StemCell Therapy

On May 25, 1968, surgeons in Richmond, Virginia, performed a successful heart transplant, one of the world's first, on a white businessman. The heart that they used was taken from a Black patient named Bruce Tucker who had been brought to the hospital the day before, unconscious and with a fractured skull and traumatic brain injury. He was pronounced brain dead less than 24 hours later.

Tucker's still-beating heart was then removed without his family's knowledge or prior permission; their horrified discovery from the local funeral director that Tucker's heart was missing was a devastating blow.

The surgeons' actions, which led to America's first civil suit for wrongful death, are brought to light in the new book "The Organ Thieves: The Shocking Story of the First Heart Transplant in the Segregated South" (Simon and Schuster, 2020) by Pulitzer Prize-nominated journalist Charles "Chip" Jones. Jones raises troubling questions about the ethics of this pioneering transplant, revealing its deep roots in racism and discrimination toward Black people in health care.

Related: 7 Reasons America still needs civil rights movements

The first human organ transplant, a kidney, took place in 1954, and by the late 1960s, "superstar" surgeons were vying to be the first to successfully transplant a human heart, Jones told Live Science.

"In terms of science, it was the medical parallel to the space race," Jones said.

Dr. Richard Lower and Dr. David Hume, surgeons at the Medical College of Virginia (MCV) in Richmond, were at the forefront of that race, but it was South African surgeon Dr. Christiaan Barnard who performed the first heart transplant on Dec. 3, 1967. In May of 1968, MCV admitted to its hospital a patient with severe coronary disease who was a promising candidate for a heart transplant. But Lower and Hume had yet to find a viable heart donor.

And with time running out for their sick patient, they needed one fast.

Tucker, a Richmond factory worker who had sustained a serious head injury in a fall, was brought to the MCV Hospital on May 24, 1968. Though Tucker's personal effects included one of his brother's business cards, officials were unable to locate a family member on behalf of the unconscious man. And because the hospital claimed Tucker had no family and had liquor on his breath (he had been drinking prior to his accident), he was profiled as a "charity patient" and marked as a potential heart donor.

"He was in the wrong place at the wrong time," Jones said.

Tucker was connected to a ventilator, unable to breathe on his own. A junior medical examiner performed an electroencephalogram (EEG) to determine electrical activity in Tucker's brain; the examiner declared that there was none. The surgeons pronounced this to be sufficient evidence of brain death; Tucker was removed from the ventilator, and Hume and Lower removed Tucker's heart for the transplant, Jones wrote.

Related: What happens to your body when you're an organ donor?

Decades later, in 1981, the Uniform Determination of Death Act provided a legal definition of death: "irreversible cessation of circulatory and pulmonary functions" and "irreversible cessation of all functions of the whole brain," which means that the entire brain including the brain stem has ceased to function, according to Johns Hopkins Medicine.

But in 1968, the legal concept of death was not as clearly defined, Jones said.

"There was no statutory framework that would let doctors know how to proceed in a situation like this, where they had a patient that they legitimately thought had no chance of recovery," Jones explained. "And time was of the essence, in their view, to save a very sick man." However, the doctors were also quick to presume that Tucker was indigent and without family a racially motivated judgment, according to Jones.

Related: The 9 most interesting transplants

Tucker's family learned that his heart was missing from the funeral director; they pieced together what had happened from news reports (Tucker's identity was not initially released to the public, Jones wrote). Eventually, Tucker's family would file a civil lawsuit for wrongful death, which went to trial in 1972. Representing them was attorney L. Douglas Wilder, who later became the first elected Black governor in the U.S.

According to Wilder, Lower "willfully, wrongfully, wantonly and intentionally pronounced Bruce O. Tucker dead ahead of his actual death, in violation of the law, well knowing that he was not legally qualified to do so." State law required family notification and waiting for 24 hours before performing surgery.

"They skirted the process that was in place in Virginia because they were so eager to finally do the operation," Jones said.

The famous case of Henrietta Lacks presents a similar collision between medical ethics and racism. Lacks, a Black woman (also from Virginia), was diagnosed in 1951 with cervical cancer. A doctor collected cells from one of her tumors and then reproduced them indefinitely in the lab; after Lacks' death, those cells were then distributed widely among scientists for years without her family's knowledge or permission. Known as the HeLa cell line, they were used in research that led to cancer treatments and to the discovery of the polio vaccine, but decades passed before Lacks' family learned of her medical "immortality."

In 2013, the National Institutes of Health (NIH) reached an agreement with the family for permitting future research involving data from HeLa cells; the new process requires application through a panel that includes descendants and relatives of Lacks, Live Science previously reported.

The injustices experienced by Lacks, Tucker and their families stemmed from racism that is deeply embedded in America's medical infrastructure, Jones noted. In fact, when medical colleges in America adopted a more hands-on approach to anatomical studies during the 19th century, instructors frequently trained their students in human anatomy using cadavers of Black people that were stolen from African American cemeteries, Jones wrote.

Grave robbing was technically illegal, but when Black people were the victims, authorities tended to look the other way, according to Jones. Medical schools would hire a "body man" (also known as a "resurrectionist") to procure bodies; at MCV, the designated grave robber was a Black man named Chris Baker, a janitor at the school who lived in the basement of the college's Egyptian Building.

Most of the country's medical schools abandoned this racist method of procuring cadavers by the mid-1800s, but records suggest that it continued in Virginia until at least 1900, Jones said.

"There were news reports of bodies being 'snatched' from the Virginia state pen, which is about five blocks from the medical college," he said.

Jones unexpectedly discovered a reminder of this crime while researching his book, in a mural displayed in MCV's McGlothlin Medical Education Center. Painted between 1937 and 1947 by Richmond artist George Murrill, the mural celebrates the medical college's history. And it includes the image of a corpse being furtively carried away from a grave in a wheelbarrow.

"It shows how the legacy of racism is literally right under people's noses," Jones said.

"The Organ Thieves" is available to buy on Aug. 18; read an excerpt here .

Originally published on Live Science.

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Landmark transplant in 1960s Virginia performed with heart stolen from a Black man - Live Science

Chemotherapeutic drug resistance is one reason cancer remains an unsolved clinical problem despite the efforts ever since President Nixon declared his "War on Cancer" in 1971. Cancer cells, due in part to the genetic destabilization characteristic of the disease, are capable of expressing genes (normal or aberrant) that permit the cell to avoid the cytotoxic effect of such drugs with the patient providing the situs of selection for and growth of resistant cells. The phenomenon is certain tumor types can have more deleterious consequences than in others, and this is particularly true for glioblastomas (and their non-malignant counterparts, gliomas), cancer of the cells that protect neurons in brain. That organ, confined to the skull, cannot accommodate tumor growth without damaging the brain with which it is confined.

The chemotherapeutic drug of choice for treating glioblastomas is temezolomide (TMZ), an oral alkylating agent that had its chemotherapeutic effect by introducing alkyl groups onto nucleotide bases (preferably at the N-7 and O-6 positions of guanine and N-3 position of adenine) in tumor cell DNA preferentially (due to the greater amount of DNA synthesis occurring in these cells) and disrupting the process leading to cell death (the O-6 methylation having the greatest capacity to induce apoptosis or programmed cell death).O-6-methylguanosnine DNA methyltransferase (MGMT) is the cellular enzyme responsible for repairing alkylated bases in DNA and reduced expression of this gene (e.g., by hypermethylation of the MGMT promoter) is a biomarker for TMZ sensitivity in gliomas and glioblastomas. Recently, a multinational team of researchers* reported genetic rearrangements associated with TMZ resistance, in a paper entitled "MGMT genomic rearrangements contribute to chemotherapy resistance in gliomas" published in Nature Communications. This paper shows a subset of gliomas with rearrangements in the MGMT gene that produce overexpression of the gene and resistance as a result. These authors screened 252 TMZ-treated recurrent gliomas by RNA sequencing and found eight different MGMT genetic fusions (designated BTRC-MGMT,CAPZB-MGMT,GLRX3-MGMT,NFYC-MGMT,RPH3A-MGMT, andSAR1A-MGMTin high-grade gliomas, HGG, andCTBP2-MGMTandFAM175B-MGMT in low-grade gliomas, LGG, in the paper) in seven patients (6 females) with recurrent disease, created by chromosomal rearrangement (see Figure 1c from paper; shown below). These individuals' tumors showed "significantly higher" expression of the rearranged MGMT gene product.

Upon further study, the authors report that five of the eight rearranged genes were located on Chromosome 10 in the vicinity of the MGMT gene itself. The breakpoint in the MGMT was uniformly found at the boundary of exon 2 of the MGMT gene, at a point 12 basepairs upstream of the ATG translation "start" codon. In three of the rearrangements, the breakpoint in the partner gene in the genetic fusion was found in the 5' untranslated region (UTR). All fusions were found to be in-frame (i.e., the reading frame of the MGMT transcript was not disrupted) and the functional regions of the MGMT protein (the methyltransferase domain and DNA-binding domain) were intact. A more fine-structure mapping experiment in the genetic rearrangement resulting in FAM175B-MGMTfound that the fusion was the consequence of a deletion of 4.8 Mb.

The effect of these rearrangements on MGMT expression was elucidated using CRIPSR-Cas9 to produce the BTRC-MGMT, NFYC-MGMT, SAR1A-MGMT, and CTBP2-MGMT rearrangements in cells of two glioblastoma cell lines, U251 and U87. When these cells and their untreated counterparts were challenged by growth in vitro with TMZ, only cells bearing the rearrangements (as confirmed by PCR analysis) were shown to be TMZ resistant. Unlike genetic rearrangements in other cancers that produce fusion proteins (such as the abl-bcr gene produced in chronic myelogenous leukemia bearing the diagnostic Philadelphia chromosome), because most of the rearrangements found involving the MGMT gene were located upstream of the initiation codon of the MGMT gene these authors reasoned that these rearrangements produce increased expression of MGMT leading to TMZ resistance because the cells were better able to repair the methylation injury and replicate functionally. This hypothesis was supported by real-time quantitative PCR analysis of MGMT transcripts in cells bearing the rearrangements, that showed a "striking" increase in expression of MGMT-encoding transcripts (an observation also found in tumors from patients whose gliomas or glioblastomas showed these rearrangements), and Western blot analysis confirmed higher expression levels of the MGMT protein. In two of the rearrangements (BTRC-MGMT and NFYC-MGMT), higher molecular weight fusion proteins were detected as predicted from the genetic data. These results were also replicated in patient tumor-derived stem cells for the BTRC-MGMTandSAR1A-MGMT rearrangements.

These results, and the researchers' conclusion that these rearrangements caused TMZ resistance by overexpression of MGMT, were confirmed by re-establishing TMZ sensitivity in these cells in the presence of O6-benzylguanine (O6-BG), an MGMT inhibitor. These results were further confirmed by detection of double-strand breaks in DNA in these cells in the presence of TMZ and O6-BG.

The relevance of these results to TMZ resistance in vivo was demonstrated using nude mouse xenograft models bearing tumors produced using BTRC-MGMT U251 cells and U251 cells without the rearrangement as control; these cells also contained a recombinant luciferase gene. Mice containing the rearrangement showed no significant prolongation of lifespan in the presence or absence of TMZ, indicating tumor cell resistance, whereas TMZ treatment of nave U251 cells showed improved survival.

While hypomethylation of the native MGMT promoter is the most frequently change associated with TMZ resistance, the results presented in this paper illustrate an alternative mechanism for glioblastomas and gliomas to acquire resistance to TMZ, the only current chemotherapeutic drugs for these maladies. Because these rearrangements were found in patients with recurrent tumors, these authors hypothesize that the rearrangements were selected or by TMZ treatment. A similar rearrangement has also been found in another cancer, medulloblastoma, after TMZ relapse. These authors also suggest that detection of these rearrangements can be used clinically to determine appropriate treatment modalities, particularly for recurrent disease.

