Interview: The Grinch at Universal Orlando Islands of Adventure for Grinchmas 2013
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Hawaiian Islands Nickname: Mokupuni o Hawaii
True color satellite image of the Hawaiian Islands
United States
The Hawaiian Islands (Hawaiian: Mokupuni o Hawaii) are an archipelago of eight major islands, several atolls, numerous smaller islets, and undersea seamounts in the North Pacific Ocean, extending some 1,500 miles (2,400 kilometres) from the island of Hawaii in the south to northernmost Kure Atoll. Once known as the "Sandwich Islands", the name chosen by James Cook in honour of the then First Lord of the Admiralty John Montagu, 4th Earl of Sandwich, the archipelago now takes its name from the largest island in the cluster. The United States state of Hawaii occupies the archipelago almost in its entirety, with the sole exception of Midway island, which is instead an unincorporated territory within the United States Minor Outlying Islands.
The Hawaiian Islands are the exposed peaks of a great undersea mountain range known as the Hawaiian-Emperor seamount chain, formed by volcanic activity over a hotspot in the Earth's mantle. The islands are about 1,860 miles (3,000km) from the nearest continent.[1]
Captain James Cook visited the islands on January 18, 1778 and named them the "Sandwich Islands" in honor of John Montagu, 4th Earl of Sandwich, who was one of his sponsors as the First Lord of the Admiralty.[2] This name was in use until the 1840s, when the local name "Hawaii" gradually began to take precedence.[3]
The Hawaiian Islands have a total land area of 6,423.4 square miles (16,636.5km2). Except for Midway, which is an unincorporated territory of the United States, these islands and islets are administered as the state of Hawaiithe 50th state of the United States of America.
The eight main islands of Hawaii (also called the Hawaiian Windward Islands) are listed here. All except Kahoolawe are inhabited.
Smaller islands, atolls, and reefs (all west of Niihau are uninhabited) form the Northwestern Hawaiian Islands, or Hawaiian Leeward Islands:
The state of Hawaii counts 137 "islands" in the Hawaiian chain.[13] This number includes all minor islands and islets offshore of the main islands (listed above) and individual islets in each atoll. These are just a few:
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A 13-year study of coral reefs spontaneously recovering in the Cayman Islands offers hope of refuting often doomsday forecasts about the worldwide decline of the colorful marine habitat.
By Barbara Liston
ORLANDO, Florida (Reuters) - A 13-year study of coral reefs spontaneously recovering in the Cayman Islands offers hope of refuting often doomsday forecasts about the worldwide decline of the colorful marine habitat.
Scientists monitoring the Cayman reefs noted a 40 percent decline in live coral cover between 1999 and 2004 during a period of warmer seas in the Caribbean.
However, seven years later, the amount, size and density of the live coral had returned to 1999 levels as sea temperatures eased, according to Tom Frazer, professor of aquatic ecology at the University of Florida and part of the research team.
"People have said these systems don't have a chance," Frazer told Reuters. "What we are saying is: 'Hey, this is evidence they do have a chance.'"
Coral reefs account for 0.01 percent of the marine environment. They harbor up to 25 percent of the different species of marine organisms and generate millions of dollars for the fishing and tourism industries, the report states.
"They're kind of like the rain forest of the sea," Frazer said.
The reefs are dying around the world. In 2012, the Australian Institute of Marine Science reported that coral coverage of the Great Barrier Reef had declined by half over the previous 27 years.
The Cayman Islands study, conducted with the Central Caribbean Marine Institute there, was published in the November online issue of the San Francisco-based Public Library of Science and highlighted in last month's issue of the Science journal.
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JAMES GIBBARD/Tulsa WorldSouthern Miss forward Norville Carey prepares to go up for a shot guarded by UTEP's Julian Washburn during the Conference USA Tournament in Tulsa in March. Carey will visit his hometown in the Virgin Islands when USM travels to a tournament there.
JAMES GIBBARD TULSA WORLD
HATTIESBURG -- Southern Miss sophomore Norville Carey figures to see a few friends and relatives this week when the Golden Eagles play in the BVI Tropical Shootout in the Virgin Islands.
The site of the tournament, you see, is in Tortola, British Virgin Islands, the home of Carey.
Just how far is it from Carey's home to the arena?
"About a 10 or 15-minute walk," he said.
Carey said he didn't know how any people would be at the game against Coppin State at 9 p.m. today or the one Saturday against either Jacksonville State or Arkansas-Little Rock.
But Southern Miss basketball coach Donnie Tyndall said the sky's the limit.
"The tournament director actually contacted us because our guy, Norville Carey, he's a folk hero over there," Tyndall said. "People love him, and people are so proud of the fact that he's one of the few guys who have gotten out of the country and are playing at a major Division I school."
