Publisher Health

Scientists at Osaka Metropolitan University utilized a Japan-developed, objective, and simple nutritional indicator called the Nutrition Risk Index (NRI) to unveil a long-suspected yet unverified relationship between sarcopenia and malnutrition in end-stage kidney disease patients. Their findings confirmed that malnutrition contributes to sarcopenia, which can be detected through NRI.
End-stage kidney disease patients undergoing maintenance hemodialysis (MHD) often struggle with malnutrition and sarcopenia, a form of musculoskeletal atrophy that amplifies mortality. Untangling the long-suspected relationship between malnutrition and sarcopenia has bedeviled researchers due to the lack of a diagnostic standard for nutritional health or status. Scientists from Osaka Metropolitan University took a step toward explaining this relationship using a convenient, objective, Japan-developed nutritional risk index, a new approach for early detection of sarcopenia in MHD patients. Their findings were published in Frontiers in Nutrition.
Conventionally, investigating malnutrition in MHD patients has involved complicated nutritional screening tools that often require examiners’ subjective assessments, making them time-consuming and irreproducible. Moving beyond this practice, the research team made use of the Japanese nutritional risk index (NRI), a nutrition indicator designed for MHD patients. “The NRI score is calculated from four objective and routinely measured variables, namely creatinine, total cholesterol, serum albumin, and BMI,” elaborated Dr. Masafumi Kurajoh, first author of this study. “A high NRI score signals malnutrition.”
Sarcopenia is characterized by losses of muscle mass, strength, and function. The researchers collected data on the NRI scores, muscle mass, muscle strength, and physical performance of 315 MHD patients, who were divided into low-risk and medium/high-risk groups according to their NRI scores. The patients with low muscle mass along with either low muscle strength or low physical performance were diagnosed with sarcopenia. Those experiencing all three conditions were considered to have severe sarcopenia.
Results of multiple regression analysis show significant relationships between the NRI score or the NRI score-based medium/high-risk group and sarcopenia and severe sarcopenia, as well as low muscle mass, strength, and physical performance. These findings confirm that malnutrition contributes to sarcopenia and does so through diminishing the MHD patients’ muscle mass, strength, and physical performance. Furthermore, the results indicate the usefulness of the NRI score as a sarcopenia detection tool.
“Our findings suggest the NRI score as a simple and objective nutritional screening tool for early detection of sarcopenia,” concluded Dr. Kurajoh. “The significant relationship between malnutrition and sarcopenia found in our study also signals the need for therapeutic strategies targeting nutritional status to prevent the onset and progression of sarcopenia.”
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Researchers at Kyushu University have identified a number of key blood biomarkers for pathological social withdrawal, known as Hikikomori. Based on their findings, the team was able to distinguish between healthy individuals and hikikomori patients as well as determine the severity of the condition.
According to Japan’s Ministry of Health, Labour, and Welfare, hikikomori is a condition in which individuals do not to leave their dwelling and isolate themselves away from society and family for a period exceeding six months. Also identified as ‘pathological social withdrawal,’ hikikomori is estimated to afflict more than one million people in Japan today. While it has been historically identified as a Japanese culture-bound syndrome, evidence over the last few decades has shown that it is becoming a global phenomenon, with some fearing the COVID-19 pandemic catalyzing a global wave of hikikomori patients.
In 2013, the Kyushu University Hospital established the world’s first outpatient clinic for hikikomori research in hopes of developing support systems for patients through biological, psychological, and social understanding of the condition.
In a report published in Dialogues in Clinical Neuroscience, lead researcher Takahiro A. Kato of Kyushu University’s Faculty of Medical Sciences explains that while the sociological underpinnings of the condition are carefully studied, major gaps remain in the understanding of the biological aspects of hikikomori.
“Mental illnesses such as depression, schizophrenia, and social anxiety disorder are occasionally observed in hikikomori individuals. However, our past research shows that it is not that simple, and that it is a complex condition with overlaps of different psychiatric and non-psychiatric elements,” explains Kato. “Understanding what happens biologically will help us greatly in identifying and treating hikikomori.”
