Electrons moving around in a molecule might not seem like the plot of an interesting movie. But a group of scientists will receive the 2023 Nobel Prize in physics for research that essentially follows the movement of electrons using ultrafast laser pulses, like capturing frames in a video camera.

However, electrons, which partly make up atoms and form the glue that bonds atoms in molecules together, don’t move around on the same time scale people do. They’re much faster. So, the tools that physicists like me use to capture their motion have to be really fast – attosecond-scale fast.

One attosecond is one billionth of a billionth of a second (10⁻¹⁸ second) – the ratio of one attosecond to one second is the same as the ratio of one second to the age of the universe.

Attosecond pulses

In photography, capturing clear images of fast objects requires a camera with a fast shutter or a fast strobe of light to illuminate the object. By taking multiple photos in quick succession, the motion of the object can be clearly resolved.

The time scale of the shutter or the strobe must match the time scale of motion of the object – if not, the image will be blurred. This same idea applies when researchers attempt to image the ultrafast motion of electrons. Capturing attosecond-scale motion requires an attosecond strobe. The 2023 Nobel laureates in physics made seminal contributions to the generation of such attosecond laser strobes, which are very short pulses generated using a powerful laser.

Imagine the electrons in an atom are constrained within the atom by a wall. When a femtosecond (10⁻¹⁵ second) laser pulse from a high-powered femtosecond laser is directed at atoms of a noble gas such as argon, the strong electric field in the pulse lowers the wall.

This is possible because the laser electric field is comparable in strength to the electric field of the nucleus of the atom. Electrons see this lowered wall and pass through in a bizarre process called quantum tunneling.

As soon as the electrons exit the atom, the laser’s electric field captures them, accelerates them to high energies and slams them back into their parent atoms. This process of recollision results in creation of attosecond bursts of laser light.

Attosecond movies

So how do physicists use these ultrashort pulses to make movies of electrons at the attosecond scale?

Conventional movies are made one scene at a time, with each instant captured as a frame with video cameras. The scenes are then stitched together to form the complete movie.

Attosecond movies of electrons use a similar idea. The attosecond pulses act as strobes, lighting up the electrons so researchers can capture their image, over and over again as they move – like a movie scene. This technique is called pump-probe spectroscopy.

However, imaging electron motion directly inside atoms is currently challenging, though researchers are developing several approaches using advanced microscopes to make direct imaging possible.

Typically, in pump-probe spectroscopy, a “pump” pulse gets the electron moving and starts the movie. A “probe” pulse then lights up the electron at different times after the arrival of the pump pulse, so it can be captured by the “camera,” such as a photoelectron spectrometer.

The information on the motion of electrons, or the “image,” is captured using sophisticated techniques. For example, a photoelectron spectrometer detects how many electrons were removed from the atom by the probe pulse, or a photon spectrometer measures how much of the probe pulse was absorbed by the atom.

The different “scenes” are then stitched together to make the attosecond movies of electrons. These movies help provide fundamental insight, with help from sophisticated theoretical models, into attosecond electronic behavior.

For example, researchers have measured where the electric charge is located in organic molecules at different times, on attosecond time scales. This could allow them to control electric currents on the molecular scale.

Future applications

In most scientific research, fundamental understanding of a process leads to control of the process, and such control leads to new technologies. Curiosity-driven research can lead to unimaginable applications in the future, and attosecond science is likely no different.

Understanding and controlling the behavior of electrons on the attosecond scale could enable researchers to use lasers to control chemical reactions that they can’t by other means. This ability could help engineer new molecules that cannot be created with existing chemical techniques.

The ability to modify electron behavior could lead to ultrafast switches. Researchers could potentially convert an electric insulator to a conductor on attosecond scales to increase the speed of electronics. Electronics currently process information at the picosecond scale, or 10⁻¹² of a second.

