StemCell Therapy

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Zika Grabs Neural Stem Cell Protein to Cause Damage The Scientist The presence of the Musashi-1 protein greatly increases production of Zika virus (green), making neural stem cells particularly vulnerable to cell death following viral infection. GENERATED BY THE GERGELY LABWhen the Zika virus enters neural stem cells ... New insights into how the Zika virus causes microcephalyMedical Xpress New insights into how Zika causes microcephalyWellcome Trust all 3 news articles »

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Zika Grabs Neural Stem Cell Protein to Cause Damage - The Scientist

June 1, 2017 by Peter Tarr Researchers have discovered that a chromatin-regulating protein called BPTF must be present for stem cells in the breast to perform their normal functions maintaining a supply of stem cells and seeding the breast with specialized new cells when needed, for instance, during pregnancy. At the mouse equivalent of mid-pregnancy, there is normally (left side) a proliferation of milk ducts (the small purple structures in both images). When BPTF is knocked out in mouse mammary stem cells early in pregnancy, however, there is a drastic decline in the number ductal structures (right side). Dos Santos and colleagues suggests that knocking out BPTF in breast cancer cells could suppress or kill them. Credit: dos Santos lab, CSHL

For years, cancer experts have realized that cancerous cells behave in certain ways like stem cells, unspecialized cells that when exposed to certain signals, can "differentiate."

When a stem cell differentiates, it starts down a one-way path that will result in its specialization and eventually its death. For instance, a stem cell in the breast can become a luminal cell, one of the breast's "milk factories." Such cells have a limited life span. Cancer cells resemble stem cells not because they can turn into other cell types, but because in developmental terms, they seem to go in the opposite direction: they begin to run through multiple layers of stop signs and barricades and just keep on multiplying.

Assistant Professor Camila dos Santos of Cold Spring Harbor Laboratory (CSHL) is studying stem cells in the breast for clues about what changes occur when normal breast cells become cancerous. Today, a team led by dos Santos, in collaboration with Assistant Professor William Pomerantz at the University of Minnesota and Professor Gregory Hannon of Cancer Research UK, Cambridge Institute, identify a protein that they show must be present in order for mammary stem cells to perform their normal functions.

When the researchers genetically removed or chemically inhibited the protein, called BPTF, stem cells could no longer maintain their "renewing" state and began to take on the character of specialized breast cellsand then soon died.

"That was very exciting for us," says dos Santos, "because that's exactly what we want to drive breast cancer cells to do. We want to take away their stem cell-like qualitiesespecially their ability to multiply indefinitely. We are testing the idea that a drug that inhibits BPTF might have the same effect in cancer cells as in stem cellsit could cause them to differentiate and then die."

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When studying how normal cells change into cancer cells, dos Santos and other cancer researchers pay close attention to gene expression. Every cell in the breast, including stem cells, contains the full human genome. One way of thinking about what differentiates a breast cell from a heart cell is that each cell type expresses different subsets of genes.

The same is also true within each organ. In the breast, the ducts designed to carry milk during and after pregnancy are composed of two highly specialized cell types and a niche of stem cells that gives rise to both types. Each of these different cell types expresses different groups of genes at different times over the lifespan of an individual.

As the illustration below indicates, the hollow "tube" that forms the milk duct is built from luminal cells; these are surrounded by a thin layer of cells called myoepithelial cells. Receptors on the surface of the myoepithelial cells are designed to interact with a hormone, oxytocin, released during lactation. This interaction causes the myoepithelial cellson the outer layer of the ductal structureto contract, squeezing the luminal cells within. Those luminal cells are the breast's milk factories.

BPTF's epigenetic role in exposing and hiding genes

BPTF, identified by dos Santos and colleagues as essential for mammary stem cell maintenance, is a protein with a very specialized function. It is what biologists call a chromatin remodeling factor. Chromatin is the packaging that enables six linear feet of DNA in each of our cells to be compressed inside the microscopic nucleus.

With so much DNA squished into such a small space, it stands to reason that expressing a gene in the "middle" of the bundle might require loosening the packing material to expose that segment of DNA to the machinery that copies it into an RNA molecule. This copying is the first step in using the gene's "blueprint" to manufacture a needed protein. Chemical modifications to chromatinand even more specifically, to the histone proteins that provide "spools" around which the DNA is woundare called epigenetic modifications.

"It has become very clear that the opening up or tightening of chromatin, to expose or hide genes in our chromosomes, plays a role in cancer progression," dos Santos says. "For instance, exposing a gene at a particular moment might help a cancer cell bypass a 'stop sign' in a growth pathway."

The research published today shows that BPTF is part of a regulatory system that opens chromatin and changes gene expression, specifically in mammary stem cells. This opening of the chromatin turns out to be critical in the ability of the stem cell to remain "immortal"to give rise to daughter stem cells that will also help maintain a tissue such as the breast, and seeding it, at different times of life, with specialized cells. For example, during puberty, when the breast develops, or during pregnancy, when the breast gears up to produce milk.

"We now know that mammary stem cells are highly dependent on BPTF. The next task is to explore if can we use that dependency to target stem cell-like programs in breast cancer cells," dos Santos says.

The research discussed here was supported by CSHL Cancer Center Support Grants 5P30CA045508 and 5P30CA045508-28; P01 award #2P01CA013106; the Sidney Kimmel Cancer Foundation; the Pershing Square Innovator Award; the Rita Allen Scholar Award; the V Foundation Scholar Award; and the Manhasset Coalition Against Breast Cancer Award.

"BPTF maintains chromatin accessibility and the self-renewal capacity of mammary gland stem cells" appears online June 1, 2017 in Stem Cell Reports. The authors are: Wesley D. Frey Anisha Chaudhry Priscila F. Slepicka, Adam M. Ouellette, Steven E. Kirberger, William C. K. Pomerantz, Gregory J. Hannon and Camila O. dos Santos.

Explore further: Study identifies RNA molecule that shields breast cancer stem cells from immune system

More information: "BPTF maintains chromatin accessibility and the self-renewal capacity of mammary gland stem cells" Stem Cell Reports, 2017.

