Human Behavior

Scientists document collapse of the white-lipped peccary – WSU News

PULLMAN, Wash. White-lipped peccaries have declined by as much as 87% to 90% from their historical range in Central America, signaling a population collapse of a key species in the region, according to a study published recently in the journal Biological Conservation. The research was conducted by a team of 50 scientists from 30 organizations including Washington State University, the Wildlife Conservation Society (WCS) and El Colegio de Frontera Sur.

A pig-like animal that is an important food source for large animal predators and humans alike, the white-lipped peccary (Tayassu pecari)also plays a critical ecological role by dispersing seeds and creating water holes that benefit other animals. The study found that current IUCN estimates underestimated the population decline. The study results are a 63% drop from the current IUCN range estimates for the region.

White-lipped peccary populations are in more of a critical condition than previously thought, said lead author Dan Thornton of Washington State University. While these results are sobering, they also offer a roadmap on how to conserve this iconic, ecologically important species.

The researchers say that human influence and loss of forest cover are the primary causes of the decline, and that peccaries now remain in increasingly threatened pockets of forest mostly found along transboundary areas. Outside of transboundary landscapes, remaining populations were generally scattered and isolated.

Due to their social behavior and anti-predatory defense of grouping together when threatened, white-lipped peccaries are highly sensitive to hunting. Their large area needs and reliance on widely dispersed fruit and water sources also makes this species highly vulnerable to forest loss and fragmentation.

The study found that the largest contiguous blocks of habitat for white-lipped peccaries occur in several major transboundary reserves. This includes the Maya Forest of Guatemala, Mexico and Belize, the Moskitia Forest complex of Honduras and Nicaragua, the Indio Maiz and Tortuguero National Park complex of Nicaragua and Costa Rica, and the Darien/Los Katios National Park complex between Panama and Colombia.

Although population estimates for white-lipped peccaries are difficult to calculate precisely, experts estimated that these same transboundary areas likely harbor the highest populations of remaining peccaries. For example, the entire Maya Forest, in Mexico, Belize, and Guatemala, hosts the largest white-lipped peccary population stronghold in Mesoamerica, with an estimated population of around 5000 individuals. The remote forests in the bi-national Moskitia, spanning Nicaragua and Honduras, may harbor around 3000 white-lipped peccaries.

Of particular concern to the plight of white-lipped peccaries in Mesoamerica is the status of the Maya Forest of Guatemala, Mexico, and Belize, the Moskitia Forest of Honduras and Nicaragua, and the Darien Forest in Panama and Colombia, all of which are under particularly grave threat from human activities. For example, in the past 15years, wildlands (those areas with limited human influence) have been reduced by 30 percent in the Rio Platano/Bosawas complex and by 25 percent in the Maya Forest. Ninety percent of recent deforestation is due to cattle ranching, and these two forests are at imminent risk of losing their contiguity due to expansion of both sugar cane and cattle ranching.

Based on this study, we believe that the white-lipped peccary should be uplisted to a higher category of threat in Mesoamerica from Vulnerable to Endangered in the IUCN Red List. We cannot afford to lose such an interesting species that has a unique social behavior of moving in large cohesive groups in a way that we still do not totally understand said co-author Dr. Rafael Reyna of ECOSUR in Mexico and WCS Associate Researcher.

Mesoamericas 5 Great Forests, spanning from Mexico to Colombia, and covering an area three times the size of Switzerland, are the most critical bastions for peccaries and other wildlife, and also provide services such as carbon sequestration, clean water, and food security to five million people. WCS is part of an alliance of countries, NGOs, Indigenous Peoples, and local communities committed to protect these remaining areas.

Without Mesoamericas five great forests, the white-lipped peccary will almost certainly go extinct in the region, with cascading impacts on forests, other wildlife, and people said study co-author Jeremy Radachowsky, Director of WCSs Mesoamerica and Caribbean Program. We must all work together to protect these incredibly important forests.

CONTACT: Sara Zaske, WSU News and Media Relations, 509-335-4846, sara.zaske@wsu.edu

Top right photo by Apolinar Basora

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Scientists document collapse of the white-lipped peccary - WSU News

Human Behavior

The Motels’ Martha Davis on surviving the ’80s, the subconscious art of songwriting, and the tragic side of motherhood – Detroit Metro Times

Farm animals have a friend in Martha Davis. The 69-year-old Motels frontwoman lives on a 72-acre farm outside Portland, Oregon, where she cares for alpacas, a squad of dogs, and chickens, one of which, named Ruthie, has found refuge indoors to escape her natural sexual predators.

"Roosters are very rapey," Davis says. "So I brought her inside the house to give her a little hospice from being raped all the time."

Davis describes her home as a sanctuary and admits she's never actually seen all of her sprawling property, but envisions taking a machete this spring to clear out some of the overgrown brush and create a walking path. Despite having been raised in Berkeley, California, and, later, in Los Angeles, Davis says she's always been a bit of a "dirt" girl and says she spent a lot of time in her yard as a child exploring.

"I'm much more at home here than I ever was."

