Category Archives: Cell Biology

Leading cancer researcher, NMSU alum to lecture May 1 – Las Cruces Sun-News

Minerva Baumann, For the Sun-News 4:00 p.m. MT April 29, 2017

NMSU alumnus Don W. Cleveland, professor and chair of the Department of Cellular and Molecular Medicine at the University of California at San Diego and member of the Ludwig Institute for Cancer Research, will visit with students and give a lecture about his research into treatment for neurodegenerative disease at NMSU on Monday, May 1.(Photo: Courtesy photo)

LAS CRUCES A Las Cruces native and field-leading researcher in the areas of cancer genetics and neurosciences will give a talk at New Mexico State University about breakthrough discoveries that could impact future treatment of diseases such as Lou Gehrigs disease, Huntingtons disease and Alzheimers disease.

Don W. Cleveland, a professor and chair of the Department of Cellular and Molecular Medicine at the University of California at San Diego as well as a member of the Ludwig Institute of Cancer Research, will return to NMSU on Monday, May 1, to share insights about his research with students and the community. Cleveland will spend the day meeting with different groups, touring the campus, talking with NMSU students in biology, chemistry and physics and giving a public lecture about his research titled Gene silencing therapy for human neurodegenerative disease, which will begin at 3:30 p.m. May 1 in the Domenici Hall Yates Auditorium, Room 109.

Its a real pleasure to visit NMSU and Las Cruces again, said Cleveland, who graduated from Las Cruces High School and earned a bachelors degree from NMSU in physics in 1972. They gave me a great start in my scientific career and made me into a lifelong New Mexican (no matter where I live).

After NMSU, Cleveland earned a doctorate at Princeton and moved to California to continue his groundbreaking research into neurodegenerative disorders. Cleveland has uncovered the mechanisms underlying the major genetic forms of amyotrophic lateral sclerosis (ALS), commonly known as Lou Gehrigs disease, and developed gene silencing therapies using designer DNA drugs that have entered clinical trials for four neurodegenerative diseases, including ALS and Huntingtons diseases.

Cleveland initially identified tau, the protein that accumulates abnormally in Alzheimers disease. It is also the protein whose misfolding underlies chronic traumatic brain injury, which is now receiving nationwide attention from the National Football League.

We are proud to welcome Dr. Cleveland back to NMSU, said Enrico Pontelli, interim dean of the College of Arts and Sciences. This is part of our Alumni Connections series, which seeks to connect our Arts and Sciences alumni with our students. One of the keys to students long-term success is the connections they build, not only with their professors and fellow students but also with alumni like Dr. Cleveland, who are leaders in their field of study.

Cleveland has earned numerous awards for his work. Among them, three National Institutes of Health Merit Awards, the Wings Over Wall Street MDA Outstanding Scientist award and The Sheila Essey Prize from the ALS Association and American Academy of Neurology as well as the Judd award from Memorial Sloan-Kettering Cancer Center.

NMSU biology professor Brad Shuster remembers Cleveland as a mentor when Shuster was a graduate student. He also invited Cleveland to NMSU for a seminar several years ago.

Don has made enormous contributions to our understanding of the basic structure and function of cells, and has lent profound insights into pathologies such as cancer and neurodegenerative diseases, said Shuster. His leadership has extended well beyond the bench, serving as president of the American Society for Cell Biology and an editor of our disciplines top journal. Plus, hes a great guy and one of the most successful scientists NMSU has ever produced.

Pontelli believes Clevelands engagement with NMSU students one-on-one will be just as valuable for them as the knowledge of his cutting-edge research.

This is an amazing opportunity for our faculty and students, Pontelli said. We are fortunate Dr. Cleveland is making the time to share his research and insights.

Clevelands lecture is free and open to the public. Campus parking passes for visitors are available at http://auxadminforms.nmsu.edu/ParkingForms/ePermit.aspx.

Minerva Baumannwrites for University Communications and can be reached atmbauma46@nmsu.edu

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Leading cancer researcher, NMSU alum to lecture May 1 - Las Cruces Sun-News

Kimmel Scholar Award propels immune cell cancer research – Davis Enterprise

UC Davis assistant professor Sean Collins of the department of microbiology and molecular genetics has received a prestigious, two-year $200,000 award that will help advance the use of immune cells for cancer therapies.

The Kimmel Scholar Award is given to 15 of the nations most promising young researchers leading the fight against cancer.

Collins seeks to understand how immune cells process information, make decisions and respond to threats in the human body. His research explores the basic molecular mechanisms that allow immune cells to navigate to infection sites.

When there is an injury or infection, our bodies respond by sending specialized immune cells to evaluate and intercept foreigner invaders. These immune cells also help defend the body against tumors. However, in order to fight infections or tumors, the cells must first find the right location in the body, and the path to get there can be complicated.

