Imagine a chicken that could speak or a pigeon with a voice rivaling that of the most musical songbirds.

Granted, the world probably doesn’t need any gossiping chickens or pigeons breaking out in song. But why some birds learn to create a deep repertoire and others are unable to has long been a research focus of the neurobiologist Erich D. Jarvis.

“Vocal learning, just like spoken language itself, is a rare trait,” said Dr. Jarvis, who directs the Neurogenetics of Language laboratory at Rockefeller University in New York.

He studies the small group of species capable of speech, focusing on birds and mice, and he has long hoped to genetically engineer an animal that can vocalize in new ways. Introducing manipulated genes into the brain of a bird or a mouse that doesn’t vocalize could create that ability and provide new clues into the origins of speech. It may also one day help in finding treatments for people with speech problems or brain disorders.

Dr. Jarvis, 60, didn’t start his career in neuroengineering. He once hoped to become a professional dancer, performing ballet at Manhattan’s renowned High School for the Performing Arts and then studying at the Alvin Ailey dance school. He was a member of the Westchester Ballet Company when he began wondering how the brain was able to create dance movements.

His mentor at Rockefeller was Fernando Nottebohm, the researcher who discovered in the early 1980s that songbird brains generate new neurons each spring to enable them to sing. That revolutionary understanding of neurogenesis led to further findings that all brains, including human ones, grow new neurons throughout life. Until then, it had been scientific gospel that people came into the world with a fixed number.

From 2002 to 2005, Dr. Jarvis helped lead the Avian Brain Nomenclature Consortium, a project that renamed the regions of the avian brain to show that it was remarkably sophisticated. The research undermined the use of the term “bird brain” as a pejorative.

That same year, he won the Alan T. Waterman Award, and then he won the National Institutes of Health Director’s Pioneer Award three years later.

Dr. Jarvis’s efforts to understand birdsong have led him to other projects, including ones working with high-quality genome assemblies — maps that allow researchers to identify which genes are related to different traits. Because of that, he was appointed as chairman of the Vertebrate Genomes Project, a global effort to sequence the genomes of 70,000 vertebrate species.

The project involved building the Genome Ark, a reference database for research and conservation, especially for endangered species. The first sequencing phase of that project, involving 260 species, is nearly complete. Dr. Jarvis is also working to sequence the genomes of all bird species, which number about 10,500.

Parsing the smallest components of vocal learning is part of that work. Dr. Jarvis and a fellow researcher, Robert B. Darnell, also at Rockefeller, announced in February 2025 that they had discovered an amino acid in a single gene that might have contributed to the evolution of complex human language.

Swapping an altered gene into a mouse “changed how the mice spoke to each other,” Dr. Darnell said. “Baby mice called to their mothers differently, and male mice looking to lure a female for mating tried to attract her attention with altered vocalizations.”

Mammal and bird brains descended from one source brain before a divergence took place more than 320 million years ago. They took separate evolutionary paths from there and now appear very different: The structure of human brains is likened to a layer cake while bird brains resemble a fruit cake. But some regions are remarkably similar, including those where vocal learning mechanisms are located. Independently acquiring similar traits is called convergent evolution.

“If we study that convergence and find the similarities, it would mean that we can understand human speech from studying these birds,” Dr. Jarvis said.

Matt Biegler, a postdoctoral researcher in Dr. Jarvis’s lab listed some questions needing answers: “What are the origins of speech? How did it evolve? Why did it evolve? And what are the mechanisms that make it happen?”

To that end, Dr. Jarvis and his colleagues were also able to engineer a new vocal pathway in a mouse, as documented in a paper published by the lab. “We have been able to change the expression pattern of that gene in the mouse brain, make it more human and songbird-like,” he said. “These mice are singing a greater diversity of variations.”

“The goal is be able to move this ability to species that wouldn’t have it,” said Matt Davenport, a post-doctorate researcher in Dr. Jarvis’s lab. “It opens up a brave new world where higher-order traits are engineerable. It gives us new insights into communication disorders, autism and stuttering.”

Orange and gray zebra finches, raised in captivity, are the bird species of choice for this kind of research, as their neural networks are strikingly similar to those of humans. But the lab has also studied the brains of wild birds. Dr. Jarvis used to lure hummingbirds to a feeder with sugar water. “They’ll find the food source and in the morning, as part of the dawn chorus, they will sing next to it” to claim their territory, he said.

The song activates a messenger molecule. If the brain were removed and examined quickly enough, within a half-hour, Dr. Jarvis could trace the chemical that created the song.

Gaining a better understanding of vocal learning circuitry holds significant promise, he said, adding that it was worth the sacrifice of some birds.

“If we can figure it out in birds, we can figure out how to similarly repair circuits damaged in stroke and trauma in people,” Dr. Jarvis said. Perhaps it would be possible to extrapolate from the findings to aid in the discovery of new drugs that help people regain speech after a stroke, say, or lead to a cure for stuttering, a brain-based condition that also occurs in some birds.

“I probably won’t finish this in my lifetime, but I am going to try,” he said.

Along the way, Dr. Jarvis has made other observations, perhaps drawing from his years of studying dance.

