Meet the World’s First Truly Universal Cable

There’s a new USB. Its mission: to kill proprietary plugs.

The best new technology of the past year wasn’t some phone or an app.

Believe it or not, it was a new kind of USB cable.

Now, before you suspect that I’ve inhaled a bit too much of that new-tablet smell, consider:

The new cable, called USB Type-C (or USB-C), is the same on both ends, so you never have to fiddle with it. The connector is also identical on both sides—there’s no upside down.

USB-C can replace four different jacks on your gadget: data, video, power and, soon, audio. That’s right: A single connector can handle flash drives, hard drives, screens, projectors, charging and headphones (simultaneously, if you have a splitter). Yet the connector is tiny enough for phones and tablets and sturdy enough for laptops and PCs.

Every device from every brand can use the same cable. You can use the charger from my Google phone to charge your Apple laptop or someone else’s Microsoft tablet. No more drawers full of mismatched power bricks.

In other words, USB-C represents the dawning of the universal cable.

That USB-C even exists at all is something of a miracle, considering what a big business accessories have become. Apple, for example, makes a staggering amount of money selling cables. Cynical observers accuse it of changing connector types deliberately, just to drum up accessory sales. For example, good luck using a 2009 power cord with a 2013 MacBook.

Apple’s not alone. A typical charger for a Windows laptop costs $60 to $80.

Several of these big companies worked together to come up with the USB Type-C standard, and even more have adopted it.

The question is: Why? Why would these archrivals work together to create a charger that works interchangeably across devices and brands, wiping out the proprietary-charger industry in one fell swoop?

Brad Saunders, who works for Intel, is chair of the USB 3.0 Promoter Group, a group of six companies that designed USB Type-C (including Intel, Hewlett-Packard and Microsoft). He says that the original reason to design it was speed; the 20-year-old regular USB connector couldn’t be made any faster.

“At the same time,” he says, “PCs were changing, becoming thinner and lighter. The existing USB connector was just way too big. And it’s not as user-friendly as we’d like: you can plug it in the wrong way.”

But surely, I asked him, these companies knew that designing One Cable to Rule Them All meant that they’d lose big bucks in sales of their proprietary chargers.

“Well, job one is making money for your company,” he admits. “But over time we became motivated by the fact that we could change the world from a green perspective. If we could standardize all these power supplies, we could reduce waste. We started to realize we could have a real impact.”

It’s weird to imagine all these blood rivals working together, side by side, to create a new standard for everyone’s mutual benefit. How often does the world work that way?

“Standards work is kind of odd,” says Jeff Ravencraft, president of the USB Implementers Forum. “Companies work together to bake a bigger pie, to expand the market for their products. But once it’s over, they have to compete for how big a piece of the pie they’ll get. You cooperate at the beginning, and then you compete like hell at the end.”

And the cable is already here. Some of the latest phones, tablets and laptops from Google, Apple, Microsoft, Samsung and others come with USB-C jacks built in.

You might think that only the nerdiest nerds could get excited about USB-C. And yet in the coming years this invention could save you hundreds of dollars in duplicate cords, adapters and chargers. It will permit our gadgets to get smaller and faster. It will save space in our drawers, packages, purses and laptop bags. It will keep tons of e-waste out of the landfills.

If that doesn’t qualify USB-C as the invention of the year, I don’t know what does.

World’s First 3D-Printed Vertebrae Saves Man With Chordoma Cancer From Becoming A Quadriplegic

What a time it is for 3D printing in health care. Over the past year alone, doctors have successfully separated conjoined twins, given a cancer patient a titanium rib cage, and created muscle, bone, and ears from 3D-printing materials. This list continues to grow; in December 2015, a man in his 60s received the first 3D-printed vertebrae. Without it, he would have become fully paralyzed.

The patient, Drage Josevski, suffers from a condition known as Chordoma cancer, a type of malignant tumor that “can occur in the bones of the spine and base of the skull,” according to the American Academy of Orthopaedic Surgeons. It’s so rare, in fact, that it occurs in only 1 percent of all malignant bone tumors, which make up about 0.2 percent of all cancers. One case per million are diagnosed each year, and about one in 125,000 people currently live with the disease.

