Friday, September 19, 2014



Publisher: bhakragani - Friday, September 19, 2014

Wednesday, September 17, 2014

Sunday, September 14, 2014

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Comparing depression to cancer doesn't help anyone

Comparing depression to cancer doesn't help anyone

By David Pilgrim, University of Liverpool

Robin Williams’s suicide has led many to open up about depression in an effort to raise awareness about how many people are living in misery. One of the most common themes in this public discussion has been that depression is a disease like any other.

In the days after the news of Williams’s death broke, Tony Blair’s former communications director, Alistair Campbell, wrote:

Depression has nothing to do with how popular or famous, unpopular or unknown, you are. It just is. Like cancer is. Like asthma is. Like diabetes is. Some people get it, some people don’t. It is a truly horrible illness, and must be viewed and treated as such.

But is depression just like cancer, asthma or diabetes? Making these comparisons can be useful in a personal sense, but if the analogy is not backed up by research, it may be standing in the way of helping people in need.

To be clear at the outset, some of us some of the time are so profoundly distressed about our lives that we may consider suicide or carry it through. Most of us at some time in our life will experience distress and that experience might include low mood and a pessimistic outlook. Some people inhabit that distressed state from time to time, others will experience it chronically. Some of us experience it more profoundly and more often than others.

This social-existential spectrum can be called a disease. But to call something a disease is only worthy if it illuminates our humanity rather than dims our sense of what it is to be human and if turning profound sadness into a medical condition brings with it the prospect of corrective action.

So before we medicalise misery consider the following things.

No test for depression

Depression has no blood test to validate it as a medical condition. Like other psychiatric diagnoses it is defined using presenting complaints (symptoms) to make the diagnosis. The problem is, these symptoms are then explained by the existence of the putative disease. This circular logic goes something like this:

Q: How do we know that this woman is depressed?
A: Because she has very low mood and a deeply pessimistic outlook on life.
Q: Why is she so miserable?
A: Because she is suffering from depression.

The diagnosis of depression is now so common that it has entered the vernacular, and so it has become a self-evident fact for us all. However, as American psychologist Martin Seligman famously commented, “depression is the common cold of psychiatry, familiar yet mysterious.”

The problem of definition

Depression commonly occurs in conjunction with other symptoms, especially anxiety. Some psychiatrists now argue that another diagnosis of common neurotic misery would be more valid. Until the late 20th century, neurotic misery was not even designated by many psychiatrists as a proper mental illness. Now even bereavement is being designated by the American Psychiatric Association as a mental disorder called depression.

Depression has been framed by medicine sometimes as a form of madness (psychosis) and sometimes as common misery (neurosis).

Do the drugs work?

Depression can be treated medicinally but the outcome is unpredictable. If a person with type 1 diabetes receives insulin, their distressing symptoms disappear and their measurable blood sugar alters at once. Without insulin they soon die. If a person with a diagnosis of depression is prescribed an antidepressant it may or may not have a beneficial impact. Sometimes it does and sometimes it does not. Sometimes the adverse effects of the drugs make patients feel worse.

According to research, those treated with a combination of drugs and psychological therapy are more likely to improve, but relapse is common, even in optimally treated cases. Some who improve still report low grade misery in their lives.

Other ways to help

All of this suggests that human misery is common, recurring and fairly impervious to clinical intervention. It ebbs and flows, mainly because it relates to personal circumstances, such as poverty, bereavement, divorce, job loss or the development of painful illness. A simple diagnosis of depression as a matter of “brain chemistry” can render the complex politics of daily life irrelevant. Poverty, domestic violence, child abuse, insecure employment can be ignored as sources of distress and dysfunction in troubled lives.

Depression is bound up for us all in the condition of being alive among inequality, oppression and multiple forms of recurring loss. Why would we expect to convert all of that complexity into a simple disease that can be measured and manipulated by medical technology just like diabetes or asthma?

Instead of making depression a disease like any other, to be treated with a technological fix, we must stand back and find a way of appreciating the role of suffering in human life and of helping ourselves and others when we are miserable.
The Conversation

David Pilgrim does not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article, and has no relevant affiliations.
This article was originally published on The Conversation.
Read the original article.

photo credit: Helga Weber via photopin cc
Publisher: bhakragani - Sunday, September 14, 2014

Friday, September 12, 2014

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Airstrikes on IS in Syria's backyard are high-risk if Assad objects

Airstrikes on IS in Syria's backyard are high-risk if Assad objects


By Ben Rich, Monash University

The expansion of airstrikes against Islamic State (IS) into Syria announced yesterday by US President Barrack Obama marks a predictable, if necessary, escalation of coalition operations against the Jihadist insurgent group. Debates over the wisdom of the operation aside, any military campaign aiming to cripple IS (also known as ISIL or ISIS) as an organisation must target its core logistical and command and control hubs. Most of these appear still to be based in Syria’s east.

The Syrian government, however, remains understandably suspicious of coalition intentions in its backyard. A senior minister in the Assad government, Ali Haidar, warned that any action undertaken without the approval of Damascus would be considered “an aggression against Syria”.

Haidar’s statement reflects a common concern among Assad loyalists. They view the prospect of any coalition activity inside Syria proper as a potential precursor to direct intervention and regime change. But after three-and-a-half gruelling years of war, is the Syrian regime still in a position to resist outside aerial encroachment and threaten coalition operations?

Down but not out

The simple answer is yes. The civil war has taken a heavy toll on the ground troops and air power of the Syrian Arab Armed Forces (SAAF), but its air defences have remained largely unaffected. While not the most advanced in the world, Syrian anti-air systems still pose a considerable threat.

According to the annual defence report of the International Institute for Strategic Studies, Damascus has access to modern Russian platforms. These include the Pantsir-S1, the Strela-10 and the likely culprit in the MH17 tragedy, the Buk/Buk-M2. Despite repeated discussions over the potential deployment of the formidable theatre-level S-300 system, its status in Syrian hands remains ambiguous.

Such weapons were responsible for the downing of a Turkish warplane along the Syrian periphery in 2012, sparking a minor diplomatic crisis. Closer to home and several decades earlier in 1983, the SAAF used similar platforms to down two US Navy aircraft in Lebanese airspace, much to the consternation of the Reagan administration. Last year, Israel had concerns over the deployment of the Buk in southern Syria and its potential transfer to Lebanese Hezbollah. The IDF launched a devastating airstrike near Damascus to destroy the weapons before they could reach their destination.

Syria has the air-defence capabilities to threaten coalition aircraft.
EPA/Syrian News Agency

The Syrian regime couldn’t hope to fend off a direct assault by the US and its partners. However, it could disrupt an operation against IS. This could have severe political consequences and lead to a rapid escalation and regionalisation of the conflict.

Given IS' positioning inside Syria, coalition air strikes will likely be centred on the eastern city of Raqqah, where the group has made a serious effort to establish itself. While SAAF forces have lost considerable ground since 2011, they nevertheless hold territory within 50 kilometres of the city. This counts much of the government arsenal out, but still leaves systems like the Buk as a credible threat to coalition aircraft.

As the 1999 NATO bombing of Yugoslavia showed, even the stealthiest of aircraft can be downed by relatively low-grade Russian and Soviet equipment.

Dealing with the devil

Until now, the US and its allies have been able to engage IS in Iraq with impunity. The greatest threats they face have been pilot error and equipment failure. Syria is not Iraq, however, and the replication of such invulnerability in Levantine airspace is predicated on an understanding between the Assad government and intervening forces.

Given that much of the coalition has spent the past three years calling for the regime’s immediate dissolution and has just committed to expanding support for its opposition, this is a daunting task on both sides of the aisle.

Some may bank on the regime simply taking a step back and allowing one enemy to kill another. It seems to have been more than happy to employ this strategy against warring factions in the opposition. Yet not securing some form of information-sharing relationship between Washington and Damascus leaves far greater room for mishap.