The team conducted blood biochemical tests and collected data on the plasma metabolome — small molecules found in blood such as sugars, amino acids, and proteins — from 42 unmedicated hikikomori individuals and compared it with data from 41 healthy volunteers. In total, data for 127 molecules were analyzed.
“Some of our key findings showed that, in the blood of men with hikikomori, ornithine levels and serum arginase activity were higher while bilirubin and arginine levels were lower,” states first author of the paper Daiki Setoyama. “In both men and women patients, long-chain acylcarnitine levels were higher. Moreover, when this data was further analyzed and categorized, we were able to distinguish between healthy and hikikomori individuals, and even predict its severity.”
Ornithine is an amino acid produced from the amino acid arginine with the help of the enzyme arginase. These molecules are vital in many bodily functions, including blood pressure regulation and the urea cycle.
Bilirubin is made when the liver breaks down red blood cells and is often used as a marker for proper liver function. Patients with major depression and seasonal affective disorder have been reported to have lower blood bilirubin levels.
Finally, acylcarnitines play an important role in supplying energy to the brain. Its levels decrease when patients with depression take selective serotonin reuptake inhibitors. However, patients with hikikomori differ from patients with depression in that only the long-chain acylcarnitines are elevated in hikikomori whereas short-chain acylcarnitines remain the same.
Says Kato, “Identifying the biomarkers of hikikomori is the first step in uncovering the biological roots of the condition and connecting them to its severity. We hope these findings will lead to better specialized treatments and support for hikikomori.”
“Many questions remain, including understanding the root causes behind these biomarkers. Today, hikikomori is spreading worldwide, thus, we must conduct international investigations to understand the similarities and differences between patients with hikikomori globally,” he concludes.
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Researchers at Kobe University and Hiroshima University have successfully developed a biomarker that will enable Parkinson’s disease to be rapidly and inexpensively diagnosed from blood serum samples.
It is hoped that being able to diagnose the disease faster will also lead to the development of new treatment methods. This would be greatly beneficial, especially for aging societies like Japan.
This study was conducted by Professor IMAISHI Hiromasa and Academic Researcher IHARA Kohei et al. of Kobe University’s Biosignal Research Center, and Assistant Professor OGURO Ami’s research group at Hiroshima University’s Graduate School of Integrated Sciences for Life. These research results were published in Springer Nature’s open journal Scientific Reports on April 22, 2022.
Main Points Japan is a super-aging country. As the elderly population continues to increase, it is predicted that the number of patients suffering from neurodegenerative diseases will also rise. Parkinson’s disease is a type of neurodegenerative disease for which a simple diagnosis method had yet to be developed. Currently, various biomarkers are in development that can be used to evaluate diseases. These biomarkers can detect the presence of a disease, as well as monitor its progress and the effectiveness of treatment. In a world-first, the researchers succeeded in developing a biomarker that can be used to easily and inexpensively assess Parkinson’s disease. It requires a mere approx. 30μ of serum from the patient. It is hoped that this biomarker can be used to develop diagnosis and treatment methods for Parkinson’s, as well as to advance research into discovering the molecular mechanism behind this disease.Research Background
Japan has the fastest growing elderly population in the world and is consequently facing related issues such as the decline in elderly people’s Quality of Life (QoL) and pressure on the caregiving sector.As people age, their risk of developing various diseases increases. In particular, neurodegenerative diseases such as Parkinson’s disease have a significant impact on the sufferer’s QoL. In addition, Parkinson’s is the second most common neurodegenerative disease in the world; believed to affect around 1~2% of the over 60s population. Furthermore, it is predicted to cost the global market 19.9 billion US dollars (including treatment costs) in 2030.

New research demonstrates that by killing essential gut bacteria, antibiotics ravage athletes’ motivation and endurance. The UC Riverside-led mouse study suggests the microbiome is a big factor separating athletes from couch potatoes.
