The 2004 Indian Ocean earthquake was an underseamegathrust earthquake that occurred at 00:58:53 UTC on Sunday, 26 December 2004, with an epicentre off the west coast of Sumatra, Indonesia. The quake itself is known by the scientific community as the Sumatra–Andaman earthquake.[5][6] The resulting tsunami was given various names, including the 2004 Indian Ocean tsunami, South Asian tsunami, Indonesian tsunami, the Christmas tsunami and the Boxing Day tsunami.[7]
The earthquake was caused when the Indian Plate was subducted by the Burma Plate and triggered a series of devastating tsunamis along the coasts of most landmasses bordering the Indian Ocean, killing over 230,000 people in fourteen countries, and inundating coastal communities with waves up to 30 meters (98 ft) high.[8] It was one of the deadliest natural disasters in recorded history. Indonesia was the hardest-hit country, followed by Sri Lanka, India, and Thailand.
With a magnitude of Mw 9.1–9.3, it is the third largest earthquake ever recorded on a seismograph. The earthquake had the longest duration of faulting ever observed, between 8.3 and 10 minutes. It caused the entire planet to vibrate as much as 1 centimetre (0.4 inches)[9] and triggered other earthquakes as far away as Alaska.[10] Its epicentre was between Simeulue and mainland Indonesia.[11]
The plight of the affected people and countries prompted a worldwide humanitarian response. In all, the worldwide community donated more than $14 billion (2004 US$) in humanitarian aid.[12]
Earthquake characteristics
The earthquake was initially documented as moment magnitude 8.8. In February 2005 scientists revised the estimate of the magnitude to 9.0.[13] Although the Pacific Tsunami Warning Center has accepted these new numbers, the United States Geological Survey has so far not changed its estimate of 9.1. The most recent studies in 2006 have obtained a magnitude of Mw 9.1–9.3. Dr. Hiroo Kanamori of the California Institute of Technology believes that Mw 9.2 is a good representative value for the size of this great earthquake.[14]
The hypocentre of the main earthquake was approximately 160 km (100 mi), in the Indian Ocean just north of Simeulue island, off the western coast of northern Sumatra, at a depth of 30 km (19 mi) below mean sea level (initially reported as 10 km (6.2 mi)). The northern section of the Sunda megathrust, ruptured; the rupture having a length of 1,300 km (810 mi).[11] The earthquake (followed by the tsunami) was felt simultaneously in Bangladesh, India, Malaysia, Myanmar, Thailand, Singapore and the Maldives.[15]Splay faults, or secondary "pop up faults", caused long, narrow parts of the sea floor to pop up in seconds. This quickly elevated the height and increased the speed of waves, causing the complete destruction of the nearby Indonesian town of Lhoknga.[16]
Great earthquakes such as the Sumatra-Andaman event, which are invariably associated with megathrust events in subduction zones, have seismic moments that can account for a significant fraction of the global earthquake moment across century-scale time periods. Of all the seismic moment released by earthquakes in the 100 years from 1906 through 2005, roughly one-eighth was due to the Sumatra-Andaman event. This quake, together with the Good Friday Earthquake (Alaska, 1964) and the Great Chilean Earthquake (1960), account for almost half of the total moment. The much smaller but still catastrophic 1906 San Francisco earthquake is included in the diagram below for perspective. Mw denotes the magnitude of an earthquake on the moment magnitude scale.
Since 1900 the only earthquakes recorded with a greater magnitude were the 1960 Great Chilean Earthquake (magnitude 9.5) and the 1964 Good Friday Earthquake in Prince William Sound (9.2). The only other recorded earthquakes of magnitude 9.0 or greater were off Kamchatka, Russia, on 4 November 1952 (magnitude 9.0)[17] and Tōhoku, Japan (magnitude 9.0) in March 2011. Each of these megathrust earthquakes also spawned tsunamis in the Pacific Ocean. However, the death toll from these was significantly lower, primarily because of the lower population density along the coasts near affected areas and the much greater distances to more populated coasts and also due to the superior infrastructure and warning systems in MEDCs (More Economically Developed Countries) such as Japan.
