In her laboratory in Barcelona, Spain, Miki Ebisuya has built a clock without cogs, springs, or numbers. This clock doesn’t tick. It is made of genes and proteins, and it keeps time in a layer of cells that Ebisuya’s team has grown in its lab. This biological clock is tiny, but it could help to explain some of the most conspicuous differences between animal species.
Animal cells bustle with activity, and the pace varies between species. In all observed instances, mouse cells run faster than human cells, which tick faster than whale cells. These differences affect how big an animal gets, how its parts are arranged, and perhaps even how long it will live. But biologists have long wondered what cellular timekeepers control these speeds, and why they vary.
A wave of research is starting to yield answers for one of the many clocks that control the workings of cells. There is a clock in early embryos that beats out a regular rhythm by activating and deactivating genes. This ‘segmentation clock’ creates repeating body segments such as the vertebrae in our spines. This is the timepiece that Ebisuya has made in her lab.
“I’m interested in biological time,” says Ebisuya, a developmental biologist at the European Molecular Biology Laboratory Barcelona. “But lifespan or gestation period, they are too long for me to study.” The swift speed of the segmentation clock makes it an ideal model system, she says.
Topics: Biology, COVID-19, Dark Humor, Existentialism, Mathematics, Politics
Figures often beguile me, particularly when I have the arranging of them myself; in which case the remark attributed to Disraeli would often apply with justice and force: “There are three kinds of lies: lies, damned lies, and statistics.”
The current US population is 332,494,997 from Worldometers.info. Each link updates minute-by-minute, so by the time you read this, these figures will have changed.
(US COVID deaths/current US population) x 100 = 0.17%. Round up to 0.2%.
That's pretty low.
For the "freedom-loving libertarians" spring breaking in Miami, or Fort Lauderdale, Florida, and Corpus Christi, Texas - a thought experiment:
100,000 of you are about to dive into the ocean.
There is a 0.2% = 0.2/100 chance some of you will get devoured by sharks.
100,000 x (0.2/100) = 200 dead spring breakers.
So, out of 100,000 - 200 = 99,800, or 99.8% have a very good chance of not becoming "chicken of the sea," and surviving your spring break. The dilemma is, there will still be blood in the water. Blood that carries pathogens that despite your "Y" swimming lessons and the saline environment, you might ingest red tide, and suffer the consequences.
The problem is, your 0.2% chance is not zero. Under normal circumstances (and pandemics are once-in-a-century "not normal"), there's no libertarian case for this:
CDC is closely monitoring these variants of concern (VOC). These variants have mutations in the virus genome that alter the characteristics and cause the virus to act differently in ways that are significant to public health (e.g., causes more severe disease, spreads more easily between humans, requires different treatments, changes the effectiveness of current vaccines).
Topics: Biology, Chemistry, DNA, Nobel Prize, Research, Women in Science
This year’s (2020) Nobel Prize in Chemistry has been awarded to two scientists who transformed an obscure bacterial immune mechanism, commonly called CRISPR, into a tool that can simply and cheaply edit the genomes of everything from wheat to mosquitoes to humans.
The award went jointly to Emmanuelle Charpentier of the Max Planck Unit for the Science of Pathogens and Jennifer Doudna of the University of California, Berkeley, “for the development of a method for genome editing.” They first showed that CRISPR—which stands for clustered regularly interspaced short palindromic repeats—could edit DNA in an in vitro system in a paper published in the 28 June 2012 issue of Science. Their discovery was rapidly expanded on by many others and soon made CRISPR a common tool in labs around the world. The genome editor spawned industries working on making new medicines, agricultural products, and ways to control pests.
Many scientists anticipated that Feng Zhang of the Broad Institute, who showed 6 months later that CRISPR worked in mammalian cells, would share the prize. The institutions of the three scientists are locked in a fierce patent battle over who deserves the intellectual property rights to CRISPR’s discovery, which some estimate could be worth billions of dollars.
“The ability to cut DNA where you want has revolutionized the life sciences. The genetic scissors were discovered 8 years ago, but have already benefited humankind greatly,” Pernilla Wittung Stafshede, a chemical biologist at the Chalmers University of Technology, said at the prize briefing.
