Posts Tagged ‘disease’


Ionocytes (orange) extend through neighboring epithelial cells (nuclei, cyan) to the surface of the respiratory epithelial lining. This newly identified cell type expresses high levels of CFTR, a gene that is associated with cystic fibrosis when mutated.

by ABBY OLENA

Two independent research teams have used single-cell RNA sequencing to generate detailed molecular atlases of mouse and human airway cells. The findings, reported in two studies today (August 1) in Nature, reveal the gene-expression patterns of thousands of lung cells, as well as the existence of a previously unknown cell type that expresses high levels of the gene mutated in cystic fibrosis, the cystic fibrosis transmembrane conductance regulator (CFTR).

“These papers are extremely exciting,” says Amy Ryan, a lung biologist at the University of Southern California who was not involved in either study. “They’ve interrogated the cellular composition and the cellular hierarchy of the airways by using a single-cell RNA-sequencing technique. That kind of information is going to have a significant impact on advancing the research that we can do, and hopefully the derivation of new therapeutic approaches for any number of airway diseases.”

Jayaraj Rajagopal, a pulmonary physician at Massachusetts General Hospital and Harvard University and coauthor of one of the studies, had been studying lung regeneration and wanted to use single-cell sequencing to look at differences in the lungs’ stem-cell populations. He and his colleagues teamed up with Aviv Regev, a computational biologist at the Broad Institute of MIT and Harvard University, and together, the two groups characterized the transcriptomes of thousands of epithelial cells from the adult mouse trachea.

Rajagopal, Regev, and colleagues uncovered previously unknown differences in gene expression in several groups of airway cells; identified novel structures in the lung; and found new paths of cellular differentiation. They also described several new cell types, including one that the team has named the pulmonary ionocyte, after salt-regulating cells in fish and amphibian skin. These lung cells express similar genes as fish and amphibian ionocytes, the team found, including a gene coding for the transcription factor Foxi1, which regulates genes that play a role in ion transport.

The team also showed that pulmonary ionocytes highly express CFTR, and are in fact the primary source of its product, CFTR—a membrane protein that helps regulate fluid transport and the consistency of mucus—in both mouse and human lungs, suggesting that the cells might play a role in cystic fibrosis.

“So much that we found rewrites the way we think about lung biology and lung cells,” says Rajagopal. “I think the entire community of pulmonologists and lung biologists will have to take a step back and think about their problems with respect to all these new cell types.”

For the other study, Aron Jaffe, a biologist at Novartis who studies how different airway cell types are made, combined forces with Harvard systems biologist Allon Klein and his team. Klein’s group had previously developed a single-cell RNA-sequencing method that Jaffe describes as “the perfect technology to take a big picture view and really define the full repertoire of epithelial cell types in the airway.”

Jaffe, Klein, and colleagues sequenced RNA from thousands of single human bronchial epithelial and mouse tracheal epithelial cells. The atlas generated by their sequencing analysis revealed pulmonary ionocytes, as well as new gene-expression patterns in familiar cells. The team examined the expression of CFTR in human and mouse ionocytes in order to better understand the possible role for the cells in cystic fibrosis. Consistent with the findings of the other study, the researchers showed that pulmonary ionocytes make the majority of CFTR protein in the airways of humans and mice.

“Finding this new rare cell type that accounts for the majority of CFTR activity in the airway epithelium was really the biggest surprise,” Jaffe tells The Scientist. “CFTR has been studied for a long time, and it was thought that the gene was broadly expressed in many cells in the airway. It turns out that the epithelium is more complicated than previously appreciated.”

These studies are “very exciting work [and] a wonderful example of how new technologies that have come online in the last few years—in this case single-cell RNA sequencing—have made a very dramatic advance in our understanding of aspects of biology,” says Ann Harris, a geneticist at Case Western Reserve University who did not participate in either study.

In terms of future directions, the authors “have shown that transcription factor [Foxi1] is central to the transcriptional program of these ionocytes,” says Harris. One of the next questions is, “does it directly interact with the CFTR gene or is it working through other transcription factors or other proteins that regulate CFTR gene expression?”

According to Jennifer Alexander-Brett, a pulmonary physician and researcher at Washington University School of Medicine in St. Louis who was not involved in the studies, the possibility that a rare cell type could be playing a part in regulating airway physiology is “captivating.”