Other studies have examined the way that exercise affects the microbiome, but this study is one of few to examine the reverse — how gut bacteria also impact voluntary exercise behaviors. Voluntary exercise involves both motivation and athletic ability.
The researchers’ methods and results are now detailed in the journal Behavioural Processes.
“We believed an animal’s collection of gut bacteria, its microbiome, would affect digestive processes and muscle function, as well as motivation for various behaviors, including exercise,” said Theodore Garland, UCR evolutionary physiologist in whose lab the research was conducted. “Our study reinforces this belief.”
Researchers confirmed through fecal samples that after 10 days of antibiotics, gut bacteria were reduced in two groups of mice: some bred for high levels of running, and some that were not.
Neither group of mice exhibited any signs of sickness behavior from the antibiotic treatment. So, when wheel running in the athletic mice was reduced by 21 percent, researchers were certain the microbiome damage was responsible. In addition, the high runner mice did not recover their running behavior even 12 days after the antibiotic treatment stopped.

Researchers have long known that memory is represented by changes in the part of the brain called the hippocampus.
One of the well-established changes in the hippocampus that has been associated with memory is the presence of so-called sharp wave ripples (SWR). These are brief, high-frequency electrical events generated in the hippocampus, and they are believed to represent a major event occurring in the brain in the so-called episodic memory. This type of memory refers to episodes that took place in the life of an individual, such as childhood memories, recollection of the first date with a partner or memory of an old cell phone number.
However, what happens in the famous seahorse-shaped structures of the brain – the hippocampus – when SRWs are generated has not been well understood.
Now a new study sheds light on the existence of a neuron type in the mouse hippocampus that might be a key to better understanding of episodic memory.
Professor Marco Capogna and Assistant professor Wen-Hsien Hou from the Department of Biomedicine at Aarhus University have contributed to the discovery of the novel neuron that is associated with sharp wave ripples and memory. The study was recently published in the scientific journal Neuron in collaboration with Professor Ivan Soltesz’ group at Stanford University.
Might be disrupted in dementia and Alzheimer’s
The study reports the novel neuron type – or nerve cell – in the hippocampus, defines its functional role in the brain, discloses its connectivity with other nerve cells and brain areas and progresses the understanding of brain circuits underlying fast brain waves that are often associated with memory.

About 3 grams daily of omega-3 fatty acids, consumed in foods or supplements, appears to be the optimal daily dose to help lower blood pressure, according to a research review published today in the Journal of the American Heart Association, an open access, peer-reviewed journal of the American Heart Association.
Omega-3 fatty acids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) are typically found in fatty fish, such as salmon, tuna, sardines, trout, herring and oysters. Some people also take combined DHA and EPA in supplements. While some studies suggest that consumption of omega-3 fatty acids may lower blood pressure, the optimal dosage needed to lower blood pressure has not been clear. The National Institutes of Health has established an adequate intake of omega-3 fatty acids for healthy people at 1.1- 1.6 grams daily, depending on age and sex.
“According to our research, the average adult may have a modest blood pressure reduction from consuming about 3 grams a day of these fatty acids,” said study author Xinzhi Li, M.D., Ph.D., assistant professor and program director of the School of Pharmacy at Macau University of Science and Technology in Macau, China.
Researchers analyzed the results of 71 clinical trials from around the world published from 1987 to 2020. The studies examined the relationship between blood pressure and the omega-3 fatty acids DHA and EPA (either individually or combined) in people aged 18 and older with or without high blood pressure or cholesterol disorders. There were nearly 5,000 participants combined, ranging in age from 22 to 86 years. Participants took dietary and/or prescription supplement sources of fatty acids for an average of 10 weeks.