* Seve Ballesteros Foundation Brain Tumor Group, Molecular Oncology Programme, Spanish National Cancer Research Center; Division of Life Science, Department of Chemical and Biological Engineering, Center of Systems Biology and Human Health and State Key Laboratory of Molecular Neuroscience, The Hong Kong University of Science and Technology; Beijing Neurosurgical Institute, Capital Medical University; Department of Neurosurgery, Samsung Medical Center, Sungkyunkwan University School of Medicine; Department of Systems Biology, Columbia University; The Jackson Laboratory for Genomic Medicine; and Molecular Cytogenetics Group, Human Cancer Genetics Program, Spanish National Cancer Research Center, CNIO, 28029, Madrid, Spain

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Chromosomal Rearrangements Associated with Chemotherapeutic Drug Resistance | McDonnell Boehnen Hulbert & Berghoff LLP - JD Supra

How worried should we be that the President of the United States recently described as very impressive a woman who claims that doctors make medicine using DNA from aliens? Or that he shows no sign of recognizing the magnitude of the COVID-19 pandemic? Its simply not possible to worry too much.

I thought her voice was an important voice, Donald Trump said, after a reporter asked him why he would retweet the claims of Stella Immanuel, a Houston pediatrician with a long history of bizarre statements about medicine and human sexuality. Immanuel also shares Trumps unfounded enthusiasm for hydroxychloroquine. The drug has been repeatedly discredited as a treatment for this disease. She insists that it is a cure. Its tempting to write off this episode purely as evidence of Trumps disrespect for science. But the problem it represents is much bigger; it is the clearest sign yet that political interests and personal whims have eclipsed the rigor of some of our most important scientific institutions.

Twenty years ago, reporting from South Africa, I saw firsthand what happens when a national leader forces his people to subsist on lies and magic. From 2000 to 2005, according to a definitive study by researchers at the Harvard School of Public Health, Thabo Mbeki, then the President of South Africa, let as many as three hundred and thirty thousand of his fellow-citizens die and thirty-five thousand babies be born with H.I.V., by refusing to permit the countrys health service to treat AIDS with antiretroviral drugs. Mbeki and his health minister, Manto Tshabalala-Msimang, insisted that antiviral medicine was the product of a plot by Western pharmaceutical companies to kill Africans. The Harvard study concluded that the drugs were withheld largely because of Mbekis well-known refusal to initially accept that AIDS is caused by a virus, H.I.V.

No single national leader would have been able to prevent the coronavirus pandemic. But Trumps denialism and hostility toward public-health officials has greatly increased Americas share of suffering and death. On Fox & Friends, on Wednesday, he said that the virus is spreading in a relatively small portion of the country, and that children are virtually immune; both statements are false. And, as he has done many times before, he declared at a briefing that the pandemic would just go away.

Trump has had one consistent response to the pandemic: he attacks leading experts when they attempt to tell the truth. Last week, when Deborah Birx, the cordinator of the White House coronavirus task force, characterized the epidemic as extraordinarily widespread, Trump tweeted that she was pathetic. Earlier this year, when Anthony Fauci, the nations leading infectious-disease expert, was asked at a briefing to discuss his view on hydroxychloroquine, Trump prevented him from answering. The Presidents refusal either to lead or to recognize the leadership of others has made it impossible to develop a national plan to combat this virus.

Without such a plan, the nation has been subjected to a giant game of viral roulette. With no coherent system of rapid tests, contact tracing is all but useless. Since we have neither a vaccine nor any general therapy, tests and tracing offer the only near-term hope of controlling the pandemic. States have largely been left to fend for themselves. Last week, seven governors, Republicans and Democrats, formed their own testing coalition.

On Wednesday, Fauci was asked if the United States had the worlds worst COVID-19 outbreak. It is quantitatively, if you look at it, he said. I mean, the numbers dont lie. Trump is asked similar questions nearly every day. And, although the numbers may not lie, the President does. As he put it in a recent tweet, You will never hear this on the Fake News concerning the China Virus, but by comparison to most other countries, who are suffering greatly, we are doing very well. No amount of statistical massaging could make that statement true.

This war on reality has deeply wounded Americas public-health system. In March, under relentless pressure from Trump and his trade adviser, Peter Navarro (who has no medical training), the Food and Drug Administration issued an emergency-use authorization (E.U.A.) for hydroxychloroquine. That allowed doctors to administer the drug to patients who were severely ill, but it was not an approval of the drug for general use. As Janet Woodcock, who runs the F.D.A.s Center for Drug Evaluation and Research, put it in an interview with Stat, We simply said its possible from the in vitro data this may have a beneficial effect and the benefits may outweigh the risks. Few people understood that distinction, and, goaded on by the President, few listened to those who urged caution.

Trump announced on national television that hydroxychloroquine could be a game changer. It wasnt. Former F.D.A. officials were astonished by the rushed action. I understand the desire to find hope, but we need more evidence than is currently available before we encourage widespread use, Margaret A. Hamburg said at the time. She served as the F.D.A. commissioner for six years under Barack Obama.

In June, when the drugs ineffectiveness had become apparent, the F.D.A. revoked the E.U.A. It was a remarkable retreat. While it is reassuring that the agency finally made a decision based on data, the drug should not have been released for this use in the first place. But, when politics takes precedence, facts no longer matter. Rick A. Bright, one of the nations experts on pandemic preparedness and the chief of BARDA (the Biomedical Advanced Research and Development Authority), had objected to the use of the drug and tried to stop it. He was fired. As the Times reported on Monday, Stephen Hahn, the current F.D.A. commissioner, is not allowed to speak to the press unless Michael Caputo, an assistant secretary of the Department of Health and Human Services, or another official, is also on the line. Caputo has long been associated with Trump, once serving as his driver.

We have recently witnessed an even more pernicious example of an American scientific colossus bowing to Trumps ignorance. In May, the Centers for Disease Control and Prevention issued stringent guidelines to determine when and if schools should reopen this fall. Trump has insisted, against all scientific advice, that all schools should open. He tweeted, I disagree with the @CDCgov on their very tough & expensive guidelines for opening schools. While they want them open, they are asking schools to do very impractical things. I will be meeting with them!!!

Robert Redfield, the director of the C.D.C., immediately issued an update to the guidelines, announcing that it is critically important for our public health to open schools this fall. The reversal was stunning; past C.D.C. directors were not immune to politics, and they understood that a President might overrule them. But there has always been an understanding at the agency that all public-health decisions made there would have to be governed by data.

No agency or scientist is infallible. Early in the pandemic, the C.D.C. failed to introduce accurate test kits; many of the kits it distributed were contaminated and useless. The agency used highly sensitive tests based on PCR technology, which is a kind of molecular copying machine that makes millions (or billions) of copies of a DNA sample. That makes it much easier for clinicians to detect any specific sequence of DNA, including those in the coronavirus. The technology has been used routinely for more than three decades, but it is sensitive to small errors, and there were several in the C.D.C. kits. The misstep delayed accurate data collection throughout the United States at one of the most critical moments in the pandemic.

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Trumps Unprecedented Attacks on Our Public-Health System - The New Yorker

While humans are all too familiar with the ravages of getting older, many trees seem to handle ageing a lot better.

Certain trees can live for thousands of years and appear to be immortal.

But not everyone is convinced these old timers can escape death due to old age.

Regardless, could humans with their relatively puny lifespans have something to learn from these ancient trees? Some scientists think so.

Establishing how old the oldest living tree is depends a bit on which plants are in the running for the title.

You could argue that Australia's Wollemi pine, which has been cloning itself for more than 60 million years, deserves the title. But that's kind of cheating because this involves multiple stems growing from the one rootstock.

This is why the oldest tree in the world is generally regarded as a single-stemmed bristlecone pine called Pinus longaeva.

This species can live to around 5,000 years and does well where most other plants cannot even grow in rocky, dry, high-altitude areas in the United States.

What's amazing is that scientists have not so far been able to show that getting older directly affects the health of such millennial trees, plant biologist Sergi Munne-Bosch from the University of Barcelona says.

It's because of this, some have suggested these trees are essentially immortal.

But in a recent article, Professor Munne-Bosch argues that it's likely even ancient trees could die from old age assuming something else doesn't kill them first.

He emphasises that there's a difference between ageing, which is about how long an organism has lived, and age-related deterioration, which is referred to as senescence.

"Just because we can't track senescence in long-lived trees doesn't mean they are immortal."

Professor Munne-Bosch points to recent research on centuries-old Ginkgo biloba trees that found no evidence of senescence.

The study was the first to look for evidence of age-related changes in cells of the cambium, a layer just beneath the bark that contains cells that can produce new tissue throughout the plant's life.

It confirmed the long-lived trees, which in this case were up to 667 years old, were just as healthy as younger ones says Professor Munne-Bosch.

"They grow very well, they produce seeds, they produce flowers, so they are healthy."

He points out that even though a 667-year-old tree seems old when compared to a human, it is relatively young for a ginkgo.

"This species can live for more than two millennia."

Professor Munne-Bosch argues that the ginkgo researchers' data shows that older trees had thinner vascular tissue and that this hints at possible age-related deterioration that would be more obvious in even older trees.

Yet despite this deterioration, he says these trees are more likely to die from insects, disease, fire, drought or loggers, than old age.

"For a species that can live for millennia, aging is not really a problem in evolutionary terms because they are much more likely to die of something else."

The problem is there are so few of these long-lived trees that it's hard to get the data to know for certain whether they can die of old age.

"We cannot prove it either way," Professor Munne-Bosch says, adding that age-related deterioration is likely to happen in these trees at such a different pace compared to in humans.

"For a Ginkgo biloba, six centuries is not as physiologically relevant as it is to us."

Brenda Casper, a professor of biology at the University of Pennsylvania says it's not clear that the changes found in the older Ginkgo biloba trees were necessarily detrimental to the tree.

But she agrees the low number of millennial trees makes it hard to study their longevity.

"It's difficult to find statistical evidence for senescence."

Even if there were enough trees, she says some of the age-related deterioration may be hard to detect, or we may not know what to look for.

"It's not just internal physiology per se but it's the interaction of the tree with its environment."

For example, she says it would be hard to measure whether age had made a tree more susceptible to disease, or less structurally sound so it's more likely to fall over in a windstorm.

Even if the jury is out on whether millennial trees are immortal, some experts say their longevity could be inspirational for medical research.

Professor Munne-Bosch says such trees can draw on a bag of tricks to help them "postpone death".

First is having a simple body plan with modular-like branches and roots. This means they can compartmentalise any damaged or dead roots or branches and work around them.

"They can lose part of leaves or roots and continue to be healthy..

And he says although 95 per cent of the trunk of a tree might be dead, the living cambium just beneath the bark is "one of the secrets of longevity" in trees.

Millennial trees have used the combination of these features to their best advantage and Professor Munne-Bosch says these tricks are providing a model for scientists researching the negative effects of ageing.

"Imagine if we could regenerate our lungs or circulatory system every year, we would be much healthier than we are."

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Professor of biomedical engineering at the University of New South Wales, Melissa Knothe Tate is one researcher who is inspired by millennial trees.

"They have units and if one unit breaks you can replace it with another unit."

Only a small percentage of an individual long-lived tree may be alive, but she argues it's all about survival of the cells that are able to regenerate the tree.

"Those that survive best, survive longest."

"Millennial trees are the best survivors because they've seen a lot."

While a tree and a human might seem worlds apart, Professor Knothe Tate sees the similarities, pointing to the role of stem cells in maintaining bones in humans.

She says cells add new layers to bone, like tree rings, to increase girth and when bone is injured, stem cells quickly help repair it.

"We're constantly renewing our bones and trees do something similar."

Professor Knothe Tate says she is using stem cells and new biomaterials that emulate tree cambium, to create replacement tissue in the lab, and has several patents for the work.

"I think about plants a lot when I'm up in the mountains and amongst the trees."

Professor Knothe Tate, who draws on her training in philosophy, biology and mechanical engineering for her work, sees other similarities that can inspire research.

For example, she likens the human brain to the network of roots and branches that helps a tree remain resilient if one part is damaged, another part can sometimes take up the slack.

"As parts of the brain are injured or die, it's remarkable what functionality we can retain,

"If we knew which of the brain's networks were essential for certain functions, we may be able to grow them."

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Professor Knothe Tate also set up a science education project for girls that explores the parallels between the biomechanics of trees and bones. It was inspired by her observation of how huge trees sway like a blade of grass in the wind.

She has high hopes for the potential of regenerative medicine research that draws on knowledge from other disciplines like plant biology to extend human life.

"We can then start to think about making ourselves immortal."