The short wavelength of attosecond pulses, which is typically in the extreme-ultraviolet, or EUV, regime, may see applications in EUV lithography in the semiconductor industry. EUV lithography uses laser light with a very short wavelength to etch tiny circuits on electronic chips.

In the recent past, free-electron lasers such as the Linac Coherent Light Source at SLAC National Accelerator Laboratory in the United States have emerged as a source of bright X-ray laser light. These now generate pulses on the attosecond scale, opening many possibilities for research using attosecond X-rays.

Ideas to generate laser pulses on the zeptosecond (10⁻²¹ second) scale have also been proposed. Scientists could use these pulses, which are even faster than attosecond pulses, to study the motion of particles like protons within the nucleus.

With numerous research groups actively working on exciting problems in attosecond science, and with 2023’s Nobel Prize in physics recognizing its importance, attosecond science has a long and bright future.

Niranjan Shivaram receives funding from the National Science Foundation and U.S. Department of Energy.

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Living cells work better than dying cells, right? However, this is not always the case: your cells often sacrifice themselves to keep you healthy. The unsung hero of life is death.

While death may seem passive, an unfortunate ending that just “happens,” the death of your cells is often extremely purposeful and strategic. The intricate details of how and why cells die can have significant effects on your overall health.

There are over 10 different ways cells can “decide” to die, each serving a particular purpose for the organism. My own research explores how immune cells switch between different types of programmed death in scenarios like cancer or injury.

Programmed cell death can be broadly divided into two types that are crucial to health: silent and inflammatory.

Quietly exiting: silent cell death

Cells can often become damaged because of age, stress or injury, and these abnormal cells can make you sick. Your body runs a tight ship, and when cells step out of line, they must be quietly eliminated before they overgrow into tumors or cause unnecessary inflammation where your immune system is activated and causes fever, swelling, redness and pain.

Your body swaps out cells every day to ensure that your tissues are made up of healthy, functioning ones. The parts of your body that are more likely to see damage, like your skin and gut, turn over cells weekly, while other cell types can take months to years to recycle. Regardless of the timeline, the death of old and damaged cells and their replacement with new cells is a normal and important bodily process.

Silent cell death, or apoptosis, is described as silent because these cells die without causing an inflammatory reaction. Apoptosis is an active process involving many proteins and switches within the cell. It’s designed to strategically eliminate cells without alarming the rest of the body.

Sometimes cells can detect that their own functions are failing and turn on executioner proteins that chop up their own DNA, and they quietly die by apoptosis. Alternatively, healthy cells can order overactive or damaged neighbor cells to activate their executioner proteins.

Apoptosis is important to maintaining a healthy body. In fact, you can thank apoptosis for your fingers and toes. Fetuses initially have webbed fingers until the cells that form the tissue between them undergo apoptosis and die off.

Without apoptosis, cells can grow out of control. A well-studied example of this is cancer. Cancer cells are abnormally good at growing and dividing, and those that can resist apoptosis form very aggressive tumors. Understanding how apoptosis works and why cancer cells can disrupt it can potentially improve cancer treatments.

Other conditions can benefit from apoptosis research as well. Your body makes a lot of immune cells that all respond to different targets, and occasionally one of these cells can accidentally target your own tissues. Apoptosis is a crucial way your body can eliminate these immune cells before they cause unnecessary damage. When apoptosis fails to eliminate these cells, sometimes because of genetic abnormalities, this can lead to autoimmune diseases like lupus.

Another example of the role apoptosis plays in health is endometriosis, an understudied disease caused by the overgrowth of tissue in the uterus. It can be extremely painful and debilitating for patients. Researchers have recently linked this out-of-control growth in the uterus to dysfunctional apoptosis.

Whether it’s for development or maintenance, your cells are quietly exiting to keep your body happy and healthy.

Going out with a bang: inflammatory cell death

Sometimes, it is in your body’s best interest for cells to raise an alarm as they die. This can be beneficial when cells detect the presence of an infection and need to eliminate themselves as a target while also alerting the rest of the body. This inflammatory cell death is typically triggered by bacteria, viruses or stress.

