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Autoimmune Disease, Behavioral Science, Immunology, Pediatrics, Research

What happens when the immune system attacks the brain? Stanford doctors investigate

What happens when the immune system attacks the brain? Stanford doctors investigate

SM PANS image - smallerThe first time he flew into a psychotic rage, Paul Michael Nelson was only 7 years old. He stabbed at a door in his family’s home with a knife, tore at blankets with his teeth, spoke in gibberish. His very worried parents, Paul and Mary Nelson, rushed him to their local emergency room, where the medical staff thought that perhaps the little boy had simply had a bad temper tantrum.

But his rages got worse. Over the weeks and months that followed the first March 2009 emergency room visit, as Paul Michael cycled in and out of psychiatric hospitals, his parents and doctors struggled to understand what was wrong. Finally, they came to a surprising conclusion: Paul Michael had an autoimmune disease. His immune system appeared to be attacking his brain.

As strange as the case seems, the Nelsons are far from alone. As I describe in a recent story for Stanford Medicine magazine, Paul Michael was the first of more than 70 children who have been evaluated at a new clinic at Lucile Packard Children’s Hospital Stanford for pediatric acute-onset neuropsychiatric syndrome, a disease (or, more likely, a group of diseases) that doctors are still working to define. The suddenness and severity of the syndrome are frightening. Healthy children abruptly begin to show psychiatric symptoms that can include severe obsessive-compulsive behavior; anorexia; intense separation anxiety at the thought of being away from a parent; deterioration in their school work, and many other problems. From my story:

“In some ways, it’s like having your kid suddenly become an Alzheimer’s patient, or like having your child revert back to being a toddler,” says Jennifer Frankovich, MD, clinical assistant professor of pediatric rheumatology at the School of Medicine and one of the clinic’s founders.

“We can’t say how many kids with psychiatric symptoms have an underlying immune or inflammatory component to their disorder, but given the burgeoning research indicating that inflammation drives mood disorders and other psychiatric problems, it’s likely to be a large subset of children and even adults diagnosed with psychiatric illnesses,” says Kiki Chang, MD, professor of psychiatry and behavioral sciences.

To shed light on the disease, Frankovich and Chang are working with scientists from around the world on defining the parameters of the illness and launching urgently-needed research. In a special issue of the Journal of Child and Adolescent Psychopharmacology that published online this month, the researchers lay out several aspects of the problem. The Stanford experts are co-authors of a scientific article describing how doctors should evaluate children with the disease, known by its acronym, PANS. Other researchers have written about disordered eating in PANS and given a detailed description of the disease phenotype.

Recognition and treatment of the disease are still an uphill battle, but the growth of research efforts is a hopeful step. As Frankovich says at the conclusion of the Stanford Medicine story, “We cannot give up on this. There are so many of these cases out there.”

Previously: Stanford Medicine magazine traverses the immune system and My descent into madness – a conversation with author Susannah Cahalan
Illustration by Jeffrey Decoster

Imaging, Immunology, Infectious Disease, Neuroscience, Research, Stanford News

Some headway on chronic fatigue syndrome: Brain abnormalities pinpointed

Some headway on chronic fatigue syndrome: Brain abnormalities pinpointed

patchbrainHow can you treat a disease when you don’t know what causes it? Such a mystery disease is chronic fatigue syndrome, which not so long ago was written off by many physicians as a psychiatric phenomenon because they just couldn’t figure out what else might be behind it. No one was even able to identify an anatomical or physiological “signature” of the disorder that could distinguish it from any number of medical lookalikes.

“If you don’t understand the disease, you’re throwing darts blindfolded,” Stanford neuroradiologist Mike Zeineh, MD, PhD, told me about a week ago. Zeineh is working to rip that blindfold from CFS researchers’ eyes.

From a release I wrote about some breaking CFS research by Zeineh and his colleagues:

CFS affects between 1 million and 4 million individuals in the United States and millions more worldwide. Coming up with a more precise number of cases is tough because it’s difficult to actually diagnose the disease. While all CFS patients share a common symptom — crushing, unremitting fatigue that persists for six months or longer — the additional symptoms can vary from one patient to the next, and they often overlap with those of other conditions.

