more than 1.9 million cumulative citations from 2008–2018.^[2] In the mass media, PNAS has been described variously as 'prestigious',^[3][4] 'sedate',^[5] 'renowned',^[6] and 'high impact'.^[7]

PNAS commits to immediately and freely sharing research data and findings relevant to the novel coronavirus (COVID-19) outbreak. See the free collection of PNAS coronavirus papers and learn more about our response to COVID-19. CRISPR (/ ˈ k r ɪ s p ər /) (clustered regularly interspaced short palindromic repeats) is a family of DNA sequences found in the genomes of prokaryotic organisms such as bacteria and archaea. These sequences are derived from DNA fragments of bacteriophages that had previously infected the prokaryote. They are used to detect and destroy DNA from similar bacteriophages during subsequent.

PNAS is a delayed open access journal, with an embargo period of 6 months that can be bypassed for an author fee (hybrid open access). Since September 2017, open access articles are published under a Creative Commons license. Since January 2019, PNAS is online-only, although print issues are available on-demand.

History[edit]

PNAS was established by the National Academy of Sciences (NAS) in 1914,^{[note 1][8][9]:30} with its first issue published in 1915. The NAS itself had been founded in 1863 as a private institution, but chartered by the United States Congress, with the goal to 'investigate, examine, experiment, and report upon any subject of science or art'.

Prior to the inception of PNAS, the National Academy of Sciences published three volumes of organizational transactions, consisting mostly of minutes of meetings and annual reports. For much of the journal's history, PNAS published brief first announcements of Academy members' and associates' contributions to research.^[10] In December 1995,^[11]PNAS opened submissions to all authors without first needing to be sponsored by an NAS member.

Members were allowed to communicate up to two papers from non-members to PNAS every year. The review process for these papers was anonymous in that the identities of the referees were not revealed to the authors. Referees were selected by the NAS member.^[10][12][13]PNAS eliminated communicated submissions through NAS members as of July 1, 2010, while continuing to make the final decision on all PNAS papers.^[14]

95% of papers are peer reviewed Direct Submissions and 5% are contributed submissions.^[15][16]

American national security concerns[edit]

In 2003, PNAS issued an editorial stating its policy on publication of sensitive material in the life sciences.^[17]PNAS stated that it would 'continue to monitor submitted papers for material that may be deemed inappropriate and that could, if published, compromise the public welfare.' This statement was in keeping with the efforts of several other journals.^[18][19] In 2005 PNAS published an article titled 'Analyzing a bioterror attack on the food supply: The case of botulinum toxin in milk',^[20] despite objections raised by the U.S. Department of Health and Human Services.^[21] The paper was published with a commentary by the president of the Academy at the time, Bruce Alberts, titled 'Modeling attacks on the food supply'.^[22]

Editors[edit]

The following people have been editors-in-chief of the journal:

• 1914–1918: Arthur A. Noyes
• 1918–1940: Raymond Pearl
• 1940–1949: Robert A. Millikan
• 1950–1955: Linus Pauling
• 1955–1960: Wendell M. Stanley
• 1960–1968: Saunders Mac Lane
• 1968–1972: John T. Edsall
• 1972–1980: Robert Louis Sinsheimer^[23]
• 1980–1984: Daniel E. Koshland, Jr.
• 1985–1988: Maxine Singer
• 1988–1991: Igor B. Dawid
• 1991–1995: Lawrence Bogorad
• 1995–2006: Nicholas R. Cozzarelli
• 2006–2011: Randy Schekman
• 2011–2017: Inder Verma^[24]
• 2018–2019: Natasha Raikhel
• 2019–present: May Berenbaum

The first managing editor of the journal was mathematician Edwin Bidwell Wilson.

Notes[edit]

1. ^The Stankus book reference states 1918 as the year instead of 1914.

References[edit]