By identifying key principles and molecular pieces, we hope to reengineer these processes to direct immune cells to tumor locations, Collins said.

The hope is that by guiding the seek and destroy ability of these immune cells, in combination with other therapeutic strategies, they will be able to more effectively target and destroy tumors.

Ive spent most of my career so far focused on understanding basic mechanisms like how a cell processes information about its environment, Collins said, but this is a new direction to try and apply some of those findings in a direct, medically relevant way to help develop strategies for cancer therapy.

From sports statistics to cell biology Professor Wolf-Dietrich Heyer, chair of the department of microbiology and molecular genetics, recognizes Collins as a rising star with a bright future.

Professor Collins work is an elegant combination of cutting-edge cell biology paired with rigorous quantitative analysis and creative mathematical modeling, Heyer said. His focus on immune cells will provide the underpinning for novel approaches in harnessing the bodys immune system in anti-cancer therapy.

Collins interest in science grew from a childhood fascination with solving problems.

At some level, it started with an interest in computer programming and statistics in sports, he said.

As a child, Collins and his twin brother were big sports statistics buffs, and would play sports simulation games on the computer. One day, their game malfunctioned, displaying a cryptic error message. So the two brothers spent the next few months figuring out how the game worked and eventually fixed it.

The Kimmel Scholar Award is sponsored by the Sidney Kimmel Foundation, which has funded more than 260 cancer researchers since its founding in 1993. Collins is the second researcher from UCD to be honored with this award, after professor Ken Kaplan of the department of molecular and cellular biology in 2001.

UC Davis News

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Kimmel Scholar Award propels immune cell cancer research - Davis Enterprise

Researchers 3-D Bioprint Cartilage – Laboratory Equipment

A team of researchers at Sahlgrenska Academy has managed to generate cartilage tissue by printing stem cells using a 3D-bioprinter. The fact that the stem cells survived being printed in this manner is a success in itself. In addition, the research team was able to influence the cells to multiply and differentiate to form chondrocytes (cartilage cells) in the printed structure.

The findings have been published in Natures Scientific Reports magazine. The research project is being conducted in collaboration with a team of researchers at the Chalmers University of Technology who are experts in the 3D printing of biological materials. Orthopedic researchers from Kungsbacka are also involved in the research collaboration.

The team used cartilage cells harvested from patients who underwent knee surgery, and these cells were then manipulated in a laboratory, causing them to rejuvenate and revert into pluripotent stem cells, i.e. stem cells that have the potential to develop into many different types of cells. The stem cells were then expanded and encapsulated in a composition of nanofibrillated cellulose and printed into a structure using a 3D bioprinter. Following printing, the stem cells were treated with growth factors that caused them to differentiate correctly, so that they formed cartilage tissue.

The publicationis the result of three years of hard work.

In nature, the differentiation of stem cells into cartilage is a simple process, but its much more complicated to accomplish in a test tube. Were the first to succeed with it, and we did so without any animal testing whatsoever," says Stina Simonsson, Associate Professor of Cell Biology, who lead the research teams efforts.

Most of the teams efforts had to do with finding a procedure so that the cells survive printing, multiply and a protocol that works that causes the cells to differentiate to form cartilage.

"We investigated various methods and combined different growth factors. Each individual stem cell is encased in nanocellulose, which allows it to survive the process of being printed into a 3D structure. We also harvested mediums from other cells that contain the signals that stem cells use to communicate with each other so called conditioned medium. In laymans terms, our theory is that we managed to trick the cells into thinking that they arent alone, clarifies Simonsson. "Therefore,the cells multiplied before we differentiated them."

A key insight gained from the teams study is that it is necessary to use large amounts of live stem cells to form tissue in this manner.

The cartilage formed by the stem cells in the 3D bioprinted structure is extremely similar to human cartilage. Experienced surgeons who examined the artificial cartilage saw no difference when they compared the bioprinted tissue to real cartilage, and have stated that the material has properties similar to their patients natural cartilage. Just like normal cartilage, the lab-grown material contains Type II collagen , and under the microscope the cells appear to be perfectly formed, with structures similar to those observed in samples of human-harvested cartilage.

The study represents a giant step forward in the ability to generate new, endogenous cartilage tissue. In the not too distant future, it should be possible to use 3D bioprinting to generate cartilage based on a patients own, backed-up stem cells. This bioprinted tissue can be used to repair cartilage damage, or to treat osteoarthritis, in which joint cartilage degenerates and breaks down. The condition is very common one in four Swedes over the age of 45 suffer from some degree of osteoarthritis.

In theory, this research has created the opportunity to generate large amounts of cartilage, but one major issue must be resolved before the findings can be used in practice to benefit patients.

