EARLY DIFFERENTIATION
Scientists find clues of cell division in 550-million-year-old fossilized embyos, say it's a "window on the past"
Life's complexity seen in fossilized embryos
WASHINGTON
A team of scientists from five countries examining fossil embryos that are more than 550 million years old has found evidence of cell differentiation. The findings were reported in the October 13 issue of Science, in the article "Cellular and Subcellular Structure of Neoproterozoic Animal Embryos."
The team of 15 scientists also identified what appeared to be cells about to divide. They used X-ray imaging technologies that produce higher resolutions than hospital CT, and digitally extracted cells from the embryos of ancient animals that have been preserved in the Doushantuo Formation, a fossil site in South China.
"We're learning something about how the very earliest multicellular animal formed embryos and how the embryos developed," said one of the authors, Rudolf Raff of Indiana University and the University of Sydney. "This gives us an enormous and entirely surprising look at half-a-billion-year-old embryos in the act of cleaving. What a window on the past. We've had no prior idea what they might have done."
The team examined 162 relatively pristine envelope-bound and spheroidal embryos in which recurrent biological structures and cleavage patterns could be distinguished from inorganic artifacts.
"We digitally extracted each cell from the embryos and then looked inside the cells," said another member of the research team, Shuhai Xiao of Virginia Tech. "We found some kidney-shaped structures within the cells, which could be nuclei or other subcellular structures. It is amazing that such delicate biological structures can be preserved in such an ancient deposit." In some four-cell embryos, each cell had two kidney-shaped subcellular structures, "so they were caught in the process of splitting during cell division," Xiao added.
James Hagadorn of Amherst College, a member of the international research team, said the findings "cast serious doubt on previous claims that these embryos represent more derived or advanced groups of animals, for example, bilaterally symmetrical animals." "Rather, all the available evidence suggests that they represent relatively simple forms, akin to sponge ancestors."
Headway on new malaria treatment
STOCKHOLM
A new treatment against the most severe form of malaria has been shown successful on rats and monkeys, animals whose "mechanisms are similar" to humans. "There's a lot of hope. I am very optimistic because we know that the mechanisms we are looking at in the two models are very similar to the mechanism that we have in humans," said Anna Vogt, a member of the team that conducted the research at Karolinska Institute in Stockholm.
The treatment concerns the most acute form of malaria, caused by the parasite Plasmodium falciparium, which kills two million people each year. The substance developed by the team both prevents and helps cure blood cells infected with the parasite.
"The parasite ... infects the red blood cells, which then accumulate in large amounts, blocking the flow of blood in the capillaries of the brain and other organs," the researchers said.
Because P. falciparum exists only in humans, the researchers had to inject it into the rats and monkeys. "We have developed two short-term models where we inject the animals with infected human red blood cells and look at the binding phenomenon in the lungs of rats and monkeys," Vogt said. "Then we treat the animals and we can see that the infected cells are released in the circulation, enabling the blood to circulate freely again. But of course there are a lot of additional factors in humans that we can't control in animals."
Vogt stressed that the treatment would serve as a complement to other treatments, as it targets the symptoms that lead to severe malaria. "Then you have to use an antimalaria drug that will release the parasite from the circulation."
Tests on humans are scheduled to begin within a year or two.
The research results were published in the online journal PLoS Pathogens of the Public Library of Science.
3D map tracks genes at work in brain
WASHINGTON
A three-dimensional map tracking genes at work in the mouse brain has been completed and posted online, a boon for researchers studying neurological disorders, an institute founded by Microsoft cofounder Paul Allen announced.
The Allen Brain Atlas is an Internet-based, 3D map plotting the regions in which 21,000 genes "express" themselves in the brain of the mouse, 90 percent of which are the same as in the human genes.
"This project is an unprecedented union of neuroscience and genomics," said Allen, whose US$100 million launched the project in 2003. "The comprehensive information provided by the atlas will help lead scientists to new insights and propel the field of neuroscience forward dramatically," he said.
Because humans share more than 90 percent of their genes with mice, researchers can refer to the map to try to understand Alzheimer and Parkinson diseases, epilepsy, schizophrenia, autism, addiction, and other disorders.
The map pinpoints regions in which certain genes are active or "expressed" in the brain and links them to brain functions, most of which are the same in mammals. "This is a multidisciplinary project of unprecedented scale," said Allan Jones, the institute's scientific officer. "It combines the scientific disciplines of math, physics, neuroscience and genomics to define where those 21,000 genes are expressed and activated in the brain. There's no other information set like this."
In the course of the study, researchers discovered that about 80 percent of genes are turned on in the brain, more than the 60 to 70 percent previously known. In a related discovery, very few genes are turned on in only one region of the brain, providing opportunities for understanding benefits and side effects of brain treatment.