Carey, at 6-foot-7, is averaging 3.2 points and 1.9 rebounds per game this season. He has played in nine
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Virgin Islands tournament serves as homecoming for USM's Carey
MINI DEATH CAKES (The Hidden)
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I #39;M EVIL AGAIN (The Hidden)
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Human genetics is the study of inheritance as it occurs in human beings. Human genetics encompasses a variety of overlapping fields including: classical genetics, cytogenetics, molecular genetics, biochemical genetics, genomics, population genetics, developmental genetics, clinical genetics, and genetic counseling.
Genes can be the common factor of the qualities of most human-inherited traits. Study of human genetics can be useful as it can answer questions about human nature, understand the diseases and development of effective disease treatment, and understand genetics of human life. This article describes only basic features of human genetics; for the genetics of disorders please see: Medical genetics.
Inheritance of traits for humans are based upon Gregor Mendel's model of inheritance. Mendel deduced that inheritance depends upon discrete units of inheritance, called factors or genes.[1]
Autosomal traits are associated with a single gene on an autosome (non-sex chromosome)they are called "dominant" because a single copyinherited from either parentis enough to cause this trait to appear. This often means that one of the parents must also have the same trait, unless it has arisen due to a new mutation. Examples of autosomal dominant traits and disorders are Huntington's disease, and achondroplasia.
Autosomal recessive traits is one pattern of inheritance for a trait, disease, or disorder to be passed on through families. For a recessive trait or disease to be displayed two copies of the trait or disorder needs to be presented. The trait or gene will be located on a non-sex chromosome. Because it takes two copies of a trait to display a trait, many people can unknowingly be carriers of a disease. From an evolutionary perspective, a recessive disease or trait can remain hidden for several generations before displaying the phenotype. Examples of autosomal recessive disorders are albinism, cystic fibrosis, Tay-Sachs disease.
X-linked genes are found on the sex X chromosome. X-linked genes just like autosomal genes have both dominant and recessive types. Recessive X-linked disorders are rarely seen in females and usually only affect males. This is because males inherit their X chromosome and all X-linked genes will be inherited from the maternal side. Fathers only pass on their Y chromosome to their sons, so no X-linked traits will be inherited from father to son. Men cannot be carriers for recessive X linked traits, as they only have one X chromosome, so any X linked trait inherited from the mother will show up.
Females express X-linked disorders when they are homozygous for the disorder and become carriers when they are heterozygous. X-linked dominant inheritance will show the same phenotype as a heterozygote and homozygote. Just like X-linked inheritance, there will be a lack of male-to-male inheritance, which makes it distinguishable from autosomal traits. One example of a X-linked trait is Coffin-Lowry syndrome, which is caused by a mutation in ribosomal protein gene. This mutation results in skeletal, craniofacial abnormalities, mental retardation, and short stature.
X chromosomes in females undergo a process known as X inactivation. X inactivation is when one of the two X chromosomes in females is almost completely inactivated. It is important that this process occurs otherwise a woman would produce twice the amount of normal X chromosome proteins. The mechanism for X inactivation will occur during the embryonic stage. For people with disorders like trisomy X, where the genotype has three X chromosomes, X-inactivation will inactivate all X chromosomes until there is only one X chromosome active. Males with Klinefelter syndrome, who have an extra X chromosome, will also undergo X inactivation to have only one completely active X chromosome.
Y-linked inheritance occurs when a gene, trait, or disorder is transferred through the Y chromosome. Since Y chromosomes can only be found in males, Y linked traits are only passed on from father to son. The testis determining factor, which is located on the Y chromosome, determines the maleness of individuals. Besides the maleness inherited in the Y-chromosome there are no other found Y-linked characteristics.
A pedigree is a diagram showing the ancestral relationships and transmission of genetic traits over several generations in a family. Square symbols are almost always used to represent males, whilst circles are used for females. Pedigrees are used to help detect many different genetic diseases. A pedigree can also be used to help determine the chances for a parent to produce an offspring with a specific trait.
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Dr. Karin Blakemore
Dr. Blakemore is the Director of Maternal Fetal Medicine and Prenatal Genetics whose clinical practice focuses on caring for expectant mothers and their deve...