Apart from investigating the potential role for ionocytes in lung function, Alexander-Brett says that researchers can likely make broad use of the data from the studies—particularly details on the expression of genes coding for transcription factors and cell-surface markers. “One area that we really struggle with in airway biology . . . is [that] we just don’t have good markers” to differentiate cell types, she explains. But these papers are “very comprehensive. There’s a ton of data here.”

D.T. Montoro et al., “A revised airway epithelial hierarchy includes CFTR-expressing ionocytes,” Nature, doi:10.1038/s41586-018-0393-7, 2018.

L.W. Plasschaert et al., “A single-cell atlas of the airway epithelium reveals the CFTR-rich pulmonary ionocyte,” Nature, doi:10.1038/s41586-018-0394-6, 2018.

https://www.the-scientist.com/news-opinion/new-lung-cell-identified-64594?utm_campaign=TS_DAILY%20NEWSLETTER_2018&utm_source=hs_email&utm_medium=email&utm_content=64924537&_hsenc=p2ANqtz-_M5n43mM_3CJb8-lIkjE6yt4ij2HduxgVeZi_X5bG7ATrAOGkvtsg4DpCbuAc0NAG8lx4myMxN3kiH4C1qc9OdlQkAGg&_hsmi=64924537

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by Leigh Hopper

Tnew stroke-healing gel created by UCLA researchers helped regrow neurons and blood vessels in mice whose brains had been damaged by strokes. The finding is reported May 21 in Nature Materials.

“We tested this in laboratory mice to determine if it would repair the brain and lead to recovery in a model of stroke,” said Dr. S. Thomas Carmichael, professor of neurology at the David Geffen School of Medicine at UCLA. “The study indicated that new brain tissue can be regenerated in what was previously just an inactive brain scar after stroke.”

The results suggest that such an approach could some day be used to treat people who have had a stroke, said Tatiana Segura, a former professor of chemical and biomolecular engineering at UCLA who collaborated on the research. Segura is now a professor at Duke University.

The brain has a limited capacity for recovery after stroke. Unlike the liver, skin and some other organs, the brain does not regenerate new connections, blood vessels or tissue structures after it is damaged. Instead, dead brain tissue is absorbed, which leaves a cavity devoid of blood vessels, neurons or axons — the thin nerve fibers that project from neurons.

To see if healthy tissue surrounding the cavity could be coaxed into healing the stroke injury, Segura engineered a hydrogel that, when injected into the cavity, thickens to create a scaffolding into which blood vessels and neurons can grow. The gel is infused with medications that stimulate blood vessel growth and suppress inflammation, since inflammation results in scars and impedes functional tissue from regrowing.

After 16 weeks, the stroke cavities contained regenerated brain tissue, including new neuronal connections — a result that had not been seen before. The mice’s ability to reach for food improved, a sign of improved motor behavior, although the exact mechanism for the improvement wasn’t clear.

“The new axons could actually be working,” Segura said. “Or the new tissue could be improving the performance of the surrounding, unharmed brain tissue.”

The gel was eventually absorbed by the body, leaving behind only new tissue.

The research was designed to explore recovery in acute stroke, the period immediately following a stroke — in mice, that period lasts five days; in humans, it’s two months. Next, Carmichael and Segura plan to investigate whether brain tissue can be regenerated in mice long after the stroke injury. More than 6 million Americans are living with long-term effects of stroke, which is known as chronic stroke.

The other authors of the paper are Lina Nih and Shiva Gojgini, both of UCLA.

The study was supported by the National Institutes of Health.

http://newsroom.ucla.edu/releases/biomaterial-ucla-regrow-brain-tissue-after-stroke-mice

Activating something called the behavioral immune system puts a damper on dating, new research shows.

About a decade ago, evolutionary psychologists suggested that humans have evolved a first line of defense against disease: this behavioral immune system or BIS.

The theory is that perceiving, rightly or wrongly, the threat of disease unconsciously activates this system. Although we cannot see microorganisms with the naked eye, we are nevertheless able to identify cues—such as coughs, unpleasant smells, or skin lesions—that hint at the possible presence of pathogens, whether or not these are actually present or represent real health threats.

Scientists have suggested that the activation of the BIS leads to prejudiced and avoidant attitudes and behavior towards those who display superficial cues connoting disease.