Home for Davis is also in the studio, something she says she would be dead without. Belonging has long since been a theme in the Motels' songwriting, as evidenced by the band's two most successful hits, 1982's "Only the Lonely" and 1983's "Suddenly Last Summer." The latter finds Davis living through the memory of a never-ending summer cut short. "It happened forever, for a short time/A place for a moment, an end to dream/Forever I loved you, forever it seemed," Davis sings in her bright tonality that's somewhere between a command and a whisper, surrounded by melancholic synths, and a dreamy bassline.

"They're old friends," she says of the hits. "They're wonderful. It was my birthday when we played Boston, and the crowd couldn't have been sweeter, and I swear to god they applauded for like five minutes. I was just standing there almost embarrassed. When a song gets to a point where it represents that much to people, it's breathtaking," she says. "However that song happens, [it evolves] and art keeps going even after it's made it turns into something else."

It's been 41 years since the Motels released their self-titled debut, which came as a result of years of missed opportunities, lineup changes, and lack of label interest as the band's previous incarnations, the Warfield Foxes and, later, as Angels of Mercy. The debut, or as Davis says, "the one without the hits," is her personal favorite, rivaling 2018's The Last Few Beautiful Days, Davis' vibrant and deeply personal return to the Motels and the first record since the death of her eldest daughter, Maria.

"The record became a story, and all the songs fit together in a way where it basically kind of mapped out what I saw as my life, you know, with my kids and trying to become this rock star and then trying to make it. It just, all of a sudden, became very, very, very personal. And and that's the beauty of art. It will take you on the journeys. I never tried to touch the steering wheel. I literally sit in the backseat [and] go, 'OK, where are we going?'" she says. "I don't know where it comes from. Like I picked up my guitar and I'm just sitting there and literally just started playing "Only the Lonely" like it had already been written. You have to get the fuck out of your own way."

The Last Few Beautiful Days, arguably the most cohesive and focused record in Davis' discography, confronts a number of hot topics, though through the lens of ambiguity and written as stories rather than protest songs. Inspired by human behavior and the turbulent world in which we live, the record is true to the Motels, particularly on "Lucky Stars," which could easily fit on the tracklisting for Careful, the Motels' sophomore release, which turns 40 this year. Though the record pans out to paint a sweeping portrait of a world in crisis, The Last Few Beautiful Days is also an examination of a mother, her daughters, and the cost of fame. The song "Criminal," Davis says, could be about a number of men, but is targeted at the suits of big pharma.

"My oldest daughter died of fentanyl overdose, and that was because she became addicted to oxy like everyone else," Davis says. "And so as far as I'm concerned, the medical industry or the pharmaceutical industry, they murdered my daughter, and I figure if you can draw one or two dots together they killed her. And there's absolutely no consequences. They don't even get a slap on the wrist."

The record's opener, "Punchline," addresses Davis' relationship with her youngest daughter, Patricia, with whom she is no longer in contact with. "I've basically lost both of my daughters," she says. "It breaks me."

When Davis was 15, she gave birth to Maria, and moved to Tampa, Florida, with her Air Force husband, a man Davis describes as being a stranger and the same man rumored to be the subject of the Motels' "Celia" ("He wasn't gonna kill you/He was just gonna fuck up your pretty face"). Soon after, she gave birth to her second child. And when Davis was about 20, her mother killed herself.

"Well, I was a mess. I was a mess at that time and there were a lot of reasons for that. I hadn't processed the death of my parents when that happened, I was trying to be a mom and I was a bad mom," Davis confesses. "And there was a lot that was going wrong. And it was going wrong because I was taken up in the whirlwind of wanting to be loved,"she says. "I mean, basically any artist most of us are insecure, most of us were very shy and awkward youngsters. That's why we scampered off to our rooms and grabbed our instruments and made our own world. That becomes easy picking for the dark side."

Davis reflects on her mother's influence, recalling the times her mother read from Henry Miller books and the revelations Davis had after finding her mother's diary following her death. While her dad urged Davis to go back to school or pursue secretary training, she found inspiration in her late mother's unfulfilled dreams of being an author, an artist.

"I could feel that she just wanted to be an artist, but she'd write, Oh I have to go to the PTA and this, that, and the other, and I saw her frustration, which possibly killed her, that she didn't do what her heart wanted her to do," Davis recalls. "So I sat my kids down when they were very tiny and I said, 'I don't know how this is going to work, but I'm going to try to be a musician, this is going to be hard.' And I tried, and it worked sort of. I mean, my oldest daughter, I was very much in tune with her for the last five years of her life. She'd go, 'Mom we're making our own Grey Gardens here.' She was hilarious and she was beautiful and I miss her so much. I miss them both so much."

The Last Few Beautiful Days marked a turning point for the Motels. It was the first record released on Davis' label, Remarkable Records, a decision that has allotted the singer the freedom she requires to create without some of the luxuries of label support, like paid studio time and tour stipends. She admits to couch surfing to save money when she travels and refers to her farm as a "money grabber," but with the financial struggle comes yet another record, titled Escape From Planet Earth, a double album composed of new and old material that is already written and mostly recorded. Davis credits her career's sustainability to one thing: peaking and not maintaining that level of fame.

