Gwede Mantashe missed a golden opportunity to revitalise our electricity sector. When he announced the IRP, the minister should have taken the time to demonstrate his willingness to be bold, decisive and constructive in ensuring South Africas energy security. There were four distinct steps that should have been announced, but werent.

First, the minister should have walked away from the pipe dream that is the Grand Inga project. South Africa signed an agreement with the Democratic Republic of the Congo in 2013 to take up at least 2500MW from the project (roughly 5% of South Africas installed capacity), at an estimated cost in excess of R200-billion. But Inga 3, the dam intended to supply this electricity, has been stalled since the 1990s. Now the Congolese government are looking to scale down the project and the Chinese-Spanish consortium that was awarded the construction contract, are at loggerheads. And apart from the construction challenges, there are transmission issues too: to get the power to South Africa, the power lines would have to cross thousands of kilometers of foreign soil and be subject to the vagaries of various threats. We recently saw the impact of weather on the Cahora Bassa power lines, which resulted in extended rolling blackouts earlier this year. Rather than standing guarantor for this unlikely source of power, South Africa should be investing in domestic power production.

The second thing Mantashe should have done is to immediately open up Bid Window Five for renewable electricity independent power producers (IPPs). Renewable energy has been identified as the quickest and one of the lowest cost solutions to South Africas electricity supply gap the shortfall between supply and demand that has arisen because Eskoms aging power plant fleet can no longer meet the needs of our people, and our economy. Various reports indicate that the supply of electricity from new renewable energy IPPs could be brought online in two years, compared to the lengthy build time for other types of power plants. Renewables also address our commitment to reducing our carbon emissions, something Eskom is fundamentally incapable of doing.

Earlier this week, Mantashe told the Portfolio Committee on Mineral Resources and Energy that renewables would not be given preference over other forms of new generation. When we open applications for new generation, everybody will be able to bid for that, including renewable producers, he said.

Sadly, Mantashe seems to regard anyone who proposes renewables as a potential solution as a lobbyist for foreign technologies and companies intent on destroying South African jobs. Nothing could be further from the truth. This is not about killing Eskom or destroying our coal industry. The reality is that our country needs electricity to ensure economic growth. We need foreign investment to help create employment. We need to clean up our polluted atmosphere especially in Mpumalanga. We need quick fixes, at affordable prices something renewable energy IPPs can assist with. Mantashes ideological and union-based opposition to opening Bid Window Five is counter-productive. The stop-start process that has been followed to date has seen component manufacturers go into liquidation and investors pulling out.

Third, the IRP highlights the decommissioning of the Grootvlei (1120MW nominal capacity), and Komati (904MW nominal capacity), coal-fired power stations in 2020. Both plants are past their projected lifespans. But, in both cases, they have among the highest availability factors of the entire Eskom fleet at 89% and 87% respectively. Mantashe should have proposed further life extension measures to keep these plants active in the short term, to ameliorate the shortfall in electricity supply from the other Eskom plants.

Last, we would have expected Mantashe to make two significant regulatory announcements. The first would be a ministerial determination to allow those municipalities which have the technical ability and financial resources to purchase electricity directly from IPPs. This falls under Section 34 of the Electricity Regulation Act and is a direct responsibility of the minister. His (and his predecessors) failure to do so has resulted in the City of Cape Town taking the minister and the Department of Mineral Resources and Energy to court to force him to act wasteful expenditure that could be avoided if Mantashe was prepared to work in the best interests of the country, rather than kowtow to the unions and failed ANC ideology.

The second pronouncement that would assist our beleaguered electricity sector would be to ease the regulatory and registration requirements on small-scale embedded generation systems. This would need to be done in conjunction with the National Energy Regulator of South Africa (NERSA), but the announcement and commencement of a dialogue in this regard would incentivise more South Africans to invest in off-grid and grid-tied solutions and thereby relieve some of the demand on Eskom.

Mantashes failure to seize the moment has long-term consequences for South Africa. Instead of opening our grid to competition and ensuring energy security from a domestic perspective, he has defaulted to the status quo, and we are left marking time, waiting for Eskom to switch the lights off. Again. DM

Kevin Mileham MP is the DA Shadow Minister of Mineral Resources and Energy

Kevin Mileham is a Democratic Alliance Member of Parliament and a Shadow Minister of Mineral Resources and Energy

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OPINIONISTA: Mantashe's Integrated Resource Plan could have been so much better - Daily Maverick

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NORTH PLATTE When Levi Thoene was just past six months old, his parents were told he had a rare genetic condition that meant he probably wouldnt reach his second birthday.

Called spinal muscular atrophy, it meant his body couldnt produce enough of a protein that certain nerve cells in his spinal cord need to survive. The condition leads to weakened muscles, including those needed for vital functions like breathing and swallowing.

On Tuesday, Levi turned 2. And in defiance of his earlier prognosis, his parents are seeing signs that hes making gains.

He can now sit up for 15 minutes or more, said mom Morgan Thoene (pronounced Tay-nee) of Ralston. Hes moving his arms and hands more, and he can do more to signal his wants and needs. His cough is stronger, and hes starting to say words, including no, the staple of toddler vocabulary.

Brandon Thoene, left, and Morgan, right, sit with their son Levi sit up during a visit to his doctor at Children's Hospital on Friday, October 18, 2019. Levi, who has spinal muscular atrophy, a month ago received a new gene therapy called Zolgensma and has been recently able to sit up on his own for the first time.

Anything he does is a surprise, and a blessing, that hes doing it as well as he is, said Brandon Thoene, his dad.

A month ago, Levi became the first child in Nebraska to receive a new gene therapy for spinal muscular atrophy called Zolgensma.

Approved by the Food and Drug Administration in May, it made headlines as one of the first gene therapies with the potential to stop the progression of possibly cure a genetic condition.The one-time treatment also comes with a price tag of $2.1 million.

About 1 in 11,000 babies are born with SMA, according to Cure SMA, an advocacy group. There are four main types, with Type 1, the version Levi has, being the most serious of those and the most common.

Before starting the new treatment, Levi had been getting a different therapy called Spinraza, the first drug available to treat the condition.

While Spinraza gives a defective gene in SMA patients an assist, Zolgensma replaces it, said Dr. Geetanjali Rathore, neurology division chief and director of the neuromuscular clinic at Childrens Hospital & Medical Center in Omaha.

No studies have yet been done to compare the two drugs. While plenty of questions remain unanswered, including about the therapies' long-term performance, both are preventing progression of the disease and resulting in improvements, Rathore said.

Dr. Geetanjali Rathore examines Levi Thoene just before his second birthday at Children's Hospital on Friday, October 18, 2019. Thoene has spinal muscular atrophy and recently received a new gene therapy called Zolgensma.

As a result, doctors for the first time have treatments to offer patients and their families, beyond feeding tubes, ventilators and other supportive care.

I think thats huge, thats huge for us and the SMA population, said Rathore, who well remembers her first SMA patient. A beautiful, 6-month-old girl and her parents first child, she was too old for the early Spinraza trials available at the time. She didnt survive her first year.

Last week, Rathore saw Levi for his one-month follow-up since starting the gene therapy. Hes also getting weekly lab tests to check for any side effects and make sure the treatment isnt affecting his liver or heart.

While its still early days, Rathore said shes very pleased with the progress Levi is making. Hes had no side effects and his lab tests are stable.

I am hoping to continue to see much more improvement, she said. Doctors typically see more measurable motor milestones starting at three months after treatment. At six months, they'll do a formal assessment of motor function.

Brandon Thoene, left, fist-bumps his son Levi during a visit to his doctor at Children's Hospital on Friday, October 18, 2019. Levi, who has spinal muscular atrophy, a month ago received a new gene therapy called Zolgensma and has been recently able to sit up on his own for the first time.

Meantime, the availability of treatments is creating new urgency to begin treatment for SMA as soon as possible, before the lack of the needed protein leads to permanent loss of neurons and function.

Unpublished data presented at medical conferences indicates that very young children treated before they develop symptoms all are doing extremely well, developing almost normally, Rathore said.

That calls for earlier diagnosis. Federal health officials added SMA to their list of recommended screenings for newborns in 2018.

The Nebraska Newborn Screening Advisory Committee voted in March to recommend adding SMA to the states newborn screening panel, the tests all babies are given at birth. State health officials anticipate that legislation to require the screening will be introduced in January.Ten states, including Missouri and Minnesota, already have implemented the testing,according to Cure SMA. Iowawilldecide whether to add it in 2021, pending successful completion of a pilot project expected to start next summer.

Rathore, who spoke in favor of adding the test, said the SMA screening can be performed using the same heel-prick blood sample now collected from newborns before they leave the hospital.

The tests, which now check for more than 30 conditions, look for conditions that would not be apparent just by looking at a baby and that can be treated effectively if identified early. Theyre credited with saving babies lives each year and preventing neurological and other developmental delays.

Morgan Thoene said the family plans to push the Nebraska Legislature to add SMA to the panel. She writes about Levis journey on the Facebook group, Life of Levi.

Morgan Thoene, left, comforts her son Levi during a visit to his doctor at Children's Hospital on Friday, October 18, 2019. Levi, who has spinal muscular atrophy, a month ago received a new gene therapy called Zolgensma and has been recently able to sit up on his own for the first time.

Starting therapy before symptoms develop, she said, could head them off. When Levi was diagnosed in April 2018, the Thoenes, both teachers at area schools, knew nothing about the condition. Levi had been hospitalized beginning in March for failure to thrive. He wasnt gaining weight, he didnt cry very loud and his cough was weak. He certainly wasnt as active as his older brother, Elliot, now 5.

Levi began receiving Spinraza, which the FDA approved in 2016, shortly after he was diagnosed. The drug must be injected into the fluid surrounding the spine every four months indefinitely. The cost is estimated at $750,000 for the first year and at $375,000 a year thereafter. Children's so far has treated 18 patients with that drug.

After Zolgensma was approved by the FDA, staff at Children's staff worked hard to get it OK'd internally for use at the hospital, Rathore said. It's federally approved for children under age 2. Levi, who started it Sept. 20, made it just under the wire.

"Spinraza was great because it allowed him to get a lot of gains," Morgan Thoene said. "But this has produced even more."

The gene therapy, given intravenously, is delivered by a virus that has had its genetic material removed. It's replaced with the gene that codes for the lacking protein. But rather than integrating with the patient's DNA, it sits on the side and goes to work to increase production of the protein.

In Levi's case, the costs were shared by Blue Cross Blue Shield of Nebraska and Medicaid.

Multiple studies, she said, found that the cost of caring for patients with SMA Type 1 think ventilators, wheelchairs, hospitalizations significantly outpaced the annual cost of Spinraza. Those studies haven't yet been done yet for Zolgensma, but the therapy is expected to be cost effective in the long term, particularly if it proves to be a one-time therapy.

Efforts are under way to expandboth treatments to more kids. Children's is on the list to become a center for trials of Zolgensma in children older than 2 who have less severe forms of the disease.

The hospital also has begun a study to gauge improvements in quality of life in such patients. That will focus on more subtle but still important changes such as whether patients can eat by themselves and how much help they need to move. It's new territory, Rathore said, because the focus with SMA patientshas for so long been on survival.

The Thoenes celebrated Levi's big milestone at home, just the four of them. They planned tomark the occasion with extended family and friends Sunday with a gathering at an area pizzeria.

For now, they're celebrating the progress he's made.Said Morgan Thoene, "He's doing fantastic."

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Boy, 2, first in Nebraska to receive $2.1 million therapy for rare disorder. 'He's doing fantastic' - Kearney Hub

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Nathaly Sweeney, a neonatologist at Rady Children's Hospital-San Diego and researcher with Rady Children's Institute for Genomic Medicine, attends to a young patient in the hospital's neonatal intensive care unit. Jenny Siegwart/Rady Children's Institute for Genomic Medicine hide caption

Nathaly Sweeney, a neonatologist at Rady Children's Hospital-San Diego and researcher with Rady Children's Institute for Genomic Medicine, attends to a young patient in the hospital's neonatal intensive care unit.

When Nathaly Sweeney launched her career as a pediatric heart specialist a few years ago, she says, it was a struggle to anticipate which babies would need emergency surgery or when.

"We just didn't know whose heart was going to fail first," she says. "There was no rhyme or reason who was coming to the intensive care unit over and over again, versus the ones that were doing well."

Now, just a few years later, Sweeney has at her fingertips the results of the complete genome sequence of her sickest patients in a couple of days.

That's because of remarkable strides in the speed at which genomes can be sequenced and analyzed. Doctors who treat newborns in the intensive care unit are turning to this technology to help them diagnose their difficult cases.

Sweeney sees her tiny patients in the neonatal intensive care unit of Rady Children's Hospital in San Diego. Doctors there can figure out what's wrong with about two-thirds of these newborns without a pricey DNA test. The rest have been medical mysteries.

"We had patients that were lying here in the hospital for six or seven months, not doing very well," she says. "The physicians would refer them for rapid genome sequencing and would diagnose them with something we didn't even think of!"

Rady's Institute for Genomic Medicine, which has been pioneering this technology, has now sequenced the genomes of more than 1,000 newborns.

In a building across the street from the hospital, three $1 million sequencing machines form the core of the operation. Technicians tending to the NovaSeq 6000s can put DNA from babies (and often their parents) into the machine in the late afternoon and have a complete genome sequence back by 11 a.m. or noon the next day, says clinical lab scientist Luca Van der Kraan.

That fact is worth repeating: An entire genome is decoded in about 16 hours.

Kasia Ellsworth is one of the experts waiting in a nearby office to analyze the information. That task has shrunk from months to typically just four hours, thanks to increasingly sophisticated software.

Ellsworth inputs the baby's symptoms into the software, which then spits out a long list of genetic variants that might be related to the illness. She scrolls down the screen.

"I'm looking through a list of those variants and then basically deciding whether something may be truly contributing to the disease or not," she says.

About 40% of the time, a gene stands out, giving doctors a tentative diagnosis. Follow-up tests are often requested, and those can take several days. But in the meantime, doctors can sometimes act on the information they have in hand.

When she or a colleague makes a diagnosis, "You always feel very relieved, very happy and excited," she says. "But at the same time you kind of need to put it in perspective. What does it mean for the family, for the patient, for the clinician as well?"

Often it's a sense of relief. And for a minority of cases, it can affect the baby's treatment.

"We now are at the point where I think the evidence is overwhelming that a rapid genome sequence can save a child's life," says Dr. Stephen Kingsmore, the institute's director and the driving force behind this revolution.

By his reckoning, the results change the way doctors manage these cases about 40% of the time.

Treatments are available for only a small share of these rare diseases. In other cases, the information can help parents and doctors understand what's wrong with their baby even if there is no treatment or learn whether death is inevitable. "And there it's a very different conversation," Kingsmore says. "We help guide parents through picking an appropriate point at which to say enough is enough" and to end futile treatments.

Of course, Kingsmore highlights the happier outcomes. One example is a bouncy girl named Sebastiana, now approaching her third birthday.

As a newborn, Sebastiana Manuel was diagnosed with a rare disease after rapid genome sequencing. She is seen here at 11 months of age. Jenny Siegwart/Rady Children's Institute for Genomic Medicine hide caption

As a newborn, Sebastiana Manuel was diagnosed with a rare disease after rapid genome sequencing. She is seen here at 11 months of age.

He showed off her case recently in front of the Global Genes conference, a meeting of families with rare genetic conditions.

"She was critically ill in our intensive care unit," he tells the audience, "and in a couple of days we gave the doctors the answer. It's Ohtahara syndrome. It comes with this specific therapy. And she hasn't had a seizure in 2 1/2 years. She doesn't take any medication."

The audience applauds enthusiastically at an outcome that sounds miraculous. But when you meet Sebastiana and her mother, Dolores Sebastian, a more complicated story emerges.

Ohtahara syndrome isn't actually what made Sebastiana ill it's a term doctors use to describe newborn seizures. Those are actually a symptom of deeper brain issues. That was apparent the day she was born.

"She was acting weird and screaming and crying and turning purple and we weren't sure why," her mother says.

The hospital where Sebastiana was born rushed her to the neonatal intensive care unit, across town at Rady. She was having frequent seizures. The following days were a nightmare for Sebastian and her husband.

"I can't even describe it," she says. "I always keep on saying that at that moment I was kind of like dead, but I was walking."

The hospital ran a battery of tests to look for severe brain damage. They couldn't get to the bottom of it.

"They came in and offered us the genomic testing," Sebastian said. "They never told us how quick it would be."

She was surprised when the results were back in four days. The doctor told her they had identified a gene variant that can trigger seizures as well as do other harm to the brain.

"He said this is how we're going to go ahead and change her medications now and treat her," she says. And that made a "huge difference, [an] amazing difference."

Sebastiana was already on a medication that was helping control her seizures, but they sedated her to the extent that she needed a feeding tube. On the new medication, carbamazepine, she was alert and able to eat, and her seizures were still under control. Sebastian says her daughter is still taking that drug.