With a considerable portion of the international community now committed to direct involvement in the Syrian conflict, the possible ramifications of such avoidable errors are dire.
The Conversation

Ben Rich does not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article, and has no relevant affiliations.
This article was originally published on The Conversation.
Read the original article.

Publisher: bhakragani - Friday, September 12, 2014
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Damage to the cockpit gives a clue to loss of flight MH17

Damage to the cockpit gives a clue to loss of flight MH17


By Geoffrey Dell

Investigations into the downing of Malaysia Airlines flight MH17 have revealed the aircraft’s cockpit was punctured by a number of “high-energy objects”.

The Dutch Safety Board has revealed the findings this week in a preliminary report into the downing of the passenger aircraft in the Ukraine on July 17. The Boeing 777 had just left Amsterdam airport with 283 passengers and 15 crew on board, heading for Kuala Lumpur airport in Malaysia.

The report confirms that the flight was proceeding as planned, at 33,000 feet and above the level of the restricted airspace over the Ukraine. It was communicating with all relevant air traffic controllers until about 1.20pm local time when the MH17 air crew stopped responding.

See: MH17 Infographic

The wreckage of the aircraft was later found spread over a large area (10km by 5km) near Rozsypne and Hrabove in eastern Ukraine, an area held by separatist rebel forces.

No malfunction of aircraft

The recovered flight data and voice recorders showed no alert or malfunction in the aircraft and the report says the crew “gave no indication that there was anything abnormal with the flight”.

So far the damage in the area of the cockpit is giving the strongest clue to what caused the accident. Australian Prime Minister Tony Abbott said the findings in the preliminary report are consistent with the Australian government’s view “that MH17 was shot down by a large surface-to-air missile”.

Part of the inside cockpit roof showing penetration by objects from outside.
DCA/Dutch Safety Board

The photographs (one above) included in the Dutch report clearly show this damage is atypical to that evident on the rest of the fuselage skin surfaces, which can be seen in other photographs of the wreckage.

These new photographs clearly show sections of forward fuselage structure with multiple holes where the skin is bent inwards around the circumference of each hole. This is consistent with the penetration of small high-energy projectiles, which would be the case with the proximity detonation of the warhead of a missile.

There is also evidence of similar penetrations in the cockpit floor. This suggests some of the projectiles from any warhead entered through the fuselage skin above the cockpit and then exited through the cockpit floor.

Under the cockpit floor

Below the cockpit floor of the Boeing 777 – as in most modern airliners – is the Electronics and Engineering (E&E) compartment, which houses most of the aircraft’s avionics, flight-management computers and other critical “black boxes”. Penetration of the E&E compartment by the high-speed projectiles would no doubt have caused catastrophic damage to critical control systems.

The evidence from the cockpit voice recorder and flight data recorder clearly show the aircraft operating quite normally with nothing unusual at all up to the abrupt end of the recording. This suggests that right up to the time the power supply to the recorders was terminated operations were normal.

It would be easy to jump to a conclusion from that evidence that the effect of any missile detonation was indeed rapid. Yet there is a need for the investigation to continue to provide answers to other questions.

For example, it is possible, although maybe unlikely, that shrapnel from any missile severed the power supply to the recorders, causing them to stop recording, but the aircraft may have continued flying for a short time. The penetration of the cockpit area by shrapnel from a missile may also explain why the crew were unable to get any mayday call away if that were the case.

What the pilots can still tell

Post-mortem examination of the pilots, if their bodies were among those recovered from the scene, would also shed important light on those last critical seconds.

The identification of the bodies that have been recovered from the crash site is apparently continuing. There is still no word as to whether the bodies of any of the pilots or other cockpit crew have been found, identified and examined.

While the report says the distribution of the pieces show the aircraft “broke up in the air”, the wreckage pattern itself will provide clues to those vital last few seconds.

Other parts of the aircraft have been found scattered across the crash site, including parts of the wings, both engines, landing gear and a portion of fuselage. The vertical tail was also located still attached to the upper rear of the fuselage.

The last location of the aircraft in flight taken from the flight data recorder (FDR). Wreckage distribution is grouped per section of the aircraft.
Dutch Safety Board

It is of interest too that the area map of the flight path in the report showed the main accident scene many degrees off the flight path the aircraft was supposedly on.

This may have been due to simple errors in the depiction on the map. But if the map was accurate, it opens speculation that the aircraft did not immediately or completely break up when the missile detonated.

If so, the heavy components, in particular the engines, would most likely have followed ballistic trajectories to the ground on roughly the same bearing as the direction of flight.

Lessons to be learned

For those who are only interested in bringing those who perpetrated this heinous crime to justice, the rest of the investigation may appear somewhat academic. But it is important to know exactly what took place, in order to make sure all lessons are learned.

For example, if the aircraft did fly on, for any time at all, but the recorders stopped recording due to power failure, recorder design might need to be reviewed to prevent that happening in future. Understanding what happens to airliners when attacked by missiles will also very usefully inform future airliner and aircraft systems design.

Aviation safety has evolved over the past 100 years by learning from the failures that have occurred. Learning all that can be learnt from this disaster will ensure all those lives were not lost entirely in vain.

There seems no doubt the governments involved in the investigation will allow it to run its natural course. This must include the recovery of all the wreckage from the field so that proper forensic analysis can be carried out.

The longer that takes, the less will be learned with certainty from this tragedy.
The Conversation

Geoffrey Dell does not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article, and has no relevant affiliations.
This article was originally published on The Conversation.
Read the original article.

Publisher: bhakragani - Friday, September 12, 2014

Sunday, September 7, 2014

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Try 5 Ways Iron Can Improve a Woman's Life

Back when I was a teenager, my mother told me I had to eat liver at least once a week because women needed their iron. Bless her heart, that’s the only thing mom knew about iron for women’s health, and fortunately I went on to learn some things of my own.

Did you know, for example, that 3 ounces of dark chocolate containing 45% to 69% cacoa solids provides more iron than does 5 ounces of beef liver? If mom had known that, our relationship could have been entirely different.
But seriously, getting a sufficient amount of iron can make a big difference in a woman’s health. Similarly, if you take too much (e.g., taking iron supplements when they are not necessary) can cause problems as well.

Are you tired?

One of iron’s main tasks is to transport oxygen to your tissues, which it does via hemoglobin in red blood cells. If your iron levels are too low, you can experience symptoms associated with too little oxygen, such as fatigue, shortness of breath, problems with concentration and memory, reduced ability to perform work, cold hands and feet, paleness, and apathy.
These are symptoms of iron deficiency anemia. Women can develop this type of anemia if they do not get enough iron in their diet and/or they experience heavy menstrual flow or other types of bleeding.

Do you catch colds?

Low iron means your B vitamins will not be metabolized optimally and your immune system will not operate as well, making you more susceptible to infections. Although most people experience the common cold, you can reduce your chances by getting enough iron.

Do you exercise?

New research published in the Journal of Nutrition notes that women who took iron supplements experienced an improvement in their performance. In fact, this study represented the first time investigators have confirmed that taking iron supplements can benefit exercise performance.
Specifically, the authors found that iron supplements allowed women to do a specific exercise with greater efficiency and with a lower heart rate than those who did not take the supplement. So if you exercise (and even if you don’t), the authors have suggested you have your iron levels checked with a simple blood test.
A pregnant woman
A pregnant woman (Photo credit: Wikipedia)

Are you pregnant?

A number of studies of the impact of iron intake among women who are pregnant show that
  • Pregnant women who have anemia are at greater risk of giving birth to a low-weight infant
  • Low intake of iron (but not necessarily having anemia) even before pregnancy and extending into the first trimester can have a negative effect on the developing brain
  • Women who took sufficient amounts of iron, vitamin A, and folic acid while they were pregnant were more likely to give birth to children who had better working memory, fine motor skills, and inhibitory control than those who took only vitamin A
Read about iron and pregnancy

Are you worried about Alzheimer’s disease?

