​‘Mystery’ respiratory virus spreads across several US states .


A mysterious respiratory virus, similar to the common cold but far more pernicious, is affecting thousands across 10 US states – hospitalizing hundreds of children, affecting those with asthma or those under the age of 5.

Reuters/Mohamed Alhwaity

The disease has yet to be officially identified, but officials suspect it is the rare respiratory virus called human enterovirus 68. The Center for Disease Control and Prevention said the virus is related to the rhinovirus, which is what causes the common cold.

Enterovirus 68 causes respiratory illness in children. It can attack the central nervous system and cause paralysis or even death.

Some US states are reporting 70 new cases a day including Kansas, Illinois, Ohio, and Indiana, but Colorado and Missouri have been hit the hardest, according to a local media report.

There is no vaccine for human enterovirus 68 according to Missouri health officials, adding “there is also no specific treatment for the virus.”

Since the virus is not treatable with antibiotics, doctors have been giving patients steroids and medication to help improve breathing. Respiratory problems seem to be the most threatening symptom, and some children and teenagers are being put in intensive care, the Atlanta Journal-Constitution reports.

HLN quoted one doctor saying, “What’s troubling about this virus is it starts out with cold-like symptoms including fever, sneezing, coughing, and body aches – making it difficult to properly diagnose until more serious symptoms show up.”

Dr. Christine Nyquist at Children’s Hospital Colorado said the virus usually “appears similar to a severe cold.”“The kids are coming in with respiratory symptoms, where their asthma is exacerbated,” Nyquist told ABC News. “Kids with no wheezing are having severe wheezing.”

Children’s Hospital Colorado locations reported treating more than 900 children for severe respiratory illnesses since August 18, with 86 of them needing to be admitted to hospital, according to 7News.

Officials told CNN that enteroviruses are not uncommon, but it is unusual that so many children have been hospitalized.

Variation in Decisions to Forgo Life-Sustaining Therapies in US ICUs


BACKGROUND:  The magnitude and implication of variation in end-of-life decision-making among ICUs in the United States is unknown.

METHODS:  We reviewed data on decisions to forgo life-sustaining therapy (DFLSTs) in 269,002 patients admitted to 153 ICUs in the United States between 2001 and 2009. We used fixed-effects logistic regression to create a multivariable model for DFLST and then calculated adjusted rates of DFLST for each ICU.

RESULTS:  Patient factors associated with increased odds of DFLST included advanced age, female sex, white race, and poor baseline functional status (all P < .001). However, associations with several of these factors varied among ICUs (eg, black race had an OR for DFLST from 0.18 to 2.55 across ICUs). The ICU staffing model was also found to be associated with DFLST, with an open ICU staffing model associated with an increased odds of a DFLST (OR = 1.19). The predicted probability of DFLST varied approximately sixfold among ICUs after adjustment for the fixed patient and ICU effects and was directly correlated with the standardized mortality ratios of ICUs (r = 0.53, 0.41–0.68).

CONCLUSION:  Although patient factors explain much of the variability in DFLST practices, significant effects of ICU culture and practice influence end-of-life decision-making. The observation that an ICU’s risk-adjusted propensity to withdraw life support is directly associated with its standardized mortality ratio suggests problems with using the latter as a quality measure.

Pembrolizumab Approved by FDA .


The U.S. Food and Drug Administration (FDA) announced the highly anticipated approval of the cancer immunotherapeutic pembrolizumab (Keytruda) for the treatment of certain patients with metastatic melanoma, the most deadly form of skin cancer.

3D structure of a melanoma cell
3D structure of a melanoma cell (Source: Sriram Subramaniam, National Cancer Institute)

Pembrolizumab is the first in a new class of cancer immunotherapeutics called PD-1 inhibitors to be approved by the FDA. While the FDA decision came earlier than initially expected, the excitement surrounding it has been palpable for a while because pembrolizumab, as well as other PD-1 inhibitors, has been yielding dramatic and durable responses for patients with metastatic melanoma. In fact, many patients are continuing to benefit from pembrolizumab more than one year after starting treatment.

