(PRWEB) July 21, 2012

[Olez INCEPTION is the first hair straightening product line to take advantage of apple stem cells excellent strengthening and anti-aging properties.

Apple stem cells from a rare Swiss apple, called the Uttwiler Sptlauber, are rich in hydrogen, phytonutrients, antioxidants, proteins and age resistant cells. These apple stem cells are being utilized for the first time within a hair straightening product line. It makes perfect sense, since the stem cells have excellent strengthening and anti-aging properties that enhance the longevity of the hair follicles and protect the hairs own stem cells. Currently, apple stem cells are the most exciting breakthrough ingredient within the cosmetics industry.

Olez INCEPTION is the first professional hair system to incorporate the use of Apple Stem Cell technology along with the finest natural ingredients. Apple stem cells slow down the deterioration of hair follicles, allowing INCEPTIONs straight and shiny results to last for up to 6 months, something other straightening brands have not been able to achieve. Olez INCEPTION provides a unique Naturally Straight look; in contrast to the processed look other treatments offer.

Everything needed for beautiful and healthy hair and to create a wow! factor comes in Olez INCEPTIONs convenient 4 product kit: Cleansing and Nourishing Shampoo, Action Apple Stem Cell Solution, Sealer and Stem Cell Masque.

Leading industry lab faculty, Kosmo Science Laboratories, performed months of testing on the product. A stress test conducted on curly hair simulated the successful longevity of the treatment beyond 6 months.

Olez INCEPTIONs product line includes two home care products:

INCEPTION Stem Cell Masque utilizes stem cells from the rare Uttwiler Sptlauber apple as well as the finest of natural ingredients including Muru-Muru, Cupuau and Carite butters for incredibly sleek, silky, soft hair.

INCEPTION Argan & Pracaxi Natural Oil Spray comes in an eco friendly aerosol that dispenses the unique formula, a blend of Argan and Pracaxi natural oils. It hydrates and conditions, while protecting the hair with antioxidants. The Spray is also effective in combating the damaging effects of UV rays while maintaining silky, shiny, and smooth hair.

Salons have a unique opportunity to carry the Olez INCEPTION line, thereby providing a treatment to their clients that features breakthrough technology and provides significant profit potential.

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Can Apple Stem Cells Give Women Straight Hair?

Public release date: 19-Jul-2012 [ | E-mail | Share ]

Contact: Anne Rahilly arahilly@unimelb.edu.au 61-390-355-380 University of Melbourne

The study, published in the journal Stem Cell, adds to our understanding of the role of stem and next stage progenitor cells in tissue regeneration and in the diagnosis and treatment of cancer.

While stem cells are known to reside in organs such as the liver and pancreas, they are difficult to isolate. The new findings show that an antibody developed by the team can be used to capture the stem cells.

Professor Pera, program leader for Stem Cells Australia and Chair of Stem Cell Sciences at the University of Melbourne, said the antibody was able to detect progenitor cells in disease states such as cirrhosis of the liver, and in cancers such as pancreatic adenocarcinoma and oesophageal carcinoma.

"By being able to identify these cells, we hope to be able to learn more about their role in tissue regeneration and in cancer especially in the diagnosis and treatment of pancreatic cancer," he said.

"Cancers of the liver, pancreas and oesophagus are often very difficult to detect and challenging to treat."

The large collaboration of scientists from around the world working on this study evolved over many years with research undertaken in Professor Pera's laboratories at the then Australian Stem Cell Centre and at the University of Southern California.

Professor Pera and one of the co-authors on the paper, Dr Kouichi Hasegawa, were recently awarded an Australia-India Strategic Research Fund grant to continue their search for novel markers for liver, pancreatic and gut stem cells. Dr Hasegawa, who recently undertook a three month sabbatical at Stem Cells Australia, holds positions at Kyoto University's Institute for Integrated Cell-Materials Sciences and at the Institute for Stem Cell Biology and Regenerative Medicine at the National Centre for Biological Sciences in Bangalore, India.

"This funding will support us to develop more antibodies that can be used to assist in the identification and prospective isolation of stem and progenitor cells in these tissues and lead to the development of novel diagnostic and therapeutic reagents." Said Professor Pera.

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Stem cell research aids understanding of cancer

ScienceDaily (July 18, 2012) To build a tooth, a detailed recipe to instruct cells to differentiate towards proper lineages and form dental cells is needed. Researchers in the group of Professor Irma Thesleff at the Institute of Biotechnology in Helsinki, Finland have now found a marker for dental stem cells. They showed that the transcription factor Sox2 is specifically expressed in stem cells of the mouse front tooth.

