ELK GROVE (CBS13) Hes only 17, but hes already making big waves in the science community.

A local high school senior was selected as a semi-finalist in the 2015 Intel Science Talent Search. His research on stem cells set him apart from the rest. Out of hundreds of applicants, Ryan Fong, a senior at Sheldon High School in Elk Grove, is being recognized for his research in stem cells. Its an opportunity he says he wont soon forget.

Each of these cells is genetic material from one cell, he explains.

He doesnt come from a line of doctors or medical researchers. Fong is just a teenager interested in stem cells.

Its such a young field and it holds so much potential to redefine what we think is medically possible, he says.

Fong wasnt always intrigued by science, but a couple of years ago, at the request of a teacher, he decided to enter the Teen Biotech Challenge and happened to win an internship at the UC Davis School of Medicine.

I didnt know anything about research and I didnt know what I was getting into, but I dived in head first, said Fong.

That internship became a launching pad for Fong. He was published in a medical peer review journal called Stem Cells. And this past summer, he spent his time in Stanford among doctors and researchers working on reprogramming cells from a layer of skin so that it can match any cell type in the body.

So were taking someones cells from their skin and turning them into cells that can be found in the lungs, said Fong.

Their research on the topic won Fong a spot as a semi-finalist in the 2015 Intel Science Talent Search, and a $1,000 scholarship.

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Local Teen Selected As Semi-Finalist In Intel Science Talent Search

A new procedure can quickly and efficiently increase the length of human telomeres, the protective caps on the ends of chromosomes that are linked to aging and disease, according to scientists at the Stanford University School of Medicine.

Treated cells behave as if they are much younger than untreated cells, multiplying with abandon in the laboratory dish rather than stagnating or dying.

The procedure, which involves the use of a modified type of RNA, will improve the ability of researchers to generate large numbers of cells for study or drug development, the scientists say. Skin cells with telomeres lengthened by the procedure were able to divide up to 40 more times than untreated cells. The research may point to new ways to treat diseases caused by shortened telomeres.

Telomeres are the protective caps on the ends of the strands of DNA called chromosomes, which house our genomes. In young humans, telomeres are about 8,000-10,000 nucleotides long. They shorten with each cell division, however, and when they reach a critical length the cell stops dividing or dies. This internal "clock" makes it difficult to keep most cells growing in a laboratory for more than a few cell doublings.

'Turning back the internal clock'

"Now we have found a way to lengthen human telomeres by as much as 1,000 nucleotides, turning back the internal clock in these cells by the equivalent of many years of human life," said Helen Blau, PhD, professor of microbiology and immunology at Stanford and director of the university's Baxter Laboratory for Stem Cell Biology. "This greatly increases the number of cells available for studies such as drug testing or disease modeling."

A paper describing the research was published today in the FASEB Journal. Blau, who also holds the Donald E. and Delia B. Baxter Professorship, is the senior author. Postdoctoral scholar John Ramunas, PhD, of Stanford shares lead authorship with Eduard Yakubov, PhD, of the Houston Methodist Research Institute.

The researchers used modified messenger RNA to extend the telomeres. RNA carries instructions from genes in the DNA to the cell's protein-making factories. The RNA used in this experiment contained the coding sequence for TERT, the active component of a naturally occurring enzyme called telomerase. Telomerase is expressed by stem cells, including those that give rise to sperm and egg cells, to ensure that the telomeres of these cells stay in tip-top shape for the next generation. Most other types of cells, however, express very low levels of telomerase.

Transient effect an advantage

The newly developed technique has an important advantage over other potential methods: It's temporary. The modified RNA is designed to reduce the cell's immune response to the treatment and allow the TERT-encoding message to stick around a bit longer than an unmodified message would. But it dissipates and is gone within about 48 hours. After that time, the newly lengthened telomeres begin to progressively shorten again with each cell division.

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Telomere extension turns back aging clock in cultured human cells, Stanford study finds

20 hours ago

Transcription factor Twist1 is involved in many processes where cells change shape or function. Thereby, Twist1 is crucial for embryonic development, but has also been implicated in cancer progression. However, the precise contribution of Twist1 to these processes is under much debate. Scientists from the Helmholtz Zentrum Mnchen describe a new mode of action: a short-term, transient activation of Twist1 primes cells for stem cell-like properties. By contrast, prolonged, chronic Twist1 activity suppresses stem cell-like traits. These results, published in the journal Cell Reports, help to unravel seemingly contradictory observations and illuminate the complexities of transcription factor action in regeneration and tumor progression.

Team leader Christina Scheel summarizes the results: "Twist1 is a developmental master regulator that has also been implicated in cancer progression. We show that transient Twist1 activation primes certain cells for stem-cell-like properties and cellular plasticity. Said differently, induction of these traits depends on Twist1, but they are only displayed by the cells after Twist1 deactivation. By contrast, chronic Twist1 activity suppresses stem-cell-like properties and promotes a phenotype that is characterized by extreme changes in cell shape and function, effectively locking the cells into an invasive, non-proliferative phenotype. Thereby, our results provide an integrative view of seemingly contradictory results concerning the effects of Twist1 in physiological and pathological processes."

