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Category Archives: Iowa Stem Cells
Cancer requires more tutoring, with Meyer continuing to Teaching Cancer a lesson – News – vintontoday.com
Posted: January 20, 2021 at 6:47 pm
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Click to view a previous story about Carly's battle.
October 30th brought a second challenge to Vinton-Shellsburg Kindergarten teacher, Carly Meyer. After battling her first round of leukemia, she suffered another relapse with a second diagnosis of leukemia.
"I thought I was done with these updates... but should have known 2020 wasnt done messing stuff up yet!" Carly shared. "For those of you who don't know, I was diagnosed with Acute Myeloid Leukemia in August 2019 and completed chemo treatments in December 2019, but unfortunately my lab results on October 30, showed some "blasts", which are the cancerous cells in my blood." She explained back in November that her lab results also showed that my WBC's the infection fighting cells, were very low.
At the beginning of November, she had another bone marrow biopsy which Wes, her husband believes is her 6th. She was then admitted to the University of Iowa Hospital for a month long stay.
Carly finished up her 5 days of chemotherapy on November 11th with only a couple of side effects (fatigue and loss of appetite) which are a couple of the more common side effects with chemotherapy treatments. Unfortunately, she suffered from dehydration as well and this caused her to pass out a couple of times, and one of the falls caused her to hit her head. This of course triggered a trip for a CT Scan just to make sure she was alright, fortunately, she didn't have any side effects from the fall.
"It is fairly common for leukemia patients to spike fevers and to get random bugs because we are neutropenic and our body cant fight off simple things they normally would," Carly explained. She did come down with an infection during this time but it was able to be pinpointed and treated right away. On Thanksgiving, she was able to return home 10 days earlier from her hospital stay than had been anticipated,
Her journey continues to beat cancer with a trip back to the hospital at the end of December, to begin preparation for her bone marrow transplant. "My hero of a brother started getting shots December 30 to prep and will be donating his Stem Cells on Monday, January 4th." Carly explained how the process works. Her brother Kyle was hooked up to a machine she said it is similar to donating blood/plasma and that the procedure lasts for about 5 hours. Fortunately, her brother Kyle was a 100% perfect match to be her donor.
The stem cells were then put into her IV Powerline over about 30 minutes while they closely monitored Carly for any side effects. "Then its just a waiting game after that," she said.
After the transplant, Carly's immune system was down to zero. Unfortunately, it is common for SCT patients to spike fevers and even get an infection after transplant.
New Year, New Me has never rang more true than this year Carly said.
She is hoping to be home at the end of the week. She said that this last stay has been "extremely exhausting mentally and physically." Developing mucositis, extreme sores and pain in her mouth, it has made it very hard to eat or drink anything. Mucositis is very common after receiving the strong chemo that she received just before her bone marrow transplant. She is slowly recovering from this.
She said that she is excited to be coming home with her husband and fur-baby Maverick if all goes well, by the end of the week.
"I am so lucky to have an amazing support system (especially my husband) to get me through this tough time," she said.
Please keep the couple in your prayers as Carly continues to heal.
Posted: August 26, 2020 at 7:56 pm
Article In Brief
Scientists identified several cellular abnormalities in the developing cortex from fetal tissues carrying the mutant gene implicated in Huntington's disease. The findings suggest that the disease alters human development at an early age.
Teams of French researchers have found cellular changes that alter cortical development in the brains of human fetuses who carry the mutant huntingtin gene (mHTT) implicated in Huntington's disease (HD).
The finding adds a new wrinkle to the puzzle of HD as many people who carry the mutation can live healthy lives for four decades or longer before the onset of symptoms.
No one knows why, but this is a common thread in other late-onset genetically-driven neurodegenerative conditions like Alzheimer's and Parkinson's disease, the researchers said. And a growing number of researchers believe that it is best to treat people with the HD mutation as early as possible.Now, findings from this study, published online July 16 in Science, beg the question: How early?
The researchers, led by Sandrine Humbert, PhD, research director of INSERM (the French National Institute for Health and Medical Research) and group leader at the Grenoble Institut des Neurosciences, and Alexandra Durr, MD, PhD, professor at Sorbonne University and team leader of the Paris Brain Institute at Pitie-Salptrire Hospital, had access to fetal tissue from families that terminated their pregnancy in the context of a prenatal test. The developing fetus carried the mHTT.
Other mouse and neuroimaging studies with pre-manifest mutation carriers have suggested that the mutation might affect neurodevelopment but this is the first time that scientists have looked to the human fetus to know for sure.
Dr. Durr works with people undergoing genetic testing and counseling for Huntington's disease. Her team was able to collect cortical tissue from four HD mutation carriers when the pregnancies were terminated at around 13-weeks' gestation and tissue from four healthy controls.
This age is an opportune time to assess the tissue, the study authors noted, because at this stage the cortical neurons that project to the striatumthose that become dysfunctional and die during the course of the diseaseare being born from progenitor cells at the ventricular zone.
Thirteen weeks gestation is the time point when you need a lot of cells to be generated, Dr. Humbert explained. At this stage in development cells are massively cycling. The implications for the fetal brain with an HD mutation is that there is a shift to differentiate early and, as a result, you generate fewer neurons, at least at this specific time point during development.
The scientists identified several cellular abnormalities in the developing cortex, including mislocalization of the mutant huntingtin protein and other junction proteins that keep the neuroepithelium sealed. They observed abnormal ciliogenesis and changes in mitosis and cell-cycle progression, which correlated with defects in the balance between renewal and differentiation of progenitors.
In neuroprogenitor cells, this balance is tightly regulated to provide the right amount of neurons along the development of the cortex. Fewer proliferating cells and more progenitors prematurely began to differentiate in the tissues of HD carrierssubtle findings that are changing the landscape of the cortex.
Huntington's definitely has a neurodevelopmental component in addition to a neurodegenerative disease, Dr. Humbert explained. Studies in mice have found similar cellular abnormalities.
These data are supported by similar findings in mice that show mutant HTT impairs neuroprogenitor cell division, migration, and maturation, and that these changes result in a thinner cortex. Additional studies have revealed that early exposure to mutant HTT is enough to trigger signs of HD when the mice grow up. Neuroimaging studies with pre-symptomatic mutation carriers, even children, have shown smaller intracranial volume in HD mutation carriers.
What is also intriguing is that these events occurred even though the fetuses had small pathological expansions39, 40, and 42 repeats that would typically cause an adult onset of HD.
The findings trigger a number of questions: Why aren't there any obvious clinical problems until mid-life? Do these early developmental changes set the stage for symptoms decades down the road? Are other brain cells compensating for the changes and it takes 40-plus years for symptoms to develop?