Plant biologist Professor Munne-Bosch is also enthusiastic.

"The future of medicine is very similar to what has evolved in millennial trees."

But while regenerating tissues will help humans live much longer, he doubts we will ever be immortal.

"It won't be forever, because we are more likely to die of something else, whether it be an accident or a pandemic."

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Are very long-lived trees immortal and what can they teach humans? - ABC News

It is a widely known fact that cancer is one of the major diseases causing death throughout both the developed and developing world, including South Africa.

Approximately 115 000 South Africans are diagnosed with cancer each year, and with a 6/10 survival rate it is easy to understand how news of such a diagnosis can fuel fear and anxiety for individuals and their families.

Against this background, one can easily understand why the need for hope from various sources becomes the lifeline for families dealing with cancer.When one thinks of the words hope, determination and inspiration, Richard Wright, when you meet him, embodies the meaning of these three words.

Having survived brain cancer three times, Richard has first-hand experience of how important holding on to hope fuelled his ability to stay emotionally strong when the disease weakened his body.

I didnt think Id see the age of 50, and am acutely aware of the gift ones age represents, said Richard.

As a result of his journey, Richard became acquainted with The Sunflower Fund and has become an inspiration to the staff as well as supporters of the cause at events in the past.

As part of my 50th birthday celebration, I am encouraging the public to take part in my #LoveYourAgeChallenge, in hopes of raising funds for The Sunflower Fund to assist patients who suffer from life-threatening blood disorders, continued Richard.

Join Richard in celebrating his age by celebrating your age. The challenge encourages individuals to create an activity of their choice, whether it is a 50-minute hike, baking 50 cakes or 50 minutes of meditation, making it relative to your age. Post your event selfie or video using the hashtag #LoveYourAgeChallenge and you could win great prizes.

Richard encouraged participants to spread the love by donating any amount to The Sunflower Fund to give hope. Any amount, no matter how big or small to reflect your age R5, R50 or R50 000.

The Sunflower Fund is a stem cell donor recruitment centre and registry that fights blood diseases by helping patients in need of a transplant find their life-saving matching donor. When a patient needs a transplant, the donor needs to be a DNA or genetic match, which is not as simple as matching a blood type. Patients have a 25 per cent chance of this match existing within the family. The remaining 75 per cent chance is based on finding a match from a database of strangers who have signed up to save a life should they match a patient.

An added factor is that the likelihood of this match most often exists within the same ethnic and cultural mix as the patient. As such, The Sunflower Fund is committed to building an ethnically diverse registry of donors, to give patients the best hope of a cure.

Our ambassador of hope programme is one of the key ways we work with people from various walks of life to help us raise awareness about the urgent need for blood stem cell donors, said Alana James, CEO of The Sunflower Fund. This awareness is vital to increasing the number of registered donors and we are pleased to have Richard on board as an Ambassador of Hope.

Richard is a husband, father, motivational speaker and advocate for determination and strength. He is a storyteller, skilled at using his experiences to inspire and transform the thinking of his audiences.

I also want to encourage individuals to be the hope by becoming stem cell donors. People have the power to change their mindset from just cancer awareness to being a part of the solution. As I always say mindset matters, added Richard.

Individuals between the ages of 18 and 55 can register as donors. If you have a consistent body weight of more than 50kgs and a BMI of less than 40, you could be eligible to be a donor.

For additional information on The Sunflower Fund, or to become a donor, visit https://www.sunflowerfund.org/

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#LoveYourAgeChallenge: Join cancer Ambassador of Hope in this fund-raiser - Brakpan Herald

- NCCN Guideline Updates Highlight Need for Maximum CIN Prevention and Resource Allocation for COVID-19 Patients -

- First Patient Dosed in the U.S. Avoided Grade 4 Neutropenia in Cycle 2 with Plinabulin and Pegfilgrastim, Despite Experiencing Grade 4 Neutropenia in Cycle 1 with Pegfilgrastim Alone -

NEW YORK, Aug. 11, 2020 (GLOBE NEWSWIRE) -- BeyondSpring Inc.(the Company or BeyondSpring) (NASDAQ: BYSI), a global biopharmaceutical company focused on the development of innovative immuno-oncology cancer therapies, today announced that the Company has initiated an Expanded Access Program (EAP) to enable doctors across the U.S. to use BeyondSprings late-stage asset, Plinabulin, to prevent cancer patients chemotherapy-induced neutropenia (CIN), both alone and in combination with G-CSFs (the current standard of care), during the COVID-19 pandemic. Dr. Emad Ibrahim enrolled the first patient at Redlands Community Hospital in California on July 28, 2020.

In response to COVID-19, the National Comprehensive Cancer Network (NCCN) recently updated its treatment guidelines for the prophylaxis of CIN, with the objective of preserving hospital and ER resources for COVID-19 patients and maximizing protection for cancer patients against CIN development. This is designed to help necessitate healthcare interactions, and avoidance of hospital / ER visits will also minimize cancer patients risk of contracting COVID-19. In light of these NCCN guideline updates, BeyondSpring initiated an Expanded Access Program to enable the use of Plinabulin by oncologists to better protect cancer patients against CIN with the use of myelosuppressive chemotherapies under the current COVID-19 challenges.

Dr. Emad Ibrahim enrolled the first patient under this EAP at Redlands Community Hospital in California:

The recent updates to the NCCN guidelines aim to protect cancer patients from developing CIN in the most effective way possible and enable the healthcare system to reserve precious resources for COVID-19 patients, said Ramon Mohanlal, BeyondSprings Chief Medical Officer and Executive Vice President, Research and Development. In our CIN studies, Plinabulin, in combination with Pegfilgrastim, provided superior protection against CIN, compared to the standard of care alone. The observation in this first EAP patient who completely avoided Grade 4 CIN when given Plinabulin and Pegfilgrastim is a significant achievement for us. At BeyondSpring, we strive to play our part in serving patients and healthcare providers to the highest degree while working through the many challenges imposed by COVID-19.

Preventing CIN during chemotherapy is extremely important, as this will enable cancer patients to receive the full regimen of chemotherapy and achieve treatment goals. The onset of CIN is the No. 1 reason for treatment modifications, such as downgrading the strength of chemotherapy or stopping chemotherapy altogether. When a patient develops CIN, the treating physician is required to delay the next round of chemotherapy until a patients white blood cell count recovers. These changes can have a profoundly negative impact on patient outcomes.

For more information on BeyondSprings Plinabulin Expanded Access Program, please visit http://www.beyondspringpharma.com/EAP/. Supplies may be limited.

If you are a physician in the U.S. who would like to request Plinabulin EAP access for your patient, please email expandedaccess@beyondspringpharma.com.

About BeyondSpringHeadquartered in New York, BeyondSpring is a global, clinical-stage biopharmaceutical company focused on developing innovative immuno-oncology cancer therapies to improve clinical outcomes for patients with high unmet medical needs. BeyondSprings first-in-class lead immune asset, Plinabulin, is a potent antigen-presenting cell (APC) inducer. It is currently in two Phase 3 clinical trials for two severely unmet medical needs indications: one is for the prevention of chemotherapy-induced neutropenia (CIN), the most frequent cause for a chemotherapy regimen doses decrease, delay, downgrade or discontinuation, which can lead to suboptimal clinical outcomes. The other is for non-small cell lung cancer (NSCLC) treatment in EGFR wild-type patients. As a pipeline drug, Plinabulin is in various I/O combination studies to boost PD-1 / PD-L1 antibody anti-cancer effects. In addition to Plinabulin, BeyondSprings extensive pipeline includes three pre-clinical immuno-oncology assets and a drug discovery platform dubbed molecular glue that uses the protein degradation pathway.

About PlinabulinPlinabulin, BeyondSprings lead asset, is a differentiated immune and stem cell modulator. Plinabulin is currently in late-stage clinical development to increase overall survival in cancer patients, as well as to alleviate chemotherapy-induced neutropenia (CIN). The durable anticancer benefits of Plinabulin have been associated with its effect as a potent antigen-presenting cell (APC) inducer (through dendritic cell maturation) and T-cell activation (Chem andCell Reports, 2019). Plinabulins CIN data highlights the ability to boost the number of hematopoietic stem / progenitor cells (HSPCs), or lineage-/cKit+/Sca1+ (LSK) cells in mice. Effects on HSPCs could explain the ability of Plinabulin to not only treat CIN but also to reduce chemotherapy-induced thrombocytopenia and increase circulating CD34+ cells in patients.

Cautionary Note Regarding Forward-Looking StatementsThis press release includes forward-looking statements that are not historical facts. Words such as "will," "expect," "anticipate," "plan," "believe," "design," "may," "future," "estimate," "predict," "objective," "goal," or variations thereof and variations of such words and similar expressions are intended to identify such forward-looking statements. Forward-looking statements are based on BeyondSpring's current knowledge and its present beliefs and expectations regarding possible future events and are subject to risks, uncertainties and assumptions. Actual results and the timing of events could differ materially from those anticipated in these forward-looking statements as a result of several factors including, but not limited to, difficulties raising the anticipated amount needed to finance the Company's future operations on terms acceptable to the Company, if at all, unexpected results of clinical trials, delays or denial in regulatory approval process, results that do not meet our expectations regarding the potential safety, the ultimate efficacy or clinical utility of our product candidates, increased competition in the market, and other risks described in BeyondSprings most recent Form 20-F on file with the U.S. Securities and Exchange Commission. All forward-looking statements made herein speak only as of the date of this release and BeyondSpring undertakes no obligation to update publicly such forward-looking statements to reflect subsequent events or circumstances, except as otherwise required by law.

Media ContactsCaitlin Kasunich / Raquel ConaKCSA Strategic Communications212.896.1241 / 212.896.1276ckasunich@kcsa.com / rcona@kcsa.com

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BeyondSpring Initiates Expanded Access Program with Plinabulin for Patients Suffering from CIN in the US - BioSpace

Overview

We are a clinical stage biopharmaceutical company focused on the discovery,development and commercialization of drugs for the treatment of cancer. We aredeveloping proprietary drugs independently and through research and developmentcollaborations. Our core objective is to leverage our proprietary phospholipiddrug conjugate (PDC) delivery platform to develop PDCs that are designed tospecifically target cancer cells and deliver improved efficacy and better safetyas a result of fewer off-target effects. Our PDC platform possesses thepotential for the discovery and development of the next generation ofcancer-targeting treatments, and we plan to develop PDCs both independently andthrough research and development collaborations. The COVID-19 pandemic hascreated uncertainties in the expected timelines for clinical stagebiopharmaceutical companies such as us, and because of such uncertainties, it isdifficult for us to accurately predict expected outcomes at this time. We havenot yet experienced any significant impacts as a result of the pandemic and havecontinued to enroll patients in our clinical trials. However, COVID-19 mayimpact our future ability to recruit patients for clinical trials, obtainadequate supply of CLR 131 and obtain additional financing.

Our lead PDC therapeutic, CLR 131 is a small-molecule PDC designed to providetargeted delivery of iodine-131 directly to cancer cells, while limitingexposure to healthy cells. We believe this profile differentiates CLR 131 frommany traditional on-market treatment options. CLR 131 is the company's leadproduct candidate and is currently being evaluated in a Phase 2 study inrelapsed/refractory (r/r) B-cell malignancies, including multiple myeloma (MM),chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL),lymphoplasmacytic lymphoma/Waldenstrom's macroglobulinemia (LPL/WM), marginalzone lymphoma (MZL), mantle cell lymphoma (MCL), and diffuse large B-celllymphoma (DLBCL).CLR 131 is also being evaluated in a Phase 1 dose escalationstudy in pediatric solid tumors and lymphoma. The U.S. Food and DrugAdministration ("FDA") granted CLR 131 Fast Track Designation for both r/r MMand r/r DLBCL and Orphan Drug Designation (ODD) of MM, LPL/WM, neuroblastoma,rhabdomyosarcoma, Ewing's sarcoma and osteosarcoma. CLR 131 was also grantedRare Pediatric Disease Designation (RPDD) for the treatment of neuroblastoma,rhabdomyosarcoma, Ewing's sarcoma and osteosarcoma. Most recently, the EuropeanCommission granted an ODD for r/r MM.