A study just published in Radiology may help to resolve those ambiguities. Comparing brain images of 15 CFS patients with those from 14 age- and sex-matched healthy volunteers with no history of fatigue or other conditions causing similar symptoms, Zeineh and his colleagues found distinct differences between the brains of patients with CFS and those of healthy people.

The 15 patients were chosen from a group of 200 people with CFS whom Stanford infectious-disease expert Jose Montoya, MD, has been following for several years in an effort to identify the syndrome’s underlying mechanisms and speed the search for treatments. (Montoya is a co-author of the new study.)

In particular, the CFS patients’ brains had less overall white matter (cable-like brain infrastructure devoted to carrying signals rather than processing information), aberrant structure in a portion of a white-matter tract called the right arcuate fasciculus, and thickened gray matter (that’s the data-crunching apparatus of the brain) in the two places where the right arcuate fasciculus originates and terminates.

Exactly what all this means is not clear yet, but it’s unlikely to be spurious. Montoya is excited about the discovery. “In addition to potentially providing the CFS-specific diagnostic biomarker we’ve been desperately seeking for decades, these findings hold the promise of identifying the area or areas of the brain where the disease has hijacked the central nervous system,” he told me.

No, not a cure yet. But a well-aimed ray of light that can guide long-befuddled CFS dart-throwers in their quest to score a bullseye.

Previously: Unbroken: A chronic-fatigue patient’s long road to recovery, Deciphering the puzzle of chronic-fatigue syndrome and Unraveling the mystery of chronic-fatigue syndrome
Photo by Kai Schreiber

Autoimmune Disease, Chronic Disease, Immunology, Stanford News, Videos

Unbroken: A chronic fatigue patient’s long road to recovery

Unbroken: A chronic fatigue patient’s long road to recovery

“Fatigue is what we experience, but it is what a match is to an atomic bomb,” said Laura Hillenbrand, the author of Unbroken, about how it feels to live with chronic fatigue syndrome.

I recently finished a Stanford Medicine story and video (above) about another CFS patient, “Erin,” who asked that her real name not be used. After an acute illness in rural Mexico, Erin went from being an elite soccer player to one of the 17 million people worldwide who suffer from the condition.

Most people who acquire hit-and-run infections go back to their normal lives after a few days. But these patients don’t. They become virtual shut-ins, prisoners of a never-ending cycle of flu-like symptoms, many of them bedridden for years. CFS, also called myalgic encephalomyelitis or ME/CFS, has no known cause or cure, frustrating both patients and physicians.

What makes Erin’s CFS story somewhat rare is its happy ending. With the help of Stanford infectious disease expert José Montoya, MD, and cardiac electrophysiologist Karen Friday, MD, Erin is back to working fulltime and playing soccer.

“Dr. Montoya and doctors like him are heroes for taking up an unpopular disease and patients that most doctors shun,” said Lori Chapo-Kroger, a registered nurse and CEO of the patient charity, PANDORA Org. “He combines his medical expertise and a creative approach with a truly caring heart for suffering patients.”

Dr. Montoya is also collaborating with immunologist Mark Davis, PhD, on the Stanford Initiative on Infection-Associated Chronic Diseases, a research project using cutting-edge technologies to identify the biomarkers and root causes of ME/CFS. Working at the Human Immune Monitoring Center, team members are searching 600 blood samples for infectious microbes, inflammation-related molecules and genetic flaws. In addition, they’re conducting brain scans and physical exams to look for physical abnormalities among these patients.

Early results are promising — the team has discovered a number of measurable biological markers that indicate that ME/CFS patients may be suffering from out-of-control inflammation.

The team’s goal: To find out what is wrong with the immune systems of patients with infection-triggered diseases such ME/CFS and Lyme disease, then figure out how to help them get better.

Previously: Deciphering the puzzle of chronic fatigue syndrome

The HIMC is partially funded by Spectrum, Stanford’s NIH Clinical and Translational Science Award.

Immunology, Infectious Disease, Microbiology, Public Health, Research, Stanford News

Paradox: Antibiotics may increase contagion among Salmonella-infected animals

Paradox: Antibiotics may increase contagion among Salmonella-infected animals

cattleMake no mistake: Antibiotics have worked wonders, increasing human life expectancy as have few other public-health measures (let’s hear it for vaccines, folks). But about 80 percent of all antibiotics used in the United States are given to livestock – chiefly chickens, pigs, and cattle – at low doses, which boosts the animals’ growth rates. A long-raging debate in the public square concerns the possibility that this widespread practice fosters the emergence of antibiotic-resistant bugs.