Dr. Humbert and her colleagues said that the defects we observed likely render the cortico-striatal circuitry more vulnerable to the later dysfunctions characteristic of HD. The path to degeneration is complex, however, and weaves together both pathogenic and compensatory mechanisms.
They cited a recent pair of studies in Neurology by Peg Nopoulos, MD, and her colleagues at the University of Iowa, Carver College of Medicine that looked at children who are HD mutation carriers. They showed initial striatal enlargement with hyper-connectivity between the striatum and the cerebellum. Over time, the striatum decreases and the connections weaken. Although the cerebellar connections initially may help compensate for the abnormally developed striatum, it is the loss of these connections that may ultimately lead to motor abnormalities. Again, it will be decades before any obvious motor signs develop.
Once there are disease-modifying therapies, we know we should treat as early as possible or differently in pre-manifest compared to symptomatic stages of the disease, or it may not be sufficient, said Dr. Humbert.
She said she is now interested in understanding how these early defects contribute to adult pathology, and how their compensation could be regulated during the silent symptom-free period. This should give access to new molecules of interest, either as treatments or biomarkers, she added.
It is a beautiful paper, said Christopher A. Ross, MD, PhD, director of neurobiology and professor of psychiatry and behavioral sciences at Johns Hopkins Medicine. The concept fits with ideas people have had. Their study is groundbreaking.
It's unclear how these cell-cycle abnormalities alter normal development, said Dr. Ross. I have been doing pre-manifest genetic testing for years, and my belief is that asymptomatic people who are far from their predicted onset but test positive are clinically completely normal.
These data are very interesting, said Sarah Tabrizi, MD, PhD, professor of clinical neurology at University College London Institute of Neurology. There has been debate in the HD field regarding the existence of a neurodevelopmental deficit, and evidence is accruing that this may be the case based on differentiating HD induced pluripotent stem cell systems, mouse development, and now these studies of early human development.
We recently found that HD gene carriers ~24 years before predicted disease onset had essentially completely normal brains including normal cortico-striatal connectivity on advanced neuroimaging, apart from a slightly smaller striatum, which we hypothesized resulted in selective vulnerability of the striatum to subsequent neurodegeneration in HD (Lancet Neurology 2020). Importantly, our HD gene carriers performed as well as matched controls on a range of stringent cognitive and motor assessments.
This all suggests that we need to treat as early as possible with disease-modifying therapies to enable us to delay or prevent symptom onset, Dr. Tabrizi said, and means that there is still great potential for therapies to potentially prevent the neurodegeneration occurring if we treat early enough. We need to understand more about the very earliest manifestations of neurodegeneration and then intervene at the optimal stage.
Dr. Ross believes that the brain figures out a workaround of these developmental alterations but agrees that it may leave the brain more vulnerable later in life. He added, These findings are conceptually very important, though not necessarily with immediate implications for patients or those who are asymptomatic but test positive.
He said that this finding represents a paradigm shift that will lead scientists to look for developmental abnormalities in other neurodegenerative diseases.
It is important to emphasize how the Huntington gene (HTT) affects the brain in the context of a lifetime trajectory, added Dr. Nopoulos, the Paul W. Penningroth professor of psychiatry and chair in the department of psychiatry at University of Iowa Carver College of Medicine. This gene is vital for brain development. Our group has shown that HTT drives brain development and that repeats in HTT are beneficial, and the higher the repeat, the higher the IQ. For individuals with repeats in the range of 39-42, like those in the fetal tissue study, HTT likely contributed to the development of a cerebellar-striatal-cortical circuit that was initially advantageous (which is why they are found to be asymptomatic in the Tabrizi study), but later in life, vulnerable to degeneration. Therefore, although the findings in the fetal tissue study are reported as abnormalities, they are more likely to be evidence of differences since the changes are not pathologic until much later in life.
However, she added, everything about HTT is on a spectrumthe classic dose effect of repeats on the age of onset is a good example where greater repeats result in earlier onset. The same is likely true for development.
Human brain development is prolonged, lasting until roughly age 30, she continued. Those with repeats in the low mutant range (36-42) will have a chance for full brain development before the vulnerable cerebellar-striatal-cortical circuit begins to degenerate and disease manifests. However, in those with longer repeats (above 50), the vulnerable brain circuit may begin to degenerate before full brain maturation is complete.
In this range of repeats, the ultimate effect of mHTT on brain development may be detrimental. These considerations are vitally important when considering when to intervene with preventive therapies such as gene knock-down drugs. In those with low mutant repeats, knocking down the gene early in life (before age 30) may be detrimental to brain development, yet in those with high repeats, rescue may need to be much earlier (adolescence).
Drs. Humbert, Durr, Ross, and Nopoulos had no relevant disclosures.
Posted: April 29, 2020 at 11:49 am
It now seems apparent that COVID-19 will dominate American life for months to come, quite possibly through the national election in November.
That means the disease, and efforts to respond to it, will likewise dominate the 2020 campaign and make it largely about something it has never been about before.
That something is science.
It is hard to think of a time when hard science biology, virology, epidemiology has been so much the core of our political conflict. Issues from evolution to stem cells to vaccination have long been a part of our political conversation, but not at the forefront of presidential elections.
This virus crisis has largely taken over the political conversation. Americans are all learning new, polysyllabic vocabulary and complex truths about threats they cannot see.
And that is likely to bring out all of the culture's ambivalence about science.
Trust in science
Last summer, a Pew Research Center survey found that 86% of Americans expressed "a fair amount or a great deal of faith" that scientists act in their best interests.
But the survey's co-author told NPR, "It tends to be kind of soft support." In fact, only 48% were willing to say that medical doctors "make fair and accurate research statements and recommendations all or most of the time." And only 32% were willing to say as much for "medical research scientists."
A YouGov poll in April 2017 found an even less sanguine attitude, as reported in Scientific American. That measure found only 35% of Americans had "a lot of confidence" in scientists. A plurality (45%) had "a little," while those with "none at all" had grown substantially since YouGov polled the same question in 2013.
Little wonder then that political figures such as Texas Lt. Gov. Dan Patrick, a Republican, and media personalities such as Fox News' Tucker Carlson pounce on the difference between various projections of deaths from COVID-19.
They interpret lower death totals (thus far) as evidence that the threat was overblown, even though public health experts consider it proof that shutdowns and social distancing are working and note that the threat is not over.
Scientific experts, like experts in general, have fared poorly in the populist atmosphere of the past decade in Europe and the United States.
"Voters say they reject expertise because experts, whom they think of as indistinguishable from governing elites, have failed them," writes Tom Nichols, a professor of national security affairs at the U.S. Naval War College.
Nichols published a book in 2017 called The Death of Expertise: The Campaign Against Established Knowledge and Why It Matters. Summing up his argument for Politico, Nichols observed that Americans have always had a healthy skepticism about "eggheads" of various kinds.