Our product pipeline also includes one preclinical PDC chemotherapeutic program(CLR 1900) and several partnered PDC assets. The CLR 1900 Series is beingtargeted for solid tumors with a payload that inhibits mitosis (cell division) avalidated pathway for treating cancers.

We have leveraged our PDC platform to establish four collaborations featuringfive unique payloads and mechanisms of action. Through research and developmentcollaborations, our strategy is to generate near-term capital, supplementinternal resources, gain access to novel molecules or payloads, accelerateproduct candidate development and broaden our proprietary and partnered productpipelines.

Our PDC platform provides selective delivery of a diverse range of oncologicpayloads to cancerous cells, whether a hematologic cancer or solid tumor, aprimary tumor, or a metastatic tumor and cancer stem cells. The PDC platform'smechanism of entry does not rely upon specific cell surface epitopes or antigensas are required by other targeted delivery platforms. Our PDC platform takesadvantage of a metabolic pathway utilized by all tumor cell types in all stagesof the tumor cycle. Tumor cells modify specific regions on the cell surface as aresult of the utilization of this metabolic pathway. Our PDCs bind to theseregions and directly enter the intracellular compartment. This mechanism allowsthe PDC molecules to accumulate over time, which enhances drug efficacy, and toavoid the specialized highly acidic cellular compartment known as lysosomes,which allows a PDC to deliver molecules that previously could not be delivered.Additionally, molecules targeting specific cell surface epitopes face challengesin completely eliminating a tumor because the targeted antigens are limited inthe total number on the cell surface, have longer cycling time frominternalization to being present on the cell surface again and available forbinding and are not present on all of the tumor cells in any cancer. This meansa subpopulation of tumor cells always exist that cannot be targeted by therapiestargeting specific surface epitopes. In addition to the benefits provided by themechanism of entry, PDCs offer the ability to conjugate payload molecules innumerous ways, thereby increasing the types of molecules selectively deliveredvia the PDC.

The PDC platform features include the capacity to link with almost any molecule,provide a significant increase in targeted oncologic payload delivery and theability to target all types of tumor cells. As a result, we believe that we cangenerate PDCs to treat a broad range of cancers with the potential to improvethe therapeutic index of oncologic drug payloads, enhance or maintain efficacywhile also reducing adverse events by minimizing drug delivery to healthy cells,and increasing delivery to cancerous cells and cancer stem cells.

We employ a drug discovery and development approach that allows us toefficiently design, research and advance drug candidates. Our iterative processallows us to rapidly and systematically produce multiple generations ofincrementally improved targeted drug candidates.

In June 2020, the European Medicines Agency (EMA) granted us Small andMedium-Sized Enterprise status by the EMA's Micro, Small and Medium-sizedEnterprise office. SME status allows us to participate in significant financialincentives that include a 90% to 100% EMA fee reduction for scientific advice,clinical study protocol design, endpoints and statistical considerations,quality inspections of facilities and fee waivers for selective EMA pre andpost-authorization regulatory filings, including orphan drug and PRIMEdesignations. We are also eligible to obtain EMA certification of quality andmanufacturing data prior to review of clinical data. Other financial incentivesinclude EMA-provided translational services of all regulatory documents requiredfor market authorization, further reducing the financial burden of the marketauthorization process.

A description of our PDC product candidates follows:

Our lead PDC therapeutic, CLR 131 is a small-molecule, PDC designed to providetargeted delivery of iodine-131 directly to cancer cells, while limitingexposure to healthy cells. We believe this profile differentiates CLR 131 frommany traditional on-market treatments and treatments in development. CLR 131 iscurrently being evaluated in a Phase 2 study in r/r B-cell lymphomas, and twoPhase 1 dose-escalating clinical studies, one in r/r MM and one in r/r pediatricsolid tumors and lymphoma. The initial Investigational New Drug (IND)application was accepted by the FDA in March 2014 with multiple INDs submittedsince that time. Initiated in March 2017, the primary goal of the Phase 2 studyis to assess the compound's efficacy in a broad range of hematologic cancers.The Phase 1 study is designed to assess the compound's safety and tolerabilityin patients with r/r MM (to determine maximum tolerated dose) and was initiatedin April 2015. The FDA previously accepted our IND application for a Phase 1open-label, dose escalating study to evaluate the safety and tolerability of asingle intravenous administration of CLR 131 in up to 30 children andadolescents with cancers including neuroblastoma, sarcomas, lymphomas (includingHodgkin's lymphoma) and malignant brain tumors. This study was initiated duringthe first quarter of 2019. These cancer types were selected for clinical,regulatory and commercial rationales, including the radiosensitive nature andcontinued unmet medical need in the r/r setting, and the rare diseasedeterminations made by the FDA based upon the current definition within theOrphan Drug Act.

In December 2014, the FDA granted ODD for CLR 131 for the treatment of MM.Multiple myeloma is an incurable cancer of the plasma cells and is the secondmost common form of hematologic cancers. In 2018, the FDA granted ODD and RPDDfor CLR 131 for the treatment of neuroblastoma, rhabdomyosarcoma, Ewing'ssarcoma and osteosarcoma. The FDA may award priority review vouchers to sponsorsof rare pediatric disease products that meet its specified criteria. The keycriteria to receiving a priority review voucher is that the disease beingtreated is life-threatening and that it primarily effects individuals under theage of 18. Under this program, a sponsor who receives an approval for a drug orbiologic for a rare pediatric disease can receive a priority review voucher thatcan be redeemed to receive a priority review of a subsequent marketingapplication for a different product. Additionally, these priority reviewvouchers can be exchanged or sold to other companies for them to use thevoucher. In May 2019, the FDA granted Fast Track designation for CLR 131 for thetreatment of multiple myeloma in July 2019 for the treatment of DLBCL, inSeptember, CLR 131 received Orphan Drug Designation from the European Union forMultiple Myeloma, and in January 2020, the FDA granted Orphan Drug Designationfor CLR 131 in lymphoplasmacytic lymphoma (LPL).

Phase 2 Study in Patients with r/r select B-cell Malignancies

In February 2020, we announced positive data from our Phase 2 CLOVER-1 study inpatients with relapsed/refractory B-cell lymphomas. Relapsed/Refractory MM andnon-Hodgkin lymphoma (NHL) patients were treated with three different doses(<50mCi, ~50mCi and ~75mCi total body dose (TBD). The <50mCi total body dose wasa deliberately planned sub-therapeutic dose. CLR 131 achieved the primaryendpoint for the study. Patients with r/r MM who received the highest dose ofCLR 131 showed a 42.8% overall response rate (ORR). Those who received ~50mCiTBD had a 26.3% ORR with a combined rate of 34.5% ORR (n=33) while maintaining awell-tolerated safety profile. Patients in the studies were elderly with amedian age of 70, and heavily pre-treated, with a median of five prior lines oftreatment (range: 3 to 17), which included immunomodulatory drugs, proteasomeinhibitors and CD38 antibodies for the majority of patients. Additionally, amajority of the patients (53%) were quad refractory or greater and 44% of alltreated multiple myeloma patients were triple class refractory. 100% of allevaluable patients (n=43) achieved clinical benefit (primary outcome measure) asdefined by having stable disease or better. 85.7% of multiple myeloma patientsreceiving the higher total body dose levels of CLR 131 experienced tumorreduction. The 75mCi TBD demonstrated positive activity in both high-riskpatients and triple class refractory patients with a 50% and 33% ORR,respectively.

Patients with r/r NHL who received ~50mCi TBD and the ~75mCi TBD had a 42% and43% ORR, respectively and a combined rate of 42%. These patients were alsoheavily pre-treated, having a median of three prior lines of treatment (range, 1to 9) with the majority of patients being refractory to rituximab and/oribrutinib. The patients had a median age of 70 with a range of 51 to 86. Allpatients had bone marrow involvement with an average of 23%. In addition tothese findings, subtype assessments were completed in the r/r B-cell NHLpatients. Patients with DLBCL demonstrated a 30% ORR with one patient achievinga complete response (CR), which continues at nearly 24 months post-treatment.The ORR for CLL/SLL/MZL patients was 33%. Current data from our Phase 2 CLOVER-1clinical study show that four LPL/WM patients demonstrated 100% ORR with onepatient achieving a CR which continues at nearly 27 months post-treatment. Thismay represent an important improvement in the treatment of relapsed/refractoryLPL/WM as we believe no approved or late-stage development treatments forsecond- and third-line patients have reported a CR. LPL/WM is a rare, indolentand incurable form of NHL that is composed of a patient population in need ofnew and better treatment options.

The most frequently reported adverse events in r/r MM patients were cytopenias,which followed a predictable course and timeline. The frequency of adverseevents have not increased as doses were increased and the profile of cytopeniasremains consistent. Importantly, these cytopenias have had a predictable patternto initiation, nadir and recovery and are treatable. The most common grade ?3events at the highest dose (75mCi TBD) were hematologic toxicities includingthrombocytopenia (65%), neutropenia (41%), leukopenia (30%), anemia (24%) andlymphopenia (35%). No patients experienced cardiotoxicities, neurologicaltoxicities, infusion site reactions, peripheral neuropathy, allergic reactions,cytokine release syndrome, keratopathy, renal toxicities, or changes in liverenzymes. The safety and tolerability profile in patients with r/r NHL wassimilar to r/r MM patients except for fewer cytopenias of any grade. Based uponCLR 131 being well tolerated across all dose groups and the observed responserate, especially in difficult to treat patients such as high risk and tripleclass refractory or penta-refractory, and corroborating data showing thepotential to further improve upon current ORRs and durability of thoseresponses, the study has been expanded to test a two-cycle dosing optimizationregimen of CLR 131.

In July 2016, we were awarded a $2,000,000National Cancer Institute (NCI)Fast-Track Small Business Innovation Research grant to further advance theclinical development of CLR 131. The funds are supporting the Phase 2 studyinitiated in March 2017 to define the clinical benefits of CLR 131 in r/r MM andother niche hematologic malignancies with unmet clinical need. These nichehematologic malignancies include Chronic Lymphocytic Leukemia, Small LymphocyticLymphoma, Marginal Zone Lymphoma, Lymphoplasmacytic Lymphoma and DLBCL. Thestudy is being conducted in approximately 10 U.S. cancer centers in patientswith orphan-designated relapse or refractory hematologic cancers. The study'sprimary endpoint is clinical benefit response (CBR), with additional endpointsof ORR, progression free survival (PFS,) median Overall Survival (mOS) and othermarkers of efficacy following a single 25.0 mCi/m2 dose of CLR 131, with theoption for a second 25.0 mCi/m2dose approximately 75-180 days later. Based onthe performance results from Cohort 5 of our Phase 1 study in patients with r/rMM, reviewed below, we have modified the dosing regimen of this study to afractionated dose of 15.625 mCi/m2 administered on day 1 and day 8.

In May 2020, we announced that the FDA granted Fast Track Designation for CLR131 in LPL/WM in patients having received two prior treatment regimens or more.

Phase 1 Study in Patients with r/r Multiple Myeloma

In February 2020, we announced the successful completion of our Phase 1 doseescalation study. Data from the study demonstrated that CLR 131 was safe andtolerated at total body dose of approximately 90mCi in r/r MM. The Phase 1multicenter, open-label, dose-escalation study was designed to evaluate thesafety and tolerability of CLR 131 administered as a 30-minute I.V. infusion,either as a single bolus dose or as two fractionated doses. The r/r multiplemyeloma patients in this study received single cycle doses ranging fromapproximately 20mCi to 90mCi total body dose. To date, an independent DataMonitoring Committee determined that all doses have been safe and well-toleratedby patients.