"I'm really glad that my career didn't stay on that trajectory," she says, "because I don't think there is anything more detrimental to humans than fame I really don't. I mean, it's beautiful, it's glorious, all my bills are taken care of. But at the height of it, I mean, I got so removed from reality, you know, in terms of, like, day to day ... how regular people live, and that's a bad bubble to be in. Your feet are definitely not on the ground, and your sense of empathy gets screwed with. It's a very happening place to be there's limo rides and there's champagne and drugs and all that stuff that's really crazy. There's so many pitfalls."

Davis admits to not really paying any attention to pop radio, name-dropping Taylor Swift like a curse word. She much prefers NPR and classical music, yet she can't help but catch the undeniable influence of the Motels and other artists of the era/genre in passing. She finds it flattering, but thinks derivative contemporary artists may have missed the point.

"The one thing that we wanted more than anything else in the world was not to sound like anyone else. No two bands sounded the same. Everybody wanted to look different. It was all about individuality," she says of the '80s.

"And so when I hear bands copying these things, I'm like, that wasn't the point. The point was to be as different as you can from anything," she says. "Blondie didn't sound like Chrissie [Hynde], you know? I call it the '80s wont-go-awaytees. And they won't they don't seem to."

The Motels will perform wsg Bow Wow Wow at 6 p.m. on Sunday, Feb. 9 at the Machine Shop; 3539 S. Dort Hwy., Flint; 810-715-2650; themachineshop.info. Tickets are $29+.

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The Motels' Martha Davis on surviving the '80s, the subconscious art of songwriting, and the tragic side of motherhood - Detroit Metro Times

Immunology

Illuminating The Intersection Of Art, Science And Technology – KPBS

An ambitious new exhibition at San Diego Art Institute paired local artists with cutting-edge research scientists to create revelatory works ofart

Photo by Bhavna Mehta

Above: A close up of "Fault Lines," a new installation by Bhavna Mehta at San Diego Art Institute.

Decades of scientific progress will converge with the work of dozens of San Diego artists in a major new group show, "Illumination," at San Diego Art Institute (SDAI) in Balboa Park.

One component of the exhibition paired 16 San Diego artists with local scientists studying in a field of interest to the artist. Scientists like Zbigniew Mikulski from the La Jolla Institute of Immunology, Lu-Lin Jiang from Sanford Burnham Prebys Medical Discovery Institute, Krishna Vadodaria from the Salk Institute, Ben Frable from Scripps Institute of Oceanography and more.

The artists spent time in the lab with their matched scientists, furthering their knowledge of a particular research project and developing a piece of work that reflected the science itself, the interactions with the research or researchers or anything that sprung from the collaboration.

When curator Chi Essary asked San Diego-based paper artist and sculptor Bhavna Mehta to participate and to pitch a topic she'd like to work with, Mehta took a gamble: Pitch something too specific. Mehta, who was stricken with polio as a child, selected contagious diseases of the spinal cord, assuming that the idea was too narrow, and it would be unlikely that the project would find a willing scientist for a pairing. It was a last-ditch effort of steering her work away from something she hadn't yet tackled as an artist: her own spine.

"It was a true dread," she said about making art about her own body. "It's not that I've been avoiding it, it's just that I haven't found the language to do it."

Essary, however, delivered. Mehta visited Dr. Samuel Pfaff at the Salk Institute's Gene Expression Laboratory, which specifically studies motor neurons and diseases of the spinal cord. "I have a real deep personal connection with the Salk Institute," Mehta said. Researchers from the lab also visited Mehta's studio to learn more about her work.

One revelation for Mehta throughout the process was the fundamental intersections of art and science: the value of questions and the pursuit of the unexpected.

"I don't make a lot of art expecting something, because I think you're always disappointed," she said, and felt similarity with the scientists. "You're willing to be surprised by what you find."

Mehta's piece, a massive installation called "Fault Lines," uses hundreds of small paper cut forms and pins to create a cross section of her spinal cord.

The spinal cord is like a superhighway of activity and information, with motor neurons sending messages through the entire body and controlling activity, sensation and what Mehta described as "the involuntary dance of organs." These elements are represented by gray, white, yellow, vivid orange and purple shapes, pinned directly to the wall in 3-dimensional relief. These are the specific tiny things that polio ravages, blown up to 200 times their size.

"It's always going to be painful for me," Mehta said, about the process of creating this piece and understanding her own history. "But the purpose of art is not to show but to discover."

Another impactful pairing in the project was that of scientists Zbigniew Mikulski ("Dr. Z") and Dr. Sara McArdle with filmmaker Cy Kuckenbaker.

"It was very much like giving a little kid a video game joystick for the first time," Kuckenbaker said. With access to one of the La Jolla Institute of Immunology's microscopes over the course of three extended visits to the lab, he began to understand the magnitude of the information stored in each cell in the human body.

Kuckenbaker's project includes a video installation, but strikingly, he also printed out all of the data included in a single chromosome, one of the smallest: chromosome 22. "It took five days to print," he said.