The structure of the cellulose we used might not be optimal for use in the human body. Before we begin to explore the possibility of incorporating the use of 3D bioprinted cartilage into the surgical treatment of patients, we need to find another material that can be broken down and absorbed by the body so that only the endogenous cartilage remains, the most important thing for use in a clinical setting is safety explains Simonsson.

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Researchers 3-D Bioprint Cartilage - Laboratory Equipment

Management Team Strengthened; Executive Level New Hire and Internal Promotion – Yahoo Finance

WOBURN, Mass.--(BUSINESS WIRE)--

Frequency Therapeutics, a company developing a pipeline of new drugs that activate progenitor cells within the body and restore healthy tissue, today announced the expansion of its management team with the promotion of Raj Manchanda, Ph.D. to Chief Development Officer and the appointment of Steven Dworetzky, Ph.D., to Senior Vice President of Molecular and Cell Biology. Dr. Dworetzky brings over 27 years of experience in key research and development roles to Frequency and will be working closely with senior leadership on scientific strategy and program development.

Frequency continues to rapidly advance our Progenitor Cell Activation (PCA) platform with a lead program addressing hearing loss. I am very pleased to have a proven scientist and businessman like Steven lead the Frequency team in our Farmington, CT location, said David Lucchino, President, CEO and Co-founder of Frequency. I am also honored to announce the well-deserved promotion of Raj to Chief Development Officer. Rajs leadership has been critical in transforming Frequency to a highly efficient development stage organization since joining us from Biogen.

Raj Manchanda, Ph.D., has been promoted to Chief Development Officer from his prior role as the Senior Vice President of Pharmaceutical Development and Technical Operations. He will continue to spearhead development activities including formulation and analytical development, manufacturing and non-clinical safety studies to facilitate clinical trials and broaden Frequencys drug development pipeline. Raj joined Frequency in 2016 from Biogen where he held a series of leadership positions, most recently as Vice President of Neurodegeneration. While at Biogen, he led the CMC development for approval and commercialization for Tecfidera, the leading oral therapy for MS. Before Biogen, held key R&D positions at Avid Radiopharmaceuticals (acquired by Eli Lilly), PerkinElmer, and Diatide (acquired by Schering AG). During his 20 years in the pharmaceutical industry, he has worked on over 25 INDs and 6 NDAs, including two Fast Track programs. Raj holds a Ph.D. in Chemistry from Yale University and was the Anna Fuller Postdoctoral Fellow at MIT.

Steven Dworetzky, Ph.D. joins Frequency as Senior Vice President of Molecular and Cell Biology Research. Dr. Dworetzky rose to the level of Senior Principal Scientist in the Neuroscience department at Bristol-Myers Squibb, with experience leading interdisciplinary programs to the clinic. Stevens ion channels team was responsible for bringing multiple compounds into clinical study. Post BMS and prior to joining Frequency, Steven was Chief Scientific Officer and Senior Vice President of Discovery Research at Knopp Biosciences. While there, he implemented a fully integrated drug discovery team for ALS and other neurology indications, as well as new directions in hematopoiesis studies. Steven received his Bachelors degree in Biology and Chemistry from Skidmore College and his Ph.D. in Molecular and Cellular Biology from the University of Florida in Gainesville.

Frequencys PCA platform presents outstanding opportunities for the development of new medicines in indications with high unmet medical needs, said Dr. Dworetzky. I look forward to lending my experience and expertise to continue the work started by Bob Langer and Jeff Karp, and bolstering the Company goals in driving the next wave of regenerative medicine.

ABOUTPROGENITOR CELL ACTIVATION (PCA) Frequencys precise and controlled approach transiently causes Lgr5+ progenitor cells to divide and differentiate, much like what is seen in naturally regenerating tissues such as the skin and intestine. Frequency activates stemness through mimicking signals provided by neighboring cells (the stem cell niche) with small molecules, and this proprietary approach is known as the Progenitor Cell Activation (PCA) platform. Frequency believes that PCA has the potential to yield a whole new category of disease-modifying therapeutics for a wide range of degenerative conditions. To fuel its drug discovery programs, Frequency is leveraging a PCA screening platform using primary human cells, including cochlear progenitor cells and adult human progenitor cells from the GI tract. Frequencys initial focus is on chronic noise induced hearing loss. Other potential applications include skin disorders, gastrointestinal diseases and diabetes.

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ABOUT FREQUENCY THERAPEUTICS Frequency Therapeutics develops small molecule drugs that activate progenitor cells within the body to restore healthy tissue. Through the transient activation of these progenitor cells, Frequency enables disease modification without the complexity of genetic engineering. Our lead program re-creates sensory cells in the inner ear to treat chronic noise induced hearing loss, which affects over 30 million people in the U.S. alone. http://www.frequencytx.com.