Controlling her seizures isn't a cure. Children who have this genetic variant, in a gene called KCNQ2, can have a range of symptoms from benign to debilitating. Sebastiana falls somewhere in between. For example, she has only a few words in her vocabulary as she approaches the age of 3.

"She took her first steps when she was 2 years old, so she's delayed in some things," Sebastian says, "but she's catching up very quickly. She has [physical therapy]; she's going to start speech therapy. She gets a lot of help but everything's working."

Sebastiana Manuel (second from left) with members of her family: Domingo Manuel Jr. (from left), Dolores Sebastian and Tony Manuel. Jenny Siegwart/Rady Children's Institute for Genomic Medicine hide caption

Sebastiana Manuel (second from left) with members of her family: Domingo Manuel Jr. (from left), Dolores Sebastian and Tony Manuel.

KCNQ2 variants are the most common genetic factor in epilepsy, causing about a third of all gene-linked cases and about 5% of all epilepsies. Sebastiana's case could have been diagnosed with a less expensive test. For example, Invitae geneticist Dr. Ed Esplin says his company offers a genetic screen for epilepsy that has a $1,500 list price and a two-week turnaround.

Rady's whole-genome test costs $10,000, Kingsmore says. But it casts a wider net, so it might provide useful information if a baby's seizures are caused by something other than epilepsy.

And Kingsmore says his test costs about as much as a single day in the NICU. "In some babies we avoid them being in the intensive care unit literally for months," he says.

Kingsmore and colleagues have published some evidence that their approach is cost-effective, based on an analysis of 42 cases.

Even so, most insurance companies and state Medicaid programs are still balking at the cost. Kingsmore says private donors are helping support this effort at Rady, which sequences about 10% of the babies in the NICU, and at more than a dozen others scattered from Honolulu to Miami. They send their samples to Rady for analysis.

Kingsmore is pushing to expand his network in the next few years, to reach 10,000 babies at several hundred children's hospitals.

Other providers are also starting to offer whole-genome sequencing. But Dr. Isaac Kohane, chair of the department of biomedical informatics at Harvard Medical School, worries that the technology is too unreliable.

Knowledge of genes and disease is evolving rapidly, so these analyses run the risk of either missing a diagnosis or making a mistaken one. Kohane says there's still a lot of dubious information there a typical person has 10 to 40 gene variants that the textbooks incorrectly identify as causing disease.

Kohane is part of a medical network that helps diagnose people with baffling diseases. A study from 2018 found "a third of the patients who actually come to us already had full genome sequences and interpretations," Kohane says. "They were just not correct."

Even so, Kohane sees this use in the NICU as a relatively fruitful use of gene sequencing. "This is one of the few areas where I think the Human Genome Project is really beginning to pay off in health care," he says, "but buyer beware, it's not something ready to be practiced in every hospital." (He supports the work at Rady in fact, he is a science adviser.)

Kingsmore is already looking ahead. "We want to solve the next bottleneck, which is, 'I don't have a great treatment for this baby,' " he says. That's a far greater challenge, and it's especially difficult for a mutation that has altered a baby's development in the womb. Those problems may often not be reversible.

Kingsmore is undeterred. "It's going to be an incredibly exciting time in pediatrics," he says.

You can contact NPR science correspondent Richard Harris at rharris@npr.org.

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Genome Sequencing In NICU Can Speed Diagnosis Of Rare Inherited Diseases : Shots - Health News - NPR

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The new horror flick on Netflix, Eli, released just in time for Halloween, borrows from The Exorcist and Rosemarys Baby, with touches of The Shining. And it all takes place in what looks like Downton Abbey with the cleaning staff gone.

Eli works; its scary. But the set-up using gene therapy gone awry is unfortunate, superfluous, and even offensive. (Beware, spoilers ahead)

The film opens with 11-year-old Eli dreaming about being able to go outside without his hazmat suit and breathing without his skin reddening and blistering. He awakens and hes inside, in a bubble.

David was diagnosed, four years earlier, with a rare formof severe combined immune deficiency (SCID). It slashes his ability to make the antibodies that protect against infection, unleashes inflammation that reddens his skin, while at the same time turns his immune system against his own tissues, an autoimmune response.

The parents, caring Rose and weirdo Paul, bundle Eli up to take him to a doctor whos going to cure him with a new treatment. Once at the supposedly clean Downton Abbey haunted house, Eli has a decontamination shower.

When the boy meets the doc, she explains that his immune system makes too many bad immunoglobulins, using that word instead of antibodies because it sounds more technical.Eli quickly responds, spouting out that he has mutations in the RAG1 and RAG2 genes (recombination-activating genes).

Elis body cant make the enzymes that mix and match antibody parts, and the proportions of a bunch of immune system cells and proteins go out of whack. His condition is also called Omenn syndrome.

Dr. Horn has two nurses, and all three of them wear purple uniforms.

Good news! Dr. Horn will administer viral gene therapy! I will make you better, like my other patients, she assures the boy.

Rose gingerly begins to unwrap the blue layers that encase her son, bending down and looking like Laura Dern examining dino poo in Jurassic Park or Princess Leia releasing the hologram from R2D2. Mom and boy can finally hug!!!

At night, the house creaks. Eli wanders the spooky halls, glimpsing kids in the windows, mirrors, and reflections, including ghostly girls who look like the twins at the end of the hallway in The Shining.

A redheaded girl outside, Sadie Sink, apparently escaped from playing Max on Stranger Things, seems real.

Im allergic to the world, Eli tells her. Not exactly.

The next morning, Dr. Horn blames Elis ghost sightings on a side effect from immunosuppressants. Why is she trying to suppress an immune system already so impaired?

Next Eli, who looks so much like Tom Petty that I expected him to shriek I Wont Back Down, is strapped down to a table with a contraption holding his head in place, as Dr. Frankenstein asks her nurses to take a reading.

Dr. Horn at first seems to have gotten the basic idea of gene therapy correct: introducing a working copy of the mutant gene aboard viruses into stem cells from bone marrow. And poof! Like a magic trick! itll work, she proclaims.

She proceeds to extract a hunk of pinkish gunk after drilling into a bone, as the immobilized boy twists and grimaces on the table. Satisfied, the doc plops the glob into a Petri dish.

It burns! Eli shrieks.

That means its working, replies the doc. Within seconds, the doctored viruses have apparently hit their targets.

Then Eli awakens. It all seems a dream, but its foreshadowing.

A ghost appears in a bloody nightgown.

The house breathes at night.

A scrawny, dagger-nailed hand grabs Eli and the apparition turns into his father.

When Eli writes his name on a window, the letters rearrange to spell Lie, like Redrum becoming Murder in the mirror in The Shining. Later on, with the E written like a 3, Eli scratched into various furniture surfaces in the house becomes 317317317. What can it mean?

When Eli reports these events, Dr. Horn barks, Its the medication, as if sophisticated gene therapy has suddenly become as mundane as a tab of Tylenol. Shell have to lower the dosage because the second of the three treatments is coming up.

Treatment 2 is indeed brutal. Eli is held in a contraption like the one Hannibal Lecter wears to keep him from eating people and his head bolted like hes Frankenstein.

Were confident that the gene therapy virus is correcting the mutation, Dr. Horn declares, adding that this will burn a little bit, as she presumably delivers more.

When Eli turns red and screams, she assures him that this is supposed to happen. The virus is penetrating the blood-brain barrier, as if said barrier is a superhighway requiring that the bolts hold his head still.

I was speechless.

Barrier refers to the blood vessels in the brain that are closed to large molecules, which keeps toxins out. A widely-used gene therapy vector, AAV9 (adeno-associated virus 9), has been known for a decade to naturally cross the barrier. And that doesnt require torture hardware.

Heres a photo of one of the kids I write about receiving AAV9 gene therapy for a rare neurological disease through an intravenous delivery in her hand!

The doc then attributes Elis reaction to his body initially rejecting the new cells, like any transplant. But if his gene therapy consists of viruses traipsing across the blood-brain barrier, where did cells suddenly come from? Is it the doctoring of stem cells from bone marrow that was in Elis dream, or delivering viruses into the bloodstream?

Elis nocturnal adventures continue. Hes pushed and pulled from unseen forces as the floor turns transparent, revealing scary medical people. As he keeps bellowing the doc orders Haldol and his mom pushes Valium.

The mysterious 317 opens a key pad to an inner sanctum, which looks like the set of the second Indiana Jones film. We see insects alighting, so the place was never a clean room after all.

Eli finds a notebook with case histories of the past patients and the pieces start to fit. Perry. Agnes. Lucas.

After treatment 2, the kids eyes look haunted, their complexions gray, like Eli. After treatment 3, their heads exploded.

Then the religion clues start to fall out.

Eli discovers a photo of nuns that includes his medical team. A huge iron cross sheaths a dagger. The surgical table with Eli across it resembles Christ on the cross.

One reviewer posits that the plot is about gay conversion, pointing to a scene in which Eli literally crawls out of a closet to tell his parents the truth.

The action speeds up and twists as treatment 3 looms.

Dr. Horn dons religious garb, makes the sign of the cross, flings holy water, and babbles about Jesus and the archangel. The boy, having discovered the medical records, has become a liability.

I thought I could cure Eli. The gene therapy would have worked, if he wasnt so strong. But he cant leave here! the enraged doc yells.

But when Eli is tied down and Dr. Crazy is coming at him with the dagger pulled from the cross, he suddenly summons his inner Regan MacNeil (from The Exorcist) and stops the knife in mid-air, turns it around, and forces the doctor to stab herself. She mutters may you find peace and forgiveness in the name of the Lord, channeling Father Damien KarrasThe power of Christ compels you! as he attempts to exorcise Regan.

With the plunging of the dagger, Eli, red-eyed and screaming, rips off his restraints. His parents are thrown to the floor while the nurses and the doc, somehow still living with the dagger in her chest, try to leave.

But Eli, like Anthony in the cornfield episode of the Twilight Zone, points at them and they turn in unison and then elevate, like Regan rising from her bed. The purple ones then float around the room in an eerie circle emanating an unearthly blue glow, as if theyre on one of those centripetal force amusement park rides.

A conspiracy revealed

It turns out that all are in on whats happening, even the nice-seeming mom. And Eli realizes hes never been sick.

What has she been putting inside me? What have you been putting inside me? he shrieks at his parents, conjuring images of Rosemarysdevil spawn.

At that the nurses and doc suddenly flip upside down, the horror equivalent of Regans rotating head, and slam to the floor.

What am I?

Our son.

Eli sets the nurses and doc on fire.

Are you my dad?

I prayed every day! answers dad.

Prayed to whom? the boy bellows.

The Lord didnt answer me, but your father did, Rose utters mysteriously.

And we know.

Eli never had a SCID. Its a twist on Munchausen Syndrome by Proxy, the cause of his symptoms the holy water that mom and then doc sprinkled on him.

But the ultimate cause? Dad is the devil. At that realization, Eli makes his dads head explode.

The other kids, whose bodies indeed turn up, were Elis half-siblings, even Haley. Dad the Devil got around.

Eli is fun, fast and scary. But why did the writers have to tarnish gene therapy? Why use a genetic disease at all? And especially an ultra rare one? I cant help but wonder what motivated the writers to do this.

Ive devoted the past decade to learning about families who have rare genetic diseases and have kids who have had, or wish they could have, gene therapy, writing about them, and accompanying some of them on their journeys.

In addition to my posts here and at my blog DNA Science, I wrote the only book on gene therapy, The Forever Fix, which chronicles the efforts of a few families. The first gene therapy was FDA-approved in late 2017. The technology has indeed been like the mythical phoenix bird, arising from the ashes.

For the families, I resent the use of gene therapy as a plot point.

After viewing the film the other night, I did a final Facebook check. The first thing that popped up: a photo of an exquisite child, on a page for families dealing with Sanfilippo syndrome, a devastating neurological condition.

The boy was now free of the cruel disease, free to be at peace. He was 11. Elis age.

Genetic disease, and especially attempts to treat it, shouldnt be the stuff of horror films.

Ricki Lewis is the GLPs senior contributing writer focusing on gene therapy and gene editing. She has a PhD in genetics and is a genetic counselor, science writer and author of The Forever Fix: Gene Therapy and the Boy Who Saved It, the only popular book about gene therapy. BIO. Follow her at her website or Twitter @rickilewis

Continue reading here:
Viewpoint: Netflix's new horror movie 'Eli' is a fright. But why did they have to 'tarnish gene therapy'? - Genetic Literacy Project

Recommendation and review posted by Bethany Smith

Two decades ago, a patient with HER2-positive breast cancer had a single targeted drug option. Now a plethora of new and emerging treatments fill the landscape.

BY Meeri N. Kim, Ph.D.

Over the summer, Gulley had noticed a hard lump in her right breast. Having experienced fibroadenomas benign, noncancerous breast lesions in the past, she mostly ignored it. During Gulleys annual gynecological exam in November, even her doctor didnt seem too concerned but asked her to keep an eye on it for the next few weeks. When the lump hadnt gone away by December, Gulley scheduled a mammogram and ultrasound.Although I didnt officially get the diagnosis until January 2018, they were already 100% sure that it was cancer, says Gulley, now 33. I have no family history of breast cancer whatsoever, and I thought at the time that breast cancer was always hereditary, so it was very shocking. Getting that news is really overwhelming, and I had no idea what was to come.

Because of her young age, her doctors wanted to start treatment right away. They took three biopsies, which revealed a subtype of breast cancer known as HER2 positive. Women with HER2-positive breast cancers have tumors with higher levels of a growth-promoting protein called HER2, which stands for human epidermal growth factor receptor 2. As a result, these cancers grow and spread more aggressively than other types of breast cancer. About one out of every five breast cancers has extra copies of the HER2 gene (known as gene amplification) that leads to an overexpression (high levels) of the HER2 protein.

Jennifer Campisano received a diagnosis of HER2- positive breast cancer in 2011, also at an early age. HER2- positive status is more common among younger patients with breast cancer, with mutation incidence at 29.9% in patients ages 15 to 29 and 25.5% in those ages 30 to 39. When Campisano was 32, she and her husband, Chris, had their first child, a boy named Quinn. When he was just 3 1/2 months old, Campisano noticed a walnut-size lump in her right breast.

After two OB-GYNs told her it was probably nothing, she eventually saw a surgeon who sent her straight to the radiology department for a mammogram and ultrasound.

In my head, I still wasnt thinking cancer, but the radiologist told me, Im 99% sure this is cancer, says Campisano, who lives in Phoenix. After the biopsies, they called me and confirmed that it was HER2-positive breast cancer. It was rough. I had to wean my son overnight, which was really painful.

Fortunately, the treatment landscape for this type of disease has evolved considerably over the past two decades, with the development of drugs that target the HER2 protein. Even today, treatment options continue to emerge for patients like Campisano and Gulley, who both received newer agents as part of their regimens for earlier-stage disease and remain cancer-free.

In the past, HER2-positive breast cancer was known as a more aggressive disease with a worse prognosis than HER2-negative breast cancer, says Dr. Janice Lu, clinical professor of medicine at the University of Southern California Norris Comprehensive Cancer Center. But with the development and approval of five drugs now that specifically target HER2, being HER2 positive is no longer any worse for patients than being HER2 negative.

In clinical trials, researchers are testing several other agents for HER2-positive breast cancer with a high likelihood of approval by the Food and Drug Administration (FDA). They are mostly focused on treating patients in the metastatic setting, meaning the disease has spread beyond the breast, and those whose disease is resistant to more commonly used drugs.

A LARGE TOOLBOX OF TREATMENTSIn 1987, oncologist Dr. Dennis Slamon at UCLA discovered that the HER2 protein was present at high levels in certain breast cancers. The protein is also found on the surface of normal breast cells, but some breast cancer cells have 40 to 100 times more HER2, which stimulates the tumor cells to divide and grow. This overexpression of HER2, which became known as HER2 positivity, was linked to a higher likelihood of metastasis and relapse in patients, along with a decrease in overall survival, or the length of life measured from the start of treatment.After this discovery, Slamon and his colleagues had a novel idea: What if HER2 proteins activity could be blocked? Shouldnt that, in theory, halt the aggressive growth of the cancer cells? This train of thought led to the groundbreaking development and FDA fast-track approval of the first drug to target HER2 in 1998. In fact, it was the first drug to target a protein that contributes to the development and growth of any cancer: Herceptin (trastuzumab).

Herceptin is a monoclonal humanized antibody, a laboratory-created molecule that attaches to cancer cells, inhibits the growth factor function of HER2 and attracts attack by the immune system. In a phase 3 clinical trial, adding Herceptin to chemotherapy was associated with more responses, longer time until cancer progression and better survival in patients with metastatic HER2-positive breast cancer compared with chemotherapy alone. In 2006, it was approved with chemotherapy for use after surgery, to help prevent recurrence, in earlier-stage HER2-positive breast cancers.

