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Back in August 2014, researchers at Michigan State University created a fully transparent solar concentrator, which could turn any window or sheet of glass (like your smartphone’s screen) into a photovoltaic solar cell. Unlike other “transparent” solar cells that we’ve reported on in the past, this one really is transparent, as you can see in the photos throughout this story. According to Richard Lunt, who led the research at the time, the team was confident the transparent solar panels can be efficiently deployed in a wide range of settings, from “tall buildings with lots of windows or any kind of mobile device that demands high aesthetic quality like a phone or e-reader.”

Now Ubiquitous Energy, an MIT startup we first reported on in 2013, is getting closer to bringing its transparent solar panels to market. Lunt cofounded the company and remains assistant professor of chemical engineering and materials science at Michigan State University. Essentially, what they’re doing is instead of shrinking the components, they’re changing the way the cell absorbs light. The cell selectively harvests the part of the solar spectrum we can’t see with our eye, while letting regular visible light pass through.

Scientifically, a transparent solar panel is something of an oxymoron. Solar cells, specifically the photovoltaic kind, make energy by absorbing photons (sunlight) and converting them into electrons (electricity). If a material is transparent, however, by definition it means that all of the light passes through the medium to strike the back of your eye. This is why previous transparent solar cells have actually only been partially transparent — and, to add insult to injury, they usually they cast a colorful shadow too.

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March 28 (UPI) — Researchers at Northwestern University created a synthetic version of the female reproductive system that can be used to test drug therapies.

The system is shaped like a cube and consists of a series of small tubes, each containing cells from a different part of the female reproductive system, including the uterus, cervix, vagina, fallopian tubes and liver.

The system is called Evatar, like avatar but with an E for Eve, because it reproduces the female reproductive tract and mimics the hormones of the full-size reproductive system.

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LIMA, Peru (AP) — If human beings finally reach Mars, they may find themselves depending on the humble, if hardy potato.

Scientists in Peru have used a simulator that mimics the harsh conditions on the Red Planet to successfully grow a small potato plant.

It’s an experiment straight out of the 2015 Hollywood movie “The Martian” that scientists say may also benefit arid regions already feeling the impact of climate change.

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Mushroom buildings, jurassic park and terraforming.

Did you ever hear about synthetic biology? No? Imagine that we could alter and produce DNA from scratch just like an engineer. Doesn’t it sound like one of the greatest interdisciplinary achievements in recent history?

Think about it, a bio-technologist is doing more or less the work of a programmer but instead of using a computer language he’s doing it by arranging molecules embedded in every living cell. The outcome, if ever mastered, could reshape the world around us dramatically.

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A look at Rapamycin the life extending drug with some serious drawbacks.


If any drug has performed consistently and unequivocally well in anti-aging trials, it’s rapamycin. Dr. Matt Kaeberlein’s Dog Aging Project is among the most recent trials investigating its longevity-promoting potential in mammals, but it’s also been the subject of numerous trials in mice, worms, flies and yeast. And although it acts through a mechanism which has been most closely associated cancer prevention, this drug appears to stave off all maladies related to aging.

Even more encouraging are the indications that it could be beneficial well into old age. Trials done in the National Aging Institute’s ITP, a testing protocol that collects its data from three independent labs, found that when mice started rapamycin treatment at 600 days old (roughly 60 in human years), they lived an average of 11% longer than control counterparts. Longevity interventions that hold up well even in late-life are few and far between, and even the traditionally successful method of caloric restriction has limited utility when begun late.

Coincidentally, some think that caloric restriction works via the same pathway as rapamycin: by inhibiting the enzyme mTOR. Among its numerous functions, mTOR helps to drive cell growth and proliferation. Halting out of control cell division is key to cancer prevention, and so it’s not too surprising that rapamycin treatment counters development of certain types of tumors by inhibiting mTOR. It can have detrimental effects on nutrient sensing, the factor behind metabolic diseases like diabetes, by promoting activation of insulin receptors. And since mTOR is responsible for increasing energy consumption and cellular metabolism, it can also produce oxidative stress by way of the free radicals created by overactive mitochondria.

Advanced capabilities in electrical recording are essential for the treatment of heart-rhythm diseases. The most advanced technologies use flexible integrated electronics; however, the penetration of biological fluids into the underlying electronics and any ensuing electrochemical reactions pose significant safety risks. Here, we show that an ultrathin, leakage-free, biocompatible dielectric layer can completely seal an underlying array of flexible electronics while allowing for electrophysiological measurements through capacitive coupling between tissue and the electronics, without the need for direct metal contact. The resulting current-leakage levels and operational lifetimes are, respectively, four orders of magnitude smaller and between two and three orders of magnitude longer than those of other flexible-electronics technologies. Systematic electro­physiological studies with normal, paced and arrhythmic conditions in Langendorff hearts highlight the capabilities of the capacitive-coupling approach. These advances provide realistic pathways towards the broad applicability of biocompatible, flexible electronic implants.

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A review of senescent cell removal therapies.


Aging at the cellular level is called “cell senescence”, and it contributes profoundly to whole-body aging. The most promising near-term prospects for a leap in human life expectancy come from drugs that eliminate senescent cells. Programs in universities and pharmaceutical labs around the world are racing to develop “senolytic” drugs, defined as agents that can kill senescent cells with minimal harm to normal cells.

Apoptosis is cell suicide, and (from the perspective of the full organism) it’s the best thing that can happen to senescent cells. The authors of this newest Dutch study ask how it is that senescent cells escape apoptosis.

FOXO is a protein that controls gene expression, a master transcription factor associated with aging and development. (It is the homolog in mammals of the pivotal life extension protein first identified in worms as DAF16 in the 1990s.) FOXO4 activiation in a cell can block apoptosis. P53 is the most common trigger of apoptosis, the first protein biochemists usually think of in connection with apoptosis. P53 has multiple functions in the cell nucleus, but as a trigger for apoptosis, it works through the mitochondria. FOXO4 binds to p53 and blocks its induction of apoptosis.