The fossil record as Darwin knew it seemed to suggest that the major metazoan groups appeared in a few million years of the early to mid-Cambrian, and even in the 1980s this still appeared to be the case.[15][16]
However, evidence of Precambrian metazoa is gradually accumulating. If the Ediacaran Kimberella was a mollusc-like protostome (one of the two main groups of coelomates),[20][61] the protostome and deuterostome lineages must have split significantly before 550million years ago (deuterostomes are the other main group of coelomates).[94] Even if it is not a protostome, it is widely accepted as a bilaterian.[65][94] Since fossils of rather modern-looking Cnidarians (jellyfish-like organisms) have been found in the Doushantuolagerstätte, the Cnidarian and bilaterian lineages must have diverged well over 580million years ago.[94]
Trace fossils[59] and predatory borings in Cloudina shells provide further evidence of Ediacaran animals.[95] Some fossils from the Doushantuo formation have been interpreted as embryos and one (Vernanimalcula) as a bilaterian coelomate, although these interpretations are not universally accepted.[48][49][96] Earlier still, predatory pressure has acted on stromatolites and acritarchs since around 1,250million years ago.[44]
The presence of Precambrian animals somewhat dampens the "bang" of the explosion: not only was the appearance of animals gradual, but their evolutionary radiation ("diversification") may also not have been as rapid as once thought. Indeed, statistical analysis shows that the Cambrian explosion was no faster than any of the other radiations in animals' history.[note 5] However, it does seem that some innovations linked to the explosion – such as resistant armour – only evolved once in the animal lineage; this makes a lengthy Precambrian animal lineage harder to defend.[98] Further, the conventional view that all the phyla arose in the Cambrian is flawed; while the phyla may have diversified in this time period, representatives of the crown-groups of many phyla do not appear until much later in the Phanerozoic.[53] Further, the mineralized phyla that form the basis of the fossil record may not be representative of other phyla, since most mineralized phyla originated in a benthic setting. The fossil record is consistent with a Cambrian Explosion that was limited to the benthos, with pelagic phyla evolving much later.[53]
Ecological complexity among marine animals increased in the Cambrian, as well later in the Ordovician.[5] However, recent research has overthrown the once-popular idea that disparity was exceptionally high throughout the Cambrian, before subsequently decreasing.[99] In fact, disparity remains relatively low throughout the Cambrian, with modern levels of disparity only attained after the early Ordovician radiation.[5]
The diversity of many Cambrian assemblages is similar to today's,[100][91] and at a high (class/phylum) level, diversity is thought by some to have risen relatively smoothly through the Cambrian, stabilizing somewhat in the Ordovician.[101] This interpretation, however, glosses over the astonishing and fundamental pattern of basal polytomy and phylogenetic telescoping at or near the Cambrian boundary, as seen in most major animal lineages.[102] Thus Harry Blackmore Whittington's questions regarding the abrupt nature of the Cambrian explosion remain, and have yet to be satisfactorily answered.[103]
This is the structure of the Tet enzyme with DNA. Note the purple ball at the active site, close to which one DNA base is flipped out of the double helix. Also note the degree to which the double helix is bent. Credit: Xiaodong Cheng, Emory University
The finding is important for the field of epigenetics because Tet enzymes chemically modify DNA, changing signposts that tell the cell's machinery "this gene is shut off" into other signs that say "ready for a change."
Tet enzymes' roles have come to light only in the last five years; they are needed for stem cells to maintain their multipotent state, and are involved in early embryonic and brain development and in cancer.
The results, which could help scientists understand how Tet enzymes are regulated and look for drugs that manipulate them, are scheduled for publication in Nature.
Researchers led by Xiaodong Cheng, PhD, determined the structure of a Tet family member from Naegleria gruberi by X-ray crystallography. The structure shows how the enzyme interacts with its target DNA, bending the double helix and flipping out the base that is to be modified.
"This base flipping mechanism is also used by other enzymes that modify and repair DNA, but we can see from the structure that the Tet family enzymes interact with the DNA in a distinct way," Cheng says.
Cheng is professor of biochemistry at Emory University School of Medicine and a Georgia Research Alliance Eminent Scholar. The first author of the paper is research associate Hideharu Hashimoto, PhD. A team led by Yu Zheng, PhD, a senior research scientist at New England Biolabs, contributed to the paper by analyzing the enzymatic activity of Tet using liquid chromatography–mass spectrometry.
Using oxygen, Tet enzymes change 5-methylcytosine into 5-hydroxymethylcytosine and other oxidized forms of methylcytosine. 5-methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC) are both epigenetic modifications of DNA, which change how DNA is regulated without altering the letters of the genetic code itself.
5-mC is generally found on genes that are turned off or on repetitive regions of the genome. 5-mC helps shut off genes that aren't supposed to be turned on (depending on the cell type) and changes in 5-mC's distribution underpin a healthy cell's transformation into a cancer cell.
In contrast to 5-mC, 5-hmC appears to be enriched on active genes, especially in brain cells. Having a Tet enzyme form 5-hmC seems to be a way for cells to erase or at least modify the "off" signal provided by 5-mC, although the functions of 5-hmC are an active topic of investigation, Cheng says.
Alterations of the Tet enzymes have been found in forms of leukemia, so having information on the enzymes' molecular structure could help scientists design drugs that interfere with them.