Duration of Twist1 activity decisive

Scientists from the Institute of Stem Cell Research and the Institute of Experimental Genetics at the Helmholtz Zentrum Mnchen (HMGU) examined the effects of Twist1 activation on breast epithelial cells, paying particular attention to the duration of the Twist1-signal. To their surprise, cells were permanently altered after a short dose of Twist1-activation: they proliferated under very stringent conditions usually permissive only for stem cells and were able to generate complex multicellular structures, suggesting a gain of cellular plasticity.

Twist1 may fuel regeneration

A high level of plasticity implies regenerative potential. However, when activated during tumor development, Twist1 promotes aggressive behaviour in tumor cells. With their investigations, the team was able to reveal a new aspect of how Twist1 regulates cell shape and function and, thereby, impacts regeneration, but also tumor progression.

"Our results offer important insights for further mechanistic studies of regeneration in healthy and tumour cells", explains first author Johanna Schmidt. "The precise delineation of the different modes of action by Twist1 provide the basis for future studies aiming to manipulate its activity either to promote regeneration or target advanced tumors ," adds co-author Elena Panzilius.

Explore further: New mechanism involved in skin cancer initiation, growth and progression

More information: Schmidt, J. et al. (2015), Stem-Cell-like Properties and Epithelial Plasticity Arise as Stable Traits after Transient Twist1 Activation, Cell Reports, DOI: 10.1016/j.celrep.2014.12.032

See original here:
Twist1: Complex regulator of cell shape and function

(Tokyo-AFP) - Japanese scientists say they are on their way to being able to create custom-made skin, bone and joints using a 3D printer.

Several groups of researchers around the world have developed small masses of tissue for implants, but now they are looking to take the next step and make them functional.

Tsuyoshi Takato, a professor at the University of Tokyo Hospital, said his team had been working to create "a next-generation bio 3D printer", which would build up thin layers of biomaterials to form custom-made parts.

His team combines stem cells -- the proto-cells that are able to develop into any body part -- and proteins that trigger growth, as well as synthetic substance similar to human collagen.

Using a 3D printer, they are working on "mimicking the structure of organs" -- such as the hard surface and spongy inside for bones, Takato said.

In just a few hours, the printer crafts an implant using data from a Computer Tomography (CT) scan.

These implants can fit neatly into place in the body, and can quickly become assimilated by real tissue and other organs in the patient, the plastic surgeon said.

"We usually take cartilage or bone from the patient's own body (for regular implants), but these custom-made implants will mean not having to remove source material," Takato said.

The technology could also offer hope for children born with bone or cartilage problems, for whom regular synthetic implants are no good because of the rate of their body's growth.

The main hurdle was the heat generated by conventional 3D printers, which damages living cells and protein.

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Japan researchers target 3D-printed body parts

(MENAFN - The Peninsula) Japanese scientists say they are on their way to being able to create custom-made skin, bone and joints using a 3D printer.

Several groups of researchers around the world have developed small masses of tissue for implants, but now they are looking to take the next step and make them functional.

Tsuyoshi Takato, a professor at the University of Tokyo Hospital, said his team had been working to create "a next-generation bio 3D printer", which would build up thin layers of biomaterials to form custom-made parts.

His team combines stem cells - the proto-cells that are able to develop into any body part - and proteins that trigger growth, as well as synthetic substance similar to human collagen.

Using a 3D printer, they are working on "mimicking the structure of organs" - such as the hard surface and spongy inside for bones, Takato said.

In just a few hours, the printer crafts an implant using data from a Computer Tomography (CT) scan. These implants can fit neatly into place in the body, and can quickly become assimilated by real tissue and other organs in the patient, the plastic surgeon said.

"We usually take cartilage or bone from the patient's own body (for regular implants), but these custom-made implants will mean not having to remove source material," Takato said.

The technology could also offer hope for children born with bone or cartilage problems, for whom regular synthetic implants are no good because of the rate of their body's growth. The main hurdle was the heat generated by conventional 3D printers, which damages living cells and protein.

"We haven't fully worked out how to avoid heat denaturation but we already have some models and are exploring which offers the most efficient method," he said.

The artificial protein Takato and his team use was developed by Fujifilm, which has been studying collagen used in photographic films. Since it is modelled on human collagen and does not derive from animals, it can be easily assimilated in human bodies, reducing the risk of infections such as mad-cow disease.

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Japan scientists target 3D-printed body parts

FRESNO, Calif. (KFSN) --

Our bodies contain 23 pairs of them, 46 total. But if chromosomesare damaged, they can cause birth defects, disabilities, growth problems, even death.

