Wednesday, August 12, 2009

miles

Named after an obscure Celtic and Gallic god, Toutatis is a yam-shaped space rock that measures 1.92 kilometers (1.2 miles) by 2.29 kilometers (1.4 miles) by 4.6 kilometers (2.9 miles). Toutatis has one of the strangest rotation states observed in the solar system. Instead of spinning around a single axis, as do the planets and the vast majority of astero

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ids, it "tumbles" somewhat like a football after a botched pass. Its rotation is the result of two different types of motion with periods of 5.4 and 7.3 Earth days, which combine in such a way that Toutatis's orientation, with respect to the solar system, never repeats.

at

The next comparable Earth flyby for asteroid 1994 CC will occur in the year 2074 when the space rock trio flies past Earth at a distance of two-and-a-half million kilometers (1.6 million miles).

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at

The next comparable Earth flyby for asteroid 1994 CC will occur in the year 2074 when the space rock trio flies past Earth at a distance of two-and-a-half million kilometers (1.6 million miles).

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at

The next comparable Earth flyby for asteroid 1994 CC will occur in the year 2074 when the space rock trio flies past Earth at a distance of two-and-a-half million kilometers (1.6 million miles).

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Earth

Prior to the flyby, very little was known about this celestial body. 1994 CC is only the second triple system known in the near-Earth population. A team led by Marina Brozovic and Lance Benner, both scientists at NASA's Jet Propulsion Laboratory in Pasadena, Calif., made the discovery.

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around

1994 CC consists of a central object about 700 meters (2,300 feet) in diameter that has two smaller moons revolving around it. Preliminary analysis suggests that the two small satellites are at least 50 meters (164 feet) in diameter. Radar observations at Arecibo Observatory in Puerto Rico, led by the center's director Mike Nolan, also detected all three objects, and

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the combined observations from Goldstone and Arecibo will be utilized by JPL scientists and their colleagues to study 1994 CC's orbital and physical properties.

oestrogen

The WEHI team, together with the Eaves group in Vancouver, have found that the breast stem cell in mice is ‘triple negative’ for oestrogen, progesterone and Her2 receptors but does express certain ‘basal cell’ markers. These characteristics also define the basal subtype of breast cancer, which is more commonly seen in tumours that develop in wome

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n who are carriers of the breast cancer predisposing gene BRCA1.

question

This possibility has generated great interest in understanding the composition of normal breast cells including the stem cell. A question of particular interest is whether the breast stem cell expresses receptors for oestrogen and progesterone and the marker ‘Her2’, since these help define the subtypes of breast cancer; and also guide current approaches to th

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erapy.

have

Victorian Breast Cancer Research Consortium scientists from The Walter and Eliza Hall Institute, using mouse models, have discovered that breast stem cells do not express receptors for the female hormones oestrogen or progesterone. These and other features of the stem cell resemble the aggressive ‘basal’ subtype of breast cancer.

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heterogeneous

There is increasing evidence that breast cancer is not simply a single disease. Scientists now view breast cancer as a heterogeneous disease, made up of various subtypes. This observation has led to speculation that breast tumours are derived from different cell types that could include the breast stem cell or its descendents that have suffered genetic accidents.

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-

Chemotherapy works by targeting cells that are dividing rapidly, which is typical behaviour of cancer cells. But an errant stem-like cell may be more resistant to chemotherapy because it divides more slowly. So while chemotherapy can eliminate the bulk of cancer cells, the tumour factory itself – a breast cancer stem cell – may survive months or years later.

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apparently

For many years, scientists and clinicians have been puzzled by the fact that women whose breast cancer cells have been apparently eliminated by chemotherapy sometimes experience a recurrence of their cancer. A cancerous stem cell could provide one possible explanation for such a recurren

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ce.

accumulation

Under normal circumstances, the newly identified breast stem cell will produce healthy tissue. But it is believed that an accumulation of genetic errors, perhaps combined with external influences and a family predisposition, could cause the breast stem cell or a "daughter" cell to produce faulty cells. In effect, the errant breast cell can become a tumour factory.

