-Douglas Fisher, computer scientist, Vanderbilt University
-Douglas Fisher, computer scientist, Vanderbilt University
Russia may be cooler than us: Raiders of the lost lake
“Arguably the most exciting — and certainly the most controversial — scientific endeavour in Antarctica's history is close to a breakthrough.”
(Original article: 17 January 2011, Nature 469, 275 2011)
Twenty years ago Russian researchers began a project to drill down 3,650 meters to get test samples of the largest subglacial lake on the planet, Lake Vostok in Antartica. They believe that in a matter of weeks they will hit this subglacial lake (methods found in original article). Samples from this lake will potentially provide us with an insight into life up to 35 million years ago. Imagine what could live under a 3,650 meters of ice, cut off from the atmosphere for millions of years (hint: bound to be cooler than arsenic bacteria)!
A new impact factor: How famous are you really?
“This is a new way to measure a scientist's influence. It captures fame on the grandest scale, weighing the cultural footprint of scientists across societies and throughout history.”
(Original article: 14 January 2011, Science 331 - 6014)
Adrian Veres and John Bohannon have created a database of the most noted scientists in the last 200 years ranked by their appearance of people’s names in books. Jean-Baptiste Michel and Erez Lieberman Aiden made this endeavor possible by creating an enormous data set based on trillions of words within Google Books (raw data, try it yourself).
Introducing the Science Hall of Fame (SHoF) (Don’t forget to look at their tips for being a famous scientist).
My science grandfather (Stanley Falkow) ranks at 4 milliDarwins, know anyone famous?
Visualizing the tiny: Malaria caught on tape
Watch the live video via New Scientist
(Original article: 20 January 2011, Cell Host & Microbe 9: 9-20)
David Rigler and David Richard, et al. have shown for the first time a live video of P. falciparum, a parasite from the genus Plasmodium, the causative agent of Malaria. They recorded the invasion of a human erythrocyte by P. falciparum. Not only is this just awesome to watch, this insight will help shed light on the complex mechanisms used by parasites to invade their host.
|Artist's rendition of Kepler (JPL)|
Information about Kepler 10-b comes from the draft paper Kepler’s First Rocky Planet: Kepler-10b by Natalie Batalha, et al. [2010 Jan 10].
That there was a such thing as a planet.
That there were other planets in our solar system.
That the Sun is a star, meaning that all the stars are like the Sun, but farther away.
Stars and their planets formed in the same place out of the same stuff, so properties of a star are likely to be relevant to what’s inside the planet. For example, we know that stars with higher metallicity (and when astronomers use the word “metal,” they mean anything heavier than Helium) are more likely to have more massive planets (Marcy, et al., 2005).
Andrew Cumming, R. Paul Butler, Geoffrey W. Marcy, et al. (2008). "The Keck Planet Search: Detectability and the Minimum Mass and Orbital Period Distribution of Extrasolar Planets". Publications of the Astronomical Society of the Pacific 120: 531–554.
Lunine, J; Macintosh, B; Peale, S. (2009). "The Detection and Characterization of Exoplanets". Physics Today 62 (46): 47-51.
G. Marcy et al. (2005). "Observed Properties of Exoplanets: Masses, Orbits and Metallicities". Progress of Theoretical Physics Supplement 158: 24–42.
Mayor, D. Queloz (1995). "A Jupiter-mass companion to a solar-type star". Nature 378: 355–359.
Wolszczan, A.; Frail, D. A. (1992). "A planetary system around the millisecond pulsar PSR1257+12". Nature 355 (6356): 145–147.
Generally when I think of antibiotics I imagine taking a pill that delivers tiny death packages to individual bacteria that have invaded my body. These micro-molecules float through my blood stream to be delivered to my organs, obliterating any foreign cells they can find, taking no prisoners.
In addition to these pilled, bottled and administered antibiotics, there are inherent antimicrobial activities your cells have evolved to combat pathogens & escape infection. One specific cell type has been shown to have potent antimicrobial activity for over 100 years, feared by all microbes large and small: the neutrophil (Metchnikoff, 1901).
Aside from being notorious for forming pus at the site of infected wounds, neutrophils are known for their immediate response to infection by migrating via the circulatory system to the site of inflammation (for an excellent review on neutrophils: Nature Immuno Reviews, Nathan, 2006). Once at the site of infection, neutrophils engage in full-contact battle by engulfing the pathogen in a membrane-bound vesicle called the phagosome. This phagosome will mature into the phagolysosome where microbes are exposed to antimicrobial peptides and reactive oxygen species. After maturation of the phagosome, most neutrophils undergo apoptosis, controlled and anti-inflammatory cell death. Recently scientists found that, in addition to apoptosis, neutrophils also have a very distinct and interesting cell death pathway that results in formation of neutrophil extracellular traps (NETs) (Brinkmann et al., 2004) (Fig 1).
What are NETs?
Brinkmann, et al. (2004) first described NETs as “extracellular fibers… composed of granule and nuclear constituents that disarm and kill bacteria extracellularly.” NETs get their fibrous structure from DNA, the major structural component. DNA is naturally negatively charged and binds to positively charged proteins and cationic antimicrobial peptides (CAMPs). Other enzymes such as neutrophil elastase (NE), an enzyme that degrades virulence factors of bacteria, also bind to NETs (Weinrauch, 2002). Bacteria secrete virulence factors to evade host antimicrobial mechanisms, & their degradation weakens the defense of the invading bacteria. In addition, like in the nucleus, DNA binds to histones (Fig 2), naturally bactericidal proteins (Hirsh, 1958).
But is the production of NETs an early pre-determined cellular fate, or is this pathway a late reaction to infection? Recently Papayannopoulos, et al. (2010), found that NE and myeloperoxidase (MPO) (Fig 2), two antimicrobial peptides that bind to DNA in NETs, regulate chromatin density during the formation of NETs. Chromatin decondensation is necessary for the relaxation and release of DNA, required for NET formation. This is excellent data, but we need to collect additional data to identify the beginning steps of NET formation in order to determine how and when neutrophil NET fate is determined.
Why I find this interesting?
I love the idea that our body has evolved countless mechanisms to fight bacteria – including a mechanism that involves cellular suicide and antimicrobial agents binding to a giant extracellular DNA net. Generally we think of DNA in the nucleus wound up around histones, occasionally being read by polymerases – but this new antimicrobial mechanism shows that there is versatility and that endless eukaryotic cellular components have dual functions. NETs showcase how beautifully we have evolved.
Hirsch JG, J Exp Med 108(6), 925 (1958)
Weinrach Y, et al. Nature 417, 91 (2002)
Metchnikoff E, Limmunité Dans Les Maladies Infectieuses (1901)
Papayannopoulos V, J Cell Bio, 191(3), 677 (2010)
Brinkmann, V. (2004). Neutrophil Extracellular Traps Kill Bacteria Science, 303 (5663), 1532-1535 DOI: 10.1126/science.1092385