Case Western scientist Anthony Wynshaw-Boris is studying how to repair damaged chromosomes with the help of a recent discovery. He's taking skin cells and reprogramming them to work like embryonic stem cells, which can grow into different cell types.

"You're taking adult or a child's skin cells. You're not causing any loss of an embryo, and you're taking those skin cells to make a stem cell." Anthony Wynshaw-Boris, M.D., PhD, of Case Western Reserve University, School of Medicine told ABC30.

Scientists studied patients with a specific defective chromosome that was shaped like a ring. They took the patients' skin cells andreprogrammed them into embryonic-like cells in the lab. They found this process caused the damaged "ring" chromosomes to be replaced by normal chromosomes.

"It at least raises the possibility that ring chromosomes will be lost in stem cells," said Dr. Wynshaw-Boris.

While this research was only conducted in lab cultures on the rare ring-shaped chromosomes, scientists hope it will work in patients with common abnormalities like Down syndrome.

"What we're hoping happens is we might be able to use, modify, what we did, to rescue cell lines from any patient that has any severe chromosome defect," Dr. Wynshaw-Boris explained.

It's research that could one day repair faulty chromosomes and stop genetic diseases in their tracks.

The reprogramming technique that transforms skin cells to stem cells was so ground-breaking that a Japanese physician won the Nobel Prize in medicine in 2012 for developing it.

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Stem Cells to Repair Broken Chromosomes: Medicine's Next Big Thing?

Researchers have successfully improved the ability of muscle to repair itself - by artificially increasing levels of the BMI1 gene in the muscle-specific stem cells of mice with muscular dystrophy.

The BMI1 gene has been previously linked to the body's ability to regenerate tissue cells in areas such as blood or skin.

Led by Queen Mary University of London and published in the Journal of Experimental Medicine, the study provides the first proof of concept that manipulating the activity of this gene enhances the regeneration of the dystrophic muscle to a level where strength is visibly improved. For example, the mice were able to run on a treadmill for a longer time period and at a faster pace.

This line of research will now be further developed and scientists aim to one day apply the treatment to patients with chronic muscle wasting such as muscular dystrophy.

Muscular dystrophy is a devastating and incurable condition. Duchenne Muscular Dystrophy - the deadliest form of the muscle-wasting disease - is caused by mutations in a gene which eventually cause muscle fibres to become damaged and waste away.

Duchenne Muscular Dystrophy is characterised by repeated cycles of muscle damage and repair, resulting in exhaustion of the muscle repair cells. It affects one in 3,500 boys and normally proves fatal by early adulthood.

Professor Silvia Marino, Lead Author, Queen Mary University of London, comments: "This study has given us the first 'proof of concept' that harnessing the gene BMI1 can significantly enhance the regeneration of dystrophic muscles to a level where strength is visibly improved. We plan to continue our research and hope to establish whether this concept can be successfully applied to patients with muscular dystrophy, but possibly other degenerative conditions or even traumatic muscle damage."

###

This research was funded by the MRC and the charity Muscular Dystrophy Campaign.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.

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Hope for muscular dystrophy patients: Harnessing gene helps repair muscle damage

Squamous cell carcinoma (SCC) represents the second most frequent skin cancer with more than half million new patients affected every year in the world. Cancer stem cells (CSCs) are a population of cancer cells that have been described in many different cancers, including skin SCCs and that feed tumor growth, could be resistant to therapy thus being responsible for tumor relapse after therapy. However, still very little is known about the mechanisms that regulate CSCs functions.

In a new study published and making the cover of Cell Stem Cell, researchers led by Pr. Cdric Blanpain, MD/PhD, professor and WELBIO investigator at the IRIBHM, Universit libre de Bruxelles, Belgium, report the mechanisms regulating the different functions of Twist1 controlling skin tumour initiation, cancer stem cell function and tumor progression.

Benjamin Beck and colleagues used state of the art genetic mouse models to dissect, the functional role and molecular mechanisms by which Twist1 controls tumor initiation, cancer stem cell function and tumor progression. In collaboration with Dr Sandrine Rorive and Pr Isabelle Salmon from the department of Pathology at the Erasme Hospital, ULB and the group of Jean-Christophe Marine (VIB, KUL Leuven), they demonstrated that while Twist1 is not expressed in the normal skin, Twist1 deletion prevents skin cancer formation demonstrating the essential role of Twist1 during tumorigenesis. "It was really surprising to observe the essential role of Twist1 at the earliest step of tumor formation, as Twist1 was thought to stimulate tumor progression and metastasis" comments Benjamin Beck, the first author of this study.

The authors demonstrate that different levels of Twist1 are necessary for tumor initiation and progression. Low level of Twist1 is required for the initiation of benign tumors, while higher level of Twist1 is necessary for tumor progression. They also demonstrate that Twist1 is essential for tumor maintenance and the regulation of cancer stem cell function. The researchers also uncovered that the different functions of Twist1 are regulated by different molecular mechanisms, and identified a p53 independent role of Twist1 in regulating cancer stem cell functions.