But a new study led by Stanford bacteriologist Denise Monack, PhD, and just published in Proceedings of the National Academy of Sciences, adds a brand new wrinkle to concerns about the broad administration of antibiotics: the possibility that doing so may, at least  sometimes, actually encourage the spread of disease.

Take salmonella, for example. One strain of this bacterial pathogen, S. typhimurium, is responsible for an estimated 1 million cases of food poisoning, 19,000 hospitalizations and nearly 400 deaths annually in the United States. Upon invading the gut, S. typhimurium produces a potent inflammation-inducing endotoxin known as LPS.

Like its sister strain S. typhi (which  causes close to 200,00o typhoid-fever deaths worldwide per year), S. typhimurium doesn’t mete out its menace equally. While most get very sick, it is the symptom-free few who, by virtue of shedding much higher levels of disease-causing bacteria in their feces, account for the great majority of transmission. (One asymptomatic carrier was the infamous Typhoid Mary, a domestic cook who, early in the 20th century, cheerfully if unknowingly spread her typhoid infection to about 50 others before being forcibly, and tragically, quarantined for much of the rest of her life.)

You might think giving antibiotics to livestock, whence many of our S. typhi-induced food-poisoning outbreaks derive, would kill off the bad bug and stop its spread from farm animals to those of us (including me) who eat them. But maybe not.

From our release on the study:

When the scientists gave oral antibiotics to mice infected with Salmonella typhimurium, a bacterial cause of food poisoning, a small minority — so called “superspreaders” that had been shedding high numbers of salmonella in their feces for weeks — remained healthy; they were unaffected by either the disease or the antibiotic. The rest of the mice got sicker instead of better and, oddly, started shedding like superspreaders. The findings … pose ominous questions about the widespread, routine use of sub-therapeutic doses of antibiotics in livestock.

So, the superspreaders kept on spreading without missing a step, and the others became walking-dead pseudosuperspreaders. A lose-lose scenario all the way around.

“If this holds true for livestock as well – and I think it will – it would have obvious public health implications,” Monack told me. “We need to think about the possibility that we’re not only selecting for antibiotic-resistant microbes, but also impairing the health of our livestock and increasing the spread of contagious pathogens among them and us.”

Previously: Did microbes mess with Typhoid Mary’s macrophages?, Joyride: Brief post-antibiotic sugar spike gives pathogens a lift and What if gut-bacteria communities “remember” past antibiotic exposures?
Photo by Jean-Pierre

Immunology, Mental Health, Stanford News

Stanford Medicine magazine traverses the immune system

Stanford Medicine magazine traverses the immune system

cover_fall2014_2If you want to understand the human immune system, try studying humans – not mice. That’s what Mark Davis, PhD, urges in a special report on the immune system in the new issue of Stanford Medicine magazine.

For decades, most research on the immune system has used mice. Davis, director of Stanford’s Institute for Immunology, Transplantation and Infection, launched Stanford’s Human Immune Monitoring Center a few years ago to change the immunology research paradigm.

“Inbred mice have not, in most cases, been a reliable guide for developing treatments for human immunological diseases,” Davis says in the special report, titled “Balancing act: The immune system.”

As the editor of the magazine, I wanted to feature a story that showed how human-focused immunology research plays out. So I was glad to learn that the center is in the midst of its largest study so far – one to figure out the cause of chronic fatigue syndrome. A team led by Stanford professor of infectious diseases José Montoya, MD, is looking for meaningful patterns in the components of blood samples gathered from 200 patients with chronic fatigue syndrome and 400 healthy subjects.

“It’s like dumping a hundred different puzzles on the floor and trying to find two pieces that fit,” Davis says in our story. We also have a video about a patient’s seven-year battle with chronic fatigue, from despair to recovery.