Although scientists were not surprised Doudna and Charpentier won the prize, Charpentier was stunned. “As much as I have been awarded a number of prizes, it’s something you hear, but you don’t completely connect,” she said in a phone call with the Nobel Prize officials. “I was told a number of times that when it happens, you’re very surprised and feel that it’s not real.”
At a press briefing today, Doudna noted she was asleep and missed the initial calls from Sweden, only waking up to answer the phone finally when a Nature reporter called. "She wanted to know if I could comment on the Nobel and I said, Well, who won it? And she was shocked that she was the person to tell me."
1 Soap, shampoo, and worm-like micelles Soaps and shampoos are made from amphiphilic molecules with water-loving (red) and water-hating (blue) parts that arrange themselves to form long tubes known as “worm-like micelles”. Entanglements between the tubes give these materials their pleasant, sticky feel. b The micelles can, however, disentangle themselves, just as entangled long-chain polymer molecules can slide apart too. In polymers, this process can be modeled by imagining the molecule sliding, like a snake, out of an imaginary tube formed by the surrounding spatial constraints. c Worm-like micelles can also morph their architecture by performing reconnections (left), breakages (down), and fusions (right). These operations occur randomly along the backbone, are in thermal equilibrium, and reversible. (Courtesy: Davide Michieletto)
Topics: Biology, DNA, Physics, Polymer Science, Research
DNA molecules are not fixed objects – they are constantly getting broken up and glued back together to adopt new shapes. Davide Michieletto explains how this process can be harnessed to create a new generation of “topologically active” materials.
Call me naïve, but until a few years ago I had never realized you can actually buy DNA. As a physicist, I’d been familiar with DNA as the “molecule of life” – something that carries genetic information and allows complex organisms, such as you and me, to be created. But I was surprised to find that biotech firms purify DNA from viruses and will ship concentrated solutions in the post. In fact, you can just go online and order DNA, which is exactly what I did. Only there was another surprise in store.
When the DNA solution arrived at my lab in Edinburgh, it came in a tube with about half a milligram of DNA per centimeter cube of water. Keen to experiment on it, I tried to pipette some of the solution out, but it didn’t run freely into my plastic tube. Instead, it was all gloopy and resisted the suction of my pipette. I rushed over to a colleague in my lab, eagerly announcing my amazing “discovery”. They just looked at me like I was an idiot. Of course, solutions of DNA are gloopy.
I should have known better. It’s easy to idealize DNA as some kind of magic material, but it’s essentially just a long-chain double-helical polymer consisting of four different types of monomers – the nucleotides A, T, C, and G, which stack together into base pairs. And like all polymers at high concentrations, the DNA chains can get entangled. In fact, they get so tied up that a single human cell can have up to 2 m of DNA crammed into an object just 10 μm in size. Scaled up, it’s like storing 20 km of hair-thin wire in a box no bigger than your mobile phone.
a, Manhattan plot of a genome-wide association study of 3,199 hospitalized patients with COVID-19 and 897,488 population controls. The dashed line indicates genome-wide significance (P = 5 × 10−8). Data were modified from the COVID-19 Host Genetics Initiative2 (https://www.covid19hg.org/). b, Linkage disequilibrium between the index risk variant (rs35044562) and genetic variants in the 1000 Genomes Project. Red circles indicate genetic variants for which the alleles are correlated to the risk variant (r2 > 0.1) and the risk alleles match the Vindija 33.19 Neanderthal genome. The core Neanderthal haplotype (r2 > 0.98) is indicated by a black bar. Some individuals carry longer Neanderthal-like haplotypes. The location of the genes in the region is indicated below using standard gene symbols. The x-axis shows hg19 coordinates.
Topics: Biology, COVID-19, Genetics, Research
Abstract
A recent genetic association study1 identified a gene cluster on chromosome 3 as a risk locus for respiratory failure after infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). A separate study (COVID-19 Host Genetics Initiative)2 comprising 3,199 hospitalized patients with coronavirus disease 2019 (COVID-19) and control individuals showed that this cluster is the major genetic risk factor for severe symptoms after SARS-CoV-2 infection and hospitalization. Here we show that the risk is conferred by a genomic segment of around 50 kilobases in size that is inherited from Neanderthals and is carried by around 50% of people in South Asia and around 16% of people in Europe.