The analysis found: Compared to adults who did not consume EPA and DHA, those who consumed between 2 and 3 grams daily of combined DHA and EPA omega-3 fatty acids (in supplements, food or both) had reduced systolic (top number) and diastolic (bottom number) blood pressure by an average 2 mm Hg. Consuming more than 3 grams of omega-3 fatty acids daily may have added blood pressure-lowering benefit for adults with high blood pressure or high blood lipids: At 3g a day of omega-3s, systolic blood pressure (SBP) decreased an average of 4.5 mm Hg for those with hypertension, and about 2 mm Hg on average for those without. At 5g a day of omega-3s, SBP declined an average of nearly 4 mm Hg for those with hypertension and less than 1 mm Hg on average for those without. Similar differences were seen in people with high blood lipids and among those older than age 45.About 4-5 ounces of Atlantic salmon provide 3 grams of omega 3 fatty acids. A typical fish oil supplement contains about 300 mg of omega-3s per pill, but doses vary widely.
“Most of the studies reported on fish oil supplements rather than on EPA and DHA omega-3’s consumed in food, which suggests supplements may be an alternative for those who cannot eat fatty fish such as salmon regularly,” Li said. “Algae supplements with EPA and DHA fatty acids are also an option for people who do not consume fish or other animal products.”
The U.S. Food and Drug Administration (FDA) announced in June 2019 that it did not object to the use of certain health claims that consuming EPA and DHA omega-3 fatty acids in food or dietary supplements may reduce the risk of hypertension and coronary heart disease. However, they noted that the evidence was inconclusive and highly inconsistent.
“Our study supports the FDA guidance that EPA and DHA omega-3 fatty acids may reduce the risk of coronary heart disease by lowering high blood pressure, especially among people already diagnosed with hypertension,” he said. “However, while our study may add a layer of credible evidence, it does not meet the threshold to make an authorized health claim for omega-3 fatty acids in compliance with FDA regulations.”
Limitations of the review include differences in how blood pressure was measured, and whether the studies examined omega-3 intake from supplements or diet, which may affect the strength of the conclusions.
The American Heart Association recommends eating two servings (3-4 ounces cooked) of fish per week (particularly fatty fish such as salmon) as part of a heart-healthy diet.
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A 4-year-old in Ohio is one of hundreds of children worldwide who have developed unexplained liver problems in recent months.It was three days before Christmas, and Elizabeth Widders was perched in her upstairs bathroom, fastening red and green bows in the hair of her 4-year-old daughter, Liviah. But as Liviah stood in the morning light, her mother noticed that the whites of her eyes had turned yellow.She hustled Liviah downstairs to ask her husband, Jack, for a second opinion. He saw the yellow tint, too.Liviah and her two siblings all had jaundice as babies, and their parents, from Mason, Ohio, were familiar with the telltale signs. “I knew: This is liver stuff,” Mrs. Widders recalled.They took Liviah to the emergency room, where she was diagnosed with acute hepatitis, an inflammation of the liver. Less than two weeks later, doctors removed her failing liver and replaced it with a new one.Over the past eight months, hundreds of other families have been caught in similar whirlwinds, as their otherwise healthy children developed hepatitis, seemingly out of the blue. Six hundred and fifty probable cases have been reported in 33 countries, according the World Health Organization. At least 38 children have required liver transplants, and nine have died.The cases have stumped experts, who are investigating a variety of potential causes. One leading hypothesis is that an adenovirus, a family of common viruses that typically cause flu- or cold-like symptoms, may be responsible, but many questions remain.The revelation that Liviah’s case might be part of a larger phenomenon has galvanized her parents, who have started sharing their story in hopes of educating others about the key warning signs.The cases are exceedingly rare, experts emphasize, and even then, most do not require transplants. “The odds of something like this happening are extremely small,” said Jack Widders, Liviah’s father.But without a solid explanation, it feels like lightning that could strike any family.Liviah, rear, and her sister, Juliana, swinging outside their home in Mason, Ohio.Maddie McGarvey for The New York TimesLiviah is not shy about showing off her transplant scar, which she calls her “princess