In conclusion, this work shows that Twist1, a well-known regulator of tumor progression, is necessary for tumor initiation, regulation of cancer stem cell function and malignant progression. "It was really interesting to see that different levels of Twist1 are required to carry out these different tumor functions and that these different Twist1 functions are regulated by different molecular pathways. Given the diversity of cancers expressing Twist1, the identification of the different mechanisms controlled by Twist1 are likely to be relevant for other cancers" comments Cdric Blanpain, the last and corresponding author of this study.

Story Source:

The above story is based on materials provided by Libre de Bruxelles, Universit. Note: Materials may be edited for content and length.

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Skin cancer: New mechanism involved in tumor initiation, growth and progression

Researchers at King's College London have identified a new mechanism by which skin damage triggers the formation of tumours, which could have important therapeutic implications for patients suffering with chronic ulcers or skin blistering diseases.

The study, published today in Nature Communications, highlights an innate sensing of bacteria by immune cells in the formation of skin tumours. This molecular process could tip the balance between normal wound repair and tumour formation in some patients, according to researchers.

Although an association between tissue damage, chronic inflammation and cancer is well established, little is known about the underlying cause. Epidermolysis Bullosa (EB), for instance, is one of several rare inherited skin conditions associated with chronic wounding and increased risk of tumours.

However, this study - funded primarily by the Medical Research Council (MRC) and the Wellcome Trust - is the first to demonstrate that bacteria present on the skin can contribute to the development of skin tumours.

Researchers found that when mice with chronic skin inflammation are wounded they develop tumours at the wound site, with cells of the immune system required for this process to take place. They discovered that the underlying signalling mechanism involves a bacterial protein, flagellin, which is recognised by a receptor (Toll-like receptor 5) on the surface of the immune cells.

Although the direct relevance to human tumours is yet to be tested, researchers have shown that a protein called HMGB1 - found to be highly expressed in mice with chronic skin inflammation - is increased in human patients with Epidermolysis Bullosa (EB). The study found a reduction in HMGB1 levels in mice when the TLR-5 receptor was removed from immune cells. This raises the possibility of future treatments aimed at reducing levels of the flagellin bacterial protein on the skin surface, or targeting the TLR-5 receptor.

Professor Fiona Watt, lead author and Director of the Centre for Stem Cells and Regenerative Medicine at King's College London, said: 'These findings have broad implications for various types of cancers and in particular for the treatment of tumours that arise in patients suffering from chronic ulcers or skin blistering diseases.

'In the context of chronic skin inflammation, the activity of a particular receptor in white blood cells, TLR-5, could tip the balance between normal wound repair and tumour formation.'

Professor Watt added: 'Our findings raise the possibility that the use of specific antibiotics targeting bacteria in wound-induced malignancies might present an interesting clinical avenue.'

###

Continued here:
Bacteria could contribute to development of wound-induced skin cancer

Fat cells shield against skin infections

(IANS) / 3 January 2015

For the study, the researchers exposed mice to Staphylococcus aureus, a common bacterium and major cause of skin and soft tissue infections in humans.

New York: Researchers have discovered that fat cells below the skin help protect you from bacteria.

These skin fat cells known as adipocytes produce antimicrobial peptides that help fend off invading bacteria and other pathogens, the findings showed, pointing to a previously unknown role for the dermal fat cells.

It was thought that once the skin barrier was broken, it was entirely the responsibility of circulating (white) blood cells like neutrophils and macrophages to protect us from getting sepsis, said principal investigator Richard Gallo, professor at University of California, San Diego School of Medicine.

But it takes time to recruit these cells (to the wound site). We now show that the fat stem cells are responsible for protecting us, Gallo added.

It was not known that adipocytes could produce antimicrobials, let alone that they make almost as much as a neutrophil, Gallo said.

For the study, the researchers exposed mice to Staphylococcus aureus, a common bacterium and major cause of skin and soft tissue infections in humans.

They detected a major increase in both the number and size of fat cells at the site of infection within hours.

Originally posted here:
Fat cells shield against skin infections

January 2, 2015

Credit: Thinkstock

Chuck Bednar for redOrbit.com Your Universe Online

Fat cells located beneath a persons skin could help protect them from bacterial infections, according to a new study published Thursday in the journal Science.

In the study, Dr. Richard Gallo, a professor and chief of dermatology at the University of California, San Diego School of Medicine, and his colleagues report that they had discovered a previously unknown function of these dermal fat cells, also known as adipocytes: they produce antimicrobial peptides that help combat bacteria and other types of pathogens.

It was thought that once the skin barrier was broken, it was entirely the responsibility of circulating (white) blood cells like neutrophils and macrophages to protect us from getting sepsis, explained Gallo. But it takes time to recruit these cells (to the wound site).

