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Tag Archives: Prevents
UK’s Activision Buyout Block Prevents Microsoft from Trying Again for 10 Years – Push Square
- UK’s Activision Buyout Block Prevents Microsoft from Trying Again for 10 Years Push Square
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New Innovative Treatment Prevents Diabetes
Diabetes is a chronic condition characterized by high levels of sugar (glucose) in the blood. It is caused by a problem with the hormone insulin, which regulates the amount of glucose in the body. There are two main types of diabetes: Type 1, in which the body does not produce enough insulin, and Type 2, in which the body does not properly use the insulin it produces.
Researchers from the Liston lab at the Babraham Institute have recently published a study on a preventative therapy for diabetes in mice. They were able to prevent the onset of diabetes in mice by modifying signaling pathways in pancreatic cells to prevent stress-induced cell death. The therapy targets a pathway that is common to both types of diabetes, making it a promising treatment option with huge therapeutic potential when translated into a clinical setting.
Dr. Kailsah Singh, a former research fellow in the Liston lab, described their findings: “Our results show that MANF could prevent the beta cell damage by preventing the inflammation in islets, which is a hallmark of type 1 diabetes.”
For over 35 years there have been failed attempts to prevent type 1 diabetes development. Previous approaches have sought to target the autoimmune nature of the disease, but Dr. Adrian Liston, senior Group Leader in the Immunology research program, wanted to investigate if there was more causing the deterioration in later stages than just the immune response.
The Liston lab sought to understand the role of cell death in the development of diabetes and therefore approached this problem by identifying the pathways that decide whether stressed insulin-producing cells of the pancreas live or die, and therefore determine the development of disease.
Their hope was to find a way to stop this stress-related death, preventing the decline into diabetes without the need to focus solely on the immune system. First, the researchers had to know which pathways would influence the decision of life or death for the beta cell. In previous research, they were able to identify Manf as a protective protein against stress-induced cell death, and Glis3 which sets the level of Manf in the cells. While type 1 and 2 diabetes in patients usually has different causes and different genetics, the GLIS3-MANF pathway is a common feature for both conditions and therefore an attractive target for treatments.
In order to manipulate the Manf pathway, the researchers developed a gene delivery system based on a modified virus known as an AAV gene delivery system. The AAV targets beta cells, and allows these cells to make more of the pro-survival protein Manf, tipping the life-or-death decision in favor of continued survival. To test their treatment, the researchers treated mice susceptible to the spontaneous development of autoimmune diabetes. Treating pre-diabetic mice resulted in a lower rate of diabetes development from 58% to 18%. This research in mice is a key first step in the development of treatments for human patients.
“A key advantage of targeting this particular pathway is the high likelihood that it works in both type 1 and type 2 diabetes”, explains Dr. Adrian Liston. “In type 2 diabetes, while the initial problem is insulin-insensitivity in the liver, most of the severe complications arise in patients where the beta cells of the pancreas have been chronically stressed by the need to make more and more insulin. By treating early type 2 diabetes with this approach, or a similar one, we have the potential to block progression to the major adverse events in late-stage type 2 diabetes.”
Reference: “Gene Delivery of Manf to Beta-Cells of the Pancreatic Islets Protects NOD Mice from Type 1 Diabetes Development” by Kailash Singh, Orian Bricard, Jeason Haughton, Mikaela Björkqvist, Moa Thorstensson, Zhengkang Luo, Loriana Mascali, Emanuela Pasciuto, Chantal Mathieu, James Dooley and Adrian Liston, 16 November 2022, Biomolecules.
DOI: 10.3390/biom12101493
The study was funded by the Biotechnology and Biological Sciences Research Council, Vlaams Instituut voor Biotechnologie, and The Research Foundation – Flanders.
Scientists develop a vaccine that kills AND prevents untreatable brain cancer that killed Beau Biden
Scientists develop a vaccine that destroys AND prevents untreatable brain cancer which killed Beau Biden and John McCain
- A new Glioblastoma treatment uses living cancer cells to reduce brain tumors
- Cells are removed, modified, and returned to induce a strong immune response
- The cell therapy method, so far tested only on mice, produced promising results
A new experimental vaccine may hold hope for sufferers of the incurable brain cancer glioblastoma.
The dual-action shot – so far only tested in mice – eliminates existing tumors and prevents future cancer from returning.