Main
The COVID-19 pandemic has caused considerable morbidity and mortality and has resulted in the death of over a million people to date3. The clinical manifestations of the disease caused by the virus, SARS-CoV-2, vary widely in severity, ranging from no or mild symptoms to rapid progression to respiratory failure4. Early in the pandemic, it became clear that advanced age is a major risk factor, as well as being male and some co-morbidities5. These risk factors, however, do not fully explain why some people have no or mild symptoms whereas others have severe symptoms. Thus, genetic risk factors may have a role in disease progression. A previous study1 identified two genomic regions that are associated with severe COVID-19: one region on chromosome 3, which contains six genes, and one region on chromosome 9 that determines ABO blood groups. Recently, a dataset was released by the COVID-19 Host Genetics Initiative in which the region on chromosome 3 is the only region that is significantly associated with severe COVID-19 at the genome-wide level (Fig. 1a). The risk variant in this region confers an odds ratio for requiring hospitalization of 1.6 (95% confidence interval, 1.42–1.79) (Extended Data Fig. 1).
The genetic variants that are most associated with severe COVID-19 on chromosome 3 (45,859,651–45,909,024 (hg19)) are all in high linkage disequilibrium (LD)—that is, they are all strongly associated with each other in the population (r2 > 0.98)—and span 49.4 thousand bases (kb) (Fig. 1b). This ‘core’ haplotype is furthermore in weaker linkage disequilibrium with longer haplotypes of up to 333.8 kb (r2 > 0.32) (Extended Data Fig. 2). Some such long haplotypes have entered the human population by gene flow from Neanderthals or Denisovans, extinct hominins that contributed genetic variants to the ancestors of present-day humans around 40,000–60,000 years ago6,7. We, therefore, investigated whether the haplotype may have come from Neanderthals or Denisovans.
Anthony Fauci has advised seven presidents on public health, most recently serving as chief medical advisor to President Joe Biden. | NIAID
Topics: Biology, COVID-19, Research, Science
Anthony Fauci – Director of the National Institute of Allergy and Infectious Diseases, an expert on HIV and immunoregulation, and the de facto public face of a science-based recovery from COVID-19 – has been named the winner of the 2021 Philip Hauge Abelson Prize, awarded annually by the American Association for the Advancement of Science to a scientist or public servant who has contributed significantly to the advancement of science in the United States.
Fauci is “an outstanding scientist with more than a thousand publications” and “an exceptional public servant, having been at the forefront of the world’s efforts to combat diverse infectious diseases for over 40 years,” wrote Alan Leshner, former chief executive officer of AAAS, in nominating Fauci for the prize. The prize committee cited Fauci’s “extraordinary contributions to science and medicine” and his service that has shaped research and public policy.
Bioinspiration and biomimicry involve studying how living organisms do something and using that insight to develop new technologies. Pit vipers have two special organs on their heads called loreal pits that allow them to “see” the infrared radiation given off by their warm-blooded prey. Now, Pradeep Sharma and colleagues have worked out that the snakes use cells that act as a soft pyroelectric material to convert infrared radiation into electrical signals that can be processed by their nervous systems. As well as potentially solving a longstanding puzzle in snake biology, the work could also aid the development of thermoelectric transducers based on soft, flexible structures rather than stiff crystals.
Topics: Biology, Civics, Civil Rights, COVID-19, Existentialism, Human Rights
I have taken the following vaccines this year: Pneumonia, Seasonal Influenza (Flu), Shingles in two booster shots.
Therefore, I am very likely to take the Coronavirus vaccine either offered by Pfizer or Moderna.
Pfizer is pushing back on the Trump administration's suggestion that the company is having trouble producing its COVID-19 vaccine, saying it's ready to ship millions more doses – once the government asks for them. As the company spoke out, several states said their vaccine allocations for next week have been sharply reduced.
Here's what the key players are saying about a complicated situation:
What Pfizer says
"Pfizer is not having any production issues with our COVID-19 vaccine, and no shipments containing the vaccine are on hold or delayed," CEO Albert Bourla said via Twitter. His company says it has completed every shipment the U.S. government has requested.
"We have millions more doses sitting in our warehouse but, as of now, we have not received any shipment instructions for additional doses," Pfizer said in a statement.