Each page is a combination of base pairs represented by the letters GCAT in sequences for 10,000 pages, or 5,000 sheets of paper. That's just for one chromosome. Each cell contains a whopping 46 of these chromosomes including the copies, and the human body contains trillions of cells. For Kuckenbacker, creating a tangible work of art from these quantifiable but astronomic facts is a way of understanding and relating something unfathomable.

The pages are bound into a book that, when set on the floor, reaches about knee height. For Kuckenbaker, it shows the "extraordinary efficiency in nature."

To round out the show, SDAI invited 10 more local artists to show pieces. These artists all routinely create work that deals with technology, climate, global health or other scientifically relevant themes, including Yasmine Kasem, and Los Angeles-based Young Joon Kwak, who created a bright pink twisted neon sculpture for the exhibition.

The exhibition opens Saturday, Feb. 8 with an opening reception, and runs through May 3 at SDAI in Balboa Park. Admission is free to San Diego Art Institute for the entirety of 2020.

Correction: An earlier version of this story incorrectly identified base pairs. The story has been updated to reflect the change.

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Julia Dixon Evans Arts Calendar Editor and Producer

I write the weekly KPBS Arts newsletter and edit and produce the KPBS Arts calendar. I am interested in getting San Diegans engaged with the diversity of art and culture made by the creative people who live here.

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Illuminating The Intersection Of Art, Science And Technology - KPBS

Immunology

State-of-the-art cancer care at a university level close to home – Freeport Journal-Standard

Yesterday, Feb. 4, was World Cancer Day, an international call to action established in 2000 at the World Summit Against Cancer for the New Millennium in Paris. The day isnt an attempt to raise awareness of any certain type of cancer, but instead the fight that thousands of people and their health care teams are fighting, every day.

We at the Leonard C. Ferguson Cancer Center at FHN Memorial Hospital in Freeport are proud to be part of that fight. In just the past few years, our talented team of professionals has cared for patients fighting 20 different types of cancer, right here on our Freeport campus.

Our medical oncologist-hematologist Arshad Shaikh, MD, offers our patients treatments that are on the front line of immunology, which gives a patients own immune system the power to fight certain cancer cells.

Our radiation oncology team, led by Bobby Koneru, MD, and Gary Shultz, DO, from the Paramount Oncology Group in Dubuque, provides our patients state-of-the-art treatments usually only available in university hospitals. Volumetric Modulated ARC Therapy (VMAT) also called Smart Arc or RapidArc radiation therapy allows our experts to more precisely target cancer cells for treatment, leaving surrounding healthy tissue unharmed.

Though patients dont usually see him at the center, our team includes surgical oncologist Spyridon Theodorakis, MD, FACS. He served fellowships in surgical oncology at Tulane University in New Orleans and at Roswell Park Memorial Hospital in Buffalo, New York, and has made it possible for breast cancer patients to consult and have reconstruction surgery in the same place as their lumpectomy or mastectomy, right here at FHN.

Our center is more than high-tech, though: From the moment a patient walks in our door, were part of his or her team. Our outstanding staff genuinely cares about our patients, and were honored to take time to get to know them and their needs.

Perhaps most importantly, we understand that being diagnosed with cancer is a big, frightening deal. Thats why we offer a three-day guarantee: Youll have a follow-up appointment within three business days of your referral. In addition, you may contact us, even if you arent a regular FHN patient.

When you are diagnosed with cancer, you want a top-notch team of experts working on your treatment as soon as possible. At the Leonard C. Ferguson Cancer Center at FHN Memorial Hospital in Freeport, youve got just that. Call us at 815-599-7000 to get your team together.

Julie Nampel MSN, RN, is the director of the Leonard C. Ferguson Cancer Center at FHN Memorial Hospital in Freeport.

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State-of-the-art cancer care at a university level close to home - Freeport Journal-Standard

Immunology

FDA just approved the first treatment for peanut allergies – The Daily Briefing

FDA on Friday approved Aimmune TherapeuticsPalforzia, the first-ever treatment for life-threatening peanut allergies.

Infographic: 6 ways your pharmacist can save the day

Theincidenceof peanut allergies in children in the United States has increased by 21% since 2010, according to theAmerican College of Allergy, Asthma, and Immunology. The latest estimates suggest about 2% to 5% of U.S. children have a peanut allergy.

There's a significant debate among providers about how to prevent or treat peanut allergies. Recent guidelines have recommended parents begin feeding their children peanuts at a young age to help their immune systems learn how to tolerate peanuts.

Researchers and some providers have tested a similar approach, known as oral immunotherapy, on kids who already have developed a peanut allergy. The technique involves slowly introducing children to small amounts of peanutsbut according to The Atlantic, many providers view such experiments as risky.

Palforzia is a capsule that contains small amounts of peanut powder.

For the treatment, doctors prescribe and administer a small dose of the drug, which can be mix with applesauce or another food. After the initial dose, patients must take the drug daily with doctors increasing the dose 11 times over several months until the patient is ingesting the equivalent of about one peanut. Doctors must administer each dosage increase, and if the patient tolerates the increase they may continue that dosage at home.