Nearly two-thirds of the people with Alzheimer’s disease are women, according to the Alzheimer’s Association. One possible way to help reduce this greater risk is to not overdo your iron intake. Yes, too much iron may cause health problems beyond causing constipation.

According to the findings of a new study in Frontiers in Aging Neuroscience, higher intake of iron and potassium was associated with an increased risk of developing mild cognitive impairment and other mild cognitive disorders. About 15 percent of people with mild cognitive impairment progress to Alzheimer’s disease each year.

How much iron do you need?

According to the Food and Nutrition Board, women ages 19 to 50 need 18 milligrams (mg) daily and 27 mg if they are pregnant. Women age 51 years and older need 8 mg. The Board also recommends women who are vegetarians or vegan increase those figures by 1.8 times since the iron in meat and fish (called heme iron) is more available to the body than is non-heme iron (found in plants).
If you are looking for food sources of iron, be sure to add these iron-rich items to your diet. For women who want to avoid red meat and other animal products, there are plenty of great plant-based sources of iron from which to choose.

Cherbuin N et al. Dietary mineral intake and risk of mild cognitive impairment: the PATH through Life Project. Frontiers in Aging Neuroscience 2014 Feb 4: 6:4
Pasricha S-R et al. Iron supplementation benefits physical performance in women of reproductive age: a systematic review and meta-analysis. Journal of Nutrition 2014 Jun 1

photo credit: Lorenia via photopin cc
Publisher: bhakragani - Sunday, September 07, 2014
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Lifestyle factors including eating baked or boiled fish promote brain health

There has been a great deal of hype surrounding reports that eating a lot of fish is good for your cardiovascular health. There has also been interest surrounding reports that eating fish is good for your brain health. It has generally been conjectured that the positive health benefits of fish are due to omega-3 fatty acids in fish. New research shows baked or boiled fish is good for your brain independent of omega-3 fatty acid content.

Brain health may be affected by modifiable lifestyle factors

It has been observed that brain health may be affected by modifiable lifestyle factors and that eating fish and antioxidative omega-3 fatty acids may decrease brain structural abnormality risk reported the American Journal of Preventive Medicine. Researchers decided to investigate whether dietary fish consumption is associated with brain structural integrity in cognitively normal elders.

Consumption of baked or broiled fish was positively associated with gray matter volumes

The researchers found that weekly consumption of baked or broiled fish was positively associated with gray matter volumes in various critical regions of the brain. These findings were not altered when omega-3 fatty acid estimates were included in the analysis. The researchers came to the conclusion that eating baked or broiled fish is associated with larger gray matter volumes in the brain independent of omega-3 fatty acid content. It has been suggested by these findings that a confluence of lifestyle factors influences brain health.

Consuming baked or boiled fish weekly boosts brain health

Researchers at the University of Pittsburgh School of Medicine have stated that consuming baked or boiled fish weekly boosts brain health regardless of the omega-3 fatty acid content reports the University of Pittsburgh Schools of the Health Sciences. These findings, which have been recently published online in the American Journal of Preventive Medicine support growing evidence that lifestyle factors contribute to brain health later in life.

Greater than 80 million people will have dementia by 2040

It has been estimated by scientists that greater than 80 million people will have dementia by 2040. There have been predictions by some studies that lifestyle changes including a decrease in rates of physical inactivity, smoking and obesity could lead to significantly fewer cases of Alzheimer’s disease and other conditions of cognitive impairment in elderly people.

Anti-oxidant effects of omega-3 fatty acids, which are found in large amounts in fish, seeds and nuts, and certain oils, also have been associated with improved overall health and particularly improved brain health. This study shows that people who ate a diet which included baked or broiled, but not fried, fish have larger brain volumes in regions of the brain which are associated with memory and cognition.

Lifestyle factors instead of biological factors contribute to structural changes in the brain 

The researchers noted that in this study there was no relationship found between omega-3 levels and these brain changes. Lead investigator Cyrus Raji, M.D., Ph.D., who now is in radiology residency training at UCLA, and the research team pursued an analysis of this data from 260 people who provided information on their dietary intake, had high-resolution brain MRI scans, and who were cognitively normal at two points during their participation in the study.

The research group concluded that there are a more general set of lifestyle factors which are affecting brain health of which diet is just one part. Senior investigator James T. Becker, Ph.D. said these findings suggest that lifestyle factors, in this case eating fish, instead of biological factors contribute to structural changes in the brain.

Dr. Becker has made significant observation that a confluence of lifestyle factors are likely to be responsible for better brain health. This is a very important point in view of the fact that the American psychiatrists have taken the position that what they label as mental illness is due to structural defects and not functional impairments of the brain.

The finding that lifestyle factors, including diet, influences brain structure and brain health raises serious questions about the generally defeatist positions of the American psychiatrists that their patients suffer from structural defects of the brain and therefore can never actually be cured. The position of the psychiatrists becomes totally unacceptable with this more refined scientific understanding of brain health.
source: EmaxHealth
photo credit: libraryman via photopin cc
Publisher: bhakragani - Sunday, September 07, 2014

How dirty is your local grocery store?

Mouse droppings, aisle 2

A baseball bat used to grind meat. A thousand shiny mouse droppings. Leaking pink goop on a meat counter cutting board.
Welcome to your neighborhood supermarket.
At least once a year, inspectors from the New York State Department of Agriculture and Markets visit every grocery store in the state. We’ve combed through their reports to find what the inspectors call “critical deficiencies” — issues the state deems “an immediate threat to the public health and welfare” — in New York City supermarkets over the last five years.
By typing in an address, intersection, zip code or neighborhood, you can see which chain grocery stores have had serious violations between Jan. 2008 and July 2013, and what those violations were. You can also see if conditions in that store have been getting better or worse.

So which markets are crawling with the most vermin, caked with the most filth and oozing with unknown substances of all colors?
In some cases, they’re some of the more upscale ones in town. Poultry grinders encrusted with old food and fresh mouse droppings near the bakery and loading area were among the 12 serious violations received by the Whole Foods market on Columbus Avenue on the Upper West Side from July 2012 to July 2013, the third-highest number of all the city’s chain supermarkets during that period.
In that same period, the Melrose Ave. location of Pioneer Supermarkets in the Bronx was written up 13 times. Inspectors found hundreds of “fresh shiny appearing rat droppings” in several areas of the store. In 2012, inspection reports showed that about 200 “live adult and nymph German cockroaches” were found crawling in the store’s basement as well as inside boxes of Goya beverages.
Inspectors documented rodent infestations and more at Pioneer Market on Melrose Ave. in the Bronx. Photo: Sebastien Malo
Inspectors documented rodent infestations and more at Pioneer Market on Melrose Ave. in the Bronx. Photo: Sebastien Malo
The grocery store with the highest number of critical deficiencies in the most recent year, ending in July, is the Garden of Eden in Brooklyn Heights, with 20 offenses. Among them: old encrusted meat residues on food contact surfaces, mold and grime in the area of the seafood area ice machine and “deep knife scores containing imbedded/dark matter across food contact surfaces.”
Shoppers at Whole Foods in upper Manhattan expressed surprise at the high number of citations. Whole Foods spokesman Michael Sinatra did not respond to multiple requests for comment.
Alecia Smith, 27, who shops at Whole Foods on a regular basis, said she usually prefers to buy her fruits and vegetables at farmers’ markets anyway.
“On meat and fish, I’m iffy,” she added. “I never know where to shop.”
According to Joe Morrissey, spokesman for the Department of Agriculture and Markets, the total number of violations statewide has decreased 11 percent since 2000. In the city, too, supermarkets appear to be getting cleaner: They saw 597 serious violations in 2012, nearly half the almost 1,100 that inspectors found in 2008.
Still, the state records show there’s plenty of filth to go around.

What’s wrong with my grocery store exactly?