The company also noted that in the past week, it shipped 2.9 million doses of the vaccine it developed with BioNTech in what is widely seen as a breakthrough in the nation's fight against the coronavirus.
Unlike the 1918 pandemic, I don't think it will take us a decade to come to some sense of normalcy. I am concerned, from a cultural perspective, that the vaccine spreads equitably.
We have a reason to be suspicious. The Tuskegee Experiment happened over four decades, affected hundreds of lives, allowing syphilis to infect men, women, and children. It makes trusting authorities with our lives a bit problematic. As I've said, if it helps anyone reading this entry, I will take the vaccine. I would like to get back to some sense of normalcy.
The revelation of the recent Russian hacks is the equivalent of a Cyber Pearl Harbor. Our nuclear triad material, three states (including Austin, Texas), the Central Intelligence Agency, Treasury, NASA, Commerce, et al. This is a stickup. Think the city, lights: sewage. Like a burglar, we could all be held hostage by a foreign power. To paraphrase a false claim attributed to Nikita Khrushchev, Putin could literally "bury us without firing a shot."
The shenanigans of the current obtuse, malignant, narcissistic, and incompetent administration will come to an end. Vaccines will go out, modeled by an incoming administration that like previous democratic ones before them, have to shovel the country out of the smoldering ruin that the previous republican one left the country in. They will, of course, delay vaccines, they will of course, try to sabotage on the way out. They are the steroids equivalent of Clinton-to-Bush removing the W keys, and costing the government approximately $15,000. It was disappointing and sophomoric. This stunt is petty, malevolent, and deadly. We have crossed the Rubicon of 300,000 dead Americans. At a rate of a 9/11 per day, we'll reach 400,000 by inauguration. Delay during a pandemic will kill more Americans, but I guess that's not a big concern to a malignant narcissist.
But I am hopeful for a brighter spring.
Mango Mussolini can do a lot of damage in 33 days, but it's 33 days at noon when he loses access to the nuclear football, he loses the presidential immunity that protects him from an indictment, not that Letitia James, Cyrus Vance, SDNY, or EDNY are bothered by his threats of family and self pardons. His crimes in New York are state felonies, likely involving inflating his wealth, or decreasing it when it suited him. We'll likely find out he's not as rich as he claims to be. He cashed a series of diminishing value checks sent as a gag by Spy Magazine, proving himself a bit player in the New York Real Estate market. He'll need every penny he's grifting from his deluded followers to stay out of prison. Not that I'm sympathetic: but grift on this constant level has to be exhausting, and depleting of finance, and bodily constitution.
The evil energizer bunny has to run out of gas sometimes. His tweets will reach a limited audience. Cities that haven't YET gotten paid for his previous rallies will refuse to book him. He's proposing bringing back The Apprentice because his "power" is his celebrity, and that dwindles quickly without cameras on you constantly. He can call it Apprentice, 2024: Finding a Vice President (a tacit admittance Pence didn't help him win re-election). Several sources say Twitter might finally remove him, not the conviction to "do the right thing," just that if his followers dwindle, they have no one to gather metadata from for marketing purposes. It's business, and a one-term president probably isn't good for the bottom-line.
That's all fine and good, Donald unless you're spending your evenings at Riker's. Maybe they'll station you at the Queens Detention Complex. He can see the old neighborhood, while the rest of us heal from his madness. We will get through this.
With COVID-19 reaching the most dangerous levels the U.S. has seen since the pandemic began, the country faces a problematic holiday season. Despite the risk, many people are likely to travel using various forms of transportation that will inevitably put them in relatively close contact with others. Many transit companies have established frequent cleaning routines, but evidence suggests that airborne transmission of the novel coronavirus poses a greater danger than surfaces. The virus is thought to be spread primarily by small droplets, called aerosols, that hang in the air and larger droplets that fall to the ground within six feet or so. Although no mode of public transportation is completely safe, there are some concrete ways to reduce risk, whether on an airplane, train or bus—or even in a shared car.