As I discussed in an earlier blog post, “Cancer Immunotherapy: Breaking Through to the Standard of Care,” PD-1 inhibitors work by releasing the PD-1 brake on cancer-fighting immune cells called T cells. Once the PD-1 brake is released, the T cells are able to carry out their natural function and can destroy cancer cells.

Louis M. Weiner, MD, director of the Georgetown Lombardi Comprehensive Cancer Center and a spokesman for the American Association for Cancer Research, told the New York Times: “This is really opening up a whole new avenue of effective therapies previously not available. It allows us to see a time when we can treat many dreaded cancers without resorting to cytotoxic chemotherapy.”

The patients who will benefit from yesterday’s FDA approval are those with metastatic melanoma that does not respond, or has stopped responding, to another cancer immunotherapeutic, ipilimumab (Yervoy). Ipilimumab targets another T-cell brake, CTLA4. A substantial number of patients with metastatic melanoma are still benefiting from ipilimumab more than five years after starting treatment, and it is hoped that pembrolizumab and other PD-1 inhibitors will have a similar impact so that significant inroads can be made against metastatic melanoma – a disease that has an overall five-year survival rate of only 16 percent.

Metastatic melanoma is a cancer diagnosis projected to be received by more than 3,000 U.S. residents in 2014 alone. With PD-1 inhibitors also showing tremendous promise in clinical trials as a potential treatment for other types of cancer, in particular non-small cell lung cancer – a disease that more than 180,000 individuals in the United States are expected to be diagnosed with in 2014 – it is hoped that additional FDA approvals for this groundbreaking class of drugs lie in the near future.

Liberia’s Ebola problem far worse than imagined, says WHO .


The World Health Organization (WHO) has released a statement saying problems related to the Ebola outbreak in Liberia are increasingly dire.

Ebola virus (blue) budding from an infected monkey kidney cell (yellow).

Situation in Liberia: non-conventional interventions needed

8 September 2014

During the past weeks, a WHO team of emergency experts worked together with President Ellen Johnson Sirleaf and members of her government to assess the Ebola situation in Liberia.

Transmission of the Ebola virus in Liberia is already intense and the number of new cases is increasing exponentially.

The investigative team worked alongside staff from the Ministry of Health, local health officials, and other key partners working in the country.

All agreed that the demands of the Ebola outbreak have completely outstripped the government’s and partners’ capacity to respond. Fourteen of Liberia’s 15 counties have now reported confirmed cases.

Some 152 health care workers have been infected and 79 have died. When the outbreak began, Liberia had only one doctor to treat nearly 100,000 people in a total population of 4.4 million people. Every infection or death of a doctor or nurse depletes response capacity significantly.

Liberia, together with the other hard-hit countries, namely Guinea and Sierra Leone, is experiencing a phenomenon never before seen in any previous Ebola outbreak. As soon as a new Ebola treatment facility is opened, it immediately fills to overflowing with patients, pointing to a large but previously invisible caseload.

Of all Ebola-affected countries, Liberia has the highest cumulative number of reported cases and deaths, amounting, on 8 September, to nearly two thousand cases and more than one thousand deaths. The case-fatality rate, at 58%, is also among the highest.

Situation in Montserrado county

The WHO investigation concentrated on Montserrado county, which includes Liberia’s capital, Monrovia. The county is home to more than one million people. The teeming West Point slum, which has no sanitation, little running water, and virtually no electrical supplies, is also located in Monrovia, and is adjacent to the city’s major market district.

In Montserrado county, the team estimated that 1000 beds are urgently needed for the treatment of currently infected Ebola patients. At present only 240 beds are available, with an additional 260 beds either planned or in the process of being put in place. These estimates mean that only half of the urgent and immediate capacity needs could be met within the next few weeks and months.

The number of new cases is moving far faster than the capacity to manage them in Ebola-specific treatment centres.

For example, an Ebola treatment facility, hastily improvised by WHO for the Ministry of Health, was recently set up to manage 30 patients but had more than 70 patients as soon as it opened.

WHO estimates that 200 to 250 medical staff are needed to safely manage an Ebola treatment facility with 70 beds.