CLR 131 in combination with dexamethasone is currently under investigation inadult patients with r/r MM. Patients must have been refractory to or relapsedfrom at least one proteasome inhibitor and at least one immunomodulatory agent.The clinical study is a standard three-plus-three dose escalation safety studyto determine the maximum tolerable dose. Multiple myeloma is an incurable cancerof the plasma cells and is the second most common form of hematologic cancers.Secondary objectives include the evaluation of therapeutic activity by assessingsurrogate efficacy markers, which include M protein, free light chain (FLC), PFSand OS. All patients have been heavily pretreated with an average of five priorlines of therapy. CLR 131 was deemed by an Independent Data Monitoring Committee(IDMC) to be safe and tolerable up to its planned maximum single, bolus dose of31.25 mCi/m2. The four single dose cohorts examined were: 12.5 mCi/m2(~25mCiTBD), 18.75 mCi/m2 (~37.5mCi TBD), 25 mCi/m2(~50mCi TBD), and 31.25mCi/m2(~62.5mCi TBD), all in combination with low dose dexamethasone (40 mgweekly). Of the five patients in the first cohort, four achieved stable diseaseand one patient progressed at Day 15 after administration and was taken off thestudy. Of the five patients admitted to the second cohort, all five achievedstable disease however one patient progressed at Day 41 after administration andwas taken off the study. Four patients were enrolled to the third cohort and allachieved stable disease. In September 2017, we announced results for cohort 4,showing that a single infusion up to 30-minutes of 31.25mCi/m2 of CLR 131 wassafe and tolerated by the three patients in the cohort. Additionally, all threepatients experienced CBR with one patient achieving a partial response (PR). Weuse the International Myeloma Working Group (IMWG) definitions of response,which involve monitoring the surrogate markers of efficacy, M protein and FLC.The IMWG defines a PR as a greater than or equal to 50% decrease in FLC levels(for patients in whom M protein is unmeasurable) or 50% or greater decrease in Mprotein. The patient experiencing a PR had an 82% reduction in FLC. This patientdid not produce M protein, had received seven prior lines of treatment includingradiation, stem cell transplantation and multiple triple combination treatmentsincluding one with daratumumab that was not tolerated. One patient experiencingstable disease attained a 44% reduction in M protein. In January 2019, weannounced that the pooled mOS data from the first four cohorts was 22.0 months.In late 2018, we modified this study to evaluate a fractionated dosing strategyto potentially increase efficacy and decrease adverse events.

Following the determination that all prior dosing cohorts were safe andtolerated, we initiated a cohort 7 utilizing a 40mCi/m2 fractionated doseadministered 20mCi/m2 (~40mCi TBD) on days 1 and day 8. Cohort 7 was the highestpre-planned dose cohort and subjects have completed the evaluation period. Finalstudy report and study close-out will be completed later this year.

In May 2019, we announced that the FDA granted Fast Track Designation for CLR131 in fourth line or later r/r MM. CLR 131 is our small-moleculeradiotherapeutic PDC designed to deliver cytotoxic radiation directly andselectively to cancer cells and cancer stem cells. It is currently beingevaluated in our ongoing CLOVER-1 Phase 2 clinical study in patients withrelapsed or refractory multiple myeloma and other select B-cell lymphomas.

Phase 1 Study in r/r Pediatric Patients with select Solid tumors, Lymphomas andMalignant Brain Tumors

In December 2017 the Division of Oncology at the FDA accepted our IND and studydesign for the Phase 1 study of CLR 131 in children and adolescents with selectrare and orphan designated cancers. This study was initiated during the firstquarter of 2019. In December 2017, we filed an IND application for r/r pediatricpatients with select solid tumors, lymphomas and malignant brain tumors. ThePhase 1 clinical study of CLR 131 is an open-label, sequential-group,dose-escalation study evaluating the safety and tolerability of intravenousadministration of CLR 131 in up to 30 children and adolescents with cancersincluding neuroblastoma, sarcomas, lymphomas (including Hodgkin's lymphoma) andmalignant brain tumors. Secondary objectives of the study are to identify therecommended Phase 2 dose of CLR 131 and to determine preliminary antitumoractivity (treatment response) of CLR 131 in children and adolescents. In 2018,the FDA granted OD and RPDD for CLR 131 for the treatment of neuroblastoma,rhabdomyosarcoma, Ewing's sarcoma and osteosarcoma. Should any of theseindications reach approval, the RPDD would enable us to receive a priorityreview voucher. Priority review vouchers can be used by the sponsor to receivepriority review for a future New Drug Application ("NDA") or Biologic LicenseApplication ("BLA") submission, which would reduce the FDA review time from 12months to six months. Currently, these vouchers can also be transferred or soldto another entity.

Phase 1 Study in r/r Head and Neck Cancer

In August 2016, the University of Wisconsin Carbone Cancer Center ("UWCCC") wasawarded a five-year Specialized Programs of Research Excellence ("SPORE") grantof $12,000,000 from the National Cancer Institute and the National Institute ofDental and Craniofacial Research to improve treatments and outcomes for head andneck cancer, HNC, patients. HNC is the sixth most common cancer across the worldwith approximately 56,000 new patients diagnosed every year in the U.S. As a keycomponent of this grant, the UWCCC researchers completed testing of CLR 131 invarious animal HNC models and initiated the first human clinical trial enrollingup to 30 patients combining CLR 131 and external beam radiation with recurrentHNC in Q4 2019. This clinical trial was suspended due to the COVID-19 pandemicbut has now been reopened for enrolment.

We believe our PDC platform has potential to provide targeted delivery of adiverse range of oncologic payloads, as exemplified by the product candidateslisted below, that may result in improvements upon current standard of care("SOC") for the treatment of a broad range of human cancers:

Research and development expense. Research and development expense consist ofcosts incurred in identifying, developing and testing, and manufacturing productcandidates, which primarily include salaries and related expenses for personnel,cost of manufacturing materials and contract manufacturing fees paid to contractmanufacturers and contract research organizations, fees paid to medicalinstitutions for clinical trials, and costs to secure intellectual property. TheCompany analyzes its research and development expenses based on four categoriesas follows: clinical project costs, preclinical project costs, manufacturing andrelated costs, and general research and development costs that are not allocatedto the functional project costs, including personnel costs, facility costs,related overhead costs and patent costs.

General and administrative expense. General and administrative expense consistsprimarily of salaries and other related costs for personnel in executive,finance and administrative functions. Other costs include insurance, costs forpublic company activities, investor relations, directors' fees and professionalfees for legal and accounting services.

Three Months Ended June 30, 2020 and 2019

Research and Development. Research and development expense for the three monthsended June 30, 2020 was approximately $2,465,000 compared to approximately$1,810,000 for the three months ended June 30, 2019.

The following table is an approximate comparison summary of research anddevelopment costs for the three months ended June 30, 2020 and June 30, 2019:

General research and development costs 1,018,000 384,000 634,000

The overall increase in research and development expense of $655,000, or 36%,was primarily a result of increased general research and development costsresulting from increased personnel related costs and in clinical project costs.Manufacturing and related costs decreased due to a decrease in materialsproduction processes and related costs. Pre-clinical study costs were relativelyconsistent.

General and administrative. General and administrative expense for the threemonths ended June 30, 2020 was approximately $1,157,000, compared toapproximately $1,391,000 in the three months ended June 30, 2019. The decreaseof approximately $234,000, or 17%, was primarily a result of lower stock-basedcompensation expense.

Six Months Ended June 30, 2020 and 2019

Research and Development. Research and development expense for the six monthsended June 30, 2020 was approximately $5,082,000 compared to approximately$4,118,000 for the six months ended June 30, 2019.

The following table is a comparison summary of research and development costsfor the six months ended June 30, 2020 and June 30, 2019:

General research and development costs 1,779,000 914,000 865,000

The overall increase in research and development expense of approximately$964,000, or 23%, was primarily a result of increased general research anddevelopment costs resulting from increased personnel related costs and inclinical project costs. Manufacturing and related costs decreased due to adecrease in materials production processes and related costs. Pre-clinical studycosts were relatively consistent.

General and Administrative. General and administrative expense for the sixmonths ended June 30, 2020 was approximately $2,499,000, compared toapproximately $2,712,000 in the six months ended June 30, 2019. The decrease ofapproximately $213,000, or 8%, was primarily a result of lower stock-basedcompensation expense.

Liquidity and Capital Resources

As of June 30, 2020, we had cash and cash equivalents of approximately$22,450,000 compared to $10,615,000 as of December 31, 2019. This increase wasdue primarily to the approximately $18,300,000 of net proceeds received inconnection with the June 5, 2020 public offering. Net cash used in operatingactivities during the six months ended June 30, 2020 was approximately$6,562,000.

Our cash requirements have historically been for our research and developmentactivities, finance and administrative costs, capital expenditures and overallworking capital. We have experienced negative operating cash flows sinceinception and have funded our operations primarily from sales of common stockand other securities. As of June 30, 2020, we had an accumulated deficit ofapproximately $119,251,000.

We believe that the cash balance is adequate to fund our basic budgetedoperations for at least 12 months from the filing of these financial statements.However, our future results of operations involve significant risks anduncertainties. Our ability to execute our operating plan beyond that timedepends on our ability to obtain additional funding via the sale of equityand/or debt securities, a strategic transaction or otherwise. We plan toactively pursue all available financing alternatives; however, there can be noassurance that we will obtain the necessary funding. Other than theuncertainties regarding our ability to obtain additional funding, there arecurrently no known trends, demands, commitments, events or uncertainties thatare likely to materially affect our liquidity. Because we have had recurringlosses and negative cash flows from operating activities, and in light of ourexpected expenditures, the report of our independent auditors with respect tothe financial statements as of December 31, 2019 and for the year ended December31, 2019 contains an explanatory paragraph as to the potential inability tocontinue as a going concern. This opinion indicated at that time, thatsubstantial doubt existed regarding our ability to remain in business.

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CELLECTAR BIOSCIENCES : Management's Discussion and Analysis of Financial Condition and Results of Operations (form 10-Q) - marketscreener.com

As Buettner shares on the mindbodygreen podcast, oregano, sage, or rosemary (or a combo of all three!) make for quite the beneficial sip. "All three of those herbs are anti-inflammatory," he notes."They're also diuretic, so they can lower your blood pressure."

Take a peek at the research: Studies have shown that the flavonoids and phenolic acid in an oregano brew can help manage inflammatory conditions and oxidative stress; similarly, rosemary tea is touted for its antimicrobial properties, and sage has been shown to lower blood sugar levels.

If you're well-versed in the benefits of herbal tea, this recipe for longevity might not feel incredibly groundbreaking. But, as Buettner says, it's not just the herbs themselves that lend so many benefitsit's the fact that people drink them all day, every day that makes them so powerful.

During his anthropological adventure to discover the aforementioned Blue Zones, Buettner noticed that communities (specifically small villages in Korea) who lived well into the autumn of life were sipping these brews all day long. "Because they couldn't afford coffee, they were drinking these teas," he adds. "It's not because they drink these teas once in a while but because they drink them every day for years or decades that probably is adding to their longevity."

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So "Longevity Tea" Is A Thing & It's Easier To Make Than You'd Expect - mindbodygreen.com

In my previous two articles, I focused on the social and dietary influences on longevity. This week I will be looking at the impact of the environment on our life expectancy. How timely then, to build on the positive effects of the recent pandemic on the change in our behaviours. Over the last 5 months of lockdown, we have experienced a dramatic improvement in air quality and climate change. There has never been a better time to take responsibility for both our health and our planet.