Herceptin is generally well-tolerated, causing mild to moderate side effects such as muscle aches, dizziness, headache, fever/chills and runny nose. However, it does come with a small risk of cardiotoxicity especially for women who were also treated with anthracycline chemo- therapy which usually manifests as cardiac dysfunction, primarily a condition known as cardiomyopathy, which can lead to congestive heart failure.

We are getting long-term data on outcomes with trastuzumab after its FDA approval 20-plus years ago, and today if women are diagnosed with HER2-positive breast cancer, we can tell them their prognosis is as good as those with HER2- negative disease, says Dr. Sara Hurvitz, a medical oncologist at UCLA. Although trastuzumab has leveled the playing field, it isnt a cure for 100% of patients by any means. For early-stage cancer that recurs as metastatic disease, trastuzumab can improve outcomes and help patients live with the disease, but it does not cure, for the most part.

More recently, patients have also benefited from a newer HER2-targeting therapy called Perjeta (pertuzumab), which was approved in 2012. Similar to Herceptin, Perjeta is a monoclonal antibody that attaches to HER2 receptors on the surface of breast cancer cells and prevents them from receiving growth signals. It targets a different area on the HER2 receptor than Herceptin, which means it can act as a complementary treatment or serve as an alternative therapy for Herceptin-resistant disease.

This drug is used in both earlier-stage and metastatic HER2-positive breast cancers.

For women with early-stage HER2-positive breast cancer, the standard of care is currently chemotherapy plus Herceptin. Typical chemotherapy regimens include AC-TH, or Adriamycin (doxorubicin) and Cytoxan (cyclophos- phamide), followed by a taxane that is given concurrently with Herceptin. Recently, it has become more common to use TCHP, which includes docetaxel and carboplatin given concurrently with Herceptin and Perjeta.

This minimizes the cardiac risks associated with Adriamcyin along with Herceptin. Patients on either regimen will end with Herceptin (and Perjeta if used with chemotherapy) after completing the chemotherapy portion, such that a full year of antibody therapy is given.

In the metastatic setting, the standard of care for initial treatment is a combination of Herceptin, chemotherapy and Perjeta. Studies have found that 15% to 25% of patients with early-stage, HER2-positive breast cancer eventually experience metastatic recurrence after initial treatment. Then, the prognosis is poor, with most recurrences involving incurable metastatic disease, although some patients can survive for many years with their cancer controlled by several available medications.

In the metastatic setting, were not curing the vast majority of patients with HER2-positive disease, and resistance does occur, says Dr. Sara Tolaney, associate director of the SusanF. Smith Center for Womens Cancers at Dana-Farber Cancer Institute in Boston. But patients continue to live longer because they can go from one treatment to the next. There are now multiple options to go to as resistance develops, and there are also clever ways to overcome resistance.

In 2012, Campisano started the TCH regimen along with surgery and radiation therapy. When it looked like her cancer recurred, her doctors gave her newly approved Perjeta, along with Herceptin and chemotherapy. Less than a week after her 2018 wedding, Gulley was also treated with Perjeta in conjunction with the AC-TH regimen following her mastectomy. The agent had already been approved for more than five years to treat both metastatic HER2-positive breast cancer and early-stage disease prior to surgery, and in 2017 it won approval to be given after surgery for early-stage disease.

I was on Perjeta for a year, and my doctors warned me about diarrhea being a common side effect, Gulley says. I definitely noticed that in the beginning of treatment, but my body got used to it, I guess, because at the end of the year, I wasnt as bad. I used over-the-counter Imodium and things like that to combat it.

With the combination of Perjeta and Herceptin, Campisano experienced very mild side effects itchy skin and a runny nose but they were nothing compared to how she felt during chemotherapy. Unfortunately, her scans still showed what looked like cancer after her initial treatment, so she started on Kadcyla (ado-trastuzumab emtansine, also known as T-DM1).

Kadcyla is a type of antibody-drug conjugate, an emerging class of agents comprised of an antibody linked to a highly potent anti-cancer drug. They combine the heat-seeking ability of targeted therapy with the cancer-killing power of chemotherapy. In 2013, Kadcyla was approved for patients with metastatic HER2- positive breast cancer who were previously treated with Herceptin and taxanes. Earlier this year, it gained approval for use in the adjuvant (postsurgical) setting for early-stage disease. Common side effects include fatigue, nausea, bone and joint pain, muscle pain and constipation.

In the phase 3 KATHERINE study, Kadcyla given after surgery significantly reduced the risk of invasive breast cancer recurrence or death from any cause by 50% compared with Herceptinin patients who had residual disease after neoadjuvant (presurgical) therapy. An analysis showed that of 1,486 patients in the trial, 165 in the Herceptin group and 91 in the Kadcyla group had experienced invasive disease or death. In addition, at three years, 88.3% of those who took Kadcyla versus 77% of those who took Herceptin were free of invasive disease.

Campisano took Kadcyla for almost three years. In 2016, a lung biopsy revealed that what had appeared to be cancer in her lungs was actually an autoimmune disease that can mimic cancer on scans. She was taken off treatment and finally tested cancer-free. Even if she didnt need T-DM1, she refers to it as a wonder drug.

Another option in both early-stage and metastatic HER2- positive breast cancer is Nerlynx (neratinib). In early-stage disease, the drug is approved for extended postsurgical therapy after chemotherapy and Herceptin to reduce the risk of recurrence. Nerlynx is a kinase inhibitor, which blocks enzymes that promote cell growth. Specifically, it inhibits the activity of HER2 and other enzymes in its family. In a phase 3 clinical trial, 94% of those who took Nerlynx experienced no disease progression over two years versus 91% in a placebo group. Common side effects included diarrhea, vomiting and nausea.

The results from a more recent phase 2 trial showed that combining Nerlynx with a chemotherapy drug called capecitabine has an effect on patients with HER2-positive breast cancer who have brain metastases.

Neratinib is notable because it has activity with HER2- positive brain metastases, which occurs in about 50% of patients with metastatic disease, Tolaney says. It already has FDA approval in the adjuvant setting for patients who have completed a year of trastuzumab, and it will likely get approval in the near future for the metastatic setting based on the results of the trial.

Finally, the kinase inhibitor Tykerb (lapatinib) was approved in 2007 for the first-line treatment of HER2-positive metastatic breast cancer, first with the chemotherapy Xeloda (capecitabine) and later with the hormone-blocking drug letrozole for postmenopausal women with hormone-driven breast cancer that over- expresses the HER2 receptor. A 2009 study showed that adding Tykerb was associated with a 5.2-month increase in median time without disease progression compared with taking letrozole alone (8.2 months with the drug combination versus 3.0 months with letrozole only).

NEW DRUGS HOLD PROMISEPatients have a lot of options, and there are multiple new therapies in clinical trials, some of which are very prom- ising, Hurvitz says. Three in particular deserve mention: tucatinib, a pill that appears to be safer than neratinib and lapatinib because it doesnt cause as much diarrhea; DS-8201, another antibody-drug conjugate with a different chemo payload than Kadcyla; and margetuximab, which is similar to trastuzumab.

All three investigational agents have shown tremendous promise in fighting HER2-positive disease and are expected to gain FDA approval in the near future. The HER2CLIMB trial is currently investigating tucatinib, a HER2-specific tyrosine kinase inhibitor, with Herceptin andcapecitabine in patients with metastatic HER2-positive breast cancer. It can penetrate the blood-brain barrier better than antibody drugs like Herceptin and Perjeta and demonstrated abrain-specific response in five of 12 patients with brain metastases. Hurvitz expects tucatinibto gain FDA approval within the next six to 12 months.

DS-8201 (trastuzumab deruxtecan) links Herceptin with a chemotherapeutic drug a topoisomerase inhibitor called deruxtecan, which interrupts DNA replication in cancer cellsand is guided more specifically to HER2-positive cells while mostly sparing normal cells.

The FDA granted this experimental antibody-drug conjugate breakthrough therapy designation, expediting its development and review, as a potential treatment for patients with HER2-positive, locally advanced or metastatic breast cancer who have been previously treated with Herceptin and Perjeta and have disease progression after T-DM1. In a phase 1 study, 54.5% of HER2-positive women treated with DS-8201 saw their cancer respond to the drug.

DS8201 is an up-and-coming drug that everyone is very excited about. It delivers a different payload into the cancer cell than TDM-1 and also uniquely allows for the bystander effect, Tolaney said. This means that some of the drug that enters one cancer cell can pass through its cell membrane into neighboring cancer cells, which then kills them.

A more recently studied monoclonal antibody, margetuximab, has been described as an optimized version of Herceptin. A section of the antibody was engineered to better engage the immune system in fighting the disease. In the phase 3 SOPHIA trial, patients with metastatic HER2-positive breast cancer who took the investigational drug with chemotherapy had a median progression-free survival of 5.8 months compared with 4.9 months for those treated with Herceptin and chemotherapy.

These new drugs are rising stars in the metastatic setting, and many other agents are currently being tested, Lu says. Patients with HER2-positive breast cancer should discuss with their doctors what is the standard of care, next steps for treatment, any clinical trials that are potentially available and, of course, possible side effects.

Although they continue to adjust to a new normal after cancer, Gulley and Campisano are grateful to be cancer-free and hopeful about the growing availability of treatment options for their disease. Gulley had a left-side mastectomy in February of this year, after a mammogram revealed calcifications in her remaining breast. She was also put into a chemical menopause at age 33, which means hot flashes, night sweats and fatigue.

After my wedding, instead of going on a honeymoon, I started my chemotherapy. This has all been such a whirlwind, Gulley said. Being newly married, its really hard. Menopause has a lotof bad side effects, sexually and otherwise. That fear of recurrence is always there too, but Im so thankful for the two medicines that were available to treat me.

Campisano also went through early menopause, induced by chemotherapy. She eventually emerged from that menopause and, surprisingly, became pregnant with her second child. But the chaos of having a newborn, then a cancer diagnosis and treatment, followed by another baby left her physically and mentally exhausted.

I dont think I had time to process anything in the beginning. My husband and I had not even been married three years when I was diagnosed, and today Im left with range-of-motion issues, body image issues, a bilateral mastectomy and post-traumatic stress disorder, Campisano says. I know that we dont have a cure for metastatic HER2-positive breast cancer, but its wonderful that these new drugs do work for some people.

Read the rest here:
From One to Many: The Growing Treatment Landscape of HER2-Positive Breast Cancer - Curetoday.com

Recommendation and review posted by Bethany Smith

Dr Mukesh Batra, the owner of Dr Batras clinics.

Mitchelle DSouza, Sub-editor/Reporter

The founder and chairman of Dr Batras group of companies, Dr Mukesh Batras name has become a byword for homeopathy.

The pioneering Indian doctor-cum-entrepreneur has built a legacy which includes a network of clinics, day-care aesthetic centres, and health and wellness products.

We caught up with Dr Batra at his Healthcare City clinic in Dubai, where he spoke at length about the workings of homeopathy and introduced us to the new Geno-Homeopathy treatment launched by the brand.

Can you explain what homeopathy treatment is for those who dont have a clear understanding? How does it work in comparison to conventional medicine?

Theres actually a misconception that its not well known. For emergencies and conventional problems, allopathy is the go-to. Like a heart attack, surgeries, gunshot wounds and so on.

However, homeopathy is safe for anything that is chronic and long lasting such as psychosomatic problems like stress, anxiety, and depression related issues; allergies, skin and hair problems.

We treat a wide range of illnesses such as asthma, arthritis, anxiety, depression, backache, cervical spondylitis, kidney stones in primary stage, warts, piles, PCOD, nasal polyps etc.

It has no side-effects and is completely painless and non-invasive. It goes to the root of the problem, nipping it in the bud, rather than just supressing it temporarily with pain killers.

"People are getting disillusioned with chemical medication, its side effects and opting for substances that are natural and safe, and holistic remedies, which homeopathy includes.

Is it true that homeopathy is slower in addressing an ailment in comparison to allopathy?

Its partly true, but not entirely. If you come to allopathy for a chronic sinus problem, you pop a pill and supress it. Similarly for a skin allergy, an ointment will supress the symptoms. The moment you stop, it flares up again.

So when you look at suppression, it is quick in allopathy, but thats not a cure. In conventional medicine, treatment is as slow as homeopathy or maybe even slower

For instance, a patient may be supressing his/her migraine or skin problem for the last 10 years with allopathy by taking pain killers and anti-inflammatories but without a proper solution.

However, if he/she were to take homeopathy for just 10 months, it would cure it, and hence that makes it much faster and effective as it gets to the root of the cause.

The reason it may feel seemingly long is because most illnesses are chronic, long-standing and deep-rooted.

Geno-Homeopathy treatment employs a gene test to predict, pre-empt and treat an illness. Charles Bertram/TNS

Can you give us an insight into the new Geno-Homeopathy treatment launched in the UAE?

As you may be aware, genetic DNA studies have been around for some years and have become more popular off late, thanks to Angelina Jolie creating awareness by positively testing herself for a cancer gene.

This helps predict and pre-empt an illness. How this works is that you have genes that are inherited, with 99.9 per cent of them being normal. But 0.1 per cent genes can be faulty and that percentage decides what diseases we carry.

A gene is like a finger print, it never changes. So just like you would use your finger print or pupil for identity, this is used for gene mapping through a simple sputum test. Now that 0.1 percentage gene decides how healthy I can be and which diseases I am likely to suffer from.

So with Geno-Homeopathy we can now analyse those 0.1 per cent genes. We completed one year in India in September and did 15,000 cases of genetic mapping.

This technique gives you your disease propensity and can tell you, for example, whether youll go bald five or 10 years from now; if youre prone to heart attack or diabetes it will tell you when youre likely to get it.

Post an analysis, a homeopathic treatment is offered to the patient to treat a condition. So this can be almost life-saving and is now within peoples reach in the UAE.

Angelina Jolie found out through genetic testing similar to Geno-Homeopathy that she is at a high risk of developing breast cancer.Marechal Aurore/TNS

There are a lot of cynics out there who question the scientific basis of homeopathy. What do you have to say to that?

A research we conducted three to four years ago found that a majority of people in Indian metros were taking homeopathy as the first choice of treatment. Pharma is growing at 10 per cent while homeopathy is growing at 30 per cent all over the world.

People are getting disillusioned with chemical medication, its side effects and opting for substances that are natural and safe, and holistic remedies, which homeopathy includes.

To give you a little perspective, there are around 300 people dying of drug reaction in America alone everyday which is equal to a Boeing crash. But it doesnt get as much attention, which can be pinned on the strong medical lobby.

So theres a gradual shift happening from allopathy to homeopathy not just in India but all over the world.

That being said, there are a lot of cynics and the lobbies that plant various stories. In spite of all this homeopathy is growing exponentially. The proof of the pudding is in eating it, so people should give it a try before denouncing it.

See the article here:
Dr Batra's have launched a new genetics-based therapy that predicts future diseases - Gulf Today

Recommendation and review posted by Bethany Smith

The statistics are all too clear Black women in the U.S. are 42% more likely to die from breast cancer than white women, according to 2016 findings from the American Cancer Society. In fact, one in nine African-American women will be diagnosed with the disease in her lifetime. These numbers are far more frightening when you consider that Black women are often subject to discriminatory practices that impact the care they receive from medical professionals. Yet every day, Black women who find themselves face-to-face with this battle suit up and fight like hell. And many of them are winning.

Dr. April Spencer, the founder of Dr. Spencer Global Breast Health & Wellness Center in Atlanta and a Know Your Girls ambassador, spoke to ESSENCE exclusively about just how much breast cancer is impacting Black women and girls. What makes African-American women unique is that the younger women, defined as women before the age of 45, have the highest rate of new breast cancer incidents, she says. That is alarming, and it is what makes our desire to [encourage] Black women to receive mammograms and testing even more significant.

Reducing your risk of breast cancer involves several factors, and Dr. Spencer breaks it all down for us, simple as ABC.

A Is For Awareness

You need to be aware of your body, your breasts, and what they feel like. Be aware of changes to your breast size, shape and changes to the skin underneath your arms. Ive had lots of patients diagnosed with breast cancer who didnt suspect it because they didnt have a lump.

B Is For Behavior

There are things that women can do to lower their risk of breast cancer. They including maintaining a healthy weight, exercising daily and limiting alcoholic intake. In terms of your culinary choices, be mindful of what youre eating. Theres no magic bullet in terms of the best diet, but there has been lots of research on the benefits of a Mediterranean diet, which is high in healthy fats like olive oil, and unsaturated fat like salmon. Every time you sit down [to eat], youre either feeding disease or fighting disease. Also, women who have undergone menopause should limit their use of hormone therapy, as it can increase your risk.

C Is For Chemoprevention

Chemoprevention is just some women that may have the breast cancer gene may not be prepared to do a surgical option like removing their breast or removing their ovaries, but there are certain medications that can block the hormone estrogen that has been known to feed breast cancer, and so those medications, they have risks, so its important to talk to your doctor about the risk versus benefit of taking those medications, but that can lower the risk as well.

So ABC. Awareness of the body, B is behavior, and C is chemoprevention.

