U.W. EXPERTS SHARES LATEST SCIENCE ON MARIJUANA AND YOUTH

What's up with our kids and marijuana?  Lots of users look to minimize the known risks with a shrug and an attitude that says, after all it's not fentanyl, it's just weed    Well, here's a chance to find out what science says..

An informational session titled  Beyond “It’s Just Weed”  will be presented by Dr. Jason Kilmer this Friday May 10th from 7:30am to 9:30 at ESD 105 in Yakima.  Dr. Kilmer is an associate professor in psychiatry and behavioral sciences at the University of Washington.

Up for discussion is the evidence-based science behind marijuana and how it affects our community’s youth.

Health Officer Teresa Everson notes that research has shown that people are more likely to develop addictions if they start using drugs at a young age with some research showing one out of every six people who start using marijuana before age 18 will develop a marijuana use disorder such as problems with problem-solving skills, attention and memory.

This event is free and available to all ages Friday May 10th, 2019 from 7:30am to 9:30 am at the Educational School District 105: 111 S. 2nd Ave, Yakima, WA 98902.

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Synthetic biology used to target cancer cells while sparing healthy tissue

Synthetic proteins engineered to recognize overly active biological pathways can kill cancer cells while sparing their healthy peers, according to a new study.

Synthetic proteins engineered to recognize overly active biological pathways can kill cancer cells while sparing their healthy peers, according to a study by researchers at the Stanford University School of Medicine.

The customizable approach, which the researchers call RASER, relies on just two proteins: The first is activated in the presence of an "always on" growth signal often found in cancer cells, and the second carries out a researcher-programmed response, such as triggering the expression of genes involved in cell death.

Although the experiments were confined to cells grown in the laboratory, the researchers believe the results could lead to a new type of cancer therapy in which synthetic proteins deliver highly targeted and customizable treatments to sidestep the sometimes devastating side effects of current options.

"We're effectively rewiring the cancer cells to bring about an outcome of our choosing," said Michael Lin, MD, PhD, associate professor of neurobiology and of bioengineering. "We've always searched for a way to kill cancer cells but not normal cells. Cancer cells arise from faulty signals that allow them to grow inappropriately, so we've hacked into cancer cells to redirect these faulty signals to something useful."

A paper describing the work will be published May 2 in Science. Lin is the senior author. Former graduate student Hokyung Chung, PhD, is the lead author.

Signals from receptors

Many cancers rely on a series of signals that originate from proteins called receptors that span the membrane of the cell. These signaling cascades, or pathways, are used by healthy cells to grow in response to external cues, for example during development or recovery from injury. Often, however, these receptor proteins are mutated or overexpressed in cancer cells in ways that render the receptor protein "always on," providing the cell with constant, unwarranted signals for growth. The researchers focused on two receptors, EGFR and HER2 -- members of a family of receptors called the ErbB receptors -- that often drive the growth of brain, lung and breast cancers. HER2, for example, is targeted by Herceptin in breast cancer.

Many common anti-cancer drugs, including Herceptin, work by blocking the cascade of signals triggered by receptor activation. Unfortunately, however, these drugs have no way to discriminate between cancerous cells, in which the pathway is always activated, and healthy cells going about their business as usual. That's where Lin and his team come in.

"We haven't had a drug that can tell the difference between a pathway signaling normally and one that is abnormally active," Lin said. "We knew we needed a better strategy, a more rational way of treating cancer. But we've not had a way to do it until recently."

Designing a synthetic protein

Chung and her colleagues designed a synthetic protein consisting of two natural proteins fused together -- one that binds to active ErbB receptors and another that cleaves a specific amino acid sequence. They then engineered a second protein that binds to the inner surface of the cell membrane and contains a customizable "cargo" sequence that can carry out specific actions in the cell. When the first protein binds to an active ErbB receptor, it cuts the second protein and releases the cargo into the interior of the cell.

"When the receptor protein is always on, as it is in cancer cells, the released cargo protein accumulates over time," Chung said. "Eventually enough accumulates to have an effect on the cell. In this way, the system produces an effect only in cancer cells, and we can convert the always-on state of the receptor into different outcomes through the choice of cargo protein."

After several rounds of tinkering, the team saw that their RASER system, which stands for "rewiring of aberrant signaling to effector release," was highly specific for cancer cells dependent on ErbB receptor activity. For their first test they chose to use a protein involved in triggering cell death as the RASER cargo.

