Brain Implant Could Be the Next Computer Mouse

Eight years ago, a patient lost her power of speech because of ALS, or Lou Gehrig’s disease, which causes progressive paralysis. She can still make sounds, but her words have become unintelligible, leaving her reliant on a writing board or iPad to communicate.

Now, after volunteering to receive a brain implant, the woman has been able to rapidly communicate phrases like “I don’t own my home” and “It’s just tough” at a rate approaching normal speech.

That is the claim inpaper published over the weekend on the website bioRxiv by a team at Stanford University. The study has not been formally reviewed by other researchers. The scientists say their volunteer, identified only as “subject T12,” smashed previous records by using the brain-reading implant to communicate at a rate of 62 words a minute, three times the previous best.

Philip Sabes, a researcher at the University of California, San Francisco, who was not involved in the project, called the results a “big breakthrough” and said that experimental brain-reading technology could be ready to leave the lab and become a useful product soon.

The performance in this paper is already at a level which many people who cannot speak would want, if the device were ready,” says Sabes. “People are going to want this.” People without speech deficits typically talk at a rate of about 160 words a minute. Even in an era of keyboards, thumb-typing, emojis, and internet abbreviations, speech remains the fastest form of human-to-human communication.

The new research was carried out at Stanford University. The preprint, published January 21, began drawing extra attention on Twitter and other social media because of the death the same day of its co-lead author, Krishna Shenoy, from pancreatic cancer.

Shenoy had devoted his career to improving the speed of communication through brain interfaces, carefully maintaining a list of records on his laboratory website. In 2019, another volunteer Shenoy worked with managed to use his thoughts to type at a rate of 18 words a minute, a record performance at the time.

Source: https://www.technologyreview.com/

Synthetic, Tumor-Targeting Molecule Promotes Immune Activation

Activating the immune system at the site of a tumor can recruit and stimulate immune cells to destroy tumor cells. One strategy involves injecting immune-stimulating molecules directly into the tumor, but this method can be challenging for cancers that are not easily accessible. Now, Stanford researchers have developed a new synthetic molecule that combines a tumor-targeting agent with another molecule that triggers immune activation. This tumor-targeted immunotherapy can be administered intravenously and makes its way to one or multiple tumor sites in the body, where it recruits immune cells to fight the cancer.
Three doses of this new immunotherapy prolonged the survival of six of nine laboratory mice with an aggressive triple negative breast cancer. Of the six, three appeared cured of their cancer over the duration of the monthslong study. A single dose of this molecule induced complete tumor regression in five of 10 mice. The synthetic molecule showed similar results in a mouse model of pancreatic cancer.

An immunotherapy molecule administered intravenously to mice was shown to target tumors.

We essentially cured some animals with just a few injections,” said Jennifer Cochran, PhD, the Shriram Chair of the Department of Bioengineering. “It was pretty astonishing. When we looked within the tumors, we saw they went from a highly immunosuppressive microenvironment to one full of activated B and T cells — similar to what happens when the immune-stimulating molecule is injected directly into the tumor. So, we’re achieving intra-tumoral injection results but with an IV deliver.”

A paper describing the study published online in Cell Chemical Biology.  The lead authors are Stanford graduate student Caitlyn Miller and instructor of medicine Idit Sagiv-Barfi, PhD.

Source: https://med.stanford.edu/

Rejuvenation by Controlled Reprogramming

On 19 January 2022, co-founders Rick Klausner and Hans Bishop publicly launched an aging research initiative called Altos Labs, with $3 billion in initial investment from backers including tech investor Yuri Milner and Amazon founder Jeff Bezos. This is the latest in a recent surge of investment in ventures seeking to build anti-aging interventions on the back of basic research programs looking at epigenetic reprogramming. In December, cryptocurrency company Coinbase’s cofounder Brian Armstrong and venture capitalist Blake Byers founded NewLimit, an aging-focused biotech backed by an initial $105 million investment, with the University of California, San Francisco’s Alex Marson and Stanford’s Mark Davis as advisors.

The discovery of the Yamanaka factors’ — four transcription factors (Oct3/4, Sox2, c-Myc and Klf4) that can reprogram a differentiated somatic cell into a pluripotent embryonic-like state — earned Kyoto University researcher Shinya Yamanaka a share of the Nobel prize in 2012. The finding, described in 2006, transformed stem cell research by providing a new source of embryonic stem cell (ESC)-like cells, induced pluripotent stem cell (iPSCs), that do not require human embryos for their derivation. But in recent years, Yamanaka factors have also become the focus for another burgeoning area: aging research.