Researchers employed by Aimmune in 2018 published clinicaltrialresults in theNew England Journal of Medicineshowing that after a one-year period, two-thirds of children taking the treatment could safely consume two peanuts in a controlled setting, compared to 4% of patients who did not take Palforzia, according to the Associated Press.

FDA on Friday approved Palforzia, making it the first drug to receive FDA approval to treat life-threatening peanut allergies. The goal of the treatment is to reduce the risk of a life-threatening allergic reaction, not to make it so that individuals with peanut allergies can regularly eat peanuts. Aimmune CMO Daniel Adelman said Palforzia is only "intended to desensitize patients to peanut protein. So while they still must practice avoidance, it can mitigate allergic reactions after accidental consumption."

The drug is approved for children ages four to 17 who have a confirmed diagnosis of peanut allergy. According to FDA, "Those who take Palforzia must continue to avoid peanuts in their diets."

Researchers assessed the effectiveness of Palforzia in a randomized, double-blind, placebo-controlled study that enrolled about 500 people who were allergic to peanuts. Researchers found 67.2% of participants who took Palforzia recipients tolerated a 600 mg dose of peanut protein after six months, compared to 4.0% of participants who received the placebo.

Researchers assessed safety using two double-blind, placebo-controlled studies in about 700 people with peanut allergies. Researchers found the most common side effects were abdominal pain, nausea vomiting, tingling in the mouth, itching (including in the mouth and ears), cough, runny nose, throat irritation and tightness, hives, wheezing and shortness of breath, and anaphylaxis. The risk of anaphylaxis is why FDA required patients to take the initial dose and the increased dosages in the presence of a doctor.

The medication will cost $890 per month, but Aimmune said it will offer an assistance program that will reduce the patient's share of the cost to as low as $20 for some patients.

Some providers said the drug could be a "big deal" for patients who live in constant fear of making contact with peanuts.

Subhadra Siegel, chief of pediatric allergy and immunology at New York Medical College, said, "The thought of relieving that anxiety and being able to eat in a restaurant without worry. These are huge debilitating things for families with food allergies."

Two separate surveys found that allergists favor Palforzia as a treatment for patients with peanut allergies, with analysts predicting the drug will make about $52 million in 2020 and as much as $830 million in 2023.

Given the drug would be the first ever to treat life-threatening peanut allergies, Aimmune projects that Palforzia's annual sales could exceed $1 billion.

However, some experts said the new drug is simply an overpriced version of peanut flour, which can be sold as a dietary supplement at a much lower cost.

A study by the Institute for Clinical and Economic Review found that there was no sufficient evidence that using Palforzia would be more effective than avoiding peanuts or another oral immunotherapy.

But Thomas Casalechief medical adviser atFood Allergy Research & Education(FARE), a nonprofit advocacy and lobbying group that helped create Aimmuneargued that, even though supplement manufacturers can offer cheaper versions of peanut flour, having an FDA-approved version makes the treatment safer and more accessible to patients.

Still setting aside price, the drug raises other concerns.

While researchers in an Aimmune clinical trial found that patients showed greater tolerance of peanuts in a clinical setting, outside of the laboratory they actually experienced more serious allergic events. According to The Atlantic, 14% of those receiving the peanut powder pill reported a severe allergic reaction during the study period, compared with just 3% in the placebo group. Ameta-analysispublished inThe Lancetconfirmed the risk.

Jeff Tice, a physician and health policy analyst at the University of California at San Francisco who examined the product, said, "This is just what we're trying to preventhaving to get taken to the ER sort of outcome." He added, "The trials clearly demonstrated desensitization [to peanuts], but apparently at the cost of more harm, and no clear evidence of long-term benefit" (Hamblin,The Atlantic, 9/13/19; Johnson, Washington Post, 1/31; Loftus, Wall Street Journal, 1/31; FDA release, 1/31; Feurstein, STAT+, 2/3).

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FDA just approved the first treatment for peanut allergies - The Daily Briefing

Immunology

Trinity researchers in potential MS treatment breakthrough – The Irish Times

An important discovery that could lead to more effective treatments for people living with multiple sclerosis (MS) and other autoimmune diseases such as psoriasis and rheumatoid arthritis, has been made by scientists from Trinity College Dublin.

The researchers have identified the role played by a specific immune molecule, known as IL-17, in priming cells that cause the disease. Rather than being directly involved in damaging the nervous system, IL-17 kick-starts the disease-causing immune response that mediates the damage, they believe

Their work, published in Immunity scientific journal, also suggested there is significant potential in drugs that target the IL-17 molecule, both for MS and psoriasis/rheumatoid arthritis.

MS is a debilitating disease that affects some 2.3 million people globally and over 9,000 people in Ireland. It is associated with infiltration of immune cells into the brain and spinal cord that cause damage to nerves, leading to neurological disabilities.

However, the cause and precise immunological basis to this autoimmune disease is still unclear.

Studies in a mouse model of MS, called experimental autoimmune encephalomyelitis (EAE), have shown that immune T cells, which secrete IL-17, cause damage to the myelin sheath that surrounds nerves in the central nervous system (CNS).

Early clinical trials with antibody-based drugs that block IL-17 are showing promise in the treatment of relapsing-remitting MS and have already been licensed for the treatment of psoriasis.