In the last five years, inspectors have seen an awful lot of animal poop: They have slammed New York City’s supermarkets 1,964 times for likely contamination from “insect, rodent, bird or vermin activity.” In more than 700 of those cases, inspectors found “fresh appearing mouse droppings.”
The Whole Foods on Columbus Ave. has been cited for 27
The Whole Foods on Columbus Ave. has been cited by state inspectors for 27 “critical deficiencies” since the beginning of 2008. Photo: Sebastien Malo
Dirty surfaces and unclean equipment, such as meat grinders, also make frequent appearances. In 752 cases since 2008, inspectors cited that food had been in contact with equipment, utensils or surfaces that had not been “properly sanitized and likely to contribute to contamination.”
Shoppers may also want to take a closer look at the refrigerators: In more than 260 cases, foods were not stored at the right temperatures, which can lead to food-borne illness. When such violations are found at grocery stores, they have to be rectified right away.
During an inspection at the Garden of Eden on 14th Street in 2009, an inspector ordered the store throw 66 pounds of prosciutto di Parma after it found the product hanging over a deli counter at 70ºF for an “undetermined period of time.” The costly lesson apparently didn’t stick: the following year, and the next year an inspection at the same location led to the destruction of more than 6 pounds of salami for similar reasons.

The award for most disgusting supermarket goes to…

Dating back to 2008, Met Foods on Fulton Street in Cypress Hills, Brooklyn, comes in at first place for the most serious violations, with a whopping 72 in all. Inspectors have found hundreds of mouse droppings, six mouse carcasses, and rodenticide on the bread shelves.
The Met Foods on Amsterdam Ave. near 125th Street has received more critical deficiencies than any store in Manhattan. Photo: Sebastien Malo
The Met Foods on Amsterdam Ave. near 125th Street has been cited for more critical deficiencies than any store in Manhattan. Photo: Sebastien Malo
Cesar, a manager at the Met Foods on Fulton street who declined to give his last name, said that in order to keep the store clean and the vermin out of the basement, cleaning crews come in every day to keep the place as spotless as possible. A fumigator comes by every week, he said.
Manhattan’s worst offender is also a Met Foods outlet, on Amsterdam Avenue near 125th Street, with a total of 48 critical deficiencies, followed by the Gristedes on Third Ave. in Murray Hill, with a total of 44.

Best and worst chains

Trader Joe’s peppy workforce isn’t just throwing smiles: they also keep one of the cleanest grocery store chains in New York City, with only one critical deficiency reported, at its Sixth Ave. location, since 2008.
By far the scummiest chain, as measured by health inspector citations, is Associated, a network of independently operated stores with more than 130 outlets in the metropolitan area: Over the past five years, state inspectors have cited its member stores for 739 critical deficiencies. The silver medal goes to two other franchise-style networks: Key Food, with 668 violations, followed by C-Town with 447.
Joe Estrada, 72, the manager of the Associated Supermarket on 14th St. and Eighth Ave. in Chelsea, said that inspectors come often, and always unannounced. Standing in front of the certificate that proves the store passed its inspection on May 13, 2013, without any serious violations, he acknowledged that in the past the store has seen violations — five, since 2008.
“It’s been 20 years,” he said. “We’re not going to be perfect all the time.”
He said that an exterminator usually comes twice a week to keep the rats and mice at bay. But the store has been cited for having not having a sink for employees to wash their hands in the kitchen, warm cold cuts and (inevitably) rodent droppings.

Cleanest and dirtiest neighborhoods

Access to fresh food is so rare in East New York that the city offers special tax incentives to get grocery stores selling fresh food to open in the Brooklyn neighborhood. The neighborhood needs all the help it can get. The nine supermarkets in zip code 11208 have seen 189 critical deficiencies in the last five years. Also grungy: midtown West, where eight supermarkets have been hit with 151 violations. In Highbridge and Morrisania in the Bronx — zip code 10456 — inspectors found 128 critical deficiencies in the past five years.
Shoppers seeking cleaner aisles and counters should head for Queens, where markets in Astoria, Richmond Hill, Kew Gardens, Woodside, Addisleigh Park and Queens Village have nearly spotless records. Stores in Sheepshead Bay, Brooklyn and Manhattan’s West Village also score high.

So now what?

The supermarket industry argues that in the fierce competition of the marketplace, cleaner grocery stores will prevail. Jay Peltz, vice president of public affairs at the trade group Food Industry Alliance, said that because the market is so competitive, “you have to operate a clean store.” The Food Industry Alliance represents many of New York state’s major supermarket chains, including C-Town, Pathmark and Shoprite.
“Our member stores have been in substantial compliance with the law,” Peltz says.
The Garden of Eden market on E. 14 St. in Manhattan had the highest number of serious violations of any market in 2012. Photo: Sebastien Malo
The Garden of Eden market on E. 14 St. in Manhattan had the highest number of serious violations of any market in the most recent year measured. Photo: Sebastien Malo
The state gives them lots of encouragement. Morrissey, the spokesman for the New York State Department of Agriculture and Markets, said that grocery stores hit with violations have to clean up their act — otherwise, they can expect “progressive legal action including civil penalties, license revocation and injunctive action.”
The state revoked a dozen licenses across the state in 2012, said Morrissey, and a few more in 2013.
When violations are recorded, inspectors return a few months afterward to check on the progress. If a store keeps failing its inspection fines can go up to a calculated total of $1,200 per critical deficiency and $200 for minor infractions.
Robert Gravani, a food science professor at Cornell University and the director of the National Good Agricultural Practices Program, said he hopes that shoppers will stop going to a particular store if they notice serious violations or apparent health hazards.
Besides having the effect of grossing people out, the critical deficiencies can lead to some serious health consequences, Gravani said. The lack of hot water for employees to wash their hands, for example, can bring bacteria to the food they’re handling. Those bacteria can lead to food-borne illnesses.
Gravani suggests social media has helped keep store managers on their best behavior. “All of that publicity,” he said, “has tremendous consequences.”
When shoppers see something dirty in a store, Gravani continued, they should tell managers at or even call the Department of Agriculture and Markets and voice their complaints.
“Some things out there,” said Gravani, “are really easy to take care of.”
Sebastien Malo contributed reporting.
Publisher: bhakragani - Sunday, September 07, 2014

5 Ways To Improve A Relationship And Stop Boredom

5 Ways To Improve A Relationship And Stop Boredom
by Jon Allo

If you want to save your relationship, think about this. Before you and your partner got together, if you had to choose between a romantic relationship and one that was dull and boring, which one would you choose? One of the reasons you chose your partner was that he, or she was romantic, full of life and passion. A passionate romantic relationship was fun when you were single, so why couldn't it still be today even though you're a little older and perhaps even married?

Is it because you have more important things to do and worry about now? Like paying the bills, working or sorting out the kids? But are these really ways to improve a relationship if it is having problems? Obviously, there are important things to do but, to save your relationship from dying of boredom, you need to make quality time for one another. Many long term relationships and marriages have suffered, even to the point of splitting up, when it's all about the labour and not the love.

5 Ways To Improve A Relationship.

1. Be Positive.

If you're trying to save your relationship you have to focus on the positive. Stop only seeing the negative side of your partner and look at the positive qualities. They're there if you look. To save your relationship you have to communicate with your partner about the good aspects of your relationship, and not just the bad. Being able to listen to your partner when they need it encourages them to talk when they need to.

2. Don't Forget The Romance.

To experience romance and intimacy you don't have to be newlyweds. One of the ways to improve a relationship is to keep in mind what you did when you began dating and do it again. You did lovely, considerate things while getting to know one another. You swapped gifts, went for walks and went to romantic restaurants. You may think you know every little thing about your partner and if that is the case, why aren't they happy? Why aren't you happy?

3. Become Young Again.

Getting older too often means getting serious. Often too serious. Act like a kid again. You don't have to do this all the time to save your relationship, but once in a while do something silly together and laugh. Go to the park and push each other in a swing, jump rope, do a dance that was popular "back then." You don't have to do it long, but loosen up and give it a go. It's likely you'll both be laughing before you make it to a bench to sit down and rest.

