Category Archives: Utah Stem Cells

Utah author Gretchen Day has a newly released childrens STEM book, Olivias Tower: The Building Power of Cells. The book introduces young readers to the scientific process, and the parts of the cell, but more importantly it shows kids the importance of asking questions, finding answers, and learning about the world around them.

It was inspired by Gretchens childhood experience of watching her mom, a molecular biologist, work in a lab. Gretchenworked in the lab with her mom for a short time after high school, and it left a big impression the rooms full of microscopes, the opportunities to learn, and the people who came from around the world to work and study.

Gretchen works as a journalist, but she always knew she wanted to write a childrens book, and she decided the lab was the perfect setting. Books allow kids to explore their interests, learn about themselves, and think about their future. STEM jobs are growing in demand, yetwomen account for only 24 percent of the STEM workforce, according to a study from the U.S. Department of Commerce. Its fun for young girls and boys to see themselves working in STEM related fields in books and other media. Regardless of a childs future career interests, they can gain knowledge and confidence when they learn about the world.

Olivias Tower: The Building Power of Cells was released on October 3rd from Storybook Genius Publishing. Its available on Amazon, Barnes & Noble online, or atoliviastower.com

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Childrens book, Olivias Tower: The Building Power of Cells - ABC 4

Is Utah Cord Bank Peddling Dangerous (and Ineffective) Stem Cell Products?

A Pittsburgh woman claims she suffered horrific injuries after being injected by a stem cell product called StemVive marketed by the Utah Cord Bank. Last month Marianne Cornetti filed a lawsuit against the maker of the product and the chiropractors office where she received the injection.

We have long warned about the dangers of stem cell products. Although the industry is still in its infancy, there is great promise for life changing therapies. Unfortunately, several products have received FDA approval for limited purposes, the marketplace still resembles the wild west. Some companies produce untested and poor quality products in garages while other companies make wild claims just like the traveling snake oil salesmen of the 1800s.

In this post we will share Marianne Cornetts story and then discuss how to separate the good companies from the bad and how to sue if you are injured by a defective stem cell product.

Mariannes story begins in May 2019 after she saw an ad for stem cell injections. The business behind the ad campaign was Verri Chiropractic Associates and its owner, Dr, Frank Verri. She attended a seminar sponsored by the chiropractic office and the Utah Cord Bank. During the seminar she heard that stem cell injections could be used as a treatment for arthritis.

She says that seminar promoted a product called StemVive. The seminar touted the safety, efficacy, approval and certification of the product, for the treatment of degenerative joint disease including arthritis.

Marianne became a patient of Dr. Verris clinic. On May 14th, she received multiple stem cell injections in both knee joints. The injections were either made or sold by Utah Cord Bank and were administered by a nurse practitioner.

What is unusual is that a representative of Utah Cord Bank was present for the injections.

Marianne says she was told the StemVive product contained viable stem cells, that the product would grow stem cell colonies, that the cell forming properties of the product exceeded the capabilities of her own bone marrow, that the FDA had approved the product for the treatment of degenerative joint arthritis and that the product was safe. According to her lawsuit, all of those claims are false.

Shortly after receiving the injections, Marianne says she suffered from a wide variety of side effects including:

There are several interesting twists to Mariannes complaint.

First, the stem cell advertisement and subsequent seminar were sponsored by a chiropractor. Depending on the state, in many locations advising patients on stem cell therapies is outside their scope of practice.

Despite our belief that stem cells should only be prescribed by a medical doctor, many chiropractors have jumped on the stem cell bandwagon and see the product as an extra revenue source.

We believe that Marianne was pressured to sign up while attending a seminar. If I have arthritis, my doctor doesnt invite me to a seminar. We meet her in office, discuss options and agree on a treatment plan. Because many insurances dont pay for non-FDA approved treatments and products, stem cell hucksters use seminars as a way to woo new patients into forking over thousands of dollars in return for a miracle cure. Its also probably why a representative of the Utah Cord Bank was present when she was injected; many of these seminars are high pressure meaning they want patients to sign up and pay immediately before they change their mind.

If the patients are lucky, they just lose their money. If they are like Marianne, they have permanent disabling injuries.

Next, Marianne sued not only the Utah Cord Bank but also Dr. Verri, his chiropractic office and the nurse practitioner who did the actual injection. In our experience, many garage based stem cell makers and distributors dont have much in the way of insurance. Physicians, healthcare clinics and nurses, on the other hand, usually have good liability insurance.

Finally, Marianne says the stem cell products werent viable. We agree and that is a huge problem. To get the benefits of live stem cells, they must be living. Many companies, however, sell freeze dried product. If it was flash frozen, any living cells are dead.

An expos from a competitor said the product they obtained from Utah Cord Bank was frozen. It shouldnt be surprising then, that the StemVive sample had no active colonies.

In May, 2019, the New Yorker ran a story that claims two former employees of the Utah Cord Bank says the company used expired chemicals and reagents in their lab. The company denied those allegations.

Because the lawsuit was just filed, we dont know how any of the defendants will respond. Utah Cord Banks website claims, We Change Lives. If you ask Marianne Cornetti, the change she experienced is not very good.

Some stem cell products have received FDA approval and are already on the market. Others have obtained an FDA investigational new drug designation. According to the National Institutes of Health (NIH), more than 1,000 clinical trials examining stem cell therapies are currently underway.

All manufacturers of FDA-regulated stem cell products must adhere to strict FDA safety guidelines regarding manufacturing practices to ensure safety, potency, and purity. Patients injured by contaminated products have the right to file a stem cell lawsuit for financial compensation, including money to pay for past and future medical expenses, lost wages, pain and suffering, and other damages. (If a patient receives dead cells or if the company selling the cell products makes inaccurate claims about the effectiveness of its products, you may also have a claim.)

Since properly prepared stem cell therapies rarely cause serious complications, you may be eligible to file a stem cell lawsuit if you suffered serious injury due to a stem cell product.[See our contact information at the end of this post.]

To meet FDA current good manufacturing practices (cGMP) requirements, stem cell companies must maintain a sterile facility to prevent risk of contamination. Live stem cells must be irradiated to ensure no bacterial or viral contamination is present.

Many stem cell products are manufactured overseas, making efficient FDA regulation difficult. With an FDA staffing shortage, overseas stem cell companies arent worried about surprise inspections and often fail to maintain a sterile facility or have proper quality control testing.

The dangerous products lawyers at Mahany Law are interested in hearing from anyone who has experienced serious complications after stem cell therapy.

Working with our national network of dangerous drug lawyers, we can help you receive answers and compensation. Stem cell products may be the future of modern medicine. Unfortunately, there are far too many companies rushing into the field with untested or dangerous products and making wild claims of miracle cures.

To learn more, visit our Stem Cell Injury Lawsuit page. Ready to see if you have a claim for your injuries (or if you are an insider with information that can help patients) contact us by email at *protected email*, by phone at 202-800-9791, or online.

