StemCell Therapy

A specific fragment of a protein secreted by the parasitic worm liver fluke (Fasciola) has been found to protect the articular cartilage of joints from being destroyed by the bodys aberrant immune system, thus preventing rheumatoid arthritis from progressing. Besides protecting the cartilage from further destruction, the team of researchers from the Central Drug Research Institute (CSIR-CDRI) also found that the protein prevented the joint bone from being destroyed. In rheumatoid arthritis, the joint bone starts getting destroyed following cartilage destruction.

Liver flukes secrete certain specialised proteins that help the parasites to evade recognition by the host immune system and also blunt the killing machinery of the immune system by dialling down the inflammatory responses.

The protein Fasciola helminth defence molecule-1 (FhHDM-1) secreted by liver fluke has similarity with a human protein that mitigates inflammatory responses. So the team led by Naibedya Chattopadhyay isolated a specific fragment of this protein having a high anti-inflammatory function. They then synthesised and tested it in a cell culture system followed by animal testing.

The results were published in FASEB Journal.

A mouse model that is vulnerable to rheumatoid arthritis was used for testing the protective effect of the protein. The type-II collagen protein the major component present in the cartilage matrix of the joints but not as a whole protein seen in blood was introduced in large quantities to trigger an autoimmune response. With this, the process of cartilage destruction was set in motion.

Twenty days after introducing the antigen protein to trigger an autoimmune response, the researchers introduced the synthesised peptide every second day to evaluate its potential to protect the collagen from destruction. The peptide rapidly stopped further damage to the cartilage. The cartilage that has already been damaged was not repaired because the damage is irreversible in the case of rheumatoid arthritis, says Yasir Akhtar Khan from the Department of Zoology at the Aligarh Muslim University, Aligarh, and the first author of the paper. Besides preventing cartilage destruction, the peptide also prevented the joint bone from destruction.

The cartilage of animals that only received the type II collagen but not the peptide was completely destroyed by the end of the experiment (46 days), while the cartilage of the treatment group that received the peptide for four weeks was protected from further damage.

The effect of treatment in controlling cartilage destruction was assessed externally during the course of treatment by measuring paw swelling every day. By 25 days of treatment, there was complete abolition of paw swelling compared with the diseased animals that did not receive any treatment, says Dr. Khan. All the animals were sacrificed at the end of 46 days and the joints examined.

There was extensive structural damage to the cartilage in mice that did not receive the peptide. The barrier that insulates the cartilage was destroyed leading to disease progression, he says. In the treatment group, the barrier was intact and comparable to the control group that did not have rheumatoid arthritis. We also did not see any immune cells in the joints of the treated animals.

In contrast to the currently used anti-rheumatic drug (methotrexate), the biggest advantage of using the liver fluke peptide is that it does not produce a wholesale suppression of the immune system. Even the monoclonal antibodies that act against individual inflammatory molecules have inherent problems. For instance, the monoclonal antibodies target and suppress the tumour necrosis factor (TNF alpha), which is the first line of defence against Mycobacterium. In the Indian context, the anti-rheumatic drug and even the monoclonal antibodies that target TNF alpha will leave the person susceptible to infections, including TB.

The liver fluke peptide only produces selective protection to the joints and does not alter the systemic immune system. So the bodys ability to combat bacterial pathogens will remain intact. Dr. Chattopadhyay says. We are yet to study the mechanism of selective joint protection (cartilage and bone) provided by the peptide.

Thus, in the Indian scenario, the peptide that specifically prevents joint inflammation and destruction without affecting the bodys overall immune function might prove a game-changer in treating rheumatoid arthritis if further tests and trials find it effective.

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New molecule for rheumatoid arthritis may be effective in preventing cartilage destruction - The Hindu

Basic ingredients and dietary supplements such as Saccharomyces cerevisiae yeast can have functional properties in the diet and yield satisfactory results when added to feed as active cells (autolysed or hydrolysed) inactive cells or as cell wall components.

It is known that the fermentation environment that will provide the fundamental differences in the final product composition is more important than yeast strain. The strains used in sugarcane processing to obtain ethanol will result in a product with a higher -glucans concentration. Yeast culture goes through numerous fermentation cycles, which makes cell wall denser, resulting in higher carbohydrate rates and lower fat content, making it less digestible in the gastrointestinal tract.

Photo: Henk Riswick

With the restrictions imposed by regulations in Brazil and abroad, as well as the demand of the consumer market for natural and healthy products in animal feed, several alternatives have been tested and used in the animal industry. However, many factors are considered by producers to obtain the highest cost-effectiveness, such as the action of these compounds on animal metabolis.

Natural additives found on the market are capable of providing compounds that stimulate the body to respond more efficiently to the stressful stimuli imposed in the field. Among the options available, ImmunoWall and Hilyses stand out for being natural Saccharomyces cerevisiae yeast-based products, with no use restrictions to any animal species.

ImmunoWall is composed of Saccharomyces cerevisiae cell wall and contains a high concentration of -glucans (> 35%) and mannan-oligosaccharides, MOS (~ 20%). Due to the processing conditions to which cells are subjected, the wall becomes denser compared to other yeast cell walls on the market. This yeast cell wall structure is resistant to degradation by digestive tract enzymes and bacteria, and its resistance to digestion in the gastrointestinal tract and fermentation in the large intestine are one of the main criteria for its use as prebiotic. Prebiotics are considered excellent contributors to animal health because they stimulate the immune system and contribute to intestinal mucosa integrity, prevent adhesion of enteropathogenic microorganisms, and have the ability to bind and inactivate mycotoxins in the intestinal lumen.

Mannan-oligosaccharide (MOS) is known for its ability to agglutinate pathogens. By providing a binding site for harmful bacteria present in the intestinal tract that have type 1 and 4 fimbriae, MOS prevents the colonisation of pathogens in the intestine. Since -glucans are not digested, trapped bacteria are excreted with faecal material. Importantly, to achieve full functionality, yeast cell walls must have low digestibility in the intestine. -glucans constitute the indigestible portion of the yeast cell wall so that the higher its concentration, the lower yeast cell wall digestibility.

-glucans are considered immunomodulators that improve immune response effectiveness and agility in animals. These polysaccharides are natural and effective stimulants of the innate immune system, and phagocytic cells, when in contact with -glucans, are stimulated, producing cytokines. Cytokine production provokes a chain reaction, improving animal immunity and allowing the body to fight opportunistic infections. One of these immune system reactions is the increased number of goblet cells responsible for mucus production. With increased mucus production and release in the intestinal lumen, the mucosa (villus protection barrier and the medium that allows the action of various enzymes) increases, providing greater protection to intestinal cells and villi.

Dietary nucleotide supplementation has been studied in several species, and although not considered essential nutrients, these additives play an important role in various metabolic processes and, in particular, in some body tissues and stages of animal life characterised by very high energetic demand due to high cell multiplication.

Free nucleosides and nucleotides can be immediately absorbed by enterocytes in the intestine, and are especially important for rapidly multiplying tissues and due to limited de novo synthesis (major nucleotide production pathway), such as intestinal epithelial cells, blood cells, hepatocytes and cells of the immune system. And this occurs especially in animals undergoing fast-growing stages (early stages), reproduction, stress, and challenges.

Hilyses is a great natural choice of exogenous free nucleosides and nucleotides, obtained through the processing of Saccharomyces cerevisiae yeast used in the fermentation of sugarcane to obtain ethanol. The process consists of cell autolysis (cell membrane rupture), where intracellular content is extravasated, and after this process, some specific enzymes are inserted for hydrolysis (breakdown) of RNA into nucleotides and nucleosides (which form the nitrogenous bases of the structure). This end product is highly digestible as it contains amino acids, peptides, and short-chain polypeptides and glutamine, and is highly recommended for animal nutrition. It also contains mannan-oligosaccharides (MOS, an effective tool against Salmonella and E. coli.) and high levels of -glucans (immunomodulators that stimulate the innate immune system for a faster and more effective response).

Supplementing diets with natural additives that provide support for animals to better respond to the challenges posed by the field is fundamental in farming systems. ImmunoWall and Hilyses act as prophylactic agents, increasing animal resistance, minimising contamination and high mortality rates, and improving weight gain and health. In highly challenging environments, such as in intensive animal production, strengthening the immune system is crucial for greater productivity gains.

