The recently-formed supergroup The New Stew, featuring all-star members from Living Colour, The Lee Boys, The Aquarium Rescue Unit and more, has been captivating audiences with their soul drenching, funk heavy tribute to the great music of Bill Withers by performing the 1972 album Live At Carnegie Hall in its entirety! The band made its way to the Brooklyn Bowl on Monday, May 9th, and have two more shows coming up in Asheville, NC and Atlanta, GA.Watch All-Star Musicians Join Forces For ‘Lean On Me’ At Bill Withers Tribute ShowThe New Stew includes Corey Glover (Living Colour, Galactic) on vocals, Roosevelt Collier (The Lee Boys) on Lap Steel/ Pedal Steel, Yonrico Scott (Derek Trucks Band, Royal Southern Brotherhood) on percussion, Dave Yoke (Susan Tedeschi Band, Dr. John, Scrapomatic) on guitar, Jared Stone (Stone’s Stew) on drums, and Matt Slocum (Oteil and the Peacemakers, Col. Bruce Hampton & Aquarium Rescue Unit, The Lee Boys) on piano. Enjoy full audio from the rockin’ Brooklyn show, thanks to taper Eric McRoberts:Here’s a fan-shot video of “Better Off Dead”:The New Stew Tour Dates5/11 Wed- The Orange Peel – Asheville, NC5/12 Thu – Center Stage – Atlanta, GA
In recent years investigators have discovered that breast tumors are influenced by more than just the cancer cells within them. A variety of noncancerous cells, which in many cases constitute the majority of the tumor mass, form what is known as the “tumor microenvironment.” This sea of noncancerous cells and the products they deposit appear to play key roles in tumor pathogenesis.Among the key accomplices in the tumor microenvironment are mesenchymal stem cells (MSCs), a group of adult progenitor cells, which have been shown to help breast cancers maneuver and spread to other parts of the body.Now, new research sheds further light on how this spreading is happening. Led by investigators at Harvard-affiliated Beth Israel Deaconess Medical Center (BIDMC), the research demonstrates that the lysyl oxidase (LOX) gene is spurred to production in cancer cells as a result of their contact with MSCs, and once produced, can help ensure the spread of otherwise weakly metastatic cancer cells from primary tumors to the lung and bones. Described online in the Proceedings of the National Academy of Sciences (PNAS), this discovery not only provides key insights into the basic biology of tumor formation, but also offers a potential new direction in the pursuit of therapies for the treatment of bone metastasis.“We don’t have a lot of therapies that can target breast cancer once it has metastasized, particularly once cancer cells have lodged in the bone,” says senior author Antoine Karnoub, an investigator in the Department of Pathology at BIDMC and assistant professor of pathology at Harvard Medical School. “When breast cancer cells reach the skeleton, one way in which they cause damage is by breaking down bone tissue, which results in the bone’s rich matrix releasing numerous factors. These factors, in turn, feed the cancer cells, setting in motion a vicious cycle that leaves patients susceptible to fractures, pain, and further metastasis.”MSCs are nonhematopoietic progenitor cells predominantly produced in the bone marrow that generate bone, cartilage, fat, and fibrous connective tissue. They additionally support immune cell development and are recruited to inflammatory sites throughout the body to help shut down immune responses and regenerate damaged tissues, as might occur during wound healing. Several years ago, as a postdoctoral researcher at the Whitehead Institute of the Massachusetts Institute of Technology, Karnoub began exploring the idea that MSCs were migrating to tumors after mistaking the cancer sites for inflammatory lesions in need of healing.“We discovered that once MSCs had reached the tumor sites, they were actually helping in cancer metastasis, causing primary cancer cells to spread to other sites in the body,” he explains. In this new research, Karnoub wanted to find out — in greater molecular detail — how breast cancer cells respond to the influences of MSCs in order to better understand how cancer cells cross talk with recruited cells in the microenvironment.His scientific team first embarked on a straightforward experiment. “We took two dishes of cells, cancer cells and MSCs, and mixed them together,” Karnoub explains. After three days, the researchers removed the cancer cells and studied them to see how they had changed.“We found that the lysyl oxidase gene was highly upregulated in the cancer cells,” Karnoub says. “It turns out that when a cancer cell comes in contact with an MSC, it flips on this LOX gene, turning it up by a factor of about 100. So our next question was: What happens to the cancer cells when they encounter this boost of LOX that they themselves have produced?”The answer, as revealed in subsequent experiments, was that LOX was setting in motion a cell program called epithelial-to-mesenchymal transition (EMT). During EMT, cancer cells that usually clump together undergo a transformation into cells that exhibit decreased adhesion to their neighbors and go their own way. As a result, these cancerous cells are able to migrate, significantly enhancing their ability to metastasize.