He says that skepticism renewed itself in the "social and political traumas" of the 1960s and 1970s. But since then, he argues, "Globalization and technological advances have created a gulf between people with enough knowledge and education to cope with these changes and people who feel threatened and left behind in the new world of the 21st century."
Lacking "scientific merit"
The plain fact is that for many, science is a source of wisdom but by no means the only one. There can be a "balancing" of science with religious teaching or humanistic ethics or what people may regard as their own common sense.
That is why so many Americans may identify with President Trump's overeagerness about potential drug therapies for COVID-19 that have worked on other diseases.
Trump's hopefulness for the antimalarial hydroxychloroquine, for example, was apparently not shared by one of the administration's own leading vaccine scientists, Richard Bright. Bright tried to limit broad use of the drug because its application lacked "scientific merit." As a result, he says, he was removed as director of the Biomedical Advanced Research and Development Authority.
In a statement released by his attorneys last week, Bright sounded the alarm: "To combat this deadly virus, science, not politics or cronyism, has to lead the way."
Also this past week, the president stood at the podium of the White House briefing room and cast doubt on the survival of the coronavirus in the fall. He then deferred to his top scientific adviser on the question.
"We will have the virus in the fall," said Dr. Anthony Fauci of the National Institutes of Health.
Trump also insisted the head of the Centers for Disease Control and Prevention had been misquoted about the difficulties of managing COVID-19 in the fall. Dr. Robert Redfield took the lectern to say he had not been misquoted.
But all this was prelude to the Thursday night stunner, when the president extended his embrace of "game-changer" therapy ideas to raising the question of whether injecting a disinfectant (which can kill the coronavirus on a surface) into a person could kill the virus (in reality, doing so would be toxic).
This prompted such immediate blowback from scientists, hospital personnel and even the makers of Lysol that the president later insisted he had made the comment sarcastically. And the next evening's briefing was cut off at just 22 minutes, with the president taking no questions.
A long-term struggle
The crisis is spreading through the body politic even as it spreads through the human population. It will stress both in myriad ways. Americans' conflicted relationship with science will play a role in how they deal with that stress.
For the moment, most are accepting the scientific approach of social distancing in service of a greater good. But there are rejections of stay-at-home orders in street protests and in some statehouses.
Saturday night, Trump repeated a line used to argue for reopening the country sooner rather than later: "Remember, the Cure can't be worse than the problem itself." He added, "Be careful, be safe, use common sense!"
The struggle has been joined, and it will likely outlast both this one campaign season and this one pandemic.
Posted: March 29, 2020 at 4:44 am
Nearly two weeks ago, Alessandro Laurenzi, a biologist working as a consultant in Bologna, Italy, was mowing the grass in his garden when a friend stopped him and said the mower reeked of fuel. I couldnt smell anything at all, he tells The Scientist. That was in the morning. A few hours later, he went to have lunch and realized he couldnt smell the food he was about to eat and when he took a bite, he couldnt taste it either. Within a few days, he developed symptoms of COVID-19 and called his doctor to ask if he could get tested. Because his symptoms were mild, Laurenzi says, his doctor said no.
Laurenzi had heard anecdotally that many COVID-19 patients in Italy suffered from a loss of smell, so he started reading all the scientific papers he could find to see if his anosmia and ageusia would ever abate. One of the papers, a review published March 13, mentioned that SARS-CoV-2, like other coronaviruses such as SARS-CoV and MERS-CoV, could target the central nervous system, possibly infecting neurons in the nasal passage and disrupting the senses of smell and taste.
Some of the purely respiratory symptoms that you might attribute to the disease, the inability to get air into the lungs, might actually be defects in respiration controlled by the nervous system.
Matthew Anderson, Beth Israel Deaconess Medical Center
Reading this, Laurenzi immediately reached out to the corresponding author, Abdul Mannan Baig, a researcher at Aga Khan University in Pakistan, and asked if his symptoms were reversible. The evidence, Mannan told Laurenzi and reiterated to The Scientist, indicates they will abate, possibly because the loss of sense is caused by inflammation in the area as the body fights the virus, so those symptoms could disappear in seven to 14 days. Lets hope so, Laurenzi tells The Scientist.
Documenting such peculiar symptoms is important, Mannan tells The Scientist, because the loss of smell and taste could be an early warning sign of SARS-CoV-2 infection. Based on the literature, British ear, nose, and throat doctors have now called for adults who lost those senses to quarantine themselves in an attempt to tamp down the spread of the disease, The New York Times reports. The symptoms, Mannan adds, also suggest that the virus has the ability to invade the central nervous system, which could cause neurological damage and possibly play a role in patients dying from COVID-19.
This is something to keep a careful eye on, says Matthew Anderson, a neuropathologist at Beth Israel Deaconess Medical Center in Boston. Theres been some intriguing observations in previous studies on viruses, including coronaviruses, to show that they have the capacity to enter the nervous system. Its important that this be considered for SARS-CoV-2 and for people to do the experiments, including autopsies, to look for signs of this damage.
Because COVID-19 has symptoms similar to the flu, much of the attention could get diverted towards the pulmonary aspect of SARS-CoV-2, while neural involvement may remain covert, Mannan says. When a patient begins to exhibit severe neurological symptoms, such as a loss of involuntary breathing, it may be too late to prevent fatalities.
In a review article first published February 27, Yan-Chao Li of Jilin University in China and colleagues argue that if SARS-CoV-2 infects nerve cells, particularly neurons in the medulla oblongata, which is part of the brain stem that serves as the control center for the heart and the lungs, the damage could contribute to acute respiratory failure of patients with COVID-19.
The epidemiological evidence supports the hypothesis that neurons in the medulla can become infected with SARS-CoV-2 and contribute to a patients breathing problems and potential death. Li and colleagues explain that the time it takes for COVID-19 to progress from first symptoms to difficulty breathing is typically five days; patients are then admitted to the hospital roughly two days later, and a day after that put into intensive care. The latency period is enough for the virus to enter and destroy the medullary neurons, they write.
SARS-CoV-2 enters human cells using a receptor called ACE2. Researchers have reported that ACE2 regulates cardiovascular function, and according to a search of protein databases, many human cell types express ACE2, including lung, heart, kidney, intestine, and brain tissue, Mannan says. There are also multiple ways that the virus could invade the central nervous system, he explains. It might circulate through the blood and then attack ACE2 receptors in the endothelia that lines blood capillaries in the brain, breaching the blood-brain barrier and invading neurons through that route. A breached blood-brain barrier could also cause brain swelling, compressing the brain stem and affecting respiration, Mannan says. The cells innervating the lungs could also become infected, making involuntary respiration more difficult.