We now show that the fat stem cells are responsible for protecting us. That was totally unexpected, he added. It was not known that adipocytes could produce antimicrobials, let alone that they make almost as much as a neutrophil.

A persons body launches a complex, multi-tiered defense against microbial infection, the authors said. Several different types of cells are involved, and the process ends with the arrival of specialized cells known as neutrophils and monocytes that target and destroy pathogens.

Before any of that can happen, a more immediate response is required one that can counter the ability of pathogens to rapidly increase their numbers, however. That task is typically performed by epithelial cells, mast cells and leukocytes residing in the area of infection.

Previous research conducted in Gallos lab detected Staphylococcus aureus, a common type of bacteria and a major source of skin infection on humans, in the fat layer of the skin. Antibiotic-resistant forms of this bacterial have become a significant health issue throughout the world, so the study authors looked to see what role adipocytes played in preventing skin infections.

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Fat cells may actually not be so bad

When it comes to skin infections, a healthy and robust immune response may depend greatly upon what lies beneath. In a new paper published in the January 2, 2015 issue ofScience, researchers at the University of California, San Diego School of Medicine report the surprising discovery that fat cells below the skin help protect us from bacteria.

Richard Gallo, MD, PhD, professor and chief of dermatology at UC San Diego School of Medicine, and colleagues have uncovered a previously unknown role for dermal fat cells, known as adipocytes: They produce antimicrobial peptides that help fend off invading bacteria and other pathogens.

"It was thought that once the skin barrier was broken, it was entirely the responsibility of circulating (white) blood cells like neutrophils and macrophages to protect us from getting sepsis," said Gallo, the study's principal investigator.

"But it takes time to recruit these cells (to the wound site). We now show that the fat stem cells are responsible for protecting us. That was totally unexpected. It was not known that adipocytes could produce antimicrobials, let alone that they make almost as much as a neutrophil."

The human body's defense against microbial infection is complex, multi-tiered and involves numerous cell types, culminating in the arrival of neutrophils and monocytes - specialized cells that literally devour targeted pathogens.

Skin graphic image via Shutterstock.

Read more at EurekAlert.

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The good role fat cells play in protecting us from disease

Why are some types of cancer so much more common than others? Sometimes its due to faulty genes inherited from ones parents and sometimes to behaviors like smoking a pack of cigarettes every day. But in most cases, it comes down to something else stem cells.

This is the intriguing argument made by a pair of researchers from Johns Hopkins University. In a study published Friday in the journal Science, they found a very high correlation between the differences in risk for 31 kinds of cancer and the frequency with which different types of stem cells made copies of themselves.

Just how strong was this link? On a scale that goes from 0 (absolutely no correlation) to 1 (exact correlation), biostatistician Cristian Tomasetti and cancer geneticist Bert Vogelstein calculated that it was at least a 0.8. When it comes to cancer, thats high.

No other environmental or inherited factors are known to be correlated in this way across tumor types, Tomasetti and Vogelstein wrote.

Researchers have long recognized that when cells copy themselves, they sometimes make small errors in the billions of chemical letters that make up their DNA. Many of these mistakes are inconsequential, but others can cause cells to grow out of control. That is the beginning of cancer.

The odds of making a copying mistake are believed to be the same for all cells. But some kinds of cells copy themselves much more often than others. Tomasetti and Vogelstein hypothesized that the more frequently a type of cell made copies of itself, the greater the odds that it would develop cancer.

The pair focused on stem cells because of their outsided influence in the body. Stem cells can grow into many kinds of specialized cells, so if they contain damaged DNA, those mistakes can spread quickly.

The researchers combed through the scientific literature and found studies that described the frequency of stem cell division for 31 different tissue types. Then they used data from the National Cancer Institutes Surveillance, Epidemiology and End Results database to assess the lifetime cancer risk for each of those tissue types. When they plotted the total number of stem cell divisions against the lifetime cancer risk for each tissue, the result was 31 points clustered pretty tightly along a line.

To put this notion in concrete terms, consider the skin. The outermost layer of the skin is the epidermis, and the innermost layer of the epidermis contains a few types of cells. Basal epidermal cells are the ones that copy themselves frequently, with new cells pushing older ones to the skins surface. Melanocytes are charged with making melanin, the pigment that protects the skin from the suns damaging ultraviolet rays.

When sunlight hits bare skin, both basal epidermal cells and melanocytes get the same exposure to UV. But basal cell carcinoma is far more common than melanoma about 2.8 million Americans are diagnosed with basal cell carcinoma each year, compared with roughly 76,000 new cases of melanoma, according to the Skin Cancer Foundation. A major reason for this discrepancy, Tomasetti and Vogelstein wrote, is that epidermal stem cells divide once every 48 days, while melanocytes divide only once every 147 days.

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Scientists explain how stem cells and 'bad luck' cause cancer

When it comes to skin infections, a healthy and robust immune response may depend greatly upon what lies beneath. In a new paper published in the January 2, 2015 issue of Science, researchers at the University of California, San Diego School of Medicine report the surprising discovery that fat cells below the skin help protect us from bacteria.