This article originally appeared in the October 2019 issue of ESSENCE Magazine, on newsstands now.

The rest is here:
Dr. April Spencer's ABC's Of Breast Cancer Prevention - Essence

Recommendation and review posted by Bethany Smith

I never imagined every woman in my family would get breast cancer. It started in 1998 when my aunt was diagnosed at 58-years-old. In 2010, my mom was diagnosed at 65. Two years later, my cousin (my aunts daughter) was diagnosed at 42 with Stage 1 Triple Negative breast cancer, the most aggressive and fastest-growing type. Had it been discovered just a year later, it would have grown to Stage 4. I joined the club in 2014, just two weeks shy of my 35th birthday. All four of us tested negative for the BRCA gene mutation.

In the simplest terms, thats code fortheBReastCAncer geneand is split into two categories: BRCA1 and BRCA2. Though we all have BRCA genes, they are believed to increase a persons chances of developing the disease when mutated. Dr. Sunil Hingorani, a family friend and pancreatic cancer specialist, once told me It doesnt mean there isnt a gene link, it just means they havent found the gene yet.Eek. Then I thought, Oh, maybe theyll name it after us. Cool. Wait. Nope, not cool.

After being told we werent BRCA gene mutation carriers, I morphed into a boob spy named Erin Boobivich to investigate exactly what the culprit was. My cousin believes it has something to do withthe water in Connecticut. Not only had each of us lived there for at least 30 years prior to our diagnosis (Boobivich knows her number-crunching); its also home to some of the countryshighest breast cancer rates. My brother thinks the microwave we grew up using is to blame. My mom thinks my aunt got it from eating too much barbecue. Im convinced it has something to do with potato chips. (What?! Theyre a carcinogen! I read an article once and now I dont eat potato chips). Okay, thats the extent of my research, but it could be all or any of those things, plus a bag of genes.

Reasoning aside, whats really worth sharing goes beyond statistics. Ultimately,breast cancercompletely changed our lives collectively and individually. And while its important to share the commonalities weaved throughout, our individual experiences carry lessons that should be amplified, too.

My aunt, who left India for America in the 70s, was diagnosed withHER2 neu positive, a very aggressive type of breast cancer. She had a lumpectomy (aka breast-conserving surgery that removes abnormal tissue) and more than 20 lymph nodes removed to determine if it had spread throughout her body. This was followed by debilitating chemotherapy that left her extremely ill for months. From the outside, you could never tell she was in pain because her sense of humor made cancer seem fun. She was always upbeat and cracking super inappropriate jokes, like the one where she called me in 2003 and joked her cancer was back, then cackled loudly and said she was kidding.Ha. Ha.

During chemo, she chose not to wear a wig, and insteadwore headwrapsand proudly flew bald. She just didnt seem to care. Her hair never really grew back. If you ask my aunt to take a picture with you today, she will refuse, claiming she hates pictures. The truth is cancer changes how you feel about your body. Her hair didnt grow back to its former glory, but thankfully, neither did her cancer. She just hit her 21 year clear MRI on October 8, 2019.

My moms cancer washormone-based. She was told by a doctor that she would need a lumpectomy, radiation and chemotherapy. Our family friend Dr. Hingorani insisted she go toDana Farber, a renowned cancer institute in Boston, for a second opinion. My mom balked at it, but my father and Hingorani insisted. Its a good thing she listened. The doctors there confirmed chemotherapy wouldnt be beneficial. At all. Had she gone through with it, she would have lost her hair and who knows what else. forNo. Benefit. At. All. With that being said, get second opinions. Get thirds. Make sure you have all the info you need.

By the way, after her lumpectomy and radiation, Mom was put onArimidex, a drug specifically for post-menopausal women to reduce the risk of cancer coming back. She just hit 9 years clear and was told on October 9, 2019 that she no longer needs to take it.

My cousin was diagnosed in November 2012 in early November and went through at least 5 biopsies well into 2013. Because her cancer was especially aggressive, a combo of lumpectomy, radiation, and chemotherapy was the only choice. At the time her children were 11, 9 and 7 years old, respectively.

At our Christmas dinner, a month before she began chemotherapy, I remember asking if I could get a picture of her, my aunt and the kids with my new camera. Priya responded, Sure, since itll be the last time I have hair like this. And she was right. Her hair has never returned to what it was that day.

She endured 8 rounds of chemo within 4 months and each infusion took 4 to 6 hours. We took turns accompanying her to Boston. Her husband, Douglas, did the first round. But when he tried to unplug the chemo machine to charge his Blackberry, lets just say he wasnt invited to return.

Priyas hair fell out, her nails turned blue, and her eyebrows disappeared. My cousin is a very strong and stoic individual to a fault. She never wanted to admit she was in pain or needed help. I understood. With three young children, she didnt want them to feel unsafe or think that their mother was dying. One morning she couldnt protect them from what was going on, and while they were having breakfast, she fainted in the pantry. Thankfully, Douglas wasnt charging his Blackberry, ran to the pantry, and moved the kids out of the kitchen so he could help her. He was scared. So were the kids.

She was told that chemotherapy would only improve her chance of no recurrence by 3-5%. It seems like nothing right? But with three kids, she said she would do whatever was necessary. Today, shes 7 years clear. But in addition to her hair thinning, chemo also affected her brainspecifically her attention span and memory. It took her two years to be able to get through a long book again. And like a lot of women, chemo threw her into early menopause at just 43.

My mother and I got the exact same type of cancer. Same boob. Same exact spot. Like mother, like daughter. The only difference was age; my diagnosis came much earlier in life (30 years before Mom, to be exact.) It sucked. I always thought Id have children of my own. Unfortunately, this diagnosis changed that.

Prior to getting the bad news, everyone in my family begged me to get screened; specifically, after my cousins diagnosis. I finally did a year later. I thought there was no way I could to get cancer at such a young age. Thats what we all thought.

But then they saw something on my right boob. After two mammograms, 1 ultrasound and a biopsy, I got an all-clear. Phew. Relief. No cancer. But then something strange happened. In my right underarm, I got a swelling that was extremely painful. So on Christmas day, my uncle drove me around to see if we could find an urgent care center. The doctor who had previously ordered my biopsy, asked for an MRI. It revealed everything was fine on the right breastand a tumor on the left. The latter was missed on two mammograms and an ultrasound.

My mom said when I called her on March 4, 2014 to break the news, it was one of the most shocking moments in her life. I remember bursting into tears and Im not a crier. That doctor told me, So listen, you can get a lumpectomy, radiation, maybe chemo. Or you can just get a mastectomy and not have to worry about any of that. Wow. (That was the most glossed-over statement that was ever said to me). My cousin called Dr. Alexandra Heerdt, her breast surgeon atMemorial Sloan Kettering Cancer Center, who later told me a mastectomy wasnt something shed recommend.

By the time my lumpectomy was done on April 9, 2014, I had been through 2 mammograms, 2 ultrasounds, and 3 biopsies. Two days after my surgery, I developed cording, despite only having 3 sentinel nodes removed. Its a traumatic reaction your body has when the muscles and nerves in that same area wrap around each other. It was one of the most painful experiences of my life and took 5 months of physical therapy to treat.

Radiation nukes everything. The doctors told me if I ever had kids, I wouldnt be able to breastfeed on my left side. It also charred my boob and literally turned it black. Thankfully, my cancer had not spread, so chemotherapy was eliminated. However, I had to go on a drug (like Mom) to inhibit the hormones that caused my cancer in the first place.

My doctor initially recommended shutting down my ovaries for 5 years. What the ever loving?! Yes, thats correct. He went over the side effects, which include but arent limited to hair loss, decreased libido, and joint pain. No thanks. So I talked to Dr. Rachel Freedman, my other doctor at Dana Farber (who also happens to be my cousins oncologist). She said the research wasnt there to confirm ovarian shutdown as the best option. Instead, she recommended I start withTamoxifenand if a new study was done on ovarian shutdown, I could switch. A few weeks later, a new study became available and my main oncologists recommendation aligned with Dr. Freedmans.

He also said pregnancy is a hormone storm for your body. You cant for at least 5 years. That was probably the hardest thing to hear. I chose to not freeze my eggs, because quite frankly, getting rid of cancer and going through treatment was enough to deal with at the time. I worry that I will regret this decision.

This year, I hit 5 years clear. I will have to take Tamoxifen for a total of 10 years, or until Im 46. Ill probably enter menopause shortly before or after that. It sucks. Thankfully, Tamoxifen hasnt thrown me intoearlymenopause; at least not yet. For this reason, I actually get excited for the period I used to curse each month. As long as Im still getting it, maybe theres still a chance I can have kids.

My cousin Priya has two daughters, Bella, age 16 and Emma, age 14. About 2 months ago, we were out to lunch with my Aunt Veena, their grandmother. The topic ofbreast cancercame up, and Emma, Bella and I made some jokes as our family is apt to do. My aunt looked horrified, and Emma lightly said, What Nani? We know were probably going to get it.

I hope they never join this club. And with research and progress over the next few years, maybe they wont. Today, all of us are diligently scanned and have annual MRIs and mammograms. I have blood tests every 3 months. And when we get clear tests, we text our family group chat to report the news because were all scared on some level. The fear that its going to come back never goes away. Sometimes, the further I get from it, the more I fear I experience.

So cancer does change things. A lot. But with a good boob squad friends, family, and doctors it will be ok. My friends saved me when I was going through all of this. In fact, this post-it my friend Marisa found on her desk from 2014 says it all. (Seriously, if you get cancer, you can get your friends to do stuff for you). And remember, every day they are discovering new genes and new treatments. So get your mamms, maams.

View post:
Every Woman in My Family Had Breast Cancer & None of Us Have the BRCA Gene Mutation - SheKnows

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Healthcare is an industry that is currently being transformed using the latest technology, so it can meet the challenges it is facing in the 21st century. Technology can help healthcare organizations meet growing demand and efficiently operate to deliver better patient care. Here are 9 technology trends that will transform medicine and healthcare in 2020.

The 9 Biggest Technology Trends That Will Transform Medicine And Healthcare In 2020

AI and Machine Learning

As the world population continues to grow, and age, artificial intelligence, and machine learning offer new and better ways to identify disease, diagnose conditions, crowdsource and develop treatment plans, monitor health epidemics, create efficiencies in medical research and clinical trials, and make operations more efficient to handle the increased demands on the healthcare system. By 2020, medical data will double every 73 days. McKinsey estimates that there could be $100 billion in annual savings for medicine and pharma by leaning on big data as well as the artificial intelligence and machine learning tools to process it. Artificial intelligence algorithms powered by recent advances in computational power learn from the data and can predict the probability of a condition to help doctors provide a diagnosis and treatment plans. Ultimately, AI and machine learning can assist with many clinical problems as long as governing and regulatory bodies can determine how to regulate the use of algorithms in healthcare.

Robotics

When it comes to life or death, would you trust a robot with yours? Currently, collaborative robotssuch as the da Vinci surgical robot are already assisting humans with tasks in the operating room. However, the potential for robots in healthcare expands beyond surgical uses. With tremendous growth expected in the industrythe global medical robotics market is expected to reach $20 billion by 2023theres no doubt that robots used in healthcare will continue to conduct more varied tasks. These already include helping doctors examine and treat patients in rural areas via telepresence," transporting medical supplies, disinfecting hospital rooms, helping patients with rehabilitation or with prosthetics, and automating labs and packaging medical devices. Other medical robots that are promising include a micro-bot that can target therapy to a specific part of the body, such as radiation to a tumor or clear bacterial infections.

Computer and Machine Vision

Training computers to "see" the world and understand visual input is no small feat. Since there has been significant progress in machine vision, there are more ways computers and machine vision are being used in medicine for diagnostics, viewing scans and medical images, surgery, and more. Machine vision is helping doctors definitively know how much blood a woman loses in childbirth so that appropriate care can be given to reduce the mortality of mothers from post-partum hemorrhaging. Computers provide accurate intel, while previously this was a guessing game. The applications where computers are being used to view CT scans to detect neurological and cardiovascular illnesses and spot tumors in X-ray images are growing rapidly.

Wearable Tech

Wearable fitness technology can do much more than tell you how many steps you walk each day. With more than 80% of people willing to wear wearable tech, there are tremendous opportunities to use these devices for healthcare. Today's smartwatches can not only track your steps but can monitor your heart rhythms. Other forms of wearable devices are ECG monitors that can detect atrial fibrillation and send reports to your doctor, blood pressure monitors, self-adhesive biosensor patches that track your temperature, heart rate, and more. Wearable tech will help consumers proactively get health support if there are anomalies in their trackers.

Genomics

Artificial intelligence and machine learning help advance genomic medicinewhen a person's genomic info is used to determine personalized treatment plans and clinical care. In pharmacology, oncology, infectious diseases, and more, genomic medicine is making an impact. Computers make the analysis of genes and gene mutations that cause medical conditions much quicker. This helps the medical community better understand how diseases occur, but also how to treat the condition or even eradicate it. There are many research projects in place covering such medical conditions as organ transplant rejection, cystic fibrosis, and cancers to determine how best to treat these conditions through personalized medicine.

3D Printing

Just as it's done for other industries, 3D printing enabled prototyping, customization, research, and manufacturing for healthcare. Surgeons can replicate patient-specific organs with 3D printing to help prepare for procedures, and many medical devices and surgical tools can be 3D printed. 3D printing makes it easier to cost-effectively develop comfortable prosthetic limbs for patients and print tissues and organs for transplant. Also, 3D printing is used in dentistry and orthodontics.

Extended Reality (Virtual, Augmented and Mixed Reality)

Extended reality is not just for entertainment; its being used for important purposes in healthcare. The VR/AR healthcare market should reach $5.1 billion by 2025. Not only is this technology extremely beneficial for training and surgery simulation, but it's also playing an important part in patient care and treatment. Virtual reality has helped patients with visual impairment, depression, cancer, and autism. Augmented reality helps provide another layer of support for healthcare practitioners and aided physicians during brain surgery and reconnecting blood vessels. In mixed reality, the virtual and real worlds are intertwined, so it provides important education capabilities for medical professionals as well as to help patients understand their conditions or treatment plans.

Digital Twins

A digital twin is a near real-time replica of something in the physical worldin healthcare, that replica is the life-long data record of an individual. Digital twins can assist a doctor in determining the possibilities for a successful outcome of a procedure, help make therapy decisions, and manage chronic diseases. Ultimately, digital twins can help improve patient experience through effective, patient-centric care. The use of digital twins in healthcare is still in its early stages, but its potential is extraordinary.

5G

As the capabilities for healthcare centers to provide care in remote or under-served areas through telemedicine increase, the quality and speed of the network are imperative for positive outcomes. 5G can better support healthcare organizations by enabling the transmission of large imaging files so specialists can review and advise on care; allow for the use of AI and Internet of Things technology; enhance a doctor's ability to deliver treatments through AR, VR and mixed reality; and allow for remote and reliable monitoring of patients.

These technologies offer incredible opportunities to provide better healthcare to billions of people and make help our healthcare systems cope with the ever-increasing demands.

Originally posted here:
The 9 Biggest Technology Trends That Will Transform Medicine And Healthcare In 2020 - Forbes

Recommendation and review posted by Bethany Smith

Photo courtesy of Bacan Family

Brynlee Bacan, five, was diagnosed with Rett Syndrome when she was 18 months old.

Posted: Friday, November 1, 2019 10:59 am

Community awareness and a local familys strength By Kelly Riibe Leadercourier-times.com

Nicole Bacan, of McCook Lake, is seeing purple this month and not just because her three daughters attend Dakota Valley. October is Rett Syndrome Awareness Month and it is recognized by wearing the schools popular purple color. Raising awareness means a lot to Bacan and her husband, Brett, because their youngest daughter, Brynlee, was diagnosed with Rett Syndrome in 2016.

Its considered a neurodevelopmental disease or disorder, and it is a mutation of a gene, Bacan detailed. Its the MECP2 gene on the X chromosome. And that apparently makes a protein, and its in the brain, and it goes to all the systems, which is why all the systems are affected.

Rett Syndrome is rare and usually found in girls. Babies with Rett typically do not show signs of concern until they are six-12 months, or older, and begin to miss or lose ground with developmental milestones.

We didnt notice anything until she was almost one and not crawling yet, Bacan recalled. So we knew that there was something physically that we were missing. We talked to our doctor. We got set up with early intervention services with physical therapy coming into the home. And then the physical therapist actually was the one who had noticed that she [Brynlee] had a little bit of a head tremor when she would stand her up... and thats indicative of neurological stuff.

See full story in this weeks Dakota Dunes / North Sioux City Times.

Posted in News on Friday, November 1, 2019 10:59 am.

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Community awareness and a local family's strength - Leadercourier-times.com

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A committee for the US Food and Drug Administration now recommends that the approval of Makena, a drug used to reduce the risk of preterm births, should be withdrawn and some women who have used the medication are sounding the alarm.