Evidence from experiments in mice also suggest that the virus might target the nervous system through the olfactory bulb. In a 2008 study, immunologist Stanley Perlman of the University of Iowa and colleagues showed that SARS-CoVthe virus that caused the SARS outbreak that killed more than 770 people in 2003entered the brains of transgenic mice expressing human ACE2 through neurons in the nose. The virus then rapidly spread to connecting nerve cells. The extensive nerve damage was the major cause of death, the team reported, even though low levels of the virus were detected in the animals lungs.
Although this has not been demonstrated, SARS-CoV-2 could potentially enter the nervous system through the olfactory bulb, as SARS-CoV does in mice.
Death of the animal likely results from dysfunction and/or death of infected neurons, especially those located in cardiorespiratory centers in the medulla, the team wrote. A study with the MERS virus in mice expressing ACE2 showed a similar result, Perlman tells The Scientist. The brain certainly can be readily infected in mice, he notes. Whether this occurs in humans to any great extent is really unknown, but not very likely at this point, given how much larger rodents olfactory bulbs are relative to the overall size of their brains compared with humans and the paucity of evidence in humans.
Still, he says, the fact that COVID-19 patients have lost their sense of smell or taste is interesting because, if the virus infects the nose, it would use the exact same neurons as in the mouse studies to enter the brain. If taking this path, SARS-CoV-2 could work its way up to the olfactory mucosa, which consists of epithelium cells, blood vessels, and the axons from olfactory neurons. This area is connected to the olfactory bulb, via small, sieve-like, tiny openings called the cribriform plate that is located at the base of the frontal lobes of the brain, Mannan explains. Because the brains frontal lobes are close to the olfactory bulb where neurons may be infected, the tissue deeper in the brain could be endangered too.
Infection of the brainstem could cause changes that would affect involuntary respiration, which suggests some of the purely respiratory symptoms that you might attribute to the disease, the inability to get air into the lungs, might actually be defects in respiration controlled by the nervous system, Anderson says.
Mannan emphasizes that the neurological data on SARS-CoV-2, though preliminary, could be important for doctors deciding how to treat patients. Asking about neurological symptomsloss of taste or smell, twitching, seizurescould factor into who might go into acute respiratory failure, or at least who might suffer from it soonest, and allow for more efficient triaging of patients, with a close eye kept on those with neurological symptoms. It is important to screen the patients for neurological signs early and late in the course of COVID-19, he says, as this could be life-saving in our fight against COVID-19 pandemic.
Anderson and Perlman add that postmortem examinations of the brains of patients who died from COVID-19 are essential to understanding the role nerve damage might play in the progression of the disease. Few, if any, autopsies of these patients are being done because of fear of contracting the disease, and if the autopsies are being done, its not likely that examiners are looking at the brain, only the lungs. Theyre just not thinking that the brain could be the site of the problem, Anderson says, and so thats the really important aspect of these reviews, getting that idea out there.
Ashley Yeager is an associate editor atThe Scientist. Email her firstname.lastname@example.org. Follow her on Twitter@AshleyJYeager.
Posted: March 14, 2020 at 7:48 am
Stem Cell Treatment for Cartilage Regeneration Posted at 28 Mar by invigo
Cartilage degeneration is a common disease or condition known as osteoarthritis. As the term indicates, it occurs when the cartilage between the joints degenerates, or breaks down with the passing of time. The cartilage is vital to the joint as it acts as a cushion for impact and movement. When this cushion wears down, the joints are subject to pain and stiffness. However, there are treatments that can help with this condition. Here are some notes to better understand cartilage degeneration and what you as a patient can do to get pain relief and regain joint function.
Although there is no specific cause for cartilage degeneration, your risk of suffering from it increases with age and use. Another contributing factor is genetics certain genes may cause an inadequate production of collagen, an essential component of cartilage. Misshapen bones may also increase your risk for osteoarthritis as they put pressure on the joint that the joint is not designed to handle.
Then there are environmental and lifestyle factors that can contribute to cartilage degeneration. Being overweight, for instance, adds extra pressure to the joints. Excessive exercise, especially if it is repetitive on the same joint, can increase wear and tear of joints. Inflammatory conditions like rheumatoid arthritis also increase the risk of cartilage damage.
There are a number of symptoms that can result from cartilage degeneration. Depending on which joint is affected, you may experience:
Household chores may become more difficult due to stiffness of fingers. If your hips or knees are affected, you should take extra caution when getting out of bed or going up and down the stairs. Stiffness of the lower limbs and weakness of the hip can increase your risk of falling and sustaining a serious injury.
There are great advances being made with stem cell technology, which is a viable and effective treatment option if you are looking for relief from joint pain cause by cartilage degeneration.
At our facility in Cedar Rapids, Iowa, we offer stem cell treatment for those who are suffering and in need. Healthy cells from unaffected areas of your body (we harvest stem cells from adipose tissue in the abdomen or love-handles) can be used to repair, heal and regenerate areas injured or damaged tissue, ligaments or cartilage. Through a natural process called differentiation, the stem cells can adapt and change into any cell in the human body. A major advantage of using stem cell treatment is the ability to avoid risky and painful surgery with long recovery times.
So, if you are tired of the pain caused by cartilage degeneration/osteoarthritis, and would like to regain a pain-free and active lifestyle, we encourage you to come into our office to discuss your treatment options. Our clinic director, Dr. Sunny Kim can give you a comprehensive consultation. And in the case that stem cell therapy is not suitable for you, we will be glad to find you another course of action for recovery. Call us at (319) 774-8143.
Posted: February 22, 2020 at 11:42 am
After several Mennonite children suffered fatal cardiac arrests and there were no answers to why, a team of UI doctors set out to discover an unknown genetic mutation that caused these deaths.
After several children died from sudden cardiac arrests, a team of doctors discovered a genetic mutation to be the cause of their fatal heart arrhythmias a disorder of the movement of the heart that disturbs its typical contracting rhythm.
Ian Law, pediatric cardiologist at the University of Iowa Hospitals and Clinics, said a Mennonite family moved to Iowa in 2013 just before one of the children died suddenly of cardiac arrests.
Doctors ran further tests and found other Mennonite children to be at a similar risk for heart problems, Law said, and had been so for years. Ultimately, the cardiac arrests were the result of genetically inherited heart arrhythmias.
We determined that the children had inherited gene mutations and the mother and father both had one good copy and one bad copy, causing their children to have different combinations of the gene, Law said.
One bad copy plus one good copy would give a child more of a predisposition to the heart defects but not make them at risk, two bad copies would mean they are indeed at risk of the fatal mutation, while two good copies would mean they bear no trace of the gene, Law said.
As of right now, Law said, there is no cure for the recently discovered genetic mutation, but physicians can prophylactically place pacemaking devices or beta blockers in children who test positive for the gene before they have an episode.
