Stem cell fillings repair cavities and may prevent root canals.


A huge breakthrough in modern dentistry allows dentists to fill cavities with stem cells that stimulate the teeth to regrow.

Discovered by researchers at the University of Nottingham and Harvard University, the tooth can be filled with this stem cell concoction via drill, just like traditional fillings.  Once filled, the stem cells stimulate the growth of dentin, the bony material that makes up the majority of the tooth.

“We have designed synthetic biomaterials that can be used similarly to dental fillings but can be placed in direct contact with pulp tissue to stimulate the native stem cell population for repair and regeneration of pulp tissue and the surrounding dentin,” Adam Celiz, a Marie Curie research fellow at the University of Nottingham, told Newsweek.

The Royal Society of Chemistry described it as a “new paradigm for dental treatments,” and harkens it as an end to the age of tooth decay.

Under old circumstances, an untreated cavity could cause an infection in the roots of the tooth; from there the infection can spread into your sinuses and even your brain, which can cause death.  This new treatment prevents the infection from getting ahold by regrowing the tooth rapidly and boxing it out.

Stem cells are amazing.

Nothing can strike fear into a grown man’s heart quite like being told he’s in need of a root canal, but a new stem cell dental implant may one day make this painful operation a thing of the past. Researchers from the University of Nottingham and Harvard University have developed a dental filling that stimulates tooth regrowth, and allows teeth to repair themselves while preventing any further dental damage.

The innovative tooth filling can be drilled and implanted into the decaying tooth just like a traditional filling. However, it’s what happens once implanted that makes this product so impressive. Rather than simply filling a hole, the implants stimulate stem cells to encourage the growth of dentin — the bony material that makes up the majority of the tooth, Newsweek reported.

Normally, when you receive a filling, a dentist will drill into your tooth and implant a permanent fixture, usually porcelain, a tooth-colored filling material, gold, or other metal alloys, into the pulp tissue inside the tooth. This soft tissue is very much alive and made up of nerves and blood vessels, hence why drilling hurts oh so very much.

“We have designed synthetic biomaterials that can be used similarly to dental fillings but can be placed in direct contact with pulp tissue to stimulate the native stem cell population for repair and regeneration of pulp tissue and the surrounding dentin,” Adam Celiz, a Marie Curie research fellow at the University of Nottingham, told Newsweek.

Sometimes the tooth decay is too far along and the filling is not enough to prevent further infection. Although today we may think of tooth decay as an annoying but otherwise harmless problem, in very rare cases, tooth decay can spread and become extremely dangerous if left untreated. Infection in an upper back tooth can spread to the sinus behind the eye, from which it can enter the brain and cause death.

When an ordinary filling fails to control an infection, a dentist will recommend a root canal. This procedure involves removing the tooth pulp, nerves and all, to prevent further tooth decay, BGR reported. The now hollowed-out tooth chamber is then filled with a permanent object known as a gutta-percha to keep the tooth free from further decay. Unfortunately, because the living material in the tooth has been removed, it is far more likely to fall out over time.

The new device could prevent the need for these painful procedures by ensuring that tooth decay never gets this bad in the first place and allowing patients to “regrow” their damaged chompers.

Already, the innovative new dental fillings were recently awarded a prize from the Royal Society of Chemistry after judges described it as a “new paradigm for dental treatments,” Newsweek reported. The scientists are now hoping to develop the technique with industry partners in order to make it available for commercial use. And while it’s far too soon to see this new tool available at your local dentist’s office, it does suggest that the dark days of painful tooth decay may soon be over.

Sex Hormones Maintain Stem Cells, May Explain Why 95% Of Supercentenarians Are Women


Supercentenarian woman
Emerging stem cell research suggests there may be a link between estrogen and longevity.

Centenarians say positivity is the key to longevity (one woman said it’s Dr. Pepper) — but newresearch suggests a long life comes down to an individual’s sex hormones, especially for supercentenarians. Of the 53 living supercentenarians, or men and women who’ve lived past their 110th birthday, 51 are female.