So-called partial reprogramming consists in applying Yamanaka factors to cells for long enough to roll back cellular aging and repair tissues but without returning to pluripotency. Several groups, including those headed by Stanford University’s Vittorio Sebastiano, the Salk Institute’s Juan Carlos Izpisúa Belmonte and Harvard Medical School’s David Sinclair, have shown that partial reprogramming can dramatically reverse age-related phenotypes in the eye, muscle and other tissues in cultured mammalian cells and even rodent models by countering epigenetic changes associated with aging. These results have spurred interest in translating insights from animal models into anti-aging interventions. “This is a pursuit that has now become a race,” says Daniel Ives, CEO and founder of Cambridge, UK-based Shift Bioscience.

The Yamanaka factors that can reprogram cells into their embryonic-like state are at the heart of longevity research

We’re investing in this area [because] it is one of the few interventions we know of that can restore youthful function in a diverse set of cell types,” explains Jacob Kimmel, a principal investigator at Alphabet subsidiary Calico Life Sciences in South San Francisco, California. The zeal is shared by Joan Mannick, head of R&D at Life Biosciences, who says partial reprogramming could be potentially “transformative” when it comes to treating or even preventing age-related diseases. Life Biosciences, a startup co-founded by David Sinclair, is exploring the regenerative capacity of three Yamanaka factors (Oct4, Sox2 and Klf4).

Source: https://www.nature.com/

Synthetic Molecule Seeks out and Destroys Cancer Tumors

Activating the immune system at the site of a tumor can recruit and stimulate immune cells to destroy tumor cells. One strategy involves injecting immune-stimulating molecules directly into the tumor, but this method can be challenging for cancers that are not easily accessible.  Now, Stanford researchers have developed a new synthetic molecule that combines a tumor-targeting agent with another molecule that triggers immune activation. This tumor-targeted immunotherapy can be administered intravenously and makes its way to one or multiple tumor sites in the body, where it recruits immune cells to fight the cancer

Three doses of this new immunotherapy prolonged the survival of six of nine laboratory mice with an aggressive triple negative breast cancer. Of the six, three appeared cured of their cancer over the duration of the monthslong study. A single dose of this molecule induced complete tumor regression in five of 10 mice. The synthetic molecule showed similar results in a mouse model of pancreatic cancer.

We essentially cured some animals with just a few injections,” said Jennifer Cochran, PhD, the Shriram Chair of the Department of Bioengineering. “It was pretty astonishing. When we looked within the tumors, we saw they went from a highly immunosuppressive microenvironment to one full of activated B and T cells — similar to what happens when the immune-stimulating molecule is injected directly into the tumor. So, we’re achieving intra-tumoral injection results but with an IV delivery.”

A paper describing the study has been published online in Cell Chemical Biology. Cochran shares senior authorship with Carolyn Bertozzi, PhD, the Baker Family Director of Stanford ChEM-H, Anne T. and Robert M. Bass Professor in the School of Humanities and Sciences and professor of chemistry; and Ronald Levy, MD, the Robert K. and Helen K. Summy Professor in the School of Medicine. The lead authors are graduate student Caitlyn Miller and instructor of medicine Idit Sagiv-Barfi, PhD.

Source: https://med.stanford.edu/
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Google Launches a Dermatology AI App in EU

Billions of times each year, people turn to Google’s web search box for help figuring out what’s wrong with their skin. Now, Google is preparing to launch an app that uses image recognition algorithms to provide more expert and personalized help. A brief demo at the company’s developer conference last month showed the service suggesting several possible skin conditions based on uploaded photos.

Machines have matched or outperformed expert dermatologists in studies in which algorithms and doctors scrutinize images from past patients. But there’s little evidence from clinical trials deploying such technology, and no AI image analysis tools are approved for dermatologists to use in the US, says Roxana Daneshjou, a Stanford dermatologist and researcher in machine learning and health.

Many don’t pan out in the real world setting,” she says.

Google’s new app isn’t clinically validated yet either, but the company’s AI prowess and recent buildup of its health care division make its AI dermatology app notable. Still, the skin service will start small—and far from its home turf and largest market in the US. The service is not likely to analyze American skin blemishes any time soon.

At the developer conference, Google’s chief health officer, Karen DeSalvo, said the company aims to launch what it calls a dermatology assist tool in the European Union as soon as the end of this year. A video of the app suggesting that a mark on someone’s arm could be a mole featured a caption saying it was an approved medical device in the EU. The same note added a caveat: “Not available in the US.”