mark.” Maddie McGarvey for The New York Times‘Where would she have gotten hepatitis?’The first signs of trouble came on Dec. 11, when Liviah began throwing up. At first, her parents chalked it up to overindulgence; Liviah had spent the previous night with her grandmother, who was known to spoil the children with treats. “We called it a ‘grandma hangover,’” Mrs. Widders recalled.Liviah, a lively, athletic child, bounced back quickly, but the next day, her 6-year-old brother, Jaxson, also fell ill. He spiked a high fever and was sick for days. Liviah — who returned to school, visited a trampoline park and decorated cookies with the neighbors — seemed to have dodged the worst of it.Until, a week and a half later, when her mother noticed her eyes. Her urine was orange, too, Liviah divulged to her.Understanding HepatitisAn inflammation of the liver generally caused by a virus, hepatitis carries a host of complicating factors, side effects and stigma. Personal Accounts: What is it like to live with the disease? Six individuals shared their experience. Symptoms in Children: Understand the warning signs of hepatitis parents should watch out for as a series of rare, but unusual cases are reported across the United States.Preventing Transmission: With infections on the rise, most adults should be getting screened for hepatitis.Pandemic’s Effect: A wave of diagnostics ushered in by Covid could help revive flagging efforts to eliminate hepatitis C, one of the most common forms of the disease.The hepatitis diagnosis came as a shock. The condition has a wide variety of potential causes, including exposure to toxins, heavy drinking and the hepatitis B and C viruses, which are often associated with intravenous drug use. Mrs. Widders stared at her husband in disbelief: “Where would she have gotten hepatitis?”(Hepatitis can also be caused by other viruses, although Mrs. Widders did not know that at the time.)That evening, Liviah was admitted to the Cincinnati Children’s Hospital Medical Center. “She came in in acute liver failure,” said Dr. Anna Peters, a pediatric transplant hepatologist who was part of Liviah’s medical team. “She was quite ill.”Over the following days, Liviah’s condition deteriorated.One of the liver’s primary roles is to process toxic substances, including ammonia that is naturally produced in the body; when the organ is not working properly, these toxins can travel to the brain, causing cognitive and behavioral changes. As Liviah’s ammonia levels rose, she became irritable and enraged, screaming at her mother without provocation.The damage to her liver, which produces proteins that help the blood to clot, also slowed her natural clotting response, leaving her at high risk for bleeding problems.Doctors gave Liviah steroids to reduce inflammation and a compound called lactulose to help flush out the ammonia. She had blood transfusions, CT scans, ultrasounds and a liver biopsy. Mr. and Mrs. Widders slept at the hospital, while relatives looked after Jaxson and their 1-year-old daughter.Liviah spent part of Christmas Day sedated, but woke up long enough to open some gifts, includingthe game Hungry Hungry Hippos. “She doesn’t remember a lot of Christmas, but she does know that Santa came,” Mr. Widders said.Liviah getting a scan during her stay at Cincinnati Children’s Hospital in December, before her transplant.via Jack and Liz WiddersLiviah returned briefly to the hospital after a liver rejection episode. She is taking medications to prevent another.Maddie McGarvey for The New York TimesTop of the listDespite the treatments, Liviah’s clotting problems persisted and her ammonia levels remained high. She woke up agitated and confused. She asked the same questions — Could she go for a walk? Where was her brother? — again and again. She could barely get through a game of Candyland with her grandmother, who was heartbroken. “Seeing her the way that we were seeing her, just rapidly deteriorate before our eyes, it’s like, ‘How much more time do we have?” her mother recalled.On Dec. 28, doctors broke the news: Liviah had been placed on the transplant list. Status 1A — the top priority.Doctors decided to start Liviah on liver dialysis to remove some of the toxins from her blood while they waited for a match. The call came just days later, while Liviah’s aunt was visiting. Mrs. Widders put the transplant coordinator on speakerphone: They had a liver for Liviah.It was a complicated moment for Liviah’s parents, their joy tempered with grief for the family of the deceased donor.“We were staring death in the face,” Mrs. Widders said.