Ta Cong Son, Tran Manh Cuong, Le Quang Dung and Le Van Dung
Theor. Probability and Math. Statist. 111 (), 153-165.
Abstract, references and article information

Bero Roos
Theor. Probability and Math. Statist. 111 (), 137-151.
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Olha Prykhodko and Kostiantyn Ralchenko
Theor. Probability and Math. Statist. 111 (), 123-135.
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Lutz Mattner
Theor. Probability and Math. Statist. 111 (), 45-122.
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Claudio Macci and Barbara Pacchiarotti
Theor. Probability and Math. Statist. 111 (), 21-43.
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Chris A.J. Klaassen
Theor. Probability and Math. Statist. 111 (), 9-19.
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Abdessamad Dehaj and Mohamed Guessous
Theor. Probability and Math. Statist. 111 (), 1-8.
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Lasse L. Wolf and Hong-Wei Zhang
Proc. Amer. Math. Soc. 152 (), 5445-5453.
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Shengyu Tang
Proc. Amer. Math. Soc. 152 (), 5381-5394.
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Ferdinand Ihringer
Proc. Amer. Math. Soc. 152 (), 5355-5365.
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Yongqiang Liu, Laurentiu Maxim and Botong Wang
Proc. Amer. Math. Soc. 152 (), 5279-5288.
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Lauri Hitruhin and Sauli Lindberg
Proc. Amer. Math. Soc. 152 (), 5265-5278.
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Sudip Ranjan Bhuia
Proc. Amer. Math. Soc. 152 (), 5249-5263.
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Frederic Heihoff
Proc. Amer. Math. Soc. 152 (), 5229-5247.
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Lawford Hatcher
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Anh Tuan Nguyen, Tómas Caraballo and Nguyen Huy Tuan
Proc. Amer. Math. Soc. 152 (), 5175-5189.
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Simão Correia
Proc. Amer. Math. Soc. 152 (), 5117-5136.
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Jan Draisma and Thomas Karam
Proc. Amer. Math. Soc. 152 (), 5083-5093.
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Donghyeok Lim and Christian Maire
Proc. Amer. Math. Soc. 152 (), 5013-5024.
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Naoki Endo and Shiro Goto
Proc. Amer. Math. Soc. 152 (), 5007-5011.
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E. P. Ushakova and K. E. Ushakova
St. Petersburg Math. J. 35 (), 571-595.
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T. A. Suslina
St. Petersburg Math. J. 35 (), 537-570.
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N. Kuznetsov
St. Petersburg Math. J. 35 (), 467-472.
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R. Gibara and D. Kinzebulatov
St. Petersburg Math. J. 35 (), 445-460.
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E. Voronetsky
St. Petersburg Math. J. 35 (), 433-443.
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Roland Donninger
Bull. Amer. Math. Soc. 61 (), 659-685.
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Alin Bostan, Xavier Caruso and Julien Roques
Bull. Amer. Math. Soc. 61 (), 609-658.
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Math educator Joan Ferrini-Mundy was one of eight new members named to the National Science Board, announced by President Biden on October 15.

Ferrini-Mundy is the 21st president of the University of Maine and its regional campus, the University of Maine at Machias. She is also Vice Chancellor for Research and Innovation for the University of Maine System. Prior to her presidency, Ferrini-Mundy was the chief operating officer of the National Science Foundation (NSF), which followed six years leading NSF’s Directorate for Education and Human Resources.

An active leader in the math community, Ferrini-Mundy is immediate past chair of the Conference Board of the Mathematical Sciences (CBMS) and a member of the Transforming Post-Secondary Education in Mathematics (TPSE) board.

The National Science Board was established via 1950 legislation that created the National Science Foundation. The Board, together with the NSF Director, helps determine the NSF’s strategic direction. It also serves as an independent body of advisors to both the President and the Congress on policy matters related to science and engineering, including education in science and engineering. The Board consists of 25 members, appointed by the President. Members serve six-year terms and one-third are appointed every two years.

Contact: AMS Communications

* * * * *

The American Mathematical Society is dedicated to advancing research and connecting the diverse global mathematical community through our publications, meetings and conferences, MathSciNet, professional services, advocacy, and awareness programs.

PROMOTED RACING, CHAPELTON MAROONS RENEW RIVALRY IN JPL - A16 FUNCAANDUN SET FOR FIFTH STRAIGHT WIN - A21

UK-based, Jamaica-born dancehall artiste Dubbi believes latest single, ' Side Chick' is a bona fide hit as its popularity has surged on the dancehall scene in the United Kingdom. "It is also streaming well in France and seems to be a real hit on...