Access to the atlas is free at www.alleninstitute.org.
Protein key to Lou Gehrig disease identified
WASHINGTON
Abnormal accumulation of a protein in brain cells seems to play a key role in Lou Gehrig disease and in frontotemporal dementia (FTD). Postmortem analysis on the brain tissue of 72 people who suffered from these incurable conditions all showed an excess of this protein, called TDP-43, University of Pennsylvania School of Medicine scientists said.
"These findings open up new avenues of research into how the crumpling or misfolding of specific brain proteins (TDP-43) leads to strange, sometimes even criminal, behavior (in FTD), as well as paralysis [in Lou Gehrig disease], which depends upon whether these toxic waste products get dumped in the frontal and temporal lobes (the part of brain controlling judgment and comportment), or the spinal-cord motor neurons (the control centers regulating the ability to walk, run and other types of movement)," they said.
A link between these two disorders long been sought, and TDP-43 is the common pathologic protein linking them, said the researchers, whose work appears in the October 6 issue of Science.
Researchers attack melanoma with gene therapy
WASHINGTON
A team of US researchers successfully turned back advanced melanoma by manipulating the genes of white blood cells to get them to attack the cancer. National Cancer Institute scientists showed the ability to get a sustained regression in melanoma, a highly dangerous and frequently fatal form of skin cancer, by reprogramming through gene-therapy patients' own lymphocytes to recognize and fight the cancer cells.
They tried out the method on 17 patients in three groups, injecting into them the patients' own lymphocytes altered by the genetic introduction of T-cell receptors, which steer the cells to find and destroy tumor cells. The method failed to stall the disease in the first group of three. So the researchers modified the treatment to make sure the genetically manipulated lymphocytes were injected into the patients at the cells' most active growth phase.
That generated better results: Of the remaining 14 patients, the cancer regressed in two patients, who remained free of the disease for one year. Moreover, one month after receiving the gene therapy, all patients in the latter two groups continued to have significant levels of the cancer-fighting cells.
"These results represent the first time gene therapy has been used successfully to treat cancer," said Elias Zerhouni, director of the National Institutes of Health, which oversees the National Cancer Institute. "We hope is will be applicable not only to melanoma, but also for a broad range of common cancers, such as breast and lung cancer," he said.
The study was published by Science.
Plant-derived cream offers cancer protection
PARIS
Scientists have devised a paint-on cream that on mice tans skin without the need for sunlight while appearing to offer some protection against cancer-causing ultraviolet rays, according to a study published in Nature.
Researchers at the Dana-Farber Cancer Institute and Children's Hospital in Boston genetically engineered a batch of hairless fair-skinned mice that, tests showed, suffered burned skin when exposed to high doses of ultraviolet light. The team smeared the rodents with a plant-derived compound, forskolin, which is known to stimulate melanin. The forskolin, derived from the root of an Indian plant called forskohli, turned the mice's skin dark.
In a second batch of experiments, a strain of cancer-prone mice that were also engineered to have deficient receptors were exposed to daily doses of Florida-level noonday sun for one to two hours for 20 weeks. Nine mice that did not receive forskolin developed 11 skin tumors while nine mice that received the forskolin developed six tumors and showed fewer signs of skin damage. In addition, the tumors among forskolin mice showed up three times later than the tumors among the untreated mice. Put together, this amounts to significant skin protection, say the scientists.
"It remains to be seen whether topical melanization will be achievable in man, and whether it would afford measurable protection against UV skin damage and cancer," they caution.
Computer model detects colon-cancer risk
WASHINGTON
A new computer model can predict genetic defects that lead to colon cancer based on family history, according to a study in the Journal of the American Medical Association.
"Genetic defects can be passed from parents to their children. As a result, colon cancer runs in families. Our model will help identify individuals likely to have particular genetic defects," said Sining Chen, who wrote the study for the Johns Hopkins University School of Public Health. "The results will give them useful information about their colon-cancer risk before they decide whether to undergo invasive screenings or expensive genetic testing."
The test pinpoints persons with Lynch syndrome, also known as hereditary nonpolyposis colon cancer and is caused by the mutation of three principal genes: MSH2, MLH1, and MSH6, which are "mismatch repair genes" (MMR). The MMR genes help fix errors in the genetic code as it is copied in the creation of each new cell.
Persons with defects in these genes have about a 50-percent chance of getting colon cancer by age 70. Women with these defective genes have a 50-percent chance of developing endometrial cancer.
The report said the new MMRpro detection model is more effective at detection than the currently used Bethesda guidelines and the Amsterdam criteria.
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