In a letter written to Law at UIHC, the mother of the children affected said that the family was thankful for the doctors putting in implantable cardioverter defibrillators the children, and understands that they need to pay more attention to how the kids take medications daily and watch their activity when sick because most of the cardiac episodes occurred when they were feeling under the weather.
[We are] glad to know if we can do a blood test to find out if the children and grandchildren will be affected I still have a hard time fully believing we can totally rely on these tests, the letter said.
The new genetic mutation is unnamed at the moment, because it had not been discovered or identified before now, Law said. Moving forward, precaution against it can now be taken.
Knowledge is power, so ideally what will happen is that we genetically test those who want to get married and counsel them, whether or not they have any trace of the mutated gene, Law said.
RELATED: Labs from UI, Texas share credit for simultaneous genetic discovery
Hannah Bombei, a genetic counselor in pediatric cardiology at the Stead Family Childrens Hospital, defined genetic arrhythmias as an abnormal heart rhythm which can stem from a variety of causes.
You can think about this like a factory assembly line. The genetic code is the blueprint to make certain products such as calcium, potassium, or sodium channels in the heart muscle cells, Bombei said. If the blueprints arent correct due to a genetic mutation, the resulting products wont be produced and/or function properly.
In the future, Bombei said doctors hope to move toward more personalized medicine. This means they would determine the most effective treatment based on the particular underlying genetic cause of an anomaly in a patients heart.
UI pediatric cardiology Professor Emerita Dianne Atkins said there are multiple mutations similar to this one which has been found only in Mennonite families, and that by the doctors discovered it they were anxious and then moved on to figure out why it happened.
Now that we have found this specific mutation it is very likely that we will continue to find it other communities and families, Atkins said.
RELATED: UI researchers find potential link between DNA changes and suicidal behavior
Its hard to pinpoint how many people are affected by arrhythmias, Atkins said, because the condition presents very differently in different people and doctors only know about those who show symptoms. Some are extremely rare, she said, and others are more common.
This mutation differs from others because doctors can discover who is at risk and who isnt, Atkins added, so treatment can begin before a fatal event.
Atkins said this discovery was important as a collaboration because doctors agreed that they were all helping patients with unclearly defined abnormalities and had to work together to find answers.
Law said they had to work to define the mutation itself, as well as keep track of who carried and showed symptoms of it.
Persistence, curiosity and teamwork is key, Law said. If we didnt have a community working together, these people and those in similar positions, would have continued to die.
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UI doctors discover new genetic mutation that causes fatal heart arrhythmias - UI The Daily Iowan
Posted: February 9, 2020 at 6:43 am
Having written for various publications for the past 30 years, I have for the most part avoided extending predictions or trends beyond the coming year or two.
But as we close out the decade and move into the new, Ive taken some time to reflect on the past 10 years and look ahead to what I believe are exciting things to come.
Making predictions might be best summarized by being either naive or foolish. Perhaps today, you get a bit of both. But I believe these technological advancements will significantly impact our lives during the next decade.
AI is growing at a pace perhaps not previously seen in human history.
Not only will AI impact the obvious areas predictive analytics and computer-assisted living devices in the home and workplace but even more critically in the field of medicine.
Humans, by 2030, will be helped through computer-assisted living.
Just as contact lenses can monitor diabetic insulin levels, AI will lead to a host of invasive and non-invasive sensors to collect and interpret tens of thousands of human body data points. The information can be shared against a database of millions of other patients to detect anomalies (while never compromising individual privacy).
The shared economy taking root in health care will enable AI to make determinations faster and more mobile.
AI will detect potential issues long before the patient feels sick. And it also will enable providers to create custom treatment plans specific to each patient and his or her symptoms based on the best outcome of treatment by aggregating the non-identifiable data of millions of other individuals.
Lab-grown meat is a dangerous prediction, being both from Iowa and personally loving a quality steak.
That said, with a population that could reach almost 9 billion by 2030, lab-grown meat (from the stem cells of real animals) has the chance to:
Reduce the environmental impact of raising animals.
Reduce the energy input required to raise a pound of fresh meat.
Use tiny spaces to grow significantly large quantities that can feed the world especially calorie-rich food products in countries where raising animals is not a viable option.
The U.S. could be a laggard in this regard, but lab-grown meat has the potential to play a significant role in feeding the world.
The smartphone, or the smart device we carry, will become the go-to for all things technology.
During the next 10 years, we will continue to see the mass deployment of thousands, if not tens of thousands, of micro-satellites that will enable individuals to be as connected to the web as if they were at their desktop at the office regardless of world locale.
The phone will continue to play a less and less significant role in the device. Added features will help run the household, collect volumes of health-related data points and, coupled with AI, suggest products, services and appointments based on complex algorithms.
By 2030, we will indeed have a significant time-saving device at our disposal. Think Siri and Alexa to a power of 10.
Higher education will see a considerable shift in delivery during the upcoming decade.
Some futurists predict as many as 50% of all higher education schools could close, merge or reinvent themselves before 2030. While I believe this prediction is high, I see higher education undergoing the most radical reinvention it has endured since its modern-day existence.
School debt is not sustainable. And some large countries are reporting wages for new graduates to be marginally better than the monthly earnings of unskilled labor.
The upcoming decade will press higher education to deliver knowledge and skills that are immediately transferable to the workplace, and job-training programs will continue to expand. Four-year brick and mortars will continue to be challenged by three-year online programs and, in some cases, 2.5-year programs.
Open-source education will gain increased value with employers by 2030. The cost will put downward pressure on the amount of time necessary to obtain an undergraduate, graduate and terminal degree.
Finally, be prepared to say goodbye to dozens of Fortune 500 companies.
The staying power of a Fortune 500 company has never been shorter. We are in a period of massive disruption.
A dozen or more of the top 100 companies in 2030 have yet to form as a company. And some of the names we trust and hold dear will quietly work their way into obsolescence.
Change is constant, and these predictions highlight the speed at which businesses, organizations and people are expected to change.
Todd Link is Senior Vice President of Risk Management and Remote Delivery at Dupaco Community Credit Union in Dubuque.
Posted: January 9, 2020 at 9:52 am
Dick Hakes, Taking Liberties Published 10:13 a.m. CT Jan. 2, 2020 | Updated 10:49 a.m. CT Jan. 3, 2020
Finn is shown with his father, John Hall, during the nearly 18-month period about ten years ago in which the boy battled cancer through chemotherapy, radiation and immunotherapy.(Photo: Special to the Press-Citizen)
John Hall of Iowa City recalls how it all started in early 2009.
Before his son Finns third birthday, the boy started spiking fevers. Then he complained of stiff legs. Then a black eye showed up that would not go away.
A CT scan eventually produced what John said was the worst call I ever received.
A tumor on Finns cheek was traced to another on his adrenal gland. It was stage four neuroblastoma. He had about a 35% to 40% chance to survive it.