Family, friends, and community members gathered on Saturday at the Falmouth First Assembly Church to celebrate the life of 15-year-old Jahmarie Reid, a William Knibb High student who tragically lost his life at sea on August 27 in what is believed...

PORT-AU-PRINCE, Haiti (AP) — Haiti's main airport remained closed on Tuesday, a day after violence erupted as the country swore in its new prime minister in a politically tumultuous transition.

If you connect to a FTP/TLS server that is configured to use implicit FTP/TLS, FILENAME FTP/TLS might fail with the following error:

Recent studies have suggested that innate immune responses exhibit characteristics associated with memory linked to modulations in both vertebrates and invertebrates. However, the diverse evolutionary paths taken, particularly within the invertebrate taxa, should lead to similarly diverse innate immunity memory processes. Our understanding of innate immune memory in invertebrates primarily comes from studies of the fruit fly Drosophila melanogaster, the generality of which is unclear. Caenorhabditis elegans typically inhabits soil harboring a variety of fatal microbial pathogens; for this invertebrate, the innate immune system and aversive behavior are the major defensive strategies against microbial infection. However, their characteristics of immunological memory remains infantile. Here we discovered an immunological memory that promoted avoidance and suppressed innate immunity during reinfection with bacteria, which we revealed to be specific to the previously exposed pathogens. During this trade-off switch of avoidance and innate immunity, the chemosensory neurons AWB and ADF modulated production of serotonin and dopamine, which in turn decreased expression of the innate immunity-associated genes and led to enhanced avoidance via the downstream insulin-like pathway. Therefore, our current study profiles the immune memories during C. elegans reinfected by pathogenic bacteria and further reveals that the chemosensory neurons, the neurotransmitter(s), and their associated molecular signaling pathways are responsible for a trade-off switch between the two immunological memories.

Animals can sense the presence of microbes in their tissues and mobilize their own defenses by recognizing and responding to conserved microbial structures (often called microbe-associated molecular patterns (MAMPs)). Successful host defenses may kill the invaders, yet the host animal may fail to restore homeostasis if the stimulatory microbial structures are not silenced. Although mice have many mechanisms for limiting their responses to lipopolysaccharide (LPS), a major Gram-negative bacterial MAMP, a highly conserved host lipase is required to extinguish LPS sensing in tissues and restore homeostasis. We review recent progress in understanding how this enzyme, acyloxyacyl hydrolase (AOAH), transforms LPS from stimulus to inhibitor, reduces tissue injury and death from infection, prevents prolonged post-infection immunosuppression, and keeps stimulatory LPS from entering the bloodstream. We also discuss how AOAH may increase sensitivity to pulmonary allergens. Better appreciation of how host enzymes modify LPS and other MAMPs may help prevent tissue injury and hasten recovery from infection.

Knockout mouse models have been extensively used to study the antiviral activity of IFIT (interferon-induced protein with tetratricopeptide repeats). Human IFIT1 binds to cap0 (m7GpppN) RNA, which lacks methylation on the first and second cap-proximal nucleotides (cap1, m7GpppNm, and cap2, m7GpppNmNm, respectively). These modifications are signatures of “self” in higher eukaryotes, whereas unmodified cap0-RNA is recognized as foreign and, therefore, potentially harmful to the host cell. IFIT1 inhibits translation at the initiation stage by competing with the cap-binding initiation factor complex, eIF4F, restricting infection by certain viruses that possess “nonself” cap0-mRNAs. However, in mice and other rodents, the IFIT1 orthologue has been lost, and the closely related Ifit1b has been duplicated twice, yielding three paralogues: Ifit1, Ifit1b, and Ifit1c. Although murine Ifit1 is similar to human IFIT1 in its cap0-RNA–binding selectivity, the roles of Ifit1b and Ifit1c are unknown. Here, we found that Ifit1b preferentially binds to cap1-RNA, whereas binding is much weaker to cap0- and cap2-RNA. In murine cells, we show that Ifit1b can modulate host translation and restrict WT mouse coronavirus infection. We found that Ifit1c acts as a stimulatory cofactor for both Ifit1 and Ifit1b, promoting their translation inhibition. In this way, Ifit1c acts in an analogous fashion to human IFIT3, which is a cofactor to human IFIT1. This work clarifies similarities and differences between the human and murine IFIT families to facilitate better design and interpretation of mouse models of human infection and sheds light on the evolutionary plasticity of the IFIT family.