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Synergistic use of yeast-based products - All about feed

At the annual San Antonio Breast Cancer Symposium, MSK investigators presented the latest research on detection and screening methods for people at high risk;immunotherapy for breast cancer;and the underlying causes of resistance to targeted therapies, among other topics.

Here are some of the noteworthy studies that featured contributions from MSK investigators.

Mammography screening has been shown to reduce breast cancer mortality by about 30% in the general population. But in women at an increased risk for the disease, additional imaging is recommended. This group includes people who carry a BRCA or other genetic mutation. Other risk factors include a family or personal history of breast cancer, certain high-risk lesions, or having undergone chest radiation at a young age.

At SABCS, diagnostic radiologist Maxine Jochelson discussed newer imaging technologies and the advantages they have over mammograms alone for detecting cancer in high-risk women. People in the high-risk group may need supplemental imaging to improve early detection, Dr. Jochelson says.

She explains that this approach would incorporate vascular imaging techniques. These methods can highlight areas of increased blood flow, a hallmark of tumor growth. This technology includes MRI and contrast-enhanced mammography. It can find tumors that mammograms may miss. Although vascular imaging costs more and generally takes longer to perform, its use is justified in high-risk women because ofthe increased chance of finding cancer, she says.

Mammograms & Other Types of Breast Exams

Learn about the different types of breast exams that can help detect breast cancer at its earliest stages, before symptoms develop.

Its undisputed that vascular imaging is better at detecting cancers than purely anatomical imaging, Dr. Jochelson adds. She emphasizes the need to fine-tune imaging strategies based on each persons specific risk factors.

Some of the imaging approaches she discussed during her presentation include:

We need to continue improving ways of assessing an individuals risk so we can stratify them and determine which type of imaging will most benefit each patient, Dr. Jochelson says. The true test will be studies to demonstrate that these newer technologies actually save lives.

Immunotherapy that uses genetically engineered cells, such as chimeric antigen receptor (CAR) T cells, has proven effective in treating some forms of blood cancer. So far, efforts to create immune cells that can effectively target solid tumors, including breast cancer, have been disappointing. At SABCS, MSK physician-scientist Christopher Klebanoff presented research from his lab on a novel tactic for enabling the immune system to better target and kill breast cancer cells while sparing healthy tissue.

We believe a major limiting challenge in successfully developing immunotherapy for breast cancer has been the identification of antigens. These are targets that the immune system can recognize, Dr. Klebanoff explains. Weve become very interested in the possibility that common mutations in breast cancer may produce antigens that can be recognized as foreign by the immune system.

The Klebanoff labs current research focuses on a gene called PIK3CA, which is mutated in about 40 to 45% of hormone receptor-positive breast cancers. It is also mutated in some HER2-positive and triple-negative breast cancers. Mutations inPIK3CA cause cancer cells to grow in an uncontrolled manner. In May 2019, the US Food and Drug Administration approved a pill called alpelisib (Piqray), which targets mutations in this gene. However, the drug has the potential for significant side effects, and tumors ultimately develop resistance to this medicine. Dr. Klebanoff and his colleague Smita Chandran, a senior research scientist in his lab and the scientific lead on this study, decided to look for a way to target antigens created by this mutation using immune cells designed to recognize them.

We believe a major limiting challenge in successfully developing immunotherapy for breast cancer has been the identification of antigens.

A challenging aspect of this approach was that mutated PIK3CA is found on the inside of cancer cells, allowing it to hide from many components of the immune system, such as antibodies. Physiological processes present in all cells, including cancer cells, allow mutated PIK3CA to be broken down into shorter fragments and loaded onto a molecular basket, called HLA, which is shuttled to the surface of the cell, Dr. Klebanoff says. This process allows immune cells to functionally look inside of other cells.

The researchers identified a specialized molecule, known as a T cell receptor, that has the ability to recognize this mutated PIK3CA-HLA complex. Immune cells specific for this complex recognize the target cell as being cancerous and destroy it. Healthy cells without the mutation remain untouched. The T cell receptors are matched to a patients unique complement of HLA molecules. As with a stem cell transplant, HLA must be matched for this immunotherapy to be effective.

Right now we are focused on the most common HLA types that are seen in a large proportion of our patients. The big-picture goal is to build a library of T cell receptors that can work in people with different HLA molecules and can target other common cancer mutations, Dr. Chandran explains. This work is still early and so far has only been done in the laboratory and not in humans. We are nonetheless excited about the prospect of working toward developing a more effective and less toxic immunotherapy customized to the genetic attributes of a patients tumor.

CDK4/6 inhibitors are an important class of drugs to treat estrogen receptor-positive breast cancer. These drugs stop the growth of breast cancer cells by targeting enzymes that are important in cell division. They are given in addition to hormone therapy. But about 10 to 15% of people who get these drugs dont respond to CDK4/6 inhibitors, and others later develop resistance.

MSK physician-scientist Sarat Chandarlapaty has been studying why this is the case. Understanding this resistance could contribute to the development of new targeted drugs. In December 2018, he published a study that reported on two genes that play a critical role in promoting this resistance. At SABCS, he presented his latest research on this area.

Weve been delving deeper into the role of these genes, as well as others, to try to understand some of the principles that could guide the next generation of therapies, Dr. Chandarlapaty says. By working out these detailed mechanisms, we will have the tools needed to design more potent and selective inhibitors for these refractory breast cancers.

Dr. Chandarlapaty explains that because tumors outsmart CDK4/6 inhibitors in different ways, he doesnt expect to find a one-size-fits-all approach for new drugs. There are some key principles for why these drugs fail, he says. For some tumors, making a more potent drug of the same general class will work. Other tumors bypass the pathway in a way that renders many of the old therapies weve used ineffective. For them, a completely different approach is needed.

Researchers Identify Why Women May Develop Resistance to a New Class of Breast Cancer Drugs

Clues emerge about why promising new breast cancer drugs sometimes dont work and what might be done about it.

Follow this link:
Updates from SABCS 2019: Detection and Screening, Immunotherapy Advances, and Therapy Resistance - On Cancer - Memorial Sloan Kettering

Unpersuaded by hundreds of pleading and occasionally hostile parents, a state Senate panel voted Thursday to eliminate religion as an acceptable reason for New Jersey children to avoid vaccines required for school attendance.

After seven years of stalled efforts to compel better vaccine compliance and a recent reemergence of measles, state lawmakers are moving quickly to end the religious exemption that allowed 14,000 students to decline their shots last year.

The Senate Health, Human Services and Senior Citizens Committee approved the bill (A3818) by a 6-4 vote Thursday. Even before the hearing, the measure was listed on Mondays agenda for action by the full 40-member body.

But hundreds of parents amassed outside the Statehouse in Trenton anyway. The crowds started arriving hours before the afternoon hearing. Hundreds of sign-waving, child-toting parents queued up in the first-floor hallway waiting for space inside the committee room. Before the hearing began, the audience recited the Serenity Prayer."

They said they were outraged by what they see as government intrusion in violation of their First Amendment right of religious freedom. They vowed to pull their children out of school or move out of New Jersey.

Alan Weller, president of the New Jersey chapter of the American Academy of Pediatrics, said as doctors, we all have a responsibility to protect...children in schools who cannot be vaccinated because of a compromised immune system.

"Your right to practice religion freely does not include...exposing the community or a child to a communicable disease, Weller said.

Many opponents say they object because embryonic tissue extracted from aborted fetuses in the 1960s is used to make the measles, mumps, rubella (MMR) vaccine. Others said they trusted that God had created their bodies strong enough without vaccines.

I love God with my whole heart, said 7-year-old Emelia Walls of Cape May. He made our immune systems perfect. We take really good care of our bodies because that makes God happy."

Emelia, a second-grader, said she would be heartbroken" if the law passed and she had to leave school. I have a bright future ahead of me. I am going to change the world, she said.

Pediatric oncologist Andrew Silverman at Jersey Shore Medical Center asked the committee to consider his 6-year-old leukemia patient, who has undergone aggressive chemotherapy. The boys mother informed him there is a child in his first-grade class who is not vaccinated for religious reasons. Should he go to school?

Silverman said no.

The oncologists in my practice agree, unvaccinated students are a major risk, he said. Its not safe for him to attend school.