Killing only overactive cells

The team compared the RASER system to two therapies currently used for metastatic breast cancer -- a chemotherapy regimen and a drug that blocks ErbB activity -- on several types of cultured cells: breast and lung cancer cells in which the ErbB pathway was overly active; breast cancer cells in which ErbB activity was normal; and noncancerous breast and lung cell lines.

The researchers found that the traditional chemotherapy regimen of carboplatin and paclitaxel killed all the cells indiscriminately. The effect of the ErbB pathway inhibitor on the viability of the cells varied and did not reliably correlate with ErbB pathway activity levels. Only RASER specifically killed those cells in which the ErbB pathway was overly active while sparing those in which ErbB activity was normal.

While much work remains to be done to learn whether RASER is effective in human tumors, the researchers are excited about the possibilities of re-engineering the system to recognize other receptors mutated in cancers and swapping the cargos to achieve different outcomes. Challenges include learning how best to deliver synthetic proteins into tumors and understanding how the immune system might react to RASER. But Lin is optimistic.

"We have so much more information now about cancer genomics, signaling and how cancer cells interact with the immune system," Lin said. "It's finally becoming practical to combine this knowledge with synthetic biology approaches to tackle some of these pressing human health problems. RASER is both customizable and generalizable, and it allows us for the first time to selectively target cancer cells while sparing normal signaling pathways."

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EFCC explains latest probe on Saraki

Nigeria’s anti-graft agency Economic and Financial Crimes Commission (EFCC) Monday said the current probe on Nigeria Senate president Bukola Saraki was not in connection to his recent appointment as International Human Rights Commission (IHRC) ambassador.

“For the avoidance of doubt, the investigation into the Senate President’s activities while he held sway as the governor of Kwara State started long before his nomination and emergence as IHRC ambassador,” EFCC said in a statement.

Some Nigerian media outfits had last week reported that the EFCC launched a fresh probe to Saraki, who was former Kwara State governor, days after his appointment.

However, the EFCC said the reports were false as the probe on Saraki’s earnings while he was governor between 2003 to 2011 predate his appointment.

The anti-graft agency urged members of the public to disregard the false connect the writer sought to establish between Saraki’s IHRC ambassadorial appointment and inquiries into his earnings as a state governor.

EFCC added that it will not be distracted from any quarters in its efforts to rid the country of corruption and corrupt elements.

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Jamb Finally Fixed Examination Date

New Jamb 2019 Exam Date

The Jamb 2019 Examination was shifted from March 16th 2019 to April 11th 2019 and this is as result of the general election,

If you are among those students who has been asking for Jamb examination date 2019 the you can visit www.jamb.org.ng to find out now.

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Why we shouldn't like coffee, but we do

The more sensitive people are to the bitter taste of caffeine, the more coffee they drink, reports a new study. The sensitivity is based on genetics. Bitterness is natural warning system to protect us from harmful substances, so we really shouldn't like coffee. Scientists say people with heightened ability to detect coffee's bitterness learn to associate good things with it.

But, it turns out, the more sensitive people are to the bitter taste of caffeine, the more coffee they drink, reports a new study from Northwestern Medicine and QIMR Berghofer Medical Research Institute in Australia. The sensitivity is caused by a genetic variant.

"You'd expect that people who are particularly sensitive to the bitter taste of caffeine would drink less coffee," said Marilyn Cornelis, assistant professor of preventive medicine at Northwestern University Feinberg School of Medicine. "The opposite results of our study suggest coffee consumers acquire a taste or an ability to detect caffeine due to the learned positive reinforcement (i.e. stimulation) elicited by caffeine."

In other words, people who have a heightened ability to taste coffee's bitterness -- and particularly the distinct bitter flavor of caffeine -- learn to associate "good things with it," Cornelis said.

Thus, a bigger tab at Starbucks.

The study will be published Nov. 15 in Scientific Reports.

In this study population, people who were more sensitive to caffeine and were drinking a lot of coffee consumed low amounts of tea. But that could just be because they were too busy drinking coffee, Cornelis noted.

The study also found people sensitive to the bitter flavors of quinine and of PROP, a synthetic taste related to the compounds in cruciferous vegetables, avoided coffee. For alcohol, a higher sensitivity to the bitterness of PROP resulted in lower alcohol consumption, particularly of red wine.

"The findings suggest our perception of bitter tastes, informed by our genetics, contributes to the preference for coffee, tea and alcohol," Cornelis said.

For the study, scientists applied Mendelian randomization, a technique commonly used in disease epidemiology, to test the causal relationship between bitter taste and beverage consumption in more than 400,000 men and women in the United Kingdom. The genetic variants linked to caffeine, quinine and PROP perception were previously identified through genome-wide analysis of solution taste-ratings collected from Australian twins. These genetic variants were then tested for associations with self-reported consumption of coffee, tea and alcohol in the current study.