Also covered in this issue:

  • “I can eat it”: on a revolutionary treatment for food allergies
  • “Brain attack”: on the struggle to help children with psychiatric illness caused by a malfunctioning immune system – a condition known as PANS or PANDAS
  • “When bones collide”: on a new view on the cause of osteoarthritis: autoinflammation
  • “My rendezvous with insanity”: a Q&A with Susannah Cahalan, author of Brain on Fire: My Month of Madness, her memoir of surviving an autoimmune attack on her brain
  • “The swashbuckler”: on look back to the early days of molecular biology when Mark Davis cracked one of the greatest mysteries of the immune system

The issue also includes an article on efforts at the VA Palo Alto Health Care System to use peer-support services to help veterans with post-traumatic stress disorder, and a story on the growing concern that biomedical research results are often erroneous and efforts being made to solve the problem.

The issue was funded in part by the Institute for Immunology, Transplantation and Infection.

Previously: Stanford Medicine magazine opens up the world of surgery, Mysteries of the heart: Stanford Medicine magazine answers cardiovascular questions and From womb to world: Stanford Medicine Magazine explores new work on having a baby.
Illustration by Jeffrey Decoster

Immunology, In the News, Parenting, Pediatrics

Ivy and Bean help encourage kids to get vaccinated

Ivy and Bean help encourage kids to get vaccinated

Ivy and Bean2Last week, I took my two little boys to get their shots, including the MMR vaccine that protects against measles, mumps and rubella. Although, as a mom, it’s easy for me to understand the value of vaccines, I’m not sure my preschooler was completely convinced that getting poked in the arm was a great idea.

That’s why I am thrilled to see “Ivy and Bean vs. The Measles,” a set of posters and other educational materials that Sophie Blackall, the illustrator of the popular series of children’s books, has produced in collaboration with the Measles and Rubella Initiative. Blackall’s illustrations show Bean, one of the book’s two heroines, devising a series of unconventional strategies for avoiding the measles: wear a biohazard suit for the rest of your life, get adopted by a polar bear, or (my personal favorite) cover yourself in a 6-inch protective layer of lard.

“Or,” says Ivy, “get vaccinated!”

My son would probably be most interested in Bean’s suggestion to “Move to the moon!” He loves all things outer space-related, and I love the idea of finding something at our doctor’s office that would spark his interest and help me explain to him why he needs that brief poke in the arm.

Bravo, Ivy and Bean!

Via Shots
Previously: Side effects of childhood vaccines are extremely rare, new study finds, Measles is disappearing from the Western hemisphere and Tips for parents on back-to-school vaccinations
Artwork by Sophie Blackall

Big data, Chronic Disease, Immunology, Research, Stanford News

Out of hiding: Found lurking in public databases, type-2 diabetes drug passes early test

Out of hiding: Found lurking in public databases, type-2 diabetes drug passes early test

lurking 3Way too often, promising-looking basic-research findings – intriguing drug candidates, for example – go swooshing down the memory hole, and you never hear anything about them again. So it’s nice when you see researchers following up on an upbeat early finding with work that moves a potential drug to the next peg in the development process. All the more so when the drug candidate targets a massively prevalent disorder.

Type 2 diabetes affects more than 370 million people worldwide, a mighty big number and a mighty big market for drug companies. (Unlike the much less common type 1-diabetes, where the body’s production of the hormone insulin falters and sugar builds up in the blood instead of being taken up by cells throughout the body, in type-2 diabetes insulin production may be fine but tissues become resistant to insulin.) But while numerous medications are available, none of them decisively halt progression, much less reverse the disease’s course.

About two-and-a-half years ago, Stanford data-mining maven Atul Butte, MD, PhD, combed huge publicly available databases, pooled results from numerous studies and, using big-data statistical methods, fished out a gene that had every possibility of being an important player in type 2 diabetes, but had been totally overlooked. (For more info, see this news release.) Called CD44,  this gene is especially active in fat tissue of insulin-resistant people and, Butte’s study showed, had a strong statistical connection to type-2 diabetes.

Butte’s study suggested that CD44′s link to type-2 diabetes was not just statistical but causal: In other words, manipulating the protein CD44 codes for might influence the course of the disease. By chance, that protein has already been much studied by immunologists for totally unrelated reasons. The serendipitous result is that a monoclonal antibody that binds to the protein and inhibits its action was already available.

So, Butte and his colleagues used that antibody in tests they performed on lab mice bioengineered to be extremely susceptible to type-2 diabetes, or what passes for it in a mouse. And, it turns out, the CD44-impairing antibody performed comparably to or better than two workhorse diabetes medications (metformin and pioglitazone) in countering several features of type 2 diabetes, including fatty liver, high blood sugar, weight gain and insulin resistance. The results appear in a study published today in the journal Diabetes.