4. Touch Each Other.

Give each other a hug everyday. Back home, give each other a massage. Start with the feet and see where it goes from there. The better you make someone else feel, the better you will feel. The following day, have breakfast in bed. Who knows where that will lead? Before you say goodbye for the day, slip a love note in a handbag or pocket. You'll know what to say.

5. Take A Break Away.

A romantic trip can help remove stress in a relationship and allows you to be more yourself with your partner. Choose somewhere that you can have some fun together while getting to know your partner a little more. More relationship problems are reported from couples who have not been on a trip together in the last six years of being together.

More Information:

When a relationship is in trouble or breaks up it is often very difficult to know what to do for the best. For help in reconciling couples, regaining the trust and passion lost due to whatever reasons that caused the relationship to break down and genuine advice on exactly what to do and what to say to really get your relationship back on track - especially if you are the only one trying, please visit

Publisher: bhakragani - Sunday, September 07, 2014

Saturday, September 6, 2014

Who is to blame when iCloud is 'hacked' – you or Apple?

By Grant Bollmer, University of Sydney

A hacker’s release of personal photos of actress Jennifer Lawrence and other female celebrities on the internet on the weekend has again drawn our attention to the security of our personal information online. Are we really aware of what we upload? And how can we make sure the information we intend for private viewing remains private?

With new devices incorporating features for recording personal data, such as the health monitoring technologies used in Samsung’s Gear and the Apple Health app, should we be even more concerned about our ability to control our private data?

Most of the hacked images were reportedly obtained through Apple’s iCloud service which can automatically back up personal data from Apple products to its servers.

Cloud confusion

How iCloud works is baffling even to some computer security experts.

The response from Apple has been unequivocal. While the tech giant said it was “outraged”, the official response noted:

None of the cases we have investigated has resulted from any breach in any of Apple’s systems including iCloud or Find my iPhone.

So individual users were responsible for any failure to take the proper precautions to make sure personal data remains in personal control.

Back in 2011, then Apple CEO Steve Jobs unveiled iCloud as a way to allow Apple users to automatically sync their information with any compatible Apple device.
EPA Monoca M DAvey

The blame game

Like those who defend the hackers of stolen photos, Apple is blaming the victims of the attack without acknowledging the role its service plays in opening up private data to these attacks. This position is indefensible for several reasons.

Social media and services such as iCloud present us with countless examples of personal data doing things that seem counter to the will of the individual.

In a study I published last year, Facebook users sometimes feared their data to have a “life” that does not correspond to that of the person who “owns” the data generated.

Like our Facebook profiles, we assume what we backup with any cloud services to be “our” data. Yet the Terms and Conditions of whatever you upload to iCloud state:

[…] you grant Apple a worldwide, royalty-free, non-exclusive license to use, distribute, reproduce, modify, adapt, publish, translate, publicly perform and publicly display.

These words mirror similar statements in Facebook’s Terms of Service.

At the same time, Apple is clear to claim:

[…] you, and not Apple, are solely responsible for any Content you upload, download, post, email, transmit, store or otherwise make available through your use of the Service.

Merely using iCloud means that Apple can do what it wants with your data, but you – and only you – are responsible with what happens to that data.

Placing the blame on the individual, as Apple does, results in a common response whenever data are thought to be beyond the control of the user: delete all of your personal information online, shared intentionally or not.

This response simply is not good enough given how cloud services operate. They make multiple copies in multiple locations, stored on multiple servers and hard drives across the globe.

These files are uploaded automatically and are built into new features of our mobile devices. When an individual deletes a file, this does not mean that it is actually deleted, simply by virtue of how computer storage works.

All about trust

Apple may wish to absolve itself of responsibility when individuals lose control of their personal data. In legal terms, Apple places all burden on the individual for the management of their data.

Yet understanding the control of data as a personal matter disregards how these services actually operate. If Apple and other cloud-based services want our trust, then they have to acknowledge the role their products play in perpetuating anxieties of data-out-of-control.

They must refuse to place sole responsibility on their users – the victims of these attacks.

Grant Bollmer does not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article, and has no relevant affiliations.
This article was originally published on The Conversation.
Read the original article.
Publisher: bhakragani - Saturday, September 06, 2014

Four things you should know about gene patents

photo credit: via photopin cc


By Rodney Scott, University of Newcastle

The Federal Court’s decision that gene patenting is permitted in Australia will have ramifications for all gene patents, even though the case involved only one gene associated with breast cancer.

A gene patent means only the patent-holder has the right to undertake research and development involving that gene. These patents generally last for 20 years.

The full bench of the Federal Court heard the appeal against a ruling that private companies could patent genes in August 2013, after a Federal Court justice dismissed a challenge to the patent for a breast cancer gene, BRCA1, in February.

A landmark ruling by the US Supreme Court in June 2012 declared that naturally occurring DNA sequences were ineligible for patents in a case that involved the same breast cancer gene, and the same patent holder.

The BRCA1 and BRCA2 controversy

It’s about 20 years since Myriad Genetics patented two genes associated with a significantly increased risk of developing breast cancer. Known as BRCA1 and BRCA2, the genes are also associated with an increased risk of ovarian cancer.

When functional, BRCA1 and BRCA2 produce tumour suppressor proteins that help repair damaged DNA. But when they are altered, the protein is either not made or doesn’t function correctly, leaving DNA damage unrepaired. The cells may then develop additional genetic alterations that can lead to cancer.

Breast cancer affects approximately one in ten women at some time in their lives, although not all cases result from these genetic mutations. Studies have estimated that the frequency of BRCA1 and BRCA2 changes in the community is approximately one in 500.

Identifying these gene carriers is an important step in reducing disease in the community and in preventing transmission into subsequent generations. Indeed, any measure that can reduce breast cancer figures and help women avoid an incurable disease is something any reasonable society would aim for.

The BRCA1 and BRCA2 patents have generated significant controversy because Myriad has effectively monopolised the market for screening these genes to identify the alterations, or mutations, that render them non-functional.

Four things you should know

Here are four things you should know about gene patents that will provide some context for understanding the Federal Court decision.

1. Genetic patents hinder, or don’t foster, innovation.

The argument that gene patents foster innovation is often used to defend gene patenting, but it’s actually addressing the wrong question.

When considering gene patenting, we need to ask whether a gene is an invention, which is grounds for granting a patent, or a discovery. Isolating the actual gene itself is a discovery and, as such, should not be the focus of patent attention.

Surely only the process of how information is obtained from a gene can be the subject of a patent, and then only if it’s new. Developing new ways to interrogate a gene sequence can and should be patented as this leads to commercial drive and (hopefully) re-investment in new resources to improve testing strategies.

2. Patents have traditionally been granted for isolated genes rather than for any kind of innovation.

Until recently, patent offices viewed the isolation of genes as enough to declare the gene more than just a product of nature and a discovery.

In the United States, patents are also granted on a first-to-invent basis. This contributed to the gene patent rush as the human genome project gathered pace in the 1990s and gene discoveries became almost a weekly event. There are now an estimated 4,000 gene patents in the United States.

The US Supreme Court ruling against gene patents hinged on a decision that isolating a human gene or part of a human gene is not an act of invention, reversing the traditional patent office practice. The decision allows for synthetically produced DNA sequences to be patented.

3. Gene patents for tests create monopolies that lead to high prices.

Commercial genetic testing has been a contentious issue and few companies undertake testing for single gene disorders. But companies engaged in commercial genetic testing have tended to ensure they’re the sole provider of such tests.

This gives them a monopoly and they can set whatever price they like for the test. This is clearly not a desirable outcome for society because it means we fail to protect vulnerable people who fear they have an illness from exploitation.

4. Monopolies lead to a lack of quality assurance.

Of particular concern is a monopoly’s inability to orchestrate a quality assurance program because this would require samples to be sent to third parties for verification.

Not only does it prevent monitoring of whether internal processes are producing the correct result, it disallows people from seeking a second opinion.