But how does this affect our dating lives, where two competing needs are pitted against one another—i.e., the potential benefits of connecting and finding a mate versus the need to protect oneself from disease? McGill University scientists set out to find out, by looking at the activation of the BIS in young, single, heterosexual Montrealers in both real speed-dating events and in experimental online dating.

The results were convincing. And not very happy.

“We found that when the behavioral immune system was activated it seemed to put the brakes on our drive to connect with our peers socially,” says first author of the study Natsumi Sawada, who holds a PhD in psychology from McGill University.

“We hadn’t expected this to be the case in real life situations like dating where people are generally so motivated to connect. The results suggest that beyond how we consciously or unconsciously think and feel about each other there are additional factors that we may not be consciously aware of, such as a fear of disease that may influence how we connect with others.”

This video explains how the experiments worked:

The findings appear in the Personality and Social Psychology Bulletin. The Social Sciences and Humanities Research Council (SSHRC) and the Fonds de Recherche sur la Société et la Culture (FRQSC) supported the work.

https://www.futurity.org/behavioral-immune-system-dating-1745362-2/

Saladin may not be well known in the West, but even 800 years after his death, he remains famous in the Middle East. Born in 1137, he rose to become the Sultan of an enormous area that now includes Egypt, Syria, parts of Iraq, Lebanon, Yemen and other regions of North Africa. He successfully led armies against the invading Crusaders and conquered several kingdoms. Historians have described him as the most famous Kurd ever.

Even today, however, Saladin’s death remains a mystery. The illness began in 1193, when he was 56. After two weeks, the Sultan was dead. Some have speculated that fever was a prominent symptom of the illness.

After closely examining a range of evidence about Saladin’s condition, Stephen J. Gluckman, MD, professor of medicine at the University of Pennsylvania School of Medicine, has developed a diagnosis. Dr. Gluckman theorizes that typhoid, a bacterial disease that was very common in the region at the time, is the most likely culprit. Today of course, antibiotics could have greatly helped Saladin. But in the 12th century these medicines did not exist.

Dr. Gluckman delivered his diagnosis at the 25th annual Historical Clinicopathological Conference, held Friday, May 4 at the University of Maryland School of Medicine. The conference is devoted to the diagnosis of disorders that afflicted historical figures; in the past, experts have focused on the diseases of luminaries such as Lenin, Darwin, Eleanor Roosevelt and Lincoln.

Dr. Gluckman, an expert on parasitic disorders, has provided care and taught in many countries around the world. He carefully reviewed what is known about the Sultan’s medical history. “Practicing medicine over the centuries required a great deal of thought and imagination,” he says. “The question of what happened to Saladin is a fascinating puzzle.”

Saladin is known for destroying King Guy’s army at the Horns of Hattin in 1187 and reclaiming Jerusalem for Islam after it had been ruled for nearly a century by Christian crusaders. He is also famed for treating his enemies generously.

Typhoid fever is a potentially deadly disease spread by contaminated food and water. Symptoms of typhoid include high fever, weakness, stomach pain, headache, and loss of appetite. It is common in most parts of the world except in industrialized regions such as the United States, western Europe, Australia, and Japan. About 300 people get typhoid fever in the United States each year, and most of them have recently traveled. Globally, typhoid infects about 22 million people a year, and kills 200,000.

‌Also speaking at the conference will be Thomas Asbridge, PhD, is a reader of medieval history at Queen Mary University of London. Dr. Asbridge is an expert on Saladin and the Crusades.

The conference was founded in 1995 by Philip A. Mackowiak, MD, the Carolyn Frenkil and Selvin Passen History of Medicine Scholar-in-Residence at UMSOM. “This is an intriguing piece of medical detecting,” says Dr. Mackowiak. “If antibiotics had been around in the 12th century, history may have been quite different.”

For more information on the conference, visit:
http://medicalalumni.org/historicalcpc/home/

http://www.medschool.umaryland.edu/news/2018/Expert-Disease-Detective-Unravels-Mysterious-Illness-That-Killed-Famed-12th-Century-Sultan.html

THE FIRST HUMAN brain balls—aka cortical spheroids, aka neural organoids—agglomerated into existence just a few short years ago. In the beginning, they were almost comically crude: just stem cells, chemically coerced into proto-neurons and then swirled into blobs in a salty-sweet bath. But still, they were useful for studying some of the most dramatic brain disorders, like the microcephaly caused by the Zika virus.

