Monthly Archives: December 2020
Chemotherapy could be up to 34 per cent more effective thanks to a new technique which combines the treatment with magnetic particles that fry cancerous cells. Researchers at University College London (UCL) found the combination of heat and chemo drugs makes the process more effective. Tiny magnetic nanoparticles attach themselves to the cancerous cells of a tumour and also carry the chemotherapy drug.
When doctors apply a harmless magnetic field to the area from outside the body it activates the nanoparticles’ magnetic properties and causes them to warm up, heating the trapped cancerous cells. Research reveals this damages the tumour and makes it more vulnerable to pre-existing drugs.
The research has so far only been tested in a lab, but researchers say the early findings are significant. Human breast cancer cells, glioblastoma (brain cancer) cells, and mouse prostate cancer cells were all treated, in a test tube, with this new technique. Doxorubicin — a commonly used chemo drug — was applied to the magnetic nanoparticles. Heat and doxorubicin together killed 98 per cent of brain cancer cells after 48 hours. The drug only killed 73 per cent of cells when applied without heat. For the breast cancer cells, 89 per cent of the cancer was eliminated by the combination, and this drops to just 77 per cent for the drug alone.
‘Our study shows the enormous potential of combining chemotherapy with heat treatment delivered via magnetic nanoparticles,” said Senior author Professor Nguyen T. K. Thanh. ‘While this combination of therapy is already approved for the treatment of fast-growing glioblastomas, our results suggest it has potential to be used more widely as a broad anti-cancer therapy. ‘This therapy also has potential to reduce the side effects of chemotherapy, by ensuring it is more highly targeted on cancer cells rather than healthy issue. This needs to be explored in further pre-clinical tests.’
The results have been published in the Journal of Materials Chemistry B,
Boston Dynamics’ Atlas and Spot robots can do a lot of things: sprinting, gymnastic routines,parkour, backflips, open doors to let in an army of their friends, wash dishes, and (poorly) get actual jobs. But the company’s latest video adds another impressive trick to our future robotic overlords’ repertoire: busting sick dance moves.
The video sees Boston Dynamics entire lineup of robots — the humanoid Atlas, the dog-shaped Spot, and the box-juggling Handle — all come together in a bopping, coordinated dance routine set to The Contours’ “Do You Love Me.”
t’s not the first time Boston Dynamics has shown off its robots’ dancing skills: the company showcased a video of its Spot robot doing the Running Man to “Uptown Funk” in 2018. but the new video takes things to another level, with the Atlas robot tearing it up on the dance floor: smoothly running, jumping, shuffling, and twirling through different moves.
Things get even more incredible as more robots file out, prancing around in the kind of coordinated dance routine that puts my own, admittedly awful human dancing to shame. Compared to the jerky movements of the 2016 iteration of Atlas, the new model almost looks like a CGI creation.
Boston Dynamics was recently purchased by Hyundai, which bought the robotics firm from SoftBank in a $1.1 billion deal. The company was originally founded in 1992 as a spin-off from the Massachusetts Institute of Technology, where it became known for its dog-like quadrupedal robots (most notably, the DARPA-funded BigDog, a precursor to the company’s first commercial robot, Spot.) It was bought by Alphabet’s X division in 2013, and then by Softbank in 2017.
While the Atlas and Handle robots featured here are still just research prototypes, Boston Dynamics has recently started selling the Spot model to any company for the considerable price of $74,500. But can you really put a price on creating your own personal legion of boogieing robot minions?
Scientists in the UK have just recruited the first participants in the world to be part of a new long-acting antibody study. If the treatment is effective, it could give those who have already been exposed to SARS-CoV-2 protection from developing COVID-19.
“We know that this antibody combination can neutralise the virus,” explains University College London Hospitals (UCLH) virologist Catherine Houlihan. “So we hope to find that giving this treatment via injection can lead to immediate protection against the development of COVID-19 in people who have been exposed – when it would be too late to offer a vaccine.”