Despite the development of new bioengineering protocols, building a tooth from stem cells remains a distant goal. Demand for it exists as loss of teeth affects oral health, quality of life, as well as ones appearance. To build a tooth, a detailed recipe to instruct cells to differentiate towards proper lineages and form dental cells is needed. However, the study of stem cells requires their isolation and a lack of a specific marker has hindered studies so far.

Researchers in the group of Professor Irma Thesleff at the Institute of Biotechnology in Helsinki, Finland have now found a marker for dental stem cells. They showed that the transcription factor Sox2 is specifically expressed in stem cells of the mouse incisor (front tooth). The mouse incisor grows continuously throughout life and this growth is fueled by stem cells located at the base of the tooth. These cells offer an excellent model to study dental stem cells.

The researchers developed a method to record the division, movement, and specification of these cells. By tracing the descendants of genetically labeled cells, they also showed that Sox2 positive stem cells give rise to enamel-forming ameloblasts as well as other cell lineages of the tooth.

Although human teeth dont grow continuously, the mechanisms that control and regulate their growth are similar as in mouse teeth. Therefore, the discovery of Sox2 as a marker for dental stem cells is an important step toward developing a complete bioengineered tooth. In the future, it may be possible to grow new teeth from stem cells to replace lost ones, says researcher Emma Juuri, a co-author of the study.

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The above story is reprinted from materials provided by Helsingin yliopisto (University of Helsinki), via AlphaGalileo.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.

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One step closer to growing a tooth

Public release date: 19-Jul-2012 [ | E-mail | Share ]

Contact: Nicole Fawcett nfawcett@umich.edu 734-764-2220 University of Michigan Health System

ANN ARBOR, Mich. Breast cancer treatments such as Herceptin that target a marker called HER2 have dramatically improved outcomes for women with this type of cancer. But nearly half of these cancers are resistant to Herceptin from the start and almost all of them will eventually become resistant.

Now, researchers at the University of Michigan Comprehensive Cancer Center have discovered one reason why the cancer cells become resistant: They turn on a completely different pathway, one that is involved in inflammation, fueling the cancer independently of HER2.

The pathway at work involves a protein called Interleukin-6, or IL-6. The researchers also showed in mice that a drug that blocks IL-6 can stop this effect and overcome the Herceptin resistance.

"Resistance to HER2-targeted therapies remains a major challenge in treating breast cancer. Our study suggests that an IL-6 inhibitor in combination with Herceptin may be a valuable addition for treating HER2-positive breast cancer," says senior study author Max S. Wicha, M.D., Distinguished Professor of Oncology and director of the U-M Comprehensive Cancer Center.

Results of the study will be published in the Aug. 24 issue of Molecular Cell.

Not only are these cells resistant to Herceptin, but they develop higher proportions of cancer stem cells, the small number of cells within a tumor that fuel the growth and spread. This makes the tumor extremely aggressive and likely to spread throughout the body. The IL-6 inhibitor also was shown to prevent this increase in cancer stem cells.

"There is evidence that patients with a lot of IL-6 tend to do poorly. What we found now is that in many of the Herceptin-resistant breast cancers, the IL-6 inflammation loop is driving the cancer stem cell," says lead study author Hasan Korkaya, D.V.M., Ph.D., research assistant professor of internal medicine at the U-M Medical School.

The researchers found that blocking the IL-6 inflammatory loop almost completely blocked the cancer and the stem cells. Mice treated with the IL-6 blocker along with Herceptin immediately after the cancer developed never became resistant to Herceptin.

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Inflammatory pathway spurs cancer stem cells to resist HER2-targeted breast cancer treatment

Newswise KANSAS CITY, MO Not all adult stem cells are created equal. Some are busy regenerating worn out or damaged tissues, while their quieter brethren serve as a strategic back-up crew that only steps in when demand shoots up. Now, researchers at the Stowers Institute for Medical Research have identified an important molecular cue that keeps quiescent mouse hematopoietic (or blood-forming) stem cells from proliferating when their services are not needed.

Publishing in the July 20, 2012 issue of Cell, the team led by Stowers Investigator Linheng Li, Ph.D., report that Flamingo and Frizzled 8, a tag team best known for its role in establishing cell polarity, are crucial for maintaining a quiescent reserve pool of hematopoietic stem cells in mouse bone marrow. Their finding adds new insight into the mechanism that controls the delicate balance between long-term maintenance of stem cells and the requirements of ongoing tissue maintenance and regeneration.