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A protein that stem cells require could be a target in killing breast cancer cells - Medical Xpress

What is retinitis pigmentosa?

Retinitis pigmentosa, also known as RP, refers to a group of inherited diseases causing retinal degeneration. The retina is a thin piece of tissue lining the back of the eye. It converts light into electrical signals that the brain interprets as vision. People with RP experience a gradual decline in their vision, because photoreceptor cells in the retina degenerate.

Forms of RP and related diseases include Usher syndrome, Leber congenital amaurosis, and Bardet-Biedl syndrome, among others.

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Symptoms depend on whether rods or cones are initially involved. In most forms of RP, rods are affected first. Because rods are concentrated in the outer portions of the retina and are triggered by dim light, their degeneration affects peripheral and night vision. When the disease progresses and cones become affected, visual acuity, color perception, and central vision are diminished.

Night blindness is one of the earliest and most frequent symptoms of RP. People with mainly cone degeneration, however, first experience decreased central vision and reduced ability to discriminate colors and perceive details.

RP is typically diagnosed in adolescents and young adults. It is a progressive disorder. The rate of progression and degree of visual loss varies from person to person. Most people with RP are legally blind by age 40, with a central visual field of less than 20 degrees in diameter. It is a genetic disorder and, therefore, is almost always inherited.

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An estimated 100,000 people in the U.S. have RP, mainly caused by gene mutations (variations) inherited from one or both parents. Mutated genes give the wrong instructions to photoreceptor cells, telling them to make an incorrect protein or too little or too much protein. (Cells need the proper amount of particular proteins in order to function properly.) Mutations in dozens of genes have been linked to RP.

Genetic mutations can be passed from parent to offspring through one of three genetic inheritance patterns autosomal recessive, autosomal dominant, or X-linked.

In autosomal recessive RP, both parents carry one copy of the mutated gene, but have no symptoms themselves. Children have a 25 percent chance of being affected by inheriting a mutated copy from each parent.

In autosomal dominant RP, usually one parent is affected and is the only parent with a mutated gene. A child has a 50 percent chance of being affected through the inheritance of the mutated gene from the parent.

In families with X-linked RP, the mother carries the mutated gene on an X chromosome, and her sons have a 50 percent chance of inheriting the condition. Daughters have a 50 percent chance of becoming carriers and arent usually affected. However, some daughters are affected sometimes mildly, sometimes severely.

If a family member is diagnosed with RP, it is strongly advised that other members of the family also have an eye exam by a physician who is specially trained to detect and treat retinal degenerative disorders. Genetic counselors are excellent resources for discussing inheritability, family planning, genetic testing, and other related issues.

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Genetic testing is available for RP. It helps assess the risk of passing the disorder from parent to offspring. It also helps with attaining an accurate diagnosis. A patient with an accurate diagnosis is in a better position to keep track of new findings, research developments, and treatment approaches.

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The Foundation is supporting several promising avenues of research, including gene, stem-cell, and drug therapies.

For the latest research advances for RP, refer to the Foundation publication Retinitis Pigmentosa: Research Advances.

This information was made possible through generous gifts from people like you. Please click here to make a donation to the Foundation.

*Images courtesy of the National Eye Institute, NIH

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Retinitis Pigmentosa | blindness.org

American sanctuary cities are established by politicians who presumably seek to protect illegal immigrants from what they see as inhumane U.S. deportation policies. But by ignoring federal requests to detain them, and instead releasing suspected and convicted illegal aliens back into the community, sanctuary cities open their doors wide to the creation of a wave of additional victims in their own communities.

To appreciate the threat, look no further than the tragically avoidable murder of Kate Steinle in sanctuary city San Francisco. Kates killer, Juan Francisco Lopez-Sanchez, was deported from the U.S. five times, was on probation, and had seven felony convictions. He used a stolen government handgun to fire three shots, one of which ended Kates life on a city pier. The San Francisco sheriffs office had opted to put Lopez-Sanchez back on the street rather than handing the felon over to ICE.

Few cases are as tragic and expose the risks more clearly than Kates, which demonstrates the fact that subsequent crimes committed by criminal illegal aliens released despite the existence of ICE detainers are preventable. And the very evident risks to those new victims are what sanctuary cities willfully ignore.

There are hundreds of jurisdictions with sanctuary policies across the country. More and more are loudly vocal about their resistance; their primary cry is to accuse the Trump administration of leading a frontal attack on millions of illegal immigrants who are merely trying to eek out an existence in a better place than their homeland. In truth, the Administration is attempting to rid the country of the relatively few criminal illegal aliens whove chosen to prey on our citizens and on other undocumented aliens. To succeed, they need the assistance of state and local law enforcement authorities.

Sanctuary cities defy federal immigration authorities detainer requests, citing the reality that immigration is a federal responsibility and claiming the Feds cant impose their responsibilities on local officers without their consent. Simply put, the performance of a federal job in immigration enforcement by state and local jurisdictions is voluntary.

But the Federal government can encourage local support of immigration enforcement by conditioning the receipt of certain federal funds on cooperation with immigration functions. ICE detainers are one of the primary means used to identify and remove criminal illegal aliens from the interior of the United States. But when local sanctuary policies obstruct or ignore detainer requests and release criminal aliens back into the community, the communities are anything but more safe as a result.

A Department of Justices (DOJ) analysis in October 2014 showed that between January 1 and August 31, 2014, ICE documented 8,145 declined detainers covering individuals in 276 counties in 43 states including the District of Columbia. Of the 8145 illegal immigrants for whom detainers were declined, more than 5000 (62%) were previously charged or convicted of a crime or presented some other safety concern. Almost 3000 had prior felony charges or convictions and almost 2000 had prior misdemeanor convictions or charges to include those related to violence, threats, assaults, sexual abuse and unlawful possession of firearm or other deadly weapon.

Thats 60% of the releasees known to have committed prior crimes. Of course another segment certainly did commit prior crimes but had yet to be identified or charged. An acceptable risk? Release policies that somehow make the community safer? Not at all.

