Yet, a century ago, its discovery by Edwin Hubble, then an astronomer at Carnegie Observatories, opened humanity’s eyes as to how large the universe really is, and revealed that our Milky Way galaxy is just one of hundreds of billions of galaxies in the universe ushered in the coming-of-age for humans as a curious species that could scientifically ponder our own creation through the message of starlight. Carnegie Science and NASA are celebrating this centennial at the 245th meeting of the American Astronomical Society in Washington, D.C.

The seemingly inauspicious star, simply named V1, flung open a Pandora’s box full of mysteries about time and space that are still challenging astronomers today. Using the largest telescope in the world at that time, the Carnegie-funded 100-inch Hooker Telescope at Mount Wilson Observatory in California, Hubble discovered the demure star in 1923. This rare type of pulsating star, called a Cepheid variable, is used as milepost markers for distant celestial objects. There are no tape-measures in space, but by the early 20th century Henrietta Swan Leavitt had discovered that the pulsation period of Cepheid variables is directly tied to their luminosity.

Many astronomers long believed that the edge of the Milky Way marked the edge of the entire universe. But Hubble determined that V1, located inside the Andromeda “nebula,” was at a distance that far exceeded anything in our own Milky Way galaxy. This led Hubble to the jaw-dropping realization that the universe extends far beyond our own galaxy.

In fact Hubble had suspected there was a larger universe out there, but here was the proof in the pudding. He was so amazed he scribbled an exclamation mark on the photographic plate of Andromeda that pinpointed the variable star.

As a result, the science of cosmology exploded almost overnight. Hubble’s contemporary, the distinguished Harvard astronomer Harlow Shapley, upon Hubble notifying him of the discovery, was devastated. “Here is the letter that destroyed my universe,” he lamented to fellow astronomer Cecilia Payne-Gaposchkin, who was in his office when he opened Hubble’s message.

Just three years earlier, Shapley had presented his observational interpretation of a much smaller universe in a debate one evening at the Smithsonian Museum of Natural History in Washington. He maintained that the Milky Way galaxy was so huge, it must encompass the entirety of the universe. Shapley insisted that the mysteriously fuzzy “spiral nebulae,” such as Andromeda, were simply stars forming on the periphery of our Milky Way, and inconsequential.

Little could Hubble have imagined that 70 years later, an extraordinary telescope named after him, lofted hundreds of miles above the Earth, would continue his legacy. The marvelous telescope made “Hubble” a household word, synonymous with wonderous astronomy.

Today, NASA’s Hubble Space Telescope pushes the frontiers of knowledge over 10 times farther than Edwin Hubble could ever see. The space telescope has lifted the curtain on a compulsive universe full of active stars, colliding galaxies, and runaway black holes, among the celestial fireworks of the interplay between matter and energy.

Edwin Hubble was the first astronomer to take the initial steps that would ultimately lead to the Hubble Space Telescope, revealing a seemingly infinite ocean of galaxies. He thought that, despite their abundance, galaxies came in just a few specific shapes: pinwheel spirals, football-shaped ellipticals, and oddball irregular galaxies. He thought these might be clues to galaxy evolution — but the answer had to wait for the Hubble Space Telescope’s legendary Hubble Deep Field in 1994.

The most impactful finding that Edwin Hubble’s analysis showed was that the farther the galaxy is, the faster it appears to be receding from Earth. The universe looked like it was expanding like a balloon. This was based on Hubble tying galaxy distances to the reddening of light — the redshift — that proportionally increased the father away the galaxies are.

The redshift data were first collected by Lowell Observatory astronomer Vesto Slipher, who spectroscopically studied the “spiral nebulae” a decade before Hubble. Slipher did not know they were extragalactic, but Hubble made the connection. Slipher first interpreted his redshift data an example of the Doppler effect. This phenomenon is caused by light being stretched to longer, redder wavelengths if a source is moving away from us. To Slipher, it was curious that all the spiral nebulae appeared to be moving away from Earth.

Two years prior to Hubble publishing his findings, the Belgian physicist and Jesuit priest Georges Lemaître analyzed the Hubble and Slifer observations and first came to the conclusion of an expanding universe. This proportionality between galaxies’ distances and redshifts is today termed Hubble-Lemaître’s law.

Because the universe appeared to be uniformly expanding, Lemaître further realized that the expansion rate could be run back into time — like rewinding a movie — until the universe was unimaginably small, hot, and dense. It wasn’t until 1949 that the term “big bang” came into fashion.