The bill would only allow children to seek an exemption for medical reasons. The state Health Department would define which health conditions would qualify, and a physician, advance practice nurse or physician assistant must verify in writing the child had the disqualifying illness, according to the bill. The law would take effect six months after Gov. Phil Murphy signs it, if he does.

The bill gained momentum in January, after a measles outbreak dominated the news. There have been 19 confirmed cases of measles this year in New Jersey, and 1,276 nationwide.

Mary Iuvone | For NJ Advance Med

People attend a hearing on a vaccine bill. The Senate health committee held a hearing on a vaccine bill, which would abolish a parent's right to reject vaccines for their children, at the Statehouse Annex, in Trenton, December 12, 2019.

State Assemblyman Herb Conaway, D-Burlington, a physician who chairs the Assembly Health Committee and bill sponsor, decided to rewrite his bill to call for an outright ban on religious exemptions as measles cases have surfaced. The Assembly changed the text without a public hearing.

After nearly two hours of tearful and bitter debate, the vote was split along party lines, with five Democrats voting yes and four Republicans voting no. Three of the Democrats who voted yes substituted permanent health committee members, raising questions among opponents that they were pulling strings to guarantee the controversial bills passage.

On balance, this is the best route we can take as a society, as a matter of public health and public safety, state Sen. Joseph Vitale, D-Middlesex, the chairman of the committee and a co-sponsor of the bill.

State Sen. Michael Testa, R-Cumberland, voted no, calling the legislation unconstitutional and un-American.

State Sen. Gerald Cardinale, R-Bergen, said he doesnt oppose vaccines but voted no because I am not going to take away peoples rights.

Even though I would make a different choice from the people in this room, its their right to be wrong, Cardinale said. Its their own right to follow their conscience.

New Jersey would be the sixth state to abolish religious exemptions for childhood vaccines. The five states are California, Maine, Mississippi, New York and West Virginia.

Mary Iuvone | For NJ Advance Media

Dr. Richard Roberts of Lakewood speaks in support of a bill which would abolish a parent's right to reject vaccines for their children based on their religious convictions, He holds a book he published which he said explains how vaccinations do not violate Orthodox Jewish teachings. December 12, 2019.

Susan K. Livio may be reached at slivio@njadvancemedia.com. Follow her on Twitter @SusanKLivio. Find NJ.com Politics on Facebook.

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N.J. bill to remove religion as reason to avoid vaccinating kids enrages parents at hearing - NJ.com

Cases of the flu are on the rise throughout New York State, as flu season kicked into high gear with the holiday season approaching.

Statewide , during the week ending on Friday, Dec. 7, cases of the flu have risen by 60 percent over the previous week, with 1,839 cases reported by New Yorkers. 4,989 cases have been reported statewide during the current flu season.

In the Metro region - which is considered Long Island, Westchester, Putnam, Rockland, Orange, Dutchess, Ulster and Sullivan counties - there were 384 cases reported last week.

Locally, on Long Island, 180 new cases were reported, 94 in Nassau County and 86 in Suffolk.

According to health officials, the Department of Public Health uses multiple systems to monitor circulating influenza viruses. During the influenza season, weekly flu updates are posted from October of the current year, through May of the following year. Annual summaries are also posted for comparison. The national flu picture may vary from what we are seeing on a state level.

Flu season kicks off in earnest in October each year, though patients can still be susceptible to certain strains in September, according to the Centers for Disease Control and Prevention.

The CDC said that reported cases tend to increase in November before peaking between December and February. Flu season typically lasts through the middle of the spring. The organization estimates that flu has resulted in between 9.2 million and 35.6 million illnesses each year in the United States and several deaths. Of those illnesses, an estimated 9 percent were hospitalized.

It takes approximately two weeks following the vaccination for the antibodies to protect against the flu to develop in the body, so make plans to get vaccinated early in fall, before flu season begins.

CDC recommends that people get a flu vaccine by the end of October, though there is still time to get vaccinated. Getting vaccinated later, however, can still be beneficial and vaccination should continue to be offered throughout flu season, even into January or later.

According to the CDC, the flu infects the respiratory tract. As the infection progresses, the bodys immune system responds to fight the virus.

"This results in inflammation that can trigger respiratory symptoms such as a cough and sore throat. The immune system response can also trigger fever and cause muscle or body aches. When infected persons cough, sneeze, or talk, they can spread influenza viruses in respiratory droplets to people who are nearby. People might also get flu by touching a contaminated surface or object that has flu virus on it and then touching their own mouth or nose.

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Here's How Many Flu Cases Have Been Reported In Nassau, Suffolk - Rutherford Daily Voice

David Fajgenbaum's life went into overtime the moment a priest read his last rites in November 2010.

At least that's how the Penn Medicine immunologist views his last nine years.

That belief has reshaped the way Fajgenbaum confronts idiopathic multicentric Castleman disease, a rare immune system disorder that has dealt him five life-threatening blows. It's also changed the way he goes about his life.

"When you're in overtime, every second counts. You don't know how much time you have," said Fajgenbaum, a former quarterback at Georgetown University. "It really helps you focus in on what's important and what's not important."

For a while, Fajgenbaum said he "just hoped and prayed" that someone, somewhere, would find a cure and better treatment options for Castleman disease, which kills about 35% of its victims within five years of diagnosis. Then, he realized he might be that person.

That life lesson is among several that Fajgenbaum, 34, recounts in his new memoir, "Chasing My Cure: A Doctor's Race To Turn Hope Into Action." Fajgenbuam wrote the book partly in hopes of boosting awareness of Castleman disease, which has not gained the notoriety of other rare diseases despite its deadly nature.

"We shouldn't either hopeortake action we should hopeandtake action," Fajgenbaum said. "I'm here on the phone because of that turning point."

Idiopathic multicentric Castleman disease the most severe form of the disorder activates the bodys immune system, releasing an abundance of inflammatory proteins that can shut down the liver, kidneys and bone marrow. Relatively little is known about it.

Fajgenbaum, an assistant professor in Penn Medicine's Translational Medicine and Human Genetics division, has spearheaded efforts to identify more effective treatment options for people with Castleman disease. After all, he recognizes his clock may stop ticking at any moment.

Chemotherapy can keep the disease at bay for a while, but it's not a permanent solution, Fajgenbaum said. Patients tend to relapse after treatment, creating a vicious cycle that he knows all too well.

Thus far, the U.S. Food and Drug Administration only has approved one treatment siltuximab for Castleman disease. But it only works in about one-third of patients and Fajgenbaum is not one of them.

Fagjenbaum's research and his personal experience eventually led him to sirolimus, an immunosuppressant typically prescribed for kidney transplant patients. Because the drug inhibits activated T-cells, he suspected it might put his disease in remission.

"I knew if I did not start myself on a drug, there was no way I was going to make it," Fajgenbaum said.

Under the supervision of his doctor, Fajgenbaum began taking sirolimus after his last life-threatening hospitalization six years ago. At the time, Fajgenbaum was simply hoping he'd live long enough to marry his girlfriend, Caitlin something he said he once took for granted.

"The pre-overtime mentality is that we have all the time in the world, that if it's meant to be, it's meant to be," Fajgenbaum said. "But the overtime reality is that none of us have all the time in the world. If it's meaningful and important, then that's exactly what you should do."

Since Fajgenbaum began taking sirolimus, his symptoms have not flared up.

Now, he and Caitlin have a daughter, Amelia. And Fajgenbaum is leading clinical trials examining sirolimus' effectiveness against Castleman disease. Like siltuximab, the drug appears it may help some but not all people battling Castleman disease.

That has Fajgenbaum wondering how many other existing drugs have been overlooked as potential treatments for other diseases. It's another lesson that he expands upon in his book.

"Sometimes, solutions can be hiding in plain site," Fajgenbaum said. "This drug I'm on is in my neighborhood CVS all these years and no one had thought to try it. How many other things are like that ... in science or medicine?"

Since writing the book, Fajgenbaum said he has heard from all kinds of people who have faced challenging health diagnoses, whether it's cancer or some other rare disease.

It's definitely moving the needle, Fajgenbaum said. In September, the month the book was published, more people Googled Castleman disease than ever before. And more people have donated funds to the Castleman Disease Collaborative Network, an organization he co-founded to expedite research efforts.

"It's really been, in many ways, therapeutic to be able to share my story, the ups and the downs," Fajgenbaum said. "Even writing it was therapeutic. To bring back some tough memories, to expose them and to face them."