This might not be the first antibody treatment for COVID-19 you’ve heard of. Outgoing US President Donald Trump was given monoclonal antibodies when he came down with the disease, and in the US two different antibody treatments – casirivimab and imdevimab – received emergency approval back in November. But those antibody treatments are given to patients with mild or moderate COVID-19, who risk progressing to a severe version of the disease.
“In a clinical trial of patients with COVID-19, casirivimab and imdevimab, administered together, were shown to reduce COVID-19-related hospitalisation or emergency room visits in patients at high risk for disease progression within 28 days after treatment when compared to placebo,” the FDA explained in a press statement when the drugs were approved. This new antibody therapy, called AZD7442 and developed by UCLH and AstraZeneca, is a little different. AZD7442 is a combination of two monoclonal antibodies AZD8895 and AZD1061, which both target the receptor binding domain of the SARS-CoV-2 spike protein.
“By targeting this region of the virus’s spike protein, antibodies can block the virus’s attachment to human cells, and, therefore, is expected to block infection,” the team wrote on the US ClinicalTrials.gov website. “Amino acid substitutions have been introduced into the antibodies to both extend their half-lives, which should prolong their potential prophylactic benefit, and decrease Fc effector functionin order to decrease the potential risk of antibody-dependent enhancement of disease.”
Antibodies are little Y-shaped proteins that lock on to a particular section – called an antigen – of a virus, bacterium or other pathogen, and either ‘tag‘ it to be attacked by the immune system, or directly block the pathogen from invading our cells. Normal antibodies are produced by your body after an infection, while monoclonal antibodies are cloned in a lab and can be injected into a person already infected, to give the immune system a hand in the fight.
The researchers are hoping that AZD7442 – which is just starting the Storm Chaser study (the name for its phase 3 trial) – provides protection for those that have been exposed to the virus but do not yet have symptoms. Effectively, they’re trying to stop COVID-19 happening in the first place. “If you are dealing with outbreaks in settings such as care homes, or if you have got patients who are particularly at risk of getting severe COVID, such as the elderly, then this could well save a lot of lives,” said University of East Anglia infectious disease expert Paul Hunter.
The Astrazenezca/Oxford vaccine could be rolled out across the UK within the next fortnight as the head of the company raised hopes of the jab’s “winning formula”. The Government is aiming for mass vaccination centres to start administering patients with either the AstraZeneca/Oxford or Pfizer jab from January 4, according to told the Sunday Telegraph, as the new variant of coronavirus first found in the UK continues to spread across the world. The Medicines and Healthcare products Regulatory Agency (MHRA) could reportedly approve the homegrown jab within days, with millions poised to start receiving the jab at the start of next month.
It comes as the AstraZeneca chief said he believed researchers had found the “winning formula” using two doses and promised to publish the results.
“We think we have figured out the winning formula and how to get efficacy that, after two doses, is up there with everybody else,” Pascal Soriot told The Sunday Times. “I can’t tell you more because we will publish at some point.”
Just over 1 million people in the U.S. have received their first dose of the coronavirus vaccine as of Wednesday morning, a far cry from the federal government’s goal of inoculating 20 million Americans by the end of the year.
Now that two Covid-19 vaccines have been approved for emergency use, the biggest hurdle to the pandemic in the U.S. is getting the doses to the roughly 331 million Americans across the country. The Centers for Disease Control and Prevention said 1,008,025 shots had been administered as of Wednesday at 9 a.m. ET.
The scale of the challenge that automation poses to the jobs market needs to be met with much stronger action to upskill the workforce, finds a new report published by a committee in the UK Parliament.
The House of Lords’ select committee on artificial intelligence raised concerns at the “inertia” that is slowing down the country when it comes to digital skills, and urged the government to take steps to make sure that people have the opportunity to reskill and retrain, to be able to adapt to the changing labor market that AI is bringing about.