Recidivism in the illegal immigrant community can be every bit as common as in the broader population. The DOJ report also found of those 8,145 releasees, 23% had a subsequent criminal arrest and were charged with 4,298 offenses in just the eight month period covered by the report.

The bigger picture is grimmer. A separate DOJ report on recidivism tracked over 400,000 prisoners released in 30 states in 2005 and followed for five years.

The report found more than two thirds of the prisoners were rearrested within three years of release and more than 75% were rearrested within five years. The 400,000-plus prisoners followed accounted for almost 1.2 million arrests. Translating that recidivism rate to released criminal illegal immigrants in the DOJ study suggests over 6200 would be rearrested within five years, responsible for more than 18,000 total arrests.

The DOJ detainer report documented egregious crimes committed by criminal illegal aliens on unsuspecting, law abiding people to include murder, child sexual abuse, rape, resisting an officer causing death or severe bodily injury and other serious crimes.

Criminal illegal aliens held in sanctuary city jails, including those with a litany of prior crimes, are being released into our communities. They will commit future crimes resulting in death, sexual assault, robbery, burglary and others. They will cause great physical and psychological harm to Americans and other illegal immigrants alike. The future crimes are preventable if communities wake up to their obligation to protect their own citizens first.

No family should suffer the same fate as Kate Steinles.

W. Stephen Thayer is an associate of the Law Enforcement Action Network, a former U.S Attorney and New Hampshire Supreme Court justice.

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The Willful Blindness Of Sanctuary Cities - The Daily Caller

In a world first, surgeons in the Chinese city of Zhengzhou are planning to inject stem cells derived from human embryos into the brains of patients with Parkinson's disease with the aim of treating their debilitating symptoms.

Meanwhile, another medical team in the same city is aiming to target vision loss using embryonic stem cells (ESC) to replace lost cells in the retina, marking a new direction in China in the wake of major changes in how the country regulates stem cell treatments.

While similar treatments on Parkinson's patients have already been tested in Australia, those trials relied on cells taken from eggs that were forced to divide without first being fertilised in an effort to circumvent any ethical concerns.

Stem cells are a little like blank slates that are yet to take on a specific task. If you rewind the clock on any of your body's tissues, its cells will become less specialised, until you're left with a cell with a lot of potential to become nearly anything.

In the case of both kinds of embryonic stem cells, divided egg cells are subjected to various treatments to encourage them to develop into replacement cells that could treat a condition in a recipient.

The symptoms of Parkinson's disease are largely caused by a loss of nervous tissue deep inside the brain in an area called the basal ganglia.

Losing those cells means a loss of a neurotransmitter called dopamine, and with it a lower ability to control nervous impulses that would prevent muscles in the extremities from activating.

In the case of a condition called macular degeneration, damage to a layer of tissue called the retinal pigment epithelium at the back of the eye causes the light-catching cells above it to die.

By turning ESC into cells that can naturally develop into the tissues that have deteriorated such as the precursors to neurons that can produce dopamine, or into retinal tissue and then injecting it into the target site, the researchers hope to improve the lost functions.

Not everybody is convinced of the success of trials such as those being done in China and last year in Australia.

A stem cell biologist from the Scripps Research Institute in California, Jeanne Loring, believes the choice of cell used in both Parkinson's disease trials won't be specialised enough to match expected results.

"Not knowing what the cells will become is troubling," Loring told David Cyranoski at Nature.

But the research team in China remains confident in its decision.

Qi Zhou from the Chinese Academy of Sciences Institute of Zoology in Beijing is the stem cell specialist leading both sets of ESC trials, and says four years of animal trials conducted on monkeys have so far showed promising results.

"We have all the imaging data, behavioural data, and molecular data to support efficacy," Zhou told Nature.

He also claims the team conducting the Parkinson's trial have been selective with their potential candidates, choosing patients who will have the least chance of rejecting the ESCs from the cell bank.

In 2015, China introduced tough new regulations to deal with the growing problem of 'rogue clinics' offering stem cell treatments without due record keeping or process, making it hard to evaluate safety, or even the types of cells used in the treatments.

The changes are set to improve the ethics and safety of stem cell treatments by enforcing the use of cells through a regulatory body, ensuring informed patient consent, and permitting treatments only through authorised hospitals.

Time will tell if the regulations can be enforced, but for stem cell researchers, the changes are positive.

"It will be a major new direction for China," stem cell scientist Pei Xuetaotold Nature.

If the results are as good as the teams in Australia and China predict, it could also set new standards for the world.

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World-first trials have been launched to treat Parkinson's and ... - ScienceAlert

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Fiction Blindness and Rage: A Phantasmagoria Brian Castro Giramondo, $26.95

Throughout a distinguished career that began in 1983 with Birds of Passage, Brian Castro has consistently played intricate games with language and with literary and cultural allusions. This playfulness often extends to echoes of the lives and works of writers as diverse as Kafka (notably in After China) and, in Drift, the little-known English experimental novelist B. S. Johnson, who died in 1973.

Many diverse elements enter into the fabric of Castro's always intriguing though sometimes opaque works. Looking back over his career, it seems that finding the appropriate form for his often unusual preoccupations hasn't always been successful. There often seems to be a conflict between the demands of narrative and what really engages Castro's intellect and imagination.

His latest work has, I think, found a solution to that conundrum. Described as "a novel in 34 cantos", Blindness and Rage recounts the adventures, mostly in Paris, of the Adelaide-based writer-cum-town-planner Lucien Gracq. Cast mostly in a kind of free verse made up of lines of different lengths with the frequent use of rhymes, half-rhymes, internal rhymes and alliteration this form gives Castro greater scope for doing what he seems to like doing best, and is often very good at doing.

Blindness and Rage hops from arcane topic to arcane topic, from Adelaide to Paris to China and Hong Kong with a disarming nonchalance unconstrained by the need to tell a coherent tale. Not all of it is completely comprehensible, at least on a first (or second) reading, but most of it is lively, striking and even exhilarating.

The narrative, such as it is, is straightforward enough. Gracq has been diagnosed with a terminal liver condition. He decides to spend his last days numbering 53 he'd been assured, he insists several times in Paris.