As you know, estrogen is the female sex hormone and testosterone is the male sex hormone. Stanford University researchers cited prior studies have shown a strong link between these sex hormones and stem cell maintenance. In animal studies, estrogen directly effected stem cell population in female mice, enhancing the regenerative capacity of brain stem cells. And in male mice, estrogen supplements have been shown to increase lifespan.

Similarly, human studies have shown eunuchs, or men who have been castrated, live an estimated 14 years longer than non-eunuchs. BBC reported castration prevents most of testosterone from being produced, possibly “protecting the body from any damaging effect and prolonging lifespan.”  This is in line with the studies that concluded testosterone weakens the immune system, as well as increase risk for coronary heart disease.

Since the “functional decline of stem cells” is a hallmark sign of aging, researchers analyzed emerging stem cell research to try and answer if “the aging of stem cells differs between males and females and whether this has consequences for disease and lifespan.”

While researchers did find “sex-associated differences in stem cell aging may be associated with sexual dimorphism in lifespan,” with dimorphism referring to the physical difference between men and women, their questions remains unanswered; the work devoted to this relationship is limited and elusive. This, however, isn’t to say the data on the effects of estrogen on stem cells doesn’t offer any current value.

“At the very least,” researchers wrote, “it should emphasize the importance of controlling for sex in studies in which age is a variable, as most recent work in the field has done.”

Researchers believe it’s likely “sex plays a role in defining both lifespan and health span, and the effects of sex may not be identical for these two variables.” But until more elaborate reserach is done, the search for a definitive answer continues.

Source: Dulken B, and Brunet A. Stem Cell Aging and Sex: Are We Missing Something? Cell Stem Cell, 2015.

WHY ARE 95% OF PEOPLE WHO LIVE TO 110 WOMEN? YOU’RE AS OLD AS YOUR STEM CELLS


old-woman-574278_1280

Human supercentenarians share at least one thing in common–over 95 percent are women. Scientists have long observed differences between the sexes when it comes to aging, but there is no clear explanation for why females live longer. In a discussion of what we know about stem cell behavior and sex, Stanford University researchers Ben Dulken and Anne Brunet argue that it’s time to look at differences in regenerative decline between men and women. This line of research could open up new explanations for how the sex hormones estrogen and testosterone, or other factors, modify lifespan.

It’s known that estrogen has direct effects on stem cell populations in female mice, from increasing the number of blood stem cells (which is very helpful during pregnancy) to enhancing the regenerative capacity of brain stem cells at the height of estrus. Whether these changes have a direct impact on lifespan is what’s yet to be explored. Recent studies have already found that estrogen supplements increase the lifespan of male mice, and that human eunuchs live about 14 years longer than non-castrated males.

More work is also needed to understand how genetics impacts stem cell aging between the sexes. Scientists have seen that knocking out different genes in mice can add longevity benefits to one sex but not the other, and that males in twin studies have shorter telomeres–a sign of shorter cellular lifespan–compared to females.

“It is likely that sex plays a role in defining both lifespan and healthspan, and the effects of sex may not be identical for these two variables,” the authors write. “As the search continues for ways to ameliorate the aging process and maintain the regenerative capacity of stem cells, let us not forget one of the most effective aging modifiers: sex.”

First-Ever Human Trial Of An Induced Pluripotent Stem Cell Treatment Set To Begin


Human stem cells converted to functional lung cells.


For the first time, scientists have succeeded in transforming human stem cells into functional lung and airway cells. The advance, reported by Columbia University Medical Center (CUMC) researchers, has significant potential for modeling lung disease, screening drugs, studying human lung development, and, ultimately, generating lung tissue for transplantation. The study was published today in the journal Nature Biotechnology.

“Researchers have had relative success in turning human stem cells into heart cells, pancreatic beta cells, intestinal cells, liver cells, and nerve cells, raising all sorts of possibilities for regenerative medicine,” said study leader Hans-Willem Snoeck, MD, PhD, professor of medicine (in microbiology & immunology) and affiliated with the Columbia Center for Translational Immunology and the Columbia Stem Cell Initiative. “Now, we are finally able to make lung and airway cells. This is important because lung transplants have a particularly poor prognosis. Although any clinical application is still many years away, we can begin thinking about making autologous lung transplants — that is, transplants that use a patient’s own skin cells to generate functional lung tissue.”