Hematopoietic stem cells daily produce billions of blood cells via a strict hierarchy of lineage-specific progenitors, says Li. Identifying the molecular signals that allow hematopoietic stem cell populations to sustain this level of output over a lifetime is fundamental to understanding the development of different cell types, the nature of tumor formation, and the aging process. My hope is that these insights will help scientists make meaningful progress towards new therapies for diseases of the blood.

The current working model, which grew out of earlier work by Li and others, postulates that hematopoietic stem cells (HSC), which are part of the reserve pool sit quietly and only divide a few times a year. They jump into action only when needed to replace active HSCs damaged by daily wear and tear or to increase their numbers in response to injury or disease. But how quiescent and active hematopoietic stem cell subpopulations are maintained and regulated in vivo is largely unknown.

What is known is that both populations of cells reside in adjacent specialized microenvironments, which provide many of the molecular cues that guide stem cell activity. Frequently cycling HSCs constitute around 90 percent of all hematopoietic stem cells and are found in the central marrow, where they seek the company of endothelial and perivascular cells. The main home base of quiescent hematopoietic stem cells is trabecular bone, the spongy part typically found at the end of long bones. Here, these cells engage in a constant molecular dialog with preosteoblasts, the precursors of bone-forming osteoblasts, which are characterized by the expression of N-cadherin.

Trying to decode the nature of the conversation graduate student and first author Ryohichi Sugimura focused on Flamingo (Fmi), a surface-based adhesion molecule, and Frizzled 8 (Fz8), a membrane-based receptor. Both molecules are part of the non-canonical arm of the so-called Wnt signaling pathway, a large network of secreted signaling molecules and their receptors. The canonical arm of the Wnt-signaling pathway exerts its influence through beta-catenin and helps regulate stem cell self-renewal in the intestine and hair follicles.

After in vitro experiments had revealed that Fmi and Fz8 accumulate at the interface between co-cultured quiescent hematopoietic stem cells and preosteoblasts, Sugimura and his colleagues were able to show that Fmi also regulates Fz8 distribution in vivo. This observation provided the first hint that these cooperation partners may carry at least part of the conversation that instructs hematopoietic stem cells to sit still. It also confirmed the previous finding by Lis team that a portion of HSCs resides in the N-cadherin+ osteoblastic niche.

When Sugimura examined the expression patterns of individual members of the Wnt signaling network within quiescent HSCs microenvironment he found that levels of canonical Wnt ligands where low. Levels of non-canonical Wnt ligands and inhibitors of the canonical arm of the Wnt signaling network, on the other hand, were high.

These observations indicated that the osteoblast niche provides a microenvironment in which non-canonical Wnt signaling prevails over canonical Wnt-signaling under normal conditions, says Sugimura. It also suggested that Fmi and Fz8 may play a direct role in maintaining the pool of quiescent hematopoietic stem cells.

Mice that had been genetically engineered to lack either Fmi or Fz8 provided the crucial clue: Not only had the number of quiescent hematopoietic stem cells plummeted in these mice, their hematopoietic stem cell function was reduced by more than 70 percent as well.

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The Yin and Yang of Stem Cell Quiescence and Proliferation

ScienceDaily (July 18, 2012) New research at the Hebrew University of Jerusalem sheds light on pluripotency -- the ability of embryonic stem cells to renew themselves indefinitely and to differentiate into all types of mature cells. Solving this problem, which is a major challenge in modern biology, could expedite the use of embryonic stem cells in cell therapy and regenerative medicine.

If scientists can replicate the mechanisms that make pluripotency possible, they could create cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases.

To shed light on these processes, researchers in the lab of Dr. Eran Meshorer, in the Department of Genetics at the Hebrew University's Alexander Silberman Institute of Life Sciences, are combining molecular, microscopic and genomic approaches. Meshorer's team is focusing on epigenetic pathways -- which cause biological changes without a corresponding change in the DNA sequence -- that are specific to embryonic stem cells.

The molecular basis for epigenetic mechanisms is chromatin, which is comprised of a cell's DNA and structural and regulatory proteins. In groundbreaking research performed by Shai Melcer, a PhD student in the Meshorer lab, the mechanisms which support an "open" chromatin conformation in embryonic stem cells were examined. The researchers found that chromatin is less condensed in embryonic stem cells, allowing them the flexibility or "functional plasticity" to turn into any kind of cell.