The decision of the High Court of Australia to uphold its previous decision now puts Australia out of step with the US Supreme Court and raises the question of just how much knowledge it has on matters it does not routinely deal with.

But what it means for Australia is probably very little; the current patent held by Myriad Genetics will expire within a relatively short period of time.

Rodney Scott does not work for, consult to, own shares in or receive funding from any company or organisation that would benefit from this article, and has no relevant affiliations.
This article was originally published on The Conversation.
Read the original article.
Publisher: bhakragani - Saturday, September 06, 2014

Tuesday, September 2, 2014


How the zebra got its stripes, with Alan Turing

Where do a zebra’s stripes, a leopard’s spots and our fingers come from? The key was found years ago – by the man who cracked the
Enigma code, writes Kat Arney.

In 1952 a mathematician published a set of equations that tried to explain the patterns we see in nature, from the dappled stripes adorning the back of a zebra to the whorled leaves on a plant stem, or even the complex tucking and folding that turns a ball of cells into an organism. His name was Alan Turing.

More famous for cracking the wartime Enigma code and his contributions to mathematics, computer science and artificial intelligence, it may come as a surprise that Turing harboured such an interest. In fact, it was an extension of his fascination with the workings of the mind and the underlying nature of life.

The secret glory of Turing’s wartime success had faded by the 1950s, and he was holed up in the grimly industrial confines of the University of Manchester. In theory he was there to develop programs for one of the world’s first electronic computers – a motley collection of valves, wires and tubes – but he found himself increasingly side-lined by greasy-fingered engineers who were more focused on nuts and bolts than numbers. This disconnection was probably intentional on Turing’s part, rather than deliberate exclusion on theirs, as his attention was drifting away from computing towards bigger questions about life.

It was a good time to be excited about biology. Researchers around the world were busy getting to grips with the nature of genes, and James Watson and Francis Crick would soon reveal the structure of DNA in 1953. There was also a growing interest in cybernetics – the idea of living beings as biological computers that could be deconstructed, hacked and rebuilt. Turing was quickly adopted into a gang of pioneering scientists and mathematicians known as the Ratio Club, where his ideas about artificial intelligence and machine learning were welcomed and encouraged.

Against this backdrop Turing took up a subject that had fascinated him since before the war. Embryology – the science of building a baby from a single fertilised egg cell – had been a hot topic in the early part of the 20th century, but progress sputtered to a halt as scientists realised they lacked the technical tools and scientific framework to figure it out. Perhaps, some thinkers concluded, the inner workings of life were fundamentally unknowable.

Turing viewed this as a cop-out. If a computer could be programmed to calculate, then a biological organism must also have some kind of underlying logic too.

He set to work collecting flowers in the Cheshire countryside, scrutinising the patterns in nature. Then came the equations – complex, unruly beasts that couldn’t be solved by human hands and brains. Luckily the very latest computer, a Ferranti Mark I, had just arrived in Manchester, and Turing soon put it to work crunching the numbers. Gradually, his “mathematical theory of embryology”, as he referred to it, began to take shape.

Like all the best scientific ideas, Turing’s theory was elegant and simple: any repeating natural pattern could be created by the interaction of two things – molecules, cells, whatever – with particular characteristics. Through a mathematical principle he called ‘reaction–diffusion’, these two components would spontaneously self-organise into spots, stripes, rings, swirls or dappled blobs.
In particular his attention focused on morphogens – the then-unknown molecules in developing organisms that control their growing shape and structure. The identities and interactions of these chemicals were, at the time, as enigmatic as the eponymous wartime code. Based on pioneering experiments on frog, fly and sea urchin embryos from the turn of the 20th century – involving painstakingly cutting and pasting tiny bits of tissue onto other tiny bits of tissue – biologists knew they had to be there. But they had no idea how they worked.

Although the nature of morphogens was a mystery, Turing believed he might have cracked their code. His paper ‘The chemical basis of morphogenesis’ appeared in the Philosophical Transactions of the Royal Society in August 1952.

Sadly, Turing didn’t live long enough to find out whether he was right. He took his own life in 1954, following a conviction for ‘gross indecency’ and subsequent chemical castration – the penalty for being openly gay in an intolerant time. In those two short years there was little to signpost the twists and turns that his patterns would take over the next 60 years, as biologists and mathematicians battled it out between the parallel worlds of embryology and computing.

In a cramped office in London, tucked away somewhere on the 27th floor of Guy’s Hospital, Professor Jeremy Green of King’s College London is pointing at a screen.

A program that simulates Turing patterns is running in a small window. At the top left is a square box, filled with writhing zebra-like monochrome stripes. Next to it is a brain-bending panel of equations. “It’s astonishing that Turing came up with this out of nowhere, as it’s not intuitive at all,” says Green, as he pokes a finger at the symbols. “But the equations are much less fearsome than you think.”

The essence of a Turing system is that you have two components, both of which can spread through space (or at least behave as if they do). These could be anything from the ripples of sand on a dune to two chemicals moving through the sticky goop holding cells together in a developing embryo. The key thing is that whatever they are, the two things spread at different speeds, one faster than the other.
One component is to be auto-activating, meaning that it can turn on the machinery that makes more of itself. But this activator also produces the second component – an inhibitor that switches off the activator. Crucially, the inhibitor has to move at a faster pace than the activator through space.
The beauty of it is that Turing systems are completely self-contained, self-starting and self-organising. According to Green, all that one needs to get going is just a little bit of activator. The first thing it does is make more of itself. And what prevents it from ramping up forever? As soon as it gets to a certain level it switches on the inhibitor, which builds up to stop it.

“The way to think about it is that as the activator builds up it has a head start,” says Green. “So you end up with, say, a black stripe, but the inhibitor then builds up and spreads more quickly. At a certain point it catches up with the activator in space and stops it in its tracks. And that makes one stripe.”
From these simple components you can create a world of patterns. The fearsome equations are just a way of describing those two things. All you need to do is adjust the conditions, or ‘parameters’. Tweaking the rates of spreading and decay, or changing how good the activator is at turning itself on and how quickly the inhibitor shuts it down, subtly alters the pattern to create spots or stripes, swirls or splodges.

Despite its elegance and simplicity, Turing’s reaction–diffusion idea gained little ground with the majority of developmental biologists at the time. And without the author around to champion his ideas, they remained in the domain of a small bunch of mathematicians. In the absence of solid evidence that Turing mechanisms were playing a part in any living system, they seemed destined to be a neat but irrelevant distraction.
Well, the stripes are easy. But what about the horse part?”
Alan Turing on the zebra, quoted by Francis Crick (1972)
Biologists were busy grappling with a bigger mystery: how a tiny blob of cells organises itself to create a head, tail, arms, legs and everything in between to build a new organism.

In the late 1960s a new explanation appeared, championed by the eminent and persuasive embryologist Lewis Wolpert and carried aloft by the legion of developmental biologists that followed in his footsteps. The concept of ‘positional information’ suggests that cells in a developing embryo sense where they are in relation to an underlying map of molecular signals (the mysterious morphogens). By way of explanation, Wolpert waved the French flag.

Imagine a rectangular block of cells in the shape of a flag. A strip of cells along the left-hand edge are pumping out a morphogen – let’s call it Striper – that gradually spreads out to create a smooth gradient of signal, high to low from left to right. Sensing the levels of Striper around them, the cells begin to act accordingly. Those on the left turn blue if the level of Striper is above a certain specific threshold, those in the middle turn white in response to the middling levels of Striper they detect, while those on the far right, bathing in the very lowest amounts of Striper, go red. Et voila – the French flag.

Wolpert’s flag model was simple to grasp, and developmental biologists loved it. All you had to do to build an organism was to set up a landscape of morphogen gradients, and cells would know exactly what to become – a bit like painting by numbers. More importantly, it was clear to researchers that it worked in real life, thanks to chickens.