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Video Now Available Genetics and Genomics of Thyroid Neoplasms On Dec. 6th, Electron Kebebew, M.D., chief of the Endocrine Oncology Branch, National Cancer Institute, NIH, presented Genetics and Genomics of Thyroid Neoplasms: Moving Closer Towards Personalized Patient Care, as part of the 2013-2014 Genomics in Medicine Lecture Series, sponsored by NHGRI in collaboration with Suburban Hospital and Johns Hopkins. Video of his talk is now available. See the video Presidential Bioethics Report on Incidental Findings The Presidential Commission for the Study of Bioethical Issues released a report on Dec. 12, 2013, entitled Anticipate and Communicate: Ethical Management of Incidental and Secondary Findings in the Clinical, Research, and Direct-to-Consumer Contexts. Although not specifically focused on genomics, the report and its guidelines have implications for genomics research and medicine. Read the report Read the press release The Genomics Landscape Jumping into the deep end of genomic medicine When NHGRI published its new strategic vision for genomics in 2011, we recognized that we had a lot to learn about the research needed to apply genomics to clinical care. At the same time, it seemed critical that we begin to establish a foundation of research programs that would facilitate the implementation of genomic medicine, so we decided to jump in and start swimming! Read more Video Now Available The African Diaspora: Integrating Culture, Genomics and History Videos of the symposium "The African Diaspora: Integrating Culture, Genomics and History" are now available. The event included talks on using genomics in ancestral research and differences in health. NHGRI organized the symposium with the Smithsonian National Museum of Natural History and the National Museum of African American History and Culture. Watch the videos
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CHICAGO (AP) Dr. Janet Rowley, a pioneer in cancer genetics research, has died at age 88.
Rowley spent most of her career at the University of Chicago, where she also obtained her medical degree. She died Tuesday of ovarian cancer complications at her home nearby, the university said in a statement.
Rowley conducted landmark research with leukemia in the 1970s, linking cancer with genetic abnormalities work that led to targeted drug treatment for leukemia. She identified a genetic process called translocation, now widely accepted. By 1990, more than 70 translocations had been identified in various cancers, according to her biography on the National Library of Medicine's website.
She is a recipient of the National Medal of Science, the nation's highest scientific honor and the Presidential Medal of Freedom, the nation's highest civilian honor.
"Janet Rowley's work established that cancer is a genetic disease," Mary-Claire King, president of the American Society of Human Genetics, said recently. "We are still working from her paradigm."
Rowley, known among colleagues for her intelligence and humility, called receiving the presidential award, in 2009, "quite remarkable."
"I've never regretted being in science and being in research," Rowley said at the time. "The exhilaration that one gets in making new discoveries is beyond description."
With her silvery hair and twinkling eyes, Rowley was a recognizable figure at the University of Chicago, often seen riding her bike around the South Side campus, even up until a few months ago despite her disease. She remained active in research until close to her death and hoped that her own cancer could contribute to understanding of the disease.
Just last month, she was well enough to attend a celebration of the 50th anniversary of the presidential medal in Washington alongside other previous recipients and this year's winners, who include several scientists, former President Bill Clinton, Oprah Winfrey, baseball's Ernie Banks and Loretta Lynn.
Rowley was born in New York City in 1925 and at age 15 won a scholarship to an advanced academic program at the University of Chicago. She went to medical school there when the quota was just three women in a class of 65, the university said.
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Human evolutionary genetics studies how one human genome differs from the other, the evolutionary past that gave rise to it, and its current effects. Differences between genomes have anthropological, medical and forensic implications and applications. Genetic data can provide important insight into human evolution.
Biologists classify humans, along with only a few other species, as great apes (species in the family Hominidae). The Hominidae include two distinct species of chimpanzee (the bonobo, Pan paniscus, and the common chimpanzee, Pan troglodytes), two species of gorilla (the western gorilla, Gorilla gorilla, and the eastern gorilla, Gorilla graueri), and two species of orangutan (the Bornean orangutan, Pongo pygmaeus, and the Sumatran orangutan, Pongo abelii).
Apes, in turn, belong to the primates order (>400 species). Data from both mitochondrial DNA (mtDNA) and nuclear DNA (nDNA) indicate that primates belong to the group of Euarchontoglires, together with Rodentia, Lagomorpha, Dermoptera, and Scandentia.[1] This is further supported by Alu-like short interspersed nuclear elements (SINEs) which have been found only in members of the Euarchontoglires.[2]
A phylogenetic tree like the one shown above is usually derived from DNA or protein sequences from populations. Often mitochondrial DNA or Y chromosome sequences are used to study ancient human demographics. These single-locus sources of DNA do not recombine and are almost always inherited from a single parent, with only one known exception in mtDNA.[3] Individuals from the various continental groups tend to be more similar to one another than to people from other continents. The tree is rooted in the common ancestor of chimpanzees and humans, which is believed to have originated in Africa. Horizontal distance in the diagram corresponds to two things:
Chimpanzees and humans belong to different genera, indicated in red. Formation of species and subspecies is also indicated, and the formation of races is indicated in the green rectangle to the right (note that only a very rough representation of human phylogeny is given). Note that vertical distances are not meaningful in this representation.