Citing research carried out by Microsoft, the committee stressed that only 17% of UK employees say that they have been part of reskilling efforts, which sits well below the global average of 38%.
Microsoft also recently reported that almost 70% of business leaders in the UK believe that their organization currently has a digital skills gap, and that two-thirds of employees feel that they do not have the appropriate digital skills to fulfil new and emerging roles in their industry.Even basic digital skills are lacking: a recent Lloyds Bank survey found that 19% of individuals in the UK couldn’t complete tasks such as using a web browser.
For the past three years, the government has been offering a national retraining scheme, which aims to upskill UK citizens, partly as a result of automation. Wendy Hall, a professor of computer science at the University of Southampton, who provided evidence to the Lords for the report, said that the UK is currently “nowhere near ready” when it comes to building up the skills that are necessary to mitigate the impact of automation on jobs.
Meanwhile, found the report, AI systems are growing at a fast pace. While in 2015, the UK saw £245 million ($326 million) invested in AI, that number jumped to £1.3 billion ($1.73 billion) in 2019. Automated systems are now prevalent in many industries, ranging from agriculture to healthcare, through to financial services, retail and logistics.
React Neuro, a startup founded three years ago by veterans of Harvard Medical School (HMS) and Massachusetts General Hospital (MGH), wants to analyze how healthy your brain is.
Rudy Tanzi, a well-known Alzheimer’s disease researcher and professor of neurology at HMS and MGH, started the company in 2017 with Brian Nahed, a neurosurgical oncologist specializing in brain tumors and associate program director of neurosurgery at MGH and HMS. The two had worked with the NFL for years — Tanzi as a brain-health advisor to the New England Patriots, Nahed as a neurotrauma consultant for the league — and wanted to focus on the issue of concussions in football players. Specifically, they wanted to take a scientific approach to figuring out when a player could safely return to the sport following a concussion. The startup has evolved since then to take a holistic look at brain health through AI software and a VR headset.
“From a consumer health standpoint, the idea is essentially [that by] using software, we can assess people’s brain health and provide feedback on what’s working and what’s not working,” said React Neuro CEO Shahid Azim, who joined the company in early 2019. “What really got me interested was not so much the concussion use case, but the more fundamental question that the team was looking to ask, which was, ‘Is there a better way to measure your brain health?’”
React Neuro answers that question with digital exams administered through a custom VR headset, which is developed by Pico Interactive in San Francisco. Designed based on the tools, techniques and exams traditionally used to assess neurological conditions, the tests return results that the startup’s AI software turns into actionable insights for physicians.
Azim, a 2009 MIT Sloan School of Management grad, calls the brain assessments via headset “digital exams,” or “experiences on screen.” The exams, he said, can last anywhere from two and a half minutes to 10 minutes, depending on the use case. A general cognitive assessment typically lasts seven minutes.
“We’re using eye tracking and voice analysis [for the exams],” Azim said. “In some cases, they’re voice-based, so you’re asked to repeat something that you see on the screen.”
Studies have shown that gut microbes can influence several aspects of the host’s life, including aging. Given the complexity and heterogeneity of the human gut environment, elucidating how a specific microbial species contributes to longevity has been challenging.
To explore the influence of bacterial products on the aging process, scientists at Baylor College of Medicine and Rice University developed a method that uses light to directly control gene expression and metabolite production from bacteria residing in the gut of the laboratory worm Caenorhabditis elegans.
The team reports (“Optogenetic control of gut bacterial metabolism to promote longevity”) in eLife that green-light-induced production of colanic acid by resident Escherichia coli bacteria protected gut cells against stress-induced cellular damage and extended the worm’s lifespan. The researchers indicate that this method can be applied to study other bacteria and propose that it also might provide in the future a new way to fine-tune bacterial metabolism in the host gut to deliver health benefits with minimal side effects.