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Notch

Cancer arises as a result of the accumulation of multiple genetic lesions that ultimately result in unregulated cell cycle, and Notch activity is a key determinant of the cellular development and differentiation related to this process. As Notch signaling is activated in human breast cancer, (and a negative regulator of Notch signaling reduces the disease), the molecular me

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chanisms regulating Notch activity are of fundamental importance for future therapy.

is

The study, conducted by Dr. Richard Pestell and colleagues at Thomas Jefferson University, was the first to show that cyclin d1 is required for breast cancer growth in mice. As cyclin d1 is known to be over-expressed in human breast cancer, the findings may explain how cyclin d1 contributes to breast tumor growth, and provide the rationale for targeted thera

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pies at cancerous stem cells in humans.

and

Thus, Notch helps to orchestrate the formation of breast tissue: it plays an important role in controlling stem cell number and instructs stem cells to produce luminal cells.

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cells

Second, Notch is important for ensuring that stem cells produce the sleeve of cells that normally line breast ducts. These 'luminal' cells may be the cells that give rise to common types

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of breast cancer.

Consortium

The breast cancer team at WEHI, led by Drs Jane Visvader and Geoff Lindeman from the Victorian Breast Cancer Research Consortium, have identified important roles for Notch genes in regulating breast development

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and function.

cell

The Notch pathway sends signals from a cell's surface membrane into its nucleus. Those signals activate genes that instruct the cell to make proteins that perform various t

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asks.

cancer

Dr. Max Wicha, director of the U-M Comprehensive Cancer Center, said Maillard's results are welcome news for cancer stem cell researchers, and for the 30-patient metastatic breast-cancer drug trial that launched last month at his center, at the Baylor College of Medicine in Houston, and at the Dana-Farber Cancer Institute in Boston.

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University

The Notch findings will be published Thursday in the journal Cell Stem Cell. Maillard's team includes researchers from the University of Pennsylvania School of Medicine, the Swiss Institute for Experimental Cancer Research, and Harvard Medical School.

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effects

"That's important, since these patients typically need good blood stem cells to maintain their blood counts and recover from the effects of chemotherapy," he said.

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these

"Our data indicate that normal blood-forming stem cells should not be damaged by the Notch inhibitor drug being used in these patients," said Maillard, a hematologist and a Life Sciences Institute researcher.

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forming

New results from the U-M's Dr. Ivan Maillard and his colleagues may allay some of those fears. The researchers showed that blood-forming stem cells in mice survive just fine when the Notch signaling pathway is experimentally bloc

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ked.

biological

"These findings will impact every walk of biology," said David Allis of Rockefeller University, a leader in studying the regulation and biological roles of histone tags. "Histone modifications are highly dynamic on-off switches that the cell throws a lot. These modifications affect everything DNA does, and getting the enzyme means you've got one upstream point of regulation. T

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his will open up a wealth of new experiments."

methylation

Genes turning on at the wrong time or in the wrong place is a hallmark of cancer cells. In some tumors, high levels of methylation of H3K4 seem to play a role in activating genes that drive abnormal cell growth. The discovery of this H3K4 demethylase suggests a way to counterbalance this progrowth signal in some tumors. And if previous experience with histo

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ne deacetylases is any guide, the demethylases could one day be targets for cancer therapeutics.
Their enzyme didn't remove just any methyl group from histone. Instead, it removed a very specific methyl found on lysine 4 (K4) of histone 3 (H3). H3K4 methylation is associated with active transcription, so its removal would be consistent with the gene repression function they had identified.

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gene

The Shi lab was not among those in the hunt, but they stumbled onto the demethylase while probing the function of a new gene repressor protein. Postdoctoral fellow Yujiang Shi had exhausted the likely possibilities for how the mystery protein worked to suppress gene activity, so one day he tried an unlikely experiment. He had the purifie

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d protein in a test tube and decided to feed it methylated histones. His finding, that the enzyme could efficiently chew off the methyl group, leaving behind intact, unmodified histone left the postdoc Shi shaking with excitement. "Forty years ago some scientists speculated that histone demethylases existed," he said. "At first, I thought it was impossible that this protein was it." After reproducing the results using several different biochemical techniques, he began to feel comfortable that they had found the first demethylase.

gene

The enzyme, a histone demethylase, removes methyl groups appended to histone proteins that bind DNA and help regulate gene activity. "Previously, people thought that histone methylation was stable and irreversible," said Shi. "The fact that we've identified a demethylase suggests a more dynamic process of gene regulation via methylation of h

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istones. The idea of yin and yang is universal in biology; our results show that histone methylation is no different."

Shi

The elusive enzyme, whose presence in cells was suspected but not proven for decades, came to light in the laboratory of Yang Shi, HMS professor of pathology, and is described in a study published in the Dec. 16 online edition of Cell and appearing in the Dec. 29 print edition.

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Am vazut multe ceasuri superbe pe www.topceas.ro