Sometimes, Fajgenbaum said, it's best to face the tough times with a sense of humor. That's a lesson he gained from his late mother, who died of cancer when he was at Georgetown.

Fajgenbaum recalled flying to Raleigh, North Carolina to see his mother after she had a brain tumor removed. He tentatively walked into her room alongside his family, unsure what to expect. He found his mom sitting, her head shaved and partly covered by a gauze wrap.

She pointed to her head and joked that she looked like the Chiquita banana lady.

"It was exactly what we needed," Fajgenbaum said. "It wasn't what my mom needed. She was going through a really tough time. It wasn't going to make her feel better. But she knew that it was going to make us feel better. By making that joke, it kind of relieved everything. It was like, you're still my mom, you're still you."

A few years later, Fajgenbaum found himself walking around the hospital with his father on New Year's Eve. This time, Fajgenbaum was the patient. His stomach was filled with 30 pounds of fluid, the result of his ill-functioning kidneys and liver.

As they passed the family waiting area, they stopped to help a man who was laying on the floor, noticeably drunk. The man thanked Fajgenbaum's father, wishing him and his "pregnant wife" the best of luck.

"We just burst into laughter," Fajgenbaum said. "I turned to my dad and said, 'Man, you've got an ugly wife.'

"If I hadn't had my mom's example ... maybe I would have just burst into tears and gone back to my room. Rather, that's hilarious. This drunk guy thinks I'm a pregnant woman because of the size of my belly."

That moment, nearly nine years ago, came just several weeks into Fajgenbaum's "overtime" session. He's overcome a lot since and learned a great deal. But he knows there's more work to be done for him and for others.

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His life in 'overtime,' Penn doctor races to find better treatments for rare Castleman disease - PhillyVoice.com

ST. LOUIS The blue carpet rolled out Friday night for one of our hometown heroes.

Laila Anderson had her name in lights at the Fox Theatre as they showcased a documentary about her journey.

This die-hard blues fan captivated our hearts with her remarkable journey battling a rare life-threatening disorder, hemophagocytic lymphohistiocytosis, or HLH. Immune cells grow out of control and attack the body, causing organ damage.

Laila's journey began two years ago when she started experiencing headaches and vomiting. She went to St. Louis Children's Hospital. Numerous tests and MRIs over the span of a few weeks showed her brain condition was deteriorating.

In September 2018, almost one year after her first symptoms appeared, doctors found out she had HLH. Her immune system was attacking her brain.

Laila is just one of 15 children in the world who have had a solely neurologic manifestation of the disease. The only known treatment for HLH is a bone marrow transplant.

In October 2018, Laila started 10 weeks of chemotherapy to suppress her overactive immune system and prepare for that transplant. She had her transplant in January 2018.

TOWN AND COUNTRY, Mo. - This time last year, Laila Anderson was battling a rare and potentially deadly auto-immune disease. Thursday night, for the very first time, she had the chance to give the donor who saved her life the biggest hug an 11-year-old could muster.

Her tough journey is now taking over the big screen.

Children's Hospital created a documentary called 'Laila: The Next Season,' which dives deeper into her story.

"I'm really excited to show everyone here like what happens behind the scenes, who helped me be here today," Laila said.

The 28-minute film highlights her road to recovery and being the inspiration to the Blues with their own recovery of winning the Stanley Cup.

The movie includes her doctors and Colton Parayko.

"We as a team tried to help her out try to cheer her up. For her, she showed up to our games, cheered us up," Parayko said.

It's a movie highlighting the impact of a little girl's passion to never give up. Inspiring a city in need of a reminder that anything is possible if you just believe.

"I feel like we've taught each other some life lessons, whether it be a battle for your life or a battle to win the Stanley cup. We've all been on the road together and fighting our battles together," Laila said.

The feature will air Saturday, Dec. 14 at 6 p.m. CT before the start of the Blues vs. Blackhawks game.

The film will be made available on the St. Louis Children's Hospital's Youtube Channel about a week after it airs.

MORE LAILA STORIES

RELATED: Laila Anderson tells us what she wants to be when she grows up

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RELATED: Laila Anderson to receive the Musial Award for extraordinary character

RELATED: 'It's her whole hand' | Laila gets a Blues Stanley Cup Championship ring

RELATED: Laila returns to school after 2 years

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Laila: The Next Season | Behind the scenes of the Laila Anderson documentary premiere - KSDK.com

This past week or so, I have been plagued by a nasty cold. My sickness got me thinking about cold and flu season with Crohn's disease and IBD.Most Crohn's patients manage their disease with some form of medication: steroids, immunosuppressants, immunomodulators, antibiotics, biologics, or another type. These medications can suppress your immune system, making it harder to fight off viruses such as colds or the flu, and increasing the risk of developing pneumonia. Patients with IBD and other chronic conditions are more likely to get sick, and these illnesses can last longer than the "normal" few days. And when IBD patients get sick, they really get sick.The common cold may last a few days, but for patients with Crohns disease or otherwise weakened immune systems, it can persist for weeks and even lead to a flare-up of IBD symptoms. The Centers for Disease Control and Prevention suggests taking these precautions to avoid illness: wash your hands, wear a face mask when visiting your doctors office or hospital, dress appropriately for the weather, and avoid those who are sick.The flu, or influenza, is a viral infection, and though it shares some symptoms with the common cold, with the flu they are more severe. While an annual flu shot is recommended for most people, IBD patients should be mindful of their suppressed immune systems, which make them more susceptible to infections. IBD patients should get their flu shot as early as possible. My doctors have a

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Cold and Flu Season with Crohn's Disease and IBD - IBD News Today

Biomedical engineers at Duke University have developed a system that allows for real-time observations of individual cells in the colon of a living mouse.

Researchers expect the procedure to allow new investigations into the digestive systems microbiome as well as the causes of diseases such as inflammatory bowel disease and colon cancer and their treatments.

The procedure described online today (December 11, 2019) in Nature Communications involves surgically implanting a transparent window into a mouses abdominal skin above the colon. Similar setups are already being used to allow live looks into the detailed inner workings of the brain, spinal cord, liver, lungs and other organs. Imaging a live colon, however, is a slipperier proposition.

A brain doesnt move around a lot, but the colon does, which makes it difficult to get detailed images down to a single cell, said Xiling Shen, the Hawkins Family Associate Professor of Biomedical Engineering at Duke University. Weve developed a magnetic system that is strong enough to stabilize the colon in place during imaging to obtain this level of resolution, but can quickly be turned off to allow the colon to move freely.

This video shows green fluorescent colon neurons activated by neurostimulation in real-time. This is the first time that sacral nerve stimulation, an FDA approved therapy for colon motility disorders, has definitively been shown to activate neurons in the colon in live animals, explaining why the therapy might work.

Credit: Xiling Shen, Duke University

Immobilizing the colon for imaging is a tricky task for traditional methods such as glue or stitches. At best they can cause inflammation that would ruin most experiments. At worst they can cause obstructions, which can quickly kill the mouse being studied.

To skirt this issue, Shen developed a magnetic device that looks much like a tiny metal nasal strip and can be safely attached to the colon. A magnetic field snaps the colon into place and keeps it stable during imaging, but once turned off, leaves the colon free to move and function as normal.

A vital organ that houses much of the digestive systems microbiome, the colon can be afflicted by diseases such as inflammatory bowel disease, functional gastrointestinal disorders, and cancer. It also plays a key role in regulating the immune system, and can communicate directly with the brain through sacral nerves.

There is a great need to better understand the colon, because it can suffer from so many diseases and plays so many roles with significant health implications, Shen said. In the study, Shen and his colleagues conducted several proof-of-principle experiments that provide starting points for future lines of research.

The researchers first colonized a living mouse colon with E. coli bacteria, derived from Crohns disease patients, that had been tagged with fluorescent proteins. The researchers then showed they could track the migration, growth and decline of the bacteria for more than three days. This ability could help researchers understand not only how antagonistic bacteria afflict the colon, Shen says, but the positive roles probiotics can play and which strains can best help people with gastrointestinal disorders.

In the next experiment, mice were bred with several types of fluorescent immune cells. The researchers then induced inflammation in the colon and carefully watched the activation of these immune cells. Shen says, this approach could be used with various types of immune cells and diseases to gain a better understanding of how the immune system responds to challenges.