At a casual glance, air travel might seem like the perfect recipe for COVID transmission: it packs dozens of people into a confined space, often for hours at a time. But many planes have excellent high-efficiency particulate air (HEPA) filters that capture more than 99 percent of particles in the air, including microbes as SARS-CoV-2, the coronavirus that causes COVID. When their recirculation systems are operating, most commercial passenger jets bring in outside air in a top-to-bottom direction about 20 to 30 times per hour. This results in a 50–50 mix of outside and recirculated air and reduces the potential for the airborne spread of a respiratory virus. Many airlines now require passengers to wear a mask during flights except for mealtimes, and some are blocking off middle seats to allow more distancing between people. Companies have also implemented rigorous cleaning procedures between flights. So how does this translate into overall risk?
“An airplane cabin is probably one of the most secure conditions you can be in,” says Sebastian Hoehl of the Institute for Medical Virology at Goethe University Frankfurt in Germany, who has co-authored two papers on COVID-19 transmission on specific flights, which were published in JAMA Network Open and the New England Journal of Medicine, respectfully. Still, a handful of case studies have found that limited transmission can take place on board. One such investigation of a 10-hour journey from London to Hanoi starting on March 1 found that 15 people were likely infected with COVID-19 in-flight—and that 12 of them had sat within a couple of rows of a single symptomatic passenger in business class. (The results were published this month in the U.S. Centers for Disease Control and Prevention’s journal Emerging Infectious Diseases.) Most of these flights occurred early on in the pandemic, however, and in the case of the March 1 flight, masks were likely not worn, the researchers wrote. Meanwhile, a recent Department of Defense study modeled the risk of in-flight infection using mannequins exhaling simulated virus particles and found that a person would have to be exposed to an infectious passenger for at least 54 hours to get an infectious dose. This finding assumes the infected passenger is wearing a surgical mask, however, and it does not account for the dangers involved in removing the mask for meals or talking or in moving about on the plane.
The year 2020 has been defined by the COVID-19 pandemic: The novel coronavirus responsible for it has infected millions of people and caused more than a million deaths. Like HIV, Zika, Ebola, and many influenza strains, the coronavirus made the evolutionary jump from animals to humans before wreaking widespread havoc. The battle to control it continues. When a disease outbreak is identified—usually through an anomalous spike in cases with similar symptoms—scientists rush to understand the new illness. What type of microbe causes the infection? Where did it come from? How does the infection spread? What are its symptoms? What drugs could treat it? In the current epidemic, science has proceeded at a frenetic pace. Virus genomes are quickly sequenced and analyzed, case and death numbers are visualized daily, and hundreds of preprints are shared every day.
Some scientists rush for their microscopes and lab coats to study a new infection; others leap for their calculators and code. A handful of metrics can characterize a new outbreak, guide public health responses, and inform complex models that can forecast the epidemic’s trajectory. Infectious disease epidemiologists, mathematical biologists, biostatisticians, and others with similar expertise try to answer several questions: How quickly is the infection spreading? What fraction of transmission must be blocked to control the spread? How long is someone infectious? How likely are infected people to be hospitalized or die?
Physics is often considered the most mathematical science, but theory and rigorous mathematical analysis also underlie ecology, evolutionary biology, and epidemiology.1 Ideas and people constantly flow between physics and those fields. In fact, the idea of using mathematics to understand infectious disease spread is older than germ theory itself. Daniel Bernoulli of fluid-mechanics fame devised a model to predict the benefit of smallpox inoculations2 in 1760, and Nobel Prize-winning physician Ronald Ross created mathematical models to encourage the use of mosquito control to reduce malaria transmission.3 Some of today’s most prolific infectious disease modelers originally trained as physicists, including Neil Ferguson of Imperial College London, an adviser to the UK government on its COVID-19 response, and Vittoria Colizza of Sorbonne University in Paris, a leader in network modeling of disease spread.
This article introduces the essential mathematical quantities that characterize an outbreak, summarizes how scientists calculate those numbers, and clarify the nuances in interpreting them. For COVID-19, estimates of those quantities are being shared, debated, and updated daily. Physicists are used to distilling real-world complexity into meaningful, parsimonious models, and they can serve as allies in communicating those ideas to the public.
Alison Hill is an assistant professor in the Institute for Computational Medicine and the infectious disease dynamics group at Johns Hopkins University in Baltimore, Maryland. She is also a visiting scholar at Harvard University in Cambridge, Massachusetts.