"Taste has been studied for a long time, but we don't know the full mechanics of it," Cornelis said. "Taste is one of the senses. We want to understand it from a biological standpoint."

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To predict the future, the brain uses two clocks

One type of anticipatory timing relies on memories from past experiences. The other on rhythm. Both are critical to our ability to navigate and enjoy the world, and scientists have found they are handled in two different parts of the brain.

That moment when you step on the gas pedal a split second before the light changes, or when you tap your toes even before the first piano note of Camila Cabello's "Havana" is struck. That's anticipatory timing.

One type relies on memories from past experiences. The other on rhythm. Both are critical to our ability to navigate and enjoy the world.

New University of California, Berkeley, research shows the neural networks supporting each of these timekeepers are split between two different parts of the brain, depending on the task at hand.

"Whether it's sports, music, speech or even allocating attention, our study suggests that timing is not a unified process, but that there are two distinct ways in which we make temporal predictions and these depend on different parts of the brain," said study lead author Assaf Breska, a postdoctoral researcher in neuroscience at UC Berkeley.

The findings, published online in the Proceedings of the National Academy of Sciences journal, offer a new perspective on how humans calculate when to make a move.

"Together, these brain systems allow us to not just exist in the moment, but to also actively anticipate the future," said study senior author Richard Ivry, a UC Berkeley neuroscientist.

Breska and Ivry studied the anticipatory timing strengths and deficits of people with Parkinson's disease and people with cerebellar degeneration.

They connected rhythmic timing to the basal ganglia, and interval timing -- an internal timer based largely on our memory of prior experiences -- to the cerebellum. Both are primal brain regions associated with movement and cognition.

Moreover, their results suggest that if one of these neural clocks is misfiring, the other could theoretically step in.

"Our study identifies not only the anticipatory contexts in which these neurological patients are impaired, but also the contexts in which they have no difficulty, suggesting we could modify their environments to make it easier for them to interact with the world in face of their symptoms," Breska said.

Non-pharmaceutical fixes for neurological timing deficits could include brain-training computer games and smartphone apps, deep brain stimulation and environmental design modifications, he said.

To arrive at their conclusion, Breska and Ivry compared how well Parkinson's and cerebellar degeneration patients used timing or "temporal" cues to focus their attention.

Both groups viewed sequences of red, white and green squares as they flashed by at varying speeds on a computer screen, and pushed a button the moment they saw the green square. The white squares alerted them that the green square was coming up.

In one sequence, the red, white and green squares followed a steady rhythm, and the cerebellar degeneration patients responded well to these rhythmic cues.

In another, the colored squares followed a more complex pattern, with differing intervals between the red and green squares. This sequence was easier for the Parkinson's patients to follow, and succeed at.

"We show that patients with cerebellar degeneration are impaired in using non-rhythmic temporal cues while patients with basal ganglia degeneration associated with Parkinson's disease are impaired in using rhythmic cues," Ivry said.

Ultimately, the results confirm that the brain uses two different mechanisms for anticipatory timing, challenging theories that a single brain system handles all our timing needs, researchers said.

"Our results suggest at least two different ways in which the brain has evolved to anticipate the future," said Breska.

"A rhythm-based system is sensitive to periodic events in the world such as is inherent in speech and music," he added. "And an interval system provides a more general anticipatory ability, sensitive to temporal regularities even in the absence of a rhythmic signal."

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Engineers fly first-ever plane with no moving parts

 

Engineers have built and flown the first-ever plane with no moving parts. Instead of propellers or turbines, the light aircraft is powered by an 'ionic wind' -- a silent but mighty flow of ions that is produced aboard the plane, and that generates enough thrust to propel the plane over a sustained, steady flight.

Since the first airplane took flight over 100 years ago, virtually every aircraft in the sky has flown with the help of moving parts such as propellers, turbine blades, and fans, which are powered by the combustion of fossil fuels or by battery packs that produce a persistent, whining buzz.

Now MIT engineers have built and flown the first-ever plane with no moving parts. Instead of propellers or turbines, the light aircraft is powered by an "ionic wind" -- a silent but mighty flow of ions that is produced aboard the plane, and that generates enough thrust to propel the plane over a sustained, steady flight.

Unlike turbine-powered planes, the aircraft does not depend on fossil fuels to fly. And unlike propeller-driven drones, the new design is completely silent.