Shen and his colleagues then showed that they could tag and track colon epithelial stem cells associated with colorectal cancer throughout radiation treatment. They also demonstrated that they could watch nerves throughout the colon respond to sacral nerve stimulation, an emerging therapy for treating motility and immune disorders such as functional gastrointestinal disorders and irritable bowel disorder.

While we know electrically stimulating the sacral nerves can alleviate the symptoms of these gastrointestinal disorders, we currently have no idea why or any way to optimize these treatments, Shen said. Being able to see how the colons neurons respond to different waveforms, frequencies and amplitudes of stimulation will be invaluable in making this approach a better option for more patients.

###

Reference: An intravital window to image the colon in real time by Nikolai Rakhilin, Aliesha Garrett, Chi-Yong Eom, Katherine Ramos Chavez, David M. Small, Andrea R. Daniel, Melanie M. Kaelberer, Menansili A. Mejooli, Qiang Huang, Shengli Ding, David G. Kirsch, Diego V. Bohrquez, Nozomi Nishimura, Bradley B. Barth and Xiling Shen, 11 December 2019, Nature Communications.DOI: 10.1038/s41467-019-13699-w

This work was supported by National Institutes of Health (R35GM122465, OT2OD023849), the Defense Advanced Research Projects Agency (N66001-15-2-4059) and the National Cancer Institutes (R35CA197616).

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A Real-Time Window Into the Hidden World of the Colon of a Living Animal - SciTechDaily

Washington D.C. : Whenever you suffer fever or infection, the first thing you are referred to is taking antibiotics as these drugs destroy or slow down the growth of bacteria.

Antibiotics also lead to positive effect on human health. A new study has come up with the new benefit of destroying cancer and tumour cells in the body.

The study on mice has found that giving a dose of common antibiotic not only helped immune cells kill tumours that were directly treated with radiation but also kill cancer cells that were further away in the body, paving the way for researchers to test the approach in a human clinical trial.

The study was published in the Journal of Clinical Investigation.

In addition, hypo-fractionated doses have the ability to impact other tumours cells in the body that weren't directly treated with radiation. This is known as the abscopal effect.

The study's senior author Andrea Facciabene, PhD, says: "Our study shows that vancomycin seems to boost the effectiveness of the hypo-fractionated radiation itself on the targeted tumour site while also aiding the abscopal effect, helping the immune system fight tumours away from the treatment site."

In this study, researchers have found vancomycin specifically improved the function of dendritic cells, which are the messenger cells that T-cells rely on to know what to attack.

While researchers used melanoma, lung, and cervical cancer models for this work, they note the approach could have implications for a wide variety of cancer types.

This study also builds off the team's previous research, which showed a similar effect in T-cell therapies, meaning it adds to a growing body of evidence.

"However, what's clear is that antibiotics play a role and can potentially impact treatments and outcomes for cancer patients," adds Facciabene. The researchers are planning a phase one study to translate this approach into the clinic.

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Study suggests taking common antibiotic before radiation may help body fight cancer - ETHealthworld.com

Microsoft co-founder Bill Gates released his annual end-of-year book list on Tuesday.

"I think they're all solid choices to help wrap up your 2019 or start 2020 on a good note," the avid reader writes on his blog, Gates Notes.

For a productive start to the new decade, crack open one of Gates's favorites this holiday season.

Bill Gates' 2019 holiday book list

Source: Gates Notes

This New York Times bestseller tells the story of newlyweds Roy and Celestial, a young black couple whose lives are upturned when Roy is wrongly convicted of rape and sentened to 12 years in prison.

Tayari Jones's novel is "fundamentally a story about how incarceration hurts more than just the person locked up," writes Gates. "It's also a reminder of how draconian our criminal justice system can be especially for black men like Roy."

It's not "a light, easy read," he notes, "but it's so well-written that you'll find yourself sucked into it despite the heavy subject matter."

Read Gates's full review of "An American Marriage."

In "These Truths," Harvard historian Jill Lepore covers centuries of American history in about 800 pages.

The one-volume history "is not a deep or comprehensive account of individual events or people," says Gates. Rather, the author offers "quick glimpses at major events such as America's first presidential impeachment (only three sentences) and doesn't even get a chance to mention pivotal figures such as Lewis and Clark."

He praises it as "the most honest account of the American story I've ever read."

Read Gates's full review of "These Truths."

Written by one of Gates's favorite authors, Czech-Canadian professor Vaclav Smil, "Growth" is "a brilliant synthesis of everything we can learn from patterns of growth in the natural and human-made world," says Gates. Though, "it's not for everyone," he adds. "Long sections read like a textbook or engineering manual."

But if you stick it out, you may experience what Gates did: "I marveled over all the miracles that modern civilization is built on, including power grids, water systems, air transportation and computing. The book gave me new appreciation for how many smart people had to try things out, make mistakes and eventually succeed."

Read Gates's full review of "Growth."

Author and educator Diane Tavenner is the founder of Summit Public Schools, which has been nationally recognized for its high performance: 99% of Summit students get into a four-year college and Summit graduates finish college at twice the national average.

In her book, she shares the Summit learning philosophy which is built on self-directed learning, project-based learning and mentoring and how to prepare all kids for school and life.

"Much of the book is deeply personal," says Gates. "Diane shares stories of her childhood, growing up in a troubled family. She recounts her years as a young, idealistic teacher and administrator. And she opens up about her own experience as a parent, raising her teenage son, Rett, as he navigates his path to adulthood."

Read Gates's full review of "Prepared."

Gates used to routinely pull all-nighters in the early days of Microsoft. "Once or twice, I stayed up two nights in a row," he recalls. "I knew I wasn't as sharp when I was operating mostly on caffeine and adrenaline, but I was obsessed with my work, and I felt that sleeping a lot was lazy."

After this read, "I realize that my all-nighters, combined with almost never getting eight hours of sleep, took a big toll," he says. Author Matthew Walker, the director of UC Berkeley's Center for Human Sleep Science, "explains how neglecting sleep undercuts your creativity, problem solving, decision-making, learning, memory, heart heath, brain health, mental health, emotional well-being, immune system and even your life span."

Read Gates's full review of "Why We Sleep."

Don't miss: Bill Gates: Here's how to figure out what you'll be world-class at

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The 5 books Bill Gates recommends you read this holiday season - CNBC

WITH schools in lockdown and businesses running on half staff, the winter vomiting bug has hit us hard. Norovirus causes vomiting and diarrhoea and is one of the most common stomach bugs around.

The symptoms of this vomiting bug include severe vomiting and diarrhoea, often alongside fever, muscle aches, and weight loss too. Anyone can pick up this pesky bug, but young children, the elderly, and immunocompromised individuals are most vulnerable.

:: How do I avoid getting sick?

Prevention is always better than cure, and although it is difficult to avoid, there are a few simple things we can all do to reduce our risk.

- Keep your immune system nourished by eating a diet packed with colourful vegetables and some fruits (berries in particular). Include some protein with each meal and pack in essential fats form nuts, seeds and oily fish.

- Take a vitamin D supplement during winter months to help support your immune function and resilience to bugs.

- Support resilience to bugs by taking a daily probiotic supplement, or consuming probiotic foods and drinks like live natural yoghurt, kefir and kombucha.

- Go to bed early and get a good night's sleep.

- Keep an eye on your sugar and alcohol intake.

- Wash your hands really well with soap and water several times a day, and especially after using the loo and before preparing or handling food.

:: How can I recover quickly?

Rest is the best healer, but here are a few ideas to help support and nourish your body to help get you back on your feet.

Rest:

- When we get hit by a bug, it tends to make us feel exhausted. This is our body's way of telling us to slow down, take it easy, rest and recover. But most of us hit the ground running again as soon as we feel well enough to get back to work. After an illness it is important to give your body a little R&R. If you can find time among the Christmas card writing and present buying, to take time to rest and let your body recover.

Hydrate:

- The norovirus causes vomiting and diarrhoea, so it is crucially important to get plenty of fluids into your body after you have been sick to help prevent dehydration. You will need to drink more than you usually do. As well as drinking water, some herbal teas can be good. Ginger is thought to help settle nausea and elderberry has been shown to have anti-viral properties.

- Once your appetite starts to pick up a little, then homemade soup is a good way to get more fluid into your system, along with some much needed vitamins and minerals to help support your immune system.