“That’s right,” her husband said. “And so we knew that our joy came at the expense of — ”“Of someone else’s selfless ‘Yes,’” she continued. “Someone else’s tragedy was our miracle.”On Jan. 1, Liviah received her new liver. The next day, doctors had her out of bed, working to regain her strength.On Jan. 12, Liviah was discharged from the hospital. The Widders family celebrated Christmas again when they returned home, and the neighbors kept their decorations up for Liviah. “There was a night that everyone put them on,” Mrs. Widders said, “and we were able to drive around and see the lights.”The Widders family shared Liviah’s story to raise awareness about the signs of liver problems and to encourage people to sign up to be organ donors.Maddie McGarvey for The New York TimesMr. Widders put sunscreen on Liviah before heading outside. From the outset, doctors told Liviah’s parents that they might never know why her liver failed.Maddie McGarvey for The New York TimesSearching for a causeFrom the beginning, doctors had warned Liviah’s parents that they might never know why her liver had failed; in many cases of pediatric hepatitis, clinicians never find a cause, Dr. Peters said.In Liviah’s case, doctors ruled out a variety of common triggers, but blood tests turned up one possible culprit: an adenovirus.Although there was no sign of the virus in the liver, an adenovirus infection could have “triggered an abnormal immune response that then attacked the liver,” Dr. Peters said.It was not a totally satisfying explanation, she conceded. Adenoviruses do not typically lead to liver damage in healthy children, and Liviah’s adenovirus levels were low.The mystery did not faze Liviah’s father. “I left the hospital going, ‘You know what? She’s alive,’” he said. “I don’t really need to know what caused it.”For Mrs. Widders, accepting the unknowns was harder, especially when Liviah had a liver rejection episode that briefly landed her back in the hospital. The setback prompted her mother to wonder whether Liviah might have some kind of genetic or autoimmune disorder, but testing turned up no evidence of that. By the spring, with Liviah home for good, her parents had made peace with the possibility that they might never get answers.And then, in April, a friend sent Mr. Widders a text about a mysterious cluster of childhood hepatitis cases in Britain. Shortly thereafter, he saw an article saying that the Centers for Disease Control and Prevention was investigating a similar cluster in Alabama; all nine of the Alabama children had tested positive for an adenovirus.A rest after playing outside.Maddie McGarvey for The New York TimesThe Widders family has been adjusting to a new normal, which includes administering immunosuppressive drugs to keep Liviah’s body from rejecting her new liver. Maddie McGarvey for The New York TimesTo Mr. and Mrs. Widders, the cases sounded eerily familiar — and brought their most difficult days rushing back. “It was a little traumatic,” Mrs. Widders said. “And then there was that sorrow of, ‘Oh my gosh, this is happening to more than just Liviah.’”So far, more than 200 potential hepatitis cases have been reported in children in the United States, according to the C.D.C. Many of the affected children have tested positive for an adenovirus — in many cases, adenovirus type 41, which typically causes gastrointestinal symptoms.But the virus has not been found in all of the affected children, and scientists are not sure why a common childhood virus might suddenly be prompting liver damage. They are investigating whether the virus has changed and whether other factors may be contributing to the phenomenon.It is possible that a prior coronavirus infection — or, conversely, the lack of exposure to adenoviruses during the pandemic shutdowns — may have left children more vulnerable, although both hypotheses remain speculative. It is also possible that adenovirus infections always caused hepatitis in a small subset of healthy children and that scientists were only now recognizing the connection.“Is it an increased awareness?” said Dr. William Balistreri, the director emeritus of the Pediatric Liver Care Center at Cincinnati Children’s. “Is it a new virus? Is it a new virus in synergy with an old virus?” He added, “I don’t think we can dismiss any of those theories.”The absence of an obvious cause has bewildered parents, too. In April, Ashley Tenold received an unexpected call from a school nurse, who informed her that her daughter appeared to have jaundice. “She just turned yellow,” said Ms. Tenold, who lives in rural Wisconsin. “There was no coughing, there was no stomachaches. It was just another typical week out in the country.”Her daughter’s liver was slightly inflamed, but her case, like most, turned out to be milder than Liviah’s. She was discharged after a few days in the hospital.But the experience was still confusing and frightening, Ms. Tenold said: “It would be nice for them to get to the bottom of it so that not a whole lot more children have to deal with this.”Liviah and her mother have been making earrings to raise money for families of children with liver problems.Maddie McGarvey for The New York Times“She’s not going to remember a lot of it, which is so great,” Liviah’s father said.Maddie McGarvey for The New York TimesA new purposeIn the months since Liviah’s transplant, her parents have encouraged friends and family members to register as organ donors, and they held a blood drive in Liviah’s name. Liviah has also been helping her mother make earrings to sell to raise money for the hospital’s liver Helping Hands Fund, which provides assistance to the families of pediatric liver patients.