The separation of humans from their closest relatives, the African apes (chimpanzees and gorillas), has been studied extensively for more than a century. Five major questions have been addressed:
As discussed before, different parts of the genome show different sequence divergence between different hominoids. It has also been shown that the sequence divergence between DNA from humans and chimpanzees varies greatly. For example the sequence divergence varies between 0% to 2.66% between non-coding, non-repetitive genomic regions of humans and chimpanzees.[5] Additionally gene trees, generated by comparative analysis of DNA segments, do not always fit the species tree. Summing up:
The divergence time of humans from other apes is of great interest. One of the first molecular studies, published in 1967 measured immunological distances (IDs) between different primates.[7] Basically the study measured the strength of immunological response that an antigen from one species (human albumin) induces in the immune system of another species (human, chimpanzee, gorilla and Old World monkeys). Closely related species should have similar antigens and therefore weaker immunological response to each other's antigens. The immunological response of a species to its own antigens (e.g. human to human) was set to be 1.
The ID between humans and gorillas was determined to be 1.09, that between humans and chimpanzees was determined as 1.14. However the distance to six different Old World monkeys was on average 2.46, indicating that the African apes are more closely related to humans than to monkeys. The authors consider the divergence time between Old World monkeys and hominoids to be 30 million years ago (MYA), based on fossil data, and the immunological distance was considered to grow at a constant rate. They concluded that divergence time of humans and the African apes to be roughly ~5 MYA. That was a surprising result. Most scientists at that time thought that humans and great apes diverged much earlier (>15 MYA).
The gorilla was, in ID terms, closer to human than to chimpanzees; however, the difference was so slight that the trichotomy could not be resolved with certainty. Later studies based on molecular genetics were able to resolve the trichotomy: chimpanzees are phylogenetically closer to humans than to gorillas. However, the divergence times estimated later (using much more sophisticated methods in molecular genetics) do not substantially differ from the very first estimate in 1967.
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Human evolutionary genetics - Wikipedia, the free encyclopedia
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Newswise Singapore, 18 December 2013 A recent study led by scientists from the National University of Singapore (NUS) opens a possible new route for treatment of Spinal Muscular Atrophy (SMA), a devastating disease that is the most common genetic cause of infant death and also affects young adults. As there is currently no known cure for SMA, the new discovery gives a strong boost to the fight against SMA.
SMA is caused by deficiencies in the Survival Motor Neuron (SMN) gene. This gene controls the activity of various target genes. It has long been speculated that deregulation of some of these targets contributes to SMA, yet their identity remained unknown.
Using global genome analysis, the research team, led by Associate Professor Christoph Winkler of the Department of Biological Sciences at the NUS Faculty of Science and Dr Kelvin See, a former A*STAR graduate scholar in NUS who is currently a Research Fellow at the Genome Institute of Singapore (GIS), found that deficiency in the SMN gene impairs the function of the Neurexin2 gene. This in turn limits the neurotransmitter release required for the normal function of nerve cells. The degeneration of motor neurons in the spinal cord causes SMA. This is the first time that scientists establish an association between Neurexin2 and SMA.
Preliminary experimental data also showed that a restoration of Neurexin2 activity can partially recover neuron function in SMN deficient zebrafish. This indicates a possible new direction for therapy of neurodegeneration.
Collaborating with Assoc Prof Winkler and the NUS researchers are Dr S. Mathavan and his team at GIS, as well as researchers from the University of Wuerzburg in Germany. The breakthrough discovery was first published in scientific journal Human Molecular Genetics last month.
Small zebrafish provides insights into human neurodegenerative disease
SMA is a genetic disease that attacks a distinct type of nerve cells called motor neurons in the spinal cord. The disease has been found to be caused by a defect in the SMN gene, a widely used gene that is responsible for normal motor functions in the body.
To study how defects in SMN cause neuron degeneration, the scientists utilised a zebrafish model, as the small fish has a relatively simple nervous system that allows detailed imaging of neuron behaviour.
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Study Provides New Insights Into Cause of Human Neurodegenerative Disease
Data obtained from a Neanderthal woman's toe bone points to incest and inbreeding among early humans, an international genetics team reported on Wednesday.
The fossil's genetic map, or genome, reported from Denisova cave in Siberia's Altai Mountains dates to more than 50,000 years ago. The cave was home at separate times to both Neanderthals and the so-called Denisovans, two sister families of now-extinct early humans. (See also "New Type of Ancient Human Found.")
Adding to increasing evidence of a tangled human family tree, the new Neanderthal genome study released by the journal Nature also suggests that another previously unknown archaic human species shared its genes with some of our ancestors. The study authors suggest that it was Homo erectus, one of the earliest human species, which first arose around 1.8 million years ago. (See also "Why Am I a Neanderthal?")
The report, led by Germany's Kay Prfer of the Max Planck Institute for Evolutionary Anthropology in Leipzig, builds on recent prehistoric genetics results that argue against theories that modern humans arose completely from one "out of Africa" migration more than 60,000 years ago that spread worldwide without mating with other early humans.