- Avoid fizzy drinks and fruit juice as they could make diarrhoea worse.

Nourish:

- Once you start to feel a little better, and can start to eat again, you may find it easier to eat little and often until you recover. Bland food will be easier on you than spicy or highly flavoured foods, but avoid foods with low nutritional value, as your body will have been nutritionally depleted when you have been sick and unable to eat.

- Easily digested foods like bananas, soups, stewed apple, yoghurts, rice, pasta or potatoes can be good foods to start with.

- Avoid caffeine, high-fat foods, sugary foods and spicy foods as these are likely to upset your stomach.

- Evidence shows that our immune system is switched down a gear by eating sugar. This comfort food, that many of us crave can deplete our immune function for up to seven hours after munching our way through a sugary snack.

Supplement:

- I would suggest taking a good quality probiotic after a bout of vomiting and diarrhoea to help rebalance the levels of your friendly, beneficial probiotic bacteria. Certain Lactobacilli strains, including Lactobacillus rhamnosus GG, may inhibit norovirus and improve gut function following gastroenteritis. Try the Optibac range, available from pharmacies and health food shops.

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Nutrition with Jane McClenaghan: Norovirus prevention and support - The Irish News

Fibrosis, or scarring, is central to a number of diseases, including cirrhosis of the liver, chronic kidney disease and several lung diseases. Generally, any organ in the body can repair itself after injury. Normally, scarring occurs and then recedes, making room for normal tissue as healing occurs. But sometimes the healing goes awry and the cells that make up scar tissue continue dividing and spreading until the scar tissue itself strangles the organ it was healing. This can cause organ failure.

Researchers at the University of California-Los Angeles Health Sciences have developed a scar-in-a-dish model derived from stem cells that can mimic fibrosis. They then identified a drug that could stop the fibrotic progression and, in further animal models, actually reverse fibrosis. They published their research in the journal Cell Reports.

Millions of people living with fibrosis have very limited treatment options, said Brigitte Gomperts, a member of the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research at UCLA. Once scarring gets out of control, we dont have any treatments that can stop it, except for whole-organ transplant.

The scar-in-a-dish model utilized several different types of cells derived from human stem cells. It used induced pluripotent stem cells (iPS).

Fibrosis likely occurs as the result of interactions between multiple different cell types, so we didnt think it made sense to use just one cell type to generate a scarring model, said Preethi Vijayaraj, the reports first author and an assistant adjunct professor of pediatric hematology/oncology at the David Geffen School of Medicine at UCLA and a member of the UCLA Johnsson Comprehensive Cancer Center.

The mixture of cells they grew had many types that are believed to participate in fibrosis, including mesenchymal cells, epithelial cells and immune cells. All of them maintained some plasticity, allowing them to change cells types. This is the first known model to recreate that plasticity, which is associated with progressive fibrosis.

They then placed the cells in a rigid hydrogel that was similar to the stiffness of a scarred organ. The cells behaved the same way they would to injury, producing damage signals and activating transforming growth factor beta (TGF beta), which typically stimulates fibrosis.

The use of the gel, as opposed to tissue, meant it couldnt heal itself. This allowed the researchers to test molecules on the scarring in a way that isolated the drug and scarring tissues. They tested more than 17,000 small molecules. They identified one that stopped progressive scarring and healed the damage. They believe the compound activates the cells innate wound healing processes.

This drug candidate seems to be able to stop and reverse progressive scarring in a dish by actually breaking down the scar tissue, said Gomperts. We tested it in animal models of fibrosis of the lungs and eyes and found that it has promise to treat both of those diseases.

The next steps are to determine how the drug candidate works and also screen more molecules. The drug has not been tested in humans. The therapeutic strategy is covered by a patent application the UCLA Technology Development Group filed on behalf of the Regents of the University of California, with Gomperts and Vijayaraj listed as co-inventors. Gomperts is also a co-founder and stock owner of a biotech company, InSpira, which is focused on developing the molecule and strategy for fibrosis.

Link:
Researchers ID Molecule that Appears to Halt and Reverse Scarring in Fibrotic Diseases - BioSpace

1. Apple is offering free genetic tests to all its Silicon Valley employees  CNBC
2. Apple to offer free genetic testing for employees, report says  Business Insider
3. Apple partners with Color to provide free genetics tests to employees  Becker's Hospital Review
4. Apple Offers Free Genetic Testing to Cupertino Employees  MacRumors
5. Apple's AC Wellness offering free genetic testing to employees  AppleInsider
6. View full coverage on Google News

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Apple is offering free genetic tests to all its Silicon Valley employees - CNBC

In a new study, a high genetic risk score (GRS) was associated with an increased risk of organ damage, renal (kidney) dysfunction and mortality in people with lupus. Organ damage, cardiovascular disease, proliferative nephritis (kidney lesions), end-stage renal disease (ESRD) and presence of antiphospholipid antibodies were successfully predicted by a high GRS in people with lupus. GRSs have been applied in several fields of medicine and may be a potential tool for prediction of disease severity in lupus.

Clinical data from 1,001 people with lupus were analyzed. Their health outcomes and cumulative genetic risk were compiled and compared against the GRSs of 5,524 people with lupus and 9,859 healthy people. Lupus was more prevalent in the high-, compared with the low-GRS group Patients in the high GRS group had a 6-year earlier average disease onset, displayed higher prevalence of damage accrual, ERSD, proliferative nephritis, certain types of autoantibodies and positive lupus anticoagulant test, compared with patients in the low-GRS group. Survival analysis showed earlier onset of the first organ damage, first cardiovascular event, nephritis, ESRD and decreased overall survival in people with high GRSs compared to those with low scores.

Genetic profiling may be useful for predicting outcomes in people with lupus and aid in the clinical decision process. Understanding the genetic contribution to permanent organ damage is important for understanding how lupus develops. Learn more about the genetics of lupus.

Read the study

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Genetic Risk Scores May Predict Severity and Outcomes in People with Lupus - Lupus Foundation of America

Jens Carlsson of the UCD School of Biology is co-founder of the Area 52 research group that aims to solve a variety of genetic questions.

After completing his PhD in 2001, followed by a stint at the Danish Institute for Freshwater Research in Silkeborg, assistant professor Jens Carlsson travelled to the US in 2002 to work as a postdoc at the Virginia Institute for Marine Science.

In 2007, he was appointed a visiting associate professor at Duke University, North Carolina, to research the population structure of striped sea bass.

In 2009, he travelled to Ireland to work at University College Cork as a senior research fellow, which included work on deep sea vessels. Then, in 2012, he made the move to University College Dublin and established his research group, Area 52.

Too many people have been watching the CSI TV series and have strange ideas of how a modern genetics laboratory works JENS CARLSSON

I think I have had an interest in fish since I was introduced to fishing as a kid. While completing my BSc project, I was fascinated by the questions you could ask and answer using scientific approaches.

The freedom that academic research has for coming up with projects and then sourcing funding, to actually examine these questions, was probably the reason why I stayed on in science.

The research group Area 52 quickly developed when I started working in UCD. It is now a rather diverse group and we take on research questions from a wide range of disciplines from viral diseases in fish to identification of human remains.

It is the use of genetic methods that allows us to work with these very diverse questions and, so far, all organisms have DNA or RNA so there are a huge variety of questions that we can address.

This also means that we collaborate with a large number of colleagues. While we have the genetic expertise, we also need to work with people who understand the biology and ecology of the organisms.

When Area 52 started, it was only myself and my wife and lab manager in the lab group. But now it has grown significantly and consists of undergraduates, summer interns, visiting students, MSc students, PhD candidates, postdocs, research fellows and research scientists.

I believe that genetics has the capacity to answer questions that no other research field can do.

For example, when you look at marine fish, there are no clear barriers preventing different populations from mixing. However, this does not mean that the fish all belong to the same biological unit or population.

While fish from multiple biological units can mix at feeding areas, they often return to specific spawning sites with each spawning site representing a single biological unit.

Multiple species have been shown using genetics separated into different populations to represent different biological units. This has profound implications for the management of fisheries species, as the level where management needs to take place is natural biological units and this might differ depending on the time of the year.

You might have multiple populations mixing at feeding grounds and it is very difficult to say which fish came from which population when being caught in commercial fisheries as they tend to look the same. However, by using genetic tools we are able to say which individual belongs to which population.