He moves into a small flat near the Jardin des Plantes, and comes into contact with a shadowy group of savants, Le club des fugitifs, which offers writers who are about to die the chance to ascribe their last work to another person. Gracq is accepted into the club, intending to bestow on it his epic poem based on cultural and anthropological theories of play. He also has a brief flirtation with Catherine Bourgeois, a concert pianist, whose flat is on the same landing as his.

Castro constructs a bewildering array of allusions, quotations, literary jokes and puns around this narrative kernel. They are far too many to detail in a short review. Here are a few. At one stage Gracq considers travelling to Amsterdam to enlist the services of "the infamous Dr Nietzsche" and his euthanasia-computer. There are references to Pushkin and Kafka again, to modern French writers such as Georges Bataille and to the 18th-century pornographer Restif de la Bretonne, de Sade's antagonist. One could go on and on.

The topography of Paris also provides important elements to this "phantasmagoria", none more so than the area around the Jardin des Plantes. Gracq rents a flat at 11 Rue Linne. As it turns out the "Fugitives" hold their raucous meetings next door at No.13. The man who acts as Gracq's sponsor is called Georges Crepe their first meeting took place in a creperie near the place where 16 Carmelite nuns were guillotined in 1794.

Such random bits and pieces come together, as often with Castro, in the literary figure standing behind Gracq's adventures. Georges Perec (his surname an anagram, of course, of Crepe) spent the last years of his life at 13 Rue Linne. He was a member of OuLiPo, an eccentric group of writers, almost all of whom flit across the pages of Blindness and Rage.

Finally, Gracq was told he had 53 days left to live when he moved to Paris, and Perec's last, unfinished, work was a novel entitled 53 Days, conceived during the 53 days he spent in Australia a few months before his death. Fifty-three was also the number of days Stendhal supposed to have needed to write The Charterhouse of Parma, a factoid that might have inspired both Castro and Perec.

After all this, read Blindness and Rage and prepare to be enthralled and sometimes exasperated.

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Blindness and rage review: Brian Castro plays his customary literary ... - The Sydney Morning Herald

MF Global failed on a trade that would have made it enormously profitable. AIG's (NYSE:AIG) portfolios of "toxic waste" ended up making money - for the Federal Reserve. Bear Stearns and Lehman Brothers were ended like the others by liquidity, not losses. SemGroup (NYSE:SEMG) was another firm that went into bankruptcy during that period, but one that practically no one has heard of. It failed for largely the same deficiency.

Based in Tulsa, Oklahoma, SemGroup at one time employed 2,000 people in ostensibly the oil distribution business. The company handled 500,000 barrels of crude a day through two pipelines, using its 6.7 million barrels of storage capacity to do what oil companies do. Almost all that capacity was located in Cushing, Oklahoma, today's dumping ground for energy making up the WTI benchmark.

It wasn't the oil business specifically that ruined SemGroup, but rather oil trading. The company and especially senior management were convinced the oil market was behaving irrationally all throughout 2007 and into early 2008. There was, in their estimation, simply no reason for skyrocketing prices. They bet against it; heavily. The company was short so much oil that at one point corporate headquarters skimmed $54 million from a $120 million loan provided by GE Capital to build a pipeline from Colorado to Cushing to cover margin to maintain their shorts.

As is usually the case, SemGroup just couldn't withstand the collateral calls on them as WTI, Brent, and every other benchmark seemed headed, unreasonably, to the moon. They made one final, enormous short, one that would pay off to the tune of $5 billion - if only they could make it just two more weeks. The company couldn't, and on July 22 it was forced into bankruptcy court just days before it would have been proved fabulously correct about the oil market.

On July 15, 2008, Ben Bernanke testified before the Senate opining, wrongly, as usual, on many topics including oil prices. In his remarks, the Fed Chairman sketched out what sounded like balanced risks; weakness due to housing but with inflation that could keep on rising, as if the two opposing forces would somehow yield a Goldilocks result where the US might avoid recession altogether by nothing more than luck.

However, in light of the persistent escalation of commodity prices in recent quarters, FOMC participants viewed the inflation outlook as unusually uncertain and cited the possibility that commodity prices will continue to rise as an important risk to the inflation forecast. Moreover, the currently high level of inflation, if sustained, might lead the public to revise up its expectations for longer-term inflation. If that were to occur, and those revised expectations were to become embedded in the domestic wage- and price-setting process, we could see an unwelcome rise in actual inflation over the longer term.

The possibility of higher energy prices, tighter credit conditions, and a still-deeper contraction in housing markets all represent significant downside risks to the outlook for growth. At the same time, upside risks to the inflation outlook have intensified lately, as the rising prices of energy and some other commodities have led to a sharp pickup in inflation and some measures of inflation expectations have moved higher.

What some people took away from that testimony was that the Fed was out of the "stimulus" business any more than they were already forced into up until and immediately after Bear Stearns. Whatever slim hope there might have been on the inside of money markets for a further necessary rescue disappeared. The Fed, as Bernanke described, felt it warranted to worry about weak demand as well as commodity prices going the other way, hoping in the best case that the two would just cancel each other out avoiding recession altogether.

It was a fundamental error, of course, on many accounts, not the least of which was the precarious state of overall economic demand being led downward by a global money system that persisted in a state of malfunction. Bernanke had essentially fooled himself into thinking that things weren't so bad after all, and the oil market helped him into that position for reasons that SemGroup was right to suspect.

Oil prices rose throughout 2007 and early 2008 on the idea that the Fed would overdo its response. It was widely believed that the central bank could achieve a resolution, and in being careful given the gravity of the situation would err too far on the side of "stimulus."

It was predicated on nothing more than the idea that interest rate cuts were liquidity, or at least the impetus for the private system to provide it. Yet, from August 9, 2007, forward, there was in several key prices a constant reminder that this just was not the case. Apart from monetary conditions, it worked out the same way in economic statistics where in the mainstream, nurtured by Bernanke's optimism as well as oil prices, often severe economic warnings were simply dismissed in favor of optimism for no other reason than this conditioned disbelief.