Because of Chordoma’s proximity to so many vital structures in the head and spine, it’s very difficult to treat. In Josevski’s case, the tumor had formed on the top two vertebrae in his neck — the ones that play roles in swiveling and tilting the head. The more the tumor grew, the more of a chance Josevski had of it severing his spine, turning him into a quadriplegic.

Dr. Ralph Mobbs, an Australian neurosurgeon, took charge of treating the tumor, and relied on 3D printers and Australian medical device manufacturer Anatomics. In a combined effort, they were able to create exact replicas of the two vertebrae made out of titanium, according to Mashable. Anatomics even created entire replicas of Josevski’s spinal anatomy for doctors to conduct practice runs before the surgery.

“3D printing of body parts is the next phase of individualized health care,” Mobbs told The ABC Australia. “To restore bones, joints, [and] organs with this type of technology really is super exciting. [H]ere is our opportunity to really take it out there and to keep pushing the boundaries on the whole 3D-printed body part business.”

Mobbs described the surgery as “particularly complicated and long and difficult.” It lasted 15 hours, and involved “exposure at the top of the neck where the neck and the head meets. It’s essentially disattaching the patient’s head from his neck and taking the tumour out and reattaching his head back onto his neck.”

Though it was considered an overall success, there was one complication. The surgery was completed through Josevski’s mouth, which stayed open the entire time. Two months afterward, Josevski’s daughter said he is still struggling to speak and eat properly — Mobbs expects the complication will fix itself over the next few months. On the bright side, Josevski has full motion in his head and neck, which is tumor-free.

7 Days Of Walking Workouts To Help You Lose Weight

Perfect Week Of Walking
Want to slim down and tone up? Step to it: Researchers from the London School of Economics found that people who walked briskly for at least 30 minutes a day tended to have lower a body mass index and smaller waistlines than even those who hit the gym regularly.

The key is changing up your walking routine regularly, says Deazie Gibson, a group fitness instructor and personal trainer with Acacia TV. “Not only does it keep you interested and motivated, but it can also speed up your weight loss.” In fact, a study published in Biology Letters shows that switching up your walking pace burns up to 20% more calories than keeping a steady pace. (Burn calories and build muscle—all while boosting your mood—with our 21-Day Walk a Little, Lose a Lot Challenge!)
To help you torch more calories—and have more fun—give the following week of walking workouts a try. It mixes fast-paced intervals with total-body toning for maximum results. How fast should you step? Measure your effort, or rate of perceived exertion (RPE), on a scale of 1 to 10—with 10 being an all-out effort.

Monday: Ease into the week with a brisk walk (an effort of 6 on a scale of 1 to 10) for 20 to 30 minutes. You should be slightly above your comfort zone.

Add jumping jacks to your walking workout

Tuesday: Get your heart pumping with an interval workout. Alternate between 30 seconds of fast walking (slightly uncomfortable, 7 or 8 effort) and 30 seconds of moderate walking (4 effort), for 20 to 30 minutes.

Wednesday: Switching things up challenges your muscles—and sparks your interest. Every 3 minutes, stop to do an interval of one of the following, continuously for 30 seconds: lunges; push-ups; step with high knees; jumping jacks; sit down on a bench and stand back up (or just do squats). Repeat for a total of 20 to 30 minutes.


Thursday: Challenge your arms and shoulders by walking with a resistance band. Every 3 minutes, as you continue to walk (or step in place), hold the ends of the band straight out in front of you at shoulder height. Stretch the band out as you pull your arms directly out to your sides while keeping them at shoulder height. Do 10 to 15 repetitions, then resume your 20- to 30-minute walk at a 6 to 7 effort pace. (If you don’t have a resistance band, you can mimic the move using light dumbbells or two full water bottles.)
Friday: Combine the week’s workout into one master workout. Do 2 minutes of a brisk walk (6 effort); 2 minutes of intervals; 30 seconds of lunges, high knees, or squats, followed by 2 minutes of walking (4 to 5 effort); and 30 seconds of resistance bands followed by 2 minutes of walking (6 to 7 effort). Repeat for a total of 20 to 30 minutes.