This was a relief to Edwin Hubble’s contemporary, Albert Einstein, who deduced the universe could not remain stationary without imploding under gravity’s pull. The rate of cosmic expansion is now known as the Hubble Constant.

Ironically, Hubble himself never fully accepted the runaway universe as an interpretation of the redshift data. He suspected that some unknown physics phenomenon was giving the illusion that the galaxies were flying away from each other. He was partly right in that Einstein’s theory of special relativity explained redshift as an effect of time-dilation that is proportional to the stretching of expanding space. The galaxies only appear to be zooming through the universe. Space is expanding instead.

After decades of precise measurements, the Hubble telescope came along to nail down the expansion rate precisely, giving the universe an age of 13.8 billion years. This required establishing the first rung of what astronomers call the “cosmic distance ladder” needed to build a yardstick to far-flung galaxies. They are cousins to V1, Cepheid variable stars that the Hubble telescope can detect out to over 100 times farther from Earth than the star Edwin Hubble first found.

Astrophysics was turned on its head again in 1998 when the Hubble telescope and other observatories discovered that the universe was expanding at an ever-faster rate, through a phenomenon dubbed “dark energy.” Einstein first toyed with this idea of a repulsive form of gravity in space, calling it the cosmological constant.

Even more mysteriously, the current expansion rate appears to be different than what modern cosmological models of the developing universe would predict, further confounding theoreticians. Today astronomers are wrestling with the idea that whatever is accelerating the universe may be changing over time. NASA’s Roman Space Telescope, with the ability to do large cosmic surveys, should lead to new insights into the behavior of dark matter and dark energy. Roman will likely measure the Hubble constant via lensed supernovae.

This grand century-long adventure, plumbing depths of the unknown, began with Hubble photographing a large smudge of light, the Andromeda galaxy, at the Mount Wilson Observatory high above Los Angeles.

In short, Edwin Hubble is the man who wiped away the ancient universe and discovered a new universe that would shrink humanity’s self-perception into being an insignificant speck in the cosmos.

The discovery, announced Jan. 14 at the winter meeting of the American Astronomical Society, is the most distant object detected by the NuSTAR X-ray space telescope (which launched in 2012) and stands as one of the most highly “variable” quasars ever identified.

“In this work, we have discovered that this quasar is very likely to be a supermassive black hole with a jet pointed towards Earth — and we are seeing it in the first billion years of the universe,” said Lea Marcotulli, a postdoctoral fellow in astrophysics at Yale and lead author of a new study published Jan. 14 in The Astrophysical Journal Letters.

Quasars are among the oldest, brightest objects in the universe. Formed from active galactic nuclei (AGN) — areas at the center of galaxies where a black hole is drawing in matter — quasars emit electromagnetic radiation that can be spotted in radio, infrared, visible, ultraviolet, X-ray, and gamma-ray wavelengths. This “visibility” has made quasars a helpful proxy for trying to understand the structure and evolution of the cosmos.

For example, astronomers look to quasars to study reionization, a period less than a billion years after the Big Bang when electrically neutral hydrogen atoms became charged and the first generation of stars lit up the universe.

“The epoch of reionization is considered the end of the universe’s dark ages,” said Thomas Connor, an astronomer at the Chandra X-Ray Center and co-corresponding author of the study. “The precise timeline and source class responsible for reionization are still debated, and actively accreting supermassive black holes are one proposed culprit.”

For the study, the researchers compared NuSTAR observations of a distant quasar — designated J1429+5447 — with unrelated observations of four months earlier by the Chandra X-ray telescope. The researchers found that the quasar’s X-ray emissions had doubled in that very short time (due to relativistic effects, the four months on Earth corresponded to only two weeks for the quasar).

“This level of X-ray variability, in terms of intensity and rapidity, is extreme,” said Meg Urry, the Israel Munson Professor of Physics and Astronomy in Yale’s Faculty of Arts and Sciences and co-author of the study. “It is almost certainly explained by a jet pointing toward us — a cone in which particles are transported up to a million light years away from the central, supermassive black hole. Because the jet moves at nearly the speed of light, effects of Einstein’s theory of special relativity speed up and amplify the variability.”

The researchers said their findings offer crucial, much-needed information for astronomers studying reionization. It may also point astronomers toward other supermassive black hole candidates from the early universe.

“Finding more supermassive black holes that are potentially hosting jets raises the question as to how these black holes grew so big in such a short timescale, and what the connection may be to jet triggering mechanisms,” Marcotulli said.

NASA supported the research.