Most exciting of all: In targeting CD44, the monoclonal antibody was working quite differently from any of the established drugs used for type-2 diabetes.

These are still early results, which will have to be replicated and – one hopes – improved on, first in other animal studies and finally in a long stretch of clinical trials before any drug aimed at CD44 can join the pantheon of type-2 diabetes medications. In any case, for a number of reasons the monoclonal antibody Butte’s team pitted against CD44 is far from perfect for clinical purposes. But refining initial “prototypes” is standard operating procedure for drug developers. So here’s hoping a star is born.

Previously: Newly identified type-2 diabetes gene’s odds of being a false finding equal one in 1 followed by 19 zeroes, Nature/nurture study of type-2 diabetes risk unearths carrots as potential risk reducers and Mining medical discoveries from a mountain of ones and zeroes
Photo by Dan-Scape.co.uk

Clinical Trials, History, Immunology, Infectious Disease, Research

Stanford scientists strive to solve centuries-old puzzle: Why are young children so vulnerable to disease?

Stanford scientists strive to solve centuries-old puzzle: Why are young children so vulnerable to disease?

512px-Gabriël_Metsu_-_The_Sick_Child_-_WGA15091

Several months ago, Stanford immunologist Mark Davis, PhD, went for a stroll in Union Cemetery in Redwood City, Calif. (not far from the Stanford campus). Graves there date from the Civil War-era and Davis, who’s currently immersed in a study of childhood immunity, was intrigued.

“In the early years, you see entire families — mom, dad, and then a whole bunch of children’s headstones,” Davis told me. “It really brought home to me how differently we live now that we just take for granted a kid will survive and grow up.”

Vaccines arrived and childhood survival rates soared. Yet young children remain much more vulnerable to infectious diseases than adults. Why?

Davis and his team think vaccines trigger a set of changes that strengthens children’s immune systems — allowing them to ward off diseases they haven’t even heard of before. That’s why the researchers are conducting a group of studies, all focused on revealing new details about the immune system’s response to the flu vaccine. They need participants, particularly young children who have never received a flu vaccine before. They also need older children and twins. All participants will receive a licensed flu vaccine that will help protect from influenza this coming winter.

Davis and colleagues plan to investigate the children’s development of two types of immune cells — memory T and B cells — that are specialized to recognize certain foreign invaders. Interestingly, adults have T cells that spot diseases they’ve never been exposed to, such as HIV, Davis said. Yet newborns lack these specialized cells, leaving them vulnerable to infection.

“Somewhere between birth and adulthood we see the appearance of these memory T cells without having the particular disease,” Davis said. “It’s a real puzzle.”

Davis suspects that routine vaccines and infections may spur the development in children of a broad spectrum of memory T cells, ones that recognize all sorts of diseases. One study plans to follow children for several years, perhaps revealing how, and when, the children develop a full compliment of these memory T cells, Davis told me.

The studies are possible thanks to the development of new analytical techniques, according to virologist and immunologist Harry Greenberg, MD, who is working with Davis on the influenza studies.

“We’ve been studying influenza for half a century, but these new assays developed in the last five years offer hope we can develop better ways of protecting more people,” Greenberg told me.

More information about the flu vaccine studies and the Stanford-LPCH Vaccine Program is available here or (650) 498-7284.

Becky Bach is a proud graduate of the UC Santa Cruz Science Communication Program (go Banana Slugs!) and a science-writing intern at the Office of Communications and Public Affairs.

Previously: Q&A about enterovirus-D68 with Stanford/Packard infectious disease expert, Gut bacteria may influence effectiveness of flu vaccine and Side effects of childhood vaccines are extremely rare, new study finds
Photo by Gabriel Metsu

Biomed Bites, Immunology, Research, Transplants, Videos

Marked improvement in transplant success on the way, says Stanford immunologist

Marked improvement in transplant success on the way, says Stanford immunologist

This is the third installment of our Biomed Bites series, a weekly feature that highlights some of Stanford’s most compelling research and introduces readers to innovative scientists from a variety of disciplines.

“Boost your immune system” is practically a mantra for some health-savvy folks who chug vitamin C or oregano oil (yep!) to ward off errant germs. But sometimes having a weaker immune system is a good thing. Take transplant patients: If their immune system attacks invaders with too much gusto, then the new organ is at risk as well.