The oil market was irrational, and in mid-July 2008, it started to become rational again. It was too late for SemGroup, but what is relevant to our current condition is that irrationality in terms of some expectations would continue. In November 2008, for example, a Time Magazine article even blamed the prospect for a bankruptcy liquidation in SemGroup assets for the drastic drop in oil prices.

Clearly, demand for oil didn't fall that much, but the price of oil isn't set by demand alone. It's the product of an extremely volatile mixture of speculation, oil production, weather, government policies, the global economy, the number of miles the average American is driving in any given week and so on.

No, oil demand did fall by that much and would fall much further before it was all over. Economic demand not only cratered, it has yet to recover almost nine years later, leaving oil investors as well as economic commentary stuck in a conundrum that really isn't one. Just like the Fed has more recently created a puzzle out of the very low unemployment rate and the lack of wage growth, explanations for oil's lack of follow-through into full reflation always contain the same color of 2008-type mistakes. It is almost certainly recency bias where now the word "recency" doesn't really apply. People just can't (or won't) believe at these times the world could be stuck in such a bad place.

For oil in 2017, it takes on more than just shale or OPEC proportions. Crude prices are it, and have been "it" in both directions. The collapse in late 2014 was a crucial signal about global prospects, which again officials all over the world tried their best to characterize as something it wasn't ("supply glut"). The same to a lesser extent has happened again, this time over-emphasizing the rise in oil prices from the February 2016 trough as more than it is - or was.

That flirtation, however, has now ended; at least with oil trading in a clear downward pattern going all the way back to late February (lower highs and lower lows).

Psychologically, while it aided "reflation" in that oil prices were up on an annual comparison basis, as of now, they no longer are. The closing price today is slightly less in WTI than the closing price on May 31, 2016. I have written before that oil prices were not really up, they were merely down less than last year. Now even that first part is no longer technically true. Year-over-year WTI has regained its minus sign.

This is no trivial matter for oil as well as broader matters. The Fed searches for inflation because the unemployment rate is 4.5% when this renewed downward comparison in oil tells us exactly why they won't find it. As in 2008, they are looking for demand that simply isn't there.

Even the oil futures curve demonstrates as much. Though it remains in slight contango, the curve of late has slipped entirely below $50. That is an enormously pessimistic take on oil fundamentals, and one that is different proportionally than the more-in-contango curve earlier this year under the sentimental upturn of "reflation."

In truth, unlike the irrationality of oil in early 2008 the trajectory of oil prices has been far more rational this time around. It surged from the bottom, but for a full year now has traded almost perfectly sideways. Like so many other economic accounts, it is conspicuous only for the lack of further momentum when by all historical expectations it and the global economy should be well into unmistakable recovery.

I have to believe that the lack of further price gains have been because unlike nine years ago by now the oil market is totally aware of how powerless the Federal Reserve actually is; and that liquidity, meaning global money, and therefore economic considerations, are completely unlike how all are characterized (glowingly) in the mainstream. After all, the price collapsed at the very moment Janet Yellen and all those economists like her were most sure demand was about to truly take off, and that under QE there was no possible way for further deflation or disinflation caused by dangerous monetary illiquidity.

Bernanke in July 2008 was using a world that didn't actually exist to make all the wrong moves and say all the wrong things. Somehow, after so much time and proof, a great many people still don't see it.

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Systemic Blindness - Seeking Alpha

Centre Daily Times

Aaronsburg man doesn't let blindness slow him down Centre Daily Times And heavy too, at least judging by the size of the equipment eating up space in Ron Ream's barn-turned-wood-working emporium. Ream was gracious enough to give me a guy who once nicked himself on a rolling pin a rundown of some of the grizzlier ...

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Aaronsburg man doesn't let blindness slow him down - Centre Daily Times

June 1, 2017 An off-the-shelf contact lens with a gold trace and a specially equipped pair of glasses could provide a non-invasive, personalized therapy to treat and prevent elevated intra-ocular pressure in patients with glaucoma. The technology is being developed by Bionode LLC, a Purdue-related startup co-founded by Purdue professor Pedro Irazoqui and Murray I. Firestone. Credit: Purdue Research Foundation/Vince Walter image

A Purdue-affiliated startup, Bionode LLC, is developing a wearable neuro-modulation device that could be used as a non-invasive, personalized therapy to treat and prevent elevated intra-ocular pressure in patients diagnosed with glaucoma.

The technology was developed in Purdue's Center for Implantable Devices by Pedro Irazoqui, professor of electrical and computer engineering and biomedical engineering and lead at the center. Irazoqui serves as chief technology officer of Bionode. The company was co-founded by Irazoqui and Murray I. Firestone, CEO of Bionode.

"Glaucoma is the second leading cause of blindness in the world behind cataracts. Intraocular pressure is caused when the eye either produces too much fluid into the aqueous humor or the eye does not drain properly. The pressure then goes up. Over time, that pressure damages the optic nerve and ultimately results in blindness," said Firestone. "Current treatments for glaucoma suffer serious limitations concerning patient compliance, side effects, and efficacy. There is need for a non-invasive, effective treatment for glaucoma that solves these issues."

Bionode's technology utilizes an off-the-shelf contact lens and a pair of glasses.

"All we do to the contact lens is add a single trace of gold. That trace of gold receives an electromagnetic field that we transmit from a specially equipped pair of glasses to convert the field into a current. The current is then delivered to a very specific part of the eye's anatomy to achieve the desired therapy," Irazoqui said. "Our device can electrically stimulate the muscles around Schlemm's canal, the structure where fluid leaves the eye, to decrease the impedance to fluid flow and, thus, decrease pressure. There's no surgery, it's not invasive, it's just a contact lens that you wear with a pair of glasses and it takes about five minutes to work and has no known side effects."

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Irazoqui said the Bionode platform overcomes the limitations of existing treatments.

"Current treatments for glaucoma include eye drops which have side effects and low patient compliance and they eventually stop working. There is the option of laser eye surgery which you can do a maximum of a couple times, and beyond that there is a blood procedure, which is an open wound in the eye that leaks liquid whenever pressure goes up, this has terrible risks for infection. Additionally, all these methods take about three months to work," he said. "Most patients who opt for these solutions have visual loss within about 10 to 15 years and by 15 to 20 years go blind. The Bionode platform could be the first line of defense for Glaucoma patients."