The Irish research outlines a new role for IL-17 in EAE and, potentially, in MS. The new research shows that, instead of playing a direct part in CNS pathology, a key role of IL-17 is to mobilise and activate an army of disease-causing immune cells in the lymph nodes that then migrate to the CNS to cause the nerve damage, said Prof Kingston Mills, professor of experimental immunology at TCD.

Crucially, our findings suggest that drugs that block IL-17 may not need to get across the blood-brain-barrier to be effective in treating MS, add Dr Aoife McGinley, another member of the research team.

So, as well as shedding new light on the importance of IL-17 as a drugs target in RR MS, our research highlights the huge potential of drugs that block IL-17 in the treatment of other autoimmune diseases.

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Trinity researchers in potential MS treatment breakthrough - The Irish Times

Cell Biology

‘Stench of death’ compound helps your body feast on its own rotting cells – Livescience.com

The scent wafts from busy roadsides, broken meat lockers and grisly crime scenes; it's the signature stink of rotting flesh. Despite its putrid aroma, the chemical compound may serve an important purpose in the living human body, new research suggests.

The compound, known as putrescine, flips a switch in certain immune cells that helps them gobble up dead tissues in the body, according to a new study published online Jan. 30 in the journal Cell Metabolism. That, in turn, could help the body stave off heart disease.

The authors studied both human and mouse cells, as well as live mice, to reveal how these corpse-crunching immune cells, called macrophages, concoct putrescine from the digested remains swirling around in their bellies.

If their putrescine supply runs short, macrophages struggle to consume additional cells, leaving corpses to pile up, break down and ooze harmful substances into the body. Dead tissues that leak toxic substances can trigger inflammation and contribute to diseases, including atherosclerosis, in which fatty plaques build up in the arteries and can burst, triggering heart attacks or stroke.

These leaky, "necrotic" cells are "really a hallmark of what distinguishes relatively benign athersclerotic lesions from those that cause disease," senior author Dr. Ira Tabas, a professor of pathology and cell biology at Columbia University Vagelos College of Physicians and Surgeons, told Live Science. Putrescine is just one member of the body's housekeeping team, but understanding its role in cellular cleanup could someday help doctors treat atherosclerosis and many other ailments, such as autoimmune diseases and cancer, Tabas added.

"The ability of macrophages to eat multiple dead cells each is very, very important to avoiding these problems," he said. An estimated billions, "if not trillions," of cells die in our bodies every day, making corpse cleanup an absolutely critical component of our everyday health. "The basis of this study was to figure out what happens after [a macrophage] eats its first dead cell," Tabas said.

Related: The science of death: 10 tales from the crypt and beyond

The process of clearing dead cells from the body is called efferocytosis, a term derived from the Latin phrase "to carry to the grave," according to a statement describing the new study. Macrophages excel at engulfing and digesting cellular corpses. Other cells help remove dying and diseased tissue when necessary, but macrophages make their living gobbling up cellular debris.

An individual macrophage often has to clear dozens of cells, if not more, to keep efferocytosis running smoothly, said Dr. Nicholas Leeper, a professor of vascular surgery at Stanford University School of Medicine who was not involved in the study. But no one knew how a single macrophage could take on such a workload. "It's always been a mystery," he said.

Unraveling this mystery could be critical to treating people with atherosclerosis, Leeper told Live Science. Evidence suggests that efferocytosis becomes defective in diseased arteries, leaving mounting plaques to become unstable and leaky, according to a 2017 review in the journal Circulation. Once a plaque ruptures, proteins sequestered inside the structure burst out and signal an army of platelets to assemble at the site. The platelets perceive the rupture as a wound that needs to clot, but in effect, the platelets themselves end up clogging the artery, leading to stroke, heart attack or sudden cardiac arrest, Tabas said.

"It's the platelet plug that does us in," Tabas noted. Restoring efferocytosis to healthy levels could theoretically prevent tissue death and plaque rupture, but scientists must first understand how fully functional macrophages consume so many cells.

Related: Top 10 leading causes of death

So Tabas and his colleagues arranged a dinner party for human macrophages, complete with a buffet of dead cells.

To grab hold of a meal, macrophages use a protein called Rac1 to construct wiry filaments that extend from their cell body. The filaments latch onto cellular corpses and reel them into the macrophage, where the deceased cells then get broken down into their component parts. While consuming this snack, the macrophage also digests some of its own Rac1 proteins. The remaining Rac1 must be revitalized before the macrophage can take on another meal, the team found but first, the cell requires something to stoke its appetite.

Turns out, the first meal devoured by a macrophage helps spur the cell to eat more and more. Proteins in the dead cells get broken down into individual amino acids, including one called arginine. An enzyme takes up the arginine, transforms it into a molecule called ornithine and then passes that product off to a second enzyme. Ornithine gets turned into putrescine, which, in turn, sets off a chain reaction that drives any remaining Rac1 to flip into overdrive and build filaments more efficiently than before. The ramped-up Rac1 enables the macrophage to go after more food.