Richard Gallo, MD, PhD, professor and chief of dermatology at UC San Diego School of Medicine, and colleagues have uncovered a previously unknown role for dermal fat cells, known as adipocytes: They produce antimicrobial peptides that help fend off invading bacteria and other pathogens.

"It was thought that once the skin barrier was broken, it was entirely the responsibility of circulating (white) blood cells like neutrophils and macrophages to protect us from getting sepsis," said Gallo, the study's principal investigator.

"But it takes time to recruit these cells (to the wound site). We now show that the fat stem cells are responsible for protecting us. That was totally unexpected. It was not known that adipocytes could produce antimicrobials, let alone that they make almost as much as a neutrophil."

The human body's defense against microbial infection is complex, multi-tiered and involves numerous cell types, culminating in the arrival of neutrophils and monocytes - specialized cells that literally devour targeted pathogens.

But before these circulating white blood cells arrive at the scene, the body requires a more immediate response to counter the ability of many microbes to rapidly increase in number. That work is typically done by epithelial cells, mast cells and leukocytes residing in the area of infection.

Staphylococcus aureus is a common bacterium and major cause of skin and soft tissue infections in humans. The emergence of antibiotic-resistant forms of S. aureus is a significant problem worldwide in clinical medicine.

Prior published work out of the Gallo lab had observed S. aureus in the fat layer of the skin, so researchers looked to see if the subcutaneous fat played a role in preventing skin infections.

Ling Zhang, PhD, the first author of the paper, exposed mice to S. aureus and within hours detected a major increase in both the number and size of fat cells at the site of infection. More importantly, these fat cells produced high levels of an antimicrobial peptide (AMP) called cathelicidin antimicrobial peptide or CAMP. AMPs are molecules used by the innate immune response to directly kill invasive bacteria, viruses, fungi and other pathogens.

"AMPs are our natural first line defense against infection. They are evolutionarily ancient and used by all living organisms to protect themselves," said Gallo.

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Fat isn't all bad: Skin adipocytes help protect against infections

Cancers due to bad luck, left, and cancers due to a combination of bad luck, environmental factors, and inherited factors. Elizabeth Cook]

Cancers due to bad luck, left, and cancers due to a combination of bad luck, environmental factors, and inherited factors. / Elizabeth Cook]

Nearly two-thirds of all cancers are caused by random mutations of the body's stem cells, not by hereditary or environmental effects, according to a study released Jan. 1 by Johns Hopkins scientists.

Tissues with the most divisions of regenerative cells and hence the most chances for mutations tend to have the greatest rates of cancer, the study found.

This explains why skin cancers, for example, are far more common than bone cancers. Skin cells die constantly, so they must be replenished far more often than those that make bone, introducing more chances for errors that lead to cancer.

In effect, most cancers come down to "bad luck", the researchers say in the study.

The findings introduce new dimensions to the struggle against cancer, said two researchers who did not take part in the study.

The study was published Thursday in the journal Science. Cristian Tomasetti of the Johns Hopkins Kimmel Cancer Center at Johns Hopkins Medicine in Baltimore is first author. The study's senior author is Bert Vogelstein, also of the center, part of Johns Hopkins University.

Healthy diet and protection against carcinogens are still important, said Tomasetti, because the one-third variability is still substantial. And the proportion of randomness in each type of cancer varies. Some cancers tend to be greatly increased by environmental factors, such as lung cancer in smokers. The two-third average is a summary of the risk of cancer from all tissue types.

Strong relationship

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Most cancer is bad luck, study finds

The research involved creating human cells in a laboratory dish instead of relying on tests on mice. Photograph: corfield / Alamy/Alamy

Cells used to study dementia in a dish have led scientists to a potential new treatment strategy for an inherited form of the brain disease.

Defective stem cells grown in the lab revealed a signalling pathway linked to frontotemporal dementia (FTD), which accounts for about half of dementia cases before the age of 60.

Treatment with a drug that suppressed the pathway, known as Wnt, restored the ability of neurons affected by the disease to develop normally.

Prof Philip Van Damme, from the Leuven Research Institute for Neuroscience and Disease in Belgium, said: Our findings suggest that signalling events required for neurodevelopment may also play major roles in neurodegeneration.

Targeting such pathways, as for instance the Wnt pathway presented in this study, may result in the creation of novel therapeutic approaches for frontotemporal dementia.

Mutations in the progranulin (GRN) gene are commonly associated with FTD, which results in damage to the frontal and temporal lobes of the brain.

The fact that GRN mutations produced in mice do not display all the features of the human disorder has limited progress towards effective treatments for FTD.

Instead of relying on animal tests, the new research involved creating human cells in a laboratory dish.

