ESA’s Venus Express has been used to study the geology in a region near Venus’ equator. Using near-infrared observations collected by the Venus Monitoring Camera (VMC), scientists have found evidence that the planet’s rugged highlands are scattered with geochemically more evolved rocks, rather than the basaltic rocks of the volcanic plains. This finding is in agreement with previous studies, which used data from the spacecraft’s Visible and Infrared Thermal Imaging Spectrometer (VIRTIS) to map the planet’s surface in the southern hemisphere.
Investigations into the nature of Venus’ surface are complicated by the fact that the surface is concealed behind a dense covering of clouds. Since the 1980s, radar instruments on board orbiting spacecraft have been used to peer through these clouds to gain insight into the texture of the surface. However, in order to understand how Venus has evolved, geologists want to ‘dig a bit deeper’ and study the composition of its rocks – information that radar imaging can’t provide.
They’re eager to learn if geological features revealed in radar images, such as steep-sided domes and rugged highland terrain (called tesserae), contain materials that are rich in silicates, such as ‘felsic rocks’. On Earth, most felsic rocks – the most common of which is granite – formed in a water environment. This makes them particularly interesting with regards to planetary evolution.
Chimon-mana Tessera and areas studied with VMC. Credit: A.T. Basilevsky et al. 2012
Since Venus Express began its observations, scientists are now starting to unearth the planet’s geology. The near-infrared channels of the VMC and VIRTIS instruments have measured the intensity of 1 micron-wavelength radiation, which is dependent upon the surface temperature and emissivity of the rocks. It’s the latter that is important here, as it depends on several factors, including the surface texture and mineral composition.
In a new study, the first findings about the geology of Venus based on VMC data have been published. The study, which was led by Alexander Basilevsky from the Vernadsky Institute of Geochemistry and Analytical Chemistry in Moscow, Russia, analysed the rugged highland terrain called Chimon-mana Tessera and its surrounding volcanic plains. This region was chosen for the VMC study because its equatorial position prevented solar light from skewing the data; by observing the night-side of Venus and keeping within low latitudes (40 degrees above and below the equator), the planet eclipsed the Sun from the spacecraft.
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For the first time scientists have succeeded in taking skin cells from heart failure patients and reprogramming them to transform into healthy, new heart muscle cells that are capable of integrating with existing heart tissue.
The research, which is published online May 22 in the European Heart Journal, opens up the prospect of treating heart failure patients with their own, human-induced pluripotent stem cells (hiPSCs) to repair their damaged hearts. As the reprogrammed cells would be derived from the patients themselves, this could avoid the problem of the patients’ immune systems rejecting the cells as “foreign.” However, the researchers warn that there are a number of obstacles to overcome before it would be possible to use hiPSCs in humans in this way, and it could take at least five to ten years before clinical trials could start.
Recent advances in stem cell biology and tissue engineering have enabled researchers to consider ways of restoring and repairing damaged heart muscle with new cells, but a major problem has been the lack of good sources of human heart muscle cells and the problem of rejection by the immune system. Recent studies have shown that it is possible to derive hiPSCs from young and healthy people and that these are capable of transforming into heart cells. However, it has not been shown that hiPSCs could be obtained from elderly and diseased patients. In addition, until now researchers have not been able to show that heart cells created from hiPSCs could integrate with existing heart tissue.
Professor Lior Gepstein, Professor of Medicine (Cardiology) and Physiology at the Sohnis Research Laboratory for Cardiac Electrophysiology and Regenerative Medicine, Technion-Israel Institute of Technology and Rambam Medical Center in Haifa, Israel, who led the research, said: “What is new and exciting about our research is that we have shown that it’s possible to take skin cells from an elderly patient with advanced heart failure and end up with his own beating cells in a laboratory dish that are healthy and young — the equivalent to the stage of his heart cells when he was just born.”
