"Genetic Engineering" is a song by British band Orchestral Manoeuvres in the Dark, released as the first single from their fourth studio album Dazzle Ships. Frontman Andy McCluskey has noted that the song is not an attack on genetic engineering, as many assumed at the time, including veteran radio presenter Dave Lee Travis upon playing the song on BBC Radio 1. McCluskey stated: "I was very positive about the subject." "People didn't listen to the lyrics...I think they automatically assumed it would be anti."[2]

Charting at #20 on the UK Singles Chart, "Genetic Engineering" ended the band's run of four consecutive Top 10 hits in the UK. It was also a Top 20 hit in several European territories, and peaked at #5 in Spain. It missed the United States Billboard Hot 100 but made #32 on the Mainstream Rock chart. US critic Ned Raggett lauded the "soaring", "enjoyable" single in a positive review of Dazzle Ships for Allmusic, asserting: "Why it wasn't a hit remains a mystery."[3]

Critics in prominent music publications have suggested that the first 45 seconds of the song were a direct influence on Radiohead's "Fitter Happier", which appears on that band's 1997 album OK Computer.[3][4][5] Theon Weber in Stylus argued that the Radiohead track is "deeply indebted" to "Genetic Engineering".[4]

Side one

Side two

Side one

Side two

"Genetic Engineering" was covered by indie rock band Eggs and released as a single in 1994.[10]

It was also covered by Another Sunny Day as a limited edition single in 1989 and as an extra track on the re-release of on their 'London Weekend' album.

Optiganally Yours recorded a cover for a "very low-key tribute compilation".[11]

Read the original:
Genetic Engineering (song) - Wikipedia, the free encyclopedia

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

27-Oct-2014

Contact: Kathryn Ryan kryan@liebertpub.com 914-740-2100 Mary Ann Liebert, Inc./Genetic Engineering News @LiebertOnline

New Rochelle, NY, October 27, 2014More than half of women with children less than a year old are working, and work travel can make breastfeeding a challenge. A study of 100 U.S. airports found that few provided a suitably equipped, private lactation room, even though most described themselves as being breastfeeding friendly, as reported in Breastfeeding Medicine, the official journal of the Academy of Breastfeeding Medicine published by Mary Ann Liebert, Inc., publishers. The article is available free on the Breastfeeding Medicine website at http://online.liebertpub.com/doi/full/10.1089/bfm.2014.0112 until November 27, 2014.

In "Airports in the United States. Are They Really Breastfeeding Friendly?," authors Michael Haight, University of California, San Francisco-Fresno and Joan Ortiz, Limerick Inc. (Burbank, CA), report that while 62% of the airports surveyed answered yes to whether they were "breastfeeding friendly," only 37% provided a specific lactation room. In only 8% of the airports did that designated space offer the minimum requirements of not being used as a bathroom and having an electrical outlet, table, and chair. These included San Francisco International, Minneapolis-St. Paul International, Baltimore/Washington International, San Jose International, Indianapolis International, Akron-Canton Regional (OH), Dane County Regional (WI), and Pensacola Gulf Coast Regional (FL) airports.

"This study presents provocative data about our airports," says Ruth Lawrence, MD, Editor-in-Chief of Breastfeeding Medicine and Professor of Pediatrics, University of Rochester School of Medicine. "The good news is that 62% think they are 'breastfeeding friendly.' The bad news is that their actions do not support the claim. There is a lot of work to be done to make travel possible for breastfeeding dyads."

###

About the Journal

Breastfeeding Medicine, the official journal of the Academy of Breastfeeding Medicine, is an authoritative, peer-reviewed, multidisciplinary journal published 10 times per year in print and online. The Journal publishes original scientific papers, reviews, and case studies on a broad spectrum of topics in lactation medicine. It presents evidence-based research advances and explores the immediate and long-term outcomes of breastfeeding, including the epidemiologic, physiologic, and psychological benefits of breastfeeding. Tables of content and a sample issue may be viewed on the Breastfeeding Medicine website at http://www.liebertpub.com/bfm.

About the Publisher

Read more from the original source:
Which US airports are breastfeeding friendly?

Recommendation and review posted by Bethany Smith

DNA, or deoxyribonucleic acid, is the hereditary material in humans and almost all other organisms. Nearly every cell in a persons body has the same DNA. Most DNA is located in the cell nucleus (where it is called nuclear DNA), but a small amount of DNA can also be found in the mitochondria (where it is called mitochondrial DNA or mtDNA).

The information in DNA is stored as a code made up of four chemical bases: adenine (A), guanine (G), cytosine (C), and thymine (T). Human DNA consists of about 3 billion bases, and more than 99 percent of those bases are the same in all people. The order, or sequence, of these bases determines the information available for building and maintaining an organism, similar to the way in which letters of the alphabet appear in a certain order to form words and sentences.

DNA bases pair up with each other, A with T and C with G, to form units called base pairs. Each base is also attached to a sugar molecule and a phosphate molecule. Together, a base, sugar, and phosphate are called a nucleotide. Nucleotides are arranged in two long strands that form a spiral called a double helix. The structure of the double helix is somewhat like a ladder, with the base pairs forming the ladders rungs and the sugar and phosphate molecules forming the vertical sidepieces of the ladder.

An important property of DNA is that it can replicate, or make copies of itself. Each strand of DNA in the double helix can serve as a pattern for duplicating the sequence of bases. This is critical when cells divide because each new cell needs to have an exact copy of the DNA present in the old cell.

DNA is a double helix formed by base pairs attached to a sugar-phosphate backbone.

The National Human Genome Research Institute fact sheet Deoxyribonucleic Acid (DNA) provides an introduction to this molecule.

Information about the genetic code and the structure of the DNA double helix is available from GeneEd.

The New Genetics, a publication of the National Institute of General Medical Sciences, discusses the structure of DNA and how it was discovered.

Nature Educations Scitable offers a thorough description of DNA, including its components and organization. It also includes a short animated video.

A basic explanation and illustration of DNA can be found on Arizona State Universitys Ask a Biologist website.

See the rest here:
What is DNA? - Genetics Home Reference

Recommendation and review posted by Bethany Smith

Background

According to the American College of Medical Genetics (ACMG), an important issue in genetic testing is defining the scope of informed consent. The obligation to counsel and obtain consent is inherent in the clinician-patient and investigator-subject relationships. In the case of most genetic tests, the patient or subject should be informed that the test might yield information regarding a carrier or disease state that requires difficult choices regarding their current or future health, insurance coverage, career, marriage, or reproductive options. The objective of informed consent is to preserve the individual's right to decide whether to have a genetic test. This right includes the right of refusal should the individual decide the potential harm (stigmatization or undesired choices) outweighs the potential benefits.

DNA-based mutation analysis is not covered for routine carrier testing for the diagnosis of Tay-Sachs and Sandhoff disease. Under accepted guidelines, diagnosis is primarily accomplished through biochemical assessment of serum, leukocyte, or platelet hexosaminidase A and B levels. The literature states that mutation analysis is appropriate for individuals with persistently inconclusive enzyme-based results and to exclude pseudo-deficiency (non-disease related) mutations in carrier couples.

Testing of a member who is at substantial familial risk for being a heterozygote (carrier) for a particular detectable mutation that is recognized to be attributable to a specific genetic disorder is only covered for the purpose of prenatal counseling under plans with this benefit (seeCPB 0189 - Genetic Counseling).

Confirmation by molecular analysis of inborn errors of metabolism by traditional screening methodologies (e.g., Guthrie microbiologic assays) is covered. Rigorous clinical evaluation should precede diagnostic molecular testing.

In many instances, reliable mutation analysis requires accurate determination of specific allelic variations in a proband (affected individual in a family) before subsequent carrier testing in other at-risk family members can be accurately performed. Coverage of testing for individuals who are not Aetna members is not provided, except under the limited circumstances outlined in the policy section above.

Hereditary non-polyposis colon cancer

Hereditary non-polyposis colon cancer ([HNPCC], Lynch syndrome) is one of the most common cancer predisposition syndromes affecting 1 in 200 individuals and accounting for 13 to 15 % of all colon cancer. HNPCC is defined clinically by early-onset colon carcinoma and by the presence of other cancers such as endometrial, gastric, urinary tract and ovarian found in at least3 first-degree relatives. Two genes have been identified as being primary responsible for this syndrome: hMLH1 at chromosome band 3p21 accounts for 30 % of HNPCC2,3 and hMLH2 or FCC at chromosome band 2p22 which together with hMLH1 accounts for 90 % of HNPCC.

Unlike other genetic disorders that are easily diagnosed, the diagnosis of HNPCC relies on a very strongly positive family history of colon cancer. Specifically, several organizations have defined criteria that must be met to make the diagnosis of HNPCC.

Although HNPCC lacks strict clinical distinctions that can be used to make the diagnosis, and therefore diagnosis is based on the strong family history, genetic testing is now available to study patient's DNA for mutations to one of the mismatch repair genes. A mutation to one of these genes is a characteristic feature and confirms the diagnosis of HNPCC. Identifying individuals with this disease and performing screening colonoscopies on affected persons may help reduce colon cancer mortality.

More here:
Genetic Testing - Aetna

Recommendation and review posted by Bethany Smith

Kids with Down syndrome tend to share certain physical features such as a flat facial profile, an upward slant to the eyes, small ears, and a protruding tongue.

Low muscle tone (called hypotonia) is also characteristic of children with DS, and babies in particular may seem especially "floppy." Though this can and often does improve over time, most children with DS typically reach developmental milestones like sitting up, crawling, and walking later than other kids.

At birth, kids with DS are usually of average size, but they tend to grow at a slower rate and remain smaller than their peers. For infants, low muscle tone may contribute to sucking and feeding problems, as well as constipation and other digestive issues. Toddlers and older kids may have delays in speech and self-care skills like feeding, dressing, and toilet teaching.

Down syndrome affects kids' ability to learn in different ways, but most have mild to moderate intellectual impairment. Kids with DS can and do learn, and are capable of developing skills throughout their lives. They simply reach goals at a different pace which is why it's important not to compare a child with DS against typically developing siblings or even other children with the condition.

Kids with DS have a wide range of abilities, and there's no way to tell at birth what they will be capable of as they grow up.

While some kids with DS have no significant health problems, others may experience a host of medical issues that require extra care. For example, almost half of all children born with DS will have a congenital heart defect.

Kids with Down syndrome are also at an increased risk of developing pulmonary hypertension, a serious condition that can lead to irreversible damage to the lungs. All infants with Down syndrome should be evaluated by a pediatric cardiologist.

Approximately half of all kids with DS also have problems with hearing and vision. Hearing loss can be related to fluid buildup in the inner ear or to structural problems of the ear itself. Vision problems commonly include strabismus (cross-eyed), near- or farsightedness, and an increased risk of cataracts.

Regular evaluations by an otolaryngologist (ear, nose, and throat doctor), audiologist, and an ophthalmologist are necessary to detect and correct any problems before they affect language and learning skills.

Other medical conditions that may occur more frequently in kids with DS include thyroid problems, intestinal abnormalities, seizure disorders, respiratory problems, obesity, an increased susceptibility to infection, and a higher risk of childhood leukemia. Upper neck abnormalities are sometimes found and should be evaluated by a doctor (these can be detected by cervical spine X-rays). Fortunately, many of these conditions are treatable.

Read the original here:
Kids Health - Down Syndrome - KidsHealth - the Web's most ...

Recommendation and review posted by Bethany Smith

By Randy Dotinga HealthDay Reporter

FRIDAY, Oct. 24, 2014 (HealthDay News) -- As more genetic tests are developed that spot increased risks for certain cancers, one might think that high-risk people would be more proactive about getting screened.

But a new study suggests that, at least with colon cancer, knowledge does not change behavior: People who found out their genes doubled their risk of colon cancer were no more likely than people with average risk to get screened.

"It didn't make any difference, not at all," said study author Dr. David Weinberg, chairman of medicine at Fox Chase Cancer Center in Philadelphia.

Weinberg cautioned against using the findings to come to conclusions about the impacts of genetic tests for other cancers. Still, he said, the "modest amount of available data" suggests that genetic tests like the colon cancer one -- which don't confirm a huge increased risk of disease -- don't alter health habits.

The researchers were surprised by the results. "Our hypothesis was that this would be effective," Weinberg said, especially considering that a person's genetic makeup is so personal and "might be a more compelling motivator than something like their cholesterol level or a lifestyle choice like smoking."

Dr. Durado Brooks, director of prostate and colorectal cancer with the American Cancer Society, agreed with Weinberg that the finding was surprising.

"The theory around genetic testing is that if you tell people they're at a higher risk of disease XYZ, the hope is that they'll modify their behavior," Brooks said. "This does not support that hope or theory."

Genetic tests have been a hot topic for several years as companies have begun offering them to the public along with insight about people's risks of developing various diseases. One big question remains largely unanswered: What will people do differently, if anything, once they get a glimpse into what their medical futures may hold?

In this latest study, the researchers focused on 783 people aged 50 to 79 who hadn't been screened for colon cancer recently. Of those, 541 of them were told that their genetic tests revealed their risk of colon cancer was doubled (about 1 in 20).

Read more here:
Knowing Genetic Risk for Cancer May Not Change Behavior

Recommendation and review posted by Bethany Smith

PUBLIC RELEASE DATE:

28-Oct-2014

Contact: Charli Scouller c.scouller@qmul.ac.uk 44-770-982-5741 Queen Mary, University of London @QMUL

A large analysis of over 40,000 individuals on statin treatment has identified two new genetic variants which influence how 'bad' cholesterol levels respond to statin therapy.

Statins are widely prescribed to patients and have been shown to lower bad cholesterol levels by up to 55%, making them a highly effective method of reducing risk of heart disease. However, despite this success, patient response can vary widely.

The study, led by Queen Mary University of London and published in Nature Communications, is the largest to date and involved analysing data from six randomised clinical trials and 10 observational studies to look for genetic variants influencing patients' response to statins.

Together with multiple universities around the world, the researchers validated their findings in a further 22,318 individuals and found two new common genetic variants which significantly affected the degree to which bad cholesterol was lowered during statin treatment.

Professor Mark Caulfield, Lead Author, Queen Mary University of London and the NIHR Biomedical Research Unit, comments: "This study marks an important step toward understanding how genetic variations influence statin response. However, further research is needed to find out how we can apply this in care of patients receiving statins. We must build up a bigger picture of the genetic variation that predicts statin response. Only then will we be in a position to tell whether testing for these genetic variants is of benefit to patients who take statin therapy."

The effects of all four associated genetic variants collectively account for about 5% of the variation in inter-individual response to statins. One of the identified genetic variants was shown to enhance statin response. In contrast, the second variant, thought to have a role in the uptake of statins by the liver, decreased the effects of the drug. Together, these findings may enhance our understanding of the biological mechanisms underlying bad cholesterol response to statin therapy.

Dr Michael Barnes, Co-author, Queen Mary University of London and the NIHR Biomedical Research Unit, comments: "Statins are one of the safest and most effective drugs in clinical use. Although all share a common target, some statins are more effective than others in different individuals. This study highlights a network of interacting genes which may individually or collectively influence the way that statins act in the body. In the future, this information could help us to select the most effective statin for each patient."

Read the original post:
Scientists find genetic variants influence a person's response to statins

Recommendation and review posted by Bethany Smith

Mutants Genetics Gladiators: Reactor spins: Gothic part 11
4 tokens, no alien.

By: DeceptiveSteam6

Read more:
Mutants Genetics Gladiators: Reactor spins: Gothic part 11 - Video

Recommendation and review posted by Bethany Smith

Gregor Johann Mendel (20 July 1822[1] 6 January 1884) was a German-speaking Silesian[2][3] scientist and Augustinian friar who gained posthumous fame as the founder of the modern science of genetics. Though farmers had known for centuries that crossbreeding of animals and plants could favor certain desirable traits, Mendel's pea plant experiments conducted between 1856 and 1863 established many of the rules of heredity, now referred to as the laws of Mendelian inheritance.

Mendel worked with seven characteristics of pea plants: plant height, pod shape and color, seed shape and color, and flower position and color. With seed color, he showed that when a yellow pea and a green pea were bred together their offspring plant was always yellow. However, in the next generation of plants, the green peas reappeared at a ratio of 1:3. To explain this phenomenon, Mendel coined the terms recessive and dominant in reference to certain traits. (In the preceding example, green peas are recessive and yellow peas are dominant.) He published his work in 1866, demonstrating the actions of invisible factorsnow called genesin providing for visible traits in predictable ways.

The profound significance of Mendel's work was not recognized until the turn of the 20th century (more than three decades later) with the independent rediscovery of these laws.[4]Erich von Tschermak, Hugo de Vries, Carl Correns, and William Jasper Spillman independently verified several of Mendel's experimental findings, ushering in the modern age of genetics.

Johann Mendel was born into an ethnic German family in Heinzendorf bei Odrau, Moravian-Silesian border, Austrian Empire (now Hynice, Czech Republic). (He was given the name Gregor when he joined the Augustinian friars.) He was the son of Anton and Rosine (Schwirtlich) Mendel, and had one older sister, Veronika, and one younger, Theresia. They lived and worked on a farm which had been owned by the Mendel family for at least 130 years.[6] During his childhood, Mendel worked as a gardener and studied beekeeping. Later, as a young man, he attended gymnasium in Opava. He had to take four months off during his gymnasium studies due to illness. From 1840 to 1843, he studied practical and theoretical philosophy and physics at the University of Olomouc Faculty of Philosophy, taking another year off because of illness. He also struggled financially to pay for his studies and Theresia gave him her dowry. Later he helped support her three sons, two of whom became doctors. He became a friar because it enabled him to obtain an education without having to pay for it himself.

When Mendel entered the Faculty of Philosophy, the Department of Natural History and Agriculture was headed by Johann Karl Nestler who conducted extensive research of hereditary traits of plants and animals, especially sheep. Upon recommendation of his physics teacher Friedrich Franz,[8] Mendel entered the Augustinian St Thomas's Abbey and began his training as a priest. Born Johann Mendel, he took the name Gregor upon entering religious life. Mendel worked as a substitute high school teacher. In 1850 he failed the oral part, the last of three parts, of his exams to become a certified high school teacher. In 1851 he was sent to the University of Vienna to study under the sponsorship of Abbot C. F. Napp so that he could get more formal education. At Vienna, his professor of physics was Christian Doppler.[10] Mendel returned to his abbey in 1853 as a teacher, principally of physics. In 1856 he took the exam to become a certified teacher and again failed the oral part.In 1867 he replaced Napp as abbot of the monastery.[11]

Mendel began his studies on heredity using mice. He was at St. Thomas's Abbey but his bishop did not like one of his friar studying animal sex, so Mendel switched to plants. Mendel also bred bees in a bee house that was built for him, using bee hives that he designed.[13] He also studied astronomy and meteorology,[11] founding the 'Austrian Meteorological Society' in 1865.[10] The majority of his published works were related to meteorology.[10]

Gregor Mendel, who is known as the "father of modern genetics", was inspired by both his professors at the University of Olomouc (Friedrich Franz & Johann Karl Nestler) and his colleagues at the monastery (e.g., Franz Diebl) to study variation in plants, and he conducted his study in the monastery's 2 hectares (4.9 acres) experimental garden,[14] which was originally planted by Napp in 1830.[11] Unlike Nestler, who studied hereditary traits in sheep, Mendel focused on plants. After initial experiments with pea plants, Mendel settled on studying seven traits that seemed to inherit independently of other traits: seed shape, flower color, seed coat tint, pod shape, unripe pod color, flower location, and plant height. He first focused on seed shape, which was either angular or round. Between 1856 and 1863 Mendel cultivated and tested some 29,000 pea plants (i.e., Pisum sativum). This study showed that one in four pea plants had purebred recessive alleles, two out of four were hybrid and one out of four were purebred dominant. His experiments led him to make two generalizations, the Law of Segregation and the Law of Independent Assortment, which later came to be known as Mendel's Laws of Inheritance.

Mendel presented his paper, Versuche ber Pflanzenhybriden (Experiments on Plant Hybridization), at two meetings of the Natural History Society of Brno in Moravia on 8 February and 8 March 1865. It was received favorably and generated reports in several local newspapers.[17] When Mendel's paper was published in 1866 in Verhandlungen des naturforschenden Vereins Brnn,[18] it was seen as essentially about hybridization rather than inheritance and had little impact and was cited about three times over the next thirty-five years. Notably, Charles Darwin was unaware of Mendel's paper, according to Jacob Bronowski's The Ascent of Man. His paper was criticized at the time, but is now considered a seminal work.

After completing his work with peas, Mendel turned to experimenting with honeybees to extend his work to animals. He produced a hybrid strain (so vicious they were destroyed) but failed to generate a clear picture of their heredity because of the difficulties in controlling mating behaviours of queen bees.[dubious discuss] He also described novel plant species, and these are denoted with the botanical author abbreviation "Mendel".

After he was elevated as abbot in 1868, his scientific work largely ended, as Mendel became consumed with his increased administrative responsibilities, especially a dispute with the civil government over their attempt to impose special taxes on religious institutions.[19] Mendel died on 6 January 1884, at the age of 61, in Brno, Moravia, Austria-Hungary (now Czech Republic), from chronic nephritis. Czech composer Leo Janek played the organ at his funeral. After his death, the succeeding abbot burned all papers in Mendel's collection, to mark an end to the disputes over taxation.[20]

See original here:
Gregor Mendel - Wikipedia, the free encyclopedia

Recommendation and review posted by Bethany Smith

Gene therapy carries the promise of cures for many diseases and for types of medical treatment that didn't seem possible until recently. With its potential to eliminate and prevent hereditary diseases such as cystic fibrosis and hemophilia and its use as a possible cure for heart disease, AIDS, and cancer, gene therapy is a potential medical miracle-worker.

But what about gene therapy for children? There's a fair amount of risk involved, so thus far only seriously ill kids or those with illnesses that can't be cured by standard medical treatments have been involved in clinical trials using gene therapy.

As those studies continue, gene therapy may soon offer hope for children with serious illnesses that don't respond to conventional therapies.

Our genes help make us unique. Inherited from our parents, they go far in determining our physical traits like eye color and the color and texture of our hair. They also determine things like whether babies will be male or female, the amount of oxygen blood can carry, and the likelihood of getting certain diseases.

Genes are composed of strands of a molecule called DNA and are located in single file within the chromosomes. The genetic message is encoded by the building blocks of the DNA, which are called nucleotides. Approximately 3 billion pairs of nucleotides are in the chromosomes of a human cell, and each person's genetic makeup has a unique sequence of nucleotides. This is mainly what makes us different from one another.

Scientists believe that every human has about 25,000 genes per cell. A mutation, or change, in any one of these genes can result in a disease, physical disability, or shortened life span. These mutations can be passed from one generation to another, inherited just like a mother's curly hair or a father's brown eyes. Mutations also can occur spontaneously in some cases, without having been passed on by a parent. With gene therapy, the treatment or elimination of inherited diseases or physical conditions due to these mutations could become a reality.

Gene therapy involves the manipulation of genes to fight or prevent diseases. Put simply, it introduces a "good" gene into a person who has a disease caused by a "bad" gene.

The two forms of gene therapy are:

Currently, gene therapy is done only through clinical trials, which often take years to complete. After new drugs or procedures are tested in laboratories, clinical trials are conducted with human patients under strictly controlled circumstances. Such trials usually last 2 to 4 years and go through several phases of research. In the United States, the U.S. Food and Drug Administration (FDA) must then approve the new therapy for the marketplace, which can take another 2 years.

The most active research being done in gene therapy for kids has been for genetic disorders (like cystic fibrosis). Other gene therapy trials involve children with severe immunodeficiencies, such as adenosine deaminase (ADA) deficiency (a rare genetic disease that makes kids prone to serious infection), sickle cell anemia, thalassemia, hemophilia, and those with familial hypercholesterolemia (extremely high levels of serum cholesterol).

Continue reading here:
Gene Therapy and Children - KidsHealth

Recommendation and review posted by Bethany Smith

Walking after five years of a spinal cord injury
I was considered C5 and C6 incomplete spinal cord injury. But after five years of injury I started to walkwith a walker at first last year with a walker,and ...

By: Sarah Benj

See original here:
Walking after five years of a spinal cord injury - Video

Recommendation and review posted by sam

Walking after five years of spinal cord injury

By: Sarah Benj

View post:
Walking after five years of spinal cord injury - Video

Recommendation and review posted by sam

AGTC - Company Presentation
Presented by: Daniel Menichella, VP Chief Business Officer AGTC is developing cures for rare lung and eye diseases, offering hope to patients with unmet me...

By: Alliance for Regenerative Medicine

Read more here:
AGTC - Company Presentation - Video

Recommendation and review posted by sam

TC BioPharm - Company Presentation
Presented by: Michael Leek, Ph.D., CEO Commercializing the anti-cancer cytotoxicity exhibited by T cells, TC BioPharm is developing an autologous therapy ...

By: Alliance for Regenerative Medicine

Original post:
TC BioPharm - Company Presentation - Video

Recommendation and review posted by sam

A Harvard team has developed special stem cells that secrete toxins that kill cancer cells, and cause no harm to healthy ones.

Now, we have toxin-resistant stem cells that can make and release cancer-killing drugs, Khalid Shah, a co-author of the study and the director of the Molecular Neurotherapy and Imaging Lab at Massachusetts General Hospital and Harvard Medical School, said in an official statement.

According to Shah, experiments in mice have proven very successful.

During the tests, the main part of the brain tumor was surgically removed, followed by the application of stem cells that were placed at the site of the tumor embedded in a biodegradable gel to kill the remaining cancerous cells.

Once within the cancer cell, the toxin disrupts its ability to synthesize proteins, killing it in a matter of days.

After doing all of the molecular analysis and imaging to track the inhibition of protein synthesis within brain tumors, we do see the toxins kill the cancer cells, he declared.

Shah said that the toxins that kill cancer have been used to treat a few types of blood cancers. However, these toxins were not effective dealing with solid tumors because these cancers are not as accessible and the toxins in the stem cells dont have enough time to kill the cancer, since they only have a short half-life.

However, the new modified stem cells developed by Shahs team change this limitation. Now, we have toxin-resistant stem cells that can make and release cancer-killing drugs, he said.

The study, published in the journal Stem Cells, possibly represents a breakthrough in cancer research, since it kills cancer cells while keeping remaining, healthy cells intact.

Scientists have applied for approval from the FDA to start the clinical trials of the method.

See the rest here:
Beyond the Dish | A developmental biologist muses about ...

Recommendation and review posted by simmons

8 hours ago

In a study that will provide the foundation for scientists to better replicate natural stem cell development in an artificial environment, UCLA researchers at the Eli and Edythe Broad Center of Regenerative Medicine and Stem Cell Research led by Dr. Guoping Fan, professor of human genetics, have established a benchmarking standard to assess how culture conditions used to procure stem cells in the lab compare to those found in the human embryo.

The study was published online ahead of print in the journal Cell Stem Cell.

Pluripotent stem cells (PSCs) are cells that can transform into almost any cell in the human body. Scientists have long cultured PSCs in the laboratory (in vitro) using many different methods and under a variety of conditions. Though it has been known that culture techniques can affect what kind of cells PSCs eventually become, no "gold standard" has yet been established to help scientists determine how the artificial environment can better replicate that found in a natural state (in vivo).

Dr. Kevin Huang, postdoctoral fellow in the lab of Dr. Fan and a lead author of the study, analyzed data from multiple existing research studies conducted over the past year. These previously published studies used different culture methods newly developed in vitro in the hopes of coaxing human stem cells into a type of pluripotency that is in a primitive or ground-zero state.

Utilizing recently-published gene expression profiles of human preimplantation embryos as the benchmark to analyze the data, Dr. Huang and colleagues found that culture conditions do affect how genes are expressed in PSCs, and that the newer generation culture methods appear to better resemble those found in the natural environment of developing embryos. This work lays the foundation on the adoption of standardized protocol amongst the scientific community.

"By making an objective assessment of these different laboratory techniques, we found that some may have more of an edge over others in better replicating a natural state," said Dr. Huang. "When you have culture conditions that more consistently match a non-artificial environment, you have the potential for a much better reflection of what is going on in actual human development."

With these findings, Dr. Fan's lab hopes to encourage further investigation into other cell characteristics and molecular markers that determine the effectiveness of culture conditions on the proliferation and self-renewal of PSCs.

"We hope this work will help the research community to reach a consensus to quality-control human pluripotent stem cells," said Dr. Fan.

Explore further: Technique to make human embryonic stem cells more closely resemble true epiblast cells

See the original post here:
Team proposes benchmark to better replicate natural stem cell development in the laboratory environment

Recommendation and review posted by simmons

Stem cells are undifferentiated biological cells that can differentiate into specialized cells and can divide (through mitosis) to produce more stem cells. They are found in multicellular organisms. In mammals, there are two broad types of stem cells: embryonic stem cells, which are isolated from the inner cell mass of blastocysts, and adult stem cells, which are found in various tissues. In adult organisms, stem cells and progenitor cells act as a repair system for the body, replenishing adult tissues. In a developing embryo, stem cells can differentiate into all the specialized cellsectoderm, endoderm and mesoderm (see induced pluripotent stem cells)but also maintain the normal turnover of regenerative organs, such as blood, skin, or intestinal tissues.

There are three known accessible sources of autologous adult stem cells in humans:

Stem cells can also be taken from umbilical cord blood just after birth. Of all stem cell types, autologous harvesting involves the least risk. By definition, autologous cells are obtained from one's own body, just as one may bank his or her own blood for elective surgical procedures.

Adult stem cells are frequently used in medical therapies, for example in bone marrow transplantation. Stem cells can now be artificially grown and transformed (differentiated) into specialized cell types with characteristics consistent with cells of various tissues such as muscles or nerves. Embryonic cell lines and autologous embryonic stem cells generated through Somatic-cell nuclear transfer or dedifferentiation have also been proposed as promising candidates for future therapies.[1] Research into stem cells grew out of findings by Ernest A. McCulloch and James E. Till at the University of Toronto in the 1960s.[2][3]

The classical definition of a stem cell requires that it possess two properties:

Two mechanisms exist to ensure that a stem cell population is maintained:

Potency specifies the differentiation potential (the potential to differentiate into different cell types) of the stem cell.[4]

In practice, stem cells are identified by whether they can regenerate tissue. For example, the defining test for bone marrow or hematopoietic stem cells (HSCs) is the ability to transplant the cells and save an individual without HSCs. This demonstrates that the cells can produce new blood cells over a long term. It should also be possible to isolate stem cells from the transplanted individual, which can themselves be transplanted into another individual without HSCs, demonstrating that the stem cell was able to self-renew.

Properties of stem cells can be illustrated in vitro, using methods such as clonogenic assays, in which single cells are assessed for their ability to differentiate and self-renew.[7][8] Stem cells can also be isolated by their possession of a distinctive set of cell surface markers. However, in vitro culture conditions can alter the behavior of cells, making it unclear whether the cells will behave in a similar manner in vivo. There is considerable debate as to whether some proposed adult cell populations are truly stem cells.

Embryonic stem (ES) cells are stem cells derived from the inner cell mass of a blastocyst, an early-stage embryo.[9] Human embryos reach the blastocyst stage 45 days post fertilization, at which time they consist of 50150 cells. ES cells are pluripotent and give rise during development to all derivatives of the three primary germ layers: ectoderm, endoderm and mesoderm. In other words, they can develop into each of the more than 200 cell types of the adult body when given sufficient and necessary stimulation for a specific cell type. They do not contribute to the extra-embryonic membranes or the placenta.

See the article here:
Stem cell - Wikipedia, the free encyclopedia

Recommendation and review posted by simmons

Using stem cells from blood, researchers have been able to grow blood vessels in a week.REUTERS

Researchers at Sahlgrenska University Hospital in Sweden have been successful in transplanting blood vessels made from three spoons of blood.

Two years ago two patients at the hospital received the blood vessels made from stem cellsin the blood.

Earlier, another patient too was treated using blood vessels made by her stem cells but in that case, the researchers had to drill into the bone marrow to obtain the stem cells.

In the later cases, all they needed was three spoons of the patient's blood and a waiting period of a week.

The children did not have the vein that goes from the gastrointestinal tract to the liver. This was rectified using the new blood vessels, a treatment that holds out promise for people with varicose veins and myocardial infarction.

The method also rules out rejection normally accompanying any foreign body transplant.

Professors Olausson and Sumitran-Holgersson have treated three patients so far. Two of the three patients are still doing well and have veins that are functioning well.

They now hope to be able to grow complete organs to overcome organ shortage from donors.

Use of embryonic stem cells to treat macular dystrophy and degeneration has been proven to be safewith low rejection rates.

Continue reading here:
Blood Vessels Made from Three Spoons of Blood in a Week's Time

Recommendation and review posted by Bethany Smith

By Alison Sullivan, The Gazette

NORTH LIBERTY What would you say to the person who saved your life? For Angela Kearns it was a tearful thank you.

Kearns, of Marion, received a bone marrow transplant two years ago and on Saturday she and her bone marrow donor, Matthew Sabongi, met for the first time at the Colony Pumpkin Patch in North Liberty.

Kearns, 42, and Sabongi, 26, met in an emotional embrace surrounded by friends, family and other bone marrow donors and recipients. The two were connected by the Be the Match National Bone Marrow Donor Program, which Sabongi joined in 2011 as a medical student.

Kearns was diagnosed with acute lymphoblastic leukemia in 2009 and again in 2012. Although none of her family members were bone marrow matches, she was optimistic there would be a match somewhere.

I thought theyd find a donor, I just thought God would work it out, said Kearns, a mother of two.

Her situation isnt abnormal, according to Be the Match. Seventy percent of bone marrow recipients find matches in unrelated donors. Whether someone is a match is determined by their human leukocyte antigen, a protein found in most cells in the body.

Sabongi, of Minneapolis, said three months after he registered he got a call that he could be a possible match. After he was a confirmed match, he immediately agreed to donate.

Young donors ages 18 to 44 can make the biggest impact, said Julee Darner, donor services coordinator at the University of Iowa Marrow Donor Program. She said tudies show recipients tend to fare better in the long term with bone marrow donated from people in that age group.

The registry keeps donors and recipients anonymous until a year later, when both parties can choose whether they want to find out the others identity. So when Sabongi received a thank-you letter from Kearns a few months later, it was anonymous.

Read the original:
Marion woman meets her life saver

Recommendation and review posted by Bethany Smith

Few diseases are as terrifying as Huntington's, an inherited genetic disorder that gradually saps away at sufferers' muscle control and cognitive capacity until they die (usually some 20 or so years after initial symptoms). But scientists at Washington University School of Medicine may have provided a new glimmer of hope by converting human skin cells (which are much more readily available than stem cells) directly into a specific type of brain cell that is affected by Huntington's.

This new method differs from another technique devised at the University of Rochester last year in that it bypasses any intermediary steps rather than first reverting the cells to pluripotent stem cells, it does the conversion in a single phase.

To reprogram the adult human skin cells, the researchers created an environment that closely mimics that of brain cells. Exposure to two types of microRNA, miR-9 and miR-124, changes the cells into a mix of different types of neurons. "We think that the microRNAs are really doing the heavy lifting," said co-first author Matheus Victor, although the team admits that the precise machinations remain a mystery.

Huntington's disease especially affects medium spiny neurons, which are involved in initiating and controlling movement and can be found in a part of the basal ganglia called the corpus striatum. This part of the brain also contains proteins called transcription factors, which control the rate at which genetic information is copied from DNA to messenger RNA.

By exposing human skin cells (top) to a combination of microRNAs and transcription factors, the researchers were able to create medium spiny neurons (bottom) (Image: Yoo Lab/Washington University at St Louis)

The researchers fine-tuned the chemical signals fed into the skin cells as they were exposed to the microRNAs, with the transcription factors guiding the cells to become medium spiny neurons. Different transcription factors would produce different types of neurons, they believe, but not without the microRNAs which appear to be the crucial component, as cells exposed to transcription factors alone failed to become neurons.

When transplanted into the brains of mice, the converted cells survived at least six months while showing functional and morphological properties similar to native neurons. They have not yet been tested in mice with a model of Huntington's disease to see if this has any effect on the symptoms.

The research will nonetheless contribute to scientific understanding of the cellular properties associated with Huntington's, regardless of whether this new method leads directly to a treatment or cure.

A paper describing the research is available in the journal Neuron.

Source: Washington University in St Louis

See the article here:
Converting skin cells directly into brain cells advances fight against Huntington's disease

Recommendation and review posted by Bethany Smith

Stem Cell Therapy Help Buddy the Beagle
Buddy the beagle wasn #39;t able to walk when he first arrived at the University of Minnesota Veterinary Medical Center. With the help of the Veterinary Medical ...

By: UMN Health

Read more:
Stem Cell Therapy Help Buddy the Beagle - Video

Recommendation and review posted by Bethany Smith

Plenary Session: Cell Therapy Product Development
As more products head into later stage clinical development inevitably there will be successes and setbacks along the way. How do we educate key stakeholder ...

By: Alliance for Regenerative Medicine

Read more:
Plenary Session: Cell Therapy Product Development - Video

Recommendation and review posted by Bethany Smith

CTVNews.ca Staff Published Saturday, October 25, 2014 10:30PM EDT Last Updated Saturday, October 25, 2014 11:46PM EDT

An estimated 16,000 Canadians live with scleroderma, an incurable autoimmune disorder which causes the body to produce too much collagen, resulting in a hardening of the skin and tissue. There is no cure for the scleroderma, but some patients in Canada are now seeking a costly and experimental stem cell therapy in the U.S.

A little over a year ago, Mike Berry of Kingston, Ont., started having trouble breathing. It was the first sign of scleroderma.

Berry, 42, suffers from the systemic version of scleroderma, which attacks his internal organs. His lungs have been scarred by the disorder, with his lung capacity dropping to 41 per cent in just nine months. His disease may ultimately be fatal.

He described to CTV News how scleroderma has impacted his day-to-day life.

"I'm unable to work any longer; it affects me and everything now," he said. "It's hard to walk fast; I can't walk and talk."

Drugs to treat his scleroderma haven't worked, so now Berry is trying to fundraise more than $150,000 for an experimental U.S. stem cell treatment called Autologous Hematopoietic Stem Cell Transplantation (HSCT), in the hopes that it will save his life.

"It would give me as second chance, I guess I just have a lot to fight for," he said.

Pioneered by Dr. Richard Burt at Northwestern Memorial Hospital in Chicago, patients receiving HSCT are administered stem cells intravenously.

During the treatment, the patient's stem cells are harvested, and then the patient's over-active immune system is destroyed with powerful chemotherapy drugs. Doctors then re-program the patient's immune system with the harvested stem cells, in the hopes that the cells will "reset" the patient's immune system and stop scleroderma.

Read more:
Scleroderma patients seek experimental U.S. stem cell therapy

Recommendation and review posted by Bethany Smith

PBR Staff Writer Published 27 October 2014

Bayer HealthCare has signed a two-year collaboration agreement with Kyoto Universitys Office of Society-Academia Collaboration for Innovation (KU-SACI) in Japan to jointly discover candidates for possible collaborative research projects.

Under the deal, the two parties will focus on key areas of unmet medical need such as cardiology, oncology, hematology, gynecology and ophthalmology, by combining Kyoto University's expertise and innovative approaches in diverse research areas with Bayer's expertise in drug discovery and development.

The deal is part of Bayer's aim to collaborate with external partners from academia and industry to develop new treatments for patients across the world.

The company has recently entered into strategic research alliance in the area of gynecological therapies with the University of Oxford as well as with Dimension Therapeutics to develop and commercialize new gene therapy to treat hemophilia A.

In addition, the company has established two research incubators for young life sciences companies in the context of its open innovation approach.

The joint effort will be supported by Bayer's newly established Open Innovation Center Japan (ICJ) in Osaka, Japan.

The threefold mission of the KU-SACI is to promote collaborative research among academia, industries and the government; manage and use the university's intellectual properties through licensing & research collaboration with industries; as well as to support business start-ups by university researchers or students.

Image: Bayer and KU-SACI members during signing of the agreement. Photo: courtesy of Bayer HealthCare AG.

Read the original here:
Bayer, Kyoto University partner on collaborative research projects

Recommendation and review posted by Bethany Smith

A plan to save the cows and make milk in the lab could ease the environmental footprint of the dairy industry.(Reuters)

If the plans of a vegan duo materialise, cow's milk will soon be made minus the cow.

Genetically engineered yeast will churn out milk proteins in a liquid that tastes and feels like cow's milk.

Ryan Pandya and Perumal Gandhi who founded Muufri, a synthetic dairy start-up in San Francisco, started lab trials early this year and hope to have their synthetic cow's milkready by early 2017.

The duo want to save cows from the harrowing trials of modern-day industrial farms that feed them growth hormones, artificially inseminate them and take away the calves to make the milk available for humans, they told National Geographic.

They plan to insert DNA sequences from cattle into yeast cells, grow the cultures at a controlled temperature and harvest milk proteins.

While the proteins will come from yeast, the fat will be extracted from vegetables. Minerals, like calcium and potassium, and sugars available in the market will be added to the brew.

They intend to use healthier fat than found in natural milk and a sugar more suited to people who are lactose intolerant.

Water makes up almost 87% of milk. Casein protein, whey proteins, fat, lactose (the milk carbohydrate), glucose and some trace elements make up the rest.

Not everyone is enthused by the idea or believes it will work.

Originally posted here:
Genetic Engineering: Synthetic Milk May Be Next After Synthetic Meat

Recommendation and review posted by Bethany Smith