Living through a pandemic has resulted in phrases like RT-PCR, immune response, and aerosolized droplets becoming part of the regular vocabulary for a portion of the population. It has also underscored the important role that we all have to play as scientists in communicating science to the public. As research related to COVID-19 has moved forward at unprecedented rates, misinformation has also multiplied and spread at a terrifying pace. And no matter where you stand politically, all of this happening in an election year for the US further underscores the ways in which science has become an increasingly partisan issue.
Did I mention that the holidays are also approaching? While gatherings of family and friends may look different this year, you may still be anticipating a challenging conversation over a holiday meal with someone who has different viewpoints from yours.
Our situation comes with innumerable challenges. However, it also provides an opportunity for scientists to make a powerful contribution to society and demonstrate the value of science education. Whether or not you are engaging in research directly related to COVID-19, you can help those around you separate facts from myths, interpret the data that are available, and make better-informed decisions.
This realization occurred to me this spring. As positive cases of COVID-19 were just starting to appear in the US, I found myself talking to my physical therapist about the virus and potential treatments. Although I don’t work in drug development, I understand enough of the chemistry to know how nucleoside analogs such as the drug remdesivir function. I excitedly explained how viruses are sloppier than normal human cells when replicating their genomes and how researchers can capitalize on this to make drugs. A few days later, I found myself having a similar conversation with my mom. I wasn’t in a place to predict the efficacy of any drug, but I could at least explain why antivirals like remdesivir had a shot at working, while hydroxychloroquine was less promising. After these two conversations, it struck me that I could also share this knowledge with a broader population on social media.
Science communication is a skill that takes practice to develop, and I am still learning and growing. The stakes couldn’t be higher, but the important part is that any scientist can build this capability to communicate effectively.
Continued: It triggered a big outbreak. At least 97 people who attended the conference, or lived in a household with someone who did, tested positive.
The Biogen meeting had become a superspreading event. Eventually, the virus spread from the meeting across Massachusetts and to other states. A recent study estimates it led to tens of thousands of cases in the Boston area alone.
Superspreading
COVID-19 superspreading events have been reported around the world. They happen in all sorts of places: bars and barbecues, gyms and factories, schools and churches, and on ships.
And even at the White House.
But why do these disease clusters occur—and why are they so important?
The reproduction rate
COVID-19 and many other diseases transmit from person to person. The reproduction rate, R, determines how fast a disease can spread.
R denotes the number of people infected, on average, by a single infected person. If R is 2, the number of cases doubles in every generation: from one infected person to two, to four, to eight, and so on.
Topics: Biology, Computer Modeling, COVID-19, Research
TOKYO (Reuters) – A Japanese supercomputer showed that humidity can have a large effect on the dispersion of virus particles, pointing to heightened coronavirus contagion risks in dry, indoor conditions during the winter months.
The finding suggests that the use of humidifiers may help limit infections during times when window ventilation is not possible, according to a study released on Tuesday by research giant Riken and Kobe University.
The researchers used the Fugaku supercomputer to model the emission and flow of virus-like particles from infected people in a variety of indoor environments.
Air humidity of lower than 30% resulted in more than double the amount of aerosolized particles compared to levels of 60% or higher, the simulations showed.
The study also indicated that clear face shields are not as effective as masks in preventing the spread of aerosols. Other findings showed that diners are more at risk from people to their side compared to across the table, and the number of singers in choruses should be limited and spaced out.
Quantum dots diffuse within living cells in a nearly two-dimensional fashion. This result, which was obtained using a new 3D microscopy technique that can track single particles, sheds fresh light on intracellular diffusion – a process that is critical for moving molecules around the cell and for mediating other important activities. According to study leader Hui Li, a biophysicist at the Chinese Academy of Sciences in Beijing and Beijing Normal University, the 2D motion he and his colleagues observed is robust and stems from the complex architectures of the flat “adherent” biological cells they studied.
Quantum dots make ideal probes for studying intracellular diffusion in living cells. They are similar in size to intracellular macromolecules and can be made to mimic biological materials relatively easily, by coating their surfaces with organic molecules. Previous studies, however, relied mainly on two-dimensional measurements of their movement, with the assumption that three-dimensional diffusion is an extension of 2D diffusion and is isotropic.</em>
Why cannot we write the entire 24 volumes of the Encyclopedia Britannica on the head of a pin? Dr. Richard P. Feynman, "There's Plenty of Room at the Bottom," said to be the seminal talk that started the concept of atomic-level engineering, soon known as nanotechnology, (named by Professor Norio Taniguchi, 1974, of the Tokyo Science University).