Below, I have attempted to provide the latest understanding of the environment on our health and advise how to mitigate the risks:1.Air quality: In Europe alone, there have been thousands of fewer deaths as a result of reduced road traffic and industrial emissions due to the recent lockdown. This is largely due to the dangerous effect particulates have on our respiratory and cardiovascular systems. London has had some of the highest levels of Nitrogen Dioxide pollution in the world (just behind Beijing and New Dehli). However, the Mayor of London has made significant improvements to reduce harmful emissions (by up to 20% in the last 4 years). In addition to this, electric and hybrid vehicles could not come at a better time.2.Sun exposure: This will not only make you look older, but will cause damage to the skins genetic material and put you at risk of skin cancer. You should use a daily facial moisturiser of at least spf30 and a similar spf for your body if you are exposed. Lighter skin will require higher spf. It is a delicate balance, as the sun is also important for Vitamin D production, and one study has actually shown increased longevity with sun exposure (only by 7 months), which may be a result of those who have healthier diets, higher Vitamin D or more active lifestyles.3.Smoking: This goes without saying. There is also a non-linear relationship to the amount smoked, so even smoking a couple of cigarettes per day can have significant risks. Thankfully, the smoking ban in public places has reduced the risks of passive smoking.4.Light emission: This is a theoretical risk from backlit screens, as it impacts on your internal body clock (Circadian Rhythm) and can disrupt sleep, a factor in longevity. I would recommend wearing blue-light filter glasses after sunset, and change the settings on your phone/devices to night shift which cuts down the blue light emissions. Ideally, one should not use backlit screens within 2 hours of bedtime.5.Background radiation: Predominantly from X-rays or CT scans, although the radiation for different procedures vary widely, and usually the benefit outweighs the risk. Radon occurs naturally in the ground and areas such as Cornwall have high levels, contributing to higher levels of lung cancer, but these risks are still relatively small. We are also exposed to radiation when flying. A return transatlantic flight is the equivalent of one Chest X-ray. However, this amount of radiation is still extremely small, and unless you were travelling extensively, it would have very little overall effect. There has been a lot of debate around the effect of wireless radiation from high mobile phone use. The jury is still out and the WHO have categorized it as possibly carcinogenic , but the Health Protection Agency has found no consistent evidence that it is harmful.6.Higher Altitudes: it is difficult to know if this is due to the cleaner air, but many communities in the Blue Zones who live beyond the average life expectancy, are in mountainous regions.7.Pesticides: These have evolved over the decades, and we no longer use highly toxic pesticides such as DDT, which is still detectable in peoples bodies, even now. The regulation has become much stricter, so the residue found on produce is hundreds of times lower than the amount known to cause harm. There is ongoing debate over the advantages of organic natural over synthetic pesticides and if there is any significant benefit. It is still advisable to wash your fruit and vegetables, but mostly to prevent infections such as Coronavirus, Norovirus or E.Coli.8.The Hygiene Hypothesis: Is a popular belief that we are over sanitised leading to a dysfunctional immune system. This is a misnomer, as it is more related to changes in our diet and urban lifestyle than being too hygienic. It is a complex argument, suggesting a lack of exposure to healthy micro-organisms early in life (particularly in relation to our gut flora), which are important in shaping our immune system. Manipulation of our environment over the past century may have led to a rise in allergies and auto-immune conditions. Research has been looking at the role of probiotics in helping with this.

If you look after your environment, your environment will look after you.

Written by Dr Tim Lebens, a private GP in Central London, with a subspecialty in health optimisation and latest advances in medicine. http://www.drlebens.com

Read more from the original source:
How to live to 100: why our environment affects longevity - Tatler

The FutureBrand Index 2020 has just been released, the first comprehensive global study into the perception of global brands since the outbreak of COVID-1. And the findings show well-perceived companies can consistently align the full picture of the experiences they create with their wider corporate purpose.

FutureBrand AU CEO, Rich Curtis, told CMO brands that develop and deliver distinctive strategies and unconventional thinking perform more strongly than other brands. And in 2020, its strongly related to the coronavirus pandemic that has profoundly affected peoples lives and the new demands or expectations which have been placed upon how people buy, work, play, study and live.

We can see in this study that those brands able to take the opportunity to stand apart, and do so in a way that is authentic to who they are and what they do, outperform other brands, Curtis said.

Curtis cited the example of Netflix, which has moved beyond being a technology outfit or a streaming business, and has successfully built an emotional connection with customers through a distinctive strategy to market.

The FutureBrand Index is a global perception study that reorders PwCs Global Top 100 Companies by Market Cap on perception strength rather than financial strength. One theme stood out beyond all others, and that is individuality. The report said its a quality that distinguishes an entity from others of the same kind.

The research was conducted during the initial weeks of lockdown, as the world adjusted to a new way of living and working, to tap decision-makers about their thinking in the here and now and into the future.

The research has also identified several other themes common to companies with strong positive perceptions. Prioritising customers and their needs, even if it means forging a different path to rival firms, is one of these. And in a time of an ongoing health crisis, those companies in healthcare rate highly, along with those that care about employees as they do their customers, including a firm commitment to diversity and inclusion feature high up on the list.

Those companies which realise the true value of an open culture that fosters a happy and productive workforce and the ones that embrace innovation, change and agility to maintain resilience in the face of fast-moving, sector-specific, national and international events also have the right ingredients for positive brand perception.

In particular, Curtis said its about an organisation having a clear sense of purpose. With the COVID-19 context, it's especially important to have a clarity of purpose and mission.

A good example of that is the Melbourne Convention and Exhibition Centre. Because it has that clarity of purpose, people feel engaged and kind of bound on to that organisation. And it is able to communicate very openly and very authentically with its own employees about what is happening at the moment and what it is doing, he explained to CMO.

Looking ahead, Curtis said for organisations to survive, and even thrive, throughout and beyond the pandemic where well-being and healthcare have been elevated, forging an emotional connection is all powerful.

That is most certainly an enduring dynamic in building successful brands, he added.

Follow CMO on Twitter:@CMOAustralia, take part in the CMO conversation on LinkedIn:CMO ANZ,follow our regular updatesvia CMO Australia's Linkedin company page, or join us on Facebook:https://www.facebook.com/CMOAustralia.

Read more here:
Study: Emotional connection key to brand longevity - CMO

In ones quest to find solutions to help live a long and disease-free life, numerous theories and suggestions have been declared. Intermittent fasting has gained much notoriety over the pastyear,and according to leading healthexperts, this type of eatingcould be the answer to helping you boost your life longevity. How?

A review of past animal and human studies in The New England Journal of Medicine recommend adopting a way of eating known as intermittent fasting which can help reduce blood pressure, aid in weight loss and improve longevity.

Alternating between fasting and eating can help to improve cellular health.

Professor Mark Mattson from John Hopkins University said the way of eating can help to trigger a metabolic switch.

In metabolic switching, cells use up their fuel stores and convert fat to energy this in turns helps fat to switch from fat-storing to fat-saving and has many health benefits.

The way of eating involves daily-time restricted feeding.

This narrows the time of eating to six to eight hours per day which is also known as 5:2 intermittent fasting, in which people limit themselves to one moderate-sized meal two days each week.

Findings on intermittent fasting range in the diets effectiveness, but some studies in animals and humans have linked the practice to longer lives, healthier hearts and improved cognition.

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When finding benefits of the diet, looking at different countries who adopt this way of eating as a norm often helps.

Residents of Okinawa are known for their extreme longevity and low-calorie, nutrient-rich diet.

Their way of eating has been suggested to help contribute to their long-life spans, low number of obesity and reduced risk of diseases.

Professor Mattson says studies have shown that this switch improves blood sugar regulation, increases resistance to stress and suppresses inflammation.

The professor notes that four studies in both animals and people found intermittent fasting also helped to decrease blood pressure, blood lipid levels and resting heart rates.

Preliminary studies suggest that intermittent fasting could benefit brain health too.

A clinical trial at the University of Toronto found that 220 healthy adults who maintained a calorie restricted diet for two years showed signs of improved memory in a battery of cognitive tests.

Professor Mattson added: Patients should be advised that feeling hungry and irritable is common initially and usually passes after two weeks to a month as the body and brain become accustomed to the new habit.

Mattson suggests a gradual acclimation to fasting rather than going cold turkey will help with this.

Mattsonalsohopes this study will give better insight to physicians, who can pass that guidance on to their patients.

For an added benefit, eating a Mediterranean diet during the eating phasecouldnot only boost longevity but improve heart health too.

Read the original:
How to live longer: Diet shown to burn fat, improve heart health and to boost longevity - Express

The first time I heard nematode worms can teach us something about human longevity, I balked at the idea. How the hell can a worm with an average lifespan of only 15 days have much in common with a human who lives decades?

The answer is in their genesespecially those that encode for basic life functions, such as metabolism. Thanks to the lowly C. elegans worm, weve uncovered genes and molecular pathways, such as insulin-like growth factor 1 (IGF-1) signaling that extends healthy longevity in yeast, flies, and mice (and maybe us). Too nerdy? Those pathways also inspired massive scientific and popular interest in metformin, hormones, intermittent fasting, and even the ketogenic diet. To restate: worms have inspired the search for our own fountain of youth.

Still, thats just one success story. How relevant, exactly, are those genes for humans? Were rather a freak of nature. Our aging process extends for years, during which we experience a slew of age-related disorders. Diabetes. Heart disease. Dementia. Surprisingly, many of these dont ever occur in worms and other animals. Something is obviously amiss.

In this months Nature Metabolism, a global team of scientists argued that its high time we turn from worm to human. The key to human longevity, they say, lies in the genes of centenarians. These individuals not only live over 100 years, they also rarely suffer from common age-related diseases. That is, theyre healthy up to their last minute. If evolution was a scientist, then centenarians, and the rest of us, are two experimental groups in action.

Nature has already given us a genetic blueprint for healthy longevity. We just need to decode it.

Long-lived individuals, through their very existence, have established the physiological feasibility of living beyond the ninth decade in relatively good health and ending life without a period of protracted illness, the authors wrote. From this rare but valuable population, we can gain insight into the physiology of healthy aging and the development of new therapies to extend the human healthspan.

While it may seem obvious now, whether genes played a role in longevity was disputed for over a century. After all, rather than genes, wouldnt access to health care, socioeconomic status, diet, smoking, drinking, exercise, or many other environmental and lifestyle factors play a much larger role? Similar to height or intelligence (however the latter is assessed), the genetics of longevity is an enormously complicated and sensitive issue for unbiased studying.

Yet after only a few genetic studies of longevity, a trend quickly emerged.

The natural lifespan in humans, even under optimal conditions in modern societies, varies considerably, the authors said. One study, for example, found that centenarians lived much longer than people born around the same time in the same environment. The offspring of centenarians also have lower chances of age-related diseases and exhibit a more youthful profile of metabolism and age-related inflammation than others of the same age and gender.

Together, about 25 to 35 percent of the variability in how long people live is determined by their genesregardless of environment. In other words, rather than looking at nematode worm genes, we have a discrete population of humans whove already won the genetic lottery when it comes to aging. We just need to parse what winning means in terms of biology. Genes in hand, we could perhaps tap those biological phonelines and cut the wires leading to aging.

Identification of the genetic factors that underlie extreme human lifespan should provide insights into the mechanisms of human longevity and disease resistance, the authors said.

Once scientists discovered that genes play a large role in aging, the next question was which ones are they?

They turned to genome-wide association studies, or GWAS. This big data approach scans existing genomic databases for variations in DNA coding that could lead to differences in some outcomefor example, long versus short life. The differences dont even have to be in so-called coding genes (that is, genes that make proteins). They can be anywhere in the genome.

Its a powerful approach, but not that specific. Think of GWAS as rudimentary debugging software for biological code: it only looks for differences between different DNA letter variants, but doesnt care which specific DNA letter swap most likely impacts the final biological program (aging, in this case).

Thats a huge problem. For one, GWAS often finds dozens of single DNA letter changes, none powerful enough to change the trajectory of aging by itself. The technique highlights a village of DNA variants, that together may have an effect on aging by controlling the cells course over a lifetime, without indicating which are most important. Its also hard to say that a DNA letter change causally leads to (or protects against) aging. Finally, GWAS studies are generally performed on populations of European ancestry, which leaves out a huge chunk of humansfor example, the Japanese, who tend to produce an outsized percentage of centenarians.

So what needs to change?

Rather than focusing on the general population, the key is to home in on centenarians of different cultures, socioeconomic status, and upbringing. If GWAS are like fishing for a rare species in several large oceans, then the authors point is to focus on pondsdistributed across the worldwhich are small, but packed with those rare species.

Extremely long-lived individuals, such as centenarians, compose only a tiny proportion (~0.01 percent to 0.02 percent) of the United States population, but their genes contain a biological blueprint for healthy aging and longevity, the authors said. Theyre spared from usual age-related diseases, and this extreme and extremely rare phenotype is ideal for the study of genetic variants that regulate healthspan and lifespan.

Its an idea that would usually make geneticists flinch. Its generally thought that the larger the study population, the better the result. Here, the recommendation is to narrow our focus.

And thats the point, the authors argue.

Whatever comes out of these studies will likely have a much larger impact on aging than a GWAS fishing experiment. Smaller (genomic) pond; larger (pro-youth) fish. Whats more, a pro-youth gene identified in one European-based long-living population can be verified in another group of centenarianssay, Japaneseensuring that the gene candidates reflect something fundamental about human aging, regardless of race, culture, upbringing, and wealth.