The 9-7 vote, which took place at a meeting of the Bone, Reproductive and Urologic Drugs Advisory Committee on Tuesday, came in response to evidence suggesting that the drug was not effective.

The committee serves as an advisory group to the FDA and the voting results are not binding, said Dr. Walid Gellad, director of the Center for Pharmaceutical Policy and Prescribing at the University of Pittsburgh, who was not involved in the committee meeting.

Most of the time the FDA will make a decision that aligns with the committee, but not always, Gellad said.

One study showed FDA will go against the committee about 20% of the time. But the committee did vote that removal of the drug from the market was warranted, which is relevant for supporting any FDA decision about withdrawal, he said.

An FDA spokesperson confirmed in an email on Thursday that the committee voted 13-3 that there is not substantial evidence of effectiveness of Makena in reducing the risk of recurrent preterm birth, based on findings from two trials that were part of a study called PROLONG, published last week in the American Journal of Perinatology.

Nine members of the committee voted to pursue withdrawal of approval for Makena, and seven members voted to leave Makena on the market under accelerated approval and require a new confirmatory trial.

None voted to leave the drug on the market without requiring a new confirmatory trial.

Makena, sold by AMAG Pharmaceuticals, is a progestin hormone that gets delivered to a patient as an injection. In 2011, the FDA approved the medicine to reduce the risk of preterm birth in women who have a history of spontaneous preterm birth under the provisions of accelerated approval regulations.

Accelerated approval is a mechanism for drugs to be approved by FDA before they have proven benefit. They need to address a high need clinical condition for which there are no or few other therapies, like premature birth, and they have to show some effect on a surrogate outcome an outcome that is reasonably expected to be related to clinical benefit, Gellad said.

As a requirement for a drug that is approved through accelerated approval, the company must perform a confirmatory trial to show clinical benefit. In this case, it took eight years, and the confirmatory trial showed no benefit, he said, adding that many of the patients in the trial were not from the United States.

So one argument from the company is that the trial does not represent effectiveness in the US, and because there are no other drugs available, and a prior study showed effectiveness, and its recommended by various OB/GYN groups, that it should stay on the market and be evaluated in another trial, he said. The caveat is that this treatment existed even before accelerated approval because pharmacies could compound or make the therapy themselves so if the drug leaves the market, there is still an option to use the drug.

Current guidelines in the United States recommend the use of progesterone supplementation, such as Makena, in women with prior spontaneous preterm births.

Last week, when the results of the PROLONG study were published, the Society for Maternal-Fetal Medicine released updated clinical guidance for providers to discuss important factors with patients, including uncertainty regarding the benefit of the drug.

Meanwhile, the American College of Obstetricians and Gynecologists released a statement from its Vice President for Practice Activities, Dr. Christopher Zahn, indicating that ACOGs clinical guidance on the use of the medication will remain in effect.

ACOGs guidance is based on a review of the best available literature. As such, we will continue to monitor this topic, evaluate additional literature and any further analyses as published, and address findings as needed in relevant clinical guidance, Zahn said in the statement.

Danielle Boyce, a mother of four and research consultant based in Philadelphia, had significant preterm labor issues with her first two children, including her eldest son, Charlie. He was born preterm at 34 weeks, developed a seizure disorder as a baby and now has Lennox-Gastaut syndrome, severe intellectual disability and autism, Boyce said.

When Boyce became pregnant for a third time at age 42, she was very concerned about having another preterm birth and made the shared decision with her physician to start using Makena. Her third and fourth children came home from the hospital and did not require a NICU stay. They are both healthy and developing normally, Boyce said.

I am glad that I had the opportunity to use Makena while it was still available because it worked for me, Boyce said in an email on Thursday.

Boyce added that she respects the decision the members of the FDA panel made since it was based on evidence presented to them but noted that studies can be flawed.

As someone trained in epidemiology and statistics, as well as someone who has served on FDA panels myself, I can appreciate the difficult decision that the panel had to make given the evidence presented, Boyce said.

I agree that the study design could have been better and the statistical endpoints were not achieved, she said about the evidence. However, this is a rare case where the stakes are so high and the side effect profile is so low that an additional layer of scrutiny is warranted beyond the statistical evidence presented before a decision is made to pull this effective medication from the market.

Boyce said that she would ask the FDA panel to consider ACOGs judgment.

Meanwhile, there also have been calls for the FDA to ban Makena.

Earlier this month, the consumer advocacy nonprofit Public Citizen submitted a petition to request that the FDA immediately withdraw the approval of all medications containing hydroxyprogesterone caproate (Makena).

Meena Aladdin, a health researcher at Public Citizens Health Research Group, testified during the FDA committee on Tuesday, arguing that maintaining approval of Makena in the absence of any clinical benefits being demonstrated by Trial 002 or Trial 003 would make a mockery of the more than 50-year FDA legal standard requiring substantial evidence of a drugs effectiveness.

In response to the FDA vote, AMAG Pharmaceuticals Chief Medical Officer Dr. Julie Krop said in a statement that the company was disappointed.

We are committed to working with the FDA to identify feasible ways to generate additional efficacy data on Makena while retaining current access to the therapy for at-risk pregnant women, Krop said in the statement.

For more than a decade, health care providers have relied on hydroxyprogesterone caproate (Makena) to reduce preterm delivery in high-risk patients, which aligns with recently updated treatment recommendations of the American College of Obstetricians and Gynecologists, as well as the Society for Maternal-Fetal Medicine, she said.

The medication now remains in limbo until the FDA makes a final decision based on its committees new recommendations.

I predict FDA will remove the drug from the market, since the confirmatory trial showed no benefit, and removing the drug does not necessarily completely eliminate the opportunity for some women to receive the therapy, Gellad said. There is an 80% chance I will be right.

Excerpt from:
FDA panel recommends withdrawing approval of drug used to prevent preterm births - FOX 59 Indianapolis

Recommendation and review posted by Bethany Smith

Womens colleges provided essential opportunities for women as both professors and students. But, as Leff points out, womens colleges were colleges, so they didnt support the same type of sophisticated research that Geiringer had been doing in universities. Any research she did would be outside of her college duties and typically unpaid.

Geiringer never found in a US university a position equal to what she had in Germany and Turkey.

After accepting her post at Wheaton, Geiringer wrote to von Mises, I hope there will be better conditions for the next generations of women. In the meantime, one has to go on as well as possible.

And Geiringer did go on. She stayed at Wheaton, which granted her an honorary doctorate in mathematics, until her retirement in 1959, that same year, she was elected a fellow of the American Academy of Arts and Sciences. She still did research when she found the time, but her most significant project post-immigration was compiling, editing, and publishing von Mises unfinished book in two editions after his death in 1953: Probably, Statistics, and Truth in 1964 and Mathematical Theory of Probability and Statistics in 1957.

Even if Geiringer didnt get exactly what she wanted, she never gave up on chasing that deepest need in her life.

Missed Genius

Ask people to imagine a scientist, and many of us will picture the same thing a heterosexual white male. Historically, a number of challenges have made it much more difficult for those who dont fit that stereotype to enter fields like science, math or engineering.

There are, however, many individuals from diverse backgrounds who have shaped our understanding of life and the Universe, but whose stories have gone untold until now. With our new BBC Future column, we are celebrating the missed geniuses who made the world what it is today.

--

Portrait of Hilda Geiringer by Emmanuel Lafont.

Join one million Future fans by liking us onFacebook, or follow us onTwitterorInstagram.

If you liked this story,sign up for the weekly bbc.com features newsletter, called The Essential List. A handpicked selection of stories from BBC Future, Culture, Worklife, and Travel, delivered to your inbox every Friday.

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The woman who reshaped maths - BBC News

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Evolution is generally thought of as a linear process: Species split off from one another over time, move to different places, and adapt different traits. But species like those in the Heliconius genus make patterns of evolution more interesting.

We need to take into account in our evolutionary models that we can get gene flow between species, Edelman says.

Heliconius made sense to study because of its hybrid-making tendencies. Its also just a cool really insect. The adult Heliconius eats pollen, which no other butterfly does. And Heliconius is smart, Edelman says. It has a home range, meaning it will go to visit the same flower every day, a habit more commonly associated with mammals.

The findings have potential implications for conservation and preserving pollinator populations. Studies show that species variation is key to protecting those populations in a changing climate.

One good thing about genetic diversity is if you have a really variable and diverse population, when environmental conditions change, you have a better chance of responding to them, Edelman says.

So how does hybridization factor in? Researchers dont all agree on whether its likely to contribute to genetic diversity. But it very well might.

Its at least somewhat likely that youre going to increase your variation rather than decrease it, Edelman says.

Conservation can involve protecting species by keeping out its close relatives, to avoid hybridization or a species takeover, but for species like these butterflies, that strategy may not work as well.

Hybridization is pretty common in nature, Edelman says. In some cases it might be good to bring in other species and increase genetic diversity for conservation purposes.

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Weird butterfly genetics counter popular theory of evolution - Inverse

Recommendation and review posted by Bethany Smith

A chirping, robotic voice welcomes you, spilling from one of six speakers that swivel overhead: Welcome to the sperm bank!

French artist Anne Le Troters site-specific sound installation, which debuted at the Nasher Sculpture Center last Saturday and will run through February 2, 2020 as part of the Sightings series, presents a 17-minute piece that centers on language, like much of her work, confronting the slipperiness of the identity politics inherent in its materiality, in this case in the domain of eugenics.

In a room paneled with rose-colored carpet, six speakers rotate on circular turntables above our heads, black audio cables swung between them, drooping, being pulled up, like fishing lines or netsfor language, perhaps, or for answers.

Curator Leigh Arnold met Le Troter at the Salon de Montrouge in 2016, where Le Troters piece LApptance (Desire) stood out to her: molded blue plastic seats of the kind youd see in a Mtro station, with speakers mounted under them that emitted whisperings. Le Troter had worked with ASMR artists for the recordings. Arnold was struck by these words that appeared public in context, but heard with a hushed intimacy akin to eavesdroppingthe tension of public and private and words showcased as a site of slippage. For her Sightings piece, her first U.S. commission, Le Troters seed notion came from a flight to the U.S., when a woman seated next to her explained her work at a sperm bank. Le Troter later signed onto the website, baffled by this world. The Nasher recording, using sourced words, borrowed language from 400 donor interviews, is, similarly, an exercise in voyeurism, an intrusion on genetics.

In the gallery, the wash of words gathered and remixed is both chilling and lulling, its childlike nursery-rhyme cadence broken by artificial, scientific intrusions. He is very sweetincredibly sweetis your typical sweetheartlike a big teddy bear male and female voices drone, enumerating a litany of positive qualities and attributes that reflect our values back at us. The breakdown begins immediately. Le Troter has arranged clusters of disjointed phrases around adjectives: a very active personvery intelligent, or has his work published in several journals, or again adventurous, outdoorsy, practical, loves his dogs. I came from, a donor voice begins, while robotic voices break in with numbers, Donor 5165, 5155, a small cascade that washes and eddies in the repeated And, um, a refrain that Le Troter sees like a beating heart.

And while the soft, carpeted walls and soothing voices create a cocoon of intimacy, I feel the twinge of danger, the threat in a piece that frames desire and exchange. If the room is a womb, then a womb for what?

The pink carpet on the walls has been swabbed and color-drained with bleach: the erasure of individuality imprinted on the space. Its whiteness bleeds as pigment-absence down to the off-white carpet, which is cellophane-wrapped, asepticized. The adjective clusters remove individuality, Le Troter says: a word is more saleable than a person.

Windows that look out onto Flora Street with its slow-moving traffic and burbling fountain add to the disquieting, womb-like effect. We are looking out at the world from inside what is, quite literally, a bubble. We sit on benches, also strung with audio cable, solid as the genetics encoded in DNA. That is, solid and also not solid. Unsettling and also human. Everything about the piece both holds and destabilizes.

What, really, do we know about what we want? What would it mean to engineer a calculated linguistic expression of desire? What would it entail, ethically, to sculpt a human future? And, underlying this, are the questions of privilege.

This concludesinterviews with400 sperm donorsThank you, and goodbye, the voice intones.

Le Troter herself, wearing a soft pink sweater the color of the walls, on the Friday before the opening, discussed the crafting of the piece, the real voices taken, borrowed, not as identifiable as faces, though dots on the wall represent photographs of the donors as children. The piece is a body with organs, a machine-body made of words and the audio cables the sinews of her work. She remembered the fountain and the view of the outside world, its slow rhythm.

And this space, sequestered from other galleries, may be the best exhibiting conditions shes ever experienced, she says. At the Palais de Tokyo in Paris, another piece of hers is currently part of a group exhibition that explores the idea of a current, contemporary French scene in the art world. The fragility of a sound installation is challenging in a group show with images. Here, we have a cocoon with an aperture on language and thought and sculpture as sound.

The piece is on view at the Nasher through February 2, 2020.

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Anne Le Troter's Sound Installation Stirs Up the Politics of Language - D Magazine

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In October 1994 in the journal Science, scientists published a strong candidate underlying heritable breast cancer. Their evidence led them to mutations in the BRCA1 gene, located on a stretch of chromosome 17. A bit more than a year later, researchers traced a second suspect, BRCA2, to chromosome 13, reporting their find in Nature. Together, the transformative discoveries set off a firestorm of oncology research, andjust as significantinjected hope for the future into the lives of millions who may carry mutations in one or both genes.

Twenty-five years later, the Basser Center for BRCA within Penn Medicines Abramson Cancer Center relentlessly continues to offer up this hope, fostering advancements in science and translating them to improve lives by emphasizing outreach, prevention, early detection, treatment, and survivorship of BRCA-mutation related cancers.

The Basser Center is focused entirely on BRCA1 and BRCA2, but within that we have this broad scope of everything from basic science to clinical care to increasing awareness, says Susan Domchek, the Basser Centers executive director. So at the same time that were hoping to figure out the basic biology of why a BRCA1 mutation leads to breast cancerand theres a lot about that that we dont know yetsimultaneously we want to use the information that we already have to help people in real time.

These parallel approaches arose from the vision of Mindy and Jon Gray, Penn alums whose initial $30million gift established the Basser Center in 2012. The Centers name honors Mindy Grays sister, Faith Basser, who died from BRCA-related ovarian cancer at age 44. Including subsequent donations, the Grays have committed a total of $55 million in support of the Centers work.

True to their vision of a multi-faceted operation, in the ensuing seven years the Center has facilitated a steady clip of scientific discovery, encouraged community building around the issue of BRCA awareness, and established support systems to aid people who are considering getting tested or weighing challenging decisions about how to proceed after finding out their status.

When we talk about the lifesaving research and innovation that is happening on campus, the Basser Center is one of Penns most important initiatives, says Penn President Amy Gutmann. Its because of Mindy and Jon Grays visionary philanthropy that we can say this so proudly today.

BRCA1 and BRCA2 are named for their association with breast cancer, but mutations also increase risks of ovarian, pancreatic, and prostate cancer, among others. Everyone possesses copies of BRCA1 and BRCA2 genes; the risks arise when their sequence is altered through a genetic mutation, which can be passed from generation to generation.

In their normal form, both genes serve a protective function, creating proteins that work within complex molecular machines to repair damage to DNA. When a mutated gene gives rise to an altered version of one of these proteins, DNA damage builds up within cells, greatly increasing the risk of cancer. Women with a mutation in BRCA1 or BRCA2, for example, have up to a 75 percent chance of developing breast cancer in their lifetime, compared to a 12 percent risk in the general population; similarly, the risk of a carrier developing ovarian cancer is up to 50 percent, compared to a risk under 2 percent in the general population.

When we talk about the lifesaving research and innovation that is happening on campus, the Basser Center is one of Penns most important initiatives. Penn President Amy Gutmann

As the scientific community marks the 25th anniversary of the discovery of the BRCA genes, Basser Center scientists are notching new breakthroughs in understanding the science of heritable cancers. Roger Greenberg, director of basic science for the Basser Center, says support for fundamental laboratory science has already paid off in a number of ways.

There has been so much exchange, so many more interactions on campus because of being here, he says. This had led to grants and papers, clinical trials and philanthropy and publications. Its such an incredible impact, and theres a lot more to come.

Greenberg is a leader in studying how DNA damage repair mechanisms are affected by mutations in BRCA1 and BRCA2, and how this impaired function affects the way people respond to therapy. In recent work, his lab has begun to focus on a relatively new category of drugs called PARP inhibitors. A heartening development in the BRCA field, these agents take advantage of a vulnerability in cells with BRCA mutations, building up so much DNA damage that the cells ultimately die.

Its a very exciting field that continues to grow, says Greenberg.

His labs work has also helped unravel mysteries of how DNA damage influencesthe immune system'sresponse to cancer cells, and how PARP inhibitors themselves create immune responses.

These kinds of insights can absolutely contribute to more personalized care, Greenberg says.

An expert on cancer genetics, Katherine Nathanson, director of genetics for the Basser Center, has also seen the growing role of immunology in cancer science during her years at Penn. Nathanson, who is also deputy director of Penn Medicines Abramson Cancer Center, has contributed extensively to the fields knowledge base around cancer risks associated with particular genetic variants. In recent years, shes also brought her genetics expertise to bear in the context of new breakthroughs in understanding the role of the immune system in controlling cancer.