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Management Team Strengthened; Executive Level New Hire and Internal Promotion - Yahoo Finance

Marquette scientists discover the early stages of neurodegenerative diseases MC1 GR2 – Marquette Wire

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Marquette biologists and mathematicians are using bakers yeast to understand the early stages of neurodegenerative diseases such as Alzehimers and Parkinsons.

Dr. Anita Manogaran, an assistant professor of biological sciences, and her lab are studying the impact of basic cell biology on neurodegeneration. By understanding what goes on in a single cell, Manogarans lab was able to gain insight into the bigger picture of neurodegenerative diseases. Many neurodegenerative diseases involve misfolded proteins, or molecules sticking together and making shapes they arent supposed to. The lab used bakers yeast to observe how certain proteins misfold in individual cells.

We are doing something unorthodox by studying proteins in bakers yeast, Manogaran said. We are able to get a lot of information really fast when we use bakers yeast.

The lab utilized 4-D live cell imaging to observe how the proteins misfold in the cell in order to learn more about these early stages of formation.

Brett Wisniewski, a research technician in Manogarans lab, believes that using yeast and other simple organisms will always be an excellent starting point for understanding the most complex human diseases.

Neurodegenerative diseases are common in older patients, but this new discovery by Manogarans lab found proteins associated with these diseases misfold in the brain years before symptoms occur. Manogaran hopes this discovery can lead to future progress tohelp control and cure these diseases.

It would be rewarding to see other groups use our work to inform their experiments on more complex organisms and eventually influence therapies for neurodegenerative diseases in humans, Wisniewski said.

Neurodegenerative diseases affect millions of people worldwide, with Alzheimers disease and Parkinsons disease being the most common.

I think that it is special that the Marquette science community is being innovative in understanding the early stages of neurodegenerative diseases, Hannah Seeman, a sophomore in the College of Communication said. I value the scientists that are making strides to aid those predisposed to Alzheimers disease since it runs in my family.

The authors of this study include Jaya Sharma, a post-doctoral student in Manogarans lab. Additional researchers on the project include Stephen J. Merrill, a professor of mathematics, statistics and computer science; Emily Paulson, a graduate student in mathematics, statistics and computer science; and Joanna O. Obaoye, an undergraduate biology student.

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Marquette scientists discover the early stages of neurodegenerative diseases MC1 GR2 - Marquette Wire

A mechanism shared by healing wounds and growing tumors – The Rockefeller University Newswire

Cancerous cells in a skin tumor become locked in an abnormal state as a result of the activation of a gene-regulating element (green).

Like an image in a broken mirror, a tumor is a distorted likeness of a wound. Scientists have long seen parallels between the two, such as the formation of new blood vessels, which occurs as part of both wound healing and malignancy.

Research at The Rockefeller University offers new insights about what the two processes have in commonand how they differat the molecular level. The findings, described April 20 in Cell, may aid in the development of new therapies for cancer.

Losing identity

At the core of both malignancy and tissue mending are stem cells, which multiply to produce new tissue to fill the breach or enlarge the tumor. To see how stem cells behave in these scenarios, a team led by scientists in Elaine Fuchss lab compared two distinct types found within mouse skin.

One set of stem cells, at the base of the follicle, differentiates to form the hair shaft; while another set produces new skin cells. Under normal conditions, these two cell populations are physically distinct, producing only their respective tissue, nothing else.

But when Yejing Ge, a postdoc in the Fuchs lab, looked closely at gene activity in skin tumors, she found a remarkable convergence: The follicle stem cells expressed genes normally reserved for skin stem cells, and vice versa. Around wounds, the researchers documented the same blurring between the sets of stem cells.

Master switches

Two of the identity-related genes stood out. They code for so-called master regulators, molecules that play a dominant role in determining what type of tissue a stem cell will ultimately producein this case, hair follicle or skin. The researchers suspect that stress signals from the tissue surrounding the damage or malignancy kick off a cycle that feeds off itself by enabling the master regulators to make more of themselves.

Access to DNA is the key. To go to work, master regulators bind to certain regions of DNA and so initiate dramatic changes in gene expression. The researchers found evidence that stress signals open up new regions of DNA, making them more accessible to gene activation. By binding in these newly available spots, master regulators elevate the expression of identity-related genes, including the genes that encode the master regulators themselves.

Locked in

While wounds heal, cancer can grow indefinitely. The researchers discovered that while stress signals eventually wane in healing wounds, they can persist in cancerand with prolonged stress signaling, another region of DNA opens up to kick off a separate round of cancer-specific changes.

Tumors have been described as wounds that never heal, and now we have identified specific regulatory elements that, when activated, keep tumor cells locked into a blurred identity, Ge says.

The scientists hope this discovery could lead to precise treatments for cancer that cause less collateral damage than conventional chemotherapy. We are currently testing the specificity of these cancer regulatory elements in human cells for their possible use in therapies aimed at killing the tumor cells and leaving the healthy tissue cells unharmed, Fuchs says.