“Only vocal learning species can learn to dance to the beat of music,” he said. “There’s a relationship between learning how to imitate sounds and learning how to dance.”

Stanley M. Gartler, a molecular biologist and geneticist who helped provide the first convincing evidence that cancerous tumors develop from a single mutated cell, and uncovered shocking research errors involving the first collection of human cells to permanently thrive in a laboratory, died on May 25 at his home in Seattle. He was 102.

His death, which was not widely reported at the time, was confirmed by Dr. Richard Weiner, his nephew.

In the early 1960s, Dr. Gartler began exploring the genetic origins of cancer at the University of Washington, where he joined the genetics department faculty in 1957 and maintained an active lab until 2007.

At the turn of the 20th century, Theodor Boveri, a German zoologist, had proposed a hypothesis that a tumor begins as a single cell that divides uncontrollably. But he lacked proof.

Working with the pathologist David Linder, Dr. Gartler began studying benign uterine tumors — commonly known as fibroid tumors — that had been removed during hysterectomies in Black women.

Females typically have two X chromosomes in each cell, while males have an X and a Y. Because of a random process called X inactivation, most genes in one of the two X chromosomes in women are silenced early in embryonic development. Dr. Gartler realized that the silencing of one gene found on the X chromosome, called G6PD, gave crucial information about that cell’s fate.

In a study published in 1965 in the journal Science, Dr. Gartler and Dr. Linder reported that normal uterine tissue showed a mosaic of two gene variants — A and B — present in roughly equal amounts. In tissue from tumors, however, only one variant was present — either A or B — which implied that a tumor originates from a single cell.

“We really had to understand the biology of cancer to have any possibility of treating it,” Dr. Gail Jarvik, who leads the division of medical genetics at the University of Washington, said in an interview. “All of these chemotherapies and now very targeted therapies are based on clearly understanding that the biology is this mutation.”

Also in 1965, while studying genetic markers that vary in human cells, Dr. Gartler collected permanent human cell lines — cultures used in laboratory research that are easily cloned and are valuable in studying diseases and developing drugs and vaccines.

He found something highly improbable. In 18 supposedly independent cultures, the genetic markers were identical, containing the rare A variant of the G6PD gene, which was found almost exclusively in Black people.

It became clear to him that these purportedly unique cell cultures had been contaminated and overgrown by the first permanent human cell line, established in 1951 at Johns Hopkins Hospital in Baltimore, called the HeLa (pronounced hee-lah) line.

HeLa is an abbreviation of the first and last names of Henrietta Lacks, a Black woman who died of cervical cancer in 1951. Her genetic information, harvested from a tissue biopsy at that hospital shortly before her death, had been shipped and studied in laboratories around the world without her consent or her family’s knowledge.

The HeLa line would help with vital advancements in the polio vaccine, cancer research, cell biology, in vitro fertilization, cloning and chemotherapy. But Dr. Gartler observed an alarming problem involving the line’s cells, which, as it turned out, could easily contaminate other cultures by traveling on dust particles, lab coats or unwashed hands.

Researchers who thought they were studying cancer cells of, say, the kidney, liver or breast were, he proposed, likely studying cervical cancer cells of the HeLa line that had overtaken the original cultures. He would later blame “sloppy techniques” in laboratories for the contamination.

At a 1966 conference in Pennsylvania on cell tissue and organ culture, Dr. Gartler presented his findings. He told a stunned and skeptical audience of 700 scientists that their work on what they believed to be original cell lines was now “open to serious question” and he suggested that work “best be discarded.”

Rebecca Skloot included an account of the conference in her 2010 best seller, “The Immortal Life of Henrietta Lacks.” Michael Gold, whose 1985 book, “A Conspiracy of Cells: One Woman’s Immortal Legacy and the Medical Scandal It Caused,” said in an interview that the scientific impact of Dr. Gartler’s findings was enormous.

He “really raised the red flag,” Mr. Gold said, on a large-scale problem that “wasted countless hours and untold millions of dollars” on invalid science.

Many researchers, Mr. Gold added, “didn’t particularly want to hear that news,” but “a critical mass” reluctantly accepted Dr. Gartler’s findings.

Dr. Gartler’s discovery has been credited as a catalyst for improved quality control in labs and enhanced authentication of cell lines. The story of the HeLa line became one of the defining lessons of 20th-century medicine and raised important ethical questions about informed consent of patients, privacy and the rights of families to receive compensation for research on a relative’s cells.

In a 2012 lecture, Dr. Gartler spoke about the need for anonymity and privacy in research, a sense of dignity that had not been given to Henrietta Lacks.

“I personally wouldn’t want to be remembered for a cancer cell,” he said.

Stanley Michael Gartler was born on June 9, 1923, in Los Angeles to parents who emigrated from Romania. His father, George Gartler, owned a dry cleaning plant. His mother, Delvira (Kupferberg) Gartler, ran the household.

He entered the University of California, Los Angeles, in 1941 with an early interest in agriculture, but left the next year to enlist in the military. He served in the Army Air Forces during World War II as a radio operator and machine-gunner aboard a B-26 bomber on missions in Europe.