One thing is clear, says Nathanson. It used to be that cancer immunology and cancer genetics were very far apart. Now there is a lot of intersection and collaboration.

Nathanson was recently awarded a $3 million grant from the Gray Foundation, which is led by Mindy and Jon Gray, to probe more deeply into immune system function in BRCA mutation carriers and in those with related cancers. Those studies have the potential not only to shed more light on BRCA cancers, but on the function of the immune system in general.

Ronny Drapkin, Bassers director of gynecologic research, conducts research that straddles the lab and clinic. A dozen years ago, when Drapkin was completing his postdoctoral training and starting his own lab, he studied the tissues from women who were having prophylactic surgerymastectomies and oophorectomiesafter finding out they possessed a BRCA1 or BRCA2 mutation. His investigations revealed that many cases of ovarian cancer may in fact originate in the fallopian tubes.

That scientific observation has the potential for profound implications for patient care. In addition to be a paradigm shift in science, its also caused a shift in treatment, he says. And that was very much ushered in by the discovery of the BRCA genes 25 years ago.

The current standard of care for women with BRCA1 and BRCA2 mutations is to have their ovaries removed to reduce their cancer risk at approximately age 40. Thus, women experience what is known as surgical menopause, compressing what is normally a 5 to 7 year process into the space of a few hours. This includes experiencing all the menopause-related morbidities of heart and bone disease. Today, two multi-center clinical trials, including one enrolling patients at Penn, are investigating an alternative practice, in which a womans fallopian tubes are removed at a younger age, after child-bearing, and her ovaries are preserveduntil her 50s. These studies are extremely important to evaluate whether this approach is safe and effective.

For this disease, we dont have early detection, we dont have mammography or colonoscopy, Drapkin says. For me its been personally gratifying to see this concept progress into the clinic.

Efforts by Domchek and others in the Basser Center have led to new paradigms for treatment of BRCA-related cancers. These Penn-led studies have helped usher in three FDA approvals related to PARP inhibitor drugs: olaparib for BRCA1- and BRCA2-associated ovarian cancer and metastatic breast cancer, and rucaparib for BRCA1- and BRCA2-associated ovarian cancer. These approvals have transformed care for ovarian cancer, for which there are few other options available. And olaparib represented the first FDA-approved therapy specifically for BRCA-related breast cancer.

More recent findings spearheaded by Basser Center investigators have also suggested PARP inhibitors hold promise for treating pancreatic cancer in patients with specific genetic mutations, including in BRCA1 and BRCA2.

A major priority of the Basser Center is to take concepts not only from the lab to the clinic, but also from the clinic to the public. Since 2012, through more than 50 patient- and public-facing events, the Center has spread lifesaving messages about the importance of genetic testing to targeted communities. The Center holds an annual scientific symposium, attracting the worlds experts on inherited cancers to Penn, and a monthly seminar series to enhance the profile of this type of research more locally. The Basser Global Prize, endowed by Mindy Grays sister, Shari Potter and her husband Len Potter, awards $100,000 annually to a visionary researcher working on BRCA1 and BRCA2, while smaller grants support the work of earlier-career researchers pursuing investigations on the topic.

Thats helped nucleate expertise here at Penn, says Greenberg.

The Centers Basser Leadership Councila group of roughly 20 of the Centers strongest advocates and supportersand Young Leadership Councilwith more than 100 members across the U.S. and beyondamplify these messages so they reverberate out from Penn into communities worldwide.

The Young Leadership Council, for example, enables peer support and discussions of the issues that young people face, such as when confronting a decision about prophylactic surgeriesto reduce cancer risk.

Many of our YLC members have undergone prophylactic surgeries or are thinking about them, and they discuss the challenges of this, what that means for dating,intimacy, and family planningfor example, says Laura Ferraiolo, seniordirector of development forthe Basser Center whose team helps oversees the councils' efforts.

The group has its own, monthlye-newsletter and holds frequent events, such as a cycling fundraiser in three cities earlier this month.

Similarly, the Basser Leadership Council supports the Centers mission in a number of ways. Many of them are either affected by a mutation or have someone in their family who is, and are incredibly engaged in this work, says Beth Stearman, administrative director for the Basser Center. They are lay leaders who support us in promoting outreach events and utilize their personal and professional connections to extend our mission to people in different communities across the country.

Emphasizing the value of knowing ones BRCA status has been a through line of the Centers outreach. An emerging priority, therefore, has been to offer education on genetic testing to primary care physicians, many of whom, Domchek explains, are uncertain of when to recommend testing, and for which patients.

My last name is Domchek, its ethnically ambiguous, she explains. Ive not been asked if Im of Ashkenazi Jewish ancestry and that is a known risk factor for BRCA mutations. Why is that? Were trying to do a lot more provider outreach so physicians are educated and comfortable with these issues.

Roughly one out of 40 people with Ashkenazi Jewish ancestry have a mutation in BRCA1 or BRCA2. The Basser Center has accordingly devoted significant energy into reaching that community. A poster campaign to promote the importance of genetic testing reached 1,500 synagogues in the Centers early years, and efforts through the Basser Leadership Council and Young Leadership Counciland an emerging Parents Leadership Community aimed at issues involved in raising families as a carriercontinue those and related efforts.

Meanwhile, efforts are ramping up in the Center to continue spreading access to genetic counseling and testing across other at-risk populations.

In a New York Times op-ed published earlier this month, attorney and writer Erika Stallings noted that Mathew Knowles, Beyoncs father, had been diagnosed with breast cancer and possessed a genetic mutation in the BRCA2 gene that dramatically increased his cancer risk. Domchek is serving as Knowless oncologist, and recently appeared with him on The Dr. Oz Show, calling attention to the risk that menshare from inherited mutations.

Several years ago, Stallings, a founding co-chair of the Basser Centers Young Leadership Council, discovered that she, too, had a BRCA2 mutation, and took action to lower her risk by undergoing a double mastectomy.

While BRCA mutations are more common in people with Ashkenazi Jewish heritage, its also true that BRCA1 and BRCA2 mutations occur in people of any background, male or female, at a rate of roughly 1 in 300. Black men and women like Knowles and Stallings are no exception. And neither are Latinx individuals, like former White House aide and founder of the Well Woman Coalition Alejandra Campoverdi, a BRCA2 mutation carrier who has partnered with the Basser Center to launch LATINX & BRCA, a campaign to connect the Latinx community with resources related to BRCA-related disease.

Making its official launch at next months BasserJean Bash, a major biennial fundraising event for the Center, LATINX & BRCA has already enabled the translation of many of Bassers educational materials into Spanish, including a list of Spanish-speaking genetic counselors. The Center is planning to spin off a similar effort focusing on the African-American community next year, also working through the Penn Center for Community Health Workers to better connect with people in the Philadelphia area and across the nation.

As momentum around the importance of genetic testing builds, the Basser Center is working to meet the need for responsible genetic counseling to contextualize the testsand supporting people in their decisions of how to act on the results. The Basser Center itself has six genetic counselors on staff, but is also trialing non-traditional ways of getting appropriate counseling to patients.

Everybody working in this space is looking for alternatives to traditional genetic counseling, says Stearman.

In one effort, the Penn Telegenetics Program, launched in 2012 by Angela Bradbury, an associate professor of medicine, medical ethics, and health policy, is using a research-based approach to allowing individuals to access genetic counselors over the phone or through two-way video conferencing. Bradbury and colleagues work has shown that offering such remote cancer genetic counseling sessions can dramatically boost patient participation in counseling. Last year Abramson Cancer Center launched a pilot effort to broadly provide telegenetic counseling services to patients and providers.

Along these lines, Domchek is helping lead the BFOR study (BRCA Founder Outreach Study) that connects at-risk individuals in the Ashkenazi Jewish community with a digital health platform that takes users through disclosures and informed consent procedures through a sophisticated interactive display. Participants can be linked with their primary care providers to receive their results.

This is different from a direct-to-consumer model where people are doing this outside the medical system, Domchek explains. Were trying to create a hybrid model where its still embedded in the medical system.

At the same time that were hoping to figure out the basic biology of why a BRCA1 mutation leads to breast cancerand theres a lot about that that we dont know yetsimultaneously we want to use the information that we already have to help people in real time. Susan Domchek, the Basser Centers executive director

Another study called Point of Care has offered genetic testing to patients already being treated for metastatic prostate and pancreatic cancer, using an 8-minute video to deliver a streamlined counseling session to this specialized population who are already all-too-familiar with the possible risks of a mutation. Yet possessing that information could guide critical treatment decisions tailored to the patients cancers genetic profiles. Testing among this population rose nine-fold after the intervention.

Were still not testing all the people who should get tested, says Domchek.

Basser leaders all stress that the Centers unique efforts wouldnt be possible without its donor-supported model.

I think people dont realize that the kind of infrastructure we have built is really hard to fund out of grants, says Nathanson. And by infrastructure, she means in large part human capacity, for recruiting patients, consenting patients, biobanking samples, getting the clinical data, putting that data in a database, maintaining the database, doing longitudinal follow-up. We cant fund our outreach, our patient awareness off of grants. Philanthropy is critical to supporting these efforts.

And theyre not lowering their sights as they look ahead.

We are continuing to grow the Center, bringing in people who have the expertise we dont currently have, says Drapkin. With our vision for the future, I see us as the epicenter for this kind of research in the world. There are few places that have the basic science, the translational and clinical science that we have. Its rare that you find expertise across the spectrum that can be applied in a way that gets to the patient. We have that here.

Susan Domchek is the Basser Professor in Oncology and executive director of the Basser Center for BRCA at the University of Pennsylvania Perelman School of Medicine.

Roger Greenberg is the J. Samuel Staub, MD Professor, director of the Penn Center for Genome Integrity, and director of basic science for the Basser Center for BRCA at Penn Medicine.

Katherine Nathanson is deputy director of the Abramson Cancer Center, the inaugural Pearl Basser Professor for BRCA-Related Research, and director of genetics for the Basser Center for BRCA at Penn Medicine.

Ronny Drapkin is the Franklin Payne Associate Professor of Pathology in Obstetrics and Gynecology, director of the Penn Ovarian Cancer Research Center, and director of gynecologic cancer research for the Basser Center for BRCA at Penn Medicine.

Beth Stearman is administrative director for the Basser Center for BRCA at Penn Medicine.

Laura Ferraiolo is senior director of development for the Basser Center for BRCA atPenn Medicine.

Homepage photo: Tianpeng Zhang, a postdoctoral researcher in Roger Greenbergs lab, takes fluorescence microscopy images to investigate how the genome is faithfully maintained as it is replicated, and how damage can arise. Zhang and other members of the lab contribute to the basic science research that supports translational discoveries in the Basser Center.

Read more from the original source:
Basser Center takes aim at BRCA - Penn: Office of University Communications

Recommendation and review posted by Bethany Smith

Lump-Sum Options present questions that deserve careful consideration.

Recent changes by the IRS have perked up interest in companies offering lump-sums to recipients of monthly defined benefit pensions. Most recently, General Electric (GE) announced was freezing its defined benefit plan and would be offering lump-sum options to 100,000 retirees. Lumps-sums are not new: AT&T, Ford and GM (Salaried only), and Allstate are among a myriad of companies offering lump-sums to retirees.

GE retirees will now face a complex decision about whether to remain in a monthly pension or take a lump-sum. The mathematical calculation for a lump-sum is prescribed by IRS rules. The interest rate is a blend of three treasury rates, and the life expectancy table is also governed by IRS rules. The math is essentially similar to the calculation of a mortgage: the lump-sum is effectively the value of the mortgage, the period is the life expectancy of the retiree, and the rate is the blended rate. By way of example, a 61-year old retiree with a $6,420 monthly pension would use a 3.11% blended rate to have their lump-sum computed at about $1.3 million.

Each decision is unique and personal in nature. Retirees may share similar lump-sum offers, but have different considerations in marital status, gender, investment expertise, flexibility demands and health situations. To that end, here are some general ideas about when a lump-sum is a good idea, and when it isnt.

When a Lump-sum is likely better:

Residual Value: A lump-sum can create a residual value. Therefore, when the retiree wants to leave assets to a non-spouse beneficiary, the lump-sum can provide that durability, if invested properly.

Withdrawal Flexibility: When a retire desires withdrawal flexibility, the lump-sum provides a wide degree of flexibility. Retirees who will have other jobs, a spouse with employment, or other assets, may enjoy the flexibility of a rollover IRA. Note that IRAs are subject to Required Minimum Distribution (RMD rules).

Investment Control: With a lump-sum, the retiree assumes investment responsibility. If the retiree can manage funds or delegate responsibility and make more than the discounted return (e.g. 3.11% for the 61-year old in the above example), the lump-sum can grow. In the example above, the retiree could get a $1.3 million lump-sum versus a $6,420 monthly pension. If the retiree creates a blended portfolio and earns 6% return, and then continued to withdraw the same monthly pension, her IRA would have more than they started with by ages of 80 and 85 (note RMD rules start to apply at 70.5).

Shorter life expectancy. Lump-sums are calculated on a unisex life expectancy. For example, a 61-year-old (irrespective of sex) is calculated to have about a 24.4-year life expectancy. Obviously, a shorter life expectancy, due to terminal illness, or bad genetics, make the lump-sum more attractive. Our 61-year old with health issues that passes at age 72, who makes 6% and withdraws her same $6,420, would have an IRA balance of about $1.35 million to leave to heirs or charity.

Higher inflation and interest assumptions. Monthly pensions usually do not index to inflation. If a retiree believes inflation or interest rates may rise, the lump-sum makes more sense. A lump-sum may be managed for inflation, and higher future interest rates allow the retiree to re-invest at a rate higher than the blended rate (like the 3.11% in the 61-year-old example).

Other Assets. Retirees with significant other assets or other income sources may want to take a lump-sum to create residual value. For example, if the retiree mentioned earlier had received an inheritance that generated ample income to support her life style, she might choose the lump-sum to delay distribution until RMD date (which may change to age 72 if the SECURE Act passes), and possibly engage in a Roth conversion strategy.

When a monthly pension is likely preferable:

Safety of income stream. When a retiree desires a safe income stream, the monthly pension is a safe alternative. Defined benefit pensions are partially to fully funded and are insured by the Pension Benefit Guaranty Corporation (PBGC). The PBGC insures monthly pensions up to $5,607.95 per month at age 65. The pension is effectively a very safe annuity. Many retirees are offered commercial annuities as alternatives to the lump-sum which seems counter-intuitive: selling an annuity to buy another annuity. Given the costs of a commercial annuity, it would seem very unlikely to find a full-replacement annuity on a commercial level. Current comparison quotes on an immediate Single Premium Immediate Annuity (SPIA) for a 61-year-old female show a slightly lower monthly benefit. It should also be noted that commercial annuities are not fully insured.

Invasion of principal. This is a behavioral issue, but many recipients of lump-sums or immediate wealth tend to make bad decisions. Spending money on family, losing it to bad investments, and even outright fraud can diminish or eradicate a lump-sum. According to the National Endowment of Financial Education, 70% of lotto winners declare bankruptcy within 5 years. Similar statistics apply to NFL players. Managing a lump-sum is a disciplined task. If a retiree has a lot of credit card debt and is undisciplined with money, a lump-sum wont help the situation.

Long life expectancy. A monthly pension is for life (or joint lives); a lump sum is based on a life expectancy table. Life expectancy tables are computed on a 50% probability of being alive at a certain age. This means that half of the people will live longer, and half will live less. A very healthy individual with good genetics may collect a monthly pension for a very substantial period of time. The very first Social Security recipient, Ida Mae Fuller, lived to age 100, paid in a total of $24.75 of taxes and collected $22,888.92 in benefits. Longer life expectancy (of the collective couple) make the monthly payment more attractive.

Investment risk. With a monthly pension, the pension plan assumes all investment risk. Retirees who are risk-averse to market fluctuations will find the monthly pension more attractive.

Other assets. Retirees who have other assets, like a 401(k) plan, to counter the effects of inflation and other prospective issues, may take the monthly pension to secure the cash flow and allow the other asset to grow. Retiree could consider the monthly pension to be the equivalent of a safe bond and they can accordingly take more risk with other assets and retain the monthly pension.

Bottom Line: This is a complex decision. Its personal in nature, depends on many variables of individual circumstance, and warrants careful consideration. If a reader has a question, or wants a second opinion, feel free to contact us with your questions.

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Six Reasons A Lump-Sum Can Look Good And Five Reasons It Might Not - Forbes

Recommendation and review posted by Bethany Smith

Around noon one August day in 2011, a familiar dorsal fin rose from the sea off the coast of Massachusetts. Flecked with tiny white scars, it belonged to Salt, a female humpback whale who scientists had been studying since the 1970s and who was named for those distinctive markings.