The intricate arrangement of base pairs in our DNA encodes just about everything about us. Now, DNA contains the entirety of “The Wonderful Wizard of Oz” as well.
A team of University of Texas Austin scientists just vastly improved the storage capacity of DNA and managed to encode the entire novel — translated into the geek-friendly language of Esperanto — in a double strand of DNA far more efficiently than has been done before. DNA storage isn’t new, but this work could help finally make it practical.
Big tech companies like Microsoft are already exploring DNA-storage technology, as the biomolecule can encode several orders of magnitude more information per unit volume than a hard drive. But DNA is particularly error-prone. It can easily be damaged and erase whatever’s stored on it.
“The key breakthrough is an encoding algorithm that allows accurate retrieval of the information even when the DNA strands are partially damaged during storage,” molecular biologist Ilya Finkelstein said in a UT Austin press release.
FIG. 1. (a) Long-legs cellar spider. (b) Reeling mechanism. (c) Manufacturing process of decorating spider silk. (d) Spider silk with dome lens placed on a dedicated holder. (e) Microphotograph of dome lens. (f) Laser scanning digital microscope system for measuring dome lens. (g) Schematic diagram of the dome lens for generating PNJ.
In this work, we thoroughly investigate the shape, size, and location of the photonic nanojets (PNJs) generated from the illuminated dome lens. The silk fiber is directly extracted from the cellar spider and used to form the dome lens by its liquid-collecting ability. The solidified dielectric dome lenses with different dimensions are obtained by using ultraviolet curing. Numerical and experimental results show that the long PNJs are strongly modulated by the dimension of the dome lens. The optimal PNJ beam shaping is achieved by using a mesoscale dielectric dome lens. The PNJ with a long focal length and a narrow waist could be used to scan over a target for large-area imaging. The silk fiber with a dome lens is especially useful for bio-photonic applications by combining its biocompatibility and flexibility.
A lattice scaffold 3D printed directly onto soft living tissue. (Courtesy: Ohio State University)
Topics: 3D Printing, Bioengineering, Biofabrication, Biology, Tissue Engineering
Tissue engineering is an emerging field in which cells, biomaterials and biotechnologies are employed to replace or regenerate damaged or diseased tissues. Currently, this is achieved by generating a biomaterial scaffold outside of the body, maturation in a bioreactor and then surgically implanting the created tissue into the patient. This surgery, however, poses the added risk of infection, increases recovery time and may even negate the therapeutic benefits of the implant.
To prevent such complications, a US research team is developing a way to fabricate 3D tissue scaffolds inside a living patient – so-called intracorporeal tissue engineering. The researchers, from the Terasaki Institute, Ohio State University and Pennsylvania State University, aim to use robotic direct-write 3D printing to dispense cell-laden biomaterials (bioinks) in a highly precise, programmable manner. The printed bioinks are delivered through minimally invasive surgical incisions and the body itself acts as the bioreactor for maturation.
Any technique used to directly print tissues inside the body, however, must meet a specific set of requirements. The biomaterial must be 3D printable at body temperature (37 °C), for example, and all procedural steps should not harm the patient. For example, current methods use UV light to crosslink the constructed tissue, which is not safe for use within the body.
To meet these requirements, the team produced a specially-formulated bioink designed for printing directly in the body. They used the hydrogel gelatin methacryloyl (GelMA) as the biomaterial, and introduced Laponite and methylcellulose as rheological modifiers to enhance printability. “This bio-ink formulation is 3D printable at physiological temperature, and can be crosslinked safely using visible light inside the body,” explains first author Ali Asghari Adib.
A game-changing technique for imaging molecules known as cryo-electron microscopy has produced its sharpest pictures yet — and, for the first time, discerned individual atoms in a protein.
By achieving atomic resolution using cryogenic-electron microscopy (cryo-EM), researchers will be able to understand, in unprecedented detail, the workings of proteins that cannot easily be examined by other imaging techniques, such as X-ray crystallography.