All inquiries are kept strictly confidential. Cases handled on a contingency fee basis meaning no fees unless we win and recover money on your behalf.

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New Stem Cell Injury Lawsuit Filed StemVive & Utah Cord Bank

SALT LAKE CITY, Utah, May 14, 2020 /PRNewswire/ -- Tolero Pharmaceuticals, Inc., a clinical-stage company focused on developing novel therapeutics for hematological and oncological diseases, today announced that the first patient has been dosed with a one-hour dosing schedule for investigational agent alvocidib, a potent CDK9 inhibitor, administered in sequence after azacitidine, in the expansion of the Phase 1b/2 Zella 102 study in patients with myelodysplastic syndromes (MDS).

The Zella 102 study is being conducted in patients with previously untreated MDS and patients with MDS who have received fewer than six cycles of treatment with a hypomethylating agent. The initial study design was to evaluate the safety and efficacy of alvocidib using a 30-minute bolus followed by a four-hour intravenous infusion (IVI), in combination with decitabine. An amendment was made to the study design to include treatment with azacitidine, in sequence before a one-hour infusion of alvocidib.

"We are pleased that this study now includes both standard of care hypomethylating agents for patients with myelodysplastic syndromes. In addition, the expansion of this study offers an alternative alvocidib dosing schedule, which reduces the amount of time patients spend in infusion," said David J. Bearss, Ph.D., Chief Executive Officer, Tolero Pharmaceuticals, and Chief Scientific Officer and Global Head of Research, Global Oncology. "Preclinical research suggests that treatment with hypomethylating agents may sensitize MDS blast cells to suppression of MCL-1 through alvocidib. We look forward to building our understanding of the potential role of alvocidib in this patient population."

MDS is a form of cancer that can occur when cells in the bone marrow are abnormal and create defective blood cells, which often die earlier than normal cells. In one of three patients, MDS can progress into AML, a rapidly growing cancer of bone marrow cells.1

About the Zella 102 Study

The Zella 102 study is an open-label, dose-escalation Phase 1b/2 study evaluating the safety and efficacy of alvocidib, when administered in sequence after either decitabine or azacitidine, in patients with previously untreated MDS and patients with MDS who have received fewer than six cycles of treatment with hypomethylating agents. The primary objective of the Phase 1b portion of the study is to determine the maximum tolerated dose and recommended Phase 2 dose of alvocidib, when administered in these regimens. Secondary objectives are to determine the complete response rate and if treatment with alvocidib, administered in sequence after decitabine or azacitidine, results in improvements in transfusion dependence and/or hemoglobin level.

The primary objective of the Phase 2 portion of the study will be to determine the objective response rate of alvocidib, when administered to untreated patients with de novo or secondary MDS in sequence after a hypomethylating agent, using revised International Working Group (IWG) criteria.

The trial is being conducted at sites in the United States. Additional information on this trial, including comprehensive inclusion and exclusion criteria, can be accessed at http://www.ClinicalTrials.gov(NCT03593915).

About Alvocidib

Alvocidib is an investigational small molecule inhibitor of cyclin-dependent kinase 9 (CDK9) currently being evaluated in the Phase 2 studies Zella 202, in patients with acute myeloid leukemia (AML) who have either relapsed from or are refractory to venetoclax in combination with decitabine or azacitidine (NCT03969420) and Zella 201, in patients with relapsed or refractory MCL-1 dependent AML, in combination with cytarabine and mitoxantrone (NCT02520011). Alvocidib is also being evaluated in Zella 101, a Phase 1 clinical study evaluating the maximum tolerated dose, safety and clinical activity of alvocidib in combination with cytarabine and daunorubicin (7+3) in newly diagnosed patients with AML (NCT03298984), and Zella 102, a Phase 1b/2 study in patients with myelodysplastic syndromes (MDS) in combination with decitabine or azacitidine (NCT03593915). In addition, alvocidib is being evaluated in a Phase 1 study in patients with relapsed or refractory AML in combination with venetoclax (NCT03441555).

About CDK9 Inhibition and MCL-1

MCL-1 is a member of the apoptosis-regulating BCL-2 family of proteins.2 In normal function, it is essential for early embryonic development and for the survival of multiple cell lineages, including lymphocytes and hematopoietic stem cells.3 MCL-1 inhibits apoptosis and sustains the survival of leukemic blasts, which may lead to relapse or resistance to treatment.2,4 The expression of MCL-1 in leukemic blasts is regulated by cyclin-dependent kinase 9 (CDK9).5,6 Because of the short half-life of MCL-1 (2-4 hours), the effects of targeting upstream pathways are expected to reduce MCL-1 levels rapidly.5 Inhibition of CDK9 has been shown to block MCL-1 transcription, resulting in the rapid downregulation of MCL-1 protein, thus restoring the normal apoptotic regulation.2

About Tolero Pharmaceuticals, Inc.

Tolero Pharmaceuticals is a clinical-stage biopharmaceutical company researching and developing treatments to improve and extend the lives of patients with hematological and oncological diseases. Tolero has a diverse pipeline that targets important biological drivers of blood disorders to treat leukemias, anemia, and solid tumors, as well as targets of drug resistance and transcriptional control.

Tolero Pharmaceuticals is based in the United States and is an indirect, wholly owned subsidiary of Sumitomo Dainippon Pharma Co., Ltd., a pharmaceutical company based in Japan. Tolero works closely with its parent company, Sumitomo Dainippon Pharma, and Boston Biomedical, Inc., also a wholly owned subsidiary, to advance a pipeline of innovative oncology treatments. The organizations apply their expertise and collaborate to achieve a common objective - expediting the discovery, development and commercialization of novel treatment options.

Additional information about the company and its product pipeline can be found at http://www.toleropharma.com.

Tolero Pharmaceuticals Forward-Looking Statements

This press release contains "forward-looking statements," as that term is defined in the Private Securities Litigation Reform Act of 1995 regarding the research, development and commercialization of pharmaceutical products. The forward-looking statements in this press release are based on management's assumptions and beliefs in light of information presently available, and involve both known and unknown risks and uncertainties, which could cause actual outcomes to differ materially from current expectations. Any forward-looking statements set forth in this press release speak only as of the date of this press release. We do not undertake to update any of these forward-looking statements to reflect events or circumstances that occur after the date hereof. Information concerning pharmaceuticals (including compounds under development) contained within this material is not intended as advertising or medical advice.

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SOURCE Tolero Pharmaceuticals, Inc.

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Tolero Pharmaceuticals Announces Expansion of the Zella 102 Study in Patients with Intermediate and High-Risk Myelodysplastic Syndromes (MDS) -...

This discovery may have clinical importance in management of heart failure.

This discovery may have clinical importance in management of heart failure.Many heart diseases are linked to oxidative stress, an overabundance of reactive oxygen species. The body reacts to reduce oxidative stress where the redox teeter-totter has gone too far up through production of endogenous antioxidants that reduce the reactive oxygen species. This balancing act is called redox homeostasis.