Furthermore, Area 52 has a strong focus on developing non-invasive sampling methods for studies of terrestrial mammals such as elephants, zebras and giraffes primarily in Kenya.

It is often very difficult and invasive to collect genetic material for these animals. We focus on using scat samples that are completely non-invasive. The animal does its business and we collect the scat and use that as source of genetic material.

Area 52 often works with method development and these methods can obviously be used in the commercial world. For example, the management of fisheries species and the integrity of supply chains.

However, the main focus of the lab is in deploying the methods we develop in conservation and environmental monitoring of water ecosystems.

It is always difficult to find time to do the research. You are teaching, mentoring, doing research and administration. At the same time, you need to secure funding for your research and that is difficult.

This is not only because of the lack of time, but also because of the strong competition among researchers for the very limited funding. This means that you can spend significant time on writing a grant application and then it is not funded. I wish the success rate of grants would be higher.

Too many people have been watching the CSI TV series and have strange ideas of how a modern genetics laboratory works.

The big question is climate change and how that will affect distribution and survival of species. This is a very important question requiring collaboration among a large number of researchers from many different fields of science.

Are you a researcher with an interesting project to share? Let us know by emailing editorial@siliconrepublic.com with the subject line Science Uncovered.

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Fishy genetics: A behind-the-scenes look at UCD's Area 52 - Siliconrepublic.com

The deal will grant 1933 Industries license to the DNA brand for the production and sale of hemp-derived CBD products

1933 Industries Inc () (OTCMKTS:TGIFF) announced Thursday that it has signed a second licensing agreement with OG DNA Genetics, a globally recognized leading cannabis brand.

The agreement will grant 1933 Industries the license to the DNA brand for the production and sale of hemp-derived CBD products signaling DNAs first entry into the cannabidiol market. DNA will leverage 1933s vast distribution network of over 800 retail outlets throughout the US.

In 2018, the Farm Bill was passed through legislation federally legalizing the cultivation of hemp and permitting the sale of hemp-derived CBD products. This gives DNA the ability to expand itsreach into the rapidly developing CBD market and provide the highest-quality products to all 50 states and globally.

We are excited to expand our partnership with 1933, one of the leaders in the CBD wellness space, said Don Morris, co-founder of DNA Genetics. It feels good to build on an already strong relationship with a like-minded company committed to putting out the best quality products.

Chris Rebentisch, CEO of 1933 Industries, said DNA has the best quality products in the market.

Its fitting that we would work together to help bring the legacy brand into the CBD wellness space. We have an amazing lineup of products and are excited to leverage DNAs global reach through this agreement, Rebentisch said.

For more than 15 years, genetics developed by DNA have won more than 200 awards in all categories at the most prestigious cannabis events around the world, making DNA the global standard in breeding and growing truly best-in-class strains.

These awards include the High Times Top 10 Strain of the Year,which was inducted into The High Times seedbank hall of fame in 2009, the High Times 100 list of the most influential people in the industry and the High Times Trailer Blazers Award, for contributions made towards uniting the fields of entrepreneurship, politics and medicine.

1933 Industries, based in Chilliwack, British Columbia, owns licensed medical and adult-use cannabis cultivation and production assets, proprietary hemp-based, CBD-infused branded products, CBD extraction services and a specialized cannabis advisory firm.

Shares recently traded up 2.6% to C$0.20 in Canada.

--ADDS share price--

Contact the author: [emailprotected]

Follow him on Twitter @PatrickMGraham

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1933 Industries signs second licensing deal with OG DNA Genetics - Proactive Investors USA & Canada

This week, GEDmatch, a genetic genealogy company that gained notoriety for giving law enforcement access to its customers DNA data, quietly informed its users it is now operated by Verogen, Inc., a company expressly formed two years ago to market next-generation [DNA] sequencing technology to crime labs.

What this means for GEDmatchs 1.3 million users and for the 60% of white Americans who share DNA with those users remains to be seen.

GEDmatch allows users to upload an electronic file containing their raw genotyped DNA data so that they can compare it to other users data to find biological family relationships. It estimates how close or distant those relationships may be (e.g., a direct connection, like a parent, or a distant connection, like a third cousin), and it enables users to determine where, along each chromosome, their DNA may be similar to another user. It also predicts characteristics like ethnicity.

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An estimated 30 million people have used genetic genealogy databases like GEDmatch to identify biological relatives and build a family tree, and law enforcement officers have been capitalizing on all that freely available data in criminal investigations. Estimates are that genetic genealogy sites were used in around 200 cases just last year. For many of those cases, officers never sought a warrant or any legal process at all.

Earlier this year, after public outcry, GEDmatch changed its previous position allowing for warrantless law enforcement searches, opted out all its users from those searches, and required all users to expressly opt in if they wanted to allow access to their genetic data. Only a small percentage did. But opting out has not prevented law enforcement from accessing consumers genetic data, as long as they can get a warrant, which one Orlando, Florida officer did last summer.

Law enforcement has argued that people using genetic genealogy services have no expectation of privacy in their genetic data because users have willingly shared their data with the genetics company and with other users and have consented to a companys terms of service. But the Supreme Court rejected a similar argument in Carpenter v. United States.

In Carpenter, the Court ruled that even though our cell phone location data is shared with or stored by a phone company, we still have a reasonable expectation of privacy in it because of all the sensitive and private information it can reveal about our lives. Similarly, genetic data can reveal a whole host of extremely private and sensitive information about people, from their likelihood to inherit specific diseases to where their ancestors are from to whether they have a sister or brother they never knew about. Researchers have even theorized at one time or another that DNA may predict race, intelligence, criminality, sexual orientation, and political ideology. Even if later disproved, officials may rely on outdated research like this to make judgements about and discriminate against people. Because genetic data is so sensitive, we have an expectation of privacy in it, even if other people can access it.

However, whether individual users of genetic genealogy databases have consented to law enforcement searches is somewhat beside the point. In all cases that we know of so far, law enforcement isnt looking for the person who uploaded their DNA to a consumer site, they are looking for that persons distant relatives people who never could have consented to this kind of use of their genetic data because they dont have any control over the DNA they happen to share with the sites users.

That means these searches are nothing more than fishing expeditions through millions of innocent peoples DNA. They are not targeted at finding specific users or based on individualized suspicion a fact the police admit because they dont know who their suspect is. They are supported only by the hope that a crime scene sample might somehow be genetically linked to DNA submitted to a genetic genealogy database by a distant relative, which might give officers a lead in a case. Theres a real question whether a warrant that allows this kind of search could ever meet the particularity requirements of the Fourth Amendment.

These are also dragnet searches, conducted under general warrants, and no different from officers searching every house in a town with a population of 1.3 million on the off chance that one of those houses could contain evidence useful to finding the perpetrator of a crime. With or without a warrant, the Fourth Amendment prohibits searches like this in the physical world, and it should prohibit genetic dragnets like this one as well.

We need to think long and hard as a society about whether law enforcement should be allowed to access genetic genealogy databases at all even with a warrant. These searches impact millions of Americans. Although GEDmatch likely only encompasses about 0.5% of the U.S. adult population, research shows 60% of white Americans can already be identified from its 1.3 million users. This same research shows that once GEDmatchs users encompass just 2% of the U.S. population, 90% of white Americans will be identifiable.

Although many authorities once argued these kinds of searches would only be used as a way to solve cold cases involving the most terrible and serious crimes, that is changing; this year, police used genetic genealogy to implicate a teenager for a sexual assault. Next year it could be used to identify political or environmental protestors. Unlike established criminal DNA databases like the FBIs CODIS database, there are currently few rules governing how and when genetic genealogy searching may be used.

We should worry about these searches for another reason: they can implicate people for crimes they didnt commit. Although police used genetic searching to finally identify the man they believe is the Golden State Killer, an earlier search in the same case identified a different person. In 2015, a similar search in a different case led police to suspect an innocent man. Even without genetic genealogy searches, DNA matches may lead officers to suspect and jail the wrong person, as happened in a California case in 2012. That can happen because we shed DNA constantly and because our DNA may be transferred from one location to another, possibly ending up at the scene of a crime, even if we were never there.

All of this is made even more concerning by the recent acquisition of GEDmatch by a company whose main purpose is to help the police solve crimes. The ability to research family history and disease risk shouldnt carry the threat that our data will be accessible to police or others and used in ways we never could have foreseen. Genetic genealogy searches by law enforcement invade our privacy in unique ways they allow law enforcement to access information about us that we may not even know ourselves, that we have no ability to hide, and that could reveal more about us in the future than scientists know now. These searches should never be allowed even with a warrant.