Then they started growing up. The simple spheres matured into 3D structures, fusing with other types of brain balls and sparking with electricity. The more like real brains they became, the more useful they were for studying complex behaviors and neurological diseases beyond the reach of animal models. And now, in their most human act yet, they’re starting to bleed.

Neural organoids don’t yet, even remotely, resemble adult brains; developmentally, they’re just pushing second trimester tissue organization. But the way Ben Waldau sees it, brain balls might be the best chance his stroke patients have at making a full recovery—and a homegrown blood supply is a big step toward that far-off goal. A blood supply carries oxygen and nutrients, allowing brain balls to grow bigger, complex networks of tissues, those that a doctor could someday use to shore up malfunctioning neurons.

“The whole idea with these organoids is to one day be able to develop a brain structure the patient has lost made with the patient’s own cells,” says Waldau, a vascular neurosurgeon at UC Davis Medical Center. “We see the injuries still there on the CT scans, but there’s nothing we can do. So many of them are left behind with permanent neural deficits—paralysis, numbness, weakness—even after surgery and physical therapy.”

Last week, it was Waldau’s group at UC Davis that published the first results of vascularized human neural organoids. Using brain membrane cells taken from one of his patients during a routine surgery, the team coaxed them first into stem cells, then some of them into the endothelial cells that line blood vessels’ insides. The stem cells they grew into brain balls, which they incubated in a gel matrix coated with those endothelial cells. After incubating for three weeks, they took a single organoid and transplanted it into a tiny cavity carefully carved into a mouse’s brain. Two weeks later the organoid was alive, well—and, critically, had grown capillaries that penetrated all the way to its inner layers.

Waldau got the idea from his work treating a rare disorder called Moyamoya disease. Patients have blocked arteries at the base of their brain, keeping blood from reaching the rest of the organ. “We sometimes lay a patient’s own artery on top of the brain to get the blood vessels to start growing in,” says Waldau. “When we replicated that process on a miniaturized scale we saw these vessels self-assemble.”

While it wasn’t clear from this experiment whether or not there was rodent blood coursing through its capillaries—the scientists had to flush them to accomplish fluorescent staining—the UC Davis team did demonstrate that the blood vessels themselves were comprised of human cells. Other research groups at the Salk Institute and the University of Pennsylvania have successfully transplanted human organoids into the brains of mice, but in both cases, blood vessels from the rodent host spontaneously grew into the transplanted tissue. When brain balls make their own blood vessels, they can potentially live much longer by hooking them up to microfluidic pumps—no rodent required.

That might give them a chance to actually mature into a complex computational organ. “It’s a big deal,” says Christof Koch, president of the Allen Institute for Brain Science in Seattle, “but it’s still early days.” The next problem will be getting these cells wired into circuits that can receive and process information. “The fact that I can look out at the world and see it as spatially organized—left, right, near, far— is all due to the organization of my cortex that reflects the regularity of the world,” says Koch. “There’s nothing like that in these organoids yet.”

Not yet, maybe, but it’s not too soon to start asking what happens when they do. How large do they have to be before society has a moral mandate to provide them some kind of special protections? If an organoid comes from your cells, are you then its legal guardian? Can a brain ball give its consent to be studied?

Just last week the National Institutes of Health convened a neuroethics workshop to confront some of these thorny questions. Addressing a room filled with neuroscientists, doctors, and philosophers, Walter Koroshetz, director of the NIH’s National Institute of Neurological Disorders and Stroke, said the time for involving the public was now, even if the technology takes a century to become reality. “The question here is, as those cells come together to form information processing units, when do they get to the point where they’re as good as what we do now in a mouse? When does it go beyond that, to information processing you only see in a human? And what type of information processing would be to a point where you would say, ‘I don’t think we should go there’?”

https://www.wired.com/story/mini-brains-just-got-creepiertheyre-growing-their-own-veins/

by Jennifer Kay

Mosquitoes are a year-round downside to living in subtropical Miami, but millions of bacteria-infected mosquitoes flying in a suburban neighborhood are being hailed as an innovation that may kill off more bugs that spread Zika and other viruses.

Miami-Dade County Mosquito Control and Habitat Management Division is releasing non-biting male mosquitoes infected with teh naturally occurring Wolbachia bacteria to mate with wild female mosquitoes.