But what happens if the redox teeter-totter goes too far down, creating antioxidative stress, also known as reductive stress? Rajasekaran Namakkal-Soorappan, Ph.D., associate professor in the University of Alabama at Birmingham Department of Pathology, and colleagues have found that reductive stress, or RS/AS, is also pathological. This discovery, they say, may have clinical importance in management of heart failure.

They report that RS causes pathological heart enlargement and diastolic dysfunction in a mouse model. This study, published in the journal Antioxidants and Redox Signaling, was led by Namakkal-Soorappan and Pei Ping, Ph.D., David Geffen School of Medicine at the University of California-Los Angeles.

Antioxidant-based therapeutic approaches for human heart failure should consider a thorough evaluation of antioxidant levels before the treatment, they said. Our findings demonstrate that chronic RS is intolerable and adequate to induce heart failure.

The study used transgenic mice that had upregulated genes for antioxidants in the heart, which increased the amounts of antioxidant proteins and reduced glutathione, creating RS. One mouse line had low upregulation, and one had high upregulation, creating chronic low RS and chronic high RS, respectively, in the hearts of the mice.

The mice with high RS showed pathological heart changes called hypertrophic cardiomyopathy, and had an abnormally high heart ejection fraction and diastolic dysfunction at 6 months of age. Sixty percent of the high-RS mice died by 18 months of age.

The mice with low RS had normal survival rates, but they developed the heart changes at about 15 months of age, suggesting that even moderate RS can lead to irreversible damage in the heart over time.

Giving high-RS mice a chemical that blocked biosynthesis of glutathione, beginning at about 6 weeks of age, prevented RS and rescued the mice from pathological heart changes.

Gobinath Shanmugam, Ph.D., postdoctoral fellow in the UAB Department of Pathology, and Namakkal-Soorappan point out that a 2019 survey found about 77 percent of Americans are consuming dietary supplements every day, and within this group, about 58 percent are consuming antioxidants as multivitamins. Thus, a chronic consumption of antioxidant drugs by any individual without knowing their redox state might result in RS, which can induce pathology and slowly damage the heart.

In a related study, published in the journal Redox Biology, Namakkal-Soorappan looked at the impact of RS on myosatellite cells, which are also known as muscle stem cells. These cells, located near skeletal muscle fibers, are able to regenerate and differentiate into skeletal muscle after acute or chronic muscle injury. The regulation of myosatellite cells is of interest given the loss of skeletal muscle mass during aging or in chronic conditions like diabetes and AIDS.

Recently, Namakkal-Soorappan reported that tilting the redox teeter-totter to oxidative stress impaired regeneration of skeletal muscle. Now, in the Redox Biology paper, he has shown that tilting the redox to RS also causes significant inhibition of muscle satellite cell differentiation.

Rather than genetic manipulation to induce RS, as was done in the heart study, the researchers used the chemical sulforaphane or direct augmentation of intracellular glutathione to induce RS in cultured mouse myoblast cells. Both treatments inhibited myoblast differentiation. Finally, authors attempted to withdraw antioxidative stress by growing cells in medium without sulforaphane, which removes the RS and accelerates the differentiation. Namakkal-Soorappan and colleagues found that a pro-oxidative milieu, through a mild generation of reactive oxygen species, was required for myoblast differentiation.

The researchers also showed that genetic silencing of a negative regulator of the antioxidant genes also inhibited myoblast differentiation.

Co-authors with Namakkal-Soorappan and Ping, and first-author Shanmugam, in the Antioxidants and Redox Signaling study, Reductive stress causes pathological cardiac remodeling and diastolic dysfunction, are Silvio H. Litovsky and Rajesh Kumar Radhakrishnan, UAB Department of Pathology; Ding Wang, UCLA; Sellamuthu S. Gounder, Kevin Whitehead, Sarah Franklin and John R. Hoidal, University of Utah School of Medicine; Jolyn Fernandes and Dean P. Jones, Emory University, Atlanta, Georgia; Thomas W. Kensler, Fred Hutch Cancer Research Center, Seattle, Washington; Louis DellItalia, UAB Department of Medicine; Victor Darley-Usmar, UAB Department of Pathology; and E. Dale Abel, University of Iowa.

In the Redox Biology study, Reductive stress impairs myogenic differentiation, co-authors with Namakkal-Soorappan are Sandeep Balu Shelar, UAB Department of Pathology; Dean P. Jones, Emory University; and John R. Hoidal, University of Utah School of Medicine.

Support for both studies came from National Institutes of Health grants HL118067 and AG042860, American Heart Association grant BGIA 0865015F, the University of Utah, and UAB.

In the two studies, Namakkal-Soorappans name is listed as Namakkal S. Rajasekaran.

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Surplus antioxidants are pathogenic for hearts and skeletal muscle - The Mix

For years, scientists have predicted that 3-D printingwhich has been used it to make toys, homes, scientific tools and even a plastic bunny that contained a DNA code for its own replicationcould one day be harnessed to print live, human body parts to mitigate a shortage of donor organs. So far, researchers also used 3-D printing in medicine and dentistry to create dental implants, prosthetics, and models for surgeons to practice on before they make cuts on a patient. But many researchers have moved beyond printing with plastics and metalsprinting with cells that then form living human tissues.

No one has printed fully functional, transplantable human organs just yet, but scientists are getting closer, making pieces of tissue that can be used to test drugs and designing methods to overcome the challenges of recreating the bodys complex biology.

A confocal microscopy image showing 3-Dprinted stem cells differentiating into bone cells

The first 3-D printer was developed in the late 1980s. It could print small objects designed using computer-aided design (CAD) software. A design would be virtually sliced into layers only three-thousandths of a millimeter thick. Then, the printer would piece that design into the complete product.

There were two main strategies a printer might use to lay down the pattern: it could extrude a paste through a very fine tip, printing the design starting with the bottom layer and working upward with each layer being supported by the previous layers. Alternatively, it could start with a container filled with resin and use a pointed laser to solidify portions of that resin to create a solid object from the top down, which would be lifted and removed from the surrounding resin.

When it comes to printing cells and biomaterials to make replicas of body parts and organs, these same two strategies apply, but the ability to work with biological materials in this way has required input from cell biologists, engineers, developmental biologists, materials scientists, and others.

So far, scientists have printed mini organoids and microfluidics models of tissues, also known as organs on chips. Both have yielded practical and theoretical insights into the function of the human body. Some of these models are used by pharmaceutical companies to test drugs before moving on to animal studies and eventually clinical trials. One group, for example, printed cardiac cells on a chip and connected it to a bioreactor before using it to test the cardiac toxicity of a well-known cancer drug, doxorubicin. The team showed that the cells beating rate decreased dramatically after exposure to the drug.

However, scientists have yet to construct organs that truly replicate the myriad structural characteristics and functions of human tissues. There are a number of companies who are attempting to do things like 3-D print ears, and researchers have already reported transplanting 3-D printed ears onto children who had birth defects that left their ears underdeveloped, notes Robby Bowles, a bioengineer at the University of Utah. The ear transplants are, he says, kind of the first proof of concept of 3-D printing for medicine.

