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Not sure that I would claim 2016 as the year that AI exploded; I believe a better term for 2016 is the year that AI reinvented itself. I still see us in an evolution trend in 2017 as we still need to see more AI technology embedded in our back office platforms and apps than where we are today to claim we’re in a real AI explosion. Once we start seeing more IT organizations and CxOs embracing it in lowering their operational costs then we can claim we’re in an explosion.


Artificial intelligence isn’t a new concept. It is something that companies and businesses have been trying to implement (and something that society has feared) for decades. However, with all the recent advancements to democratize artificial intelligence and use it for good, almost every company started to turn to this technology and technique in 2016.

The year started with Facebook’s CEO Mark Zuckerberg announcing his plan to build an artificially intelligent assistant to do everything from adjusting the temperature in his house to checking up on his baby girl. He worked throughout the year to bring his plan to life, with an update in August that stated he was almost ready to show off his AI to the world.

In November, Facebook announced it was beginning to focus on giving computers the ability to think, learn, plan and reason like humans. In order to change the negative stigma people associate with AI, the company ended its year with the release of AI educational videos designed to make the technology easier to understand.

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Since their development in 1960, lasers have become an indispensable tool supporting our modern society, finding use in fields such as medicine, information, and industry. Thanks to their compact size and energy efficiency, semiconductor lasers are now one of the most important classes of laser, making possible a diverse range of applications. However, the threshold current of a typical semiconductor laser—the minimum electrical current required to induce lasing—increases with temperature. This is one of a number of disadvantages that can be overcome by using quantum dot lasers. Professor Yasuhiko Arakawa of the Institute of Industrial Science at the University of Tokyo has been researching quantum dot lasers for about 35 years, from their conception to commercialization.

An electron trapped in a microscopic box

Sunlight is composed of light of various colors. The property that determines the color of light is its wavelength, or in other words, the distance between two successive wave peaks or troughs. The location of the peaks and troughs in the waveform is known as its phase. As a laser emits light waves in a uniform phase at the same wavelength, the light can be transmitted as a beam over long distances at high intensity.

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What’s next? Nanocavities in a diamond for small devices.


Researchers have developed a new type of light-enhancing optical cavity that is only 200 nanometers tall and 100 nanometers across. Their new nanoscale system represents a step toward brighter single-photon sources, which could help propel quantum-based encryption techniques under development.

Quantum encryption techniques, which are seen as likely to be central to future data encryption methods, use individual photons as an extremely secure way to encode data. A limitation of these techniques has been the ability to emit photons at high rates. “One of the most important figures of merit for single-photon sources is brightness — or collected photons per second — because the brighter it is, the more data you can transmit securely with quantum encryption,” said Yousif Kelaita of Stanford University.

In the journal Optical Materials Express, from The Optical Society (OSA), Kelaita and his colleagues show that their new nanocavity significantly increased the emission brightness of quantum dots — nanometer-scale semiconductor particles that can emit single photons.

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Caloric restriction can help tumour supression.


Tumor suppressors stop healthy cells from becoming cancerous. Researchers from Charité — Universitätsmedizin Berlin, the Medical University of Graz and the German Institute of Human Nutrition in Potsdam-Rehbruecke have found that p53, one of the most important tumor suppressors, accumulates in liver after food withdrawal. They also show that p53 in liver plays a crucial role in the body’s metabolic adaptation to starvation. These findings may provide the foundation for the development of new treatment options for patients with metabolic or oncologic disorders. Results of this study have been published in The FASEB Journal.

Previously described as the ‘guardian of the genome’ and voted ‘Molecule of the Year’ in 1993, p53 is one of the most important proteins regulating cell growth and a major focus for oncology research. It is a protein that has the ability to interrupt the cell cycle and block the division of diseased cells. In order to better understand its physiological regulation, the researchers around Prof. Dr. Michael Schupp from Charité’s Institute of Pharmacology studied the regulation and function of p53 in normal, . After withholding food from mice for several hours, the researchers were able to show that p53 protein accumulates in the liver. In order to determine which type of cause this accumulation, the researchers repeated the experiment using cultured hepatocytes. They found that the starvation-induced accumulation of p53 was indeed detectable in hepatocytes, irrespective of whether these cells were of mouse or human origin.

“Our data also suggest that the accumulation of p53 is mediated by a cellular energy sensor, and that it is crucial for the metabolic changes associated with starvation,” explains Prof. Michael Schupp. The researchers were able to show that mice with an acute inactivation of the p53 gene in liver had difficulties in adapting their metabolisms to starvation. “Food intake seems crucial in determining the protein levels of p53 in liver, and p53 also plays an important role in normal liver metabolism,” says Prof. Schupp. The researchers are planning to study whether their observations are limited to liver cells, or whether this p53 accumulation also occurs in other tissues and organs. Prof.

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Scientists are hailing a pioneering stem cell technique that promises “off-the-shelf” treatment for people with damaged muscles without the existing risks.

Researchers have for the first time successfully implanted “synthetic” cardiac stem cells which successfully repaired muscle tissue that had been weakened by a heart attack.

Traditional stem cell therapy comes with a risk of cancer because scientists are unable to stop the cells replicating and forming tumours.

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This thing was not imagination,” he says, jabbing his index finger into the tablecloth. By Cuarón’s estimation, anyone surprised at the accuracy of his movie’s predictions was either uninformed or willfully ignorant about the way the world already was by 2006.’


Revisiting the overlooked 2006 masterpiece with director Alfonso Cuarón.

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Time to work off that Chritmas Turkey bigsmile


Making muscles burn more fat and less glucose can increase exercise endurance, but could simultaneously cause diabetes, says a team of scientists from Baylor College of Medicine and other institutions.

Mouse muscles use (carbohydrate) as fuel when the animals are awake and active and switch to fat (lipid) when they are asleep. The team discovered that disrupting this natural cycle may lead to diabetes but, surprisingly, can also enhance exercise endurance. The switch is controlled by a molecule called histone deacetylase 3, or HDAC3. This finding opens the possibility of selecting the right time to exercise for losing body fat but also raises the concern of using HDAC inhibitors as doping drugs for endurance exercise. The study appears in Nature Medicine.

“How the uses glucose is regulated by its internal that anticipates the level of its activity during the day and at night,” said senior author Dr. Zheng Sun, assistant professor of medicine—diabetes, endocrinology and metabolism, and of molecular and cellular biology at Baylor. “The circadian clock works by turning certain genes on and off as the 24-hour cycle progresses. HDAC3 is a key connection between the circadian clock and gene expression. Our previous work showed that HDAC3 helps the liver alternate between producing glucose and producing lipid. In this work, we studied how HDAC3 controls the use of different fuels in .”

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