Aboard the research vessel Shearwater, Jooke Robbins director of humpback whale research at the Center for Coastal Studies in Provincetown, Massachusetts loaded a crossbow with a dart, modified with a specialized tip and yellow float, and took aim. The bolt went flying. It hit its target but, by design, bounced harmlessly off the whales bulk, taking with it only a few cubic millimeters of flesh almost like a mosquito bite, relative to the whales size.

Robbins and her team collected the sample, preserved it in liquid nitrogen, then sent it away to be analyzed. Now, eight years later, a team supported by the Arizona Cancer Evolution Center (ACE) at Arizona State University has discovered that Salt and other cetaceans the group of mammals that includes whales, dolphins, and porpoises evolved clever ways of dealing with cancer, including an array of tumor-suppressing genes. The team published its findings in May in the journal Molecular Biology and Evolution.

The findings, along with similar work on elephants, suggest that somewhere, hiding in the genetic code and evolutionary history of large mammals, there could be a new cancer treatment for humans. But if the researchers are correct, their window to study these megafauna may be closing as humans continue to threaten the animals populations and the biodiversity of their habitats.

That whales like Salt had value was never in doubt for Robbins. There are many valid reasons to conserve large mammals, from ethical to ecological. But the idea that their genes could be useful for cancer research was a new one for her.

I did not think years ago that one of the things we would be studying with this population would be cancer, in general, let alone any kinds of cancer implications for humans, she said. Its unexpected, and very valuable, but I never would have planned it.

In theory, large, long-lived creatures like Salt should have high cancer rates. At its core, cancer begins when a cell splits it divides incorrectly, the potentially fatal mutation spreads to neighboring cells, and, if left unchecked, throughout the body.

Compared to humans, whales and elephants can have hundreds of times the number of cells and have similarly long natural lifespans but their cells mutate, become cancerous, and kill them less frequently. This quirk of nature, which the ACE team is studying, is called Petos Paradox, named for Richard Peto, a British epidemiologist. In the late 1970s, he proposed that there must be some kind of natural selection for cancer suppression, because humans live longer and are much larger than mice, but the species have similar rates of the disease.

In 2011, ACE researchers, along with scientists at 11 other institutions worldwide, first started looking at how Petos Paradox manifests itself in the genomes of humpback whales by comparing the information in Salts genes to those of other cetaceans. According to the results reported this year, the parts of a whales genome that determine how and when a cell splits evolved quickly and coincided with when the animals grew to their enormous size. Marc Tollis a biologist at Northern Arizona Universitys School of Informatics, Computing, and Cyber Systems who joined and began leading the ACE study in 2015 hopes that taking one of the amped up, cancer-fighting whale genes and putting it in the body of a smaller creature will help the latter fight off these cellular mutations: a mouse as a test, a human as a hopeful end result.

Other scientists are also studying Petos Paradox in a different group of huge animals: elephants. In 2012, Joshua Schiffman, a pediatric oncologist at the University of Utah, began investigating cancer defenses in the animals after learning that they had extra copies of a gene responsible for fighting off tumors. It was this same gene that his patients with Li-Fraumeni syndrome, a rare hereditary disorder that predisposes sufferers to cancer development, lacked.

Collaborating with ACEs Carlo Maley, Schiffman and his team worked with local zoos and the Ringling Bros. and Barnum & Bailey Circus before the circus ceased using elephants in its acts and its Center for Elephant Conservation to gather blood samples during regular checkups with veterinarians. In their 2015 paper in the Journal of the American Medical Association, they reported that the elephants extra copies of this tumor-squashing gene triggers a type of programmed cell death and a defense against cancer called apoptosis. When a cell splits and experiences some kind of DNA damage from chemical agents, for example the cell will either try to fix itself, or self destruct to prevent the mutations from spreading to other cells. Both whale and elephant cells are also likely to undergo apoptosis more often compared to humans.

People are smart, but nature is much smarter, said Schiffman. Nature has figured out the solutions to some of our health problems over hundreds of millions of years of evolution.

Its clear elephants and whales have managed to find their resistance to cancer over countless generations, Schiffman added. His team is also looking for other cancer defenses in elephant genetics and trying to transfer this phenomenon to humans.

Whats even more exciting than that [these animals] found the cure, he added, is that, through nature, they evolved ways to prevent cancer in the first place.

So far, 22 of the 90 or so existing cetacean species have had their genomes sequenced and added to the National Center for Biotechnology Information database, with more being added all the time. When Tollis began working on Salts genome in 2015, there were only five. The field moves quickly, he said, with new technologies making the process cheaper and easier.

Scientists have also sequenced the genomes of all three elephant species alive today. While its a start, scientists may not have enough data to get a full picture of how the animals thwart cancer. As human activity eats away at these populations through ecosystem destruction, climate change, and more researchers get fewer and fewer chances to collect samples. The creatures become harder to find and the regulations protecting them grow tighter, delaying research by years.

Considering the rate these species are in decline, Tollis also hopes the research will also make people consider the importance for both cancer research and the environment.

Generally, since were living in a mass-extinction event right now, he said, we need every reason for conservation we can get.

The conservation status of these large mammals is a mixed bag, according to data from the International Union for Conservation of Nature (IUCN), which, among other projects, tracks population health of the worlds animals. Some whale species, like the humpback, have recovered from centuries of hunting while others, like the North Atlantic right whale and Sei whale, are still endangered. African and Asian elephants are listed as vulnerable and endangered, respectively.

Recently, Botswana lifted its five-year ban on elephant hunting and Japan resumed commercial whaling in July. However, conservation experts are even more concerned with habitat loss and other less violent, but thoroughly insidious dangers to the species.

Elephants suffer as their former stomping grounds are turned into industrial areas or farmland, which also leads to human-elephant conflicts, said Chris Thouless, strategic advisor with Save the Elephants, a research and conservation organization based out of Kenya.

In the ocean, whales are increasingly put at risk by marine microplastics and noise from shipping, said Hal Whitehead, a cetacean specialist with the IUCN. Cetaceans use sound to hunt for food and form social bonds, as neither sight nor smell work particularly well under water, and the noise stresses out the creatures.

The species which have been hit the worst are those with the closest contact with humans, Whitehead added.

Even if these species populations recover, there are other challenges for collecting genetic data from a wealth of species. A sample from only one animal isnt necessarily representative of an entire species, said David Baillie, a molecular biologist at Simon Fraser University in Burnaby, British Columbia.

While having an accurate, representative genome of a species gleaned from many samples is valuable, so too are some of the oddities that can arise in the genomes of individuals. Genetic diversity and large population numbers leave a good deal of wiggle room for mutations that could benefit both the creature and further down the line and with the right understanding humans.

The more genomes we have, the better we come to understand the residual diversity that underlies the population structure, Baillie wrote in an email to Undark. He added that rare mutations can be very important when trying to understand disease resistance, for example.

Theres evidence that points to robust genetic variation between regional groups within the same species, and more effort is needed to catalog the genes of an animals distant cousins, Tollis said. Similarly, according to Schiffman, poaching, habitat loss, and inbreeding have caused a bottleneck that has stifled genetic diversity in many species and among the worlds largest creatures in particular.

According to Cristiana Paca Palmer, executive secretary at the UNs Convention on Biological Diversity, the impact of habitat and species loss on medical research more broadly is still unknown.

The loss of large species like elephants and whales is just a microcosm of the cataclysmic species diversity loss happening in ecosystems the world over, she wrote in an email. Really, when we act to preserve biodiversity, we are acting to preserve ourselves.

Its also unknown how, over generations, human activities are changing these animals genomes, and the potentially useful data they hold. Research out of the University of Southampton in the U.K. suggests the median size of mammals will shrink by a quarter as humans continue to pave over untamed habitats, for example. As the genetics of the worlds animals adjust to humanitys tightening grasp on the planet, the genes a species use to defeat any number of diseases and other valuable mutations could be, effectively and inadvertently, bred out of existence.

If we lost the opportunity to study these animals in the wild, and if we dont protect them, Schiffman said, we could be losing cures for many different diseases to come.

Doug Johnson is a Canadian writer, editor, and journalist

A version of this article was originally published on Undarks website as As Elephants and Whales Disappear, They Take Valuable Cancer Clues With Them and has been republished here with permission.

Link:
If we aren't careful, we could miss the chance to learn cancer-fighting secrets from threatened whales and elephants - Genetic Literacy Project

Recommendation and review posted by Bethany Smith

My first diagnosis was stage IIIC breast cancer, which is as close as you can get to stage IV without actually being stage IV, which is terminal. At that point, IIIC, youre still considered curable.

My oncologist told me that I had triple-negative breast cancer, which can be more aggressive and more difficult to treat than other forms of breast cancer. (Triple-negative breast cancer doesnt respond to some common breast-cancer treatments, such as hormone therapy.)

I went through chemotherapy and then had a double mastectomy in May of 2018. The lump was in one breast, but I felt like I would always worry that wed missed something if I hadnt had both removed. I have three sonsnow 12, 13, and 16and every step of the way, Ive wanted to do whatever I could to heal myself and be here for them.

I made the most of my (bald) 44th birthday.

The mastectomy was followed by a second round of chemotherapy, which was followed by radiation. And then my oncologist said, Youve done all the treatment thats reasonable at this point. Now you need to go back to your normal life and watch for any symptoms. Well check you out every three to six months.

After recovering from the radiation, I went back to work the first week in December. I worked for a month and then was diagnosed with stage IV cancer the first week of January.

The cancer had metastasized to my liver and lungs. I did even more chemotherapy, but a follow-up scan showed that the tumor in my liver had doubled in size in the three months since my last scan. Following treatment, some tumors will shrink or disappear. The 14-centimeter tumor in my liver didnt react that way; its there, not getting smaller. There really isnt much room left in my liver. For now, my best-case scenario is that the cancer doesnt spread further.

It was really hard to tell my kids. Ive always wanted to be really honest with them. I was honest about what I had and that it was serious. Theyre old enough that they can do their own research. There was no point in trying to mislead them from the beginning. Also, I tried to be lighthearted.

I want my sons to know and remember how much I love them. Im glad that theyre at a point where theyll remember me. And my husband can remind them.

My eldest son has thanked me a couple of times for handling things so well. He feels like the fact that Im not complaining a lot or acting down or sad or depressed has been really helpful. I really try to stay positive and make the most out of all the moments that I still do have with them.

It was hard for them to see me go bald again. Having my hair grow back was a big milestone for my kids. My youngest, especially, was so excited when my hair started to grow back. He would measure it and rub my headhe really celebrated me starting to look more normal again.

More here:
This Mom Has Terminal Breast Cancer, But Shes Still Fighting for Her Kids - Glamour

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Animal sociability through microbes

Accumulating evidence suggests that the microbiota living in and on animals has important functions in the social architecture of those animals. Sherwin et al. review how the microbiota might facilitate neurodevelopment, help program social behaviors, and facilitate communication in various animal species, including humans. Understanding the complex relationship between microbiota and animal sociability may also identify avenues for treating social disorders in humans.

Science, this issue p. eaar2016

Increasingly, it is recognized that the microbes resident in the gastrointestinal tract can influence brain physiology and behavior. Research has shown that the gastrointestinal microbiota can signal to the brain via a diverse set of pathways, including immune activation, production of microbial metabolites and peptides, activation of the vagus nerve, and production of various neurotransmitters and neuromodulators in the gut itself. Collectively, this bidirectional pathway is known as the microbiota-gut-brain axis. In the absence of a microbiota, germ-free and antibiotic-treated mice exhibit alterations to several central physiological processes such as neurotransmitter turnover, neuroinflammation, neurogenesis, and neuronal morphology. Perhaps as a result of these neurological alterations, the behavior of rodents lacking a microbiotaespecially social behavioris remarkably different from that of rodents colonized with bacteria. Conversely, supplementation of animals with certain beneficial live bacteria (e.g., Bifidobacterium and Lactobacillus) can lead to notable improvements in social behavior both in early life and in adulthood. Collectively, these results suggest that microbial signals are important for healthy neurodevelopment and programming of social behaviors in the brain. Although research on the functional and ecological implications of the gut microbiota in natural populations is growing, from an evolutionary perspective it remains unclear why and when relationships between microbes and the social brain arose. We propose that a trans-species analysis may aid in our understanding of human sociability.

Sociability comprises a complex range of interactive behaviors that can be cooperative, neutral, or antagonistic. Across the animal kingdom, the level of sociability an animal displays is variable; some are highly social (e.g., primates, termites, and honey bees), living within cooperative communities, whereas others have a mostly solitary existence (e.g., bears). Consequently, although studies on germ-free and antibiotic-treated animals have yielded insights into how the microbiota may influence social behaviors, they are perhaps too reductionist to fully appreciate the complex relationship between symbiotic bacteria in the gastrointestinal tract and host sociability when considering a broader zoological perspective. Some social interactions have evolved to facilitate horizontal transmission of microbiota. Observations across both invertebrate and vertebrate species suggest that factors such as diet and immunity generate selection pressures that drive the relationship between microbiota and social behavior. Although microbiota may influence behaviors endogenously through regulation of the gut-brain axis, some animal species may have evolved to use symbiotic bacteria exogenously to mediate communication between members of the same species. Hyenas, for example, produce an odorous paste from their scent glands that contains fermentative bacteria that is suggested to facilitate social cohesion among conspecifics. This complex relationship between animals and microbiota raises the hypothesis that microbes may have influenced the evolution of the social brain and behavior as a means to propagate their own genetic material.

Understanding the factors that affect the development and programming of social behaviors across the animal kingdom is important not only in terms of rethinking the evolution of brain physiology and behavior, but also in terms of providing greater insight into disorders of the social brain in humans [including autism spectrum disorders (ASDs), social phobia, and schizophrenia]. Evidence for a link between the microbiota and these conditions is growing, and preclinical and emerging clinical data raise the hypothesis that targeting the microbiota through dietary or live biotherapeutic interventions can improve the associated behavioral symptoms in such neurodevelopmental disorders. Larger clinical trials are required to confirm the efficacy of such interventions before they are recognized as a first-line treatment for neurodevelopmental disorders. Although such connections between gut bacteria and neurodevelopmental disorders are currently an intriguing area of research, any role for the microbiota in the evolution of social behaviors in animals does not supersede other contributing factors. Rather, it adds an additional perspective on how these complex behaviors arose.

The bidirectional pathway between the gut microbiota and the central nervous system, the microbiota-gut-brain axis, influences various complex aspects of social behavior across the animal kingdom. Some animals have evolved their own unique relationship with their gut microbiota that may assist them in interacting with conspecifics. The relationship between the gut microbiota and social behavior may help to explain social deficits observed in conditions such as autism spectrum disorders (ASDs) and could potentially lead to the development of new therapies for such conditions.

Sociability can facilitate mutually beneficial outcomes such as division of labor, cooperative care, and increased immunity, but sociability can also promote negative outcomes, including aggression and coercion. Accumulating evidence suggests that symbiotic microorganisms, specifically the microbiota that reside within the gastrointestinal system, may influence neurodevelopment and programming of social behaviors across diverse animal species. This relationship between host and microbes hints that host-microbiota interactions may have influenced the evolution of social behaviors. Indeed, the gastrointestinal microbiota is used by certain species as a means to facilitate communication among conspecifics. Further understanding of how microbiota influence the brain in nature may be helpful for elucidating the causal mechanisms underlying sociability and for generating new therapeutic strategies for social disorders in humans, such as autism spectrum disorders (ASDs).

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Microbiota and the social brain - Science Magazine

Recommendation and review posted by Bethany Smith

If you tend to wake up feeling like all you need is "just one more hour" of sleep, youre probably pretty stoked about "falling back" an hour this Halloweekend, marking the end of Daylight Saving Time. After all, when you change your clocks (or, let your iPhone do it for you) to switch back to standard time, you're gifted with an extra hour of sleep basically the best thing since the advent of the snooze button, right?

Well, according to experts, while you may gain that extra hour this weekend, the end of DST can actually have some pretty negative effects on your sleep and overall health.

In fact, although around 70 countries currently participate in DST, several are now pushing to scrap the practice altogether, citing general unpopularity and public health concerns. (One scary example? Scientists found that the pedestrian risk for being struck and killed by a car at 6 p.m. in November, when DST ends, is 11 times higher than the risk at 6 p.m. in April, when DST begins.)

Because at least for now DST isnt going anywhere in the U.S., its important to know what lies ahead. Here, experts weigh in on how Daylight Saving Time affects your health and mood and how you can squash symptoms related to the transition.

RELATED: We Tried 4 Products Designed to Help You Sleep Better

Youve probably already guessed this one, but the reason your sleep suffers as a result of the time change comes down to light (or lack thereof), says Clifford Segil, DO, a neurologist at Providence Saint John's Health Center.

"We get used to going to sleep a few hours after it gets dark, which is disrupted when all of sudden it's dark earlier than we are used to, Dr. Segil says. "Its hard for many people to continue to fall asleep at the same time or to maintain good sleep for the same amount of time as they did before a time change."