Experts take live pieces of patients’ tumors and reprogram them to attack the glioblastoma before reinjecting them into the body. From there, the re-engineered living cancer cells make a beeline to the original tumor, allowing the immune system to tag and remember them as they travel.
While it has only been tested in animals, the shot offers hope in the treatment of a deadly cancer that kills virtually all patients within five years. President Biden’s son Beau succumbed to glioblastoma in 2015 at just 46 years old. Senator John McCain died in 2018, only one year after his diagnosis.
The new vaccine works in 4 steps: First, cancer cells are removed from the tumor; Second, through gene mutation using CRISPR technology, the cells are re-engineered to produce a tumor killing agent and express factors allowing the immune system to better recognize and tag them; Third, the cells are re-inserted, and begin travelling across the brain to the tumor site, producing a strong immune defense; Finally, the tumor reduces as a result of the two-pronged attack
Glioblastoma are malignant, stage 4 tumors that develop deep in the brain and spinal cord.
Their fast growth and invasion of surrounding brain tissue makes 100% removal nearly impossible, while the changing nature of the tumor cells over time makes treatment incredibly difficult.
The new vaccine is the result of years of painstaking research by a lab at Brigham and Women’s Hospital in Massachusetts.
The treatments works by extracting live tumor cells from a Glioblastoma, and transforming them into potent, anti-cancer killers.
Most cancer vaccines in production use inactivated cancer particles to help the immune system seek and destroy them.
But the new shot turns living cells into tumor killers that will both destroy active tumor cells and allow the immune system to memorize how to combat them next time.
This method harnesses the unique ability of active cancer cells to travel vast distances across the brain to return to the site of their fellow tumor cells, much like homing pigeons returning to the roost.
The transplanted cells are transformed using CRISPR technology, a gene editor that allowed the team to reprogram the cells to release a tumor killing agent.
The lab also conditioned the tumor cells to express factors that make them more recognizable to the immune system, allowing it to tag and remember them.
The patient’s immune system is thereby primed for a long-term, anti-tumor response.
Once packaged into a vaccine, the team tested it on mice bearing cells derived from humans, mimicking how it would work on people.
Dr. Khalid Shah, one of the creators of the shot, said: ‘Our team has pursued a simple idea: to take cancer cells and transform them into cancer killers and vaccines.
‘Using gene engineering, we are repurposing cancer cells to develop a therapeutic that kills tumor cells and stimulates the immune system to both destroy primary tumors and prevent cancer.’
The team’s findings were published in Science Translational Medicine this week.
It comes as a number of new vaccines show promising results in trials.
Moderna’s new cancer vaccine uses the same mRNA technology as its Covid vaccination, using pieces of genetic code from patients’ tumors to effectively ‘teach’ the body to fight off cancer.
The shot, combined with an immunotherapy drug, reduced the chance of relapse or death in post-surgery Melanoma patients by 44 percent, compared to the drug on its own.
Another recent cancer breakthrough saw all 10 participants of a last resort Mount Sinai trial go from having just years to live, to complete or partial remission.
The vaccine they received was injected directly into the tumor itself, melting it away as well as teaching the body to hunt and kill cancer cells that have spread elsewhere.
Revolutionary Cancer Vaccine Simultaneously Kills and Prevents Brain Tumors
Researchers at Brigham and Women’s Hospital have found a way to use cancer cells to fight cancer. In a study published in Science Translational Medicine, the team led by Khalid Shah demonstrated that their cell therapy could eliminate established tumors and create long-term immunity in an advanced mouse model of glioblastoma, a type of brain cancer. The vaccine works by training the immune system to prevent cancer from returning. These results are encouraging and suggest that this approach may be effective in treating cancer in humans.
Dual-action cell therapy engineered to eliminate established tumors and train the immune system to eradicate primary tumor and prevent cancer’s recurrence.
Scientists are harnessing a new way to turn cancer cells into potent, anti-cancer agents. In the latest work from the lab of Khalid Shah, MS, PhD, at Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system, investigators have developed a new cell therapy approach to eliminate established tumors and induce long-term immunity, training the immune system so that it can prevent cancer from recurring. The team tested their dual-action, cancer-killing vaccine in an advanced mouse model of the deadly brain cancer glioblastoma, with promising results. Findings are published in Science Translational Medicine.