Ms Limor Zwi-Dantsis, who is a PhD student in the Sohnis Research Laboratory, Prof Gepstein and their colleagues took skin cells from two male heart failure patients (aged 51 and 61) and reprogrammed them by delivering three genes or “transcription factors” (Sox2, Klf4 and Oct4), followed by a small molecule called valproic acid, to the cell nucleus. Crucially, this reprogramming cocktail did not include a transcription factor called c-Myc, which has been used for creating stem cells but which is a known cancer-causing gene.
“One of the obstacles to using hiPSCs clinically in humans is the potential for the cells to develop out of control and become tumours,” explained Prof Gepstein. “This potential risk may stem from several reasons, including the oncogenic factor c-Myc, and the random integration into the cell’s DNA of the virus that is used to carry the transcription factors — a process known as insertional oncogenesis.”
The researchers also used an alternative strategy that involved a virus that delivered reprogramming information to the cell nucleus but which was capable of being removed afterwards so as to avoid insertional oncogenesis.
The resulting hiPSCs were able to differentiate to become heart muscle cells (cardiomyocytes) just as effectively as hiPSCs that had been developed from healthy, young volunteers who acted as controls for this study. Then the researchers were able to make the cardiomyocytes develop into heart muscle tissue, which they cultured together with pre-existing cardiac tissue. Within 24-48 hours the tissues were beating together. “The tissue was behaving like a tiny microscopic cardiac tissue composed of approximately 1000 cells in each beating area,” said Prof Gepstein.
Finally, the new tissue was transplanted into healthy rat hearts and the researchers found that the grafted tissue started to establish connections with the cells in the host tissue.
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Limits to growth: Scientists identify key metastasis-enabling enzyme
On the complex road to eradicating cancer, controlling or preventing metastatic growth initiated by primary tumors is high on the to-do list. A key area of such research is the development of therapies based on identifying markers of metastasis associated with altered choline metabolism in breast, ovarian, and prostate cancers. Recently, scientists at the Leibniz Research Centre for Working Environment and Human Factors (IfADO), University of Dortmund, Germany, studying the tumor metabolome – the characteristic metabolic phenotype of tumor cells fundamental to the tumor’s metastatic capacity – identified EDI3 (endometrial differential 3) as the enzyme responsible for a decreased glycerophosphocholine (GPC) to phosphocholine (PC) ratio by cleaving GPC to produce choline. The scientists concluded that since inhibiting EDI3 activity corrects the GPC/PC ratio and thereby decreases tumor cell migration capacity, it represents a possible therapeutic modality.
Not surprisingly, Dr. Jan G. Hengstler and his team – Dr. Joanna D. Stewart, Dr. Rosemarie Marchan, Dr. Michaela S. Lesjak, and other researchers – had to deal with a number of challenges in identifying EDI3 as the critical enzyme in glycerophosphocholine cleaving. “The story started,” recalls Hengstler, “when we scraped out a band from a silver gel. This band contained a gene expressed in metastasizing, but not non-metastasizing endometrial carcinomas. Nothing was known about the function of this gene, which we named EDI3 because its precursors EDI1 and EDI2 were not confirmed in independent clinical samples, and therefore not further studied.” In fact, at that point EDI3 was not yet included on the Affymetrix genomic analysis chip, which may explain why EDI3 was completely unexplored.
“Some initial attempts to understand EDI3’s function and relevance failed,” Hengstler tells Medical Xpress. “At this time the small EDI3-project was almost dead. Fortunately, persistence and some brilliant ideas from two post docs and a PhD student - Rosemarie Marchan, Joanna Stewart and Michaela Lesjak – gave the project new life. By some clever in silico studies, they came up with a small number of hypotheses on the mode of action of EDI3 – and one of them could indeed be experimentally confirmed.” EDI3 cleaves glycerophosphocholine to release choline and glycerol-3-phosphate – an important metabolic step, because choline metabolism not only provides membrane phospholipids essential for neoplastic cells, but is essential for the activation of a number of signaling proteins. “This reaction, also known as Kennedy-pathway, was already in the textbooks, Hengstler adds, “and some components of the choline metabolism were even being explored as possible targets in cancer. However, a key enzymatic protein positioned at the start of this pathway remained unidentified.”
As soon as the enzymatic mechanism was clear, the project progressed rapidly. “Through what I’d consider amazing teamwork,” says Hengstler, “Marchan, Stewart and Lesjak worked together to establish methods that allowed them to manipulate EDI3’s levels, while at the same time developing the reagents and methods needed to measure EDI3.” The latter included the development of an EDI3 antibody and an enzymatic assay to measure EDI3’s activity. “From this we learned that EDI3 has a tremendous influence on lipid patterns, particularly both lysophosphatidic acid and phosphatidic acid. Things got even more exciting when it became clear that phosphatidic acid creates membrane anchoring points for proteins that activate many intracellular signaling pathways, many that are altered in cancer. In addition, phosphatidic acid is a direct precursor to another important signaling lipid – diacylglycerol, which directly activates protein kinase C (PKC).” Activated PKC increases migration activity of several tumor cell lines, and increased migration contributes to the high metastatic capacity observed in EDI3 overexpressing carcinomas.
Hubble captures first pictures of auroras on Uranus
NASA’s Hubble space telescope has captured the first images of auroras on the ice giant Uranus.
Uranus, the seventh planet from the sun, is an oddball world. At some point in its past, the planet appears to have been knocked on its side, so now its “North Pole” sits where the equator on most planets is located.
The newly observed auroras — seen as tiny white dots in the image above — underscore just how strange Uranus really is.
Auroras, also known as the Northern Lights, appear on Earth when the solar wind – a stream of charged particles emanating from the sun — interacts with our planet’s magnetic field. While terrestrial auroras appear as giant green curtains of light and may last hours, the auroras seen recently on Uranus were relatively small and stuck around only a few minutes.
Scientists don’t know much about Uranus’ magnetic field because it has only been investigated in detail once, 25 years ago when the Voyager 2 satellite zoomed by. At that time, Voyager detected auroras but Earth-based attempts to reexamine the atmospheric phenomenon on Uranus have all failed since.
A new image of Messier 55 from ESO’s VISTA infrared survey telescope shows tens of thousands of stars crowded together like a swarm of bees. Besides being packed into a relatively small space, these stars are also among the oldest in the Universe. Astronomers study Messier 55 and other ancient objects like it, called globular clusters, to learn how galaxies evolve and stars age.
Globular clusters are held together in a tight spherical shape by gravity. In Messier 55, the stars certainly do keep close company: approximately one hundred thousand stars are packed within a sphere with a diameter of only about 25 times the distance between the Sun and the nearest star system, Alpha Centauri.
About 160 globular clusters have been spotted encircling our galaxy, the Milky Way, mostly toward its bulging centre. The two latest discoveries, made using VISTA, were recently announced. The largest galaxies can have thousands of these rich collections of stars in orbit around them.
Observations of globular clusters’ stars reveal that they originated around the same time — more than 10 billion years ago — and from the same cloud of gas. As this formative period was just a few billion years after the Big Bang, nearly all of the gas on hand was the simplest, lightest and most common in the cosmos: hydrogen, along with some helium and much smaller amounts of heavier chemical elements such as oxygen and nitrogen.
Being made mostly from hydrogen distinguishes globular cluster residents from stars born in later eras, like our Sun, that are infused with heavier elements created in earlier generations of stars. The Sun lit up some 4.6 billion years ago, making it only about half as old as the elderly stars in most globular clusters. The chemical makeup of the cloud from which the Sun formed is reflected in the abundances of elements found throughout the Solar System — in asteroids, in the planets and in our own bodies.
Sky watchers can find Messier 55 in the constellation of Sagittarius (The Archer). The notably large cluster appears nearly two-thirds the width of the full Moon, and is not at all difficult to see in a small telescope, even though it is located at a distance of about 17 000 light-years from Earth.
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