Rather than quietly shutting down, cells undergoing inflammatory cell death will make themselves burst, or lyse, killing themselves and exploding inflammatory messengers as they go. These messengers tell your immune cells that there is a threat and prompts them to treat and fight the pathogen.

An inflammatory death would not be healthy for maintenance. If the normal recycling of your skin or gut cells caused an inflammatory reaction, you would feel sick a lot. This is why inflammatory death is tightly controlled and requires multiple signals to initiate.

Despite the riskiness of this grenadelike death, many infections would be impossible to fight without it. Many bacteria and viruses need to live around or inside your cells to survive. When specialized sensors on your cells detect these threats, they can simultaneously activate your immune system and remove themselves as a home for pathogens. Researchers call this eliminating the niche of the pathogen.

Inflammatory cell death plays a major role in pandemics. Yersinia pestis, the bacteria behind the Black Death, has evolved various ways of stopping human immune cells from mounting a response. However, immune cells developed the ability to sense this trickery and die an inflammatory death. This ensures that additional immune cells will infiltrate and eliminate the bacteria despite the bacteria’s best attempts to prevent a fight.

Although the Black Death is not as common nowadays, close relatives Yersinia pseudotuberculosis and Yersinia enterocolitica are behind outbreaks of food-borne illnesses. These infections are rarely fatal because your immune cells can aggressively eliminate the pathogen’s niche by inducing inflammatory cell death. For this reason, however, Yersinia infection can be more dangerous in immunocompromised people.

The virus behind the COVID-19 pandemic also causes a lot of inflammatory cell death. Studies show that without cell death the virus would freely live inside your cells and multiply. However, this inflammatory cell death can sometimes get out of control and contribute to the lung damage seen in COVID-19 patients, which can greatly affect survival. Researchers are still studying the role of inflammatory cell death in COVID-19 infection, and understanding this delicate balance can help improve treatments.

In good times and bad, your cells are always ready to sacrifice themselves to keep you healthy. You can thank cell death for keeping you alive.

Zoie Magri does not work for, consult, own shares in or receive funding from any company or organization that would benefit from this article, and has disclosed no relevant affiliations beyond their academic appointment.

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The New York Blood Center (NYBC) is absorbing two of Talaris Therapeutics’ autologous and allogeneic cell and gene therapy facilities to expand its CDMO capabilities and geological footprint in the US.

“We now have all the pieces in the continuum of manufacturing,” Chris Hillyer, CEO of NYBC Enterprises, told Endpoints News. 

The blood center has the non-profit business unit Cell Comprehensive Solutions with a clientele of pharma companies, biotechs and academic centers. CCS offers development and manufacturing of cell and gene therapies for preclinical and commercial-stage products.

On top of boosting its CDMO services, the acquisition expands the company’s reach to donors and patients, Hillyer noted. The blood center declined to detail how much the deal is worth.

The first site acquired from Talaris is in Louisville, KY, with the 20,000 square-foot facility capable of providing manufacturing capacity for Phase III trials, including cryopreservation storage, warehouse space and testing processes. The second, 6,000 square-foot facility in Houston houses analytical and process development capacity across viral vectors, mRNA and gene expression.

On Feb. 16, Talaris announced its restructuring plan to divest all its cell therapy activity, as well as discontinue two kidney transplant trials. Talaris first reduced its workforce by 33% in February, and a further 80 employees were laid off in April, which is 95% of the company’s remaining workforce.

Chief business officer Jay Mohr told Endpoints the blood center has already taken on some of Talaris’ employees following this acquisition and is looking to bring on more, but did not add further detail.

On May 11, NYBC launched a $50 million venture fund that has since made 10 investments in blood technology startups. When asked about the company’s next steps, Hillyer told Endpoints that he foresees “M&A activity, and internal and organic growth.”

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