“Our team has pursued a simple idea: to take cancer cells and transform them into cancer killers and vaccines,” said corresponding author Khalid Shah, MS, PhD, director of the Center for Stem Cell and Translational Immunotherapy (CSTI) and the vice chair of research in the Department of Neurosurgery at the Brigham and faculty at Harvard Medical School and Harvard Stem Cell Institute (HSCI). “Using gene engineering, we are repurposing cancer cells to develop a therapeutic that kills tumor cells and stimulates the immune system to both destroy primary tumors and prevent cancer.”
Scientists developed a bifunctional therapeutic strategy by transforming living tumor cells into a therapeutic. Shah’s team engineered living tumor cells using the gene editing tool CRISPR-Cas9 and repurposed them to release tumor cell killing agent. In addition, the engineered tumor cells were designed to express factors that would make them easy for the immune system to spot, tag and remember, priming the immune system for a long-term anti-tumor response. The team tested their repurposed CRISPR-enhanced and reverse-engineered therapeutic tumor cells (ThTC) in different mice strains including the one that bore bone marrow, liver and thymus cells derived from humans, mimicking the human immune microenvironment. Shah’s team also built a two-layered safety switch into the cancer cell, which, when activated, eradicates ThTCs if needed. Credit: Kok Siong Chen and Khalid Shah
Cancer vaccines are an active area of research for many labs, but the approach that Shah and his colleagues have taken is distinct. Instead of using inactivated tumor cells, the team repurposes living tumor cells, which possess an unusual feature. Like homing pigeons returning to roost, living tumor cells will travel long distances across the brain to return to the site of their fellow tumor cells. Taking advantage of this unique property, Shah’s team engineered living tumor cells using the gene-editing tool CRISPR-Cas9 and repurposed them to release tumor cell killing agent. In addition, the engineered tumor cells were designed to express factors that would make them easy for the immune system to spot, tag, and remember, priming the immune system for a long-term anti-tumor response.
The team tested their repurposed CRISPR-enhanced and reverse-engineered therapeutic tumor cells (ThTC) in different mice strains including the one that bore bone marrow, liver and thymus cells derived from humans, mimicking the human immune microenvironment. Shah’s team also built a two-layered safety switch into the cancer cell, which, when activated, eradicates ThTCs if needed. This dual-action cell therapy was safe, applicable, and efficacious in these models, suggesting a roadmap toward therapy. While further testing and development is needed, Shah’s team specifically chose this model and used human cells to smooth the path of translating their findings for patient settings.
“Throughout all of the work that we do in the Center, even when it is highly technical, we never lose sight of the patient,” said Shah. “Our goal is to take an innovative but translatable approach so that we can develop a therapeutic, cancer-killing vaccine that ultimately will have a lasting impact in medicine.” Shah and colleagues note that this therapeutic strategy is applicable to a wider range of solid tumors and that further investigations of its applications are warranted.
Reference: “Bifunctional cancer cell-based vaccine concomitantly drives direct tumor killing and antitumor immunity” by Kok-Siong Chen, Clemens Reinshagen, Thijs A. Van Schaik, Filippo Rossignoli, Paulo Borges, Natalia Claire Mendonca, Reza Abdi, Brennan Simon, David A. Reardon, Hiroaki Wakimoto and Khalid Shah, 4 January 2023, Science Translational Medicine.
DOI: 10.1126/scitranslmed.abo4778
Disclosures: Shah owns equity in and is a member of the Board of Directors of AMASA Therapeutics, a company developing stem cell-based therapies for cancer.
Funding: This work was supported by the National Institutes of Health (grant R01-NS121096).
Revolutionary Cancer Vaccine Simultaneously Kills and Prevents Brain Tumors
Researchers at Brigham and Women’s Hospital have found a way to use cancer cells to fight cancer. In a study published in Science Translational Medicine, the team led by Khalid Shah demonstrated that their cell therapy could eliminate established tumors and create long-term immunity in an advanced mouse model of glioblastoma, a type of brain cancer. The vaccine works by training the immune system to prevent cancer from returning. These results are encouraging and suggest that this approach may be effective in treating cancer in humans.
Dual-action cell therapy engineered to eliminate established tumors and train the immune system to eradicate primary tumor and prevent cancer’s recurrence.
Scientists are harnessing a new way to turn cancer cells into potent, anti-cancer agents. In the latest work from the lab of Khalid Shah, MS, PhD, at Brigham and Women’s Hospital, a founding member of the Mass General Brigham healthcare system, investigators have developed a new cell therapy approach to eliminate established tumors and induce long-term immunity, training the immune system so that it can prevent cancer from recurring. The team tested their dual-action, cancer-killing vaccine in an advanced mouse model of the deadly brain cancer glioblastoma, with promising results. Findings are published in Science Translational Medicine.