The investigation team viewed conditions in general-purpose health facilities as well as Ebola-specific transit and treatment facilities.

The John F Kennedy Medical Center in Monrovia, which was largely destroyed during Liberia’s civil war, remains the country’s only academic referral hospital. The hospital is plagued by electrical fires and floods, and several medical staff were infected there and died, depleting the hospital’s limited workforce further.

The fact that early symptoms of Ebola virus disease mimic those of many other common infectious diseases increases the likelihood that Ebola patients will be treated in the same ward as patients suffering from other infections, putting cases and medical staff alike at very high risk of exposure.

In Monrovia, taxis filled with entire families, of whom some members are thought to be infected with the Ebola virus, crisscross the city, searching for a treatment bed. There are none. As WHO staff in Liberia confirm, no free beds for Ebola treatment exist anywhere in the country.

According to a WHO staff member who has been in Liberia for the past several weeks, motorbike-taxis and regular taxis are a hot source of potential Ebola virus transmission, as these vehicles are not disinfected at all, much less before new passengers are taken on board.

When patients are turned away at Ebola treatment centres, they have no choice but to return to their communities and homes, where they inevitably infect others, perpetuating constantly higher flare-ups in the number of cases.

Other urgent needs include finding shelters for orphans and helping recovered patients who have been rejected by their families or neighbours.

Last week, WHO sent one of its most experienced emergency managers to head the WHO office in Monrovia. Coordination among key partners is rapidly improving, aiming for a better match between resources and rapidly escalating needs.

Implications of the investigation

The investigation in Liberia yields three important conclusions that need to shape the Ebola response in high-transmission countries.

First, conventional Ebola control interventions are not having an adequate impact in Liberia, though they appear to be working elsewhere in areas of limited transmission, most notably in Nigeria, Senegal, and the Democratic Republic of Congo.

Second, far greater community engagement is the cornerstone of a more effective response. Where communities take charge, especially in rural areas, and put in place their own solutions and protective measures, Ebola transmission has slowed considerably.

Third, key development partners who are supporting the response in Liberia and elsewhere need to prepare to scale up their current efforts by three- to four-fold.

As WHO Director-General Dr Margaret Chan told agencies and officials last week in New York City and Washington, DC, development partners need to prepare for an “exponential increase” in Ebola cases in countries currently experiencing intense virus transmission.

Many thousands of new cases are expected in Liberia over the coming three weeks.

WHO and its Director-General will continue to advocate for more Ebola treatment beds in Liberia and elsewhere, and will hold the world accountable for responding to this dire emergency with its unprecedented dimensions of human suffering.

How rabies attacks the brain, seen in Israel for the first time .


Israeli scientists watch as virus hijacks neuron ‘train’ and speeds to central nervous system
An illustration of a rabies virus in the nervous system. (photo credi: Rabies image

The virus has long been known to travel along neurons, the cells that transmit the electrical and chemical signals enabling movement, feeling, and thought. Until now, though, nobody had been able to figure out how.
Using powerful live cell imaging, the scientists found that the virus hijacks the “train” that transports cell components along a neuron, and drives it full throttle into the spinal cord. From there, the virus likely takes other trains to the brain and then throughout the peripheral nervous system, they say – shutting down the body as it goes along.
A microscope image of a sensory neuron, with an inset of the rabies virus (green) binding to the p75 receptor (red). (photo credit: Courtesy)

“The rabies virus is transported through railway-like machinery in the neurons,” said Shani Gluska, a doctoral student at Tel Aviv University, who led the study along with Prof. Eran Perlson, a physiologist at the university. “With very high-end microscopy, we saw for ourselves how the virus not only hijacks the transport machinery, but also makes it go faster.”

The scientists say their findings, published in the journal PLOS Pathogens in August, could one day enable scientists to take control of the neuron train system to treat rabies, as well as other neurodegenerative diseases.

Seeing is believing
Rabies is infamous for its dramatic symptoms, like aggression, psychosis, wild movements, and “foaming at the mouth.” Without treatment in time by vaccination, rabies severely inflames the brain, ultimately leading to paralysis of the heart and lungs and, with a few recent exceptions, to death. More than 55,000 people die every year from rabies, mostly in Africa and Asia, according to the World Health Organization.