Someone whos regularly logging plenty of sleep will be able to adapt more easily to the shift. However, it can feel like the last straw if you are already dealing with not-so-great sleep habits, says Caroline Rasmussen, a meditation teacher, herbalist, and founder of brain health company, Antara.

The fix: Light cues can help your body's internal clock adjust more quickly to the time change, Dr. Segil says. If you wake up and its still dark, try to mimic morning light by turning on a nearby light or salt lamp, Dr. Segil says. He adds that the type of light isn't as important as the duration of time spent in the light and the volume of light the more the better. The same goes for when nighttime darkness begins to creep in; turn on a lamp at your desk if you can so your system knows it's not time for bed.

Maintaining a consistent sleep schedule aiming to hit the hay and wake up at the same time each day can also shorten the time it takes to feel back to normal after a time change, Dr. Segil adds.

As a result of poor sleep, your mood, productivity level, and concentration may all suffer, Dr. Segil says. Beyond feeling irritable and sluggish, theres a more serious mental health risk at play, too.

A 2016 study published in Epidemiology showed that depression diagnoses have a tendency to spike as people make the transition out of DST and into standard time. The studys authors noted that they believe the shift is related to the "psychological distress associated with the sudden advancement of sunsetwhich marks the coming of winter and a long period of short days."

This could be related to a larger condition that affects people during the winter months Seasonal Affective Disorder (aka SAD). People who experience SAD notice an increase in depressive symptoms in early fall or winter that experts say is linked to decreased exposure to light.

"The change in light information created by the time change directly influences the level of stress hormones in the body," Rasmussen says. If you already have chronically elevated cortisol levels, the time change can have an even more noticeable, negative impact on mood, she adds.

RELATED: 8 Signs You Might Have Seasonal Affective Disorder

The fix: If you think you have SAD, seek help from a mental health expert, who may recommend medication or light therapy; a 2009 study showed using a light box daily for 20 to 40 minutes resulted in significant and immediate mood improvement in people with SAD.

If its an overall feeling of irritability or stress you're experiencing, you may also want to consider adding in relaxing habits, like sipping tea. Not only is the act soothing, but Rasmussen says tea also contains L-theanine, an amino acid that can help keep stress at bay. On the supplement home front, consider popping an adaptogen, like tulsi or ashwagandha, which can help ease anxiety.

"Adaptogens help balance the stress response system for example by restoring the normal sensitivity of our cortisol receptors so that the adrenals aren't forced to pump out overly high levels of the hormone to achieve the same physiological effect," Rasmussen says.

Surprisingly, the time change and subsequent disruption of our circadian patterns can also have downstream effects on everything from our levels of inflammation to our eating habits, Rasmussen says.

"The brain is programmed for a 24-hour day, and when our internal clocks are disrupted, it leads to a domino effect, disrupting many bodily functions, including your appetite, body temperature, bowel function, and even heart and lung function," explains David Cutler, M.D., a California-based family medicine physician. Because these functions are all controlled by the brains internal clock, the end of DST can take your body on a bit of a roller coaster, he adds.

Translation: If you notice you're way hungrier than usual or that your digestion is out of wack DST may actually be partially to blame.

The fix: While there are some health factors out of your control, it never hurts to help your body along by taking care of it with diet and exercise. Aim to stick to your regular workout schedule at least 150 minutes per week of moderate-intensity aerobic activity per week or 75 minutes of vigorous aerobic activity and save protein-heavy meals (which involve more digestion and may disrupt your sleep) for earlier in the day, Rasmussen says.

View original post here:
How the End of Daylight Saving Time Can Affect Your Health - Yahoo Lifestyle

Recommendation and review posted by Bethany Smith

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Sen. Edward J. Markey (D-MA) and Rep. Earl Blumenauer (D-OR) reintroduced Tuesday legislation is designed to reduce the nations nuclear weapons budget by $75 billion over the next decade.

The Smarter Approach to Nuclear Expenditures (SANE) Act would enhance national security and cut what they deem redundant and destabilizing nuclear programs.

The United States should fund education, not annihilation; that is our future, Markey said. We need sanity when crafting Americas budget priorities and more and improved nuclear weapons defies common sense. The SANE Act cuts nuclear weapons and delivery systems that we dont need so we can invest in the people and programs that will make America safe and prosperous in the future.

The bill reduces the purchase of Columbia-class submarines from 12 to eight, cutting the existing ICBM fleet from over 400 to 150, and trims deployed strategic warheads from approximately 1,500 to 1,000; cancels development of a new air-launched cruise missile and an associated warhead life extension program; and lowers to 80 the purchase of new B-21 long-range bombers.

These disastrous weapons will never be the answer to solving our complex and ever-changing national security threats, especially with a reckless administration in charge of the codes, Blumenauer said. We should not be investing trillions of dollars of our budget on an outdated and irresponsible nuclear arsenal. There are far more important programs and initiatives that will actually help and protect the American people. This legislation will put us on the path towards a safer, nuclear-free future.

More:
Bill seeks to cut nuclear weapons budget - Homeland Preparedness News

Recommendation and review posted by Bethany Smith

Canaccord has raised its target price for Perseus from $1.05 per share to $1.20 per share (current price: 84 cents per share).

() operates two gold mines in West Africa, Edikan and Sissingu, and is developing its third mine - Yaour.

The companys share price has outperformed most of its gold producer peers since August, which can be attributed to a growing recognition of its improved operational stability and a diversified production base.

has increased its target price for Perseus to $1.20 per share (from $1.05 per share) on incorporation of Canaccords updated gold price deck and revisions to FY20 forecasts.

Following is an extract from Canaccords research update:

SepQ production in line, beat on costs: Group production of 66koz was broadly in line with CGe of 68koz, with AISC of US$922/oz lower than CGe of US$1,022/oz on improved unit costs at both operating assets. The result implies a run rate in line with H1'FY20 guidance which at this stage looks comfortably achievable, in our view. SepQ operational cashflow was strong at US$30m, with cash and bullion at quarter end of A $179m.

Edikan - lower feed grade driven by mining sequence: Edikan produced 44.1koz at AISC of US$1,027/oz, vs CGe of 49.4koz at US$1,031/oz. Production was lower on milled grade (0.91g/t vs CGe 1.03g/t) and slightly lower recovery. The grade performance was a function of mining sequence with grades expected to improve over the remainder of FY20. AISC was slightly higher on lower production offsetting lower mining and processing unit rates.

Sissingue - beat on production and costs: Sissingue produced 21.7koz at AISC of US $709/oz, vs CGe of 18.6koz at US$870/oz. Production was higher on plant throughput (453kt vs CGe 380kt) driven by better than expected mining rates following successful implementation of wet season mitigation controls. AISC was lower on higher production, compounded by lower unit rates.

Outlook: FY20 guidance is unchanged at 260-300koz at AISC of US$800-975/oz, and is weighted with a 54% split in favour of H2. Our FY20 production forecast increases slightly to 280koz at AISC US$955/oz (from CGe 277koz at US$989/oz) on incorporating higher grades at both Edikan and Sissingue in 2HFY20.

Growth - Yaoure progressing in line with forecasts; mine life extension opportunities at Sissingue : Yaoure site earth works were largely unaffected by the wet season and progressed in line with plan. Contractors began mobilising to site late in the SepQ with full construction of the processing plant expected to commence this month. Targeted construction finish and first gold pour remains on schedule for DecQ'20.

At Sissingue, regional exploration at the Zanikan prospect has identified multiple mineralised structures over a strike of 500m. Highlights from drilling include 12m at 4.5 g/t from 60m, 10m at 5 g/t from 136m and 8m at 60 g/t from 80m. While early stage, Zanikan presents as possible new satellite for Sissingue, incrementally adding to the remaining ~4 year reserve life.

Our target price increases to A$1.20/sh (from A$1.05/sh) on incorporation of our updated price deck (2019-2025 average gold price +5% to US$1,548/oz, LT +5% to US $1,603oz; LT AUD:USD -4% to 0.68) and revisions to our FY20 forecasts.

PRU has outperformed most of its gold producer peers since August, which we attribute to a growing recognition of PRU's improved operational stability and now diversified (i.e. lower risk) production base. We continue to see PRU as undervalued on both an absolute and relative basis, and maintain our BUY rating.

Read the rest here:
Perseus Mining has target price raised by Canaccord Genuity - Proactive Investors Australia

Recommendation and review posted by Bethany Smith

Sealed Air Corp (NYSE:SEE) has been given an average recommendation of Hold by the fourteen ratings firms that are covering the firm, Marketbeat Ratings reports. Four analysts have rated the stock with a sell recommendation, seven have assigned a hold recommendation and two have assigned a buy recommendation to the company. The average 12 month price objective among brokerages that have issued a report on the stock in the last year is $43.70.

A number of equities analysts recently weighed in on the stock. Citigroup reduced their target price on shares of Sealed Air from $45.00 to $42.00 and set a neutral rating for the company in a research note on Thursday, October 17th. Wells Fargo & Co upped their target price on shares of Sealed Air from $42.00 to $43.00 and gave the stock a market perform rating in a research note on Tuesday, August 6th. KeyCorp restated a sell rating and set a $39.00 price objective on shares of Sealed Air in a research note on Friday, August 2nd. Finally, ValuEngine downgraded shares of Sealed Air from a sell rating to a strong sell rating in a research note on Thursday, October 10th.

NYSE SEE traded down $0.38 on Thursday, reaching $41.31. The company had a trading volume of 63,752 shares, compared to its average volume of 722,588. The firm has a market capitalization of $6.45 billion, a price-to-earnings ratio of 16.52, a price-to-earnings-growth ratio of 1.56 and a beta of 1.08. Sealed Air has a 1-year low of $30.47 and a 1-year high of $47.13. The companys fifty day moving average is $40.88 and its 200-day moving average is $42.86.

The firm also recently disclosed a quarterly dividend, which will be paid on Friday, December 20th. Stockholders of record on Friday, December 6th will be paid a dividend of $0.16 per share. The ex-dividend date of this dividend is Thursday, December 5th. This represents a $0.64 dividend on an annualized basis and a dividend yield of 1.55%. Sealed Airs dividend payout ratio is 25.60%.

Several institutional investors have recently bought and sold shares of SEE. Motco acquired a new position in shares of Sealed Air during the 2nd quarter worth about $29,000. Doyle Wealth Management bought a new stake in shares of Sealed Air in the 2nd quarter valued at about $40,000. CSat Investment Advisory L.P. raised its holdings in shares of Sealed Air by 34.1% in the 2nd quarter. CSat Investment Advisory L.P. now owns 1,234 shares of the industrial products companys stock valued at $53,000 after purchasing an additional 314 shares during the period. Massey Quick Simon & CO. LLC bought a new stake in shares of Sealed Air in the 3rd quarter valued at about $96,000. Finally, Rockefeller Capital Management L.P. raised its holdings in shares of Sealed Air by 51.4% in the 2nd quarter. Rockefeller Capital Management L.P. now owns 2,894 shares of the industrial products companys stock valued at $124,000 after purchasing an additional 983 shares during the period. Institutional investors own 96.58% of the companys stock.

Sealed Air Company Profile

Sealed Air Corporation provides food safety and security, and product protection solutions worldwide. It operates in two segments, Food Care and Product Care. The Food Care segment offers integrated packaging materials and equipment solutions to provide food safety, shelf life extension, and total cost optimization for perishable food processors in the fresh red meat, smoked and processed meats, poultry, and dairy markets under the Cryovac, Cryovac Grip & Tear, Cryovac Darfresh, Cryovac Mirabella, Simple Steps, and Optidure brands.

Further Reading: Understanding the two types of arbitrage

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Sealed Air Corp (NYSE:SEE) Given Average Recommendation of Hold by Brokerages - Mitchell Messenger

Recommendation and review posted by Bethany Smith

SEATTLE, Oct. 31, 2019 /PRNewswire/ -- RareCyte announces an addition to the RarePlex Staining Kit product line, enabling customers to evaluate HER2 and ER expression on circulating tumor cells (CTCs) in their own laboratory. HER2 and ER are biomarkers that direct treatment recommendations for invasive breast cancer, and liquid biopsy offers a blood-based method to evaluate biomarker expression for insight into receptor status, response to treatment, and potentially therapy selection in clinical research.

The RarePlex HER2/ER CTC Panel Kit includes all the reagents necessary for immunofluorescent detection of CTCs along with HER2 and ER expression. When combined with the RareCyte platform for CTC analysis, the RarePlex HER2/ER CTC Panel Kit enables the first blood-to-result breast-specific CTC assay deployable in customer laboratories.

The HER2/ER Panel Kit was validated based on rigorous requirements set to clinical standards with guidance from CLIA and industry experts. Tad George, PhD, Sr. VP of Biology R&D at RareCyte noted "Our approach to CTC assay development and validation is centered on creating deployable products that combine the sensitivity, specificity, and precision required for multi-center trials, not only for CTC enumeration but also for classifying CTCs based on their biomarker phenotypes."

Dr. Minetta Liu, MD, Professor and Research Chair in the Department of Oncology at Mayo Clinic recently presented her work with the HER2/ER CTC Panel Kit at the Advances in Circulating Tumor Cells Conference in Corfu, Greece. "Our early work with this assay has revealed interesting patterns of HER2/ER expression that vary widely across patients. Efforts will now focus on defining thresholds for HER2 and ER positivity that are specific to CTCs. This platform will facilitate important investigations into the clinical significance of CTC heterogeneity relative to standard tissue-based definitions of HER2 positive and/or hormone receptor positive advanced breast cancer."

The HER2/ER Panel Kit is available for purchase and more information on the HER2/ER Panel Kit and the RareCyte platform is available at rarecyte.com.

RareCyte products are for research use only. Not for use in diagnostic procedures.

About RareCyte, Inc.

RareCyte offers next generation instruments, consumables and reagents for the analysis and capture of rare cells from blood and tissue, enabling its foundational liquid biopsy and tissue analysis platform. The company has deep experience in developing advanced precision life science systems used in cutting-edge labs worldwide. Our customers perform innovative research, bring new therapeutics to market, and perform a wide-range of single cell applications in oncology, prenatal testing, and infectious disease. For more information about RareCyte, visitrarecyte.com.

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RareCyte expands liquid biopsy offering with the release of a HER2/ER breast cancer CTC Panel Kit - Daily Record-News

Recommendation and review posted by Bethany Smith

Abbie Duggar is having a rough time. The 27-year-old, who is expecting her first child with husband John David Duggar, 29, has been battling severe morning sickness, the dad-to-be told Us Weekly. He called the experience scary.

Abbie who is due early next year was diagnosed with hyperemesis gravidarum, John David explained. Its a type of serious morning sickness that causes extreme nausea and vomiting. It can lead to dehydration, weight loss, and can sometimes requires hospitalization.

It hit her hard, and she was down for probably seven weeks with severe morning sickness, he told the magazine. She got diagnosed with hyperemesis gravidarum, and she was hospitalized a couple times. We made multiple visits to the ER for dehydration. She couldnt eat, pretty much, or drink, or anything. So she was actually on IVs and had IVs at home. So that was a pretty scary time.

While Abbies illness was alarming, John David stepped up to care for his wife and make sure she was as comfortable as possible.

I keep her water filled up, and her snacks for her, the Counting On star explained. I keep her eating and just comfortable. Anything I can get for her, I try to. I run to the store, [get] whatever she needs, just keep her as comfortable as possible when shes feeling bad.

Abbie says shes been grateful for her husbands help. Hes cooked for me. Hes cleaned. Hes just been an angel, she said.

Hyperemesis gravidarum affects fewer than 3% of pregnant women, according to WebMD. Many people had never heard of it until 2012, when the royal family revealed that Kate Middleton was suffering from the condition during her pregnancy with Prince George. The duchess had to be admitted to the hospital for treatment. She experienced the condition again during her second and third pregnancies.

Since then, a number of celebrities have opened up about their struggle with the condition. Amy Schumers hypermesis was so serious she had to be hospitalized.

I have hyperemesis and it blows, the comedian wrote on Instagram. Very lucky to be pregnant but this is some bullsh*t!

Amber Rose also experienced the extreme nausea and vomiting associated with the condition. Im tired and I just want to barf all day. Its just not fun. But its totally worth it, she said in an Instagram video.

Doctors arent entirely sure what causes hyperemesis gravidarum, though it might be related to changes in hormone levels, according to the Cleveland Clinic. Symptoms usually begin in the first trimester and include vomiting multiple times per day, losing a significant amount of weight, dizziness and lightheadness, and dehydration.

Women whove experienced the condition describe not being able to keep down most food, being unable to get out of bed, and feeling so awful they considered ending the pregnancy.

Treatment for hyperemesis gravidarum can include anti-nausea medications, intravenous fluids, and ginger. Some women may need to be hospitalized if the condition is severe.

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'Counting On': Pregnant Abbie Duggar Is Battling the Same Condition That Afflicted Kate Middleton - Showbiz Cheat Sheet

Recommendation and review posted by Bethany Smith