Elaine Fuchs is the Rebecca C. Lancefield Professor, head of the Robin Chemers Neustein Laboratory of Mammalian Cell Biology and Development, and a Howard Hughes Medical Institute investigator.

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A mechanism shared by healing wounds and growing tumors - The Rockefeller University Newswire

Are baby, wisdom teeth the next wave in stem cell treatment? – CNN

It's based on experimental research that suggests stem cells extracted from the pulp of these teeth might someday regrow a lost adult tooth or offer other regenerative medicine benefits -- some potentially life-saving.

"So I'll try not to get emotional here, but my husband was diagnosed with acute myeloid leukemia in 2011," said Bassetto, of Naperville, Illinois, head of a sales team at a software company.

In 2012, her husband, James, had a stem cell transplant to restore his bone marrow and renew his blood.

"He was very fortunate. He was one of six kids, and his brother was a perfect match," she said. She noted that her two children, Madeline, 23, and Alex, 19, may not be so lucky if they develop health problems, since they have only each other; the chance of two siblings being a perfect stem cell match is only 25%.

Unfortunately, her husband's stem cell transplant was not successful. He developed graft-versus-host disease, where his brother's donated stem cells attacked his own cells, and he died shortly afterward.

However, she says, the transplant had given him a chance at a longer life.

Last year, when her son saw a dentist for wisdom tooth pain, a brochure for dental stem cell storage caught Bassetto's eye and struck a chord.

"I know stem cells have tremendous health benefits in fighting disease, and there's a lot ways they're used today," she said. "Had my husband had his own cells, potentially, his treatment could have been more successful."

Medical breakthroughs happen all the time, said Bassetto. "Who knows what potential there is 20 years, 40 years down the road, when my son is an adult or an aging adult?

"Almost like a life insurance policy, is how I viewed it," she said.

Some scientists see storing teeth as a worthwhile investment, but others say it's a dead end.

"Research is still mostly in the experimental (preclinical) phase," said Ben Scheven, senior lecturer in oral cell biology in the school of dentistry at the University of Birmingham. Still, he said, "dental stem cells may provide an advantageous cell therapy for repair and regeneration of tissues," someday becoming the basis for reconstructing bone tissue, retinas and even optic neurons.

Dr. Pamela Robey, chief of the craniofacial and skeletal diseases branch of the National Institute of Dental and Craniofacial Research, acknowledges the "promising" studies, but she has a different take on the importance of the cells.

"There are studies with dental pulp cells being used to treat neurological disorders and problems in the eye and other things," Robey said. The research is based on the idea that these cells "secrete factors that encourage local cells to begin the repair process."

"The problem is, these studies have really not been that rigorous," she said, adding that many have been done only in animals and so provide "slim" evidence of benefits. "The science needs a lot more work."

Robey would know. Her laboratory discovered dental stem cells in 2003.

"My fellows, Songtao Shi and Stan Gronthos, did the work in my lab," Robey said. "Songtao Shi is a dentist, and basically he observed that, when you get a cavity, you get what's called 'reparative dentin.' In other words, the tooth is trying to protect itself from that cavity, so it makes a little bit of dentin to kind of plug the hole, so to speak."

Dentin is the innermost hard layer of tooth that lies beneath the enamel. Underneath the dentin is a soft tissue known as pulp, which contains the nerve tissue and blood supply.

Observing dentin perform reparative work, Shi hypothesized that this must mean there's a stem cell within the tooth that's able to activate and make dentin. So if you wanted to grow an adult tooth instead of getting an implant, knowing how to make dentin would be the start of the process, explained Robey.

Pursuing this idea, Shi, Gronthos and the team conducted their first study with wisdom teeth. They discovered that pulp cells in these third molars did indeed make dentin, but the cells found in baby teeth, called SHED (stem cells from human exfoliated deciduous teeth), had slightly different properties.

"The SHED cells seem to make not only dentin but also something that is similar to bone," Robey said. This "dentin osteogenic material" is a little like bone and a little like dentin -- "unusual stuff," she said.

There is a meticulous process for extracting stem cells from the pulp.

"We very carefully remove any soft tissue that's adhering to the tooth. We treat it with disinfectant, because the mouth is not really that clean," Robey said, laughing.

Scientists then use a dental drill to pass the enamel and dentin -- "kind of like opening up a clam," said Robey -- to get to the pulp. "We take the pulp out, and we digest it with an enzyme to release the cells from the matrix of the pulp, and then we put the cells into culture and grow them."

According to Laning, even very small amounts of dental pulp are capable of producing many hundreds of millions of structural stem cells.