“Red meat is high in saturated fat and has been shown in previous studies to increase the risk of type 2 diabetes and heart disease, which are both linked to reduced brain health,” said study author Dong Wang, MD, ScD, of Brigham and Women’s Hospital in Boston. “Our study found processed red meat may increase the risk of cognitive decline and dementia, but the good news is that it also found that replacing it with healthier alternatives, like nuts, fish and poultry, may reduce a person’s risk.”

To examine the risk of dementia, researchers included a group of 133,771 people with an average age of 49 who did not have dementia at the start of the study. They were followed up to 43 years. Of this group, 11,173 people developed dementia.

Participants completed a food diary every two to four years, listing what they ate and how often.

Researchers defined processed red meat as bacon, hot dogs, sausages, salami, bologna and other processed meat products. They defined unprocessed red meat as beef, pork, lamb and hamburger. A serving of red meat is three ounces, about the size of a deck of cards.

Researchers calculated how much red meat participants ate on average per day.

For processed red meat, they divided participants into three groups. The low group ate an average of fewer than 0.10 servings per day; the medium group ate between 0.10 and 0.24 servings per day; and the high group, 0.25 or more servings per day.

After adjusting for factors such as age, sex and other risk factors for cognitive decline, researchers found that participants in the high group had a 13% higher risk of developing dementia compared to those in the low group.

For unprocessed red meat, researchers compared people who ate an average of less than one half serving per day to people who ate one or more servings per day and did not find a difference in dementia risk.

To measure subjective cognitive decline, researchers looked at a different group of 43,966 participants with an average age of 78. Subjective cognitive decline is when a person reports memory and thinking problems before any decline is large enough to show up on standard tests.

The subjective cognitive decline group took surveys rating their own memory and thinking skills twice during the study.

After adjusting for factors such as age, sex and other risk factors for cognitive decline, researchers found that participants who ate an average of 0.25 servings or more per day of processed red meat had a 14% higher risk of subjective cognitive decline compared to those who ate an average of fewer than 0.10 servings per day.

They also found people who ate one or more servings of unprocessed red meat per day had a 16% higher risk of subjective cognitive decline compared to people who ate less than a half serving per day.

To measure objective cognitive function, researchers looked at a different group of 17,458 female participants with an average age of 74. Objective cognitive function is how well your brain works to remember, think and solve problems.

This group took memory and thinking tests four times during the study.

After adjusting for factors such as age, sex and other risk factors for cognitive decline, researchers found that eating higher processed red meat was associated with faster brain aging in global cognition with 1.61 years with each additional serving per day and in verbal memory with 1.69 years with each additional serving per day.

Finally, researchers found that replacing one serving per day of processed red meat with one serving per day of nuts and legumes was associated with a 19% lower risk of dementia and 1.37 fewer years of cognitive aging. Making the same substitution for fish was associated with a 28% lower risk of dementia and replacing with chicken was associated with a 16% lower risk of dementia.

“Reducing how much red meat a person eats and replacing it with other protein sources and plant-based options could be included in dietary guidelines to promote cognitive health,” said Wang. “More research is needed to assess our findings in more diverse groups.”

A limitation of the study was that it primarily looked at white health care professionals, so the results might not be the same for other race, ethnic and non-binary sex and gender populations.

The study was supported by the National Institutes of Health.

Previous studies showed that a protein called PIN1 helps cancers initiate and progress, but its exact role in tumor development has remained unclear. Now, cancer biologists at the Salk Institute have discovered that PIN1 is a significant driver of bladder cancer and revealed that it works by triggering the synthesis of cholesterol — a membrane lipid essential for cancer cells to grow.

After mapping out the molecular pathway between PIN1 and cholesterol, the researchers developed an effective treatment regimen that largely halted tumor growth in their mouse model of cancer. The therapy consists of two drugs: a PIN1 inhibitor called sulfopin, an experimental drug not yet tested in humans, and simvastatin, a statin that is already used in humans for lowering cholesterol levels to reduce the risk of cardiovascular disease.

The findings were published in Cancer Discovery, a journal of the American Association for Cancer Research, on January 14, 2025.

“We’re excited to be the first to identify PIN1’s role in bladder cancer and to describe the mechanism it uses to drive tumor growth,” says senior author Tony Hunter, American Cancer Society professor and holder of the Renato Dulbecco Chair at Salk. “Given the high costs, morbidity, and mortality rates for bladder cancer, we’re especially thrilled to discover that targeting the cholesterol pathway with this therapeutic combination was so effective in suppressing bladder tumor growth in mice, and we hope to see this approach explored in a future clinical trial, once a PIN1 inhibitor is approved for clinical use.”