The team tried blocking the production of putrescine in both human and mouse macrophages and found that the cells could no longer consume multiple meals in one sitting. The researchers wondered how low putrescine levels might contribute to atherosclerosis. In a mouse model of the disease, the team found that animals with advanced symptoms lacked a key component in the putrescine production line: the enzyme that transforms arginine into ornithine, known as arginase-1.

In an attempt to treat the animals, the team added low doses of putrescine directly to the animals' drinking water. (When dissolved and delivered in low doses, the super-stinky compound no longer gives off an offensive odor.) After the treatment, the mouse macrophages appeared to consume cells more efficiently, and the animals' plaques began to shrink.

To connect the dots from mice to humans, the team also sampled macrophages from people with early and advanced atherosclerosis and noted a similar pattern: Macrophages from those with the more advanced disease were equipped with less arginase-1. Given that the formation of putrescine works very similarly in mice and humans, theoretically, treatments that manipulate that formation could treat atherosclerosis.

"I wouldn't push putrescine as a treatment," specifically, but other therapies could be developed to boost efferocytosis in other ways, Tabas said. At high doses, putrescine can be toxic to people and animals and cause gastrointestinal distress, he said. The main point is that efferocytosis, when unfolding properly, helps maintain human health and prevent disease, Tabas said.

It may be possible that "one could drive the conversion of cells to a situation that would induce more efferocytosis and repair of damaged arteries," Dr. Ira Goldberg, director of the Division of Endocrinology, Diabetes and Metabolism at NYU Langone Health, told Live Science in an email. "More important, this process is likely to be similar to that which occurs in other situations that [involve] cell death," said Goldberg, who was not involved in the new study.

For example, research suggests that efferocytosis goes awry in autoimmune diseases like lupus, in which dead cells accumulate in the lymph nodes and disrupt immune cell function. Cancer cells avoid being eaten by macrophages by sending out so-called "don't eat me" signals, so boosting efferocytosis at tumor sites could serve as a targeted form of cancer treatment. For now, though, insight into efferocytosis could mark a "major advance" in the treatment of heart disease, Leeper said.

"The importance of a pathway linked to cardiovascular disease can't be overstated Basically all adults in the Western world have some sort of atherosclerosis," Leeper said. Plagues can begin developing as early as adolescence, he said. Leeper himself recently developed a medication that helps macrophages recognize and eat dying cells in mice with atherosclerosis. As scientists continue to uncover the various chemical reactions involved in efferocytosis, drug developers can learn to promote the process through various therapies.

Leeper said the line of research could someday result in treatments to address "several of the top killers in the world."

Originally published on Live Science.

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'Stench of death' compound helps your body feast on its own rotting cells - Livescience.com

Cell Biology

UH professor examines life cycle of drug-resistant persister cells in recurrent infections – News-Medical.net

A University of Houston engineering professor is examining the life cycle of stubborn, drug-resistant persister cells in recurrent infections to find a way to destroy them. Persister cells are non-growing cell subpopulations observed in many pathogenic bacteria and they certainly live up to their name - they persist, and are not phased in the least by current medications. Scientists believe they cause the recurrence of chronic health issues like airway infections in cystic fibrosis patients, urinary tract infections and tuberculosis.

"If we know how persister cells are formed, we can target their formation mechanisms to eliminate these dangerous cell types," said Mehmet Orman, assistant professor of chemical and biomolecular engineering, who is using a $1.9 million grant from the National Institute of Allergy and Infectious Diseases to explore persister cells.

Orman believes that self-digestion, or autophagy, stimulates persister formation. In self-digestion, cells recycle essential energy molecules by eating their own protein, lipids or other bits to stay alive or temporarily survive under starvation conditions. Self-digestion is triggered by extracellular stress conditions, such as nutrient depletion, hypoxia and overpopulation.

Orman will map the self-digestion-related mechanisms in E. coli to understand how self-digestion is linked to persister cell formation. Then, he will therapeutically explore these mechanisms to identify chemical compounds that can eliminate persister cells.

Mapping of this comprehensive bacterial pathway from its initial exogenous trigger, through its signal transduction, to the source of antibiotic tolerance, will enable us to develop affective anti-persister therapeutics."

Mehmet Orman, assistant professor of chemical and biomolecular engineering,University of Houston

Self-digestion inflicts damage on the cells and can make the cells dormant, putting them in a sleeping mode, and these dormant cells are not effected by antibiotics. The bacterium is less fit to produce protein and resume growth upon exposure to fresh nutrients, providing temporary protection against antibiotics until the self-inflicted damage is repaired.

From an evolutionary perspective, self-digestion is an important survival mechanism. This complex process, which is orchestrated by many regulatory proteins and enzymes, has been well documented in mammalian cells, but largely ignored in bacteria. "By integrating our expertise in bacterial cell biology with advanced current technologies, we aim to decipher the key components of this pathway to provide a clear and much-needed picture of bacterial self-digestion mechanisms," said Orman.

Orman, himself, is persistent. Previously he developed methods to directly measure the metabolism of persister cells. He has also discovered that persisters are mostly derived from stationary-phase cells with high metabolic activities maintained by self-digestion.