The research builds on Dr. Snoeck’s 2011 discovery of a set of chemical factors that can turn human embryonic stem (ES) cells or human induced pluripotent stem (iPS) cells into anterior foregut endoderm — precursors of lung and airway cells. (Human iPS cells closely resemble human ES cells but are generated from skin cells, by coaxing them into taking a developmental step backwards. Human iPS cells can then be stimulated to differentiate into specialized cells — offering researchers an alternative to human ES cells.)

In the current study, Dr. Snoeck and his colleagues found new factors that can complete the transformation of human ES or iPS cells into functional lung epithelial cells (cells that cover the lung surface). The resultant cells were found to express markers of at least six types of lung and airway epithelial cells, particularly markers of type 2 alveolar epithelial cells. Type 2 cells are important because they produce surfactant, a substance critical to maintain the lung alveoli, where gas exchange takes place; they also participate in repair of the lung after injury and damage.

The findings have implications for the study of a number of lung diseases, including idiopathic pulmonary fibrosis (IPF), in which type 2 alveolar epithelial cells are thought to play a central role. “No one knows what causes the disease, and there’s no way to treat it,” says Dr. Snoeck. “Using this technology, researchers will finally be able to create laboratory models of IPF, study the disease at the molecular level, and screen drugs for possible treatments or cures.”

“In the longer term, we hope to use this technology to make an autologous lung graft,” Dr. Snoeck said. “This would entail taking a lung from a donor; removing all the lung cells, leaving only the lung scaffold; and seeding the scaffold with new lung cells derived from the patient. In this way, rejection problems could be avoided.” Dr. Snoeck is investigating this approach in collaboration with researchers in the Columbia University Department of Biomedical Engineering.

“I am excited about this collaboration with Hans Snoeck, integrating stem cell science with bioengineering in the search for new treatments for lung disease,” said Gordana Vunjak-Novakovic, PhD, co-author of the paper and Mikati Foundation Professor of Biomedical Engineering at Columbia’s Engineering School and professor of medical sciences at Columbia University College of Physicians and Surgeons.

 

Stem Cells Converted Into Lung Tissue.


Lung transplant recipients have a relatively low 10 year survival rate of about 28%. Cellular rejection of the donor organ occurs about 90% of the time, which brings additional obstacles for the patient and doctors. This might be about to change, as functional lung tissue has been created from human stem cells. The research comes from Hans-Willem Snoeck from the Columbia Center for Translational Immunology and was published in the current edition of Nature Biotechnology.

A couple of years ago, Dr. Snoeck was able to convert stem cells into the precursor endoderm cells that can eventually differentiate into lung cells. This was done with human embryonic stem cells as well as human induced pluripotent stem cells, which involve a bit more work but are easier to come by. Those precursor cells were shown to actually differentiate into six different respiratory tissues, including the coveted type II alveolar cells. which facilitate gas exchange and produce surfactant.

Type 2 alveolar cells, also called pneumocytes, are responsible for producing surfactant, the compound that allows the lungs to remain inflated with air. These type II cells also aid in gas exchange and lung repair.

The lung tissue produced by stem cells could give researchers a unique perspective to study the tissue and learn more about how lung diseases originate. This could lead to better treatment options for lung diseases.

If treatments do not work and transplant becomes inevitable, physicians can use the patient’s own cells to provide a new disease-free organ. This eliminates both the potential for cellular rejection as well as the stress of waiting on the transplant list. To make a replacement lung, researchers would first remove the patient’s lung and decellularize it, leaving only a cartilaginous scaffold. The stem cells would then be used to coat the scaffold and regrow functional tissue to be put back into the patient.

Though it is a long way from getting implanted into a human body, these results are exciting. A patent has been filed by Columbia University for their technique of converting induced pluripotent stem cells into the functional tissue.