Bladder cancer is one of the most diagnosed cancers worldwide and the fourth most common cancer among men. It poses a serious threat to public health, as most cases result in either expensive, lifelong treatment, or rapid progression and mortality.

Hunter’s lab had originally discovered PIN1 in 1996 as a part of its work on phosphorylation, a process in which phosphate molecules are tacked onto proteins to change their structure and function. The lab showed that PIN1 is an enzyme that can recognize a protein when a phosphate is added to the amino acid serine while it’s next to the amino acid proline. PIN1 then changes that protein’s shape.

Phosphorylation of proteins at serine residues next to prolines is known to be a major signaling mechanism controlling cell proliferation and malignant transformation, and its dysregulation causes human cancers. PIN1 can target these phosphorylated areas and instigate structural and functional changes to the protein. Still, it’s been unclear exactly how this PIN1 activity contributes to tumor formation or which proteins PIN1 might be interacting with in bladder cancer cells.

In search of answers, the team compared normal human bladder cells with bladder cancercells, in culture dishes and implanted in mice.

First, they demonstrated that PIN1 expression was higher in bladder cancer cells — specifically in the specialized tissue layer that lines the inside of the urinary tract, called the urothelium. Then, they used genetic scissors to eliminate the PIN1 gene in the cancer cells. Without PIN1, they saw fewer cancerous cells develop, and those that did develop migrated less aggressively within and beyond the urothelium.

These findings indicated that PIN1 was contributing to the development of bladder cancer, but how?

The researchers returned to the cells that were missing PIN1 and looked to see if any other biological processes had been altered. Surprisingly, they found that one of the most affected pathways was the cholesterol synthesis pathway, mediated by a protein called SREBP2. Without PIN1, the bladder cells contained much lower levels of cholesterol.

“Cancer cells need a lot of cholesterol to accomplish their trademark excess growth,” says first author Xue Wang, a postdoctoral researcher in Hunter’s lab. “Our findings show that PIN1 plays an important role in cholesterol production, and removing it leads to lower cholesterol and therefore less out-of-control tumor growth.”

Through a series of experiments, the researchers confirmed that PIN1 was working with the SREBP2 protein to stimulate cholesterol production. Removing PIN1 effectively put a lid on the cancer’s fuel supply, but reinstating PIN1 reversed those anti-cancer effects. Without intervention, the high level of PIN1 in bladder cancer assists in tumor growth and metastasis.

How can we stop PIN1? One obvious answer is to inhibit the protein itself, but it’s also possible to inhibit an enzyme in the cholesterol pathway that PIN1 stimulates. One class of drugs, called statins, is already very widely used to control cholesterol levels. Statins work by blocking a protein in the cholesterol biosynthesis pathway called HMGCR. The idea was to attack the cholesterol pathway from two angles by combining simvastatin, a widely prescribed statin, to block HMGCR, and sulfopin to disable PIN1 and prevent its activation of SREBP2, thus drastically reducing the ability of the bladder cancer cells to make cholesterol.

When the researchers treated the mice with bladder cancer tumors with the PIN1 inhibitor sulfopin and the HMGCR inhibitor simvastatin, they found the combination suppressed cancer cell proliferation and tumor growth — importantly, the two worked better in tandem than as individual treatments.

“This is likely just one of many roles that PIN1 plays in cancers,” says Hunter. “What’s exciting about this discovery, though, is that statins are already in human use to prevent cardiovascular disease, and our work suggests an opportunity to use statins in combination with other drugs for bladder cancer therapy. And beyond this, we’ll continue to study whether PIN1 plays a similar role in other cancers, so our findings can hopefully improve lives regardless of cancer type.”

Not only did the team confirm PIN1’s role in bladder cancer progression, they also connected PIN1 to cholesterol biosynthesis and created viable treatment solutions to improve treatment outcomes.

Other authors include Yuan Sui and Jill Meisenhelder of Salk, Derrick Lee of UC San Diego, and Haibo Xu of Shenzhen University in China.

The work was supported by the National Institutes of Health (CCSG P30CA023100, CCSG CA014159, 5 R35 CA242443) and a Pioneer Fund Postdoctoral Scholar Award.

In a paper published recently in Nature Communications, the UC Irvine scientists describe their construction of complementary, internal, ion-gated, organic electrochemical transistors that are more amenable chemically, biologically and electronically to living tissues than rigid, silicon-based technologies. The medical device based on these transistors can function in sensitive parts of the body and conform to organ structures even as they grow.