Instead, it looks like early modern humans sometimes mated with archaic human cousins they met along the way. People of non-African origin broadly have genes that are 1.5 percent to 2.1 percent Neanderthal, according to the study, with proportions higher among Asians and Native Americans. Similarly, 5 percent of the genome of people of Australian and Papua New Guinea descent looks Denisovan, as does 0.2 percent of the genes of people from Asia.
"We don't have one ancestral group, but proportions of ancestral groups," says computational biologist Rasmus Nielsen of the University of California, Berkeley, who was not part of the study team. "I think they make a convincing argument."
"In my view, this paper heralds the completion of the Neanderthal genome project in terms of mapping an entire genome," says paleontologist and human origins expert Richard Potts of the Smithsonian's National Museum of Natural History in Washington, D.C. "That's pretty cool science."
Kissing Cousins
In 2010, the study's toe bone first turned up at Denisova Cave, where excellent fossil preservation conditions had allowed for the genetic mapping of the then-surprising Denisovan finger bone found in 2008. Gene tests showed the toe belonged to a Neanderthal, and Prfer and colleagues began calculating its full genetic map.
Photograph by B. Viola, MPI f. Evolutionary Anthropology
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A team of geneticists has identified a possible link between mutations that cause early cognitive impairments, such as dyslexia, and schizophrenia and autism.
The study was led by members of an Icelandic biopharmaceutical company specialising in the human genome, called deCODE genetics, and was based on work done by those before them into possible links between copy number variant (CNV) mutations and schizophrenia and autism.
CNVs occur when parts of the genome have an abnormal number of copies -- this could be represented as a deletion or duplication of a section of a particular chromosome. A number of these CNVs have in the past been identified in those suffering from psychiatric disorders, and the deCODE genetics team sought to track down how these markers alter the brain over time by comparing the genetics of sufferers of psychiatric disorders against healthy volunteers that carry those same mutations.
"In a small fraction of patients with schizophrenia or autism, alleles of CNVs in their genomes are probably the strongest factors contributing to the pathogenesis of the disease," write the authors in the paper, published in Nature. "These CNVs may provide an entry point for investigations into the mechanisms of brain function and dysfunction alike."
Working alongside the Central Institute of Mental Health in Mannheim, Germany, the team used a genealogical database of more than 100,000 Icelanders to track down carriers of the mutations. They found 26 CNV alleles, already identified as being markers for an increased predisposition of the disorders, in just 1.16 percent of candidates -- those 1,178 people carried one or more of the mutations each. According to a report by medwireNews, of these 167 carried specific neuropsychiatric-related CNVs but had not been diagnosed with any such condition.
The team then went about administering a series of neuropsychiatric and cognitive tests to those 167 individuals, along with a healthy control group, schizophrenia sufferers and carriers of other unrelated CNVs.
What they found, was a distinct link between mild cognitive impairments and CNVs linked to neuropsychiatric disorders, which makes sense, considering autism and schizophrenia are cognitive impairments. The carriers of neuropsychiatric-linked CNVs performed significantly worse in cognitive tasks than those with unrelated CNVs, and were more likely to have a history of learning disabilities such as dyslexia. They did, however, perform far better than patients with schizophrenia.
Digging further, the team broke down the specific CNVs. They found that those that performed poorly in the cognitive tasks and also had a history of dyslexia and dyscalculia carried the same CNV -- a deletion in chromosome 15, known as 15q11.2. Carrying out MRI scans of these volunteers' brains, they found the structure had altered in the same regions that are altered in patients with early signs of schizophrenia and in those with dyslexia
"This study provides one of the first footholds into biochemical understanding of humans' unique cognitive abilities," lead author on the study and deCODE genetics CEO Kari Stefansson said in a statement. "The findings also provide insight into which cognitive abilities put individuals at risk of developing schizophrenia and demonstrate that control carriers provide an opportunity to study cognitive abnormalities without the confounding effects of psychosis or medication."
This is not the first time a significant genetic link has been made between different cognitive impairments. Earlier this year a paper published in Nature Communications revealed the results of a novel study that involved the descendants of those living in isolated small towns in northern Finland, where cases of neuropsychiatric disorders are unusually common.
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Genetic markers for schizophrenia linked to unrelated cognitive impairments
Another health-care delay Listing all the delays Obama heads to Hawaii, but dont be surprised if we hear from him first Republicans again dealing with immigration and gay rights A busy next two months And the top 10 races of 2014 to watch.