“We’re stepping into this purpose that we have,” Mrs. Widders said.Liviah’s parents have also found themselves striking a delicate balance with parents worried that their own children might be next. They want others to be alert for the signs of liver problems — yellow skin and eyes, dark urine — but also to know that what happened to Liviah is rare.“You can’t react to every vomit, you can’t react to every cold,” Mr. Widders said. “But the liver signs are unmistakable.”Liviah, who is currently in physical therapy, is recovering well, her parents said. The whole family, aside from the 1-year-old Juliana, is also in psychotherapy to help process what they have been through. Liviah knows that her old liver was sick and that she has been given a new one, which she has named Teddi.Mr. and Mrs. Widders also hope to make a scrapbook for Liviah that will chronicle exactly what happened to her — or at least, as much as they, and experts, have been able to make sense of.“She’s not going to remember a lot of it, which is so great,” said her father, who has continued to record Liviah’s liver enzyme levels in a spreadsheet. “It’s way harder on the parents,” he added. “The kids are so dang resilient.”The family is still adjusting to a new normal, which includes immunosuppressive drugs for Liviah to prevent her body from rejecting the new liver and a renewed focus on hygiene to protect her from other pathogens, to which she is now more vulnerable.But Liviah returned to preschool and soccer and dance. On her school’s recent beach day, she wore a bikini so she could show off her eight-inch scar. She calls it her “princess mark.”

Infectious microbes have evolved sophisticated means to invade host cells, outwit the body’s defenses and cause disease. While researchers have tried to puzzle out the complicated interactions between microorganisms and the host cells they infect, one facet of the disease process has often been overlooked — the physical forces that impact host-pathogen interactions and disease outcomes.
In a new study, corresponding authors Cheryl Nickerson, Jennifer Barrila and their colleagues demonstrate that under low fluid shear force conditions that simulate those found in microgravity culture during spaceflight, the foodborne pathogen Salmonella infects 3-D models of human intestinal tissue at much higher levels, and induces unique alterations in gene expression.
This study advances previous work by the same team showing that physical forces of fluid shear acting on both the pathogen and host can transform the landscape of infection.
Understanding this subtle interplay of host and pathogen during infection is critical to ensuring astronaut health, particularly on extended space missions. Such research also sheds new light on the still largely mysterious processes of infection on earth, as low fluid shear forces are also found in certain tissues in our bodies that pathogens infect, including the intestinal tract.
While the team has extensively characterized the interaction between conventionally grown shake flask cultures of Salmonella Typhimurium and 3-D intestinal models, this study marks the first time that S. Typhimurium has been grown under the low fluid shear conditions of simulated microgravity and then used to infect a 3-D model of human intestinal epithelium co-cultured with macrophage immune cells, key cell types targeted by Salmonella during infection.
The 3-D co-culture intestinal model used in this study more faithfully replicates the structure and behavior of the same tissue within the human body and is more predictive of responses to infection, as compared with conventional laboratory cell cultures.

Unless you are an identical twin, you probably aren’t often mistaken for someone else. Likewise, our own sense of self as distinct from all other humans is deeply ingrained since early childhood.
The immune system, however, faces far greater challenges in distinguishing self from non-self. Should this complex surveillance network fail to identify a foreign intruder, like a bacterium or virus, the result may be serious, unchecked disease.