Harvesting dental stem cells is not a matter of waiting for the tooth to fall out and then quickly calling your dentist. When a baby tooth falls out, the viability of the pulp is limited if it's not preserved in the proper solution.

American Academy of Pediatric Dentistry President Dr. Jade Miller explained that "it's critical that the nerve tissue in that pulp tissue, the nerve supply and blood supply, still remain intact and alive." Typically, the best baby teeth to harvest are the upper front six or lower front six -- incisors and cuspids, he said.

For a child between 5 and 8 years of age, it's best to extract the tooth when there's about one-third of the root remaining, Miller said: "It really requires some planning, and so parents need to make this decision early on and be prepared and speak with their pediatric dentist about that."

Bassetto found the process easy. All it involved was a phone call to the company recommended by her dentist.

"They offer a service where they grow the cells and save those and also keep the pulp of the tooth without growing cells from it," she said. "I opted for both." From there, she said, the dentist shipped the extracted teeth overnight in a special package.

Bassetto said she paid less than $2,000 upfront, and now $10 a month for continued storage.

So is banking teeth something parents should be doing?

In a policy statement, the American Academy of Pediatric Dentistry "encourages dentists to follow future evidence-based literature in order to educate parents about the collection, storage, viability, and use of dental stem cells with respect to autologous regenerative therapies."

"Right now, I don't think it is a logical thing to do. That's my personal opinion," said Robey of the National Institute of Dental and Craniofacial Research. As of today, "we don't have methods for creating a viable tooth. I think they're coming down the pike, but it's not around the corner."

Science also does not yet support using dental pulp stem cells for other purposes.

"That's not to say that in the future, somebody could come up with a method that would make them very beneficial," Robey said.

Still, she observed, if science made it possible to grow natural teeth from stem cells and you were in a car accident, for example, and lost your two front teeth, you'd probably be "very happy to give up a third molar to use the cells in the molar to create new teeth." Third molars are fairly expendable, she said.

Plus, Robey explained, it may not be necessary to bank teeth: Another type of stem cell, known as induced pluripotent stem cells, can be programmed into almost any cell type.

"It's quite a different story than banking umbilical cord blood, which we do know contains stem cells that re-create blood," Robey said.

"So cord blood banking -- and now we have a national cord blood bank as opposed to private clinics -- so there's a real rationale for banking cord blood, whereas the rationale for banking baby teeth is far less clear," Robey said.

And there's no guarantee that your long-cryopreserved teeth or cells will be viable in the future. Banking teeth requires proper care and oversight on the part of cryopreservation companies, she said. "I think that that's a big question mark. If you wanted to get your baby teeth back, how would they handle that? How would they take the tooth out of storage and isolate viable cells?"

Provia's Laning, who has "successfully thawed cells that have been frozen for more than 30 years," dismissed such ideas.

"Cryopreservation technology is not the problem here," he said. "Stem cells from bone marrow and other sources have been frozen for future clinical use in transplants for more than 50 years. Similarly, cord blood has a track record of almost 40 years." The technology for long-term cryopreservation has been refined over the years without any substantial changes, he said.

Despite issues and doubts, Miller, of the pediatric dentistry academy, said parents still need to consider banking baby teeth.

A grandparent, he is making the decision for his own family.

"It's really at its infancy, much of this research," he said. "There's a very strong chance there's going to be utilization for these stem cells, and they could be life-saving."

He believes that saving baby teeth could benefit not only his grandchildren but also their older siblings and various other family members if their health goes awry and a stem cell treatment is needed.

"The science is strong enough to show it's not science fiction," Miller said. "There's going to be a significant application, and I want to give my grandkids the opportunity to have those options."

Aside from cost, Miller said there are other considerations: "Is this company going to be around in 30, 40 years?" he asked. "That's not an easy thing to figure out."

Having taken the leap, Bassetto doesn't worry.

"In terms of viability, you know, if something were to happen with the company, you could always get what's stored and move it elsewhere, so I felt I was protected that way," she said. She feels "pretty confident" with her decision and plans to store her grandchildren's baby teeth.

Still, she concedes that her circumstances may be rare.

"Not everybody's going to be touched by some kind of disease where it just hits home," Bassetto said. "For me, that made it a no-brainer."

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Are baby, wisdom teeth the next wave in stem cell treatment? - CNN

Scientists reveal a new mechanism mediating environment-microbe-host interactions – Phys.Org

April 24, 2017 Dr. Meng Wang is an associate professor of the Huffington Center On Aging at Baylor College of Medicine. Credit: Baylor College of Medicine

Researchers at Baylor College of Medicine have uncovered a new mechanism showing how microbes can alter the physiology of the organisms in which they live. In a paper published in Nature Cell Biology, the researchers reveal how microbes living inside the laboratory worm C. elegans respond to environmental changes and generate signals to the worm that alter the way it stores lipids.