“Our team has pursued a simple idea: to take cancer cells and transform them into cancer killers and vaccines,” said corresponding author Khalid Shah, MS, PhD, director of the Center for Stem Cell and Translational Immunotherapy (CSTI) and the vice chair of research in the Department of Neurosurgery at the Brigham and faculty at Harvard Medical School and Harvard Stem Cell Institute (HSCI). “Using gene engineering, we are repurposing cancer cells to develop a therapeutic that kills tumor cells and stimulates the immune system to both destroy primary tumors and prevent cancer.”
Scientists developed a bifunctional therapeutic strategy by transforming living tumor cells into a therapeutic. Shah’s team engineered living tumor cells using the gene editing tool CRISPR-Cas9 and repurposed them to release tumor cell killing agent. In addition, the engineered tumor cells were designed to express factors that would make them easy for the immune system to spot, tag and remember, priming the immune system for a long-term anti-tumor response. The team tested their repurposed CRISPR-enhanced and reverse-engineered therapeutic tumor cells (ThTC) in different mice strains including the one that bore bone marrow, liver and thymus cells derived from humans, mimicking the human immune microenvironment. Shah’s team also built a two-layered safety switch into the cancer cell, which, when activated, eradicates ThTCs if needed. Credit: Kok Siong Chen and Khalid Shah
Cancer vaccines are an active area of research for many labs, but the approach that Shah and his colleagues have taken is distinct. Instead of using inactivated tumor cells, the team repurposes living tumor cells, which possess an unusual feature. Like homing pigeons returning to roost, living tumor cells will travel long distances across the brain to return to the site of their fellow tumor cells. Taking advantage of this unique property, Shah’s team engineered living tumor cells using the gene-editing tool CRISPR-Cas9 and repurposed them to release tumor cell killing agent. In addition, the engineered tumor cells were designed to express factors that would make them easy for the immune system to spot, tag, and remember, priming the immune system for a long-term anti-tumor response.
The team tested their repurposed CRISPR-enhanced and reverse-engineered therapeutic tumor cells (ThTC) in different mice strains including the one that bore bone marrow, liver and thymus cells derived from humans, mimicking the human immune microenvironment. Shah’s team also built a two-layered safety switch into the cancer cell, which, when activated, eradicates ThTCs if needed. This dual-action cell therapy was safe, applicable, and efficacious in these models, suggesting a roadmap toward therapy. While further testing and development is needed, Shah’s team specifically chose this model and used human cells to smooth the path of translating their findings for patient settings.
“Throughout all of the work that we do in the Center, even when it is highly technical, we never lose sight of the patient,” said Shah. “Our goal is to take an innovative but translatable approach so that we can develop a therapeutic, cancer-killing vaccine that ultimately will have a lasting impact in medicine.” Shah and colleagues note that this therapeutic strategy is applicable to a wider range of solid tumors and that further investigations of its applications are warranted.
Reference: “Bifunctional cancer cell-based vaccine concomitantly drives direct tumor killing and antitumor immunity” by Kok-Siong Chen, Clemens Reinshagen, Thijs A. Van Schaik, Filippo Rossignoli, Paulo Borges, Natalia Claire Mendonca, Reza Abdi, Brennan Simon, David A. Reardon, Hiroaki Wakimoto and Khalid Shah, 4 January 2023, Science Translational Medicine.
DOI: 10.1126/scitranslmed.abo4778
Disclosures: Shah owns equity in and is a member of the Board of Directors of AMASA Therapeutics, a company developing stem cell-based therapies for cancer.
Funding: This work was supported by the National Institutes of Health (grant R01-NS121096).
Eagles vs. Saints score, takeaways: New Orleans prevents Philly from clinching home-field advantage in NFC
PHILADELPHIA — The Philadelphia Eagles will have one more chance to clinch home-field advantage in the NFC playoffs after failing to accomplish the task, thanks to a brutal 20-10 loss to the New Orleans Saints at Lincoln Financial Field. In what was arguably their worst offensive performance of the season, the Eagles couldn’t muster more than 10 points against the Saints defense with Jalen Hurts missing his second consecutive game.