Bionode is working to conduct a clinical trial of 100 patients to demonstrate the durability and effectiveness of its platform.

"Currently we have a working prototype and we are seeking $1.5 million in funding to conduct a full human clinical trial. We have partnered with a clinician who owns two ophthalmology institutes, one in Madrid and one in Barcelona, Spain. He is an internationally renowned ophthalmologist," Irazoqui said. "Our goal is to complete that large clinical trial, apply for CE Mark approval, and file for a FDA de Novo approval in the United States."

Firestone added that in the future the company may also look into the Bionode platforms' usefulness in post-traumatic stress disorder, urinary incontinence, gastric disorders and more.

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Non-invasive, effective contact lenses and glasses to treat glaucoma, prevent blindness - Medical Xpress

For years, the international community has grappled with the threat of chemical, biological, radiological, and nuclear terrorism. And although al Qaeda and the Islamic State (ISIS) have demonstrated interest in and some capability to develop and use such weapons, there have been no successful mass casualty terrorist attacks involving them. Attempted attacks involving radiological dispersal devices or chemical and biological means have either failed or had a very limited impact. Experts such as John Parachini, Jeffrey Bale and Gary Ackerman, Adam Dolnik, and Rajesh Basrur and Mallika Joseph argue that the reason is terrorists inability to weaponize chemical, biological, radiological, or nuclear material. Others, including Brian Michael Jenkins, believe that the lack of mass causality attacks also has to do with self-restraint: perpetrators might not be able to control the consequences of such an attack. It could end up harming the members of the communities that the terrorists are purportedly fighting for and could therefore be counterproductive.

The recent WannaCry ransomware attack, however, could force the expert community to rethink such positions. Although available information suggests that North Korean hackers were behind these attacks, in which hackers took control of about 300,000 computers in over 150 countries and held the victims hostage in exchange for a payment of $300 in bitcoin, there is reason to believe that terrorist groups such as al Qaeda and ISIS could copy the tactic. In doing so, they would cause as much damage (loss of data and equipment) and chaos (in hospitals and other public utilities) as possible, comparable to the chaos and panic that could be caused by a chemical or biological attack.

Terrorists could use cyber capabilities to target any sector. But the most vulnerable industries are those with high proportions of old infrastructure onto which new technology has been grafted. According to a report from the U.S. Bureau of Economic Analysis, in 2015, the average age of all fixed assets in the United States stood at 22.8 years, with hospitals and utilities some of the worst culprits.

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Cyberterrorism and Biotechnology - Foreign Affairs (subscription)

There are more than 52 million adults in the United States who suffer from joint inflammation caused by arthritis. Its a disabling condition that is especially prevalent among people over age 50.

Feet are especially susceptible to arthritis; each foot has 33 joints, and there is no way to avoid bearing weight on them.

The Michigan Podiatric Medical Association says symptoms of arthritis in the foot and ankle can include early morning stiffness, limitation in motion of joint, recurring pain or tenderness in any joint, redness or heat in joint, skin changes and swelling in one or more joints.

There is usually no need to endure years of painful ambulation because of arthritic feet, said Dr. Jodie Sengstock, MPMA director of professional relations. Most conditions can be diagnosed and treated either conservatively or surgically by a podiatrist.

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Arthritis of the foot and ankle can be treated in many ways, including physical therapy and exercise, orthotics or specially prescribed shoes, and joint replacement surgery. In addition, anti-inflammatory medication and/or steroid injections into the affected joint may also provide relief.

Obesity is linked to arthritis; when you take a step any step four times your body weight presses on your feet. If you weigh 200 pounds, thats 800 pounds of pressure per inch with every step. The best way to lose weight is to eat smarter.

Although it may seem counterintuitive to move your joints when theyre a source of pain, its still important to keep moving. As you age, you lose 1 percent of muscle mass a year. The more you lose, the more strain you put on your joints because muscles are the joints primary shock absorbers. You can slow that muscle loss with strength exercises. If possible walk 30 minutes a day. If walking is painful, try a stationary bike or water exercise to build strength and endurance.

Debra Kaszubski, Vitality special writer, contributed to this report.

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When it comes to arthritis, feet bear a tremendous weight - The Macomb Daily

WCVB's 5 Investigates Karen Anderson will emcee the Walk to Cure Arthritis this Saturday, June 10 starting at 9am at Canal Park in Cambridge.

Arthritis is the #1 cause of disability in the United States, affecting more than 50 million people. The Arthritis Foundation is committed to finding a cure for the millions of people who suffer from arthritis pain, including 300,000 children and their families.

Join us for the Walk to Cure Arthritis and say Yes to helping create a world where people dont have to struggle to button their shirt, tie their shoe, pick up their child or grandchild or play with their friends. As Champions of Yes, its up to us to make sure that people with arthritis have life changing resources and information to manage their disease, access to the critical medications they need to live full, healthy lives and to accelerate the path to better treatments and a cure through cutting-edge research.

Join the fight and Walk to Cure Arthritis register, fundraise, come together to support each other and walk. Another step, another victory!

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Join 5 Investigates Karen Anderson at the Walk to Cure Arthritis on Saturday, June 10th - WCVB Boston

As part of the 52 Weeks of Public Health campaign, the Kentucky Department of Public Health (DPH), within the Cabinet for Health and Family Services (CHFS), is emphasizing the negative impact of arthritis on people who live in rural areas.

A recent report by the Centers for Disease Control and Prevention (CDC) showed that one-third of adults in rural areas have arthritis and that more than one-half of that population is limited in their daily activities by the condition. In Kentucky, more than one million adults have doctor-diagnosed arthritis and more than half (570,000) of those with arthritis live in rural parts of the state. Furthermore, 45 percent of rural working-age adults report that arthritis limits their ability to work.