Even today, chicken embryos are an attractive way to study animal development. Scientists can cut a window in the shell of a fertilised hen’s egg to watch the chick inside, and even fiddle about with tweezers to manipulate the growing embryo. What’s more, chicken wings have three long bony structures buried inside the tip, analogous to our fingers. Each one is different – like the three stripes of a French flag – making them the perfect system for testing out Wolpert’s idea.
In a series of landmark experiments in the 1960s, John Saunders and Mary Gasseling of Wisconsin’s Marquette University carefully cut a piece from the lower side of a developing chick’s wing bud – imagine taking a chunk from the edge of your hand by the little finger – and stuck it to the upper ‘thumb’ side.

Instead of the usual three digits (thumb, middle and little ‘fingers’), the resulting chicken had a mirror wing – little finger, middle, thumb, thumb, middle, little finger. The obvious conclusion was that the region from the base of the wing was producing a morphogen gradient. High levels of the gradient told the wing cells to make a little finger, middling ones instructed the middle digit, and low levels made a thumb.

It was hard to argue with such a definitive result. But the ghost of Turing’s idea still haunted the fringes of biology.

In 1979 a physicist-turned-biologist and a physical chemist caused a bit of a stir. Stuart Newman and Harry Frisch published a paper in the high-profile journal Science showing how a Turing-type mechanism could explain the patterning in a chicken’s fingers.

They simplified the developing three-dimensional limb into a flat rectangle and figured out reaction–diffusion equations that would generate waves of an imaginary digit-making morphogen within it as it grew. The patterns generated by Newman and Frisch’s model are clunky and square, but they look unmistakeably like the bones of a robot hand.

They argued that an underlying Turing pattern makes the fingers, which are then given their individual characteristics by some kind of overlying gradient – of the sort proposed by the French flag model – as opposed to the gradient itself directing the creation of the digits.
“People were still in an exploratory mode in the 1970s, and Turing’s own paper was only 25 years old at that point. Scientists were hearing about it for the first time and it was interesting,” says Newman, now at New York Medical College in the USA. “I was lucky to get physics-oriented biologists to review my paper – there wasn’t an ideology on the limb that had set in, and people were still wondering how it all worked.”

It was a credible alternative to Wolpert’s gradient idea, prominently published in a leading journal. According to Newman, the reception was initially warm. “Straight after it was published, one of Wolpert’s associates, Dennis Summerbell, wrote me a letter saying that they needed to consider the Turing idea, that it was very important. Then there was silence.”

A year later, Summerbell’s view had changed. He published a joint paper with biologist Jonathan Cooke, which made clear that he no longer considered it a valid idea. Newman was shocked. “From that point on nobody in that group ever mentioned it, with one exception – Lewis Wolpert himself once cited our paper in a symposium report in 1989 and dismissed it.”

The majority of the developmental biology community did not consider Turing patterns important at all. Fans of the positional information model closed ranks against Newman. The invitations to speak at scientific meetings dried up. It became difficult for him to publish papers and get funding to pursue Turing models. Paper after paper came out from scientists who supported the French flag model.
Newman explains: “A lot of them got to be editors at journals – I knew some colleagues who felt that pressure was put on them to keep our ideas out of some of the good journals. In other areas people were as open to new ideas as you might expect, but because Wolpert and his scientific descendants were so committed to his idea it became part of the culture of the limb world. All the meetings and special editions of journals were all centred around it, so it was very difficult to displace.”
Further blows came from the fruit fly Drosophila melanogaster – another organism beloved of developmental biologists. For a while the regimented stripes that form in the fly’s developing embryo were thought to develop through a Turing mechanism. But eventually they turned out to be created through the complex interplay of morphogen gradients activating specific patterns of gene activity in the right place at the right time, rather than a self-striping system.

Newman was disappointed by the failure of the research community to take his idea seriously, despite countless hours of further work on both the mathematical and molecular sides. For decades, his and Frisch’s paper languished in obscurity, haunting the same scientific territory as Turing’s original paper.;
I’ll take spots, then,” said the Leopard, “but don’t make ’em too vulgar-big. I wouldn’t look like Giraffe – not for ever so.”
‘How The Leopard Got His Spots’, from Rudyard Kipling’s Just So Stories (1902)
High up in the Centre for Genomic Regulation in Barcelona is an office papered with brightly coloured pictures of embryonic mouse paws. Each one shows neat stripes of developing bones fanning out inside blob-like budding limbs – something the room’s decorator, systems biologist James Sharpe, is convinced can be explained by Turing’s model.

Turing’s idea is simple, so one can easily imagine how it could explain the patterns we see in nature. And that’s part of the problem, because a simple likeness isn’t proof that a system is at work – it’s like seeing the face of Jesus in a piece of toast. Telling biological Just So Stories about how things have come to be is a dangerous game, yet this kind of thinking was used to justify the French flag model too.

In Sharpe’s view it was the chicken’s fault. “If studies of limb development had started with a mouse,” he says, “the whole history would have been very different.”
In his opinion there was a built-in bias right from the start that digits were fundamentally different from each other, requiring specific individual instructions for each one (provided by precise morphogen ‘coordinates’, according to the French flag model). This was one of the primary arguments made against a role for Turing patterns being involved in limb development – they can only ever generate the same thing, such as a stripe or a spot, again and again.

So how could a Turing system create the three distinctive digits of a chick’s limb? Surely each one must be told to grow in a certain way by an underlying gradient ‘map’? But a chick only has three fingers. “If they had 20, you would see that wasn’t the case,” says Sharpe, wiggling his fingers towards me by way of demonstration. “They’d all look much more similar to each other.”
I look down at my own hand and see his point. I have four fingers and a thumb, and each finger doesn’t seem to have particularly unique identity of its own. Sure, there are subtle differences in size, yet they’re basically the same. According to Sharpe, the best evidence that they aren’t that different comes from one of the most obvious but incorrect assumptions about the body: that people always have five fingers.

In reality the number of fingers and toes is one of the least robust things about the way we’re made. “We don’t always have five,” he says, “and it’s surprisingly common to have more.” In fact, it’s thought that up to one in 500 children is born with extra digits on their hands or feet. And while the French flag model can’t account for this, Turing patterns can.

By definition Turing systems are self-organising, creating consistent patterns with specific properties depending on the parameters. In the case of a stripy pattern, this means that the same set-up will always create stripes with the same distance (or wavelength, as mathematicians call it) between them. If you disrupt the pattern, for example by removing a chunk, the system will attempt to fill in the missing bits in a highly characteristic way. And while Turing systems are good at generating repeating patterns with a consistent wavelength, such as regular-sized fingers, they’re less good at counting how many they’ve made, hence the bonus digits.

Importantly, a particular Turing system can only make the same thing over and over again. But look closely at the body and there are many examples of repeating structures. In many animals, including ourselves, the fingers and toes are more or less all the same. But, according to the flag model, structures created in response to different levels of morphogen would all have to be different. How to explain the fact that the same thing can be ‘read’ out from a higher and lower morphogen level?
Sharpe maintains that the concept of an underlying molecular ‘road map’ just doesn’t hold up. “I don’t think it’s an exaggeration to say that for a long time a lot of the developmental biology community has thought that you have these seas of gradients washing over a whole organ. And because they’re going in different directions, every part of the organ has a different coordinate.”
In 2012 – the centenary of Turing’s birth and 60 years since his ‘chemical morphogenesis’ paper – Sharpe showed that this idea (at least in the limb) was wrong.

The proof was neatly demonstrated in a paper by Sharpe and Maria Ros at the University of Cantabria in Spain, published in Science. Ros used genetic engineering techniques to systematically remove members of a particular family of genes from mice. Their targets were the Hox genes, which play a fundamental role in organising the body plan of a developing embryo, including patterning mouse paws and human hands.

Getting rid of any of these crucial regulators might be expected to have some fairly major effects, but what the researchers saw was positively freakish. As they knocked out more and more of the 39 Hox genes found in mice, the resulting animals had more and more fingers on their paws, going up to 15 in the animals missing the most genes.