Gardner Minshew sealed the Eagles’ fate by throwing an interception to Marshon Lattimore that was returned 12 yards for a touchdown with 5:10 to play. The Eagles, trailing 13-10, needed to go 91 yards for the win but the first giveaway for the team came at the worst possible time. Philadelphia never led in this one, going three-and-out on its first four possessions and allowing New Orleans to build a 13-point lead the Eagles couldn’t overcome.
The Saints took the lead on a 15-play, 75-yard drive to start the game that took 8:58 off the clock, capped by a Taysom Hill 1-yard touchdown run to put the New Orleans up 7-0. Wil Lutz hit 54- and 20-yard field goals to extend the lead to 13-0 prior to the half. The Saints hung on from there, stopping the Eagles on a fourth-and-1 quarterback sneak by Minshew in the fourth quarter and Lattimore intercepting Minshew in the fourth quarter to hang on for the victory.
Philadelphia will have to win in Week 18 against the New York Giants, who clinched a playoff spot and the No. 6 seed Sunday, to claim the NFC East crown and home-field advantage for the playoffs. New Orleans kept its shot for the NFC South alive with the win, but the Saints were eliminated from playoff contention with the Tampa Bay Buccaneers beating the Carolina Panthers Sunday.
Why the Saints won
New Orleans defense came to play against Philadelphia, holding the Eagles offense to a season-low 10 points and just 313 yards in the loss. The defense kept the Eagles offense in check by getting pressure on Gardner Minshew, only pressuring him 12 times but getting six sacks. Cameron Jordan had four pressures and three sacks in the win, taking advantage of an Eagles offensive line that didn’t have Lane Johnson.
The offense built enough of a lead early to hold on at the end, with Marshon Lattimore sealing the victory with an interception return for a touchdown off Minshew in the fourth quarter. The Saints defense has allowed just 38 points in the last three quarters.
Why the Eagles lost
Philadelphia’s offense clearly misses Jalen Hurts, as the Eagles had just one offensive touchdown in the loss. Minshew couldn’t convert a fourth-and-1 quarterback sneak with 8:35 left and threw an interception return for a touchdown on the next possession to seal the win for New Orleans. The Eagles started its first four possessions with three-and-outs, very uncharacteristic for the highest-scoring offense in football heading into Week 17. They ran the ball just twice in those possessions and had just 21 yards as the Saints built a 13-0 lead.
The Eagles were off all day, but still had a chance to win it in the fourth quarter. They’ll get Hurts back next week in a must-win game for home-field advantage.
Turning point
The Eagles were at midfield with 8:35 left in a 13-10 game and facing a fourth-and-1 in a 13-10 game. With the momentum going, Philadelphia called Minshew’s number to get the first down on a quarterback sneak — but he failed to convert. Jalen Hurts was 27 of 30 on quarterback sneaks this season while Minshew was 1 of 2 — including Sunday’s failed attempt.
Philadelphia didn’t have Hurts, but tried the sneak anyway. That showcases how valuable he is to an offense.
Play of the game
Marshon Lattimore’s interception off Gardner Minshew was the takeaway the Saints needed to steal the victory in Philadelphia. With 5:31 left in a 13-10 game, Lattimore easily read Minshew’s slant route to A.J. Brown and snatched the ball before it even got there — ending the Eagles chances at a win.
Minshew has thrown three crucial interception in the second half of his two games, all of which played a significant role in losses. The Eagles could have taken the lead, having the ball with 91 yards to score with just over six minutes left when the possession started.
The quote
“We can’t expect the season to go peaches and cream and go our way all the time. Unfortunately we put ourselves in this position and we gotta find a way to win next week.” — James Bradberry to CBS Sports on the recent adversity the Eagles are facing.
Philadelphia has failed to wrap up home-field advantage the last two weeks. The Eagles still control their own destiny, needing a win over the Giants — who have nothing to play for — next week.
Up next
The Eagles (13-3) face the New York Giants in their regular season finale, with a win needed to seal home-field advantage. The Saints (7-9) end their season against the Panthers.
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DDoS attack on ‘Overwatch 2’ servers prevents fans from playing the game on launch day
Overwatch 2’s early access launch has been marred by a few bugs and a massive DDoS attack preventing players from getting into the game. Fans have been reporting getting stuck on the loading screen and getting one error after another. They’re also put in queue behind hundreds — and in some cases, even tens of thousands — of other players also trying to get in. Blizzard president Mike Ybarra initially tweeted that the game is experiencing server issues and that the company’s teams are working hard to fix it. In a follow-up tweet, though, the executive admitted that the game is “experiencing a mass DDoS attack” on its servers causing drop and connection issues.