By Chuck Todd, Mark Murray, and Domenico Montanaro
*** Another 11th-hour health-care change:Fearing that the number of people who lose coverage could match the number who sign up for insurance this year, the administration announced a new grandfather clause Thursday night: People who received cancellation notices for their policy but are not eligible for subsidies can use the laws hardship exemption to buy a bare-bones plan. Also, the administration announced these folks will NOT get hit with a tax penalty this year if they do not have insurance by Jan. 1, NBCs Maggie Fox reports. This is just the latest of several delays and extensions offered by the administration (some items listed below). The insurance industry behind the scenes is panicking over this, thinking it will affect their cost estimates, warning that it could increase costs and could mean higher prices eventually. This is just the latest in a series of rules changes the administration has put into place as criticism of the implementation has heated up. Heres a quick list of just some of the delays put in place this year:
REUTERS/Jonathan Bachman
The federal government forms for applying for health coverage are seen at a rally held by supporters of the Affordable Care Act, widely referred to as "Obamacare", outside the Jackson-Hinds Comprehensive Health Center in Jackson, Mississippi October 4, 2013.
And thats in addition to the delayed sign up deadline that slid eight days (Dec. 15-23), the extended sign ups until March 31, 2014, open enrollment being pushed back into November, as well as the web sites back-end delays, the Spanish-language site delay, and the essentially two-month delayed functional launch of HealthCare.gov. Serious question: will there be a single uninsured American in 2014 who will end up paying the mandate penalty?
*** Wanna get away? All that could make the person in charge of this law and whose legacy rests on its implementation want to book a flight and get out of town for the holidays. President Obama is doing just that tonight when he leaves for Hawaii at 6:45 pm ET. He does not return to Washington until Jan. 5th. It would be surprising if we didnt hear from him one more time before he leaves. There is no doubt the president cant wait for 2013 to be in the books, easily his most troubled year politically. And now most of his vacation, if hes focused on work, itll be health care, so admin officials told reporters yesterday. There will be regularly updates provided to the president regarding signups. Ironically, while the president has had a terrible year politically, the economy continues to slowly and steadily improve. The economy grew at a 4.1% annual rate, according to GDP numbers out this morning, up from the 3.6% reported earlier this month. Thats the fastest pace in nearly two years. By the way, Steve Harveys interview with President Obama airs at 3 pm ET today.
*** What do Republican presidential hopefuls do about immigration? Gov. Chris Christie (R) struck a deal with the state legislature yesterday on a bill that allows in-state tuition for undocumented immigrants. He promised to do this during his campaign. It wasnt clear that he would go through with it, but he did. In-state tuition was an issue in 2012 for Rick Perry, and nearly sunk John McCains presidential aspirations in 2008. By the way, this could be a dividing line issue for Christie with another governor, who wants to make the case that he can appeal to moderates Wisconsin Gov. Scott Walker. In 2011, Walker stripped out in-state tuition rates for children of undocumented immigrants, something that had been put in there in 2009 by Democratic Gov. Jim Doyle, per NBCs Vaughn Hillyard. Of course, the wild card here is what do presidentials do if the GOP-controlled House tackles some similar immigration measures next year? Secretly, every GOPer running in 2016 would love nothing more than for the House Republicans to simply get this issue out of the way for them.
***Conservatives dont Duck this fight: From one thorny GOP issue to another To us, that Phil Robertson of Duck Dynasty saying something controversial/offensiveisnt political news, or that its political news he got suspended from A&E for saying it. After all, plenty of celebrities -- conservative or liberal -- say controversial/offensive things all the time and they usually get some slap on the wrist. But what IS political news is when prominent politicians swoop in to defend the controversial/offensive comments. Here wasLouisiana Gov. Bobby Jindal (R): The politically correct crowd is tolerant of all viewpoints, except those they disagree with. I don't agree with quite a bit of stuff I read in magazine interviews or see on TV. In fact, come to think of it, I find a good bit of it offensive. But I also acknowledge that this is a free country and everyone is entitled to express their views. (Of course, companies are also entitled to fire/suspend their employees, too.) And here was Sen. Ted Cruz (R-TX) onTwitter:If you believe in free speech or religious liberty, you should be deeply dismayed over treatment of Phil Robertson. But the real reason why this is a story is that the Jindal-Cruz comments go precisely against the RNCs autopsy recommendations. On messaging, we must change our tone especially on certain social issues that are turning off young voters, the RNC report said.These comments may feel good in the moment and appeal to the base (something certainly Jindal needs to do with sagging poll numbers). But thats all this is talking to. And it reinforces the problems Republicans have with swing voters when it comes to these issues. Thats the danger here. Republicans have three choices on things like this denounce, support, or say nothing. The safest thing for most of them is to say nothing.
*** Look at the busy couple of months ahead -- Some upcoming political dates to circle on your calendars:
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Hyderabad: Asserting that providing good health care is one of the major responsibilities of the government,Nobel laureate Venkatraman Ramakrishnan today hailed the national health service in Britain.