“When we put these cells back into mice, they not only formed tumors that metastasized to the lung, but also to the bone,” says Karnoub. “This makes you wonder whether the cancer cells in primary tumors have become so acclimated to interacting with bone-derived MSCs that they can now grow more easily in the bone once they leave the tumor.”The investigators also wanted to find out if, by going through the EMT process, cancer cells were also acquiring the phenotypes of another highly aggressive feature of malignant cancer cells, those of cancer stem cells within the cores of most tumors.“Cancer stem cells are believed to be responsible for the resurgence of tumors following chemotherapy treatment, and an increasing body of science is focused on understanding how CSCs function and how they originate,” says Karnoub. “The processes of EMT and CSC formation have been described as being closely coupled, and we asked whether LOX might be regulating CSC phenotypes, just as it was regulating EMT. To our surprise, this was not the case. This tells us that pathways that were once thought to be intimately intertwined and commonly tweaked may, in fact, be separate, and now we can start to tease out the respective circuitries with a bit more clarity.”Lastly, the investigators identified the mechanism that was enabling LOX to be turned on from outside the cell, a set of molecules called hyaluronic acid (HA) and CD44. “It turns out that the MSCs provide the HA while the cancer cells provide the CD44, and they work in tandem like a lock and key to upregulate LOX expression,” explains Karnoub, adding that antagonists to HA and CD44, already in extensive investigations and clinical exploration, might be of increased use from a clinical standpoint, perhaps in managing bone metastasis.To read the full story.
“But to see the roomful of pension scheme CIOs, trustees and managers spontaneously agreeing to take radical, decisive action now was incredible. I cannot remember being a part of a discussion like it.” Senior figures at large UK pension schemes have signed a climate change “charter”, seeking to address a sense among trustees that not enough is being done to fight climate change.Signatories pledged to recommend to their boards that every investment be scrutinised for its impact on the climate and to insist that their asset managers engage with companies about having a clear plan to move to a low-carbon future. The charter was created at a recent event held by pensions industry forum Mallowstreet, and committed individuals to action, rather than pension funds or trustee boards.Co-founder of Mallowstreet Dawid Konotey-Ahulu, who hosted the event at which the charter was created, said: “We had a chance to halt climate change 30 years ago, but we missed the opportunity, and now we are out of time. “I think the time has come for asset owners to focus on this as a core part of their investment decision making”Paul TrickettAccording to Mallowstreet, the charter has so far been signed by three senior individuals working for UK pension funds: Paul Trickett, who chairs the trustee board for Santander UK’s £11.5bn (€13.3bn) scheme, as well as working as a trustee for the Railways Pension Scheme and the Mineworkers’ Pension Scheme; Mark Tennant, chairman of the £8bn Centrica Common Investment Fund; and Rosie Lacey, group pensions manager of the £970m De La Rue Pension Scheme.Tennant said: “The problem we have with climate change is that everyone talks about it and everyone is deeply concerned, but very little is being done.”“We hold assets for future generations,” he added. “For them climate change matters. The younger generation requires us to look at the carbon footprint and the social impact of the investments we make on their behalf.”Trickett said: “I think the time has come for asset owners to focus on this as a core part of their investment decision making. I don’t know exactly how urgent it is, but I would prefer not to wait any longer.“The industry is focused on achieving its obligations to members. Establishing climate change as an issue to be considered as part of that is going to take time but if asset owners press for this it will happen more quickly.”The charter, which can be signed here, reads as follows:We, the undersigned, agree with the UK government that there is a climate emergency. We also know that current actions and responses are insufficient to avoid catastrophic damage to our planet. This climate emergency will have a material financial impact on every pension fund and all our futures.As chairs, investment committee members, pension managers and trustees, we pledge to recommend to our boards and investment committees:To ask “What is the impact on the climate?” for each and every investment that is made.To demand that the carbon impact of every investment is measured and reported on by our managers. We will work actively and collaboratively to develop complete carbon measurement standards.To insist that each of our investment managers actively engage with corporate boards underlying our investments so that every company develops and discloses both a complete measure of their carbon impact as well as a clear business plan to transition to a low carbon future. To review, and ultimately will recommend the termination of, any investment manager that fails to support and actively engage in stewarding the transition to a low-carbon future.