The scientists reprogrammed skin cells from three dementia patients into induced pluripotent stem cells (iPSCs), immature cells that mimic stem cells taken from early-stage embryos.

Original post:
Stem cell study leads to potential new dementia treatment

IMAGE:Induced pluripotent stem cells (iPSCs) derived from patients with frontotemporal dementia were genetically corrected and converted to cortical neurons. The green staining indicates the cortical marker CTIP2, the red stain... view more

Credit: Susanna Raitano/Stem Cell Reports 2014

Belgian researchers have identified a new strategy for treating an inherited form of dementia after attempting to turn stem cells derived from patients into the neurons most affected by the disease. In patient-derived stem cells carrying a mutation predisposing them to frontotemporal dementia, which accounts for about half of dementia cases before the age of 60, the scientists found a targetable defect that prevents normal neurodevelopment. These stem cells partially return to normal when the defect is corrected.

The study appears in the December 31st issue of Stem Cell Reports, the official journal of the International Society of Stem Cell Research published by Cell Press.

"Use of induced pluripotent stem cell (iPSC) technology"--which involves taking skin cells from patients and reprogramming them into embryonic-like stem cells capable of turning into other specific cell types relevant for studying a particular disease--"makes it possible to model dementias that affect people later in life," says senior study author Catherine Verfaillie of KU Leuven.

Frontotemporal disorders are the result of damage to neurons in parts of the brain called the frontal and temporal lobes, gradually leading to behavioral symptoms or language and emotional disorders. Mutations in a gene called progranulin (GRN) are commonly associated with frontotemporal dementia, but GRN mutations in mice do not mimic all the features of the human disorder, which has limited progress in the development of effective treatments.

"iPSC models can now be used to better understand dementia, and in particular frontotemporal dementia, and might lead to the development of drugs that can curtail or slow down the degeneration of cortical neurons," Verfaillie says.

Verfaillie and Philip Van Damme of the Leuven Research Institute for Neuroscience and Disease explore this approach in the Stem Cell Reports study by creating iPSCs from three patients carrying a GRN mutation. These immature cells were impaired at turning into mature, specialized cells called cortical neurons--the most affected cell type in frontotemporal dementia.

One of the top defective pathways in the iPSCs was the Wnt signaling pathway, which plays an important role in neuronal development. However, genetic correction or treatment with a compound that inhibits the Wnt signaling pathway restored the ability of the iPSCs to turn into cortical neurons. Taken together, the findings demonstrate that the GRN mutation causes the defect in cortical neuron formation by altering the Wnt signaling pathway.

"Our findings suggest that signaling events required for neurodevelopment may also play major roles in neurodegeneration," Van Damme says. "Targeting such pathways, as for instance the Wnt pathway presented in this study, may result in the creation of novel therapeutic approaches for frontotemporal dementia."

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Patient stem cells used to make dementia-in-a-dish; help identify new treatment strategy

Scientists are now creating primordial germ cells (precursors to egg and sperm) with human stem cells and even skin cells. This new work,published inCelltoday, takes us beyond what was previously just done using stem cells.

One of the first events in the early development of both mice and men is the creation of primordial germ cells (PGCs). After an egg is fertilized by sperm, embryonic stem cells begin to differentiate into various basic cell types that make up the fetus. A small number of these stem cellsdevelop into primordial germ cells, which will go on to become egg or sperm. Germ cells are immortal in the sense that they provide an enduring link between all generations, carrying genetic information from one generation to the next,Cambridges Azim Suranisays in auniversity statement.

Researchers have now figured out how to reprogram cells to act like embryonic stem cells. These induced pluripotent stem (iPS) cells have been used to develop humanretinasandintestines, for example, according to IFLScience. Researchers have also created iPS cells that could differentiate into primordial germ cells, but its only been successful in rodents.

Now, a team of researchers from the U.K. and Israel traced the genetic chain of events that directs a human stem cell to develop into a primordial germ cell. This stage in our development is called specification,and once PGCs become specified,they continue developing toward precursor sperm cells or ova pretty much on autopilot,Jacob Hanna from the Weizmann Institute of Sciencesays in anews release.

A master gene called SOX17 works to direct stem cells which in previous studies was found to direct stem cells into becoming lung, gut and pancreas cells. But the gene working as part of primordial germ cell specification is a new development.

The international team followed their discovery by actually making primordial germ cells in the lab. Using both embryonic stem cells and iPS cells (reprogrammed adult skin cells) from both males and females, the researchersmade sex cell precursors with up to 40 percent efficiency. When they compared the protein markers of their new, lab-grown PGCs with real PGCs collected from aborted fetuses,Nature reports, they were found to be very similar.

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Skin cells are being used to create artificial sperm and eggs

A UCSF spinout is growing neuronal stemcells to transplant into the brain, for potential use in treating epilepsy, spinal cord injury, Parkinsons and Alzheimers disease and investors are listening. Because one thing thatdifferentiatesNeurona Therapeutics is that its stem cells turn exclusively intointerneuron cells which are less likely to be tumorigenic than other IPS cells.