Many senior centers, local health departments, the University of Kentucky Center of Excellence for Rural Health and YMCAs offer proven exercise and self- management programs that help relieve arthritis pain, said Teri Wood, principal investigator on the CDC Arthritis grant for DPH. Our program is always seeking local organizations already serving rural populations, including churches, county extension agents, veterans service organizations, health care clinics, and community centers that might be able to collaborate to make the small-group versions of these low-cost programs more available.

DPH and the Department for Aging and Independent Living (DAIL), within CHFS, collaborate on arthritis prevention and control to increase access to programs for arthritis management. Programs such as Walk with Ease, Enhance Fitness and the Chronic Disease Self-Management Program as examples of effective arthritis management tools that are available in many communities across the state. More information can be found here: http://www.chfs.ky.gov/dph/info/dpqi/cd/arthritis.htm.

Throughout the planned 52 Weeks of Public Health promotion, DPH will spotlight a specific public health issue. Additional information about the campaign is available on the DPH website: http://chfs.ky.gov/dph/default.htm and will be posted on the CHFS Facebook page: http://www.facebook.com/kychfs where Kentuckians are encouraged to like and share posts among their networks of friends.

More information on the impact of arthritis nationwide can be found here: http://www.cdc.gov/mmwr.

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One in Three Adults in Rural Areas Have Arthritis | BereaOnline - Berea Online

OSTEOARTHRITIS,a painful condition in which the tissue between bones wears down, frequently affects people in old age and a new study finds that as many as 4 in 10 people may develop the condition in their hands.

Among women, researchers found the lifetime risk was 47 per cent while for men it was about 25 per cent. Obese people also had 11 per cent higher lifetime risk than those who were not obese.

Hand osteoarthritis can cause disability and problems with daily living, but is not often a subject of research, the study team writes in the journal Arthritis and Rheumatology. Past research shows the lifetime risk for arthritis of the knee to be 45 per cent and 25 per cent for the hip, they write.

These findings indicate that symptomatic hand osteoarthritis is very common and affects a substantial proportion of the population in their lifetimes, lead author and epidemiologist at the Centers for Disease Control and Prevention in Atlanta, Jin Qin told Reuters Health.

The researchers analysed data from a study of more than 2,000 people over age 45. The study collected data between 1999 and 2010, using self-reports of arthritis symptoms and X-ray images of the participants hands.

Based on this group, researchers estimated the proportion of people who will develop osteoarthritis in at least one hand by age 85 to be 39.8 per cent.

White people were at greater risk, at 41 per cent, for hand osteoarthritis than black people, with 29 per cent. Obese people had a lifetime risk of 47 per cent, compared to 36 per cent among the non-obese.

Some people with hand osteoarthritis have minimal or no symptoms. But for many, symptomatic hand osteoarthritis greatly affects their everyday lives, with few options for improving their symptoms, Dr. Fiona Watt, a research lecturer and honorary consultant rheumatologist at the University of Oxford told Reuters Health.

The pain can vary and tends to be worse the more people use their hands, flaring up during daily activity like carrying heavy shopping bags or typing on keyboards or phones, said Watt, who was not involved in the study.

Our hands are so important and we need to look after them, Watt said, adding that doing aerobic exercise and watching our weight can help protect against all types of osteoarthritis.

We know that injury can increase the risk of osteoarthritis, Watt said. Although we cant always prevent hand injuries, wearing supporting and protective gloves in occupations with heavy use of the hand is important.

Preventing injuries and maintaining a healthy weight may lower the risk of osteoarthritis, Qin said. Earlier diagnosis allows earlier use of interventions (e.g. physical/occupational therapy), that may help manage symptoms, maintain better function and improve quality of life.

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40 per cent lifetime risk of hand arthritis - RTN Newspaper

Experimental arthritis FLIPping the switch on macrophages Nature.com Reducing the expression of anti-apoptosis molecule FLICE-like inhibitory protein (FLIP, also known as CASP8 and FADD-like apoptosis regulator) in macrophages could protect against inflammatory arthritis, according to new findings published in Arthritis ...

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Experimental arthritis FLIPping the switch on macrophages - Nature.com

Walk into any gym, step onto any basketball or tennis court, or even take a look at the person jogging or walking down your street, and youll likely to see an assortment of braces or support aids on older (and younger) individuals.

One of the most common areas youll see this equipment is on the knee.

Knee pain is one of the most common conditions I see as a physical therapist. Often I see people after knee replacement. However, I also see people with knee pain due to osteoarthritis before surgery.

Knee osteoarthritis is a common condition and is one of the five most disabling conditions in the U.S., affecting more than a third of people over 65 years of age. Sometimes, knee pain due to arthritis will lead to the use an assistive device, such as a cane or walker, and eventually knee replacement surgery.

Chronic knee pain due to arthritis is characterized by pain, cartilage degeneration and joint space narrowing. When patients are referred to physical therapy for arthritis relief, they often dont understand how physical therapy can help. After all, if there is cartilage degeneration and joint space narrowing, wouldnt more movement just make the arthritis worse?

Fortunately, as Ive discussed at length before, the body is much more complex than that. In fact, the 2008 guidelines from the American Academy of Orthopaedic Surgeons recommend exercise as the core treatment for osteoarthritis.

As the saying goes in physical therapy, "Movement is medicine."

The right type of exercise in the appropriate dosage and intensity can help "lubricate" the joint, improve muscle strength, improve joint motion and decrease joint pain. Osteoarthritis is associated with decreased muscle strength and abnormal joint mechanics.

A 2012 review in the journal Physical Medicine and Rehabilitation reviewed resistance training interventions on knee osteoarthritis and found some studies showing up to a 43 percent reduction in pain with appropriate resistance training.

Physical therapy, and specifically resistance training, works to improve joint mechanics and muscle activation patterns. In the physical therapy clinic, the typical culprits for weakness I see are the muscles of the thigh and the hips. So my treatment usually starts with exercises targeting the thigh muscles, both quads and hamstrings, as well as the muscles that move your leg back (hip extension) and to the side (hip abduction). The hip muscles actually help control the position of the knee during functional activities, so making sure your hips are strong is a good way to help improve knee mechanics.

I also will include some calf (lower leg) strengthening as well.