He returned to U.C.L.A. to complete his bachelor’s degree, then received his Ph.D. in genetics in 1952 from the University of California, Berkeley, where he studied plant breeding and developed an interest in human genetics, which he fostered during a postdoctoral fellowship at Columbia University. He joined the University of Washington as the first faculty member in the newly formed division of medical genetics.

His wife, Marion Mitchelson Gartler, a writer and editor who also developed a vest to thwart pickpockets, died in 2016. He has no immediate survivors.

In 1962, Dr. Gartler and two colleagues published an influential paper about a girl with two different-colored eyes and atypical genitalia. It was, Dr. Jarvik of the University of Washington said, the first demonstration of mixed XX and XY cells in a human, likely from an early fusion of twin fetuses.

“It really does say sex determination is much more complex than XX and XY,” Dr. Jarvik said, “and that the human body tolerates a significant amount of variability.”

The reported illnesses this spring initially looked like the spread of a typical stomach bug on a luxury ocean liner, but the situation quickly escalated to a fatal outbreak of hantavirus, a rare rodent-borne pathogen, leading to weekslong quarantines for the ship’s passengers and a global health alert.

But the outbreak is now over, the World Health Organization announced on Thursday. Overall, there were 12 confirmed cases and one probable case aboard the cruise ship, including three deaths.

The declaration was made after the final contact of a passenger completed a quarantine period and tested negative for the virus, said the health agency, which is part of the United Nations.

The announcement ended a three-month saga that had scientists scrambling to find the origins of a rare vector for hantavirus; crew members and passengers held captive on a luxury ship; and global health officials enforcing contact tracing and quarantine protocols.

The luxury cruise liner, MV Hondius, began its trip carrying 175 passengers and crew members from nearly two dozen countries as it left Ushuaia, an Argentine city, on April 1. The first passenger sickened by the virus died less than two weeks later.

The last reported case was on May 25, Tedros Adhanom Ghebreyesus, the director general of the W.H.O., said in making the announcement.

The passengers caught in the outbreak were to enjoy a leisurely journey aboard the state-of-the-art polar expedition ship from Argentina to remote islands in the southern Atlantic Ocean, including stops in mainland Antarctica, the Falkland Islands and Cape Verde.

Several passengers who boarded the ship were passionate bird watchers interested in the landfill in Ushuaia because it is a prime location to spot the white-throated caracara, a raptor bird. For a brief period, there was speculation that the landfill was the likeliest source of the contagion.

After the outbreak began, the ship was headed to Cape Verde, where government officials did not allow it to dock, saying that it was too small a country to handle the outbreak. The ship was refused entry in multiple countries, and the passengers and crew became isolated captives in the middle of the Atlantic Ocean.

Patient zero was a Dutch man, 69 years of age, who first showed vague, flulike symptoms on April 6, five days after the cruise began. He died on board on April 11.

His wife, also 69, became ill after leaving the ship with his body on April 24 on the island of St. Helena in the South Atlantic, where the ship was finally allowed to dock. She reported “gastrointestinal symptoms,” the W.H.O. said. She died on April 26 in Johannesburg, where she was going to take a flight home to the Netherlands.

About 30 people from at least 12 countries left the ship in St. Helena, a British territory. Two days after the second death linked to the virus, on April 28, a German woman had “fever and general malaise,” and then had symptoms of pneumonia, the W.H.O. said. She died aboard the ship on May 2.

The next day, after laboratory testing, the W.H.O. confirmed that the hantavirus was on the ship, attributing one of the infections to the virus.

While the ship was moored off the coast of Cape Verde, an archipelago in the Atlantic Ocean off West Africa, government and health officials around the world raced to find a way to evacuate the sick people onboard. By then, the hantavirus outbreak had been tied to seven people on the ship, according to the W.H.O.

The government of Spain allowed the ocean liner to dock on May 9 at Tenerife, one of the Canary Islands. It was nearly six weeks after the ship had left Argentina, and, during a two-day interval, all the remaining passengers were tested and disembarked.

By May 11, many of the passengers and some crew members were either on their way to their home countries, or had already arrived. Many of them, including 18 Americans, were quarantined when they arrived home.

On May 18, the Hondius arrived at the Port of Rotterdam, in the Netherlands, with only 27 passengers and crew members placed in a special quarantine area. After the ship was inspected and samples were collected, it was cleaned and disinfected.

Dr. Tedros said that over 650 contacts of people on the ship were identified, and that health officials in about three dozen countries and territories reached out to those contacts.

The W.H.O. said it believed the outbreak originated on land and was not an infestation from the multimillion-dollar ship. The agency identified the strain as the Andes subtype, which can be transmitted between people in close contact.

The Andes subtype caused the deaths of the two first patients who traveled on the ship, the agency said. It is endemic in three provinces across Argentina’s Patagonia, with several cases reported there every year, according to the health authorities.

There are no targeted treatments for hantaviruses, which are typically carried by rodents, and no widely available vaccines.

But Dr. Tedros expressed optimism that one could arrive.

“We are also coordinating a study involving 21 countries to understand how the disease develops,” he said, “which will support the development of diagnostics, therapeutics and vaccines for future outbreaks.”