“Advanced electronics have been in development for several decades now, so there is a large repository of available circuit designs. The problem is that most of these transistor and amplifier technologies are not compatible with our physiology,” said co-author Dion Khodagholy, Henry Samueli Faculty Excellence Professor in UC Irvine’s Department of Electrical Engineering and Computer Science. “For our innovation, we used organic polymer materials that are inherently closer to us biologically, and we designed it to interact with ions, because the language of the brain and body is ionic, not electronic.”

In standard bioelectronics, complementary transistors have been composed of different materials to account for different polarities of signals, which, in addition to being unyielding and cumbersome, present the risk of toxicity when implanted in sensitive areas. The team of researchers from UC Irvine and Columbia University worked around this problem by creating its transistors in an asymmetric fashion that enables them to be operated using a single, biocompatible material.

“A transistor is like a simple valve that controls the flow of current. In our transistors, the physical process that controls this modulation is governed by the electrochemical doping and de-doping of the channel,” said first author Duncan Wisniewski, Columbia University Ph.D. candidate during the project who is now a visiting scholar in the UC Irvine Department of Electrical Engineering and Computer Science. “By designing devices with asymmetrical contacts, we can control the doping location in the channel and switch the focus from negative potential to positive potential. This design approach allows us to make a complementary device using a single material.”

He added that arraying transistors into a smaller, single-polymer material greatly simplifies the fabrication process, enabling large-scale manufacturing and opportunities to expand the technology beyond the original neurological application to almost any biopotential processes.

Khodagholy, who heads the UC Irvine Translational Neuroelectronics Laboratory, which recently moved to Irvine from Columbia University, said that his team’s work has the added benefit of scalability: “You can make different device sizes and still maintain this complementarity, and you can even change the material, which makes this innovation applicable in multiple situations.”

Another advantage highlighted in the Nature Communications paper is that the device can be implanted in a developing animal and withstand transitions in tissue structures as the organism grows, something that is not possible with hard, silicon-based implants.

“This characteristic will make the device particularly useful in pediatric applications,” said co-author Jennifer Gelinas, UC Irvine associate professor of anatomy and neurobiology as well as pediatrics, who’s also a physician at Children’s Hospital of Orange County.

“We demonstrated our ability to create robust complementary, integrated circuits that are capable of high-quality acquisition and processing of biological signals,” Khodagholy said. Complementary, internal, ion-gated, organic electrochemical transistors “will substantially broaden the application of bioelectronics to devices that have traditionally relied on bulky, nonbiocompatible components.”

Joining Khodagholy, Gelinas and Wisniewski on this project were Claudia Cea, Liang Ma, Alexander Ranschaert, Onni Rauhala and Zifang Zhao of Columbia University. The work was supported by the National Institutes of Health and the National Science Foundation.

Based on new research, we now know that college students gain the same amount of weight as older adults during the holiday season; however, they add new muscle not fat.

Obesity researcher Martin Binks, professor and chair of George Mason University’s Department of Nutrition and Food Studies, was surprised by the findings of this breakthrough research. “The differences between college students’ and older adults’ weight gain highlights the importance of understanding weight and health in the context of major life stages and transitions across the lifespan,” says Binks. “At this key transitional stage of life, the influence of the holiday season is uniquely different for college students than later in adulthood. It raises so many important scientific questions about what might be driving this.” Binks is interested in learning more about the reasons for this difference with future studies.

Binks has been a metabolic disease scientist and clinician for over 20 years. He has assisted thousands of patients with behavioral pharmacologic and surgical weight loss, health and wellness, and quality of life improvement. He has been chair of George Mason’s Department of Nutrition and Food Studies since August 2024. This publication is the result of a study that was conducted by undergraduate students who were guided by graduate students under Binks’ mentorship. “Mentoring students in conducting impactful research is at the heart of my lifelong passion and is integral to the vision of George Mason’s Nutrition and Food Studies department,” says Binks.

Obesity Science & Practice published “Holiday Weight Change in a US College Student Sample: A Prospective Observational Cohort Study” in January 2025. Additional authors include Hannah B Yoo (lead author), Casen Bigham, Sharmin Akter, Alexis Brown, Shruthi Durai, and Claire Brown from Texas Tech University; Tanisha Basu from the University of Cincinnati; Tiffany Tsai from Princeton University; and Sara Kiros from the University of Oregon.