N. gruberi is a single-celled organism found in soil or fresh water that can take the form of an amoeba or a flagellate; its close relative N. fowleri can cause deadly brain infections. Cheng says his team chose to study the enzyme from Naegleria because it was smaller and simpler and thus easier to crystallize than mammalian forms of the enzyme, yet still resembles mammalian forms in protein sequence.
Mammalian Tet enzymes appear to have an additional regulatory domain that the Naegleria forms do not; understanding how that domain works will be a new puzzle opened up by having the Naegleria structure, Cheng says. Journal reference:Nature
Most participants of National Geographic’s Genographic Project can recite their haplogroup as readily as their mother’s maiden name. Yet outside consumer genetics, the word haplogroup is still unknown. Your haplogroup, or genetic branch of the human family tree, tells you about your deep ancestry—often thousands of years ago—and shows you the possible paths of migration taken by these ancient ancestors. Your haplogroup also places you within a community of relatives, some distant, with whom you unmistakably share an ancestor way back when.
DNA Molecule
Haplogroup H1, Genographic’s most common lineage.
Let’s focus here on mitochondrial DNA haplogroup is H1, as it is the Genographic Project’s most common maternal lineage result. You inherited your mitochondrial DNA purely from your mother, who inherited it from her mother, and her mother, and so on. Yet, unlike often is the case with a mother’s maiden name, her maternal haplogroup is passed down through generations. Today, all members of haplogroup H1 are direct descendants from the first H1 woman that lived thousands of years ago. Most H1 members may know their haplogroup as H1a or H1b2 or H1c1a, etc, yet as a single genetic branch, H1 accounts for 15% of Genographic participants. What’s more, in the past few years, anthropologists have discovered and named an astonishing 200 new branches within haplogroup H1; and that number continues to grow.
Haplogroup H3, sister branch to H1
The origin of haplogroup H1 continues to be a debate as well. Most researchers suggest it was born in the Middle East between 10,000 and 15,000 years ago, and spread from there to Europe and North Africa. However, ancient DNA studies show that its ancestral haplogroup H first appears in Central Europe just 8,000 year ago. Its vast diversity and high concentration in Spain and Portugal, suggests H1 may have existed there during the last Ice Age, and spread north after glaciers melted. Yet others postulate that its young age and high frequency indicate it spread as agriculture took shape in Europe.
Any of the scenarios is possible. As technology improves, more DNA is extracted and sequenced from ancient bones, and more people contribute their DNA to the Genographic Project, we will keep learning about H1, and all other haplogroups. It is because of participants contributing their DNA, their stories, and their hypotheses to science that we can carry forward this exciting work uncovering our deep genetic connections.
Basically the researchers, lead by Dr. Srivas Chennu at the University of Cambridge, were trying to see if patients diagnosed as either in a vegetative state (VS) or minimally conscious state (MCS) could pay attention to (count) certain words, called the attended words, when they were embedded in a string of other randomly presented words, called the distracting words. Normal brain wave responses were established by performing the word testing on 8 healthy volunteers. The same testing was then applied to 21 brain damaged individuals, 9 with a clinical diagnosis of vegetative state and 12 with a diagnosis of minimally conscious state. Most of the patients did not respond to the presentation of words as did normal volunteers. But one did.
The patient, described at Patient P1, suffered a traumatic brain injury 4 months prior to testing. He was diagnosed as “behaviorally vegetative,” based on a Coma Recovery Score-Revised (CRS-R) of 7 (8 or greater = MCS). In addition to being able to consciously attend to the key words, this patient could also follow simple commands to imagine playing tennis.
Dr. Chennu was quoted as saying, “we are progressively building up a fuller picture of the sensory, perceptual and cognitive abilities in patients” with vegetative and minimally conscious states. Yes, this is true. But what does it mean if someone previously diagnosed as vegetative can now be shown to perform this sort of task? Dr. Chennu hopes that this information will spur the development of “future technology to help patients in a vegetative state communicate with the outside world.”
I think this is fascinating research and it sheds new insights into how the brain functions, but it also raises a number of important questions. For example, if I can attend to words, does it change my prognosis? Patient P1 was found to have minimal cortical atrophy. Perhaps he is just slow to transition from a vegetative to a MCS. If attending to words is associated with a better prognosis, should that make me a candidate for intensive and expensive rehabilitation? If so, who should pay for this? If I have an advanced directive that says I don’t want to continue to live in a persistent vegetative state, will this level of awareness mean I am not really vegetative. As more and more resources are poured into care for folks with severe brain damage, does it come at a societal cost?
What trade offs are we making, what services are we forgoing, as we spend money developing tools to improve communication in vegetative states
Of course no one has the answer to these questions and I suspect as researchers like those at Cambridge continue to learn more about the functioning of the severely injured brain, the more difficult it will be to clearly say what is really means to be “aware.”
Posted by Miguel Vilar on December 24, 2013 