"Microbe-host interactions have been known for a long time, but the actual molecular mechanisms that mediate the interactions were largely unknown," said senior author Dr. Meng Wang, associate professor of molecular and human genetics at Baylor and the Huffington Center On Aging. "Microbes living inside another organism, the host, can respond to changes in the environment, change the molecules they produce and consequently influence the normal workings of the host's body, including disease susceptibility."

In this study, Wang and first author Dr. Chih-Chun Lin working in the Wang Lab have dissected for the first time a molecular mechanism by which E. coli bacteria can regulate C. elegans' lipid storage.

How E. coli changes lipid storage in C. elegans

C. elegans is a laboratory worm model scientists use to study basic biological mechanisms in health and disease.

"This worm naturally consumes and lives with bacteria in its gut and interacts with them in ways that are similar to those between humans and microbes. In the laboratory, we can study basic biological mechanisms by controlling the type of bacteria living inside this worm as well as other variables and then determining the effect on the worm's physiology," Wang said.

In this study, Wang and Lin compared two groups of worms. One group received bacteria that had been grown in a nutritionally rich environment. The other group of worms received the same type of bacteria, but it had grown in nutritionally poor conditions. Both groups of worms received the same amount and type of nutrients, the only difference was the type of environment in which the bacteria had grown before they were administered to the worms.

Interestingly, the worms carrying bacteria that came from a nutritionally poor environment had in their bodies twice the amount of fat present in the worms living with the bacteria coming from the nutritionally rich environment.

The researchers then carried out more experiments and determined that it was the lack of the amino acid methionine in the nutritionally poor environment that had triggered the bacteria to adapt by producing different compounds that then initiated a cascade of events in the worm that led to extra fat accumulation. In addition, the researchers observed that the tissues showing extra fat accumulation also had their mitochondria fragmented. The activities of the mitochondria, the balance between their fusion and breaking apart, are known to be tightly coupled with metabolic activities.

A mechanism that reveals unsuspected connections

The researchers found that the bacteria were able to trigger mitochondrial fragmentation and then extra lipid accumulation because the molecular intermediates the bacteria had triggered allowed them to 'establish communication' with the mitochondria.

"We have found evidence for the first time that bacteria and mitochondria can 'talk to each other' at the metabolic level," Wang said.

Bacteria and mitochondria are like distant relatives. Evolutionary evidence strongly suggests that mitochondria descend from bacteria that entered other cell types and became incorporated into their structure. Mitochondria play essential roles in many aspects of the cell's metabolism, but also maintain genes very similar to those of their bacterial ancestors.

"It's interesting that the molecules bacteria generate can chime in the communication between mitochondria and regulate their fusion-fission balance," Wang said. "Our findings reveal this kind of common language between bacteria and mitochondria, despite them being evolutionary distant from each other."

Some components of this common language involve proteins such as NR5A, Patched and Sonic Hedgehog. The latter is of particular interest to the researchers because it has not been involved in regulating lipid metabolism and mitochondrial dynamics before.

"Microbes in the microbiome can affect many aspects of their host's functions, and here we present a new molecular mechanism mediating microbe-host communication," Wang said. "Having discovered one mechanism encourages us to investigate others that may be related to other physiological aspects, such as the stress response and aging, among others."

Explore further: How gut bacteria change cancer drug activity

More information: Microbial metabolites regulate host lipid metabolism through NR5AHedgehog signalling, Nature Cell Biology (2017). nature.com/articles/doi:10.1038/ncb3515

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Scientists reveal a new mechanism mediating environment-microbe-host interactions - Phys.Org

Scientists step closer to finding cause of multiple sclerosis – Medical News Today

As they find out more about the cell biology of multiple sclerosis, scientists are gradually unraveling the mysteries of the disease, although the exact causes are still unclear. Now, a new study continues this progress with a significant discovery about a new cellular mechanism. It suggests that high levels of the protein Rab32 disrupt key communications involving mitochondria. The disruption causes these "cellular batteries" to misbehave, leading to the toxic effects seen in the brain cells of people with multiple sclerosis.

The new study is the work of researchers from the University of Exeter in the United Kingdom and the University of Alberta in Canada. They report their findings in the Journal of Neuroinflammation.

Co-author Paul Eggleton, an immunologist and professor at the University of Exeter Medical School, says that multiple sclerosis can have a "devastating impact on people's lives," and yet, unfortunately, the present situation is that "all medicine can offer is treatment and therapy for the symptoms."

Multiple sclerosis (MS) is a disease in which the immune system mistakenly attacks tissue of the central nervous system - which comprises the brain, spinal cord, and optic nerve.

As the disease progresses, it destroys more and more of the fatty myelin sheath that insulates and protects the nerve fibers that send electrical messages in the central nervous system.