But transplant patients don’t want to completely dismantle their immune systems – and that’s where Stanford immunologist Sheri Krams, PhD, comes in. “We want to specifically temper the immune response to that new foreign organ,” Krams says about her work in the video above.

Transplant patients can survive for decades by taking immunosuppressive drugs, yet long-term use of these drugs can weaken bones, muscles and leave patients more vulnerable to infection. But through basic research, this basic transplant conundrum is changing, Krams says:

We’ve made major strides in the field of transplantation in the last few years…  We’re thinking that our research, in a very short period of time, will markedly improve the quality of life for transplant recipients and people that will be receiving stem cell transplants.

Learn more about Stanford Medicine’s Biomedical Innovation Initiative and about other faculty leaders who are driving forward biomedical innovation here.

Becky Bach is a former park ranger and newspaper reporter who now spends her time writing about science or practicing yoga. She’s currently a science writing intern in the medical school’s Office of Communication & Public Affairs.

Previously: Stanford study in transplant patients could lead to better treatmentExtracting signal from noise to combat organ rejection and Kidney-transplant recipients party without drugs — immune-suppressing anti-rejection drugs, that is

Clinical Trials, Immunology, Pain, Research, Stanford News, Surgery, Technology

Discovery may help predict how many days it will take for individual surgery patients to bounce back

Discovery may help predict how many days it will take for individual surgery patients to bounce back

pandaPost-surgery recovery rates, even from identical procedures, vary widely from patient to patient. Some feel better in a week. Others take a month to get back on their feet. And – until now, anyway – nobody has been able to accurately predict how quickly a given surgical patient will start feeling better. Docs don’t know what to tell the patient, and the patient doesn’t know what to tell loved ones or the boss.

Worldwide, hundreds of millions of surgeries are performed every year. Of those, tens of millions are major ones that trigger massive inflammatory reactions in patients’ bodies. As far as your immune system is concerned, there isn’t any difference between a surgical incision and a saber-tooth tiger attack.

In fact, that inflammatory response is a good thing whether the cut came from a surgical scalpel or a tiger’s tooth, because post-wound inflammation is an early component of the healing process. But when that inflammation hangs on for too long, it impedes rather than speeds healing. Timing is everything.

In a study just published in Science Translational Medicine, Stanford researchers under the direction of perioperative specialist Martin Angst, MD, and immunology techno-wizard Garry Nolan, PhD, have identified an “immune signature” common to all 32 patients they monitored before and after those patients had hip-replacement surgery. This may permit reasonable predictions of individual patients’ recovery rates.

In my news release on this study, I wrote:

The Stanford team observed what Angst called “a very well-orchestrated, cell-type- and time-specific pattern of immune response to surgery.” The pattern consisted of a sequence of coordinated rises and falls in numbers of diverse immune-cell types, along with various changes in activity within each cell type.

While this post-surgical signature showed up in every single patient, the magnitude of the various increases and decreases in cell numbers and activity varied from one patient to the next. One particular factor – changes, at one hour versus 24 hours post-surgery, in the activation states of key interacting proteins inside a small set of “first-responder” immune cells – accounted for 40-60 percent of the variation in the timing of these patients’ recovery.

That robust correlation dwarfs those observed in earlier studies of the immune-system/recovery connection – probably because such previous studies have tended to look at, for example, levels of one or another substance or cell type in a blood sample. The new method lets scientists simultaneously score dozens of identifying surface features and goings-on inside cells, one cell at a time.

The Stanford group is now hoping to identify a pre-operation immune signature that predicts the rate of recovery, according to Brice Gaudilierre, MD, PhD, the study’s lead author. That would let physicians and patients know who’d benefit from boosting their immune strength beforehand (there do appear to be some ways to do that), or from pre-surgery interventions such as physical therapy.

This discovery isn’t going to remain relevant only to planned operations. A better understanding, at the cellular and molecular level, of how immune response drives recovery from wounds may also help emergency clinicians tweak a victim’s immune system after an accident or a saber-tooth tiger attack.

Previously: Targeting stimulation of specific brain cells boosts stroke recovery in mice, A closer look at Stanford study on women and pain and New device identifies immune cells at an unprecedented level of detail, inside and out
Photo by yoppy

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