A genomic screen of centenarians can easily be done these days on the cheap. But thats only the first step.

The next step is to validate promising anti-aging genetic differences, similar to how scientists validated such differences in nematode worms during classic longevity studies. For example, a promising pro-youth gene variant can be genetically edited into mice using CRISPR or some other tool. Scientists can then examine how the mice grow up and grow old, compared to their non-edited peers. Does the gene make these mice more resilient to dementia? What about muscle wasting? Or heart troubles? Or hair greying and obesity?

From these observations, scientists can then use an enormous selection of molecular tools to further dissect the molecular pathways underlying these pro-youth genetic changes.

The final step? Guided by centenarian genes and validated by animal models of aging, we can design powerful drugs that sever the connection between the genes and proteins that drive aging and its associated diseases. Metformin is an experimental pill that came out of aging studies in nematode wormsimagine what studies in human centenarians will yield.

Despite enormous improvements in human health over the past century, we remain far from a situation in which living to 100 years of age in fairly good health is the norm, the authors said.

But as centenarians obviously prove, this is possible. By digging into their genes, scientists may find a path towards healthy longevitynot just for the genetically fortunate, but for all of us.

Image credit:Cristian Newman / Unsplash

See more here:
The Secret to a Long, Healthy Life Is in the Genes of the Oldest Humans Alive - Singularity Hub

Editors note: This article is part of an editorial partnership between Next Avenue and The American Federation for Aging Research (AFAR), a national nonprofit whose mission is to support and advance healthy aging through biomedical research.

Dr. Nir Barzilais research as director of the Einstein-Institute for Aging Research and AFAR scientific director explores the genetics and biology of aging through the lens of exceptional longevity. He is a pioneer in the study of centenarians and, as one step in the process of understanding how we age, looking at the cellular level to see how centenarians genes can point to opportunities to delay aging or protect against age-related disease.

He is also co-founder of biotech firms CohBar and Lifebiosciences, who are developing therapies to extend health by targeting aging, and is principal investigator for the TAME (Targeting Aging with Metformin) Trial, which aims to provide proof of concept that aging can be targeted and treated.

Barzilai recently published his first book, Age Later: Health Span, Life Span, and the Science of Longevity. We spoke with him to learn about his research on those who live past 100.

American Federation of Aging Research: What are SuperAgers and what does the study of these individuals tell you about longevity?

Dr. Nir Barzilai: SuperAgers are people who have aged more slowly than others. In other words, SuperAgers chronological age does not reflect their biological age. They do not accumulate age-related disease and require treatment, which allows them to work longer, enjoy post-retirement interests, to live life to the fullest.

Centenarians, as well as many older adults, do survive COVID-19.

In my studies, not only did SuperAgers live twenty to thirty more healthy years, they also had a contraction of morbidity. This means they spent less time being sick and therefore there is a longevity dividend among SuperAgers as medical costs are saved.

How can your study of genes in centenarians or their offspring translate to drug discovery efforts?

The interesting thing about discovering specific changes in the genes of centenarians and their offspring is that those genes can point to a mechanism that can be targeted for intervention. We can look to these mechanisms for developing drugs that inhibit or stimulate these genes.

Through the Longevity Genes Project at Einstein, we have found two such changes in genes that control the good aspect of lipid metabolism. These discoveries led to the development of a drug and successful Phase 2 studies by the pharmaceutical companies Merck and Ionis. [Barzilai is on Mercks advisory board.] The indications for the development of these drugs was cardiovascular disease, but they may impact other diseases as well.

The disproportionate impact of COVID-19 on older adults has been well documented, but what can be learned from older adults, even centenarians, who survive the virus?

Centenarians, as well as many older adults, do survive COVID-19. While we must be sensitive to the range of socioeconomic factors impacting how and who COVID-19 is affecting in America, its important to look at the hallmarks of aging.

On a cellular level, these hallmarks are processes that are considered to be the core underlying machinery controlling how our bodies age. COVID-19 vulnerability is linked to two of the hallmarks of aging: immune decline and inflammation. Some older adults experience these hallmarks at lower levels.

Further, research has shown that immunity among offspring of centenarians is better than that of others their age. Because all hallmarks of aging are involved, not just the immune system, these individuals are able to survive through a severe disease like COVID-19.

In Age Later, you pose the question: Is it possible to grow older without getting sicker? How have your thoughts on this question changed since the coronavirus pandemic?

COVID-19 has put a spotlight on how the biology of aging makes some of us more or less vulnerable to viruses and sickness. The field of aging research has been looking at this for decades, and now we can apply our expertise to COVID-19 and expand the conversation on targeting age-related diseases and extending health span our years of health as we age.

I always say that a future of healthy aging is not just a hope, but a promise: not only have we gone from the promise of targeting aging, but there are drugs that can do this in use by humans today. Those drugs can change biological age and improve immunity not only against COVID-19, but against the next pathogen.

For example, metformin is a drug that can target aging in humans. There are several papers that show COVID-19 patients on metformin were hospitalized less and had lower mortality than patients with similar problems who were not treated with metformin. We need to move rapidly to consider available drugs like this that can help defend older adults against threats like COVID-19 now and those in the future.

This also why we need the TAME Trial. At fourteen leading research institutions across the country, we hope to engage over three thousand individuals between the ages of sixty-five and seventy-nine to test whether those taking metformin experience delayed development or progression of age-related chronic diseases such as heart disease, cancer, and dementia.

The TAME Trial seeks an indication for aging from the FDA [Food and Drug Administration], and this would open the door to so many promising therapies to extend health.

Im passionate about the therapeutics that are within our reach and their promise to extend health as we grow older. My book may be called Age Later, but it really could be called Healthier Longer. The promise that we all can live healthier for longer as we grow older and decrease the pain of disease and illness is really what motivates me and my inspiring colleagues in the field.

Dr. Barzilai will be talking about his book at an online event on Thursday, Aug. 27, 2020 at 2 pm ET (RSVP required). The talk is part of AFARs Live Better Longer series with Prevention magazine, and is part of an editorial and promotional partnership with Next Avenue.

Next Avenue brings you stories that are inspiring and change lives. We know that because we hear it from our readers every single day. One reader says,

"Every time I read a post, I feel like I'm able to take a single, clear lesson away from it, which is why I think it's so great."

Your generous donation will help us continue to bring you the information you care about. What story will you help make possible?

Next Avenue - 2020. All rights reserved.

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What We Can Learn About Longevity From SuperAgers and Centenarians - Next Avenue

Maintaining a healthy lifestyle, including a well-rounded diet is crucial to prolonging your lifespan.

You could also boost your lifespan by doing regular exercise. Its the miracle cure weve all been waiting for, according to the NHS.

Making some small diet or lifestyle changes could help to increase your life expectancy and avoid an early death.

One of the best ways to make sure that you live a long and healthy life is to eat more turmeric, it's been revealed.

READ MORE: How to live longer - the amount of exercise you need to do each day

"Many people think that life expectancy is largely determined by genetics," the dietitian wrote on medical website Healthline.

"However, genes play a much smaller role than originally believed. It turns out that environmental factors like diet and lifestyle are key.

"When it comes to anti-aging strategies, turmeric is a great option. Thats because this spice contains a potent bioactive compound called curcumin.

"Due to its antioxidant and anti-inflammatory properties, curcumin is thought to help maintain brain, heart, and lung function, as well as protect against cancers and age-related diseases."

Meanwhile, you could also lower your risk of an early death by eating more nuts, it's been claimed.

They're particularly rich in proteins, fibre, antioxidants, and magnesium.

Scientists have previously revealed that they could protect against heart disease and high blood pressure.

Everyone should aim to eat a handful of nuts everyday; the equivalent to around 30g.

See the rest here:
How to live longer - the anti-ageing spice to protect against an early death and cancer - Express

The research report on Precision Medicine Software Industry market comprises of key development trends that define the industry in terms of profit potential and expansion scope. It also highlights the challenges & constraints that may negatively influence the market outlook alongside the various growth drivers and opportunities affecting the future remuneration of this business vertical. In addition, the study encompasses data regarding the impact of COVID-19 in an effort to gain insights about the projected performance over the study duration.

Major aspects from COVID-19 impact analysis:

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A summary of the geographical landscape:

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Major Points Covered in TOC:

Overview:Along with a broad overview of the global Precision Medicine Software Industry market, this section gives an overview of the report to give an idea about the nature and contents of the research study.

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Market Forecasts:Buyers of the report will have access to accurate and validated estimates of the total market size in terms of value and volume. The report also provides consumption, production, sales, and other forecasts for the Precision Medicine Software Industry market.

Regional Growth Analysis:All major regions and countries have been covered in the report. The regional analysis will help market players to tap into unexplored regional markets, prepare specific strategies for target regions, and compare the growth of all regional markets.

Segmental Analysis:The report provides accurate and reliable forecasts of the market share of important segments of the Precision Medicine Software Industry market. Market participants can use this analysis to make strategic investments in key growth pockets of the market.

Key questions answered in the report:

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Global Precision Medicine Software Industry Market 2020 Size, Share, Trends, Growth and Outlook with Company Analysis and Forecast to 2025 - CueReport

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Competitive companies and manufacturers in global market

Some of the major companies operating in the global advanced wound management technologies market are 3M, Bard Medical Division, Coloplast A/S, Derma Sciences Inc., Hartmann Group, Shire Regenerative Medicine and Baxter International Inc. In addition, some other companies operating in global advanced wound management technologies market are Ethicon Inc., Smith & Nephew Plc, Convatec Inc. and Genzyme Corporation, a Sanofi company.

Key geographies evaluated in this report are:

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Advanced Wound Management Technologies Market Table of Contents

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Advanced Wound Management Technologies Market Forecasted To Surpass The Value Of US$ XX Mn/Bn By 2015 2021 - Jewish Life News

Police are offering a $3,500 reward for information leading to Breasia Terrell, who is reportedly partially deaf and has trouble with her vision

Police, family and concerned neighbors are desperately searching for a missing 10-year-old girl who vanished in Davenport, Iowa, late last week.

According to KWQC, Breasia Terrell was last seen in the early hours of Friday morning at the 2700 block of East 53rd Street in Davenport. Breasias grandmother Donita Gardner told the Quad City Times that Breasia had gone to stay at the home of Henry Earl Dinkins on Thursday night with her cousin, who is reportedly Dinkinss son. The little girl had vanished by Friday morning.

Dinkins is a registered sex offender with a criminal history. Breasias family reportedly asked police to search Fejervary Park and a lagoon at Credit Island after they heard a tip that Dinkins mentioned something about Mother Goose. According to the Quad City Times, there is a large Mother Goose structure at the entrance to the park, where police and volunteers were seen scouring the area on Friday.

Police reportedly also searched Dinkinss apartment on Friday, and later the same day took him into custody on a sex offender violation. Dinkins allegedly failed to comply with sex-offender registry requirements, according to documents obtained by the Quad City Times. He has not been charged in connection to Breasias disappearance.

Doomsday, death & deception: Nancy Grace investigates Cult Mom Lori Vallow. Inside sources reveal brand new bombshell information. Click here to watch.

Davenport Police are reportedly offering a $3,500 reward for information leading to the missing 10-year-old girl, or information which leads to an arrest of anyone who may have taken part in her disappearance.

Breasias mother Aishia Lankford is hoping someone with information will come forward.

Lankford spoke to reporters on Saturday as she participated in a volunteer search of Credit Island, which she believes is a key location in her daughters disappearance.

Her picture is everywhere. Everywhere. And nobody has called and come forward, Lankford told WQAD on Saturday.

I had to go home last night without a baby and Ill be damned if I go home again without one, Lankford said.

Breasias mother also said that the little girl has physical disabilities related to her hearing and sight.

Her eyesight is kinda messed up out of her left eye and she cant hear out of her left ear, Lankford told the Muscatine Journal.

According to KWQC, Breasia is described as 4 feet, 5 inches tall and weighing 75 pounds. She has black hair and brown eyes, and was last seen wearing a white T-shirt, shorts, and flip-flops.

Police have urged anyone with information to call 911.

For the latest true crime and justice news, subscribe to the Crime Stories with Nancy Grace podcast.