Saturday: Go for a mindful walk. If you can, pair up with a friend. Walk at a decent pace (6 effort) and, every few minutes, remind each other about proper posture: Pull your abs in, squeeze your glutes, and push off with the heels.

Sunday: It’s your pick! Go for a leisurely 30-minute stroll to smell the roses, or challenge yourself by walking as fast as you can for 15 minutes.

Zika virus: scientists a step closer to establishing microcephaly link

Although not a concrete link to microcephaly, study shows that Zika can infect cells similar to those involved in brain development and disrupt cell growth

Scientists examining the link between the Zika virus and microcephaly in babies have discovered that the virus can infect cells similar to those involved in brain development.

Published in Stem Cell Stem the study, led by scientists at Johns Hopkins University and Florida State University, reveals that when lab-grown neuronal cells are exposed to the Zika virus, it infects the cells and is able to produce a large number of copies of itself. The researchers also found that the virus was able to disrupt pathways within the cells and limit their growth.

However, the scientists are quick to point out that their results do not prove that the mosquito-borne virus is leading to abnormal brain development of babies in the womb. “We don’t have the direct evidence to show that this will link the Zika virus to microcephaly,” said Dr Zhexing Wen, a co-author of the paper from Johns Hopkins University.

In order to probe the effect of the virus on neuronal cells, the scientists took human skin cells and “reprogrammed” them into pluripotent stem cells, which were then encouraged to grow into cells known as human cortical neural progenitor cells (human NPCs). These cells are similar to those that lead to the development of the cortex – the region of the brain that is typically underdeveloped in babies born with microcephaly.

The cells were then exposed to Zika virus. After 56 hours 65- 90% of the cells were infected with Zika; the virus was also found to be able to reproduce in large numbers within infected cells. What’s more, the Zika virus was found to interfere with cell processes and to increase cell death.

“This study hasn’t directly proved that the Zika virus causes microcephaly,” said Wen. “But it is telling that the human NPCs are very susceptible to the Zika virus and the Zika virus can cause the disruption of the human NPC growth and this may potentially correlate to the disrupted brain development in the foetus.”

While the Zika virus has previously been found to infect a range of human cells types, the latest study reveals that human NPCs showed a greater susceptibility to infection than some other cell types, including human embryonic stem cells. “We also want to know why the human NPCs are quite specific for the infection,” Wen adds.

There are, however, many more questions. “Maybe different strains of the Zika virus have different effects or maybe different people in different areas of the world may have a different response to the same Zika virus,” says Wen. But he believes the technique used by the team could help to provide answers. “We can test this out with the human NPC system,” he says.

Wen adds the team now want to use the human NPC system to screen for drugs that could prevent or eradicate infection by the Zika virus.

Responding to the paper, Prof Jonathan Ball from the University of Nottingham urges caution in interpreting the study’s findings. “There are still a number of unknowns,” he says. “It isn’t clear if the virus growing in the laboratory in these artificially generated nerve cells behaves the same way as it would in a human. We are complex organisms and lots of factors can affect how a virus infection pans out.”

However, he does believe the findings are a step towards probing the impact of Zika on the human body. “These are really interesting findings and go some way to understand how Zika virus might be causing the serious conditions that it is associated with,” he adds. “But we must remember, at the moment Zika and the link to microcephaly and Guillain-Barré [a neurological condition that can cause temporary paralysis] are only associations, and we need to know what is really happening in natural infection. Unfortunately we don’t have all of the tools to be able to do this work and the necessary experiments are tricky to do.”

Dr Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, believes such in vitro research builds on a range of studies exploring the link between the Zika virus and microcephaly. “It’s all accumulating complementary evidence,” he says.

“It is important to understand and definitively prove – or not – the direct causal relationship between infections during pregnancy and microcephaly. As the weeks and months go by there is more and more evidence that is becoming almost compelling that there is a direct causal link,” he told the Guardian.

“I think it is reasonable to make the assumption that sooner or later we will find definitive proof that Zika is related to microcephaly,” he adds. “Then we have a compelling need to protect pregnant women and women of childbearing age who will become pregnant.”