A distinct pattern of chemical modifications of chromatin structural proteins (referred to as the acetylation and methylation of histones) enables a looser chromatin configuration in embryonic stem cells. During the early stages of differentiation, this pattern changes to facilitate chromatin compaction.

But even more interestingly, the authors found that a nuclear lamina protein, lamin A, is also a part of the secret. In all differentiated cell types, lamin A binds compacted domains of chromatin and anchors them to the cell's nuclear envelope. Lamin A is absent from embryonic stem cells and this may enable the freer, more dynamic chromatin state in the cell nucleus. The authors believe that chromatin plasticity is tantamount to functional plasticity since chromatin is made up of DNA that includes all genes and codes for all proteins in any living cell. Understanding the mechanisms that regulate chromatin function will enable intelligent manipulations of embryonic stem cells in the future.

"If we can apply this new understanding about the mechanisms that give embryonic stem cells their plasticity, then we can increase or decrease the dynamics of the proteins that bind DNA and thereby increase or decrease the cells' differentiation potential," concludes Dr. Meshorer. "This could expedite the use of embryonic stem cells in cell therapy and regenerative medicine, by enabling the creation of cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases."

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Mechanisms that allow embryonic stem cells to become any cell in the human body identified

Public release date: 18-Jul-2012 [ | E-mail | Share ]

Contact: Dov Smith dovs@savion.huji.ac.il 972-258-81641 The Hebrew University of Jerusalem

New research at the Hebrew University of Jerusalem sheds light on pluripotencythe ability of embryonic stem cells to renew themselves indefinitely and to differentiate into all types of mature cells. Solving this problem, which is a major challenge in modern biology, could expedite the use of embryonic stem cells in cell therapy and regenerative medicine. If scientists can replicate the mechanisms that make pluripotency possible, they could create cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases.

To shed light on these processes, researchers in the lab of Dr. Eran Meshorer, in the Department of Genetics at the Hebrew University's Alexander Silberman Institute of Life Sciences, are combining molecular, microscopic and genomic approaches. Meshorer's team is focusing on epigenetic pathwayswhich cause biological changes without a corresponding change in the DNA sequencethat are specific to embryonic stem cells.

The molecular basis for epigenetic mechanisms is chromatin, which is comprised of a cell's DNA and structural and regulatory proteins. In groundbreaking research performed by Shai Melcer, a PhD student in the Meshorer lab, the mechanisms which support an "open" chromatin conformation in embryonic stem cells were examined. The researchers found that chromatin is less condensed in embryonic stem cells, allowing them the flexibility or "functional plasticity" to turn into any kind of cell.

A distinct pattern of chemical modifications of chromatin structural proteins (referred to as the acetylation and methylation of histones) enables a looser chromatin configuration in embryonic stem cells. During the early stages of differentiation, this pattern changes to facilitate chromatin compaction.

But even more interestingly, the authors found that a nuclear lamina protein, lamin A, is also a part of the secret. In all differentiated cell types, lamin A binds compacted domains of chromatin and anchors them to the cell's nuclear envelope. Lamin A is absent from embryonic stem cells and this may enable the freer, more dynamic chromatin state in the cell nucleus. The authors believe that chromatin plasticity is tantamount to functional plasticity since chromatin is made up of DNA that includes all genes and codes for all proteins in any living cell. Understanding the mechanisms that regulate chromatin function will enable intelligent manipulations of embryonic stem cells in the future.

"If we can apply this new understanding about the mechanisms that give embryonic stem cells their plasticity, then we can increase or decrease the dynamics of the proteins that bind DNA and thereby increase or decrease the cells' differentiation potential," concludes Dr. Meshorer. "This could expedite the use of embryonic stem cells in cell therapy and regenerative medicine, by enabling the creation of cells in the laboratory which could be implanted in humans to cure diseases characterized by cell death, such as Alzheimer's, Parkinson's, diabetes and other degenerative diseases."

The research was funded by grants from the European Union (ERC, Marie Curie), Israel Science Foundation, Ministry of Science, Ministry of Health, The National Institute for Psychobiology, Israel Cancer Research Foundation (ICRF), Abisch-Frenkel Foundation and Human Frontiers Science Program (HFSP).

The research appears in the journal Nature Communications as Melcer et al., Histone modifications and lamin A regulate chromatin protein dynamics in early embryonic stem cell differentiation.

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Researchers identify mechanisms that allow embryonic stem cells to become any cell in the human body