Blizzard developed the new free-to-play shooter for the Nintendo Switch, PlayStation 4, PlayStation 5, Windows, Xbox One and Xbox Series X|S. The new game reduces team sizes from six to five, so a team gets only one tank. It also comes with new maps, new heroes and new features, such as the ability to place a Ping on the enemy’s location to point them out to the rest of the team. Servers for the original Overwatch went offline shortly after its sequel launched, so fans have no choice but to wait for Blizzard to fix the issue before they can play the game again.
Aside from mitigating the DDoS attack, Blizzard also has to fix quite a few bugs that made themselves known upon launch. They include items and currency going missing from players’ collections, sections not populating, some areas becoming inaccessible, actions resulting in a blackscreen and Blizzard’s SMS Protect leaving the client unusable.
In a tweet, Overwatch 2 game director Aaron Keller said Blizzard will work throughout the night to deal with server issues and a second DDoS attack.
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US Navy prevents Iranian attempt to capture American maritime drone in Arabian Gulf
While US forces in the region were transiting international waters around 11 p.m. Monday, they saw an Iranian Islamic Revolutionary Guard Corps Navy support ship, Shahid Baziar, towing a US-operated maritime drone, also known as a Saildrone Explorer unmanned surface vessel, US Naval Forces Central Command said in a news release.
A US Navy patrol coastal ship, USS Thunderbolt, was “operating nearby and immediately responded,” the Navy said. After the Iranians attached a line to the maritime drone, US forces in the area communicated directly with the Iranians to say they wanted the drone back, a US defense official said.
The US Navy patrol boat then moved closer to the maritime drone, and US 5th Fleet launched an MH-60S Sea Hawk Helicopter from Bahrain and positioned moved it above the drone, the release and a US defense official said.
After the US responded with both the coastal ship and Sea Hawk helicopter, the Iranian vessel disconnected the towing line from the US drone and departed the area four hours later, the release said.
The US Navy then resumed operations “without incident,” the release added.
The incident comes at a critical time in relations between Iran and the US. Negotiations to revive the Iran nuclear deal are at a sensitive stage and US officials had voiced some optimism around the latest efforts. However, they have stressed that gaps remain between the two sides.
Vice Adm. Brad Cooper, commander of US Naval Forces Central Command, US 5th Fleet and Combined Maritime Forces, called the IRGCN’s actions “flagrant, unwarranted and inconsistent with the behavior of a professional maritime force,” in a statement about the incident.
“U.S. naval forces remain vigilant and will continue to fly, sail and operate anywhere international law allows while promoting rules-based international order throughout the region,” Cooper said in the statement.
Gen. Michael “Erik” Kurilla, Commander of US Central Command which oversees the US military presence in the Middle East, reacted strongly, saying Iran’s actions were illegal.
“The professionalism and competence of the crew of the USS Thunderbolt prevented Iran from this illegal action,” Kurilla said in a statement. “This incident once again demonstrates Iran’s continued destabilizing, illegal, and unprofessional activity in the Middle East.”
The maritime drone that the IRGCN attempted to take is “US government property and equipped with sensors, radars and cameras for navigation and data collection,” the release said. The drone “does not store sensitive or classified information,” the release added.
A Polyphenol-Rich Diet Prevents Inflammation in Older People
Summary: Polyphenols can reduce inflammation in older people by altering the intestinal microbiota and inducing the production of indole 3-propionic acid.
Source: University of Barcelona
Polyphenols in the foods that we eat can prevent inflammation in older people since they alter the intestinal microbiota and induce the production of the indole 3-propionic acid (IPA), a metabolite derived from the degradation of tryptophan due to intestinal bacteria.
This study, published in Molecular Nutrition and Food Research, was carried out by the Research Group on Biomarkers and Nutritional & Food Metabolomics of the Faculty of Pharmacy and Food Sciences of the University of Barcelona and the CIBER on Fragility and Healthy Ageing (CIBERFES).
The team, led by Professor Cristina Andrés-Lacueva, from the Faculty of Pharmacy and Food Sciences of the UB, is also a member of the Food Innovation Network of Catalonia (XIA).
Polyphenols and healthy aging
Polyphenols are natural compounds, considered probiotics, which we eat mainly through fruits and vegetables. Several dietary polyphenols have well-known antioxidant and anti-inflammatory properties and the ability to interact with bacteria present in the human gut and produce postbiotics (such as IPA), which increases their positive effects on health.