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Genetic Testing Company Acquired by Company With Ties to FBI and Law Enforcement - Truthout

Every minute of every day our bodies are bombarded with millions of different molecules that we breathe, eat and touch including bacteria, viruses, chemicals and seemingly harmless compounds like food and pollen.

For every one of these encounters, our immune system has to decide if the substance is a threat or not, if it is foreign or self and how the body should respond to stay healthy. To do this, we rely on two immune systems working in tandem.

Scientists have discovered a new human autoinflammatory disease that results from a mutation in an important gene in one of these systems.

The syndrome, now known as CRIA (cleavage-resistant RIPK1-induced autoinflammatory) syndrome causes recurring episodes of debilitating and distressing fever and inflammation.

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Our bodys first line of defence is the innate immune system that is effectively a hard wired and fast response, explains Dr Najoua Lalaoui from the Walter and Eliza Hall Institute of Medical Research (WEHI) and the Department of Medical Biology at the University of Melbourne.

This system works in the skin and mucous membranes like the mouth, making sure that any invaders like bacteria are detected and destroyed quickly, she says.

If pathogens do enter the body, the innate immune cells move to the site of infection and physically devour invaders and activate chemical messengers to alert the body.

This can lead to an inflammatory reaction where blood circulation is increased, the affected area becomes swollen and hot, and the person may experience fever. When these chemical messengers are over-active it can result in conditions like colitis, arthritis and psoriasis.

Supporting this system is the adaptive immunity system that involves antibodies that recognise and then train the body to respond to threats. This is our memory immunity and the basis of how vaccinations work.

Scientists from the WEHI, with colleagues at the National Institutes of Health (NIH) in the United States, have been working to understand why patients from three families suffered from a history of painful swollen lymph nodes, fever and inflammation.

The families had a range of other inflammatory symptoms which began in childhood and continued into their adult years.

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This type of repeated fever often indicates an issue with the innate immune system and the same disease in an extended family can indicate genetic changes that are passed from parents to their children, explains Dr Lalaoui.

Previous tests didnt identify any known cause.

But by sequencing the patients genomes, the NIH team identified a mutation in DNA that codes for a molecule known as RIPK that they suspected might cause the disease.

RIPK is a critical regulator of inflammation and the cell death pathway responsible for cleaning up damaged cells or those infected by pathogens.

Professor John Silke from the Walter and Eliza Hall Institute and his team have been studying RIPK1 for more than 10 years. His team had previously shown that damaging the RIPK1 gene could lead to uncontrolled inflammation and cell death.

RIPK1 is a potent controller of cell death, which means cells have had to develop many ways of regulating its activity, Professor Silke says.

In this paper, we showed that one way that the cell regulates its activity is by cleaving RIPK1 into two pieces to disarm the molecule and halt its role in driving inflammation.

In this condition (CRIA), the mutations are preventing the molecule from being cleaved into two pieces, resulting in autoinflammatory disease. This helped confirm that the mutations identified by the NIH researchers were indeed causing the disease, he says.

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He explains that mutations in RIPK1 can drive both too much inflammation as in autoinflammatory and autoimmune diseases and too little inflammation, resulting in immunodeficiency.

There is still a lot to learn about the varied roles of RIPK1 in cell death, and how we can effectively target RIPK1 to treat disease.

In CRIA syndrome, the mutation in RIPK1 overcomes all of the normal checks and balances that exist, resulting in uncontrolled cell death and inflammation, says Dr Steven Boyden from the National Human Genome Research Institute at the NIH.

Dr Boyden says the first clue that the disease was linked to cell death was when they delved into the patients exomes the part of the genome that encodes all of the proteins in the body.

The team sequenced the entire exome of each patient and discovered unique mutations in the exact same amino acid of RIPK1 in each of the three families.

It is remarkable, like lightning striking three times in the same place. Each of the three mutations has the same result it blocks cleavage of RIPK1 which shows how important RIPK1 cleavage is in maintaining the normal function of the cell, says Dr Boyden.

Dr Lalaoui said the WEHI researchers then confirmed the link between the RIPK1 mutations and CRIA syndrome in laboratory models.

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We showed that mice with mutations in the same location in RIPK1 as in the CRIA syndrome patients, had a similar exacerbation of inflammation, she says.

Dr Dan Kastner from NIH widely regarded as the father of autoinflammatory disease says colleagues had treated CRIA syndrome patients with a number of anti-inflammatory medications, including high doses of corticosteroids and biologics, compounds that block specific parts of the immune system.

And although some of the patients markedly improved, others responded less well or had significant side effects.

Understanding the molecular mechanism by which CRIA syndrome causes inflammation provides an opportunity to get right to the root of the problem, Dr Kastner says.

Dr Kastner noted that RIPK1 inhibitors, which are already available on a research basis, may provide a focused, precision medicine approach to treating patients.

RIPK1 inhibitors may be just what the doctor ordered for these patients. The discovery of CRIA syndrome also suggests a possible role for RIPK1 in a broad spectrum of human illnesses, such as colitis, arthritis and psoriasis.

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The genetic mutation behind a new autoinflammatory disease - Pursuit

A genetic variant found in about 3% of people of African ancestry is a more significant cause of heart failure than previously believed, according to a multi-institution study led by researchers at Penn Medicine. The researchers also found that this type of heart failure is underdiagnosed. According to their study, 44% of TTR V122Ivariant carriers older than age 50 had heart failure, but only 11% of these individuals had been diagnosed with hATTR-CM. The average time to diagnosis was three years, indicating both high rates of underdiagnoses and prolonged time to appropriate diagnosis

This study suggests that workup for amyloid cardiomyopathy and genetic testing of TTR should be considered, when appropriate, to identify patients at risk for the disease and intervene before they develop more severe symptoms or heart failure, said the studys lead author Scott Damrauer, M.D., an assistant professor of Surgery at Penn Medicine and a vascular surgeon at the Corporal Michael J. Crescenz VA Medical Center. (Penn Medicine consists of the Raymond and Ruth Perelman School of Medicine at the University of Pennsylvania and the University of Pennsylvania Health System.)

In this study, researchers from Penn Medicine and the Icahn School of Medicine at Mount Sinai used a genome-first approach, performing DNA sequencing of 9,694 individuals of African and Latino ancestry enrolled in either the Penn Medicine BioBank (PMBB) or the Icahn School of Medicine at Mount Sinai BioMe biobank (BioMe). Researchers identified TTR V122I carriers and then examined longitudinal electronic health record-linked genetic data to determine which of the carriers had evidence of heart failure.

The findings, which were published today in JAMA, are particularly important given the US Food and Drug Administrations (FDA) approval of the first therapy (tafamidis) for ATTR-CM in May 2019. Prior to tafamidiss approval, treatment was largely limited to supportive care for heart failure symptoms and, in rare cases, heart transplant.

Our findings suggest that hATTR-CM is a more common cause of heart failure than its perceived to be, and that physicians are not sufficiently considering the diagnosis in certain patients who present with heart failure, said the studys corresponding author Daniel J. Rader, M.D., chair of the Department of Genetics at Penn Medicine. With the recent advances in treatment, its critical to identify patients at risk for the disease and, when appropriate, perform the necessary testing to produce an earlier diagnosis and make the effective therapy available.

hATTR-CM, also known as cardiac amyloidosis, typically manifests in older patients and is caused by the buildup of abnormal deposits of a specific transthyretin protein known as amyloid in the walls of the heart. The heart walls become stiff, resulting in the inability of the left ventricle to properly relax and adequately pump blood out of the heart. However, this type of heart failurewhich presents similar to hypertensive heart disease is common, and the diagnosis of hATTR-CM is often not considered.

Tafamidis meglumine is a non-NSAID benzoxazole derivative that binds to TTR with high affinity and selectivity. TTR acts by transporting the retinol-binding protein-vitamin A complex. It is also a minor transporter of thyroxine in blood. Its tetrameric structure can become amyloidogenic by undergoing rate-limiting dissociation and monomer misfolding.

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Penn Team Finds Genetic Variant Largely Found in Patients of African Descent that Increases Heart Failure Risk - Clinical OMICs News