Under certain circumstances, however, the immune system can become over-vigilant, identifying our own tissues as foreign and targeting them for destruction, resulting in autoimmune disease. Autoimmune responses are also associated with some cancers.
In a new study, Arizona State University researcher Joshua LaBaer and his colleagues explore components of the immune system known as autoantibodies. While they have been implicated as central players in a range of serious autoimmune diseases, the study observes that autoantibodies are also found in healthy individuals.
This fact may make the diagnostic use of autoantibodies as sentinels of autoimmune disease more challenging, hence the importance of such investigations.
An improved awareness of the pervasiveness and role of autoantibodies in human health and disease may ultimately help in the design of better diagnostics and therapeutics against a range of illnesses.

Researchers at Washington University School of Medicine in St. Louis have developed a way to attack synovial sarcoma — a rare tumor of soft tissues, such as ligaments and muscles — using an investigational drug that triggers cell death. The drug was developed by Washington University researchers who are planning a phase 1 clinical trial to investigate its safety and effectiveness in patients who have synovial sarcoma that has spread beyond the original tumor site.
The study is available online in the journal Clinical Cancer Research.
Synovial sarcoma is rare, with 900 to 1,000 new cases diagnosed annually, and is most typically diagnosed during adolescence and into young and middle adulthood. Siteman Cancer Center at Barnes-Jewish Hospital and Washington University School of Medicine is a major center for the treatment of sarcomas nationwide, as is Siteman Kids at St. Louis Children’s Hospital.
“Synovial sarcoma is responsible for about 10% of all sarcomas, and because sarcoma in general is rare, a lot of these patients — pediatric and adult — travel from all over the country to receive treatment at our specialized Sarcoma Center,” said oncologist Brian A. Van Tine, MD, PhD, a professor of medicine. “If it’s diagnosed early, this cancer can be cured with standard care — surgery, radiation and chemotherapy. But once it spreads, we have no effective curative therapies, so we’re looking for new treatment strategies that take advantage of the genetic quirks of this rare tumor.”
The researchers found that synovial sarcoma is missing an important protein that most tumors rely on to drive their energy metabolism. The absence of this key protein — called malic enzyme 1 (ME1) — forces synovial sarcoma tumors to rely on a different metabolic pathway, which makes it uniquely vulnerable to the inhibition of that alternate pathway. The investigational drug ACXT-3102 interferes with this alternate route. The interference causes volatile waste compounds called reactive oxygen species to build up inside the cancer cells. When enough reactive oxygen species build up inside, the cell dies.
“Because they’re missing ME1, these tumor cells are already crippled in their ability to fight damage from reactive oxygen species,” said Van Tine, who leads the sarcoma program at Siteman. “So, we asked if we could use this broken defense against this cancer. When levels of these compounds skyrocket inside the cells, they die very quickly.”
The drug ACXT-3102 was developed by William G. Hawkins, MD, the Neidorff Family and Robert C. Packman Professor of Surgery, and his team, to treat pancreatic cancer. Because most pancreatic cancers still have ME1, researchers will need to find a second way to attack that tumor type. But because the metabolism of synovial sarcoma is unusual and consistent across patients — the cancer’s defining genetic mistake is present in 90% to 95% of all cases — the researchers suspect that this rare tumor could be treatable with ACXT-3102 alone.
“Synovial sarcoma is caused by a very specific genetic mutation, so it’s a relatively clean cancer, meaning it has a single specific genetic mistake that can be exploited, unlike other cancers that have a complex accumulation of many mutations whose effects are difficult to unravel,” Van Tine said. “Because of this single mutation, it’s harder for synovial sarcoma cells to adapt to an attack on their energy metabolism. Finding a weakness in cancer that we can exploit based on the biology of a rare tumor is really exciting.”
The drug ACXT-3102 was licensed to a Washington University startup company called Accuronix Therapeutics that was co-founded by Hawkins to develop new cancer therapies.
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Materials provided by Washington University School of Medicine. Original written by Julia Evangelou Strait. Note: Content may be edited for style and length.