Stem cell transplant repairs damaged gut in mouse model of inflammatory bowel disease.


A source of gut stem cells that can repair a type of inflammatory bowel disease when transplanted into mice has been identified by researchers at the Wellcome TrustMedical Research Council Cambridge Stem Cell Institute at the University of Cambridge and at BRIC, the University of Copenhagen, Denmark.

The findings pave the way for patient-specific regenerative therapies for inflammatory bowel diseases such as ulcerative colitis.

All tissues in our body contain specialised stem cells, which are responsible for the lifelong maintenance of the individual tissue and organ. Stem cells found in adults are restricted to their tissue of origin, for example, stem cells found in the  will be able to contribute to the replenishment of the gut whereas stem cells in the skin will only contribute to maintenance of the skin.

The team first looked at developing intestinal tissue in a mouse embryo and found a population of stem cells that were quite different to the  that have been described in the gut. The cells were very actively dividing and could be grown in the laboratory over a long period without becoming specialised into the adult counterpart. Under the correct growth conditions, however, the team could induce the cells to form mature intestinal tissue.

When the team transplanted these cells into mice with a form of , within three hours the stem cells had attached to the damaged areas of the mouse intestine and integrated with the gut cells, contributing to the repair of the damaged tissue.

Dr Kim Jensen, a Wellcome Trust researcher and Lundbeckfoundation fellow, who led the study, said: “We found that the cells formed a living plaster over the damaged gut. They seemed to respond to the environment they had been placed in and matured accordingly to repair the damage.

“One of the risks of  like this is that the cells will continue to expand and form a tumour, but we didn’t see any evidence of that with this immature stem cell population from the gut.”

Cells with similar characteristics were isolated from both mice and humans and the team were also able to generate similar cells by reprogramming adult human cells, so called induced Pluripotent Stem Cells (iPSCs), and growing them in the appropriate conditions.

“We’ve identified a source of gut  that can be easily expanded in the laboratory, which could have huge implications for treating human inflammatory bowel diseases. The next step will be to see whether the human cells behave in the same way in the mouse transplant system and then we can consider investigating their use in patients,” added Dr Jensen.

Scientists generate “mini-kidney” structures from human stem cells.


Diseases affecting the kidneys represent a major and unsolved health issue worldwide. The kidneys rarely recover function once they are damaged by disease, highlighting the urgent need for better knowledge of kidney development and physiology.

Now, a team of researchers led by scientists at the Salk Institute for Biological Studies has developed a novel platform to study  diseases, opening new avenues for the future application of regenerative medicine strategies to help restore kidney function.

Salk scientists generate “mini-kidney” structures from human stem cells

For the first time, the Salk researchers have generated three-dimensional kidney structures from human stem cells, opening new avenues for studying the development and diseases of the kidneys and to the discovery of new drugs that target human . The findings were reported November 17 in Nature Cell Biology.

Scientists had created precursors of kidney cells using stem cells as recently as this past summer, but the Salk team was the first to coax human stem cells into forming three-dimensional cellular structures similar to those found in our kidneys.

“Attempts to differentiate human stem cells into renal cells have had limited success,” says senior study author Juan Carlos Izpisua Belmonte, a professor in Salk’s Gene Expression Laboratory and holder of the Roger Guillemin Chair. “We have developed a simple and efficient method that allows for the differentiation of human stem cells into well-organized 3D structures of the ureteric bud (UB), which later develops into the collecting duct system.”

The Salk findings demonstrate for the first time that pluripotent stem cells (PSCs)—cells capable of differentiating into the many cells and tissue types that make up the body—can made to develop into cells similar to those found in the ureteric bud, an early developmental structure of the kidneys, and then be further differentiated into three-dimensional structures in organ cultures. UB cells form the early stages of the human urinary and reproductive organs during development and later develop into a conduit for urine drainage from the kidneys. The scientists accomplished this with both human  and induced  (iPSCs),  from the skin that have been reprogrammed into their pluripotent state.