The companyhasraised $7.6 million of a proposed $24.3 million round, according to a regulatory filing. But the companys staying a touch under the radar it lacks a website, and tis the season for calls to the company to remain unanswered.

But funding for the six-year-old company comes from 11 investors. Listed on the documents contact pages areTim Kutzkeyand David Goeddel, both partners at early stage healthcare venture firm The Column Group giving some insight into who the startupsinvestors are.

Also listed is Leo Guthart, a managing partner at New York private equity firm TopSpin Partner, and Arnold Kriegstein, director of the UCSF developmental and stem cell biology program.

Kriegsteinand his UCSF colleagues filed a patentfor the in vitro production of medial ganglionic eminence (MGE) precursor cells which are, in essence, immature cells that morphinto nerve cells. The work that led to the patent was funded bythe California Institute of Regenerative Medicine, the NIH and the Osher Foundation.

We think this one type of cell may be useful in treating several types of neurodevelopmental and neurodegenerative disorders in a targeted way,Kriegstein said in a UCSF statement last year.

Neurona Therapeutics scientific backers collaborated on a paper on these MGE cells inCell Stem Cell,finding that mouse models closely mimicked human cells inneural cell development and that human cells can successfully be transplanted into mouse brains. UCSF writes:

Kriegstein sees MGE cells as a potential treatment to better control nerve circuits that become overactive in certain neurological disorders. Unlike other neural stem cells that can form many cell types and that may potentially be less controllable as a consequence most MGE cells are restricted to producing a type of cell called an interneuron. Interneurons integrate into the brain and provide controlled inhibition to balance the activity of nerve circuits.

To generate MGE cells in the lab, the researchers reliably directed the differentiation of human pluripotent stem cells either human embryonic stem cells or induced pluripotent stem cells derived from human skin. These two kinds of stem cells have virtually unlimited potential to become any human cell type. When transplanted into a strain of mice that does not reject human tissue, the human MGE-like cells survived within the rodent forebrain, integrated into the brain by forming connections with rodent nerve cells, and matured into specialized subtypes of interneurons.

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Stem cells to transplant in the brain: Stealth UCSF spinout Neurona Therapeutics raises $7.6M

First it was stem cells from rare apples touted as a revolution in anti-aging skin care. Then every other plant (seller) decided to get into the game. So is it true, or is it a con? Can stem cells from plants benefit your skin, and if so how? Is stem cell just a buzz word that unscrupulous marketers use to dupe you into thinking they are scientifically on the leading edge?

Plant Stem Cell Basics

A fertilized ovum (egg) is the ultimate stem cell. Every animal and plant that reproduces sexually begins as a fertilized ovum, with half of its genetic material contributed by the male parent and half from the female parent. In the case of flowering plants, structures within the flower play both roles. Pollen from the stamen is the equivalent of animal sperm and the pistol is the female receptive organ. A stem cell with the ability to repeatedly sub-divide and eventually differentiate into all types of cells found within an individual animal or plant is termed totipotential.

In the animal kingdom, a fertilized ovum divides, creating daughter totipotential stem cells, for only about four days. Daughter cells subsequently differentiate into pluripotential stem cells, which can differentiate into different various types of cells, but not all types. Plants, on the other hand, have totipotential stem cells throughout their life. These cells can develop into a complete adult plant.

Totipotential plant stem cells exist in very small numbers and are found in highly specialized tissues, structures called meristems. Meristems exist in root and shoot sprouts and are the cells from which all other plant cells and structures originate. Every root and stem shoot tip contains a very small number of these extraordinarily important cells. Meristems in shoot sprouts are called apical meristems, and those on the tips of roots are called root meristems. Remove the meristem and all growth in that part of the plant ceases.

Meristem stem cells are under external control and respond to local humoral factors from adjacent cells (quiescent cells) as well as more systemic plant hormones called cytokinin and auxin. Apical and root meristems have different specific, but complementary, controlling mechanisms. Generally speaking, hormonal influences that make an apical meristem grow may be inhibitory to root meristems, and vice versa. It is an intricately coordinated process in which stem cell activity is very tightly controlled and the number of totipotential stem cells is maintained at a very sparse population in comparison to the total plant cellular number.

Of paramount interest for this discussion is the fact that both apical and root meristems have control systems that act upon them, which are controlled by the needs of the entire plant. Without these outside influences, the cells in the meristem do not divide to produce daughter cells. While indispensable for plant growth, meristem stem cells are incapable of function without external influences dictating their response. These cells are followers, not leaders.

The photos show the relative size of structures within the meristem regions of a growing plant.

In the first photo (at right), the stem cells within the root meristem and adjacent quiescent cells are colored blue. The root meristem is also extremely tiny, consisting of only a few, albeit very important cells.

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Botanical Stem Cells in Skin Care | BareFacedTruth.com