neutrinos nobel prize

Neutrinos and the Nobel Prize

Neutrino experiments are difficult and often ground-breaking. In (sometimes long-delayed) recognition of this, a number of pioneers of neutrino physics have been awarded the Nobel Prize for Physics.

1988	Leon Lederman, Melvin Schwartz, Jack Steinberger	for the neutrino beam method and the demonstration of the doublet structure of the leptons through the discovery of the muon neutrino
1995	Frederick Reines	for the detection of the neutrino
2002	Raymond Davis and Masatoshi Koshiba	for pioneering contributions to astrophysics, in particular for the detection of cosmic neutrinos

In addition, Wolfgang Pauli (1945), Enrico Fermi (1938), and Lee and Yang (1957), who made major contributions to neutrino theory, won the Nobel Prize for work not directly connected with neutrinos. Clyde Cowan did not share in the belated prize for the discovery of the neutrino because Nobel prizes are not awarded posthumously.

The Nobel Prize in Physics 2015

The Nobel Prize in Physics 2015

The Nobel Prize in Physics 2015 was awarded jointly to Takaaki Kajita and Arthur B. McDonald "for the discovery of neutrino oscillations, which shows that neutrinos have mass"

Photo © Takaaki Kajita

Takaaki Kajita

Prize share: 1/2

Photo: K. MacFarlane. Queen's University /SNOLAB

Arthur B. McDonald

Prize share: 1/2

Our own genes can block HIV

                              Our own genes can block HIV

       Two groups of researchers at the University of Massachusetts Medical School say a powerful weapon against the AIDS virus may exist in the unlikeliest of places — in our own genes.

The studies, published online yesterday in the journal Nature, found that two genes can block HIV from spreading to other cells, which researchers in the HIV/AIDS field say could open the door to promising new treatments and could even pave the way for a cure.

Two groups of UMass Medical researchers used different methods in each study, but came to the same conclusion: the SERINC5 and SERINC3 genes can shut down the virus, stopping its spread and rendering it inactive.

But a component of the virus — the protein Nef — counteracts the SERINCs inhibiting powers, which is why those genes don’t prevent people from contracting the virus.

The finding, though, could very well lead to treatments that weaken the damaging protein and allow the virus-fighting genes to fend off illness, researchers say.

“Nef is a gene that HIV evolved largely to overcome this anti-viral factor that our cells make,” said Dr. Jeremy Luban, professor of molecular medicine at UMass Medical, an investigator in one of the studies.

“The hope is that there will be 
a way to intervene, perhaps by developing a new drug that 
allows the SERINCs to escape from Nef,” Luban said.

Ideally, the discoveries will lead to the development of treatments in the next five years, though it 
is difficult to estimate, Luban said.

The research, funded primarily by the National Institutes of Health, was done in collaboration with scientists at the Univer-
sity of Trento in Italy and the University of Geneva in Switzerland.

The discovery coincides with new HIV guidelines issued yesterday by the World Health Organization, increasing the number of those infected or at risk who should seek virus-inhibiting therapy by 9 million.

“Advancing science is a critical part of what needs to happen,” said Dr. Carlos Del Rio, chairman-elect of the HIV Medicine Association.

“Gene therapy advances for HIV are very exciting. They could lead to treatments that can cure HIV,” Del Rio said.

Though there are more than 30 of these therapies available, they can cause a range of side effects, from skin rashes and nightmares to weakened bones and cardiovascular disease, according to 
Dr. Daniel Kuritzkes, chief of 
Infectious Diseases at Brigham and Women’s Hospital.

“Not everyone tolerates the currently available regimen equally well,” Kuritzkes said.

“We still need to keep looking for new and improved treatments.”

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Cell Division and Cancer

Cancer cells are cells gone wrong — in other words, they no longer respond to many of the signals that control cellular growth and death. Cancer cells originate within tissues and, as they grow and divide, they diverge ever further from normalcy. Over time, these cells become increasingly resistant to the controls that maintain normal tissue — and as a result, they divide more rapidly than their progenitors and become less dependent on signals from other cells. Cancer cells even evade programmed cell death, despite the fact that their multiple abnormalities would normally make them prime targets for apoptosis. In the late stages of cancer, cells break through normal tissue boundaries and metastasize (spread) to new sites in the body.

How Do Cancer Cells Differ from Normal Cells?

In normal cells, hundreds of genes intricately control the process of cell division. Normal growth requires a balance between the activity of those genes that promote cell proliferation and those that suppress it. It also relies on the activities of genes that signal when damaged cells should undergo apoptosis.

Cells become cancerous after mutations accumulate in the various genes that control cell proliferation. According to research findings from the Cancer Genome Project, most cancer cells possess 60 or more mutations. The challenge for medical researchers is to identify which of these mutations are responsible for particular kinds of cancer. This process is akin to searching for the proverbial needle in a haystack, because many of the mutations present in these cells have little to nothing to do with cancer growth.

Different kinds of cancers have different mutational signatures. However, scientific comparison of multiple tumor types has revealed that certain genes are mutated in cancer cells more often than others. For instance, growth-promoting genes, such as the gene for the signaling protein Ras, are among those most commonly mutated in cancer cells, becoming super-active and producing cells that are too strongly stimulated by growth receptors. Some chemotherapy drugs work to counteract these mutations by blocking the action of growth-signaling proteins. The breast cancer drug Herceptin, for example, blocks overactive receptor tyrosine kinases (RTKs), and the drug Gleevec blocks a mutant signaling kinase associated with chronic myelogenous leukemia.

Other cancer-related mutations inactivate the genes that suppress cell proliferation or those that signal the need for apoptosis. These genes, known as tumor suppressor genes, normally function like brakes on proliferation, and both copies within a cell must be mutated in order for uncontrolled division to occur. For example, many cancer cells carry two mutant copies of the gene that codes for p53, a multifunctional protein that normally senses DNA damage and acts as a transcription factor for checkpoint control genes.

New Graphene __ Black Phosphorus

NEW GRAPHENE

Atoms-thin flakes of phosphorus have a crucial property that graphene lacks

Chemists first synthesized black phosphorus over a hundred years ago. But it was only last year when anybody really took interest in the flaky black stuff. In a series of experiments reported in the first half of 2014, researchers were able to exfoliate black phosphorus into very thin films of only about 10 to 20 atoms thick. Now black phosphorus has become the new darling of two-dimensional materials research and a new hope for a postsilicon world.

The excitement around black phosphorus, which is also called phosphorene in reference to its 2-D cousin graphene, stems mainly from the fact that it has an inherent bandgap, something that graphene lacks. A bandgap, an energy band in which no electron states can exist, is essential for creating the on/off flow of electrons that are needed in digital logic and for the generation of photons for LEDs and lasers.

Black phosphorus doesn’t just have any bandgap. Its bandgap can be fine-tuned by adjusting the number of layers of the material, explains Philip Feng, an assistant professor of electrical engineering and computer science at Case Western Reserve University.

The bandgap can be dialed up from 0.3 to 2.0 electron volts. That’s a range covering a regime otherwise unavailable to all other recently discovered 2-D materials. It bridges the bandgaps of graphene (0 eV) and of transition-metal dichalcogenides such as molybdenum disulfide, which range from 1.0 to 2.5 eV.

By combining this bandgap tuning with different choices of contact materials, scientists at Sungkyunkwan University, in South Korea, were recently able to build both n-type transistors—those conducting electrons—and ambipolar transistors, which conduct both holes and electrons. Such a mix brings the material closer to mimicking the complementary logic used in today’s silicon chips.

Scientists are also excited about black phosphorus for photonics, “since optoelectronic functions, including light absorption, emission, and modulation, of semiconductor materials depend on the size of the bandgap,” says Mo Li, a photonics expert at the University of Minnesota. Black phosphorus’s bandgap range means it can absorb and emit light with wavelengths of 0.6 to 4.0 micrometers—covering the visible to infrared. That spectrum could be key to its use in sensors and in optical.

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Graphene Keeping It Cool In Electronics

By Dexter Johnson

Cooling fans and other system-level solutions are reaching their limits as circuit densities continue to grow. It’s no wonder then that graphene’s remarkable heat conductivity has led to a lot of research into using it to forthermal management in electronics.

Now an international team of researchers, organized by a team at the University of Michigan, has found that layered graphene can be an important tool for thermal management because of its ability to release heat efficiently.

In research published in the journal Nature Communications, the scientists demonstrated that the electrostatic interactions between electrically charged particles—known as Coulomb interactions—in  different layers of multi-layered graphene offers a key mechanism for dispersing heat. This occurs despite the fact that all electronic states are strongly confined within individual 2D layers.

“We believe that this cooling mechanism is not limited to multilayer graphene samples but is likely to be important in many other new, layered nanomaterials under active development by the scientific community,” said Theodore Norris, who led the research, in a press release.

This mechanism came as a bit of surprise to the researchers. They did not expect the heat building up in the electrons of the graphene to travel well through the layers because previous observations had shown that the graphene layers interact too strongly for this to occur. This stood in contrast to 3D pieces of silicon that are capable of conducting heat in any direction.

Momchil Mihnev, a doctoral student at the University of Michigan and first author on the paper, explained in the press release that while the electrons in the different layers can’t mechanically come in contact with each other, they do manage to interact with each other through their electrical charges.

When the negative charges repel each other, the electrons take on an effective size that extends between the layers. When the electrons come in contact with each other in this way, the hotter electrons transfer heat to the colder ones. This transfer of heat eventually channels down through the graphene towards the layer that is closest to the silicon carbide substrate the researchers used in these experiments. Once it gets to the final layer of graphene, the heat transfers into the silicon carbide.

The researchers have developed a detailed theory on why and how this mechanism works, and it could provide an important tool in keeping electronics cool well into the future.

cancer cell growth

Bacterial Sepsis Protein May Inhibit Cancer Cell Growth

A toxin secreted by Vibrio vulnificus, a water and food-borne bacteria that can cause rapidly lethal infections in persons with liver disease, has potential to prevent the growth of tumors, according to a new study by Northwestern Medicine scientists.

Karla Satchell, a professor in microbiology-immunology at Northwestern University Feinberg School of Medicine, and her team demonstrated in a paper in Nature Communications, that a multifunctional-autoprocessing repeats-in-toxin (MARTX) protein from Vibrio vulnificus can inhibit tumor cell growth by cutting the protein Ras. This protein is central to cell division and survival, and mutations in the gene that codes for Ras are a common cause of human malignancies.

"Ras is important for cell proliferation in cancer, so the toxin could potentially be developed as a treatment for different types of tumors," Satchell says. 'It has been known that Ras has a role in cancer development and targeting Ras has been one of the hardest challenges of cancer research and drug discovery.'

Ras also plays a role in detecting pathogens and activating an immune response. The bacterium uses the MARTX toxin protein to inactivate Ras, increasing its own virulence and allowing it to spread throughout the host.

They used cell biological, genetic and biochemical techniques to show how a specific part of the toxin, an effector domain called DUF5Vv, targets and cleaves Ras. Satchell's team also revealed the ability of this domain to slice both normal and mutant forms of Ras commonly found in cancers.

"What is unique about this study is the ability of the toxin to cleave Ras, rather than modify it, which is a novel mechanism for inactivating Ras," Satchell says.

The scientists plan to continue to study the mechanisms and biochemistry of the MARTX toxin specificity to the Ras protein.

The research was funded by National Institutes of Health grants R01AI051490, R01AI092825, R01AI098369, R01CA152601, R01CA152799, R01CA168292 and a Northwestern University Avon Center of Excellence grant and by the Northwestern Medicine Catalyst Fund.

Source: Northwestern University

http://www.infectioncontroltoday.com/news/2015/06/bacterial-sepsis-protein-may-inhibit-cancer-cell-growth.aspx

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