What followed was almost 18 months of aggressive treatment at University of Iowa Hospitals and Clinics (UIHC) chemotherapy sessions, two surgeries, two stem cell transplants, radiation and finally immunotherapy, which had just been green-lighted for broader use nationwide.
Those months became a heartbreakingly painful, sleepless, worrisome and all-encompassing ordeal for the entire family especially for Finn.
A recent photo of Finn Hall shows a smiling, cancer-free kid wearing a T-shirt promoting the Red Shamrock Foundation started by his father, John Hall.(Photo: Special to the Press-Citizen)
It worked, however, and the cancer disappeared.
We threw the cancer playbook at him, John said. I give the immunotherapy regiment credit for saving his life. It took care of the remaining cancer cells in the end. He was the first patient to complete that regiment at the U.
But it wasnt long after Finn came home and the family worked to return to a normal life that a new troubling reality emerged that led John to form the Red Shamrock Foundation.
Our only focus was getting past the cancer, he said. But now, because he had received so many harsh treatments at such a young age, we realized Finn would need some type of specialized care for the rest of his life.
Finn is 13 now and leading a pretty normal life, but because chemotherapy killed the seeds of his adult teeth, he still has all of his baby teeth, which will have to be replaced when he becomes an adult. He also has some minor hearing loss, kidney damage and must take growth hormones.
But it could have been a lot worse, John said. After cancer, kids sometimes have serious cognitive issues or chronic heart disease or secondary cancers due to the chemo and radiation. Some lose a limb or an organ.
He says he was amazed to learn that 95% of young cancer survivors can expect some type of serious chronic health condition by the time they reach age 45.
It hit me that people need to know about this, he said. I wanted to raise awareness that youre not done just because you have left the hospital.
John formed his nonprofit in 2011 with the help of friends who could handle obtaining legal status and help design a professional logo and web pages. A shamrock logo with a red heart seemed appropriate, given the familys Irish heritage.
The Red Shamrock Foundation mission is simple: Raise public awareness of the unique needs of kids who survive cancer, plus support survivorship programs and post-cancer research in Iowa.
As detailed on its website at http://www.redshamrock.org, the group sponsors three large fundraising events each year: A trail race at Regina High School in the spring, a golf outing in Mount Vernon in June and a Red Tie Gala during Childhood Cancer Awareness Month in September. Other money comes from donations and an online store operated through One Mission Fund Raising of Mount Vernon.
John Hall of Iowa City founded the Red Shamrock Foundation to raise public awareness that children who survive cancer will often face other medical challenges related to their treatment for the rest of their lives.(Photo: Dick Hakes/Special to the Press-Citizen)
As its director, John meets monthly with his board and often promotes the cause by speaking to civic groups. He says securing about $25,000 from the local 100 Men Who Careorganization a few years ago helped raise our profile in the community. All involved with Red Shamrock are unpaid volunteers.
In the past few years, the nonprofit has donated $110,000 for research projects at the university and through Passport for Care to assemble data on the health and needs of post-cancer patients.
Red Shamrock also provides educational materials for parents and teachers on how to explain cancer to kids and what to expect when a cancer survivor returns to class.
Finn was out of preschool for a year and a half, going through all he went through, then suddenly found himself back at preschool surrounded by 30 active, screaming kids, John said. The teachers were good, but Id drop him off and hed just sit in the middle of the room and cry. It took maybe six months for him to get comfortable again.
Dick Hakes(Photo: Special to the Press-Citizen)
The next step for Red Shamrock, John says, is to try to find a national partner and increase its scope beyond Iowa. A dedicated Team Red Shamrock group that participates in running events in other locations may be the catalyst for this, he said.
He has high praise for UIHC and points out that it now operates a survivorship clinic directed by Dr. Bill Terry, a pediatric oncologist.
The bottom line is to raise awareness of what pediatric cancer patients must face after theyve already fought the battle of their lives,John said. People need to understand that their fight is never over.
John is an Elkader native, a University of Iowa graduate in anthropology and a 30-year resident of Iowa City who works for Coldwell Banker in real estate. His wife Monica is a nurse at UIHC. Finn has an older brother, Sully.
Posted: December 22, 2019 at 2:41 pm
Democratic presidential candidate and former Vice President Joe Biden claimed without evidence that more people are coming home from Iraq with brain cancer than any other war. He also suggested that burn pits open air waste incineration sites are behind the purported increase.
Existing statistics do not indicate that Iraq veterans are more affected by brain cancer than other veteran groups, although no comprehensive data is available to definitively say one way or the other.
The evidence on the cancer risk of burn pits is likewise inconclusive. A 2011 report by the National Academy of Sciences on the long-term health effects of burn pit exposure in Iraq and Afghanistan found that there was inadequate/insufficient evidence to determine whether there is an association with cancer. We didnt identify any published studies addressing a link to brain cancer since the review.
Bidens comments came during a CNN town hall in Iowa on Veterans Day, when he was asked by a woman in a military family how he, as president, would address the lack of mental health care and resulting homelessness among service members.
After promising to provide more services to veterans, Biden brought up his eldest son, Beau, who served in Iraq and died from an aggressive brain cancer known as glioblastoma in 2015.
Biden, Nov. 11: And I if youre my son did a year in Iraq. He came home we lost him, but he came home and, you know, one of the things we should be looking at is those burn pits that are there. That its just like, you know, when all the firemen in New York went down to 9/11, and so many got cancer, and particularly brain cancer, well, thats whats happening. More people are coming home from Iraq with brain cancer than ever before, than any other war.
And were in a situation where theres a direct connection between those burn pits and and and taking in that that that all that toxin thats available.
And we should say, anybody who was anywhere near those burn pits, thats all they have to show, that they and they get covered, they get all their health care covered.
Bidens comments echo previous statements he made in a PBS interview about his son and a potential link between military burn pits and brain cancer. In that 2018 interview, Biden said he was not aware of any direct scientific evidence tying cancer to burn pits, but postulated that the exposure which occurred in Iraq and also perhaps in Kosovo, where Beau had gone on a civilian mission may have played a role in his sons cancer.
The younger Biden deployed to Iraq for one year, from October 2008 until September 2009, as a captain in the Delaware Army National Guard. In 2013, he was diagnosed with a brain tumor and died two years later at the age of 46.
Well present whats known about burn pits and brain cancer, and also review the available statistics on how common brain cancer is among different veteran groups.
We were unable to find any support for Bidens claim that more people are coming home from Iraq with brain cancer than ever before, than any other war. His campaign did not reply to our request asking for a source for his statement.
The little data that exists does not suggest that Iraq veterans have developed brain cancer at higher rates than those who served in earlier wars.