After generating iPSCs that demonstrated pluripotent properties and were able to differentiate into mesoderm, a germ cell layer from which the kidneys develop, the researchers made use of growth factors known to be essential during the natural development of our kidneys for the culturing of both iPSCs and embryonic stem cells. The combination of signals from these growth factors, molecules that guide the differentiation of stem cells into specific tissues, was sufficient to commit the cells toward progenitors that exhibit clear characteristics of renal cells in only four days.

The researchers then guided these cells to further differentiated into organ structures similar to those found in the ureteric bud by culturing them with kidney cells from mice. This demonstrated that the mouse cells were able to provide the appropriate developmental cues to allow human  to form three-dimensional structures of the kidney.

In addition, Izpisua Belmonte’s team tested their protocol on iPSCs from a patient clinically diagnosed with polycystic  (PKD), a genetic disorder characterized by multiple, fluid-filled cysts that can lead to decreased  and kidney failure. They found that their methodology could produce kidney structures from patient-derived iPSCs.

Because of the many clinical manifestations of the disease, neither gene- nor antibody-based therapies are realistic approaches for treating PKD. The Salk team’s technique might help circumvent this obstacle and provide a reliable platform for pharmaceutical companies and other investigators studying drug-based therapeutics for PKD and other kidney diseases.

“Our differentiation strategies represent the cornerstone of disease modeling and drug discovery studies,” says lead study author Ignacio Sancho-Martinez, a research associate in Izpisua Belmonte’s laboratory. “Our observations will help guide future studies on the precise cellular implications that PKD might play in the context of .”

What Will Stem Cells Become?


Scientists at the University of Toronto say they have developed a technique that can rapidly screen human stem cells and better control what they will turn into. The technology could have potential use in regenerative medicine and drug development, according to the researchers, who published their findings (“High-throughput fingerprinting of human pluripotent stem cell fate responses and lineage bias”) in this week’s issue of the journal Nature Methods.

“The work allows for a better understanding of how to turn stem cells into clinically useful cell types more efficiently,” explained Emanuel Nazareth, a Ph.D. student at the Institute of Biomaterials & Biomedical Engineering at the University of Toronto. The research comes out of the lab of Peter Zandstra, Ph.D., Canada Research Chair in Bioengineering at U of T.

The researchers used human pluripotent stem cells (hPSC), cells which have the potential to differentiate and eventually become any type of cell in the body. But the key to getting stem cells to grow into specific types of cells, such as skin cells or heart tissue, is to grow them in the right environment in culture, and there have been challenges in getting those environments (which vary for different types of stem cells) just right, Nazareth said.

The researchers developed a high-throughput platform, which uses robotics and automation to test many compounds or drugs at once, with controllable environments to screen hPSCs in. With it, they can control the size of the stem cell colony, the density of cells, and other parameters in order to better study characteristics of the cells as they differentiate or turn into other cell types. Studies were done using stem cells in micro-environments optimized for screening and observing how they behaved when chemical changes were introduced.

“We developed a high-throughput platform to screen hPSCs in configurable microenvironments in which we optimized colony size, cell density, and other parameters to achieve rapid and robust cell fate responses to exogenous cues,” wrote the investigators. “We used this platform to perform single-cell protein expression profiling, revealing that Oct4 and Sox2 costaining discriminates pluripotent, neuroectoderm, primitive streak, and extraembryonic cell fates.”

In essence, Oct4 and Sox2, two specific proteins found within stem cells, can be used to track the four major early cell fate types that stem cells can turn into, allowing four screens to be performed at once.

“One of the most frustrating challenges is that we have different research protocols for different cell types. But as it turns out, very often those protocols don’t work across many different cell lines,” added Nazareth.

The work also provides a way to study differences across cell lines that can be used to predict certain genetic information, such as abnormal chromosomes. What’s more, these predictions can be done in a fraction of the time compared to other existing techniques, and for a substantially lower cost compared to other testing and screening methods, pointed out Nazareth.

“We anticipate this technology will underpin new strategies to identify cell fate control molecules, or even drugs, for a number of different stem cell types,” said Dr. Zandstra said.