THE SCIENTIST STAFF

Bowles adds that researchers are still a ways away from printing more-complex tissues and organs that can be transplanted into living organisms. But, for many scientists, thats precisely the goal. As of February 2020, more than 112,000 people in the US are waiting for an organ transplant, according to the United Network for Organ Sharing. About 20 of them die each day.

For many years, biological engineers have tried to build 3-D scaffolds that they could seed with stem cells that would eventually differentiate and grow into the shapes of organs, but to a large extent those techniques dont allow you to introduce kind of the organization of gradients and the patterning that is in the tissue, says Bowles. There is no control over where the cells go in that tissue. By contrast, 3-D printing enables researchers with to very precisely direct the placement of cellsa feat that could lead to better control over organ development.

Ideally, 3-D printed organs would be built from cells that a patients immune system could recognize as its own, to avoid immune rejection and the need for patients to take immunosuppressive drugs. Such organs could potentially be built from patient-specific induced pluripotent stem cells, but one challenge is getting the cells to differentiate into the subtype of mature cell thats needed to build a particular organ. The difficulty is kind of coming together and producing complex patternings of cells and biomaterials together to produce different functions of the different tissues and organs, says Bowles.

To imitate the patterns seen in vivo, scientists print cells into hydrogels or other environments with molecular signals and gradients designed to coax the cells into organizing themselves into lifelike organs. Scientists can use 3-D printing to build these hydrogels as well. With other techniques, the patterns achieved have typically been two-dimensional, Eben Alsberg, a bioengineer at the University of Illinois, tells The Scientist in an email. Three-dimensional bioprinting permits much more control over signal presentation in 3D.

So far, researchers have created patches of tissue that mimic portions of certain organs but havent managed to replicate the complexity or cell density of a full organ. But its possible that in some patients, even a patch would be an effective treatment. At the end of 2016, a company called Organovo announced the start of a program to develop 3-D printed liver tissue for human transplants after a study showed that transplanted patches of 3-D printed liver cells successfully engrafted in a mouse model of a genetic liver disease and boosted several biomarkers that suggested an improvement in liver function.

Only in the past few years have researchers started to make headway with one of the biggest challenges in printing 3-D organs: creating vasculature. After the patches were engrafted into the mouses liver in the Organovo study, blood was delivered to it by the surrounding liver tissue, but an entire organ would need to come prepared for blood flow.

For any cells to stay alive, [the organ] needs that blood supply, so it cant just be this huge chunk of tissue, says Courtney Gegg, a senior director of tissue engineering at Prellis Biologics, which makes and sells scaffolds to support 3-D printed tissue. Thats been recognized as one of the key issues.

Mark Skylar-Scott, a bioengineer at the Wyss Institute, says that the problem has held back tissue engineering for decades. But in 2018, Sbastian Uzel, Skylar-Scott, and a team at the Wyss Institute managed to 3-D print a tiny, beating heart ventricle complete with blood vessels. A few days after printing the tissue, Uzel says he came into the lab to find a piece of twitching tissue, which was both very terrifying and exciting.

For any cells to stay alive, [the organ] needs that blood supply, so it cant just be this huge chunk of tissue.

Courtney Gegg, Prellis Biologics

Instead of printing the veins in layers, the team used embedded printinga technique in which, instead of building from the bottom of a slide upwards, material is extruded directly into a bath, or matrix. This strategy, which allows the researchers to print free form in 3-D, says Skylar-Scott, rather having to print each layer one on top of the other to support the structure, is a more efficient way to print a vascular tree. The matrix in this case was the cellular material that made up the heart ventricle. A gelatin-like ink pushed these cells gently out of the way to create a network of channels. Once printing was finished, the combination was warmed up. This heat caused the cellular matrix to solidify, but the gelatin to liquify so it could then be rinsed out, leaving space for blood to flow through.

But that doesnt mean the problem is completely solved. The Wyss Institute teams ventricle had blood vessels, but not nearly as many as a full-sized heart. Gegg points out that to truly imitate human biology, an individual cell will have to be within 200 microns of your nearest blood supply. . . . Everything has to be very, very close. Thats far more intricate than what researchers have printed so far.

Due to hurdles with adding vasculature and many other challenges that still face 3-Dprinted tissues, laboratory-built organs wont be available for transplant anytime soon. In the meantime, 3-D printing portions of tissue is helping accelerate both basic and clinical research about the human body.

Emma Yasinski is a Florida-based freelance reporter. Follow her on Twitter@EmmaYas24.

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On the Road to 3-D Printed Organs - The Scientist

Evolutionary biologist Patty Brennan had watched a lot of birds have sex. But in 2002, in Costa Rica, she saw something she never had before: a bird penis.

Most male birds don't have penises. They mate using an opening called a cloacaderived from the Latin word for sewer. It's a cavity inside a bird's anus that's a one-stop shop for the digestive, urinary, and reproductive tracts. When birds mate, the male and female cloaca touch. The male releases sperm, and it enters the females body. It's referred to, somewhat romantically, as a "cloacal kiss."

Brennan was observing a pair of Great tinamousbrown, chicken-like birds with small heads that live in the Costa Rican forest. Instead of just the subtle and brief cloacal kiss, the male bird grabbed the female by the neck. Then, the two birds started walking around still attached, as if they were fused together. When they separated, she saw a white, tentacle-looking organ hanging from his body.

"This was unlike anything I had ever seen," she said. "I was like, is this a penis?" (According to biologist Richard Prum, the tinamous penis had been seen and described by Victorian anatomists, but the appendage was forgotten to science. Her sighting was probably the first-ever observation of the tinamou penis in action," he wrote in a 2017 book.)

That unexpected bird penis launched Brennan, now an assistant professor of biological sciences at Mount Holyoke College, into a career of studying the weird and wonderful variations of genitalia in the natural world. But unlike many scientists before her who had noticed the dizzying variety of penises out there, Brennan began to ask: What about the vaginas? A long-standing misconception in evolutionary biology was that penises were incredibly diverse, but vaginas were not. In the past two decades, biologists, like Brennan, have been finding otherwise.

While doing so, they've been uncovering how gender biases might have played a role in obscuring vaginal variety, and how excluding vaginas from the study of genital evolution led to gaping holes in our understanding of why genitals look and behave the way they do. Only by examining how male and female parts evolve together can we see how sometimes, strange genitals are a result of sexual conflicteach sex trying to get the upper hand to control the reproductive act to best suit their needs. That's what Brennan learned, not through bird penises alone, but also through the vaginas with which they interact.

After her encounter in Costa Rica, Brennan wanted to continue studying bird genitalia. She shifted her focus to ducks, a more accessible subject than tinamous. At a duck farm in California's Central Valley in 2009, she captured some duck penises in action. (These ducks had been trained to ejaculate into small glass bottles for artificial insemination.)

You might remember what she and Prum discovered because, for a short while, the duck penis went viral online. Brennan found that the penises unfurl out of a duck's body at lengths of around 5 to 7 inchessome duck penises can be almost as long as the male's body. And they were spiraled, like a fleshy cavatappi pasta noodle. Male ducks forced these long corkscrew penises onto females. The internet was horrified, and also, enthralled.

In the history of people (and scientists) marveling at genitalia in nature, this is where it often stops: Look at this weird penis! In 1979, Science published a paper on the penis of the damselfly. As Dutch evolutionary biologist, Menno Schilthuizen, wrote in his book, Nature's Nether Regions, this minuscule penis carried a miniature spoon that, during mating, cleaned out the females vagina, scooping out any remaining sperm from previous males. It was an eye-opener as well as a sperm-scooper.

This finding opened biologists' eyes to the fact that even tiny creatures had strange penises. The chicken flea's penis is rolled up in its body like a coiled spring. Other insects have musical penises, where males rub them against ribbed parts of their bodies to emit loud noises. Black widow spiders have penis tips that break off to block other males sperm from entering a female. It was somewhat of an evolutionary mystery: Why were penises so different from one another if they had the same evolutionary purposeto deliver sperm to a female's eggs?

The lock and key theory was one potential explanation, proposed in the mid 19th century. It said that male genitals were like a key, and for each key there needed to be a corresponding lock (the vagina). If the key doesnt fit into the lock, mating couldn't take place. Essentially, penises varied to keep different species from mating with one another. Another guess was sexual selectionthat females detected some particular feature of the male genitalia and used it to choose a mate, pushing the male's penis evolution in bizarre off-shoots.

Still, the focus remained on male genitalia and how it was changing and evolving, even in more recent texts on genital evolution, like important work from scientist William Eberhard on sexual selection. Brennan wrote in a 2016 paper that while Eberhard noted female choice was important in shaping male genital features, he concluded that female genitalia are relatively uniform while male genitalia are diverse.

"It created this idea, from my reading of the literature later on, that the females were somehow boring," Brennan said. "We need to look at the males, because thats where all the action is.

As a result, most of the research on genital evolution has focused on males. Nearly two times as many studies have looked at male genitals compared to females. In 2014, evolutionary biologist and gender researcher Malin Ah-King and her colleagues looked at 364 studies published over the last two decades, and found that 49 percent of them only looked at male genitals, compared to 8 percent that looked only at females, and 44 percent that looked at both.

Even the language that researchers use to describe male and female genitals has differed. A study found that active words like "coercion" are used for males, while more passive words like "avoidance" or "resistance," are provided for females. As Ah-King and her co-authors wrote: Too often, the female is assumed to be an invariant container within which all this presumed scooping, hooking, and plunging occurs.

When Brennan first saw the duck penis, though, she immediately considered the duck vagina. I looked at their penis and next question was, 'wow these penises are so big. So what do the vaginas look like?' Surprisingly, no one had investigated that before, she told me. To her, it was an obvious question. As she told science writer Carl Zimmer for a New York Times article: You cant have something like that without some place to put it in. You need a garage to park the car.

When she dissected some female ducks, "I could not believe it, she said. The differences in the vagina of a duck compared to the vagina of a chicken or a finch or quail was like the difference between night and day.

What Brennan found was a vagina like a labyrinth. Yes, duck penises were spiraledbut duck vaginas were too, in the opposite direction. Rather than finding a vagina that had evolved to fit this weird penisa garage that fit the carthe duck vagina indicated a less cooperative history.

Given that duck mating was often forced, Brennan and her colleagues hypothesized that the vagina had co-evolved to actively resist the males. The ducks vagina is swirled in a clockwise coil, so the males can only completely penetrate her with their counter-clockwise penis if she chooses to relax her vaginal muscles. Even though female ducks can't stop the male ducks from forcing themselves on them, they can control if the male could successfully inseminatereclaiming some reproductive autonomy.

Brennan and her colleagues looked at other species where the males took part in forced copulation, and then at the corresponding females. In ducks and geese, they found that when male birds forced sex on the females, females also had complicated vaginas. In species where theres no forced copulation, then the females have a regular, tube-looking vagina," Brennan said.

It also meant that the duck penis size and shape wasn't solely a result of males competing with other males, or females making a choice between malesit was the female and male ducks' competition driving the evolution.

This is the core tenet of sexual conflict: Males and females dont always agree about the best way to mate. For males, mating with a large number of females is the ideal way for them to procreate. For females, who are often left with the care of the offspring, as well as giving birth and pregnancy, being selective about reproduction is her best bet for creating progeny that will survive. This creates a conflict, where the males are going for quantity and the females, for quality.

Lets say a male animal evolves a penis hook, which allows him to latch onto a female. Even if that hook hurts the female, or gives her an infection, if it benefits the male by allowing him to reproduce more, the genes for that hook will be passed to the next generation. That puts the female a step behind, so evolution might next select for females that can defend themselves against the hook, and evolve thicker walls in their vagina. (Something very similar has happened in sharks.) This is a way of understanding the evolution of genitals as a kind of conversation, even if a contentious and competitive one. And this perspective is providing new understanding for a whole host of creatures.

The males evolve these weird penises and females evolve their convoluted vaginas in response, Brennan said. This is a lot more widespread than what we had originally realized. It's just, we have to go out there and look.

Take the earwig, an insect with a male reproductive organ called a virga. The virga has a fringe-like tip that can brush away sperm from any male that mated with a female before him. Looking at the male genitals only tells one half of the story, because the females have receptacles in their bodies to store sperm that lie just out of reach of the virga. It may seem that the males are controlling the sperm, but the females have the upper hand. As science writer Ed Yong wrote: The male can scrape away all he wants; the female decides whether to keep or jettison her sperm.

Dolphins have a complex series of vaginal folds that researchers once assumed were there to keep sea water from getting inside the female reproductive tract. Theyre realizing now how intricate their vaginas are, partly by making the effort to look closer at them. In 2017, biologist Dara Orbach made silicone molds of the dolphin vagina "revealing complex folds and spirals," the New Scientist reported. Brennan said it's now thought that those folds are actually barriers to male's penises.

Paying more attention to vaginas can help explain strange mating behavior too: In water striders, bugs that live and walk on water, the females evolved a genital shield, which can block any males that try to force them into mating. That led the males to adopt new "courting" techniques. "The males have started tapping the surface of the water while mounted on a female; the resulting ripples attract fish, and since the female is under the male, she's more likely than him to become a meal," according to post on Nature's blog. "Females can avoid this grisly end by giving in to the male's intimidation and mating with him.

Without knowing that the females have a genital shield, researchers' understanding of such behavior would be incomplete. It allows us to understand all of these bizarre morphologies and behaviors that we see in the context of, essentially, an arms race, said Teri Orr, a evolutionary ecologist at The University of Utah.

Spiders are another of Orrs favorites, because they can have around a dozen different pockets in them for manipulating spermsome are for receiving sperm, or moving it around. Orr frequently studies bats, and said they will store sperm for a full year in the reproductive tract. Leaf cutter ants can store sperm for around ten years.

Female chickens can eject about 80 percent of sperm from undesirable mates. Female guppies can hold onto sperm tooone study found that one in four guppies in Trinidad and Tobago were fathered by males that had been dead for 10 months. By doing so, females could wait to reproduce at favorable times of the year.

Theyre able to keep those sperm until its a good time of year for them to become pregnant, and then carry out that pregnancy and have babies when theres food available for them, Orr said. To me, that is absolutely mind-blowing. A lot of it is almost science fiction, what these species are able to do."

It also shows how the female anatomy is anything but passive. Outside of sperm storage, the vagina is awash with muscles that control contractions and movementits as mobile as the digestive tract is, Orr said. These muscles can play a part in moving the sperm where they want it to go. We didnt know what until about a decade ago, she said. And even then, its only in cattle, horses, mice and humans that its been studied. Thats such a small part of the diversity thats out there.

In 2005, more than 200 scientists met in London at The Royal Society for a meeting titled Sexual conflict: a new paradigm? Brennan said that since then, she feels the field is moving to include vaginas, and that several of the most recent papers on genital evolution acknowledge the fact that female genitals have been overlooked. But Orr said that when she presents her work at conferences, it can still feel like its regarded as out there" or niche. It hasnt reached mainstream science yet, she said. I think its going to take a little while until its fully embraced and not just a noveltybut normal biology.

It's not as if Brennan wants the research to flip and only focus on femalesthe point is that you need both pieces of the puzzle. Ive been very adamant that when youre looking at genitalia, you cant just look at the female or the male alone," she said. "You need to look at both because of that mechanical fit. I could commit the opposite sin, in a way. I could just go look at a bunch of females and never look at the males. Thats not going to tell me much.

She hopes that the field of genital evolution become more well-rounded, and also that the public will recognize its value. When Brennan's work on duck genitalia went public, conservatives latched onto it as a waste of government money (like a lot of academic research, it was partly funded by the National Science Foundation), acquiring the moniker #DuckPenisGate. Fox News put up a poll on their site where readers could vote if the research was a worthwhile use of taxpayer money, and 89 percent voted it was not. Brennan and her co-author Prum had to write articles defending the research.

The thing about basic science, Brennan said, is that you never know when a seemingly obscure discovery in nature is going to lead to an application for humans. So could secrets to our evolutionary past (and sexual conflicts) be hidden in our genital shapes? It's true that humans also have weird penises awash with unsolved questions, Brennan said. They are disproportionately wide given our body size and MRI studies of people having sex show that the shape of the male and female genitalia can change during intercourse, for reasons that are not completely understood.

Humans don't have penile spines, unlike many of our close primate relatives. Humans have also lost the baculum, a little bone inside of the penis of many animals, like bats, rodents, and primates. We have no idea what it does, Orr said. Its buried in tons of soft tissue and so its not interacting with the female, so its quite mysterious." Even less understood is the tiny little bone some animals have inside of the clitoris which humans didn't retain.

But more often, translation from basic science will come from where you least expect it. One obvious example is how the immune system of a bacteria was developed into a revolutionary gene editing techniqueCRISPR/Cas9.

In the realm of genital evolution: duck penises grow and shrink every season, which means there are probably stem cells in the penis that allow for that growth each year. If researchers could learn what those cells are and how they work, they could have all sorts of medical or cosmetic applications. Could we actually grow penile cells that might become a treatment someday? Its perfectly possible," Brennan said.

Many of the stages where pregnancy fails in humans are the same ones where bats are able to intervene and store fertilized eggs or sperm. By looking closer at those processes, it might lead to ideas for aiding issues in human or reproduction or endocrinology, Orr said.

Hypospadias is a birth defect leading to a malformed urethra; one in every 200 boys is born with some type of hypospadias. For people with such developmental problems, or others, like malformation of the uterus, research into genitals that are naturally bifurcated could lead to an understanding of what causes those hiccups, and how to fix them.

Even if those animal-human translations aren't right around the corner, the field of genital evolution has already offered something else: Recognizing the value in seeing how gender biases and language can divert research to ignore crucial elements. Anthropologist Emily Martin's 1991 essay The Egg and the Sperm highlighted how the (often incorrect) descriptions of human sperm and eggs reflected stereotypical male and female roles. It's a reminder that it could happen again, and to examine what social constructs are currently inseminating scientific research.

And Brennan wonders if the response to her research doesn't betray how touchy and judgemental people still are about genitalia, especially vaginas. It's almost as if there was something a little perverse with that line of questioning or that particular type of research," she said. "I happen to think that we actually need to understand a lot more about sex and sexual interactions than less.

She views genitals just like any other organs. If you think about our other organs: livers, kidneys, hearts, or brainsthere's much less variation and excitement. It's a rare window into what evolution can do. Genitalia are critical biological organs to be studying, she said. Im still surprised that we know as little as we seem to know. Evolutionarily, this is where the rubber meets the road.

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Millions of people around the world have some form of sight or hearing loss, have no sense of smell or taste or have lost limbs, taking away their sense of touch. Fortunately, the science of senses is the most advanced its ever been. Biotech researchers are developing methods that merge humans and machines in ways that could restore human abilities to hear, see, taste, smell and touch. From neuro-prosthetic limbs that mimic touch to bionic eyes and smart glasses that restore sights, the innovations could drastically improve the quality of life of people around the world.

Some of the most advanced technology developed around the science of senses comes from the field of prosthetic limbs, where researchers are finding ways to connect tissue to metal. Systems called brain-machine interfaces literally wire robotic limbs to a persons nervous system. Two of the latest achievements were reported in July 2019 in the journal Science Robotics.

In the first, a team from the University of Utah connected a robotic hand and partial forearm to the remaining nerves in the mans arm. The man trained his brain to control the motion of the hand. At the same time, artificial zaps sent to the robotic hand were designed to mimic the skins natural response patterns to touch. Remarkably, the man could more easily discriminate between small and large objects as well as soft and hard items while blindfolded and wearing headphones. Another team, based at the National University of Singapore, engineered flexible, electronic skin that contains artificial nerves that transmit signals 1,000 times faster than nerves in human skin. The skin is able to sense temperature, pressure and humidity and is also durable enough to function even if it is scratched or damaged.

Since the mid-1980s, a tiny electronic device called a cochlear implant has been providing the sense of sound to hundreds of thousands of people worldwide, according to the National Institutes of Health. Part of the implant is surgically placed under the skin behind the ear, with another part attached in the same position externally. A third part is inserted inside the ear canal. Unlike a hearing aid that amplifies sound, a cochlear implant senses sounds and converts them into an electric signal that it uses to stimulate a persons auditory nerve. Even people who are profoundly deaf can learn to discern sounds as long as some fraction of their nerve still functions.

But cochlear implants are not perfect. They are only capable of sensing and transmitting part of a sound waves full audio spectrum, producing a sound that has a metallic quality. That can make it difficult to filter out background noise, such as a crowd conversations or traffic. In 2019, a team from the University of Greenwich in England reported on new research that improves upon this technology, reports MedicalXpress. It deconstructs sounds from the environment and then reconstructs them with 90% to 100% percent efficiency. This means patients will be able to better distinguish noises from background sounds.

Smell loss, called anosmia, affects about 5% of the general population, according to the Massachusetts Eye and Ear Infirmary. The condition may be the result of something temporary, such as a sinus infection or swelling or polyps in the nasal cavity or it could be the result of damage to the sensory nerves. Permanent loss of smell can impact daily enjoyment of life and even affect safety. The inability of smelling smoke or natural gas could put someone in harms way.

Although there is no proven therapy, researchers at the Massachusetts Eye and Ear have, for the first time, invented a device that stimulates different smells. Their technology, which they reported in 2018 in the International Forum of Allergy & Rhinology, uses an array of tiny electrodes to send an electrical signal to the olfactory bulb, a structure in the brain involved in smell. In a small experiment, the scientists created different electrical stimulation in five patients, producing smells similar to onions and antiseptic as well as sour and fruity aromas. Although the innovation is still in the early stage, it demonstrates a possible path forward for a cochlear implant for the nose, the scientists say.

Although smell is connected to taste, its the receptor cells on the taste buds of a persons tongue that discern sweet, salty, sour, bitter or savory flavors. Medical procedures inside the mouth or ear can alter a persons taste, as can head trauma or ear infections, according to MedicineNet. Scientists have made a couple of attempts to solve the problem with technology. Back in 2013, a team from the National University of Singapore developed a taste simulator that used a kind of electronic tongue depressor to simulate taste sensations, New Scientist reported. Later, another team at City University of London invented a similar device called Taste Buddy that also stimulated taste buds to alter the flavor of foods, reported Digital Trends.

Unfortunately, neither gadget went beyond the research lab. For now, solutions may lie within human DNA. Lynnette McCluskey, a neurobiologist at the Medical College of Georgia at Augusta University, and her team are investigating whether a protein called interleukin-1, or IL-1, secreted during an injury could help rebuild a persons sense of taste. The protein promotes inflammation and also helps regulate nerve growth. In 2018, she and her colleagues received grant money to study whether manipulating the proteins after an injury could help the nerves associated with taste recover faster, reports MedicalXpress. It could take a few more years to find out.

Worldwide, 36 million people are legally blind, according to Nature. Some biotechnological solutions, such as growing stem cells into those that can repair damage to the retina or using techniques from gene therapy to correct genetic defects, are showing promising results. But technology is also playing a big role.

A bionic eye, called the Argus II, is a retinal prosthesis system that, since its development in early 2000, has restored some vision capabilities to more than 300 people. Its reserved for people who have no vision or almost no vision due to a genetic condition called retinitis pigmentosa. Patients undergo surgery, in which a tiny electronic device is attached to the persons retina. Its connected wirelessly to a pair of smart glasses that have a portable video-processing unit that project images from the outside world onto the persons retina. Clinical trials done in 2015 showed that visual function improved in 90% of people wearing the prosthesis and that 80% of patients reported improved quality of life, according to the American Academy of Ophthalmology.

Advances in technology are allowing machines to merge with the human body. Coupled with our growing ability to correct genetic defects or repair cellular damage, the science of senses is moving into the future. One day all humans could move through the world with all five of their senses intact seeing the unseen, hearing the unheard and tasting, touching and smelling new wonders that evoke all of the pleasures of being alive.

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Since Brainstorm Cell Therapeutics Inc. (NASDAQ:BCLI) and PolarityTE Inc. (NASDAQ:PTE) are part of the Biotechnology industry, they are influenced by compare. The influences particularly affect the analyst recommendations, profitability, risk, institutional ownership, dividends, earnings and valuation of both companies.

Earnings & Valuation

Table 1 shows gross revenue, earnings per share and valuation of the two companies.

Profitability

Table 2 represents Brainstorm Cell Therapeutics Inc. (NASDAQ:BCLI) and PolarityTE Inc. (NASDAQ:PTE)s net margins, return on equity and return on assets.

Volatility and Risk

Brainstorm Cell Therapeutics Inc.s 1.19 beta indicates that its volatility is 19.00% more volatile than that of Standard and Poors 500. From a competition point of view, PolarityTE Inc. has a 1.14 beta which is 14.00% more volatile compared to Standard and Poors 500.

Liquidity

Brainstorm Cell Therapeutics Inc. has a Current Ratio of 1 and a Quick Ratio of 1. Competitively, PolarityTE Inc.s Current Ratio is 5.6 and has 5.6 Quick Ratio. PolarityTE Inc.s better ability to pay short and long-term obligations than Brainstorm Cell Therapeutics Inc.

Analyst Recommendations

Brainstorm Cell Therapeutics Inc. and PolarityTE Inc. Recommendations and Ratings are available on the next table.

Brainstorm Cell Therapeutics Inc.s consensus target price is $9, while its potential upside is 129.01%. On the other hand, PolarityTE Inc.s potential upside is 235.69% and its consensus target price is $9.5. The results provided earlier shows that PolarityTE Inc. appears more favorable than Brainstorm Cell Therapeutics Inc., based on analyst belief.

Insider & Institutional Ownership

Roughly 11.4% of Brainstorm Cell Therapeutics Inc. shares are owned by institutional investors while 45.6% of PolarityTE Inc. are owned by institutional investors. Insiders owned roughly 0.6% of Brainstorm Cell Therapeutics Inc.s shares. Competitively, 33% are PolarityTE Inc.s share owned by insiders.

Performance

In this table we provide the Weekly, Monthly, Quarterly, Half Yearly, Yearly and YTD Performance of both pretenders.

For the past year Brainstorm Cell Therapeutics Inc. has 12.96% stronger performance while PolarityTE Inc. has -64.71% weaker performance.

Summary

On 7 of the 11 factors Brainstorm Cell Therapeutics Inc. beats PolarityTE Inc.

Brainstorm Cell Therapeutics Inc., a biotechnology company, develops adult stem cell therapies for neurodegenerative disorders that include amyotrophic lateral sclerosis, multiple sclerosis, Parkinsons disease, and others. The company holds rights to develop and commercialize its NurOwn technology through a licensing agreement with Ramot of Tel Aviv University Ltd. Its NurOwn technology is based on a novel differentiation protocol, which induces differentiation of the bone marrow-derived mesenchymal stem cells into neuron-supporting cells and secreting cells that release various neurotrophic factors, including glial-derived neurotrophic factor, brain-derived neurotrophic factor, vascular endothelial growth factor, and hepatocyte growth factor for the growth, survival, and differentiation of developing neurons. The company was formerly known as Golden Hand Resources Inc. and changed its name to Brainstorm Cell Therapeutics Inc. in November 2004 to reflect its new line of business in the development of novel cell therapies for neurodegenerative diseases. Brainstorm Cell Therapeutics Inc. was founded in 2000 and is headquartered in Hackensack, New Jersey.

PolarityTE, Inc. operates as a biotechnology and regenerative biomaterials company in the United States. The company focuses on discovering, designing, and developing a range of regenerative tissue products and biomaterials for the fields of medicine, biomedical engineering, and material sciences. PolarityTE, Inc. is headquartered in Salt Lake City, Utah.

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Brainstorm Cell Therapeutics Inc. (BCLI) and PolarityTE Inc. (NASDAQ:PTE) Contrasting side by side - The Broch Herald

Since Merus N.V. (NASDAQ:MRUS) and PolarityTE Inc. (NASDAQ:PTE) are part of the Biotechnology industry, they are influenced by compare. The influences particularly affect the dividends, institutional ownership, analyst recommendations, profitability, risk, earnings and valuation of both companies.

Earnings and Valuation

Table 1 showcases the gross revenue, earnings per share (EPS) and valuation of Merus N.V. and PolarityTE Inc.

Profitability

Table 2 provides Merus N.V. and PolarityTE Inc.s return on equity, net margins and return on assets.

Liquidity

Merus N.V.s Current Ratio and Quick Ratio are 6.4 and 6.4 respectively. The Current Ratio and Quick Ratio of its competitor PolarityTE Inc. are 5.6 and 5.6 respectively. Merus N.V. therefore has a better chance of paying off short and long-term obligations compared to PolarityTE Inc.

Analyst Recommendations

Merus N.V. and PolarityTE Inc. Ratings and Recommendations are available in the next table.

Merus N.V. has a 27.47% upside potential and an average price target of $20. Meanwhile, PolarityTE Inc.s average price target is $9.5, while its potential upside is 197.81%. Based on the analysts opinion we can conclude, PolarityTE Inc. is looking more favorable than Merus N.V.

Institutional & Insider Ownership

Institutional investors held 65.8% of Merus N.V. shares and 45.6% of PolarityTE Inc. shares. 30.47% are Merus N.V.s share held by insiders. Competitively, 33% are PolarityTE Inc.s share held by insiders.

Performance

In this table we show the Weekly, Monthly, Quarterly, Half Yearly, Yearly and YTD Performance of both pretenders.

For the past year Merus N.V. has 12.5% stronger performance while PolarityTE Inc. has -64.71% weaker performance.

Summary

PolarityTE Inc. beats on 6 of the 11 factors Merus N.V.

Merus N.V., a clinical-stage immuno-oncology company, engages in developing bispecific antibody therapeutics. Its lead bispecific antibody candidate is MCLA-128, which is in Phase I/II clinical trials in Europe for the treatment of various solid tumors, including breast, gastric, and ovarian cancers. The company also develops MCLA-117, a bispecific antibody candidate that is expected to commence a Phase I/II clinical trial for the treatment of patients with acute myeloid leukemia, as well as for the treatment of myelodysplastic syndrome in pre-clinical studies, as well as developing MCLA-158, a bispecific antibody candidate, which is designed to bind to cancer stem cells for the potential treatment of colorectal cancer. Its pre-clinical bispecific antibody candidates include MCLA-134 and MCLA-145, as well as other early research projects. The company has a strategic collaboration with Incyte and ONO Pharmaceutical Co., Ltd. to develop bispecific antibody candidates based on Biclonics technology platform. Merus N.V. was founded in 2003 and is headquartered in Utrecht, the Netherlands.

PolarityTE, Inc. operates as a biotechnology and regenerative biomaterials company in the United States. The company focuses on discovering, designing, and developing a range of regenerative tissue products and biomaterials for the fields of medicine, biomedical engineering, and material sciences. PolarityTE, Inc. is headquartered in Salt Lake City, Utah.

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Merus N.V. (MRUS) and PolarityTE Inc. (NASDAQ:PTE) Contrasting side by side - The Broch Herald

Intermountain Primary Children's Hospital, along with University of Utah Health, and Intermountain Precision Genomics are teaming up to launch a pediatric center for personalized medicine that will serve the Intermountain West.

WHY IT MATTERS The center will use precision genomics to discover, address and treat genetic diseases, many of which affect infants and children and can cause life-long disability.

The Center will focus on precision diagnosis, gene therapies and novel therapeutics, and stem cell, immunologic and regenerative medicine.

Precision medicine includes applications across diagnostics, prevention and screening that takes into account individual variabilities in genes, environment, and lifestyle for every individual.

Through its work on precision diagnosis, the Center hopes to provide more targeted care to critically-ill children based on their genetic make-up, where rapid whole genome sequencing can quickly identify genetic causes of hard-to-diagnose diseases.

The initial efforts will be focused on providing answers to critically ill infants in the newborn intensive care unit, and children with severe seizures and heart conditions.

The research into gene therapies and novel therapeutics will help enable children with previously debilitating and fatal genetic diseases, with clinical trials testing gene therapy treatments for Duchenne's Muscular Dystrophy, Adrenoleukodystrophy, and other serious diseases.

The Center is also developing novel therapeutics that target specific diseases and improve health, with a release noting the Center is one of only six hospitals nationwide to provide gene therapy for the common childhood genetic condition spinal muscular atrophy.

Stem cell research uses a child's own cells, or genetically modifies a child's cells and immune system, to fight disease and promote healing, with additional research aimed at developing immunotherapy as a tool to fight pediatric brain tumors.

The organization also noted clinical trials are testing the use of stem cells in repairing diseased hearts and other tissues.

THE LARGER TRENDIntermountain has been busy on this front recently. In June, the health system announced that it is performing a massive clinical DNA study, pairing 500,000 samples drawn from Intermountain Healths patient population and analyzing them with help from deCODE, a subsidiary of Reykjavik-based Amgen.

"Better health and being able to cure common diseases is the promise of precision medicine, but its not happening fast enough," said Dr. Marc Harrison, president and CEO at Intermountain Healthcare, announcing that initiative. "For too long, the genetic code to better health has been locked. This collaboration with deCODE unlocks that insight so we can rapidly advance well-being not only for ourselves and our families, but for generations to come.

Intermountain's new pediatrics personalized medicine announcement also follows Mount Sinai's just-announced plans to build new precision medicine supercomputer, which will have 15 terabytes of memory, 14 petabytes of raw storage and a peak speed of 220 teraflops per second, to manage massive amounts of genomic data.

ON THE RECORD"Our mission is to leverage the expertise of our scientists, the clinical care of our physicians and care-givers, and the dedication of our community, to discover and develop new cures for children," said Dr. Josh Bonkowsky, Intermountain's medical director of the Primary Children's Center for Personalized Medicine, in a statement. "The work we are doing here and now is transforming pediatric medicine. We will not be done until we have put these diseases out of business."

Nathan Eddy is a healthcare and technology freelancer based in Berlin.Email the writer:nathaneddy@gmail.comTwitter:@dropdeaded209

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