Google says its skin app has been approved “CE marked as a Class I medical device in the EU,” meaning it can be sold in the bloc and other countries recognizing that standard. The company would have faced relatively few hurdles to secure that clearance, says Hugh Harvey, managing director at Hardian Health, a digital health consultancy in the UK. “You essentially fill in a form and self-certify,” he says. Google’s conference last month took place a week before tighter EU rules took effect that Harvey says require many health apps, likely including Google’s, to show that an app is effective, among other things. Preexisting apps have until 2025 to comply with the new rules.

Source: https://www.wired.com/

How To Restore Sight To The Blind

For more than a decade, researchers have been working to create artificial digital retinas that can be implanted in the eye to allow the blind to see again. Many challenges stand in the way, but researchers at Stanford University may have found the key to solving one of the most vexing: heat. The artificial retina requires a very small computer chip (nanocomputer) with many metal electrodes poking out. The electrodes first record the activity of the neurons around them to create a map of cell types. This information is then used to transmit visual data from a camera to the brain. Unfortunately, the eye produces so much data during recording that the electronics get too darn hot.

The chips required to build a high-quality artificial retina would essentially fry the human tissue they are trying to interface with,” says E.J. Chichilnisky, a professor in the Neurosurgery and Ophthalmology departments, who is on Stanford’s artificial retina team.

Members of the team, including Chichilnisky and his collaborators in Stanford’s Electrical Engineering and Computer Science departments, recently announced they have devised a way to solve that problem by significantly compressing the massive amounts of visual data that all those neurons in the eye create. They discuss their advance in a study published in the IEEE Transactions on Biomedical Circuits and Systems.

To convey visual information, neurons in the retina send electrical impulses, known as spikes, to the brain. The problem is that the digital retina needs to record and decode those spikes to understand the properties of the neurons, but that generates a lot of heat in the digitization process, even with only a few hundred electrodes used in today’s prototypes. The first true digital retina will need to have tens of thousands of such electrodes, complicating the issue further. Boris Murmann, a professor of electrical engineering on the retina project, says the team found a way to extract the same level of visual understanding using less data. By better understanding which signal samples matter and which can be ignored, the team was able to reduce the amount of data that has to be processed. It’s a bit like being at a party trying to extract a single coherent conversation amid the din of a crowded room — a few voices matter a lot, but most are noise and can be ignored.

We compress the data by being more selective, ignoring the noise and baseline samples and digitizing only the unique spikes,” Murmann says. Previously, digitization and compression were done separately, leading to a lot of extra data storage and data transfer. “Our innovation inserts compression techniques into the digitization process,” says team member Subhasish Mitra, a professor of electrical engineering and of computer science. This approach retains the most useful information and is easier to implement in hardware.

Source: https://engineering.stanford.edu/

Most Metastatic Colorectal Cancers Have Spread Before Diagnosis

Colorectal cancers often spread before the initial tumor is detected, according to a new Stanford study. Identifying patients in whom early metastasis is likely could better guide treatment decisions. Up to 80% of metastatic colorectal cancers are likely to have spread to distant locations in the body before the original tumor has exceeded the size of a poppy seed, according to a study of nearly 3,000 patients by researchers at the Stanford University School of MedicineIdentifying patients with early-stage colorectal tumors that are born to be bad may help doctors determine who should receive early treatments, such as systemic chemotherapy, to kill cancer cells lurking far from the tumor’s original location.

This finding was quite surprising,” said Christina Curtis, PhD, assistant professor of medicine and of genetics at Stanford. “In the majority of metastatic colorectal cancer patients analyzed in this study, the cancer cells had already spread and begun to grow long before the primary tumor was clinically detectable. This indicates that metastatic competence was attained very early after the birth of the cancer. This runs counter to the prevailing assumption that metastasis occurs late in advanced primary tumors and has implications for patient stratification, therapeutic targeting and earlier detection.”

Researchers and clinicians have assumed that cancers acquire the ability to metastasize through the gradual accumulation of molecular changes over time. These changes, the thinking goes, confer specific traits that eventually allow cancer cells to escape the surrounding tissue, enter the bloodstream and take up residence in new locations. In this scenario, metastasis, if it occurs, would be a relatively late event in the evolution of the primary cancer.

Curtis, who co-directs the molecular tumor board at the Stanford Cancer Institute, is the senior author of the study, which was published online June 17 in Nature Genetics. Postdoctoral scholar Zheng Hu, PhD, is the lead author.

Source: http://med.stanford.edu/