"Health care is one of the responsibilities of a government. One thing that we in Britain are proud of is the national health service. The poorest person in Britain gets the same treatment that a senior scientist at the MRC gets. There is no preference, I don't get pushed ahead in line. I have to wait my turn," the Indian-born scientist said.
"There used to be public health care in India. But somehow, it is deteriorated. I have not lived here. So, I don't know. But, this is just what I hear," said Ramakrishnan, who works at the MRC Laboratory of Molecular Biology, Cambridge, UK.
He was speaking to reporters after delivering a lecture on "Antibiotics and the Cell's Protein Factory" at CSIR-Centre for Cellular Molecular Biology (CCMB) here.
To a question, he said he cannot offer any suggestions on social health care for India, as he had not lived here, but there was no dearth of talented health care professionals in the country, and they should be consulted.
"There are hundreds, thousands of superb, dedicated Indian health professionals at the top medical schools, people who work in the field... These are people who have ideas, they should be asked what the solutions are... There is no shortage of excellent people here," he said.
He also spoke about the need for rational use of antibiotics, and favoured regulation of over the counter sale of medicines. "It should be only prescription-based," he said.
Preventive medicine was more cost-effective than later treatment, he added.
Ramakrishnan, who received Nobel Prize for Chemistry along with two others in 2009 for "studies of the structure and function of the ribosome", said that understanding how ribosomes of humans differ from ribosomes of bacteria and other related aspects are important issues.
"Ribosomes don't make all proteins at the same rate. Some proteins are made very efficiently. So, this process called translational regulation, when a proteins made, how much are made. This idea of how ribosomes are regulated, at which point they make things, that is a big step.
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Health care is government's responsibility: Venkatraman Ramakrishnan
Asserting that providing good health care is one of the major responsibilities of the government, Nobel laureate Venkatraman Ramakrishnan today hailed the national health service in Britain.
"Health care is one of the responsibilities of a government. One thing that we in Britain are proud of is the national health service. The poorest person in Britain gets the same treatment that a senior scientist at the MRC gets. There is no preference, I don't get pushed ahead in line. I have to wait my turn," the Indian-born scientist said.
"There used to be public health care in India. But somehow, it is deteriorated. I have not lived here. So, I don't know. But, this is just what I hear," said Ramakrishnan, who works at the MRC Laboratory of Molecular Biology, Cambridge, UK.
He was speaking to reporters after delivering a lecture on "Antibiotics and the Cell's Protein Factory" at CSIR-Centre for Cellular Molecular Biology (CCMB) here.
To a question, he said he cannot offer any suggestions on social health care for India, as he had not lived here, but there was no dearth of talented health care professionals in the country, and they should be consulted.
"There are hundreds, thousands of superb, dedicated Indian health professionals at the top medical schools, people who work in the field. These are people who have ideas, they should be asked what the solutions are. There is no shortage of excellent people here," he said.
He also spoke about the need for rational use of antibiotics, and favoured regulation of over the counter sale of medicines. "It should be only prescription-based," he said.
Preventive medicine was more cost-effective than later treatment, he added.
Asked about further discoveries in ribosomes, Ramakrishnan, who received Nobel Prize for Chemistry along with two others in 2009 for "studies of the structure and function of the ribosome", said that understanding how ribosomes of humans differ from ribosomes of bacteria and other related aspects are important issues.
"Ribosomes don't make all proteins at the same rate. Some proteins are made very efficiently. So, this process called translational regulation, when a proteins made, how much are made. This idea of how ribosomes are regulated, at which point they make things, that is a big step.
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Big data analytics is playing a larger role in health care, and that is changing the way in which the industry is approaching patient care and research. A new report revealed that health care leaders believe big data will have a significant and positive impact on their businesses. The lessons that they are learning parallel the experiences of midsize firms as they seek to gain greater insight into the increasing amounts of data accumulated each day.
Big Data Good for Business
According to a new study by the Society of Actuaries (SOA), more than 87 percent of health care leaders said that big data will have an important impact on the business of health care. The results, featured in the CloudTimes, also found that 66 percent of leaders are happy about the potential of big data, and more than half believe that there is a business benefit to implementing big data in their information infrastructures.
The biggest hurdle cited by executives is to effectively apply big data to health care delivery. According to the report, the insight gained has been useful, but executives want to extract greater meaning from the data and to see more of an impact. The health care industry also faces the challenge of finding and hiring staff with expertise in the optimization of big data. There is a significant need for IT professionals with big data know-how, and the report found that 45 percent of health care companies are planning to hire energetically in 2014.
Midsize Insight
Applying big data analytics is a significant undertaking for any organization. IT professionals at midsize firms around the world, as also in the health care industry, are seeking solutions that make the most of the deluge of data with which they are confronted on a daily basis. As technologies such as the cloud and virtualization become commonplace, both structured and unstructured data will pile up as never before. For firms that want to remain at their most productive, big data solutions are a worthy investment.