Next, it's important to help make sure that certain movements, such as squatting and going up and down steps, are performed with good mechanics. This usually means ensuring that when looking at the knee from the front that it stays in line with the second toe when climbing the stairs.

When bending down to sit in a chair or pick something up off the ground, it means that the knees stay outward to remain in line with the toes.

A good test to perform at home to check your mechanics is to stand sideways beside a step and perform a lateral step-up. Keeping the knee in line with toes is often difficult for most people. Often, when people have pain with stairs, fixing the mechanics helps their pain relatively quickly.

Lastly, I like to combine knee/hip strengthening and functional tasks focused on mechanics with a biking activity. It seems the continual motion of the bike helps to lubricate the joint and just helps things move a little better. If you have knee pain due to osteoarthritis, I recommend you get a bike, either recumbent or upright, and ride for 10 to 20 minutes a day to keep the knee joint loose and well-lubricated.

With the right exercises, individuals with mild to moderate osteoarthritis can experience symptom relief, decreased disability, improved function and overall improved health.

These recommendations also apply even if you dont have knee osteoarthritis. As we age, the prevalence of knee osteoarthritis increases, so its likely a good idea to perform biking, leg strengthening and biomechanics training as part of a comprehensive exercise routine.

Show caution when starting new exercises, and if you have any doubt about your mechanics, see your physical therapist for instruction. Dont push through pain with exercises. Start off slow, and progress in weight, reps and biking distance as you are able.

Nick McClary earned his doctor of physical therapy from the University of Tennessee. He is a Georgetown County native and lives and works in Pawleys Island. Send him your health and fitness questions at: nmcclaryDPT@gmail.com.

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Nick McClary column: With arthritis, movement is good medicine - South Strand news

Chondroitin Eases the Pain of Knee Arthritis New York Times As part of the trial, 604 patients with knee arthritis received either the NSAID drug celecoxib (brand name Celebrex, 200 milligrams a day), a dummy pill, or chondroitin (800 milligrams a day), a component of cartilage that cushions the joints and is ...

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Chondroitin Eases the Pain of Knee Arthritis - New York Times

Stem Cell Therapy is poised to change the face of medicine.

Thousands of published studies and or testimonialscan be wrong! Regeneration or Regenerative Medicine has the ability to change almost all facets of medicine.

Doctors are using them on themselves to help with problems and or provide with a better quality of life, in-fact one doctor sais in a recent stem cell seminar that he would be doing them every year just for preventative maintenance.

Stem Cells have been studied for decades however in the past few years a real breakthrough in using Human UmbilicalCell Tissue (HUCT) being harvested from healthy mommy / healthy baby umbilical cords.

Studies have proved that the older you get the fewer stem cells in the body, ruling out the effectiveness of stem cells extracted from your aging body or your fat.

Statin drugs have been proven to diminishstem cells

Using Concentrated Umbilical-Cord Potentcy Stem Cells (CUP STEM CELLS) give you cell counts in the millions ffrom a newborn tht may allow stem cells to duplicate every 28 hours, over 65 or so cucles making CUP STEM CELLS very favorable to all the other options available in the past.

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Stem Cell Therapy - Checkbiotech.org (press release)

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How to protect your eyesight this summer wreg.com To protect your eyesight, the most important recommendation you need to follow is to wear sunglasses that block ultraviolet radiation whenever you go outside during daylight hours, according to the National Eye Institute. This is true for everyone, no ... and more »

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How to protect your eyesight this summer - wreg.com

When the eyes of her mice looked normal, Xu Wang was certain she had done something wrong. She was blasting the mice with blinding light to study how a specific gene affected the animals response to eye injury. All the mice were given the drug tamoxifen. Half were engineered to respond to the drug by disabling the gene a step that would protect their eyes. The control mice, with all genes intact, should have lost sight as photo-receptors the light-sensitive cells in the retina died.

Instead, the retinas of the control mice looked just fine. I was kind of despondent because it didnt agree with our hypothesis, Wang says. She and her mentor, Wai Wong, both ophthalmologists at the National Eye Institute in Bethesda, Md., could have started over with another kind of mouse. But they decided to do the test again. And again.

The spared vision was no mistake. Many experiments later, Wang, Wong and colleagues have shown that tamoxifen, a drug used to treat breast cancer, can help preserve photoreceptors and sight in mice with eye injuries.

After exposure to blinding light, injured photoreceptors send distress signals to summon microglia, immune cells that are the first line of defense in the brain and spinal cord. Microglia support photoreceptors by keeping the connections between them intact. But a photoreceptor SOS brings microglia swarming in to destroy damaged photoreceptors, resulting in vision loss. The same happens in progressive genetic vision disorders such as retinitis pigmentosa. The microglias murderous tendencies are meant to protect, but, Wong notes, their enthusiastic efforts can be overkill.

Story continues after images

Exposure to blinding light killed photoreceptor cells in the retinas of mice (left, dying cells colored pink). Animals given tamoxifen before the light (right), had almost no cell death.

When mice ate chow containing tamoxifen (about six to eight times the dose usually given to humans), the microglia didnt overreact and the photoreceptors were spared, the researchers found. Tamoxifen offered the same protection in mice with a form of retinitis pigmentosa. The killing power of microglia can be reduced by tamoxifen and this resulted in protection, Wong says. The group reported its findings in the March 22 Journal of Neuroscience.

The researchers are looking into whether lower doses of the drug can be protective, too. And there are plenty of other questions, such as how exactly tamoxifen protects against microglial malfeasance. Other scientists have shown that tamoxifen and similar drugs might also reduce nerve cell damage in the spinal cord and brain. The drug is widely used to treat women with certain types of breast cancer. But the eyes present their own challenges. In rare cases, tamoxifen has been tied to vision loss in women taking the drug. The scientists didnt see any sign of that in their mice, but Wong is quick to note that mice are not people.

Wang recalls her early days with patients facing blindness. I felt so helpless, she says. I thought, I want to find a way to solve their problems. She has new optimism. It opens a new window, she says. An old drug can be used in a new way.

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Researchers stumble onto a new role for breast cancer drug - Science News