According to a 2015 Veterans Affairs post-deployment surveillance report, which the agency said was the only current published data on this topic, brain cancer prevalence was 0.04% for Vietnam veterans and 0.03% for both Gulf War veterans and those who served in Iraq and Afghanistan post-9/11. The report documents the prevalence and incidence of brain cancer, among other health conditions, for users of VA health care between April 2014 and March 2015. The Iraq War started on March 20, 2003; the conflict in Afghanistan began on Oct. 7, 2001.
The report also lists the age-adjusted frequency of brain cancer among each veteran group by fiscal quarter. While these values fluctuate, the average of these frequencies for all veteran groups is approximately the same, around 4 to 5 cases per 100,000 service members, with post-9/11 veterans on the low end and Vietnam veterans on the high end.
Robert Bossarte, an epidemiologist at West Virginia University and the director of the VAs epidemiology program at the time of the 2015 report, told us in a phone interview that the brain cancer data in the report do not show much difference between any of the veteran groups.
But he also cautioned against thinking of the post-deployment data as definitive. The statistics, Bossarte noted, only cover one point in time, and are limited to veterans using VA services. That means the figures are missing large numbers of people who have already died and those who get their health care outside of the VA. Only about half of all veterans use the VA for their health care, and usage rates vary by era. As a result, he said, its difficult to draw conclusions from the data about how the different service groups compare.
Still, he said he was not aware of a single manuscript that has suggested there is a higher rate of brain cancer among post-9/11 veterans.
A VA spokesperson told us in an email that there is no evidence of increased brain cancer among Iraq War veterans, or any post-9/11 group, and directed us to the 2015 post-deployment report. She noted that the prevalence of brain cancer increases in all populations as one ages, and said that because cancers may take a long time to develop, the VA continues to study all causes of mortality for the deployed post 9/11 Veteran population.
The agency said it expects to release an updated post-deployment report in early 2020.
Bidens other main claim was his suggestion that burn pits are the reason why some veterans are developing brain cancer. There is little evidence to indicate thats true, although scientists have not ruled out a connection.
Burn pits are open areas in which trash from a military base is burned, typically because of a lack of other waste infrastructure, including incinerators. Although the U.S. military has significantly reducedthe use of burn pits, they once were common throughout war zones in the Middle East and Central Asia.
A 2010 Government Accountability Office report explains that before 2004, burn pits were the only method of waste management that the military used in Iraq and Afghanistan. In November 2009, the report adds, U.S. Central Command reported 50 active burn pits in Afghanistan and 67 in Iraq; by April 2010, this had changed to 184 and 52, respectively, and in August 2010, to 251 and 22.
U.S. Central Command created guidelines for burn pits in 2009, including prohibitions on burning certain materials, such as hazardous waste, plastic, batteries, tires and electronics, but the GAO report found that this guidance was not always followed.
The primary issue with burn pits is that the fumes from the combusted items contain toxins that could be harmful; many soldiers who returned complained of long-term health effects, especially breathing problems, that they believe stemmed from inhaling burn pit smoke.
Given these concerns, the VA asked the National Academy of Sciences to review the evidence on the long-term health effects of burn pits, including an analysis of raw air-sampling data taken from one of the most notorious burn pit sites, Joint Base Balad a large military base outside of Baghdad that in 2007 burned up to 200 tons of waste every day.
The resulting 2011 report was largely inconclusive. While recognizing the potential for serious health concerns and recommending further study, the committee concluded that it was unable to say whether long-term health effects are likely to result from exposure to emissions from the burn pit at JBB. The committee also suggested that long-term health effects might be more generally associated with service in Iraq and Afghanistan, rather than burn pit exposure per se, because of high levels of particulate air pollution on bases as a result of military activities and natural dust storms.
Based on a review of existing epidemiology studies, which evaluated similar, but not identical exposures, such as those experienced by firefighters and incineration workers, there was inadequate/insufficient evidence to determine whether there was an association between exposure to combustion products and a variety of health outcomes, including cancer, respiratory disease and circulatory disease. There was slightly more evidence to suggest a connection to reduced pulmonary function, which the report categorized as limited/suggestive evidence.
As the GAO report later summarized, while the NAS report did not determine a linkage to long-term health effects, because of the lack of data, it did not discredit the relationship either.
For brain cancer in particular, the report explained that while a few studies identified associations between firefighting and brain cancer, the largest cohort study and the only one that quantified exposure was negative. Given the mixed results and limitations of the studies, the committee could not make a determination about a potential link but said that [b]ecause of the carcinogenic nature of many of the chemicals potentially associated with burn pit emissions, it is prudent to continue investigations of cancer end points and other health outcomes that have long latency in exposed military populations.
A follow-up report from the National Academy of Sciences in 2017, which focused on an evaluation of the VAs Burn Pit Registry, reviewed new studies published since the 2011 report relating to burn pits, but the majority were focused on respiratory diseases. None of them addressed cancer.
We also did not find any studies since these reviews that assessed a potential link between burn pits and brain cancer in the biomedical literature.
David Savitz, an epidemiologist at Brown University, and chair of the National Academy committee that conducted the 2017 review, told us in a phone interview that he was not aware of any evidence specifically linking burn pit exposures to brain cancer, and added, It seems unlikely that were going to have such evidence.
Part of this, he said, has to do with how rare brain cancer is only about 1% of new cancer cases in the U.S. every year are due to brain tumors, making it hard to study. But also, he said, brain cancer is not at the top of the list of diseases that one would expect from burn pit exposure.
We dont know what the consequences of burn pit exposure are with a high degree of confidence, he said, but they go more toward respiratory diseases and cardiovascular risks, not brain cancer.
Indeed, very little is known about what causes brain tumors in general. Jill Barnholtz-Sloan, a brain tumor researcher at Case Western Reserve University, said in a phone interview that there are a few genetic risk factors, including some inherited predisposition syndromes and single-letter DNA changes, but these do not explain the vast majority of brain tumors.
Similarly, the only well-established environmental risk factor that increases risk is ionizing radiation to the head and neck, Barnholtz-Sloan said. High doses of ionizing radiation confer a 2-to-4 fold increase in risk, she said, depending on the type of brain tumor a fact revealed by studies of children immigrating to Israel in the 1950s who had their scalps irradiated to treat ringworm infection. Smoking, interestingly, is not associated with brain cancer.
The only other well-validated factor is a history of allergies, which appears to provide some protection against developing a brain tumor. Several studies have shown that people with allergies and related conditions, such as asthma, hay fever and eczema, have a reduced risk of brain cancer. While scientists dont fully understand why this might be, Barnholtz-Sloan said the running hypothesis is that people with these diseases may have revved up immune systems, which may be able to kill cells that turn cancerous more quickly.