1. ^'Journal Citation Reports'. Clarivate. Retrieved July 9, 2020.
2. ^'InCites [v2.54] – Sign In'. error.incites.thomsonreuters.com. Archived from the original on January 8, 2019. Retrieved January 31, 2019.
3. ^'Discovery (could pave way for better diabetes treatments)'. The News-Star. 86 (264). Monroe, Louisiana. July 6, 2015. p. 2D – via Newspapers.com.
4. ^'Ben-Gurion study highlights gene that could lead to new therapies for ALS'. South Florida Sun Sentinel. September 21, 2016. p. A52 – via Newspapers.com.
5. ^Lear, John (August 11, 1986). 'On Our Knees'. The Gettysburg Times. Gettysburg, Pennsylvania. p. 4 – via Newspapers.com.
6. ^Byerman, Mikalee (October 26, 2008). 'Survival skills'. Living Green. Reno Gazette-Journal. 27 (300). Reno, Nevada. p. 7 – via Newspapers.com.
7. ^'U of U programs frequently cited as references'. School News. The Daily Spectrum. 27 (167). St. George, Utah. August 16, 1993. p. B2 – via Newspapers.com.
8. ^'Assistant professor's research gets published'. Poughkeepsie Journal. Poughkeepsie, New York. October 13, 2009. p. 1D – via Newspapers.com.
9. ^Stankus, Tony (1990). Scientific journals: Improving library collections through analysis of publishing trends. Haworth Press. ISBN0-886656-905-7 – via Internet Archive.CS1 maint: ignored ISBN errors (link)
10. ^ ^abInformation for Authors
11. ^Schekman, R. (2007). 'Introducing Feature Articles in PNAS'(PDF). Proceedings of the National Academy of Sciences. 104 (16): 6495. Bibcode:2007PNAS.104.6495S. doi:10.1073/pnas.0702818104.
12. ^Fersht, Alan (May 3, 2005). 'Editorial: How and why to publish in PNAS'. Proceedings of the National Academy of Sciences. 102 (18): 6241–6242. doi:10.1073/pnas.0502713102. PMC1088396. PMID16576766.
13. ^Garfield, Eugene (September 7, 1987). 'Classic Papers from the Proceedings of the National Academy of Sciences'(PDF). Essays of an Information Scientist. 10 (36): 247. Retrieved September 28, 2007.
14. ^Schekman, Randy (2009). 'PNAS will eliminate Communicated submissions in July 2010'. Proceedings of the National Academy of Sciences. 106 (37): 15518. Bibcode:2009PNAS.10615518S. doi:10.1073/pnas.0909515106. PMC2747149.
15. ^https://www.pnas.org/content/111/40/14311
16. ^https://www.pnas.org/page/authors/direct-submission
17. ^Cozzarelli, Nicholas R. (2003). 'PNAS policy on publication of sensitive material in the life sciences'. Proceedings of the National Academy of Sciences. 100 (4): 1463. Bibcode:2003PNAS.100.1463C. doi:10.1073/pnas.0630514100. PMC149849. PMID12590130.
18. ^Harmon, Amy (February 16, 2003). 'Journal Editors to Consider U.S. Security in Publishing'. Archives. The New York Times.
19. ^Fauber, John (February 16, 2003). 'Science articles to be censored in terror fight'. Milwaukee Journal Sentinel.
20. ^Wein, L. M. (2005). 'Analyzing a bioterror attack on the food supply: The case of botulinum toxin in milk'. Proceedings of the National Academy of Sciences. 102 (28): 9984–9989. Bibcode:2005PNAS.102.9984W. doi:10.1073/pnas.0408526102. PMC1161865. PMID15985558.
21. ^'Provocative report on bioterror online'. The Atlanta Journal-Constitution. June 29, 2005.
22. ^Alberts, B. (2005). 'Modeling attacks on the food supply'. Proceedings of the National Academy of Sciences. 102 (28): 9737–9738. Bibcode:2005PNAS.102.9737A. doi:10.1073/pnas.0504944102. PMC1175018. PMID15985557.
23. ^Sinsheimer, Robert L. (August 29, 1976). 'Caution May Be an Essential Scientific Virtue'. Los Angeles Times. XCV (270). p. IV:5 – via Newspapers.com. Robert L. Sinsheimer is head of Caltech's biology division and chairman of the editorial board of Proceedings of the National Academy of Sciences.
24. ^Robbins, Gary (December 28, 2017), 'Renowned Salk Institute scientist loses a top post due to gender discrimination claims', Los Angeles Times

External links[edit]

MATHEMATICS

Graph regularity extension to k-uniform hypergraphs

A powerful tool in graph theory is Szemerédi's regularity lemma, which roughly states that any graph splits into small graphs that are in some sense pseudorandom, which renders arbitrary graphs more manageable. Although graph theory is appropriate for describing binary relations on objects, the more general structure of hypergraphs is the appropriate tool for multiple relations. However, dealing with hypergraphs is difficult because of their complex nature, and an extension of graph regularity to hypergraphs has not been easily found. V. Rödl et al. developed a notion of hypergraph regularity, including an idea of pseudorandomness for hypergraphs, which has applications to graph theory as well as other fields such as number theory and combinatorial geometry. The main results of their work are regularity and counting lemmas for k-uniform hypergraphs for an arbitrary k ≥ 2. The combination of these two results yields a proof of Szemerédi's theorem for arithmetic progressions of length k and also gives a bound for the multi-dimensional Szemerédi theorem.

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“The hypergraph regularity method and its applications” by V. Rödl, B. Nagle, J. No live preview for excel 2016 mac. Skokan, M. Schacht, and Y. Kohayakawa (see pages 8109-8113)

ECOLOGY

Climate changes could threaten European plant species

Projected climate changes could trigger massive species loss and distribution shifts in Europe, according to Wilfried Thuiller et al. Using four climate scenarios proposed by the Intergovernmental Panel on Climate Change (IPCC) and three different climate models (HadCM3, CGCM2, and CSIRO2), the authors predicted distributions of 1,350 European plant species through 2080. The researchers reported that more than half of the species could be classified as vulnerable or threatened. Species from European mountains were found to be more sensitive to climate change, with ≈60% of species estimated to lose suitable climate in these areas. Boreal regions had the least amount of potential species loss, in part because these regions might gain species via immigration from the south. The least vulnerable ecosystems were the southern Mediterranean and Pannonian regions. Two situations were considered, no species migration and universal migration; under the no-migration constraint with the most severe climate scenario, 22% of all species could become critically endangered and 2% extinct by 2080. Under the universal migration assumption, 67% of species would be at low risk. The authors say that the most critical bioclimatic factors affecting species loss are growing-degree days and moisture availability.