Health care companies and midsize firms across industries value the security of their data. Health care data can be particularly sensitive, and certain compliance requirements need to be met. Most midsize firms cannot afford a data breach that could compromise their bottom line. Smart security measures targeted to a firm's specific needs are key to maintaining a big data solution that can empower executives to make more informed decisions.
The SOA study found that health care firms are struggling to recruit personnel to tackle big data projects, and midsize firms face similar struggles. Smaller companies have fewer resources, and they likely do not have the expert staff on hand to execute a big data implementation. As a result, they count on trusted partners to offer solutions that target their specific goals.
Midsize Demand
Small and midsize businesses (SMBs) benefit from partnering with a vendor that understands how their needs differ from those of enterprise. SMBs are constrained by limited resources, personnel and budget and cannot afford to make mistakes. As a result, they demand a quick return on investment (ROI). Midsize firms should implement well-researched methods to organize data and integrate analytics throughout their infrastructures.
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PUBLIC RELEASE DATE:
18-Dec-2013
Contact: Sarah Avery sarah.avery@duke.edu 919-660-1306 Duke University Medical Center
DURHAM, N.C. A genetic trait known to make some people especially sensitive to stress also appears to be responsible for a 38 percent increased risk of heart attack or death in patients with heart disease, scientists at Duke Medicine report.
The finding outlines a new biological explanation for why many people are predisposed to cardiovascular disease and death, and suggests that behavior modification and drug therapies could reduce deaths and disability from heart attacks.
The study appears in the Dec. 18, 2013, issue of the journal PLOS ONE.
"We've heard a lot about personalized medicine in cancer, but in cardiovascular disease we are not nearly as far along in finding the genetic variants that identify people at higher risk," said senior author Redford B. Williams Jr., M.D. director of the Behavioral Medicine Research Center at Duke University School of Medicine. "Here we have a paradigm for the move toward personalized medicine in cardiovascular disease."
Williams and colleagues built on previous work at Duke and elsewhere that identified a variation in a DNA sequence, known as a single nucleotide polymorphism (SNP), where one letter in the genetic code is swapped for another to change the gene's function. The SNP the Duke team focused on occurs on the gene that makes a serotonin receptor, and causes a hyperactive reaction to stress.
In a study published last year, the researchers reported that men with this genetic variant had twice as much cortisol in their blood when exposed to stress, compared to men without the genetic variant. Known as a "stress hormone," cortisol is produced in the adrenal gland to support the body's biological response when reacting to a situation that causes negative emotions.
"It is known that cortisol has effects on the body's metabolism, on inflammation and various other biological functions, that could play a role in increasing the risk of cardiovascular disease," said lead author Beverly H. Brummett, Ph.D., associate professor of Psychiatry and Behavioral Sciences at Duke. "It has been shown that high cortisol levels are predictive of increased heart disease risk. So we wanted to examine this more closely."
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PUBLIC RELEASE DATE:
19-Dec-2013
Contact: Scott LaFee slafee@ucsd.edu 619-543-6163 University of California - San Diego
Researchers at the University of California, San Diego School of Medicine, with colleagues in The Netherlands and United Kingdom, have produced the first map detailing the network of genetic interactions underlying the cellular response to ultraviolet (UV) radiation.
The researchers say their study establishes a new method and resource for exploring in greater detail how cells are damaged by UV radiation and how they repair themselves. UV damage is one route to malignancy, especially in skin cancer, and understanding the underlying repair pathways will better help scientists to understand what goes wrong in such cancers.
The findings will be published in the December 26, 2013 issue of Cell Reports.
Principal investigator Trey Ideker, PhD, division chief of genetics in the UC San Diego School of Medicine and a professor in the UC San Diego Departments of Medicine and Bioengineering, and colleagues mapped 89 UV-induced functional interactions among 62 protein complexes. The interactions were culled from a larger measurement of more than 45,000 double mutants, the deletion of two separate genes, before and after different doses of UV radiation.
Specifically, they identified interactive links to the cell's chromatin structure remodeling (RSC) complex, a grouping of protein subunits that remodel chromatin the combination of DNA and proteins that make up a cell's nucleus during cell mitosis or division. "We show that RSC is recruited to places on genes or DNA sequences where UV damage has occurred and that it helps facilitate efficient repair by promoting nucleosome remodeling," said Ideker.
The process of repairing DNA damage caused by UV radiation and other sources, such as chemicals and other mutagens, is both simple and complicated. DNA-distorting lesions are detected by a cellular mechanism called the nucleotide excision repair (NER) pathway. The lesion is excised; the gap filled with new genetic material copied from an intact DNA strand by special enzymes; and the remaining nick sealed by another specialized enzyme.
However, NER does not work in isolation; rather it coordinates with other biological mechanisms, including RSC.
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