There is increasing evidence that confirms that the regular consumption of polyphenols in the diet can contribute to healthy aging, especially if they are part of a healthy diet, such as the Mediterranean one, and are associated with a healthy lifestyle, that is, one including regular physical activity and excluding tobacco and alcohol, for instance.
The study shows the interaction between polyphenols and gut microbiota can induce the proliferation of bacteria with the ability to synthesize beneficial metabolites, such as IPA. IPA is a postbiotic with antioxidant, anti-inflammatory and neuroprotective properties that contribute to improving the health of the intestinal wall. This compound appears to contribute to the prevention of some diseases associated with aging.
“If we consider the beneficial effects of IPA on the gut microbiota and health in general, it is important to find reliable strategies to promote the production of this metabolite”, notes the co-first signatory of the study, Tomás Meroño, from the Department of Nutrition, Food Sciences and Gastronomy of the UB and CIBERFES.
As part of the study, the researchers carried out a multiomic analysis to monitor the IPA levels in the serum. Researchers analyzed the composition of the gut microbiota in fecal samples of fifty-one volunteers aged over sixty-five who followed a polyphenol-rich diet ( including consuming green tea, bitter chocolate, fruits including apples, pomegranate, and blueberries) for eight weeks.
Increase of IPA in blood and bacterial growth
The results show that the diet rich in polyphenols generated a significant increase in the blood IPA levels, together with a decrease in inflammation levels and changes in gut bacteria from the order of Bacteroidales.
Surprisingly, the researchers did not observe the same effects in the volunteers with kidney diseases. This could be explained due to the altered composition of their gut microbiota. These people showed lower amounts of IPA at the beginning of the trial compared to the volunteers with normal kidney function.
“These results could be clinically relevant since the low IPA levels have been associated with a rapid decline of kidney function and a chronic kidney disease”, notes Professor Cristina Andrés-Lacueva.
Therefore, a polyphenol-rich diet, including probiotic foods such as green tea, dark chocolate, and some fruits like apples, pomegranate, and blueberries could increase the production of IPA through changes in the composition of gut microbiota. This increase in the levels of a postbiotic such as IPA in the elderly could be beneficial in delaying or preventing chronic diseases that harm the quality of life.
The study also includes the participation of teams from the University of Milan (Italy), Quadram Institute (United Kingdom), and the National Institute of Health and Sciences on Ageing (INCRA, Italy), among other institutions.
About this diet and inflammation research news
Author: Rosa Martínez
Source: University of Barcelona
Contact: Rosa Martínez – University of Barcelona
Image: The image is in the public domain
See also
Original Research: Open access.
“A polyphenol-rich diet increases the gut microbiota metabolite indole 3-propionic acid in older adults with preserved kidney function” by Tomás Meroño et al. Molecular Nutrition & Food Research
Abstract
A polyphenol-rich diet increases the gut microbiota metabolite indole 3-propionic acid in older adults with preserved kidney function
Scope
Dietary polyphenols can alter the gut microbiota (GM) and promote the production of bioactive metabolites. Several indoles result of GM metabolism of dietary tryptophan have been associated with intestinal barrier integrity. Our aim is to study the changes in GM-derived indoles during a polyphenol-rich (PR) diet intervention in older adults.
Methods and Results
Randomized, controlled, crossover trial in adults ≥ 60 years living in a residential care facility during an 8-week PR versus control diet (n = 51). Seven GM-tryptophan metabolites are measured in serum, and metataxonomic analysis of GM is performed on fecal samples.
Exploratory subgroup analyses are performed based on renal function (RF). The PR-diet significantly increases serum indole 3-propionic acid (IPA) in subjects with normal RF, but not in subjects with impaired RF. Other GM-tryptophan metabolites are not affected.
Comparison of baseline GM composition shows shifts in Bacteroidales order members as well as higher abundance of Clostridiales in participants with normal RF. During the trial, variations of IPA are associated with changes in C-reactive protein (β = 0.32, p = 0.010) and GM, particularly with the Clostridiales (r = 0.35, p < 0.001) and Enterobacteriales (r = −0.15, p < 0.05) orders.
Conclusion
A PR diet increases the serum concentration of IPA in older adults with normal RF. Our findings may be important when defining appropriate dietary interventions for older adults.