“Climate change threats to plant diversity in Europe” by Wilfried Thuiller, Sandra Lavorel, Miguel B. Araújo, Martin T. Sykes, and I. Colin Prentice (see pages 8245-8250)

IMMUNOLOGY

Mouse model for coronavirus infection

Caroline Lassnig et al. have developed a mouse strain enabling the study of group 1 human coronaviruses. The transgenic mice are susceptible to infection by HCoV-229E, which causes mild respiratory disease in humans, entering cells via the human aminopeptidase N (hAPN) receptor. Lassnig et al. demonstrate that APN is not sufficient to allow infection in vivo, rendering homozygous hAPN-transgenic mice (hAPN^+/+) resistant to HCoV-229E. The researchers crossed hAPN^+/+ animals with mice lacking the Stat1 gene, generating the double-transgenic hAPN^+/+ Stat1^-/-. Immunocom-promised Stat1 null mice are known to be highly susceptible to microbial and viral infections, and, as predicted, the double-transgenic mice were vulnerable to HCoV-229E. However, the HCoV-229E strain that infects APN^+/+ primary embryonic fibroblasts in vitro did not infect any of the double-transgenic mice or the controls until it was “adapted” through four rounds of passaging in primary embryonic fibroblasts from hAPN^+/+ Stat^-/- mice at both 32°C and 37°C. When the adapted HCoV-229E was administered nasally, virus was found 3 days later in double-transgenic mouse lungs, which revealed signs of inflammation through infection.

“Development of a transgenic mouse model susceptible to human coronavirus 229E” by Caroline Lassnig, Carlos M. Sanchez, Monika Egerbacher, Ingrid Walter, Susanne Majer, Thomas Kolbe, Pilar Pallares, Luis Enjuanes, and Mathias Müller (see pages 8275-8280)

MEDICAL SCIENCES

See full list on wikihow.com. CRP does not worsen arterial plaques

Gideon Hirschfield et al. report that atherosclerosis is not exacerbated by the inflammation marker C-reactive protein (CRP). To investigate the role of CRP in arterial plaque formation, Hirschfield et al. studied apolipoprotein E (apoE) knockout mice, which are predisposed to atherosclerosis, in the presence or absence of transgenic human CRP expression. The authors examined the mice up to 56 weeks of age and determined that human CRP had no effect on mortality or development, progression, or severity of atherosclerosis. However, compared with wild-type mice, apoE^-/- mice showed higher concentrations of circulating CRP. CRP was detected within the plaques. In addition, analysis of mouse serum amyloid P component revealed no evidence of systemic inflammation, which is proatherogenic in apoE^-/- mice. This study demonstrates that human CRP transgene expression is up-regulated in apoE-deficient mice despite the absence of other systemic signs of inflammation. According to the authors, these data suggest that CRP is neither proatherogenic nor atheroprotective in vivo.

“Transgenic human C-reactive protein is not proatherogenic in apolipoprotein E-deficient mice” by Gideon M. Hirschfield, J. Ruth Gallimore, Melvyn C. Kahan, Winston L. Hutchinson, Caroline A. Sabin, G. Martin Benson, Amar P. Dhillon, Glenys A. Tennent, and Mark B. Pepys (see pages 8309-8314)

MICROBIOLOGY

Tuberculosis survival genes identified

Jyothi Rengarajan et al. have identified the set of genes in Mycobacterium tuberculosis (MTB) required for survival in host macrophages. Previous research has shown that MTB replicates in macrophages, where it inhibits IFN-γ-mediated signaling and evades immunity. Rengarajan et al. infected primary mouse macrophages unactivated or activated with IFN-γ either before or after MTB infection. By screening for poorly growing mutants, the authors found 126 genes required specifically for MTB growth in macrophages, regardless of activation state. Grouping genes with functional similarities, the authors uncovered individual members of several putative operons, such as the mce locus, which may allow molecules to transport between bacteria and host. Rengarajan et al. categorized the genes into three hierarchical clusters: (i) genes with cell-autonomous functions; (ii) genes necessary for in vivo infection but dispensable for survival in macrophages; and (iii) genes for intracellular adaptation. In addition, by comparing survival and transcriptional profiling data, the researchers observed that a majority of the genes necessary for MTB growth in macrophages were not regulated but rather appeared to be constitutively expressed.

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“Genome-wide requirements for Mycobacterium tuberculosis adaptation and survival in macrophages” by Jyothi Rengarajan, Barry R. Bloom, and Eric J. Rubin (see pages 8327-8332)

Projected European plant species loss.

Lung inflammation in hAPN^+/+ Stat1^-/- mice.

Atherosclerotic plaques in apoE^-/--hCRP⁺ mouse.

Clustering of M. tuberculosis genes required for survival in macrophages.

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