Importantly, as more Hox genes were cut and more fingers appeared, the spacing between them got smaller. So the increased number of fingers wasn’t due to larger paws, but to smaller and smaller stripes fitting into the same space – a classic hallmark of a Turing system, which had never been observed before in mouse limbs. When Sharpe crunched the numbers, Turing’s equations could account for the extra fingers Ros and her team were seeing.

That’s great for the near-identical digits of a mouse, I say, but it doesn’t explain why the chick’s three digits are so different. Sharpe scribbles on a piece of paper, drawing a Venn diagram of two scruffy overlapping circles. One is labelled “PI” for positional information à la Wolpert, the other “SO” for self-organising systems such as Turing patterns. Tapping at them with his pen, he says, “The answer is not that Turing is right and Wolpert was wrong, but that there’s a combination at work.”

Wolpert himself has conceded, to a certain extent, that a Turing system could be capable of patterning fingers. But it can’t, by definition, impart the differences between them. Morphogen gradients must work on top of this established pattern to give the digits their individual characteristics, from thumb to pinky, marrying together Wolpert’s positional information idea with Turing’s self-organising one.
Other real-life examples of Turing systems that have been quietly accumulating over the past two decades are now being noticed. A 1990 paper from a trio of French chemists described the first unambiguous experimental evidence of a Turing structure: they noticed a band of regular spots appear in a strip of gel where a colour-generating reaction was happening – the tell-tale sign of the system at work.

While studying elegantly striped marine angelfish, Japanese researcher Shigeru Kondo noticed that rather than their stripes getting bigger as the fish aged (as happens in mammals like zebras), they kept the same spacing but increased in number, branching to fill the space available. Computer models revealed that a Turing pattern could be the only explanation. Kondo went on to show that the stripes running along the length of a zebrafish can also be explained by Turing’s maths, in this case thanks to two different types of cells interacting with each other, rather than two molecules.

It turns out that the patterned coats of cats, from cheetahs and leopards to domestic tabbies, are the result of Turing mechanisms working to fill in the blank biological canvas of the skin. The distribution of hair follicles on our heads and the feathers on birds are also thanks to Turing-type self-organisation.

Other researchers are focusing on how Turing’s mathematics can explain the way tubes within an embryo’s developing chest split over and over again to create delicate, branched lungs. Even the regular array of teeth in our jaws probably got there by Turing-esque patterning.
Meanwhile in London, Jeremy Green has also found that the rugae on the roof of your mouth – the repeated ridges just above your front teeth that get burnt easily if you eat a too-hot slice of pizza – owe their existence to a Turing pattern.

As well as fish skins, feathers, fur, teeth, rugae and the bones in our hands, James Sharpe thinks there are plenty of other parts of the body that might be created through self-organising Turing patterns, with positional information laid on top. For a start, while our digits are clearly stripes, the clustered bones of the wrist could be viewed as spots. These can easily be made with a few tweaks to a Turing equation’s parameters.

Sharpe has some more controversial ideas for where the mechanism might be at work – perhaps patterning the regular array of ribs and vertebrae running up our spine. He even suspects that the famous stripes in fruit fly embryos have more to do with Turing patterning than the rest of the developmental biology community might have expected.

Given that he works in a building clad in horizontal wooden bars, I ask if he’s started to see Turing patterns everywhere he looks. “I’ve been through that phase,” he laughs. “During the centenary year it really was Turing everywhere. The exciting possibility for me is that we’ve misunderstood a whole lot of systems and how easy it can be to trick ourselves – and the whole community – into making up Just So Stories that seem to fit and being happy with them.”

Stuart Newman agrees, his 1979 theory now back out of the shadows. “When you start tugging at one thread, a lot of things will fall apart if you’re on to something. They don’t want to talk about it, not because it’s wrong – it’s easy to dismiss something that’s wrong – but probably because it’s right. And I think that’s what turned out to be the case.”;

Slowly but surely, researchers are piecing together the role of Turing systems in creating biological structures. But until recently there was still one thing needed to prove that there’s a Turing pattern at work in the limb: the identities of the two components that drive it.

That mystery has now been solved by James Sharpe and his team in a paper published in August 2014, again in the journal Science. Five years in the making, it combines delicate embryo work with hardcore number crunching.

Sharpe figured that the components needed to fuel a Turing pattern in the limb must show a stripy pattern that reflects the very early developing fingers – either switched on in the future fingers and off in the cells destined to become the gaps, or vice versa.

To find them, graduate student Jelena Raspopovic collected cells from a developing mouse limb bud, in which only the merest hint of gene activity that leads to digit formation can be seen. After separating the two types of cells, and much painstaking molecular analysis, some interesting molecular suspects popped out. Using computer modelling, Sharpe was able to exactly recapitulate a gradual appearance of digits that mirrored what they saw in actual mouse paws, based on the activity patterns of these components.

Intriguingly, unlike the neat two-part system invoked by Turing, Sharpe thinks that three different molecules work together in the limb to make fingers. One is Sox9, a protein that tells cells to “make bones here” in the developing digits. The others are signals sent by two biological messenger systems: one called BMP (bone morphogenetic protein) signalling, which switches on Sox9 in the fingers, and another messenger molecule known as WNT (pronounced “wint”), which turns it off in the gaps between fingers.

Although classic Turing systems invoke just two components – an activator and an inhibitor – this situation is a little more complicated. ;“It doesn’t seem to boil down to literally just two things,” Sharpe explains. “Real biological networks are complex, and in our case we’ve boiled it down to two signalling pathways rather than two specific molecules.”

Further confirmation came when they went the other way – from the model to the embryo. Another of Sharpe’s students, Luciano Marcon, tweaked the program to see what would happen to the patterns if each signalling pathway was turned down. In the simulation, reducing BMP signalling led to a computer-generated paw with no fingers. Conversely, turning down WNT predicted a limb made entirely of digits fused together.

When tested in real life, using tiny clumps of limb bud tissue taken from early mouse embryos and grown in Petri dishes, these predictions came true. Treating the cultures with drugs that dampen down each pathway produced exactly what the program had predicted – no fingers, or all fingers. An alternative simulation with both signals turned down at the same time predicts two or three fat fingers instead of five neat digits. Again, using both drugs at once on real mouse limb buds created exactly the same pattern. Being able to flip from the model to the embryo and back again – making testable predictions that are borne out by experiments – is a key piece of proof that things are working in the way Sharpe thinks.

And if the theory is finally accepted, and we figure out how and where Turing systems are used to create structures in nature, what can we do with this knowledge? Quite a lot, according to Jeremy Green.

“You can live without rugae but the things like your heart valves or your whole palate, they really matter,” he says. “The regenerative medics working on any stem cell technology or cell therapy in the future are going to need to understand how these are made. The growth factor research in the 1980s was the bedrock of the stem cell therapies that are starting to go into clinical trials now, but it inspired the whole world of regenerative medicine. That’s the kind of timescale we’re talking about.”
At Guy’s Hospital he sees close-up what happens when development goes awry. His department specialises in birth defects affecting the face and skull, and Green believes that understanding the underlying molecular nuts and bolts is the key to fixing them. “What we’re doing now is very theoretical, and we can fantasise about how it’s going to be useful, but in 25 years that’s the kind of knowledge we’ll need to have. It’ll probably be taken for granted by then, but we’ll need to know all this Turing stuff to be able to build a better body.”

In the last years of Alan Turing’s life he saw his mathematical dream – a programmable electronic computer – sputter into existence from a temperamental collection of wires and tubes. Back then it was capable of crunching a few numbers at a snail’s pace. Today, the smartphone in your pocket is packed with computing technology that would have blown his mind. It’s taken almost another lifetime to bring his biological vision into scientific reality, but it’s turning out to be more than a neat explanation and some fancy equations.

With thanks to Dagmar Iber for additional discussion.

This article was originally published on Mosaic.
Read the original article.
Publisher: bhakragani - Tuesday, September 02, 2014


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