“Gut microbial metabolism is associated with host longevity. However, because it requires direct manipulation of microbial metabolism in situ, establishing a causal link between these two processes remains challenging. We demonstrate an optogenetic method to control gene expression and metabolite production from bacteria residing in the host gut. We genetically engineer an E. coli strain that secretes colanic acid (CA) under the quantitative control of light,” the investigators wrote.
“Using this optogenetically-controlled strain to induce CA production directly in the C. elegans gut, we reveal the local effect of CA in protecting intestinal mitochondria from stress-induced hyper-fragmentation. We also demonstrate that the lifespan-extending effect of this strain is positively correlated with the intensity of green light, indicating a dose-dependent CA benefit on the host.
“Thus, optogenetics can be used to achieve quantitative and temporal control of [the microbiome] metabolism in order to reveal its local and systemic effects on host health and aging. “We used optogenetics, a method that combines light and genetically engineered light-sensitive proteins to regulate molecular events in a targeted manner in living cells or organisms,” said co-corresponding author Meng Wang, PhD, professor of molecular and human genetics at the Huffington Center on Aging at Baylor.
Influenza is one of the most widespread viral diseases and constitutes a major public health problem. For some, it means spending a week in bed; for others, it could lead to hospitalization or, in the most severe cases, death. Scientists at the Ecole Polytechnique Fédérale de Lausanne (EPFL)’s Supramolecular Nano-Materials and Interfaces Laboratory (SuNMIL) within the School of Engineering, working in association with the team headed by Caroline Tapparel, a professor at the University of Geneva’s Department of Microbiology and Molecular Medicine, have synthesized a compound that can kill the virus that causes influenza. Their discovery paves the way to effective drug therapies against the seasonal disease.
“With the flu virus, the risk of a pandemic is high,” says Francesco Stellacci, the EPFL professor who heads SuNMIL. “Scientists have to update the vaccine every year because the strain mutates, and sometimes the vaccine turns out to be less effective. So it would be good to also have antivirals that could limit the effects of large-scale infection.”
“Antiviral drugs already exist, and Tamiflu is the most well-known. But it has one major drawback – it has to be taken within 36 hours of infection or it loses its efficacy completely. And with influenza, symptoms generally start appearing 24 hours after infection. “By the time patients seek medical treatment, it’s often too late for Tamiflu,” explained Stellacci. “In addition, for antivirals to really work, they have to be virucidal – that is, they have to irreversibly inhibit viral infectivity. But today that’s not the case.”
The research has been published in Advanced Science.
Many neurodegenerative conditions, from glaucoma to Alzheimer’s disease, are characterized by injury to axons — the long, slender projections that conduct electrical impulses from one nerve cell to another, facilitating cellular communications. Injury to axons often leads to neuronal impairment and cell death.
Researchers know that inhibiting an enzyme called dual leucine zipper kinase (DLK) appears to robustly protect neurons in a wide range of neurodegenerative diseases models, but DLK also inhibits axonal regeneration. Until now, there have been no effective methods to modify genes to improve both the long-term survival of neurons and promote regeneration.
In a paper published December 14, 2020 in PNAS, a multi-university team led by researchers at University of California San Diego School of Medicine and Shiley Eye Institute at UC San Diego Health identified another family of enzymes called germinal cell kinase four kinases (GCK-IV kinases) whose inhibition is robustly neuroprotective, while also permitting axon regeneration, making it an attractive therapeutic approach for treating at some neurodegenerative diseases.
Example of retinal ganglion cells with axons and dendrites in the retina of a healthy eye.
“We basically figured out that there are a set of genes that, when inhibited, allow optic nerve cells to survive and regenerate,” said senior author Derek Welsbie, MD, PhD, associate professor of ophthalmology in the Viterbi Family Department of Ophthalmology at Shiley Eye Institute.
“Prior to this work, the field knew how to get these cells to survive, but not regenerate. Conversely, there are ways to promote regeneration, but then the survival was rather modest. Of course, for a successful strategy of vision restoration, you need both and this is a step in that direction.”