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UH professor examines life cycle of drug-resistant persister cells in recurrent infections - News-Medical.net

Cell Biology

As bioengineering progresses, regulation will need to follow – Highlander Newspaper

Courtesy of YouTube

The first annual conference of Please Try This at Home took place in September 2019. At the cross section of biotechnology, body autonomy and anarchy, the conference represents an inclusive group of scientists concerned with using and discussing biotechnology in the hopes of moving the field in a more progressive direction. That being said, it is indeed a solid step in the right direction, especially when one takes into consideration how misunderstood the bioengineering field has become.

To get a sense of the state of bioengineering, a biohacker by the name of Josiah Zayner livestreamed an attempt to splice his DNA to give himself bigger muscles. If it was inserted in the wrong place in his body, or in the wrong place for the code, his DNA could end up producing weakened or ineffective proteins that could affect his body functionality. While that attempt was misguided and Zayner later regretted the stunt, the implication was that this technology should be safe and easy, which is a dangerous and untrue belief to hold. As biotechnology continues to improve, more research and regulation will be needed to ensure the safety of its use.

Ensuring said safety requires a basic understanding of cellular biology, and at its core is the central dogma of molecular biology. Simply put, most genetic material is encoded in DNA, DNA transcribes to RNA and RNA translates to proteins and those proteins are responsible for most functions in the body. Generally, bioengineering works by taking a segment of foreign DNA and inserting it into the rest of the genetic code, resulting in a production of proteins that will carry out a function specific to that DNA code. The described process is extremely complex and delicate, but despite that, genetic engineering has been used to treat Parkinsons disease and sickle cell disease among others.

That said, genetic engineering has a promising future outside of simple disease treatment. To reaffirm the purpose of Please Try This at Home, genetic engineering could be used for a different form of hormone therapy for transgender individuals. In a mostly speculative procedure, a geneticist could activate the necessary genes responsible for production of a specific hormone. That being said, it is important to keep in mind that this is a hypothetical experiment, and could result in potentially greater health problems later in life. These potential problems necessitate the need for greater experimentation and regulation in order to work out the difficulties.

Experiments in gene editing on a larger scale have already been proposed to fight Lyme disease. Normally, the disease spreads when a tick bites a mouse, followed by that tick biting a human. On Nantucket Island and Marthas Vineyard, where Lyme disease is particularly virulent, a project called Mice Against Ticks is under consideration, in which mice would be genetically modified to be able to resist and prevent the spread of Lyme disease. Kevin Esvelt, the scientist spearheading this operation is also acutely aware of the potential ecological ramifications of this project, cautiously choosing an isolated island with a low human population and low chances of dispersal if the project goes awry.

Esvelts caution in choosing an experimental site calls to mind the dangers of genetic engineering: the long term effects are not yet fully known, and it is understandable to be afraid of something that is not entirely explored. The chances of cascading ecological effects from genetic engineering is as present as the possibility for abuse of genetic engineering via eugenics. Simultaneously, those possibilities are also matched by the potential to eradicate Lyme disease, malaria or leukemia.

The best way to ensure safer practices and better opportunities for the future of genetic engineering is to regulate its practice. Clear distinctions need to be made between biohackers, like Zayner and practical, controlled applications like Mice Against Ticks. Genetic engineering could have world changing effects; it just needs to be regulated and perfected.

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As bioengineering progresses, regulation will need to follow - Highlander Newspaper

Cell Biology

Bernard Robaire honoured by Society for the Study of Reproduction – McGill Reporter

The Society For The Study Of Reproduction (SSR) unveiled its 2020 award winners today, honouring seven individualswho have made outstanding contributions to the scientific discipline ofreproductive biology. BernardRobaire, cross appointed in both the Departments of Pharmacology & Therapeutics; and Obstetrics & Gynaecology, was named recipient of the SSR Jansen Distinguished Service Award. The Jansen Award recognizes an individual for their unselfish service and leadership in advancing the discipline of reproductive biology.

Robaires research interests focus on aging of the male reproductive system, male-mediated reproductive toxicology, mechanisms of androgen actions, and the structure, function, and regulation of the epididymis.

The scientific research conducted by theseseven biology scientists, physicians and professors have significantly advanced thescience of reproduction, fertility and development, said Saima Hedrick, executive director, SSR, Their original researchon a broad range of topics in the field of reproductive biologyis helping lead us toward new discoveries, more mentorship opportunities and greater professionalism in the discipline. Their work has improved the lives of millions of humans and animals.

SSRsupports the scientific study of reproductive processes in animals and humans. Pioneering scientific contributions from SSR members have been made in areas such as stem cell biology; transgenesis; treatment of infertility; contraception; livestock production; pregnancy health; treatment of reproductive system cancers; and identification of environmental contaminants.

The annual award program recognizes significant achievements and contributions to advancing the science of reproductive biology in research, academic scholarship, professional leadership, mentoring and service. Award winners will be recognized at SSRs 2020 annual conference in Ottawa, Canada from July 912.

For a description of each award winners achievements and contributions click here.

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Bernard Robaire honoured by Society for the Study of Reproduction - McGill Reporter