The fact that there are not more environmental factors may stem from the brains naturally high level of defense. Evolutionarily, if you think about your brain as the epicenter of your body your CPU its highly protected, Barnholtz-Sloan said, noting the multiple membranes surrounding the brain, along with the blood-brain barrier and skull. Environmental exposures would have to permeate a lot of layers of hard things to get in to affect cells. This is one reason why its so hard to find drugs to treat brain diseases, she said.
While Savitz said that no long-term health effects have yet been clearly linked to burn pit exposure, he said that that should not be interpreted to mean that burn pits dont cause health problems.
The absence of evidence is not the evidence of absence, he said. There may well be a problem, its just a matter of direct evidence. He is conducting a three-year study to further investigate the long-term health effects of burn pits, but is unaware of anyone doing specific research on cancer.
The VAs Airborne Hazards and Open Burn Pit Registry allows eligible service members to report health concerns related to burn pits and other airborne hazards. The National Academy of Sciences, however, identified multiple flaws in the registry that led to low completion rates, and recommended numerous changes to increase the registrys utility. The committee also stated that as a voluntary, self-reported registry, it was fundamentally unsuitable for addressing the question of whether these exposures have, in fact, caused health problems.
In an email, the VA defended its registry, saying that it had completed most of the academys suggested improvements, and that the registry is a very good tool for health surveillance. The agency also pointed to its new research hub on airborne hazards and burn pits, which opened in May 2019, and said another consensus report from the National Academy of Sciences is expected in May 2020. That report, the VA said, will focus on the hazards of burn pits and other exposures, and will include cancer outcomes.
Other groups, too, have stepped in to collect data. Burn Pit 360, a nonprofit veterans group, set up its own voluntary registry for people to report health complaints from burn pits. Rosie Torres, one of the co-founders of the organization, told us that as of March 2019, there had been 97 reports of brain cancer out of approximately 6,000 submissions.
Savitz, however, said that neither registry likely will yield any concrete answers. They can generate possibilities, they can point to where problems may exist, he said, but theyre not a substitute for carefully designed research.
Although future studies may eventually come out to change scientific opinion, there is no direct evidence that burn pits cause brain cancer, and no indication that Iraq War veterans are especially affected by brain cancer, as Biden claimed.
The rest is here:
Biden Exaggerates Science on Burn Pits and Brain Cancer - FactCheck.org
Fate Therapeutics Inc. (FATE) and KemPharm Inc. (NASDAQ:KMPH) Comparison side by side – The EN Herald
Posted: September 23, 2019 at 6:46 am
This is therefore a contrasting of the risk, analyst recommendations, institutional ownership, profitability, dividends, earnings and valuation in Fate Therapeutics Inc. (NASDAQ:FATE) and KemPharm Inc. (NASDAQ:KMPH). The two are both Biotechnology companies that compete with one another.
Valuation and Earnings
Table 1 shows top-line revenue, earnings per share (EPS) and valuation of the two companies.
Table 2 represents Fate Therapeutics Inc. (NASDAQ:FATE) and KemPharm Inc. (NASDAQ:KMPH)s net margins, return on equity and return on assets.
Volatility & Risk
A 1.62 beta indicates that Fate Therapeutics Inc. is 62.00% more volatile compared to S&P 500. Competitively, KemPharm Inc.s beta is 1.33 which is 33.00% more volatile than S&P 500.
Fate Therapeutics Inc.s Current Ratio is 6.4 while its Quick Ratio is 6.4. On the competitive side is, KemPharm Inc. which has a 1 Current Ratio and a 1 Quick Ratio. Fate Therapeutics Inc. is better positioned to pay off short and long-term obligations compared to KemPharm Inc.
The next table highlights the delivered recommendations and ratings for Fate Therapeutics Inc. and KemPharm Inc.
Fate Therapeutics Inc. has a 30.49% upside potential and a consensus price target of $23.75. Meanwhile, KemPharm Inc.s average price target is $1.05, while its potential upside is 28.83%. Based on the analysts view we can conclude, Fate Therapeutics Inc. is looking more favorable than KemPharm Inc.
Institutional and Insider Ownership
Institutional investors owned 98.8% of Fate Therapeutics Inc. shares and 33.5% of KemPharm Inc. shares. Fate Therapeutics Inc.s share owned by insiders are 0.9%. Comparatively, KemPharm Inc. has 0.5% of its share owned by insiders.
In this table we show the Weekly, Monthly, Quarterly, Half Yearly, Yearly and YTD Performance of both pretenders.
For the past year Fate Therapeutics Inc. had bullish trend while KemPharm Inc. had bearish trend.
On 8 of the 9 factors Fate Therapeutics Inc. beats KemPharm Inc.
Fate Therapeutics, Inc., a clinical-stage biopharmaceutical company, develops programmed cellular immunotherapies for cancer and immune disorders worldwide. Its immuno-oncology product candidates include FATE-NK100, a natural killer (NK) cell cancer immunotherapy that consists of adaptive memory NK cells; engineered hnCD16 induced pluripotent stem cells (iPSC)-derived natural killer cell therapy candidates for hematologic/solid tumors; and engineered chimeric antigen receptor iPSC-derived T cell therapy product candidates for hematologic/solid tumors. The companys immuno-regulation product candidates comprise ProTmune, an investigational programmed cellular immunotherapy for use as a next-generation allogeneic hematopoietic cell transplantation cell graft; and ToleraCyte for the treatment of autoimmune and inflammatory diseases; engineered iPSC-derived CD34+ cell therapy for immune disorders. Fate Therapeutics, Inc. has a research collaboration and license agreement with Memorial Sloan Kettering Cancer Center to develop off-the-shelf T-cell immunotherapies; and strategic research collaboration and license agreement with Juno Therapeutics, Inc. to identify small molecule modulators that enhance the function of T cells. Fate Therapeutics, Inc. was founded in 2007 and is headquartered in San Diego, California.
KemPharm, Inc., a clinical-stage specialty pharmaceutical company, discovers and develops new proprietary prodrugs in the United States. Its lead product candidates are KP415, an extended release d-threo-methylphenidate product candidate for the treatment of ADHD; and KP201/IR, an IR formulation of KP201, a prodrug of hydrocodone and acetaminophen for the treatment of acute pain. The company is also involved in developing KP511/ER, a prodrug of hydromorphone for the management of pain; KP511/IR for the short duration management of acute pain; KP606/IR, an IR formulation of KP606, a prodrug of oxycodone for the management of moderate to severe pain; KP746, a prodrug of oxymorphone for the management of moderate to severe pain; and KP303, a prodrug of quetiapine for the treatment of central nervous system disorders. KemPharm, Inc. was founded in 2006 and is headquartered in Coralville, Iowa.
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Fate Therapeutics Inc. (FATE) and KemPharm Inc. (NASDAQ:KMPH) Comparison side by side - The EN Herald