Link:
URGENT MISSING: After 10-year-old girl vanishes in the night, tip leads police to search lagoon and apartment of registered sex offender - CrimeOnline

DEAR DR. ROACH: Could you discuss Elmiron side effects and the pending lawsuit? I have been on this for years for interstitial cystitis and am worried about staying on it even though it is the only relief I can find. -- C.H.

ANSWER: "Interstitial cystitis" is a term used for chronic bladder pain when no other cause has been identified. It is not well understood. It appears that some of the protective layers of the bladder are damaged, allowing irritants in the urine to attack deeper layers, causing pain. There may be an autoimmune component to the disease. There does seem to be a family predisposition.

Before considering medication therapy, it's important to identify individual triggers to symptoms, whether through diet, body position or exercise. Some people do better with more fluid, some with less. Pelvic floor physical therapy can bring great relief to many with IC.

If medication is indicated, amitriptyline is usually the first tried, and is effective for many. It is not effective for all, and pentosan polysulfate (Elmiron) is then often tried. It may take three to six months to see maximum benefit. It appears to work by repairing the damaged protective layers of the bladder. Side effects of nausea and diarrhea happen 10% to 20% of the time. Hair loss may occur and is reversible with stopping the medication. Liver function abnormalities are possible but uncommon.

In 2018, a paper identified damage to the macula (the center of the retina) in people who had been taking the medication for an average of 15 years. A further study in 2019 confirmed that people taking pentosan polysulfate may develop pigment in the retina, which threatens sight.

A lawsuit claims that the drug manufacturer withheld knowledge about this potential side effect.

People with IC should be made aware of this potential side effect. Those with vision symptoms should have a visual examination by an ophthalmologist. The risk of retina damage is highest in people who have taken the most Elmiron -- 42% of people taking the highest amount of Elmiron for many years had evidence of this toxicity.

Although there is no official recommendation to do so, those who have been taking Elmiron for years should get an ophthalmologic examination, in my opinion. Knowing whether there is any toxicity is important in deciding whether to keep taking the medication, especially since there is evidence that the damage may continue even after the drug is stopped. People may still choose to continue the medication despite this toxicity. I recall when Vioxx was removed from the market, many of my patients said they wished they could continue it despite the risks. Knowing the risks is essential in order to make an informed decision.

DEAR DR. ROACH: What do you think of the enema fad? I've heard of people who take daily enemas. Some even go to the doctor for higher-up irrigation. To me this is weird and I would think not healthy. -- L.

ANSWER: Enemas are neither necessary nor recommended for everyday use and should be used only for constipation after several days' worth of no bowel movement, when other safer treatments have been ineffective. In this case, enemas can prevent impaction. Enemas, if used, should be warm water, rather than with soap, which can damage the lining of the colon.

Some people, such as those who are bedridden with chronic illness, may need enemas on a regular basis, but this is uncommon and only to be done under doctor's orders.

I was unaware there was a "fad."

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Interstitial cystitis drug can affect the macula in the eye - Martinsburg Journal

By: Parenting Desk | New Delhi | Updated: July 12, 2020 10:38:08 pm Sudden, large weight gain is linked to the possibility of preeclampsia. You may notice this weight gain is combined with swelling of the face and hands. (Source: Getty/Thinkstock)

By Dr Alka Kriplani

The constant buzz about social distancing and stay-at-home has been keeping us worried about stepping out from the home and visiting a doctor. The fear doubles when you are pregnant. But there are certain symptoms that can be life-threatening for both mother and the child, for which she needs to visit a doctor immediately. Even the recent guidelines from the World Health Organization suggested a pregnant mother to continue regular check-ups in the unlock situation.

Most hospitals are taking extra precaution in their premises as per as the checklist suggested by the various health bodies. So, it may be safe to visit hospital if you are experiencing symptoms like persistent abdomenpain, severe headache, changes in eyesight, unusual weight gain, among others. Some of these symptoms may be normal symptoms of pregnancy, but they may also be signs of something more serious, so visit your gynecologist.

ALSO READ |Childhood cancer: Understanding brain tumour in kids

Here are the lists of few conditions, which you should not take lightly:

Persistent abdominal pain: Discomfort associated with round ligament pain, for example, may be perfectly normal, but abdominal pain, with early pregnancy and fainting attacks, may be a sign that theres something wrong.

Severe headache: Headaches during pregnancy can be caused by many factors, including hormonal changes, stress, and fatigue, but if headache feels severe, it may be a sign of high blood pressure or the high blood pressure disorder called preeclampsia. Preeclampsia is aserious condition that requires medical treatment to protect a mothers health and the health of her baby.

Changes in eyesight: Changes in vision, such as temporary loss of vision, blurred vision, or light sensitivity, may be linked to complications like gestational hypertension or preeclampsia.

Fainting or dizziness: Feeling lightheaded can be a normal symptom of early pregnancy. You might also feel dizzy later during pregnancy due to things like circulation problems or low blood sugar levels. But, if this feeling of dizziness persists, if you feel faint or actually do faint, or if your dizziness is combined with other symptoms like blurred vision, vaginal bleeding, headaches, or pain in your abdomen, consult your doctor so that a cause can be identified and treated.

Unusual weight gain and swelling or puffiness: Sudden, large weight gain is linked to the possibility of preeclampsia. You may notice this weight gain is combined with swelling of the face and hands.

ALSO READ |Is it safe to go for pregnancy scans during COVID-19?

Burning sensation while you urinate: If you feel an increased urge to pee, but find only a few drops come out, or if you have a burning sensation while you urinate, it may be a sign of a urinary tract infection (UTI). Other symptoms of a UTI can include fever, chills, or blood-tinged urine. Your doctor will be able to diagnose your symptoms and treat the bacterial infection to avoid complications.

Severe pain above the stomach, under the rib cage: This pain (especially if its combined with other symptoms like blurred vision, severe headaches, or nausea) may be a sign of high blood pressure and an associated condition called preeclampsia. Your doctor will monitor your blood pressure during prenatal visits, but if you notice any of the signs of preeclampsia, then contact your doctor right away.

Vaginal bleeding: Early on in the pregnancy, it can be normal to experience spotting thats known as implantation bleeding, but bleeding could be due to placenta praevia or a cervical lesions. If in doubt, tell your doctor if you notice any spotting or bleeding during your pregnancy.

(The writer is the Director & Head, Centre for Minimally Invasive Gynecology, Obstetrics & ART, Paras Hospital)

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What could be causing unusual weight gain and swelling during pregnancy? A doctor answers - The Indian Express

Machine vision joins machine learning in a set of tools that gives consumer- and commercial-level hardware unprecedented abilities to observe and interpret their environment. In an industrial setting, these technologies, plus automation and higher-speed networking, add up to a new industrial revolution Industry 4.0. They also offer brand-new ways to conduct low-waste, high-efficiency industrial activities.

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Machine vision affects manufacturing, drilling, and mining. Further benefits are found in freight and supply chain management, quality assurance, material handling, security, and many different other processes and verticals.

Machine vision is going to be every-where before long, adding a critical layer of intelligence to the Internet of Things buildouts in the industrial world. Heres a glance at how businesses are already putting it to work.

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Machine vision is a set of technologies that gives machines greater understanding of their environments. It facilitates higher-order image recognition and decision-making predicated on that awareness.

To take advantage of machine vision, a bit of industrial equipment uses high-fidelity cameras to capture digital images of the environment, or even a workpiece. The images could be taken in an automated guided vehicle (AGV) or a robotic inspection station. From there, machine vision uses excessively sophisticated pattern recognition algorithms to produce a judgment about its position, identity, or condition.

Several lighting sources are typical in machine vision applications, including Light emitting diodes, quartz halogen, metal halide, xenon, and traditional fluorescent lighting. If part of a barcode or workpiece is shadowed, the reading may deliver one when there isnt one, or vice versa.

Machine vision combines sophisticated hardware and software to allow machines to observe and react to outside stimuli in new and beneficial ways.

The proliferation of Industrial Internet of Things (IIoT) devices marks an important moment in technological advancement. IIoT gives organizations unprecedented visibility of their operations from top to bottom. Networked sensors and cloud-based enterprise and resource planning hubs provide two-way data mobility between local and remote assets, as well as business partners.

The two-way mobility could be something no more than a mechanical piston or bearing. It can also be as large as a fleet of trucks, can yield valuable operational data with the right IoT hardware and software. Businesses can have their eyes every-where, even when theyre strapped for resources or labor.

Where does machine vision squeeze into all this? Machine vision makes existing IoT assets a lot more powerful and better able to deliver value and efficiency. We can expect it to create some brand-new opportunities.

Machine vision makes sensors through the entire IoT a lot more powerful and useful. Instead of providing raw data, sensors deliver a level of interpretation and abstraction you can use in decision-making or further automation.

Machine vision may help decrease the bandwidth requirements of large-scale IoT buildouts. Compared with capturing pictures and data at the origin and sending it to servers for analysis, machine vision on average performs its research at the source of the data. Modern industry generates millions of data points, but a great deal of it could yield actionable insights without requiring transmission to another location, thanks to machine vision and edge computing.

Machine vision complements IoT automation technologies extremely well. Robotic inspection stations can work faster and accurately than human QA employees, and they immediately surface relevant data for decision-makers when defects and exceptions are detected.

Guidance systems designed with machine vision give robots and cobots greater autonomy and pathfinding abilities, and help them work faster and more safely along side human workers. In warehouses and other settings with a high danger of error, machine vision helps robotic order pickers improve response time and limit fulfillment defects that bring about lost business.

Todays and tomorrows economy requires companies and industries that operate while wasting much less time, material, and labor. Machine vision will keep on to make drones, material handling equipment, unmanned vehicles and pallet trucks, manufacturing lines, and inspection stations better able to exchange detailed and valuable data with all of those other network.

In a factory setting, it means machines and people working in better harmony with fewer bottlenecks, overruns, and other disruptions.

When you consider each of the steps involved in a normal industrial process, its easy to see each point where machine vision can improve operations.

To manufacture just one automotive part, humans and machines collaborate to source raw materials, appraise their quality, transport them to a plant for processing, and move those items through the facility at each manufacturing stage. Ultimately, they view it successfully through the QA process and then out the door again, where one or more last leg of its journey awaits. At some later time, the retailer or end-user receives it.

Whether this product is at rest, in transit, or not really assembled yet, machine vision provides a way to automate the handling of it. It improves efficiency in most department, such as for instance assembly, and maintains higher and more consistent quality levels.

Some applications are as simple as placing a line on a warehouse floor for an unmanned vehicle to follow safely. Other machine vision tools are a lot more sophisticated, even though even the best examples could be game-changers.

Some of the very exciting samples of machine vision in the industrial world involve tasks once thought difficult or impossible to outsource to robots. As mentioned, picking from bins in warehouses is an activity thats inherently risky as it pertains to errors. Mistakes in fulfillment cost goodwill and customers.

There happen to be nearly 100% autonomous order-picking robots on the market, which can navigate safely, inspect parts and products in the bin, make the proper pick employing a manipulator arm, and transport the pick to a staging or packaging area.

Ultimately, this means businesses are at a far lesser risk of shipping damaged goods or incorrect SKUs that look similar to, but dont quite match, usually the one the customer ordered.

In some modern manufacturing settings, it will also help employers automate and improve results from the QA process, even without sacrificing human jobs. Instead, automated inspection stations tackle this high-priority work while employees learn more cognitively demanding skills.

Cobots will likely achieve a 34% share of most robotics sales by 2025. This is due in large part to improvements in machine vision and the drive to expel as much inefficiency, inaccuracy, and waste from the modern industry as possible.

Expect machine vision to keep on to evolve in the coming years and contribute further to Industry 4.0, which many call the Fourth Industrial Revolution. Eyes are already trained on newer, lower-cost products and services featuring embedded and board-level image processing with machine vision capabilities.

Machine vision capabilities will lead to a lot more widespread adoption of the IoT and machine eyesight and innovative ways for businesses to capitalize upon digital brains.

Featured Image Credit: HAHN Group, CLOSED CIRCUIT BY-SA

Megan Ray Nichols is a contract technical article writer and tumblr. She likes writing simple to know science and technology content articles on her weblog, Schooled By Science. When she is not writing, Megan enjoys observing movies and hiking along with friends.

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Machine Vision is Key to Industry 4.0 and IoT - Digital Market News