UCLA scientist uncovers biological clock able to measure age of most human tissues.


Study finds women’s breast tissue ages faster than the rest of the body.

Everyone grows older, but scientists don’t really understand why. Now a UCLA study has uncovered a biological clock embedded in our genomes that may shed light on why our bodies age and how we can slow the process.
Published in the Oct. 21 edition of the journal Genome Biology, the findings could offer valuable insights to benefit cancer and stem cell research.
Biological clock
While earlier biological clocks have been linked tosalivahormones and telomeres, the new research is the first to result in the development of an age-predictive tool that uses a previously unknown time-keeping mechanism in the body to accurately gauge the age of diverse human organs, tissues and cell types. Unexpectedly, this new tool demonstrated that some parts of the anatomy, like a woman’s breast tissue, age faster than the rest of the body.
“To fight aging, we first need an objective way of measuring it. Pinpointing a set of biomarkers that keeps time throughout the body has been a four-year challenge,” said Steve Horvath, a professor of human genetics at the David Geffen School of Medicine at UCLA and a professor ofbiostatistics at the UCLA Fielding School of Public Health. “My goal in inventing this age-predictive tool is to help scientists improve their understanding of what speeds up and slows down the human aging process.”
To create his age predictor, Horvath focused on a naturally occurring process called methylation, a chemical modification of one of the four building blocks that make up our DNA. He sifted through 121 sets of data collected previously by researchers who had studied methylation in both healthy and cancerous human tissue.
Gleaning information from nearly 8,000 samples of 51 types of tissue and cells taken from throughout the body, Horvath charted how age affects DNA methylation levels from pre-birth through 101 years. For the age predictor, he zeroed in on 353 markers linked to methylation that change with age and are present throughout the body.
Horvath tested the predictive tool’s effectiveness by comparing a tissue’s biological age to its chronological age. When the tool repeatedly proved accurate in matching biological to  chronological age, he was thrilled — and a little stunned.
“It’s surprising that one could develop a predictive tool that reliably keeps time across the human anatomy,” he said. “My approach really compared apples and oranges, or in this case, very different parts of the body — including brain, heart, lungs, liver, kidney and cartilage.”
While most samples’ biological ages matched their chronological ages, some diverged significantly. For example, Horvath discovered that a woman’s breast tissue ages faster than the rest of her body.
“Healthy breast tissue is about two to three years older than the rest of a woman’s body,” he said. “If a woman has breast cancer, the healthy tissue next to the tumor is an average of 12 years older than the rest of her body.”
The results may explain why breast cancer is the most common cancer in women. Given that the clock ranked tumor tissue an average of 36 years older than healthy tissue, it could also explain why age is a major risk factor for many cancers in both genders.
Horvath next looked at induced pluripotent stem cells, adult cells that have been reprogrammed to an embryonic stem cell–like state, enabling them to form any type of cell in the body and continue dividing indefinitely.
“My research shows that all stem cells are newborns,” he said. “More importantly, the process of transforming a person’s cells into pluripotent stem cells resets the cells’ clock to zero.”
In principle, the discovery proves that scientists can rewind the body’s biological clock and restore it to zero.
“The big question is whether the underlying biological clock controls a process that leads to aging,” Horvath said. “If so, the clock will become an important biomarker for studying new therapeutic approaches to keeping us young.”
Finally, Horvath discovered that the clock’s rate speeds up or slows down depending on a person’s age.
“The clock’s ticking rate isn’t constant,” he explained. “It ticks much faster when we’re born and growing from children into teenagers, then slows to a constant rate when we reach 20.”
In an unexpected finding, the cells of children with progeria, a genetic disorder that causes premature aging, appeared normal and reflected their true chronological age.
Horvath noted that it will take additional research to dissect the precise molecular or biochemical mechanism in the body that makes his age predictor possible.
UCLA has filed a provisional patent on Horvath’s age-predictive tool. His next studies will examine whether stopping the body’s clock halts the aging process and whether a similar clock exists in mice.
%d bloggers like this: