Archive for September, 2017

Gene-editing technology CRISPR has revealed a clue in how human embryos begin to develop, possibly reducing the risk of miscarriage in those crucial first few weeks of pregnancy.

CRISPR Cas9 can modify or snip out genetic defects thought to contribute to miscarriage, but until now it wasnt clear why some embryos continued to form into a fetus and others did not. However,findings, published Wednesday in the journal Nature, hold genetic clues.

British scientists conducting the study found that a certain human genetic marker called OTC4 played an important role in the formation and development in the early stages of embryonic development. The scientists used CRISPR Cas9 to knock out this important gene in days-old human embryos and found that without it, these embryos ceased to attach or grow properly.

The findings could not only help us better understand why some women suffer more miscarriages than others, but it could also potentially greatly increase the rate of successful in vitro fertilization (IVF) procedures.

IVF is sometimes the only way a couple can make a baby using their own genes, but even with technological improvements over the years, the rates of success are still poor.Only about 36 percent of IVF cycles result in a viable pregnancy, and a mere 24 percent produce a baby, according to the Centers for Disease Control.

Of course, this is not the first time scientists have tested on human embryos. The practice has sparked a fierce international debate, but earlier this year, U.S. scientists used CRISPR technology to cut out a gene known to cause heart defects in three-day old human embryos.

None of the embryos in that study or this latest one were meant to go on to become human beings and were discarded after the study was finished. However, both studies hint at the potential CRISPR could have in the formation of human life in the future.

It will likely take years before putting this breakthrough into practice on viable embryos meant to develop beyond a few days, and theres likely still much more research needed, but it does give hope for those whove suffered a miscarriage and wanting to ensure they can one day carry a healthy baby to full term.

Read more:
CRISPR breakthrough could drop miscarriage rates | TechCrunch

Usually, this type of study is conducted on mice, which are easier to come by and carry less ethical considerations. But, in this case, scientists knocked out the gene in 41 human embryos donated by couples who had undergone in-vitro fertilization (IVF). The researchers claim the switch allowed them to highlight key differences between the role of OCT4 in human and mouse models. The team are hoping their findings can help scientists better grasp why some women suffer more miscarriages than others. Additionally, the study could also increase the rate of successful IVF procedures.

This isn't the first time scientists have used human embryos. Earlier this year, a team of researchers from Oregon became the first to use CRISPR tech to cut out genes that cause inherited diseases in humans. Before that, scientists in China utilized the technique to repair a gene that can bring about a fatal blood disorder.

The new study is being hailed as a compelling first step. "We were surprised to see just how crucial this gene is for human embryo development, but we need to continue our work to confirm its role," Norah Fogarty of the Francis Crick Institute told CNN. "Other research methods, including studies in mice, suggested a later and more focused role for OCT4, so our results highlight the need for human embryo research."

Read the rest here:
CRISPR gene-editing could result in more successful birth rates

Our goal is to help you to improve your health and quality of life, while identifying the possible cause of your symptoms. We strive to offer you the best care possible in a professional, spa-like space and support you through the latest Naturopathic Medical practices.

Are you suffering for a health condition you need help treating? Are you generally healthy but have noticed increasing difficulty with your weight, mood, energy, focus or hormones? Thepractitioners at Marine Drive Naturopathic Clinic offer programs and treatments to help you not only to feel better, but examine the cause of your symptoms or conditions.

Our team includes Naturopathic Physicians Dr. Cathryn Coe,Dr. Cameron McIntyre, Dr. Elizabeth Miller, Dr. Lynn Klassen, and Dr. Sarah Wulkan.

Weight gain? Hot flashes? Poor sleep? We offer comprehensive thyroid and hormone testing to identify hormonal imbalances, correcting them using bioidentical hormone treatments or herbal support

Are you or your child affected by learning difficulties or cognitive problems? We offer testing and treatment for conditions such as autism spectrum disorders, Alzheimers disease and dementia, and ADD/ADHD. Our Clinical Counsellor also offers support forparents of children with autism and spectrum disorders

The clinic is conveniently located along Marine Drive in North Vancouver with plenty of free parking and direct access to public transit. Come in, relax, enjoy a cup of tea and read a magazine in our spa-like environment. At Marine Drive Naturopathic Clinic, your treatment begins the minute you walk in the door

See the article here:
Clinic North Vancouver | Bioidentical Hormone Treatments

A hormone doctor, or an endocrinologist, is a physician who treats diseases related to the endocrine system. While primary care physicians (family practitioners and internal medicine physicians) can treat many hormonal disorders without a need for specialized training, a physician may also receive advanced training and specialize in endocrinology. A primary care physician can determine whether he or she can treat a patient or whether the patient should be referred to a specialist treating only disorders of the endocrine system.

The endocrine system is composed of many glands, including the pituitary, thyroid, parathyroids, adrenals, hypothalamus, pineal body, ovaries and testicles. The islet cells of the pancreas are also part of the endocrine system. These glands secrete hormones (chemical messengers) that regulate the bodys metabolism, growth, sexual development and sexual function, by complex feedback systems comparable to a thermostat regulating room temperature.

A hormone doctor can specialize in diseases of one or two glands or treat patients in all areas of endocrinology. A large part of a typical practice could involve treating diabetes and related complications. The physician may also treat thyroid disorders, inborn metabolic disorders, over- and underproduction of hormones, osteoporosis, menopause, cholesterol disorders, hypertension, and short or tall stature. Patients with endocrine cancer are usually referred to an oncologist.

To treat non-reproductive hormonal disorders, a physician generally completes four years of medical or osteopath school and a three-year residency in either family medicine or internal medicine. He or she must pass a board examination to become board certified in family or internal medicine. To become board certified as an endocrine specialist, the physician completes a three-year endocrinology fellowship program and passes a board certification examination.

Reproductive endocrinologists complete four years of residency training in obstetrics and gynecology, rather than training in family medicine or internal medicine. They must complete two or three years of fellowship training in reproductive endocrinology and infertility and pass the board certification examination. These specialists treat infertility by using in vitro fertilization, embryo and sperm freezing, assisted embryo hatching, pre-implantation genetic diagnosis and other emerging technologies. Reproductive endocrinologists also treat a wide range of reproductive disorders, including endometriosis, polycystic ovary syndrome, gonadal dysgenesis, galactorrhea, repeat pregnancy loss, ectopic pregnancy and excess hair in women, to name just a few.

A hormone doctor may work in academic medical centers, community hospitals, private group practices or private solo practices. Each situation can involve different work hours, a different patient base, and different lifestyles. Unlike surgical specialties, hormone doctors generally do not take call hours, but they may be called on an emergency basis to see a patient in a hospital when the physician on staff cannot appropriately treat the patient.

Continue reading here:
What Is a Hormone Doctor? | Career Trend

Gene therapy is a type ofbiological therapy for cancer that is still in the early stages of research.

Genes are coded messages that tell cells how to make proteins. Proteins are the molecules that control the way cells behave. Our genes decide what we look like and how our body works.We have many thousands of separate genes.

Genes are made ofDNAand they are in the nucleus of the cell. The nucleus is the cell's control centre.Genes are grouped together to make chromosomes. We inherit half our chromosomes from our mother and half from our father.

Cancer cells are different from normal cells. They have changes (called faults or mutations) in several of their genes which make them divide too often and form a tumour. The genes that are damaged mightbe:

Many gene changes that may make a cell become cancerous are caused by environmental or lifestyle factors, such as smoking.

Some people have inherited faulty genes that increase their risk of particular types of cancer. Inherited damaged genes cause between 2 and 3 in every 100 (2% to 3%) of cancers.

Gene therapy is a type of treatment which uses genes to treat illnesses. Researchers have been developing differenttypes of gene therapyto treat cancer.

The ideas for these new treatments have come about because we are beginning to understand how cancer cells are different from normal cells. It is stillearly days for this type of treatment. Some of these treatments are being looked at in clinical trials. Otherscan now be used for some people with types of cancer such as melanoma skin cancer.

Getting genes into cancer cells is one of the most difficult aspects of gene therapy. Researchers are working on finding new and better ways of doing this. The gene is usually taken into the cancer cell by a carrier called a vector.

The most common types of carrier used in gene therapy are viruses because they can enter cells and deliver genetic material. The viruses have been changed so that they cannot cause serious disease but they may still cause mild, flu like symptoms.

Some viruses have been changed in the laboratory so that they target cancer cells and not healthy cells. So they only carry the gene into cancer cells.

Researchers are testing other types of carrier such as inactivated bacteria.

Researchers are looking at different ways of using gene therapy:

Some types of gene therapy aim to boost the body's natural ability to attack cancer cells. Ourimmune systemhas cells that recognise and kill harmful things that can cause disease, such as cancer cells.

There are many different types of immune cell. Some of them produce proteins that encourage other immune cells to destroy cancer cells. Some types of therapy add genes to a patient's immune cells. Thismakes them better at finding or destroying particular types of cancer.

There are a few trials using this type of gene therapy in the UK.

Some gene therapies put genes into cancer cells to make the cells more sensitive to particular treatments. The aim is to make treatments,such as chemotherapy or radiotherapy, work better.

Some types of gene therapy deliver genes into the cancer cells that allow the cells to change drugs from an inactive form to an active form. The inactive form of the drug is called a pro drug.

First of all you have treatment with the the carrier containing the gene, then you havethe pro drug.The pro drug circulates in the body and doesn't harm normal cells. But when it reaches the cancer cells, it is activated by the gene and the drug kills the cancer cells.

Some gene therapies block processes that cancer cells use to survive. For example, most cells in the body are programmed to die if their DNA is damaged beyond repair. This is called programmed cell death or apoptosis. Cancer cells block this process so they don't die even when they are supposed to.

Some gene therapy strategies aim to reverse this blockage. Doctors hope these new types of treatment will make the cancer cells die.

Some viruses infect and kill cells. Researchers are working on ways to change these viruses so they only target and kill cancer cells, leaving healthy cells alone.

This sort of treatment uses the viruses to kill cancer cells directly rather than to deliver genes. So it is not cancer gene therapy in the true sense of the word. But doctors sometimes refer to it as gene therapy.

A drug called T-VEC (talimogene laherparepvec)isnowavailable as a treatmentfor melanoma skin cancer. It isalso calledImlygic. It is also being looked at in trials for other types of cancer, such as head and neck cancer.

T-VEC uses a strain of the cold sore virus (herpes simplex virus)that been changed by altering the genes that tell the virus how to behave. It tells the virus to destroy the cancer cells and ignore the healthy cells.

T-VEC can beused to treatsome people with melanoma skin cancer whose cancer cannot be removed with surgery. You have T-VEC as an injectiondirectly into yourmelanoma.

Use the tabs along the top to look at recruiting,closed and results.

Continue reading here:
Gene therapy | Cancer in general | Cancer Research UK

A common and frustrating complaint we at Life Extension hear is how to stop urinary incontinence.

Our frustration has been that despite aggressive research, we could not identify a safe solution to this problem that plagues so many aging women (and men to a lesser extent).

Even more numerous are inquiries we receive from people seeking relief from frequent daytime and nighttime urinary urges.

In a breakthrough discovered by Japanese scientists, a natural plant extract combination has been shown to reduce incontinent episodes by up to 79%,1 daytime urination by up to 39%,2 and nighttime urination by up to 68%.3

This article will discuss the research findings on maturing women who found significant relief after taking this novel supplement for only six to eight weeks.

Additionally, this article will discuss more limited data obtained when men suffering from nighttime urinary urgencies were given this same plant extract.

Urinary frequency becomes more common with advancing age, with nearly half of people over 60 reporting to suffer from nocturia (two or more episodes of urination during the night).

Urinary incontinence is defined as an involuntary loss of urine. It represents a major social and hygiene problem in the aging population. About 48% of women and 17% of men over age 70 suffer urinary incontinence.4

Overactive bladder affects one in six adults over age 40, and is defined as having an urgent need to empty the bladder during the day-night, along with incontinence. Those afflicted with an overactive bladder have to go to the bathroom frequently, leak urine into their clothes, and report feeling depressed, stressed, and sleep-deprived.

In women, stress incontinence (involuntary loss of urine during physical activity such as sneezing or exercise) is usually caused by a weakening of the bladder sphincter and pelvic floor muscles. Shrinkage (atrophy) of tissues where the bladder and urethra meet also contributes to the problem. Hormonal changes occurring after menopause are thought to be an underlying cause of these anatomical changes in the bladder sphincter that lead to urinary incontinence.

In postmenopausal women, decreased androgen (testosterone) levels weaken the pelvic floor and sphincter muscles, while an estrogen deficit induces atrophy of the urethra.

Mainstream medicine offers only mediocre therapies to address urinary incontinence. Drugs commonly used for this condition are expensive and side-effect-prone. Only a small proportion of the affected population seeks treatment because most people consider their urinary symptoms a consequence of normal aging.

Fortunately, a safe, natural, and low-cost approach has been developed that has demonstrated remarkable benefits in human clinical trials.

Pumpkin seeds were traditionally used by Native American tribes to facilitate passage of urine. A European herbal encyclopedia first mentioned the use of pumpkins seeds to treat urinary problems in the year 1578. The German health regulators approve pumpkin seed as a treatment for irritable bladder.

Pumpkin seed oil has been included in products used to alleviate urinary difficulties. While some effects have been shown when using the fat-soluble (oil) fraction of the pumpkin seed, it is the water-soluble portion that demonstrated impressive symptomatic effects in recent studies.

Japanese scientists have patented a method to obtain the water-soluble constituents of the pumpkin seed, which are absorbed far more efficiently into the bloodstream.

Urinary incontinence worsens after menopause. While menopausal problems are usually associated with estrogen deficit, low levels of testosterone and progesterone are also underlying culprits.

Water-soluble pumpkin seed extract exerts an anabolic (tissue-building) effect on the pelvic floor muscles via several mechanisms. By inhibiting the aromatase enzyme, it may make more testosterone available to strengthen the pelvic muscles.5

Secondly, this water-soluble pumpkin seed fraction binds to the androgen receptor on pelvic muscle cells, thus inducing a strengthening effect. This is important because androgen receptors are expressed in the pelvic floor and lower urinary tract in humans.6 By promoting androgenic activity, water-soluble pumpkin seed extract may play an important role in female pelvic floor structural integrity and lower urinary tract disorders.5

Nitric oxide is a molecule critically involved in lower urinary tract functions. For the urination muscles to relax when the bladder is full, nitric oxide is required. When nitric oxide synthesis is inhibited, the result is bladder hyperactivity and reduced bladder volume.

The dual mechanisms of strengthening pelvic floor muscles, while increasing nitric oxide synthesis,5 help explain how water-soluble pumpkin seed extract alleviated urinary incontinence in three separate studies on aging women.1-3

Soy extracts provide standardized phyoestrogens that are potentially effective in ameliorating geriatric symptoms relating to estrogen deficit.

The ingestion of standardized soy extract has been hypothesized to decrease the atrophy of tissues where the bladder and urethra meet and thus alleviate frequent urinary urges and incontinence.

A study was done to evaluate the effects of water-soluble pumpkin seed extract in anesthetized rats to determine bladder functionality.7

As measured by a cystometrogram, bladder parameters showed a dramatic 54.5% improvement in rats receiving water-soluble pumpkin extract compared to other agents.

When the excretion frequency was measured, a 60% reduction in urine excretion frequency occurred after administration of water-soluble pumpkin seed extract. No improvement was seen in the group given inactive solvent.

Conclusions from the study showed that water-soluble pumpkin extract significantly increases maximum bladder capacity while decreasing urination frequency.

A study of 39 incontinent females (aged 55-79 years) using water-soluble pumpkin seed and soy isoflavone extracts was conducted over a six-week period.1 The objective was to evaluate the effects on frequency of daytime and nighttime urinations and number of incontinent episodes.

After six weeks, the number of nighttime urinations was reduced from 3.3 to 2.0 a 39% improvement. Daytime urinations went from 8.0 to 6.7 after six weeks a modest 16% improvement.

The number of incontinent episodes, however, plunged to a remarkably low number. Prior to receiving the water-soluble pumpkin seed-soy extract, these women experienced an average of 7.3 incontinent episodes a day. After six weeks of using this supplement, daily incontinent episodes averaged only 1.5 an astounding 79% decrease in urinary incontinence!

When these women were questioned about the effects they noticed in response to taking water-soluble pumpkin seed-soy extract, there was a 73% subjective improvement in the highest fulfilled category. When the global improvement ratio was evaluated, which included degree of satisfaction after sleeping, 81.8% of women with two to four episodes of nightly urinations reported that they were markedly improved.

A study of 50 incontinent women (aged 35-84 years) was conducted using the same water-soluble pumpkin seed-soy extract supplement to evaluate the effect on stress incontinence episodes.3

Before the pumpkin seed-soy supplement was given, these women averaged 2.1 incontinent events each day. After taking the supplement for six weeks, incontinent events fell to an average of only 0.7 a day a remarkable 67% decrease in stress-induced incontinent episodes!

A consumer test of 10 women (aged 45-65 years) was conducted using the same water-soluble pumpkin seed and soy extract supplement.2

After eight weeks, daytime urinations went from 9.3 to 5.6 a 39% reduction. Nighttime urinations went from 2.0 to 0.8 a 60% reduction.

Prior to initiating the pumpkin seed-soy supplement, there was an average of 2.3 incontinent episodes each day. After eight weeks, the frequency of incontinent episodes declined to only 1.0 per day a 57% reduction!

Link:
Relief of Overactive Bladder - page 1 | Life Extension ...

Have you heard? A revolution has seized the scientific community. Within only a few years, research labs worldwide have adopted a new technology that facilitates making specific changes in the DNA of humans, other animals, and plants. Compared to previous techniques for modifying DNA, this new approach is much faster and easier. This technology is referred to as CRISPR, and it has changed not only the way basic research is conducted, but also the way we can now think about treating diseases [1,2].

CRISPR is an acronym for Clustered Regularly Interspaced Short Palindromic Repeat. This name refers to the unique organization of short, partially palindromic repeated DNA sequences found in the genomes of bacteria and other microorganisms. While seemingly innocuous, CRISPR sequences are a crucial component of the immune systems [3] of these simple life forms. The immune system is responsible for protecting an organisms health and well-being. Just like us, bacterial cells can be invaded by viruses, which are small, infectious agents. If a viral infection threatens a bacterial cell, the CRISPR immune system can thwart the attack by destroying the genome of the invading virus [4]. The genome of the virus includes genetic material that is necessary for the virus to continue replicating. Thus, by destroying the viral genome, the CRISPR immune system protects bacteria from ongoing viral infection.

Figure 1 ~ The steps of CRISPR-mediated immunity. CRISPRs are regions in the bacterial genome that help defend against invading viruses. These regions are composed of short DNA repeats (black diamonds) and spacers (colored boxes). When a previously unseen virus infects a bacterium, a new spacer derived from the virus is incorporated amongst existing spacers. The CRISPR sequence is transcribed and processed to generate short CRISPR RNA molecules. The CRISPR RNA associates with and guides bacterial molecular machinery to a matching target sequence in the invading virus. The molecular machinery cuts up and destroys the invading viral genome. Figure adapted from Molecular Cell 54, April 24, 2014 [5].

Interspersed between the short DNA repeats of bacterial CRISPRs are similarly short variable sequences called spacers (FIGURE 1). These spacers are derived from DNA of viruses that have previously attacked the host bacterium [3]. Hence, spacers serve as a genetic memory of previous infections. If another infection by the same virus should occur, the CRISPR defense system will cut up any viral DNA sequence matching the spacer sequence and thus protect the bacterium from viral attack. If a previously unseen virus attacks, a new spacer is made and added to the chain of spacers and repeats.

The CRISPR immune system works to protect bacteria from repeated viral attack via three basic steps [5]:

Step 1) Adaptation DNA from an invading virus is processed into short segments that are inserted into the CRISPR sequence as new spacers.

Step 2) Production of CRISPR RNA CRISPR repeats and spacers in the bacterial DNA undergo transcription, the process of copying DNA into RNA (ribonucleic acid). Unlike the double-chain helix structure of DNA, the resulting RNA is a single-chain molecule. This RNA chain is cut into short pieces called CRISPR RNAs.

Step 3) Targeting CRISPR RNAs guide bacterial molecular machinery to destroy the viral material. Because CRISPR RNA sequences are copied from the viral DNA sequences acquired during adaptation, they are exact matches to the viral genome and thus serve as excellent guides.

The specificity of CRISPR-based immunity in recognizing and destroying invading viruses is not just useful for bacteria. Creative applications of this primitive yet elegant defense system have emerged in disciplines as diverse as industry, basic research, and medicine.

In Industry

The inherent functions of the CRISPR system are advantageous for industrial processes that utilize bacterial cultures. CRISPR-based immunity can be employed to make these cultures more resistant to viral attack, which would otherwise impede productivity. In fact, the original discovery of CRISPR immunity came from researchers at Danisco, a company in the food production industry [2,3]. Danisco scientists were studying a bacterium called Streptococcus thermophilus, which is used to make yogurts and cheeses. Certain viruses can infect this bacterium and damage the quality or quantity of the food. It was discovered that CRISPR sequences equipped S. thermophilus with immunity against such viral attack. Expanding beyond S. thermophilus to other useful bacteria, manufacturers can apply the same principles to improve culture sustainability and lifespan.

In the Lab

Beyond applications encompassing bacterial immune defenses, scientists have learned how to harness CRISPR technology in the lab [6] to make precise changes in the genes of organisms as diverse as fruit flies, fish, mice, plants and even human cells. Genes are defined by their specific sequences, which provide instructions on how to build and maintain an organisms cells. A change in the sequence of even one gene can significantly affect the biology of the cell and in turn may affect the health of an organism. CRISPR techniques allow scientists to modify specific genes while sparing all others, thus clarifying the association between a given gene and its consequence to the organism.

Rather than relying on bacteria to generate CRISPR RNAs, scientists first design and synthesize short RNA molecules that match a specific DNA sequencefor example, in a human cell. Then, like in the targeting step of the bacterial system, this guide RNA shuttles molecular machinery to the intended DNA target. Once localized to the DNA region of interest, the molecular machinery can silence a gene or even change the sequence of a gene (Figure 2)! This type of gene editing can be likened to editing a sentence with a word processor to delete words or correct spelling mistakes. One important application of such technology is to facilitate making animal models with precise genetic changes to study the progress and treatment of human diseases.

Figure 2 ~ Gene silencing and editing with CRISPR. Guide RNA designed to match the DNA region of interest directs molecular machinery to cut both strands of the targeted DNA. During gene silencing, the cell attempts to repair the broken DNA, but often does so with errors that disrupt the geneeffectively silencing it. For gene editing, a repair template with a specified change in sequence is added to the cell and incorporated into the DNA during the repair process. The targeted DNA is now altered to carry this new sequence.

In Medicine

With early successes in the lab, many are looking toward medical applications of CRISPR technology. One application is for the treatment of genetic diseases. The first evidence that CRISPR can be used to correct a mutant gene and reverse disease symptoms in a living animal was published earlier this year [7]. By replacing the mutant form of a gene with its correct sequence in adult mice, researchers demonstrated a cure for a rare liver disorder that could be achieved with a single treatment. In addition to treating heritable diseases, CRISPR can be used in the realm of infectious diseases, possibly providing a way to make more specific antibiotics that target only disease-causing bacterial strains while sparing beneficial bacteria [8]. A recent SITN Waves article discusses how this technique was also used to make white blood cells resistant to HIV infection [9].

Of course, any new technology takes some time to understand and perfect. It will be important to verify that a particular guide RNA is specific for its target gene, so that the CRISPR system does not mistakenly attack other genes. It will also be important to find a way to deliver CRISPR therapies into the body before they can become widely used in medicine. Although a lot remains to be discovered, there is no doubt that CRISPR has become a valuable tool in research. In fact, there is enough excitement in the field to warrant the launch of several Biotech start-ups that hope to use CRISPR-inspired technology to treat human diseases [8].

Ekaterina Pak is a Ph.D. student in the Biological and Biomedical Sciences program at Harvard Medical School.

1. Palca, J. A CRISPR way to fix faulty genes. (26 June 2014) NPR < http://www.npr.org/blogs/health/2014/06/26/325213397/a-crispr-way-to-fix-faulty-genes> [29 June 2014]

2. Pennisi, E. The CRISPR Craze. (2013) Science, 341 (6148): 833-836.

3. Barrangou, R., Fremaux, C., Deveau, H., Richards, M., Boyaval, P., Moineau, S., Romero, D.A., and Horvath, P. (2007). CRISPR provides acquired resistance against viruses in prokaryotes. Science 315, 17091712.

4. Brouns, S.J., Jore, M.M., Lundgren, M., Westra, E.R., Slijkhuis, R.J., Snijders, A.P., Dickman, M.J., Makarova, K.S., Koonin, E.V., and van der Oost, J. (2008). Small CRISPR RNAs guide antiviral defense in prokaryotes. Science 321, 960964.

5. Barrangou, R. and Marraffini, L. CRISPR-Cas Systems: Prokaryotes Upgrade to Adaptive Immunity (2014). Molecular Cell 54, 234-244.

6. Jinkek, M. et al. A programmable dual-RNA-guided DNA endonuclease in adaptive bacterial immunity. (2012) 337(6096):816-21.

7. CRISPR reverses disease symptoms in living animals for first time. (31 March 2014). Genetic Engineering and Biotechnology News. <http://www.genengnews.com/gen-news-highlights/crispr-reverses-disease-symptoms-in-living-animals-for-first-time/81249682/> [27 July 2014]

8. Pollack, A. A powerful new way to edit DNA. (3 March 2014). NYTimes < http://www.nytimes.com/2014/03/04/health/a-powerful-new-way-to-edit-dna.html?_r=0> [16 July 2014]

9. Gene editing technique allows for HIV resistance? <http://sitn.hms.harvard.edu/flash/waves/2014/gene-editing-technique-allows-for-hiv-resistance/> [13 June 2014]

Read the rest here:
CRISPR: A game-changing genetic engineering technique ...

Why it matters to you

Pigs could be a solution to the shortage of transplant organs. CRISPR gene editing makes them safer candidates.

There is a massive shortage of transplant organs worldwide, and scientists are desperate to come up with a solution whether that be boosting patients immune systems to let them accept otherwise incompatible organs, or creating technology for preserving organs after they are harvested. A new international research initiative has another approach: Using CRISPR gene editing on pigs to make them into safe organ donor candidates for humans.

The reason pigs are desirable as possible sources of organs is that their organs are similar to humans in both size and anatomy. Unfortunately, they also carry viruses known as porcine endogenous retroviruses (PERVs) embedded in their DNA. As this research demonstrated, this can be passed on to humans, although gene editing can be used to eradicate it.

Currently, the major problem of human transplants is the great shortage of transplantable human organs, Lin Lin, a researcher in the department of biomedicine at Denmarks Aarhus University, told Digital Trends. While using pig organs, we can in principle use as many as we need. Eradicating PERVs makes porcine organs safer for human transplants. However, there are still several other barriers that we have to cross in order to make pig organs better for human transplants. This is now achievable with the great development in CRISPR gene editing.

Using an optimized CRISPR-Cas9 gene editing technology and porcine somatic cell nuclear transfer, this work successfully generated viable pigs that are 100 percent PERV-inactivated.Thirty-seven PERV-inactive piglets have so far been born, with 15 remaining alive. The oldest of these is four months old, which means it will need to be monitored for a longer period of time to make sure it suffers no ill-effects.

The next major step is to solve the problem of vigorous immune responses, such as complement activation, coagulation and thrombosis, triggered by xenotransplantation, Lin said. Many previous works have demonstrated that the immunological incapability can be alleviated through tailoring the pig genome. Thus, a serial of very sophisticated gene editing and modifications will be further introduced into the PERV-inactivated pigs and tested in higher primates.

A paper describing the research was recently published in the journal Science.

See more here:
Thanks to CRISPR, gene-edited pigs could be organ donors for ...

CRISPR or CRISPR Cas9 is commonly used to refer to a revolutionary genome editing technology that enables efficient and precise genomic modifications in a wide variety of organisms and tissues.

Definition: Clustered Regularly Interspaced Short Palindromic Repeat or CRISPR (pronounced 'crisper') was identified in a prokaryotic defence system. CRISPR are sections of genetic code containing short repetitions of base sequences followed by spacer DNA segments

Identified in archaea and bacteria, short nucleic acid sequences are captured from invading pathogens and integrated in the CRISPR loci amidst the repeats. Small RNAs, produced by transcription of these loci, can then guide a set of endonucleases to cleave the genomes of future invading pathogens, thereby disabling their attacks.

Definition: CRISPR ASsociated protein 9 (Cas 9) is an endonuclease used in an RNA-guided gene editing platform. It uses a synthetic guide RNA to introduce a double strand break at a specific location within a strand of DNA

Cas9 was the first of several restriction nucleases (or molecular scissors) discovered that enable CRISPR genome editing. The CRISPR Cas9 mechanism has since been adapted into a powerful tool that puts genome editing into the mainstream.

In the laboratory, CRISPR Cas9 genome editing is achieved by transfecting a cell with the Cas9 protein along with a specially designed guide RNA (gRNA) that directs the cut through hybridization with its matching genomic sequence. When the cell repairs that break, errors can occur to generate a gene knockout or additional genetic modifications can be introduced. Our CRISPR gene editing technology is particularly good for the efficient generation of complete knockout of genes on multiple alleles.

Use of wild-type Cas 9 has been shown to lead to off-target cleavage, but a modified version introduces only single strand nicks to the DNA, which in pairs still stimulate the repair mechanisms while significantly decreasing the risk of off-target cutting.

Horizon has licensed gene editing IP from Harvard University, the Broad Institute and ERS Genomics with the goal of being able to ensure that we will be able to offer uninterrupted use of CRISPR tools to our customers. Our scientists have extensive knowledge of CRISPR technology including the benefits of using each Cas9 structure.

Other Gene Editing Systems

Genome editing can be achieved using the widely used S. Pyogenes (spCas9), and also utilising CRISPR Cas 9 protocol for S. Aureus (scCas9), Cpf1, HiFi Cas9, Nickase Cas9, Nuclease Cas9, NgAgo gDNA and even synthetic spCas9 with alternative PAM sites.

Our genome editing knowledge also includes rAAV and ZFNs.

Continue your CRIPSR/Cas9 research with ourpopular education and training webinars:

Find out more about our exciting upcoming eventwhere the future of CRISPR will be discussed:

The CRISPR Forum 2017

Barrangou R, Fremaux C, Deveau H, Richards M, Boyaval P, Moineau S, Romero DA, Horvath P. 2007.CRISPR provides acquired resistance against viruses in prokaryotes. Science 315(5819): 1709-1712.

Jinek M, Chylinski K, Fonfara I, Hauer M, Doudna JA, Charpentier E. 2012.A programmable dual-RNA-guided DNA endonuclease in adaptive bacterial immunity. Science 337(6096): 816-821.

Continued here:
CRISPR - CRISPR-Cas9 | Gene Editing

B

ioengineer Luhan Yang swiped through the photos on her phone until she got to one that made her beam: It showed her crouching down by a pudgy, wide-eyed newborn she calls my baby.

This newborn is a pig, and its the first to be born with dozens of genetic changes that could enable scientists to turn swine into a source of organs for human transplants, Yang and her colleaguesreported on Thursday in Science.

Theynamed the piglet Laika, after the first dog to orbit Earth in 1957. The new Laika, born this year in China after numerous miscarriages and other setbacks, could be a pioneer in her own right. Using the genome-editing technology CRISPR-Cas9, Yang and her team at the biotech startup eGenesis knocked out pig DNA that has long been considered a deal-breaker for efforts to use pigs as organ donors. Laika and 36 other designer piglets are completely free of it.

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There are additional Olympic-level hurdles to overcome before people facing death from organ failure get replacement kidneys, hearts, livers, or lungs from the species that provides their bacon and pork chops.Other genetic changes will be necessary. And regulators require stringent tests in lab primates before a single patient could get a CRISPRd pig organ; that will take years.

But after decades of dashed hopes, experts say, xenotransplantation might actually be in the offing.

Its an elegant tour de force of genetic engineering, so my hat is off to them, said Dr. A. Joseph Tector, of the University of Alabama, Birmingham, who has also made genetically modified pigs aimed at producing transplantable organs. But if you want to move xenotransplantation to the hospital, there are many more things youll have to do.

Doctors wont have to do much persuasion, however, to get patients to accept organs from another species. There is so much desperation among people on transplant lists, and 20 a day are dying as they wait, said Dr. Adam Griesemer, a xenotransplantation researcher and transplant surgeon at Columbia University Medical Center. This could be a path to a transplant for them. Colleagues keep asking me when were going to do it.

Pigs are scientists first choice because their organs and physiology are pretty close matches to humans, and they come with less ethical baggage than, say, chimps or baboons. But for years, the path to xenotransplantation has been paved with disappointment. Pig organs with genetic changes, transplanted into baboons and other lab animals,kept failing within weeks, even though the recipients received immune-suppressing drugs to prevent organ rejection.

Yang believes that CRISPR can accomplish what previous approaches have not: make multiple, simultaneous changes in pig DNA so that the animals organs work, and work safely, in people.

The team at Massachusetts-based eGenesis, working with scientists in China, used the Dolly recipe to clone pigs. They started with cells from adult pigs, and used an electrical jolt to fuse them with pig ova whose DNA had been removed. They grew the resulting embryos in lab dishes and then transferred healthy ones to sows, hoping for pregnancies.

The adult cells were not as nature made them, however. In a key step, the scientists used the genome-editor CRISPR to cripple all 25 copies of PERV genes DNA in the pig genome that makes potentially dangerous viruses that could infect anyone who receives a pig organ. (PERV stands for porcine endogenous retroviruses.) Initially, in about one-third of the CRISPRd pig cells, the PERV genes were almost all gone. In most of the rest, CRISPR missed its mark. That wasnt unexpected; for all the hype around CRISPR, it isnt perfect.

The unwelcome surprise was that cells that were effectively CRISPRd the ones the scientists needed to clone designer pigs were dying like orchids in the tundra. Apparently, in its zeal to attack so many PERV genes, CRISPR had shredded the cells genomes fatally.

Its quite a problem, when you move to so many targets, said Yang, the chief scientific officer at eGenesis. If there are multiple cuts in the genome at the same time, chromosomes rearrange themselves. That can happen when you make two or three [CRISPR edits], and were dealing with 25.

The eGenesis scientists, many of them alums of George Churchs lab at Harvard Medical School, scrambled for a solution. They eventually stumbled on a cocktail of molecules that both increased the number of PERV targets that CRISPR hit and, even better, kept the well-CRISPRd cells alive. We were able to get cells to grow even with very aggressive gene editing, Yang said: 100 percent of the cells doused with the chemical cocktail were 100 percent PERV-free.

As is typical with cloning, very few of the cloned embryos were healthy enough to implant into sows, and few implanted embryos resulted in births. Crucially, however, of the 37 piglets born from 17 sows, all were PERV-free. And CRISPR did not change any DNA it wasnt supposed to; there were no off-target effects.

The oldest pigs are nearly 5 months old, or adolescents; 15 remain alive. The rest were killed so the scientists could see whether their organs were developing normally.

So far, so good, Yang said, showing that pigs dont need PERVs to live: Weve shown you can produce PERV-free pigs which could serve as a source for future xenotransplants.

Among eGenesiss next experiments: see if the pigs are fertile and, if so, whether their CRISPRd genetic changes, including inactivating PERVs, are inherited. That could provide an easier source of transplantable organs than cloning.

Other scientists have also used CRISPR to produce pigs with altered genomes, including pigs in which a genethat triggers organ rejection was eliminated. Last year, scientists announcedthat hearts from genetically-modified pigs survived in baboons for up to 945 days, a record.

UABs Tector and his colleagues, with financial backing from United Therapeutics Corp., are using CRISPR not on PERVs but on other pig genes. Knocking out threein particular could protect pig organs from being attacked by the human immune system, he said; lab macaques that received kidneys from the pigs have survived as long as 499 days. We have a pig we are very confident we can make work for kidney transplants, Tector said.

There is disagreement about whether pig organs would have to be PERV-free to be successfully transplanted into people. Tector said transplant patients could take anti-retroviral drugs, just as they take immune-suppressing drugs, to kill the viruses.

Nevertheless, eGenesis scientists achievement with their 25 DNA edits, the eGenesis pigs set the record for genome modifications suggests that however many edits are needed to make pigs into organ donors might be feasible. The challenge is to identify which pig genes are necessary and sufficient to change so that the animals organs have a shot at working in people.

Senior Writer, Science and Discovery

Sharon covers science and discovery.

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CHOLLEY PhytocellBooster is ideal for smoothening wrinkles and eliminating the signs of aging or fatigue. It is a perfect product in many situations, such as after waking up in the morning, an exhausting day at work, and prior to attending a business meeting or party.

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Frozen Dead GuyHome of The Frozen Dead Guy (AKA Bredo Morstoel)The Iceman's Chronicle...Contact the Iceman for information on where to get your copy...and for booksignings and special events.Get information on events for 2013 FDGDays>>>>Get Twitter Tweets from Botheiceman@Twitter.com!!!What's the Frozen Dead Guy all about?It has a lot to do with Cryonics, which is pretty much freezing people who are about to die, in hopes that future technology will be able to "re-animate" them and cure what ailed them.It had a lot to do with the Town of Nederland and the Nederland Chamber of Commerce....and there's a year round Information Center in Ned for souvenirs of the Frozen Dead Guy Days festival (see below). The Chamber's site had all the information on upcoming FDGDaze.....but in 2011 they sold the festival to a private group who now has the only site with information on the upcoming festival. Frozen Dead Guy Days is their link.It has a big connection to Norway, as the Grandson of the FDG, Trygve, lives there with his Mother, Aud (FDG's Daughter). They are the ones responsible for maintaining the financials and micro-managing from afar. Trygve was deported in 1994 and has not set foot in the US since. Aud has visited...once. THere are long and curious tales about both of these situations, but suffice to say, neither is allowed back in the country at this time.There's some of that old history......Psychics and all, found in the Historical Archives of the Planetary Ecologists at....There's some history regarding the Great Unappearance on the Jay Leno Tonight Show..Here's some archived video of the days when Grandpa was persona non grata.....Although there is a wild and entertaining side to this story.....there is also a serious and scientific side, too.There's been some Press.......and some websites, like Dark DestinationsEven a local company who went National has played a part....Tuff Shed has made it all possible from a practical point of view.We celebrated Grandpa Bredo's 107th Birthday with an Ice Run Party at the old International Cryonics Institute, before it was dismantled.********Update.....September 2012******* In September of 2012, a labor dispute broke out and when overseas management and local labor couldn't agree on terms, a walkout ensued. The International Cryonics Institute was kicked out of it's offices and had to remove all their equipment. Scabs were hired and the fate of Grandpa Bredo now rests in the hands of some guy and a truck. The coming winter is predicted to be snowy and cold. Stay tuned for further info.... The Iceman's last day on the job...Here's a wordle from the book "Chronicles of the Colorado Iceman"....And then there's the Frozen Dead Guy Days Festival.....Frozen Dead Guy Days 2006 Frozen Dead Guy Daze of 2007.....a festival to remember!Frozen Dead guy Days of 2008...A picture GalleryFrozen Dead Guy Daze 2009...Frozen Dead Guy Daze 2010...Re-animated Tours!If, after perusing this evolving site, you have any questions or still just can't seem to figure out what the FDG is all about...Feel free to Send your query to The IcemanThis Page is deep in the throes of Creative Endeavour.......please be advised

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Frozen Dead Guy

During the last decade, an increased interest in somatic stem cells has led to a flurry of research on one of the most accessible tissues of the body: skin. Much effort has focused on such topics as understanding the heterogeneity of stem cell pools within the epidermis and dermis, and their comparative utility in regenerative medicine applications. In Skin Stem Cells: Methods and Protocols, expert researchers in the field detail many of the methods which are now commonly used to study skin stem cells. These include methods and techniques for the isolation, maintenance and characterization of stem cell populations from skin. Written in the highly successful Methods in Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible laboratory protocols, and key tips on troubleshooting and avoiding known pitfalls.

Authoritative and practical, Skin Stem Cells: Methods and Protocols seeks to aid scientists in the further understanding of these diverse cell types and the translation of their biological potential to the in vivo setting.

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Skin Stem Cells - Methods and Protocols | Kursad Turksen ...

"The event reflected the fantastic growing enthusiasm around cell and gene therapy, including small and large companies, investors and regulators. It was great to see everyone so engaged and so positive. The event really gives you the pulse of what is happening right now in cell and gene therapy."

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Great program, great people, great venue.

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Dynamic, interesting and highly interactive event that promotes exchange and networking in highly specialized field of gene therapy.

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"Phacilitate provides a unique forum, bringing together research, process development, and commercial leaders on the cutting edge of cell, gene, and immunotherapy. A great conference for anyone wanting a comprehensive view of the field."

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"It was all business. Ive never been to an event where over 80% of the conversations I had were constructive to my business objectives."

Acquisition & Business Development Manager, BioMedical Materials, Chemelot Campus B.V.

Great way to expand network with global experts in cell and gene therapy who are facing similar challenges.

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Home - Cell & Gene Therapy World 2018 - Meet the Future of ...

Objective: Adrenal insufficiency due to hypopituitarism can lead to severe hyponatremia with potentially fatal consequences. Prompt diagnosis and adequate hormonal replacement therapy are essential to block an otherwise unfavorable course and to re-establish a healthy life. Unfortunately, this condition is often misdiagnosed. Design: Case report. Setting: Intensive Care Unit of a teaching hospital. Patient: A 76-yr-old man with refractory hypotension, acute myocardial infarction, and left ventricular dysfunction, secondary to severe chronic pan-hypopituitarism, associated with severe hyponatremia. Methods and main results: The patient underwent mechanical ventilation and continuous venous-venous hemodiafiltration, for severe respiratory and renal insufficiency. A hormonal replacement therapy with T4, hydrocortisone, and nandrolone was started and the patient was discharged to a rehabilitation facility after 31 days of hospitalization. Conclusions: Hypopituitarism with secondary adrenal insufficiency is often misdiagnosed at an early stage and a high degree of suspicion is necessary for early diagnosis. Determination of plasma cortisol level in patients with hyponatremia not explained by other causes should always be obtained.

Key-wordsHyponatremiapan-hypopituitarismadrenal insufficiencymyocardial infarctionhypothyroidism

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Yatagai T, Kusaka I, Nakamura T, et al. Close association of severe hyponatremia with exaggerated release of arginine vasopressin in elderly subjects with secondary adrenal insufficiency. Eur J Endocrinol 2003, 148: 2216.

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Ishikawa SE, Saito T, Fukagawa A, et al. Close association of urinary excretion of aquaporin-2 with appropriate and inappropriate arginine vasopressin-dependent antidiuresis in hyponatremia in elderly subjects. J Clin Endocrinol Metab 2001, 86: 166571.

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Heneghan C, Goldrick P, Pham H. Management of acute symptomatic hyponatremia. BMJ 1994, 308: 203.

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Goldstein CS, Braunstein S, Goldfarb S. Idiopathic syndrome of inappropriate antidiuretic hormone secretion possibly related to advanced age. Ann Intern Med 1983, 99: 1858.

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Smith JC, Siddique H, Corrall RJM. Misinterpretation of serum cortisol in a patient with hyponatremia. BMJ 2004, 328: 2156.

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Surawicz B, Mangiardi ML. Electrocardiogram in endocrine and metabolic disorders. Cardiovasc Clin 1977, 8: 24366.

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Biondi B, Palmieri EA, Lombardi G, Fazio S. Effects of subclinical thyroid dysfunction on the heart. Ann Intern Med 2002, 137: 90414.

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Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med 2001, 344: 5019.

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Hazouard E, Piquemal R, Dequin PF, Tayoro J, Valat C, Legras A. Severe non-infectious circulatory shock related to hypopituitarism. Intensive Care Med 1999, 25: 8658.

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Al Jarallah AS. Reversible cardiomyopathy caused by an uncommon form of congenital adrenal hyperplasia. Pediatr Cardiol 2004, 25: 6756.

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Francque SM, Schwagten VM, Ysebaert DK, Van Marck EA, Beaucourt LA. Bilateral adrenal haemorrhage and acute adrenal insufficiency in a blunt abdominal trauma: a case-report and literature review. Eur J Emerg Med 2004, 11: 1647.

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Yanagi N, Maruyama T, Arita M, Kaji Y, Niho Y. Alterations in electrical and mechanical activity in Langendorff-perfused guinea pig hearts exposed to decreased external sodium concentration with or without hypotonic insult. Pathophysiology 2001, 7: 25161.

Italian Society of Endocrinology (SIE)2007

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Stem cells have the remarkable potential to develop into many different cell types in the body during early life and growth. In addition, in many tissues they serve as a sort of internal repair system, dividing essentially without limit to replenish other cells as long as the person or animal is still alive. When a stem cell divides, each new cell has the potential either to remain a stem cell or become another type of cell with a more specialized function, such as a muscle cell, a red blood cell, or a brain cell.

Stem cells are distinguished from other cell types by two important characteristics. First, they are unspecialized cells capable of renewing themselves through cell division, sometimes after long periods of inactivity. Second, under certain physiologic or experimental conditions, they can be induced to become tissue- or organ-specific cells with special functions. In some organs, such as the gut and bone marrow, stem cells regularly divide to repair and replace worn out or damaged tissues. In other organs, however, such as the pancreas and the heart, stem cells only divide under special conditions.

Until recently, scientists primarily worked with two kinds of stem cells from animals and humans: embryonic stem cells and non-embryonic "somatic" or "adult" stem cells. The functions and characteristics of these cells will be explained in this document. Scientists discovered ways to derive embryonic stem cells from early mouse embryos more than 30 years ago, in 1981. The detailed study of the biology of mouse stem cells led to the discovery, in 1998, of a method to derive stem cells from human embryos and grow the cells in the laboratory. These cells are called human embryonic stem cells. The embryos used in these studies were created for reproductive purposes through in vitro fertilization procedures. When they were no longer needed for that purpose, they were donated for research with the informed consent of the donor. In 2006, researchers made another breakthrough by identifying conditions that would allow some specialized adult cells to be "reprogrammed" genetically to assume a stem cell-like state. This new type of stem cell, called induced pluripotent stem cells (iPSCs), will be discussed in a later section of this document.

Stem cells are important for living organisms for many reasons. In the 3- to 5-day-old embryo, called a blastocyst, the inner cells give rise to the entire body of the organism, including all of the many specialized cell types and organs such as the heart, lungs, skin, sperm, eggs and other tissues. In some adult tissues, such as bone marrow, muscle, and brain, discrete populations of adult stem cells generate replacements for cells that are lost through normal wear and tear, injury, or disease.

Given their unique regenerative abilities, stem cells offer new potentials for treating diseases such as diabetes, and heart disease. However, much work remains to be done in the laboratory and the clinic to understand how to use these cells for cell-based therapies to treat disease, which is also referred to as regenerative or reparative medicine.

Laboratory studies of stem cells enable scientists to learn about the cells essential properties and what makes them different from specialized cell types. Scientists are already using stem cells in the laboratory to screen new drugs and to develop model systems to study normal growth and identify the causes of birth defects.

Research on stem cells continues to advance knowledge about how an organism develops from a single cell and how healthy cells replace damaged cells in adult organisms. Stem cell research is one of the most fascinating areas of contemporary biology, but, as with many expanding fields of scientific inquiry, research on stem cells raises scientific questions as rapidly as it generates new discoveries.

I.Introduction|Next

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Stem Cell Basics I. | stemcells.nih.gov

Researchers recently determined that an existing drug may protect premenopausal women from infertility following cancer treatments.

A study funded by the National Institutes of Health with findings published in Genetics revealed the benefits of checkpoint protein (CHK2) in mice.

Officials said women treated for cancer with radiation or certain chemotherapy drugs are commonly rendered sterile adding women are born with a lifetime reserve of oocytes or immature eggs but those oocytes are among the most sensitive cells in the body and may be wiped out by cancer treatments.

Investigators said CHK2 functions in a pathway that eliminates oocytes with DNA damage, a natural function to protect against giving birth to offspring bearing new mutations. When they irradiated mice lacking the CHK2 gene, the oocytes survived and eventually repaired the DNA damage, with the mice birthing healthy pups.

It turns out there were pre-existing CHK2 inhibitor drugs that were developed, ironically enough, for cancer treatment, but they turned out not to be very useful for treating cancer, said John Schimenti, the papers senior author and Cornell University professor in the Departments of Biomedical Sciences and Molecular Biology and Genetics. The one major concern is that even though these irradiated oocytes led to the birth of healthy mouse pups, its conceivable that they harbor mutations that will become manifested in a generation or two because we are circumventing an evolutionarily important mechanism of genetic quality control. This needs to be investigated by genome sequencing.

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Drug may reduce female cancer patient infertility risk, according to study - Life Science Daily

On Monday, the Memphis Zoo tweeted about their new baby flamingos the most recent in a long line of zoo babies we've met through the spring and summer.

Let's see ... there's been Winnie the hippo, two giraffes, a sloth, an orangutan, rare Louisiana pine snakes, a Yellow-backed Duiker, aFrancois langur, and a Spot-nosed Guenon named Grommet.

So what is going on? Has there been extra-sexy time at the zoo? Do we need to have a birds-and-the-bees talk with them? Is this all a PR stunt?

Matt Thompson, director of the zoo's Animal Programs, says that while springtime is a time for babies, reproduction at the zoo has been higher than average, and the push to get the public involved has also been higher than average.

The birth rate is all part of a bigger plan, bigger than the Memphis Zoo.

"Theres different programs for different species of animals Species Survival Plan (SSP)," Thompson explains. "For instance, there is a sloth SSP, and a hippo SSP and a giraffe SSP. What that is is a collection of zoo professionals, very smart people who analyze and look at the genetics of different lines of animals, so if the Memphis Zoo, for example, has a certain genetic line and a certain female that would really work well at the Indianapolis Zoo, they might put out a recommendation.They work their hardest to keep the gene pool healthy to prevent inbreeding and that kind of thing."

A prime example of the SSP at work is one little hippo named Winnie.

"Her mother and father both came to us from Disneys Animal Kingdom and they came as a result of an SSP recommendation. It was kind of win-win because Disney was getting a little full with hippos as you can imagine, hippos take up a lot of room," Thompson says. "We were building a new hippo exhibit and we needed a hippo or two, so we reached out to the SSP and they made recommendations based on genetics and thats how we wound up with these animals."

As for birth control, Thompson says it ranges from oral contraceptives to physically pulling the animals apart. And there are accidents. "Sure, just like with people, there are surprises. Not many, but every now and then," says Thompson.

Thompson says there are over 500 SSPs that cover all sorts of animals from pandas to lizards. The coordinator for the SSP for Louisiana Pine snakes, a rare species, is based at the Memphis Zoo.

Some of the toughest animals to breed are amphibians, and, yep, pandas.

"Its not for lack of trying," Thompson says. "Pandas are challenging because they ovulate about once a year and you have about a three-day window for them to get pregnant. Theyve got to tell you when they are ready [and] thats very challenging."

See the article here:
What's Up with All the Zoo Babies? - Memphis Flyer (blog)

A mouse ovary with proteins specific to oocytes labelled in red and yellow. The study reports that culturing such ovaries in the presence of a drug that inhibits DNA damage checkpoint enzymes protects the oocytes from lethal levels of radiation that would normally kill the entire oocyte reserve (small oocytes in picture). Credit: Schimenti Lab, Cornell University

An existing drug may one day protect premenopausal women from life-altering infertility that commonly follows cancer treatments, according to a new study.

Women who are treated for cancer with radiation or certain chemotherapy drugs are commonly rendered sterile. According to a 2006 study from Weill Cornell Medicine, nearly 40 percent of all female breast cancer survivors experience premature ovarian failure, in which they lose normal function of their ovaries and often become infertile.

Women are born with a lifetime reserve of oocytes, or immature eggs, but those oocytes are among the most sensitive cells in the body and may be wiped out by such cancer treatments.

The current study, published in the journal Genetics, was led by John Schimenti, Cornell University professor in the Departments of Biomedical Sciences and Molecular Biology and Genetics. The study builds on his 2014 research that identified a so-called checkpoint protein (CHK2) that becomes activated when oocytes are damaged by radiation.

CHK2 functions in a pathway that eliminates oocytes with DNA damage, a natural function to protect against giving birth to offspring bearing new mutations. When the researchers irradiated mice lacking the CHK2 gene, the oocytes survived, eventually repaired the DNA damage, and the mice gave birth to healthy pups.

The new study explored whether the checkpoint 2 pathway could be chemically inhibited.

"It turns out there were pre-existing CHK2 inhibitor drugs that were developed, ironically enough, for cancer treatment, but they turned out not to be very useful for treating cancer," said Schimenti, the paper's senior author. Vera Rinaldi, a graduate student in Schimenti's lab, is the paper's first author. "By giving mice the inhibitor drug, a small molecule, it essentially mimicked the knockout of the checkpoint gene," Rinaldi said.

By inhibiting the checkpoint pathway, the oocytes were not killed by radiation and remained fertile, enabling birth of normal pups.

"The one major concern," Schimenti said, "is that even though these irradiated oocytes led to the birth of healthy mouse pups, it's conceivable that they harbor mutations that will become manifested in a generation or two, because we are circumventing an evolutionarily important mechanism of genetic quality control. This needs to be investigated by genome sequencing."

When doctors recognize the need for oocyte-damaging cancer treatments, women may have their oocytes or even ovarian tissue removed and frozen, but this practice delays treatment. Also, when women run out of oocytes, women's bodies naturally undergo menopause, as their hormonal systems shift.

"That is a serious dilemma and emotional issue," Schimenti said, "when you layer a cancer diagnosis on top of the prospect of having permanent life-altering effects as a result of chemotherapy, and must face the urgent decision of delaying treatment to freeze oocytes at the risk of one's own life."

The study sets a precedent for co-administering this or related drugs and starting cancer therapy simultaneously, though such interventions would first require lengthy human trials.

"While humans and mice have different physiologies, and there is much work to be done to determine safe and effective dosages for people, it is clear that we have the proof of principle for this approach," Schimenti said.

Explore further: Protein that culls damaged eggs identified, infertility reversed

Journal reference: Genetics

Provided by: Cornell University

Read more:
Drug may curb female infertility from cancer treatments - Medical Xpress

For the new study, which was published in July in Carcinogenesis, researchers at Colorado State University, Memorial Sloan Kettering Cancer Center in New York City and the University of Michigan opted to focus on breast cancer. Epidemiological studies have shown that being physically fit is associated with lower risk for the disease, but not why.

Because they wanted to examine the role of innate fitness in the disease, the scientists turned to a famous strain of rats bred by Lauren Koch and Steven Britton at the University of Michigan. Over multiple generations, these rats were tested on treadmills. Those that ran the farthest before tiring were subsequently mated with one another, while those that pooped out early likewise were paired up, until, ultimately, the pups displayed a large difference in inborn fitness.

The researchers used female pups born to mothers with either notably high or low aerobic capacity. These young animals did not exercise, so their fitness depended almost exclusively on genetics.

Before the pups reached puberty, they were exposed to a chemical known to be a potent breast cancer trigger. The researchers then checked them frequently for palpable tumors throughout adulthood. They also looked, after the animals deaths, for signs of malignancies that had been too small to feel and microscopically examined breast cells for various markers of cell health.

The differences between the animals with high and low fitness turned out to be striking. The rats with low natural fitness were about four times as likely to develop breast cancer as the rats with high fitness were, and showed more tumors once the disease began. They also tended to contract the disease earlier and continue to develop tumors later in life compared with highly fit rats.

The contrasts between the two types of rats continued deep inside their cells. The researchers found almost inverted relationships in how certain aspects of the cells worked, and in particular, in the operation of what is known as the mTOR network. Shorthand for mammalian target of rapamycin, the mTOR network is a group of interlinked proteins within a cell that sense how much energy is available, depending on levels of oxygen and other factors, and let the cell know if there is enough energy around for it to divide and replicate.

In the rats with high fitness in this study, the mTOR networks typically produced biochemical signals that tell cells to avoid dividing much, while in the rats with low fitness, the mTOR networks pumped out messages that would generally promote cell division. Unchecked cell division is a hallmark of cancer.

Past studies have noted that women with breast cancer often show hyperactive mTOR networks.

Of course, this study involved rats, which are not people. But the findings have potential relevance for us, says Henry J. Thompson, the director of the Cancer Prevention Lab at Colorado State University and the studys lead author.

The study underscores the pervasive effects of fitness on bodily health, he says. Even without exercise, the pups born with high fitness were remarkably resistant to breast cancer in this study, he says, and showed fine-tuned cell function.

Most of us are likely to be able to raise our particular innate fitness capacity with exercise, he says.

In future studies, he and his colleagues hope to use the Michigan rats to learn more about the precise types and amounts of exercise that might best augment fitness, especially in those born with low capacity, and the subsequent effects on cell health and cancer risk.

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Fitness May Lower Breast Cancer Risk - New York Times

Dr Undenge

From Walter Nyamukondiwa in KARIBAThe Kariba South Extension Project is now 92 percent complete and on course for commissioning by end of December as Government moves to clear the power deficit.

This is part of an eight-pronged approach to increasing power generation amid indications that about $500 million is being mobilised for the Hwange Life Extension project.

With a daily deficit of between 300MW and 600MW, the shortfall is being reduced progressively.In an interview on the sidelines of the Zimbabwe Institute of Engineers biennial congress here yesterday, Energy and Power Development Minister Dr Samuel Undenge hailed the collaboration between the contractors and Zesa management.

We are very pleased with the progress so far and to date we know that the Kariba South Extension Project is now 92 percent complete and everything is on course for its commissioning on 24 December, 2017, said Dr Undenge.

We applaud the focused work and effort that is being exhibited by the contractor (Sinohydro) and Zesa management that has seen so much progress.

He said initial challenges of foreign currency to pay suppliers were being overcome with the involvement of the Reserve Bank of Zimbabwe. The two new units will add a further 300MW to the national grid.

Zimbabwe has not had load-shedding for the last 20 months, as more than 300MW are being imported to offset the supply deficit.Expansion works and implementation of new projects ties in with regional efforts within SADC to offset the 8 247MW deficit.

This is largely due to lack of meaningful investment in power generation over the last two decades.Zimbabwes major investment in the power sector was in 1987 when Hwange Stage II was commissioned.

Dr Undenge said load-shedding is a major cost and inconvenience to consumers, undermines economic growth and suppresses foreign and local investment.The Hwange Life Extension seeks to recondition the power plant and add another 25 years to its productive life.

There are also plans to increase the thermal plants generation capacity from 550MW to 750MW.Government is implementing eight strategies including optimising existing generation plants, development of renewable energy and conservation among others.

This also includes guaranteeing production at Harare II and III (40MW), Bulawayo (25MW) and Munyati (30MW) thermal power stations.The Energy minister revealed that tendering for the Batoka Gorge South Bank which will add a further 1 400MW to the national grid will be out soon.

In terms of the Batoka Gorge project there are feasibility studies that have just been completed, then tenders will be send out. So that process is underway, said the Minister.

Other projects in the pipeline include the Devils Gorge (1 000MW), Hwange Western Area (1 200MW), Tokwe-Mukosi Hydro (15MW) and Gairezi Small Hydro (30MW).

Dr Undenge said the Minister of Finance and Economic Development Patrick Chinamasa was working on incentives to make investment into the energy sector attractive.

The Minister (Chinamasa) is trying to come up with a regime of incentives so that we make investment into the energy sector by private players more attractive. We need them to augment what Government is doing, said Minister Undenge.

Originally posted here:
Kariba project 92pc complete - The Herald

SEPTEMBER 7, 2017

TWO TRENDS are on the rise, and one is about to make the other worse.

The first is epitomized in a July 2017 report in The Economist on the United Statess urban-rural divide, which noted that deaths of despair suicide, heart disease, and drug overdoses are increasing in the southeastern corner of West Virginia. Life expectancy for men is now 16.5 years lower than in neighboring Arlington. Christian H. Coopers moving essay in Nautilus entitled Why Poverty Is Like a Disease, Karin Goodwins journalism in the Guardian, and James Bloodworths op-ed in New Scientist have piled on additional accounts of how chronic stress and loss of a sense of control can be our undoing.

Meanwhile, in the second trend, biotechs rise, ever more powerful tools are being developed for in vitro fertilization, and for anti-aging and cancer technologies. Some of the latter run to six figures, which means some insurance companies may not cover them.

As economist Thomas Piketty noted in 2014, and so many have since Trumps election, the United States is embroiled in an intensifying era of class struggle, which expresses itself not only in differential impacts on health as pegged to class, but also in the growing unlikelihood that the rural poor, and indeed the poor in general, can securely provide for their children, no doubt a factor in the declining fertility rate. At the same time, the commercialization of science steadily escalates, along with its corollary: the commercialization of human life. Many life scientists hope to start a company and strike it rich. Many have. Entrepreneurial scientists now count themselves among the wealthiest of Americans, and, as the market so freely allows, some of them build their careers on the development and sale of biotech solutions. Offering a route to positive eugenics, longer life, and interventions into deadly diseases, these life-saving and life-enhancing technologies will assuredly widen the public health gap.

First, consider birth. In December 2015, I attended a meeting at the National Academy of Sciences in which a member of the American Society of Reproductive Medicine stood up to proclaim that parents have a right to use the gene-editing tool CRISPR-Cas9 and in vitro, or IVF, technologies to have a genetically connected child. These technologies could be used, he explained, to repair the code for deleterious genes that run in certain families or improve older parents chances of a birth. Bioethicist Hille Haker argued that there is a difference between a negative right, which is a freedom from harm or tyranny, and a full positive right, which is a freedom to access potential benefits. Having a healthy child is a negative right, according to Haker, meaning a right you have unless someone (such as the Chinese government) takes it away, but not a full positive right. If it were a full positive right, society would be hidebound in debt to pay for each of its citizens to have children, applying genetic tests and in vitro techniques as needed. Almost no one would contend that society has such a responsibility, she argued. You may disagree with me, but as an ethicist I put the consequential assessment in terms of rights and obligations, Haker said. There is no right to a genetically related child, it is a high value, not a right.

In August, Shoukhrat Mitalipov, at the Oregon Health & Science University in Portland,controversially became the first scientist in the United States to use the gene modification system CRISPR to alter a human embryo. He modified the gene MYBPC3; when mutated in a single copy of that gene, it can increase your risk for a rare heart condition. Forty-two of the 58 embryos he altered, or 72 percent, had two mutation-free copies of the gene in every cell, and, most importantly, there were no unintended mutations. This study suggests that any technical limitations will soon be overcome, which will then open up a landslide of ethical questions related to equity. Keep in mind that many of us carry a genetic variant that predicts risk for a serious condition. Will insurance companies pay for these gene modifications, and to what extent? Or will the wealthy alone be able to afford to modify their embryos?

This past winter, the National Academy of Sciences and National Academy of Medicine published a report entitled Human Genome Editing: Science, Ethics, and Governance that signals support for gene editing to the heritable, or germline, code, but only in cases where no safer options are available. In her book, A Crack in Creation, Jennifer Doudna, one of the inventors of CRISPR-Cas9, also signaled her openness to CRISPR-ized babies through gene modification.

Already, insurance coverage of in vitro fertilization varies widely by state, and now gene modification techniques may further challenge the concept of what is medically necessary. A mutated APP gene can predict early-onset Alzheimers. A mutated BRCA gene can predict breast or ovarian cancer. A disrupted PCSK9 can lower LDL cholesterol. The Food and Drug Administration actually thinks of CRISPR as a drug rather than a device, so in the United States, CRISPR must pass through a regulatory process for each target it modifies, even in an embryo. For some single-gene or Mendelian diseases such as Tay-Sachs and cystic fibrosis, or the immune disorders NEMO or X-SCID, CRISPR technology could be a fairly straightforward new treatment modality in vitro. Keep in mind, however, that generating an embryo without a heritable mutation can, in the vast majority of cases, already be accomplished by screening embryos before implantation. This raises the question of when CRISPR would be indispensable. In fact, genetic variants in BRCA, which tend to run in high-risk families, are nested in complex so-called epistatic relationships involving the interaction of multiple genetic variants. It would be impossible to know whether altering that single gene reduces cancer in a family in future generations. And if it did, would poor families be able to afford it? Probably not.

Marcy Darnovsky, director of the Center for Genetics and Society in Berkeley, California,and her team have counted as many as 45 countries that ban germline modification. The United States is not one of them, and instead it handles germline editing in vitro much as it does stem cell research by prohibiting funding to scientists to do this research and prohibiting funding to the FDA to review applications for clinical trials of CRISPR babies. We can be sure that entrepreneurial scientists who stand to cash in on such technologies are working to alter such policies. Using gene-editing techniques in a test tube is arguably safer than using gene modification techniques on a living person in a test tube, youre modifying a clump of 64 cells or fewer, rather than trillions of cells, and eliminating the risk of an immune reaction. But those test tube techniques still require genetic diagnostics to know something about a familys risk, not to mention requiring the capital outlay to pay for expensive genetic diagnosis and IVF treatments in short, not particularly realistic or affordable for most of us.

Ultimately, none of this would help living people who develop a disease such as cancer. New technologies such as genetically engineered T-cells combined with CRISPR will enable doctors to coax the bodys immune system into fighting cancer,the first of which wasapprovedonAugust 30, which Novartis will sell in the U.S. for$475,000, a drug price that is nine times the median income in the United States. This means that high-cost medicines will create wealthy scientists and just as surely will exacerbate the health divide. This may be the reality if the Trump administration repeals the Affordable Care Act, but it may also be the reality in a single-payer system such as the National Health Service in Britain, which isnt prepared to pay for these high-priced medicines either. Indeed, oncologist and author Siddhartha Mukherjee warned this summer at the annual American Society of Clinical Oncology meeting about dividing the world into the rich who can afford personalized cancer treatment and the poor who cannot. If health insurance is unequal or inadequate, the only solution may be to use the power of the state to regulate the cost of cancer drugs. A drug price fairness initiative is in fact already on the ballot in Ohio; and transparency laws, established in Vermont, are clarifying their cost. We may have to cap them by executive order.