The bacteria are not harmful to humans but will prevent any offspring produced when the lab-bred mosquitoes mate with wild female mosquitoes from surviving to adulthood. This drives down the population of Aedes aegypti mosquitoes that thrive in suburban and urban environments and can spread Zika, dengue fever and chikungunya.

During a six-month field trial approved by the U.S. Environmental Protection Agency, over half a billion of the mosquitoes bred by Kentucky-based MosquitoMate will be released in a suburban neighborhood split by long, narrow canals near the University of Miami, said South Miami Mayor Philip Stoddard.

Miami-Dade County is testing MosquitoMate’s insects as a potential mosquito-control method about 10 miles southwest of Miami’s hip Wynwood neighborhood, where health officials confirmed the first local Zika infections spread by mosquitoes on the U.S. mainland in July 2016.

Stoddard, a zoology professor at Florida International University, said he volunteered his city for the trial, wanting to keep the outdoor cafes in his city from becoming another ground zero for a mosquito-borne virus outbreak.

“All those diseases are still a concern,” he said. “They’re still in the Caribbean and could move to the mainland to cause problems.”

By the end of 2016, Florida health officials had confirmed 1,456 Zika infections in the state, including 285 cases spread by mosquitoes in Miami-Dade County. Just two local Zika infections were reported in Florida last year, including one Miami-Dade case.

If MosquitoMate’s bugs perform well in South Miami, Wolbachia could be added to regular mosquito control operations as a long-term preventative strategy, said Bill Petrie, Miami-Dade County’s mosquito control chief.

“It’s not a silver bullet,” he said. “You’d want to integrate it into your existing methods.”

It would not replace naled, the pesticide sprayed from airplanes during the 2016 outbreak, angering Miami residents concerned the chemicals were more dangerous than Zika. Health officials credited naled among other aggressive response efforts with stopping the outbreak.

MosquitoMate’s technology appears low-tech in the field. Infected mosquitoes are shipped weekly in cardboard tubes — similar to the ones used in paper towel rolls — from Lexington, Ky.

Each tube contains a thousand mosquitoes. In a demonstration Thursday in a city park, a cloud of mosquitoes burst from one end when a black netting cover was removed; a firm shake sent any stragglers flying out.

The trial will study how far the mosquitoes fly, how long they live in the area, and how many Aedes aegypti eggs hatch compared to untreated areas, MosquitoMate founder Stephen Dobson said.

Results from a similar trial near Key West last year are awaiting publication, he said.

Last year, the EPA approved permits for MosquitoMate to sell a related mosquito species, known as the “Asian tiger mosquito,” infected with Wolbachia as a pest control service in 20 states and Washington, D.C. Those mosquitoes also can carry viruses, but experts consider them less of a threat for triggering outbreaks than Aedes aegypti.

http://www.orlandosentinel.com/news/os-modified-mosquitoes-20180208-story.html

By SAM ROBERTS

Julius Youngner, an inventive virologist whose nearly fatal childhood illness destined him to become a medical researcher and a core member of the team that developed the Salk polio vaccine in 1955, died on April 27 at his home in Pittsburgh. He was 96.

His death was confirmed by his son, Dr. Stuart Youngner.

Dr. Youngner was the last surviving member of the original three-man research team assembled by Dr. Jonas Salk at the University of Pittsburgh to address the polio scourge, which peaked in the United States in the early 1950s when more than 50,000 children were struck by it in one year. Three other assistants later joined the group.

Dr. Salk credited his six aides with major roles in developing the polio vaccine, a landmark advance in modern medicine, which he announced on April 12, 1955.

The announcement — that the vaccine had proved up to 90 percent effective in tests on 440,000 youngsters in 44 states — was greeted with ringing churchbells and openings of public swimming pools, which had been drained for fear of contagion. Within six years, annual cases of the paralyzing disease had declined from 14,000 to fewer than 1,000.

By 1979, polio had been virtually eliminated in developed nations.

“I think it’s absolutely fair to say that had it not been for Dr. Youngner, the polio vaccine would not have come into existence,” Dr. Salk’s son, Peter L. Salk, president of the Jonas Salk Legacy Foundation and a visiting professor at the University of Pittsburgh Graduate School of Public Health, said in an email.

While Dr. Youngner, who was 34 at the time, remained at the university and made further advances in virology, he and other members of the team remained embittered that Dr. Salk had not singled them out for credit in his announcement speech.