"This is the first-ever sustained flight of a plane with no moving parts in the propulsion system," says Steven Barrett, associate professor of aeronautics and astronautics at MIT. "This has potentially opened new and unexplored possibilities for aircraft which are quieter, mechanically simpler, and do not emit combustion emissions."

He expects that in the near-term, such ion wind propulsion systems could be used to fly less noisy drones. Further out, he envisions ion propulsion paired with more conventional combustion systems to create more fuel-efficient, hybrid passenger planes and other large aircraft.

Barrett and his team at MIT have published their results in the journal Nature.

Hobby crafts

Barrett says the inspiration for the team's ion plane comes partly from the movie and television series, "Star Trek," which he watched avidly as a kid. He was particularly drawn to the futuristic shuttlecrafts that effortlessly skimmed through the air, with seemingly no moving parts and hardly any noise or exhaust.

"This made me think, in the long-term future, planes shouldn't have propellers and turbines," Barrett says. "They should be more like the shuttles in 'Star Trek,' that have just a blue glow and silently glide."

About nine years ago, Barrett started looking for ways to design a propulsion system for planes with no moving parts. He eventually came upon "ionic wind," also known as electroaerodynamic thrust -- a physical principle that was first identified in the 1920s and describes a wind, or thrust, that can be produced when a current is passed between a thin and a thick electrode. If enough voltage is applied, the air in between the electrodes can produce enough thrust to propel a small aircraft.

For years, electroaerodynamic thrust has mostly been a hobbyist's project, and designs have for the most part been limited to small, desktop "lifters" tethered to large voltage supplies that create just enough wind for a small craft to hover briefly in the air. It was largely assumed that it would be impossible to produce enough ionic wind to propel a larger aircraft over a sustained flight.

"It was a sleepless night in a hotel when I was jet-lagged, and I was thinking about this and started searching for ways it could be done," he recalls. "I did some back-of-the-envelope calculations and found that, yes, it might become a viable propulsion system," Barrett says. "And it turned out it needed many years of work to get from that to a first test flight."

Ions take flight

The team's final design resembles a large, lightweight glider. The aircraft, which weighs about 5 pounds and has a 5-meter wingspan, carries an array of thin wires, which are strung like horizontal fencing along and beneath the front end of the plane's wing. The wires act as positively charged electrodes, while similarly arranged thicker wires, running along the back end of the plane's wing, serve as negative electrodes.

The fuselage of the plane holds a stack of lithium-polymer batteries. Barrett's ion plane team included members of Professor David Perreault's Power Electronics Research Group in the Research Laboratory of Electronics, who designed a power supply that would convert the batteries' output to a sufficiently high voltage to propel the plane. In this way, the batteries supply electricity at 40,000 volts to positively charge the wires via a lightweight power converter.

Once the wires are energized, they act to attract and strip away negatively charged electrons from the surrounding air molecules, like a giant magnet attracting iron filings. The air molecules that are left behind are newly ionized, and are in turn attracted to the negatively charged electrodes at the back of the plane.

As the newly formed cloud of ions flows toward the negatively charged wires, each ion collides millions of times with other air molecules, creating a thrust that propels the aircraft forward.

The team, which also included Lincoln Laboratory staff Thomas Sebastian and Mark Woolston, flew the plane in multiple test flights across the gymnasium in MIT's duPont Athletic Center -- the largest indoor space they could find to perform their experiments. The team flew the plane a distance of 60 meters (the maximum distance within the gym) and found the plane produced enough ionic thrust to sustain flight the entire time. They repeated the flight 10 times, with similar performance.

"This was the simplest possible plane we could design that could prove the concept that an ion plane could fly," Barrett says. "It's still some way away from an aircraft that could perform a useful mission. It needs to be more efficient, fly for longer, and fly outside."

Barrett's team is working on increasing the efficiency of their design, to produce more ionic wind with less voltage. The researchers are also hoping to increase the design's thrust density -- the amount of thrust generated per unit area. Currently, flying the team's lightweight plane requires a large area of electrodes, which essentially makes up the plane's propulsion system. Ideally, Barrett would like to design an aircraft with no visible propulsion system or separate controls surfaces such as rudders and elevators.

"It took a long time to get here," Barrett says. "Going from the basic principle to something that actually flies was a long journey of characterizing the physics, then coming up with the design and making it work. Now the possibilities for this kind of propulsion system are viable."

This research was supported, in part, by MIT Lincoln Laboratory Autonomous Systems Line, the Professor Amar G. Bose Research Grant, and the Singapore-MIT Alliance for Research and Technology (SMART). The work was also funded through the Charles Stark Draper and Leonardo career development chairs at MIT.

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