This destruction can lead to brain damage, vision impairment, pain, altered sensation, extreme fatigue, problems with movement, and other symptoms.

As research into the cause of MS progresses, scientists are becoming increasingly interested in the role of mitochondria - the tiny components inside cells that produce units of energy for powering the cell.

Fast facts about MS

Learn more about MS

In earlier work, the team behind the new study was the first to provide an explanation for the role of defective mitochondria in MS through clinical and laboratory experiments.

In their new investigation, the researchers study a protein called Rab32, which is known to be involved in certain mitochondrial processes.

They found that levels of Rab32 are much higher in the brains of people with MS and hardly detectable in brains of people without the disease.

They also discovered that the presence of Rab32 coincides with disruption to a communication system that causes mitochondria to malfunction, causing toxic effects in the brain cells of people with MS.

The disruption is caused by a cell compartment called the endoplasmic reticulum (ER) being too close to the mitochondria.

The ER produces, processes, and transports many compounds that are used inside and outside the cell.

The researchers note that one of the functions of the ER is to store calcium, and if the distance between the ER and mitochondria is too short, it disrupts the communication between the mitochondria and the calcium supply.

Calcium uptake into mitochondria is already known to be critical to cell functioning.

Although they did not discover what causes Rab32 levels to increase, the team believes that the problem may lie in a defect in the base of the ER.

The study could help scientists to find ways to use Rab32 as a treatment target, as well as look for other proteins that may cause similar disruptions, note the authors.

"Our exciting new findings have uncovered a new avenue for researchers to explore. It is a critical step, and in time, we hope it might lead to effective new treatments for MS."

Prof. Paul Eggleton

Learn how a new immunotherapy reversed paralysis in mouse models of MS.

Read more:
Scientists step closer to finding cause of multiple sclerosis - Medical News Today

New insight into brain development disorder – Phys.Org

April 24, 2017 During cell division, DNA must be copied and distributed between daughter cells. A cellular structure called the mitotic spindle pulls apart the DNA-containing structures, the chromosomes. The photo shows a microscopic image of DNA (blue) in a spindle. The protein ASPM appears to play a key role in this process, as it is located at the 'poles' (yellow) in the spindle. Credit: Cell Biology Utrecht University

Two years ago, the Zika virus drew attention to microcephaly, a developmental disorder in which the brain and skull display inhibited growth. But there are other causes of microcephaly, such as congenital genetic diseases. Much is still unknown about brain development, but researchers at Utrecht University, in collaboration with their colleagues in Switzerland, have now new shed light on the molecules involved. The results of their research will be published in Nature Cell Biology.

"Biological processes are determined by molecules in our cells. We can only understand the factors that determine health and disease and find medicines to control these factors by zooming into this molecular world", explains research leader Prof. Anna Akhmanova.

Surprising discovery

The researchers began their studies by focusing on the protein ASPM. "We knew that the genetic form of microcephaly is most often caused by defects in this protein. But a surprising discovery was that ASPM appears to work closely together with another protein, called katanin", tells Akhmanova.

Essential for healthy development

It appears that precisely this collaboration is important for cell division, and therefore for the normal development of brain cells. "The interaction between ASPM and katanin is required for the proper balance between cell division and their specialisation into nerve cells. When the balance sways too much in one direction or the other, too few brain cells are produced", Akhmanova adds.

Crucial balance

For developing brain cells, this balance is especially crucial, because once they become nerve cells, they cannot divide. If new cells develop into nerve cells too quickly, not enough cells are formed, and the brain remains small.

Key position

During cell division, DNA must be copied and distributed between daughter cells. A cellular structure called the mitotic spindle pulls apart the DNA-containing structures, the chromosomes. The photo shows a microscopic image of DNA (blue) in a spindle. The protein ASPM appears to play a key role in this process, as it is located at the 'poles' (yellow) in the spindle.

Spindle position

The study shows how ASPM does its work at the molecular level, and why it is so important. In cooperation with the protein katanin, ASPM is responsible for the regulation of the organisation and positioning of the spindle. "It is this positioning that helps to determine how the daughter cells develop: will they become copies of new cells, or will they develop into nerve cells", Akhmanova explains.

Much broader insight

The fact that a deviation in the protein ASPM leads to microcephaly can now be better understood at the molecular level. However, the results of this study provide a much broader insight, which may make it possible to explain or find other causes of the disorder.

Evolutionarily unique

Akhmanova's fascination for brain development is not limited to disease, however. "Even apes, our closest relatives, have much less brain capacity than we do. Our brain makes us what we are. This means the development of our brain is evolutionarily very special."

Explore further: Scientists uncover how Zika virus causes microcephaly

More information: Microtubule minus-end regulation at spindle poles by an ASPMkatanin complex, Nature Cell Biology (2017). nature.com/articles/doi:10.1038/ncb3511

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