The printed version was prefaced with the phrase “From the Staff of the Virus Research Laboratory by Jonas E. Salk, M.D.,” and a United Press account quoted him as crediting his original three assistants, who had joined him as early as 1949 — Dr. Youngner, Army Maj. Byron L. Bennett and Dr. L. James Lewis — as well as three others.

“The really important thing to recognize is that the development of the polio vaccine at the University of Pittsburgh was a team effort,” Dr. Peter Salk wrote.

He added, “There is no question that my father recognized the importance of the team, and if there were circumstances in which that wasn’t adequately expressed, I would feel that it needs to be expressed now and very clearly so.”

In 1993, Dr. Youngner crossed paths with Dr. Salk for the first time since Dr. Salk left for California in 1961. According to “Polio: An American Story” (2005), by David M. Oshinsky, Dr. Youngner raised the 1955 announcement speech in confronting Dr. Salk.

“Do you remember whom you mentioned and whom you left out?” the book quoted him as saying to Dr. Salk. “Do you realize how devastated we were at that moment and ever afterward when you persisted in making your co-workers invisible?”

Asked later, though, whether he regretted having worked for Dr. Salk, Dr. Youngner replied: “Absolutely not. You can’t imagine what a thrill that gave me. My only regret is that he disappointed me.”

Dr. Youngner’s contribution to the team was threefold.

He developed a method called trypsinization, using monkey kidney cells to generate sufficient quantities of the virus for experiments and production of the vaccine. He also found a way to deactivate the virus without disrupting its ability to produce antibodies. And he created a color test to measure polio antibodies in the blood to determine whether the vaccine was working.

He later contributed research to understanding interferon as an antiviral agent in the treatment of cancer and hepatitis; to the development (with Dr. Samuel Salvin) of gamma interferon, which is used against certain infections; and to advances that resulted in vaccines for Type A influenza and (with Dr. Patricia Dowling) equine influenza.

“As a direct result of his efforts, there are countless numbers of people living longer and healthier lives,” Dr. Arthur S. Levine, the University of Pittsburgh’s senior vice chancellor for the health sciences and dean of its medical school, said in a statement.

Julius Stuart Youngner was born on Oct. 24, 1920, in Manhattan and raised in the Bronx, where he survived lobar pneumonia, a severe infection of the lungs. His father, Sidney Donheiser, was a businessman. His mother was Bertha Youngner. He took her surname when his parents divorced.

After graduating from Evander Childs High School in the Bronx at 15, he earned a bachelor’s degree in English with a minor in biology from New York University in 1939 and a master’s and doctorate of science in microbiology from the University of Michigan.

Drafted into the Army in World War II, he worked on the Manhattan Project at Oak Ridge, Tenn., and at the University of Rochester, testing the toxicity of uranium salts. He said he learned of the project’s goal of building an atomic bomb only when it was dropped on Japan.

He was working at the National Cancer Institute, part of the National Institutes of Health, when the University of Pittsburgh hired him as an assistant professor in 1949 to assist Dr. Salk. He was a professor of microbiology and medical genetics at the university School of Medicine and chairman of the department of microbiology (biochemistry and microbiology were added later) from 1966 until his retirement in 1989.

His first wife, the former Tula Liakakis, died in 1963. Besides their son, Stuart, a psychiatry and bioethics professor at Case Western Reserve University in Cleveland, Dr. Youngner is survived by his wife, the former Rina Balter; a daughter, Lisa, an artist, also from his first marriage; three grandchildren; and a half brother, Alan Donheiser.

Dr. Youngner’s infectious curiosity, as a colleague characterized it, generated hundreds of scholarly papers and more than 15 patents. He was president of the American Society for Virology from 1986 to 1987.

When he was 7, Dr. Youngner nearly died from the pneumonia he had contracted when bacteria ate through his chest and infected a rib. An effective vaccine for pneumonia and antibiotics would not be invented for nearly two decades.

“So they strapped my legs to a table, and two nuns held my arms and another held my head and they prayed while they operated on me,” he recalled in an oral history interview in the early 1990s with the National Council of Jewish Women. “To this day I can remember the feeling of the saw on that rib.

“Later in life, when I had to have some minor surgery,” he said, “I put it off for years because I was so affected by this episode.”

https://mobile.nytimes.com/2017/05/04/science/julius-youngner-dead-salk-polio-vaccine-researcher.html?_r=0&referer=https://www.google.com/