In the 1970s, Michel Foucault developed the influential notions of biopower and biopolitics, which gave power its access even to the body. In his words, biopolitics is the endeavour, begun in the eighteenth century, to rationalize problems presented to governmental practice by the phenomena characteristic of a group of living human beings constituted as a population: health, sanitation, birth rate, longevity, race. He defines biopower as the techniques for achieving the subjugation of bodies and the control of populations. But even Foucault had yet to conceive of how new biotechnologies could be leveraged. The industrial revolution of the human genome initiates an era in which social divisions are amplified by means of genomics technologies.

Foucault was wrong about some things, such as health and mental illness being solely the result of social forces. But he may have been only partially wrong. As neuroscientist Robert Sapolsky and so many others have noted, stress is distributed unequally across the social spectrum. Hierarchies of wealth and power institutionalize certain forms of stress, including chronic forms, and, according to a spate of recent research, social hierarchies are then embedded in body chemistry through social imprinting. If this research holds up, then it seems clear that we cant undo the damages accrued by years of poverty or poor social status by giving more funding to wealthy scientists. Theres been a clear shift to funding genetics research into mental illness, but the fact is that this research supports the drug-maker model, which then mostly benefits those who control and sell those drugs. It supports their careers through generous amounts of public funding. It does not support the disenfranchised who may need more than drug-based interventions.

The philosopher Nick Bostrom defines transhumanism as the doctrine that

holds that current human nature is improvable through the use of applied science and other rational methods, which may make it possible to increase human health-span, extend our intellectual and physical capacities, and give us increased control over our own mental states and moods.

This not-so-subtle movement includes efforts by the National Institute of Mental Health to monetize the field of psychiatry by basing research on a molecular biomarker or gene target that can be pursued as a diagnostic test or drug target, an agenda that is, in fact, now in retreat because so few reliable biomarkers or targets have actually been discovered. Clinical biomarkers and biochemical transformations have failed to make a dent in suicide rates, not to mention in the incident rates or prognosis of serious psychiatric ills. The most promising discovery coming out of research into psychiatric drugs in recent years may be a street drug called ketamine, or Special K, a worldly knowledge that experts have expropriated from regular folks.

As for the budding life-extension industry, it is built around over-the-counter drugs, such as nicotinamide mononucleotide (NMN), and the development of new drugs to degrade proteins that build up in brains and are associated with age-related diseases such as Alzheimers and Parkinsons disease. In 2013, the Time magazine cover story Can Google Solve Death? became part of the transhumanist spectacle when it noted that, for CEO Larry Page, solving cancer may not be a big enough task. The article introduced life extension company Calico, which is currently working on ways to degrade proteins that build up in the brain and are correlated with age-related diseases. But insurers may not have an incentive to pay for life-extension techniques that add bonus years, since insurance is more costly when we are older. As a result, these pursuits only contribute to the trope that life extension is a luxury pursued by wealthy Silicon Valley entrepreneurs stymied by their own loss of control. The most potent real news is precisely the connection between income and longevity. In short: The fact that such studies have led to no major societal shifts in how we value life suggests that the longevity that drug makers pursue as a financial prospect is solely about extending life for the wealthy.

An urgent question, therefore, is the following: Are our scientific institutions working on behalf of the public and fairness, and so of distributive justice, or are they working for commercial interests? And another disturbing question: Are these interests being normalized before we can even debate them? The fact that scientists themselves like to appeal to economic interests when asking for public funding should offer one clue. And of course it doesnt help that scientists want to sell us stuff.

In the famous 1971 Chomsky-Foucault Debate, Foucault argued that those who take up social justice causes are in fact doing so only because they want to take power. Chomsky demurred:

I think its too hasty to characterize our existing systems of justice as merely systems of class oppression [] they also embody a kind of groping towards the true humanly valuable concepts of justice and decency and love and kindness and sympathy, which I think are real.

Of course, institutions can be applied to advance justice and fairness, or be exploited for special interests. If authority is broadly distributed and innate to the wellsprings of the mind, then institutions are an extension of principles that reside within us and should seek to ensure access and fairness. But if scientists are working toward selling biotech solutions at the highest price the market will allow, then scientific institutions may be exploited for power and profit and thats just capitalism.

The irony is that we may need the state to ensure fair access to medicines we fund, and to prohibit genetic enhancement or reproductive advantages if all of us cant afford or access them. This is no small problem. Political scientist Francis Fukuyama called transhumanism the worlds most dangerous idea, suggesting that the commercialization of biotech would create increasing unfairness. In his book Our Posthuman Future, he qualifies his original end of history thesis, arguing that human genetic engineering and in vitro fertilization might perpetuate social divisions, putting liberal democracy at risk. If there is one imperial power left on the world stage, Fukuyama argues, it is biotech. What should we do in response to biotechnology that in the future will mix great potential benefits with threats that are either physical and overt or spiritual and subtle? he asks. The answer is obvious: We should use the power of the state to regulate it.

Here are some recommendations: the price of biologic medicines (gene and cell therapies) should be fixed or capped that is, if the public is expected to subsidize their cost through National Institutes of Health funding. If that sounds too much like socialism, then we need to stop socializing the costs and risks of drug development through NIH funding. A second point: The federal legislators and the FDA should have strong regulatory control over the creation of gene modifications to the heritable code of newborns. For the moment, they are able to constrain those enterprises as mentioned earlier, the FDA regulates gene modifications as a drug, and any specific target must pass through an extensive regulatory process. Once approved, then some sort of public insurance must make them accessible to everyone, or else biotech will assuredly exacerbate social and economic inequality, thus affecting the Freedom Index in the United States.

Scientists are readily using taxpayer funding to advance their own economic interests, thereby institutionalizing power and wealth. Indeed, many managerial scientists count themselves among the wealthiest Americans with annual salaries in the six and seven figures. If the state has a role, it is to live up to the ideals which we are groping towards, the concepts of justice and decency, rather than the current reality of scientific institutions seeding biotech startups. The fact is that scientists are increasingly testing public trust. Whether they should continue to receive tax-exempt funding ought to depend on whether they are working toward fair and equal access to medicine, lest by the time science funding reaches a commercial shelf, life is simply up for sale.

Jim Kozubek is the author ofModern Prometheus: Editing the Human Genome withCrispr-Cas9,published by the Cambridge University Press.

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Biopower in the Era of Biotech - lareviewofbooks

The cost approach requires the identity and quantification of three types of obsolescence physical, functional and economic. Assessors frequently account only for physical depreciation (although some assessors/appraisers apply a special factor in an attempt to capture functional and economic obsolescence). Physical depreciation is dependent upon accurately determining: (1) the effective age, which is the chronological age or the weighted chronological age (if physical improvements have been made) adjusted for physical condition; and (2) the appropriate service life of the facility (some also measure and apply remaining life). Needless to say, an assessor/appraiser can increase a propertys value by misstating any one of these factors. So, the taxpayer must closely review the assessment process to make sure that each factor reflects market realities and the facilitys physical condition. It is also essential that the assessor/appraiser apply an appropriate service life that considers the major components of the facility and their interaction on the life of the facility. A purchaser of the building only recognizes value to the extent that the building can continue to produce profitable net operating income at a required rate of return. An example is an old K Mart or Sears building. Physically, for retail purposes, they are likely to have short term life, as major reparations are likely necessary to make the facilities operable in todays demanding retail environment. Nonetheless, taxing jurisdictions often apply longer physical lives that are based on the effect of such reparations (i.e., life extension); even though, they have not yet been incurred and without accounting for their cost. This artificially boosts the facilitys valuation.

Bottom line, if the taxpayer does not accurately identify and quantify the physical age, condition and service life, its property will continue to be over valued by the assessor/appraiser. If economic life is applied, the appraiser needs to recognize and quantify the other non-physical forms of obsolescence captured in the economic life to avoid double counting.

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Beware of the Overstated Service Life in the Cost Approach - Lexology (registration)

The U.S. Coast Guard Cutter Eagle moors at Point Lumley Park in Old Town Sept. 4, marking the first time in 11 years that the vessel known as Americas Tall Ship returned to the Washington area.

Alexandria For the first time in 11 years, the U.S. Coast Guard Cutter Eagle arrived in the

Washington area, mooring at Old Towns Point Lumley Park Sept. 4 as part of the tall ships summer deployment.

Also known as Americas Tall Ship, Eagle is the largest tall ship flying the U.S. flag and the only active commissioned sailing vessel in American military service. Eagle is the only square-rigger in the U.S. military services and is used to train students at the U.S. Coast Guard Academy in New London, Conn.

The Eagle has a fascinating history, said Old Town resident Hal Hardaway after touring the vessel Sept. 5. Eagle was hull #508 built in the Blohm and Voss shipyard in Hamburg in 1936. That yards next hull # 509 was Bismark.

Alexandria is Eagle's final stop in its summer deployment, which has spanned

five months and included 14 ports, including multiple ports along the Eastern Seaboard, Canada and Bermuda.

Also known as the Coast Guard Barque Eagle, the ship left Baltimore April 26 bound for New London to commence the 2017 cadet summer training program. Eagle and her crew, including Capt. Matthew Meilstrup as commanding officer, have been at the Coast Guard Yard facility in Baltimore as part of a Service Life Extension Project that will keep the ship away from its home port of New London for several years.

The ship was built in 1936 in Germany and commissioned as Horst Wessel, one of three sail training ships operated by the pre-World War II German navy. At the close of World War II, Horst Wessel was taken as a war reparation by the United States, recommissioned as the U.S. Coast Guard Cutter Eagle and sailed to New London. The vessel is used for at-sea leadership and professional development training for future officers of the U.S. Coast Guard.

Eagle is scheduled to depart Point Lumley at approximately 4:30 a.m. Sept. 8. The Woodrow Wilson Bridge span will be raised at that time to allow Eagle to sail through as it makes its return to Baltimore.

For more information, visit http://www.cga.edu/eagle.

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'America's Tall Ship' - Virginia Connection Newspapers