The breakthrough, reported by two laboratories late last month, cements cryo-EM’s position as the dominant tool for mapping the 3D shapes of proteins, say scientists. Ultimately, these structures will help researchers to understand how proteins work in health and disease, and lead to better drugs with fewer side effects.
“It’s really a milestone, that’s for sure. There’s really nothing to break anymore. This was the last resolution barrier,” says Holger Stark, a biochemist and electron microscopist at the Max Planck Institute for Biophysical Chemistry in Göttingen, Germany, who led one of the studies1. The other2 was led by Sjors Scheres and Radu Aricescu, structural biologists at the Medical Research Council Laboratory of Molecular Biology (MRC-LMB) in Cambridge, UK. Both were posted on the bioRxiv preprint server on 22 May.
“True ‘atomic resolution’ is a real milestone,” adds John Rubinstein, a structural biologist at the University of Toronto in Canada. Getting atomic-resolution structures of many proteins will still be a daunting task because of other challenges, such as a protein’s flexibility. "These preprints show where one can get to if those other limitations can be addressed,” he adds.
On March 26, 1953, American medical researcher Dr. Jonas Salk announces on a national radio show that he has successfully tested a vaccine against poliomyelitis, the virus that causes the crippling disease of polio. In 1952—an epidemic year for polio—there were 58,000 new cases reported in the United States, and more than 3,000 died from the disease. For promising eventually to eradicate the disease, which is known as “infant paralysis” because it mainly affects children, Dr. Salk was celebrated as the great doctor-benefactor of his time.
Polio, a disease that has affected humanity throughout recorded history, attacks the nervous system and can cause varying degrees of paralysis. Since the virus is easily transmitted, epidemics were commonplace in the first decades of the 20th century. The first major polio epidemic in the United States occurred in Vermont in the summer of 1894, and by the 20th century thousands were affected every year. In the first decades of the 20th century, treatments were limited to quarantines and the infamous “iron lung,” a metal coffin-like contraption that aided respiration. Although children, and especially infants, were among the worst affected, adults were also often afflicted, including future president Franklin D. Roosevelt, who in 1921 was stricken with polio at the age of 39 and was left partially paralyzed. Roosevelt later transformed his estate in Warm Springs, Georgia, into a recovery retreat for polio victims and was instrumental in raising funds for polio-related research and the treatment of polio patients.
According to the link, the trials weren't without consequence:
In 1954, clinical trials using the Salk vaccine and a placebo began on nearly two million American schoolchildren. In April 1955, it was announced that the vaccine was effective and safe, and a nationwide inoculation campaign began. Shortly thereafter, tragedy struck in the Western and mid-Western United States, when more than 200,000 people were injected with a defective vaccine manufactured at Cutter Laboratories of Berkeley, California. Thousands of polio cases were reported, 200 children were left paralyzed and 10 died.
The Salk method - created in 1954 - is to inject inert forms of the virus into the bloodstream (made inactive with formaldehyde), then the body develops defenses, or antibodies against them, however it didn't prevent the virus from thriving in the intestines. His colleague, Dr. Sabin, injected an attenuated vaccine (1961), meaning it wasn't a fully inert strain so that the gut environment could be addresses. More here. The Sabin mostly eliminated Polio in the world, but the U.S. still uses the Salk method.
April 8, 1950, Mildred Dean married Robert H. Goodwin. Mom would earn an associates degree as a PN - practical nurse, and Pop worked for Hanes Dye and Finishing as an operator, under grueling conditions and few opportunities to promote until retirement. My big sister - in grade school at the time - would come along for the ride.
1954 - the year of the Polio vaccine, was also the date of Brown vs. Board of Education, where the Supreme Court reached a non-partisan, 9-0 decision, that education in America was separate and unequal.
1961 was the year the Sabin vaccine was created, and a couple who had been married twelve years got pregnant around Thanksgiving - I would be born August of 1962. I likely was beneficiary of the Sabin method at Kate Biting Hospital in Winston-Salem, NC, also the black hospital where my mother worked.
We cannot "patent the sun." But one can be grateful for the impact of invention by Dr. Salk and Dr. Sabin on the quality of life given to everyone in my generation, and forward, and African American parents wise enough to wait for it.