While there is currently no vaccine available to combat the virus, Fauci says that several are under development, with phase one trials for the first vaccine scheduled to begin towards the end of the summer. “Barring any unforeseen glitches I would think we would start that in September,” he says. “By the end of 2016, early 2017 we will know if it is safe in normal people.”

However finding out if it works could take time. “Everything is going to depend on the state of the epidemic because if [it] dies down it might take a couple of years to show that the vaccine works,” says Fauci. “If the epidemic is raging as it is now in early 2017, we may actually know whether it works by the end of 2017.”

Viral Remnants Help Regulate Human Immunity

Remnants of retroviruses that entered the human genome millions of years ago can regulate some innate immune responses. These viral sequences have previously been linked to controlling early mammalian development and formation of the placenta, among other things. A study published today (March 3) in Science establishes that one such endogenous retrovirus in human cells can also regulate the interferon response, which helps organisms quickly respond to infections. The work is one of the first reports to show that human cells could have adopted retroviral sequences to regulate their genes.

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“Before we started this project . . . we knew our genomes were full of these elements and many of them are activated during normal development in cells,” said study coauthor Edward Chuong, a postdoc at the University of Utah in Salt Lake City. “Our motivation was: How can we take the next step and figure out their potential biological consequences?”

Chuong and his University of Utah mentors Nels Elde and Cédric Feschotte began by scanning the sequences around interferon-induced genes, finding at least 27 transposable elements that likely originated from the long repeats at the ends of retroviral sequences. One such element, known as MER41, comes from a virus that invaded the genome approximately 45 million to 60 million years ago; the team found that its sequence in present-day human cells contained interferon-inducible binding sites.

The group then focused on a MER41 sequence that occurs 220 base pairs upstream of an interferon-induced gene called AIM2, which activates an inflammatory response in cells. When the researchers deleted this MER41 element in a cell line using CRISPR/Cas9 gene editing, interferon treatment could not trigger the AIM2 gene. Without the interferon-mediated response, these cells were more susceptible to viral infections, the team found.

“This is a really strong paper,” said Dixie Mager of the University of British Columbia who was not involved with the study. Although previous studies have considered the regulatory functions of endogenous retroviruses, most have been genome-wide correlations, Mager added. “[Here] they go in and delete the specific endogenous retroviruses and show an effect. That’s one of the things that sets this study apart.”

In addition to AIM2, the group found MER41 elements helped regulate at least three other interferon-inducible genes involved in human immunity. Looking across the genomes of other mammals, the researchers also found MER41-like regulatory elements in lemurs, bats, and other species.

The work is “simple and elegant,” said Todd Macfarlan of the Eunice Kennedy Shriver National Institute of Child Health and Human Development who was not involved with the study. “The novelty here is that it extends this idea that retroviruses are continually being coopted for things—not just for placental or early development, but also for other types of gene regulatory pathways. In the future the question might be: Are there any pathways where retroviruses don’t play a role?”

Whether host cells coopted the viral sequences for their regulatory needs or if ancient viruses used their regulatory abilities to control host immunity during invasion is still unknown, according to Feschotte. “We can only speculate why ancient viruses might have carried these regulatory switches to begin with, but data suggest they had these systems built into their sequence already,” he told The Scientist.

Endogenous retroviral elements make up about 8 percent of the human genome, and similar regulatory effects might be found on other mammalian gene functions, said Mager. “What’s cool about endogenous retroviruses is that their ends, known as LTRs, are optimized to have all these regulatory sequences in just 300 to 400 base pairs of DNA,” she said. “These units are powerhouses of regulatory potential.”

Future studies are needed to establish that these regulatory mechanisms are functional in animals, said Macfarlan. In subsequent work, Feschotte and his colleagues aim to extend their studies to a mouse model and immune cell lines.

To Feschotte’s mind, understanding how these sequences regulate human genes could shed light on previously unknown mechanisms of many diseases. While studies of cancer, autoimmune diseases, and other conditions have reported that endogenous retroviruses are reactivated in disease, the reasons for reactivation— and its consequences—are still unclear.

“What has plagued this field is that we don’t the consequences or molecular mechanisms by which these endogenous retroviruses contribute to disease,” he said.

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