To see how the rabies virus travels through the nervous system, the Israeli scientists grew mouse sensory neurons in the lab and infected them with the virus. They tagged the virus with a fluorescent marker, then watched and recorded its movements in real time with a high-power microscope.

‘If we can learn how rabies manipulates the system, we can maybe try to manipulate it ourselves’
The scientists saw that the virus takes a route normally reserved for nerve growth factors, proteins that are responsible for development and health of neurons. The virus enters a neuron in the peripheral nervous system by binding to a nerve growth factor receptor called p75.

Once inside, the virus boards a “train car,” a bubble-like vesicle, and departs from the cell membrane. “Engines” – nano-sized motor proteins that typically chug up and down neurons to keep them alive – then hitch themselves to the car and pull it along “tracks,” microtubules. The ride continues through the neuron’s tail-like axon, which can stretch up to a meter in length, and on to its cell body, which is located in the spinal cord.
Doctoral student Shani Gluska working in Dr. Eran Perlson’s lab at Tel Aviv University. (photo credit: Courtesy)

In the spinal cord, the scientists believe the virus catches the first available train to the brain, where it wreaks havoc before embarking on a tour of the body – though the study did not include the kinds of neurons that run directly to or from the brain. Compared to the growth factors that take the same p75 route, the virus travels much more quickly.

The scientists say the virus may speed up the train by pushing the engines harder, by dumping more “fuel,” or ATP, into the engines, or by demanding more engines or a better track. A minority of the rabies viruses in the study took other, slower routes along the neurons.

Putting the brakes on nerve disease
The results reveal what is likely a major mechanism the rabies virus uses to enter the peripheral nervous system, usually from the muscles, and to travel rapidly to the central nervous system, the scientists say.

Based on previous research, they say the virus probably travels in a similar way elsewhere in the nervous system: along motor neurons to the spinal cord, along interneurons in the spinal cord to the brain, and along motor neurons from the brain back to the peripheral nervous system.

Improved understanding of how the neuron train works could lead to new disease treatments, they say.

“If we can learn how rabies manipulates the system, we can maybe try to manipulate it ourselves,” said Perlson, who oversaw the study in his lab, which focuses on neuron signaling and transport. When it comes to rabies, interfering with the virus’ travel plans could extend the window of time for treatment, the scientists say.

The rabies vaccine is only effective until the virus reaches the central nervous system and begins causing symptoms, which usually takes one to three months. On the other hand, disruptions of the neuron train system contribute to neurodegenerative diseases, like Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS).

The scientists say getting the train back on track could treat and possibly even cure such diseases.

 

New Ebola vaccine approved for human trials — RT News


http://rt.com/news/185840-ebola-vaccine-human-trials/

From the desk of Zedie.

US has seen nearly 600 measles cases this year, CDC says .


Outbreaks linked to trend of parents not vaccinating children
• Deadly disease had been virtually eradicated in US

mmr vaccine
A bottle of combined measles, mumps and rubella vaccine. A drop in vaccination rates is being blamed for a surge in measles cases. 

The United States is experiencing a record number of measles cases since the disease was declared eliminated in 2000.

Authorities have confirmed 592 cases between 1 January and 29 August, a jump caused mainly by parents refusing to vaccinate their children, according to the latest monthly report from the Centres for Disease Control and Prevention.

The latest figures from summer continue a troubling trend reported in May when the US recorded 288 cases of measles since January – the most in a five-month period since 1994.

Eighteen outbreaks have accounted for 89% of the cases this year. Outbreaks are being driven by unvaccinated people, primarily US residents, contracting measles in other countries, bringing the virus back to the US and spreading it to others in communities with relatively low vaccination rates.

Parents who challenge the medical consensus over the safety and efficacy of inoculations are driving down the rate of vaccination. Some fear vaccines could trigger autism – a theory discredited by mainstream science.

California parents are deciding against vaccinating their kindergarten-age children at twice the rate they did seven years ago, according to the Los Angeles Times. The growth in personal-belief exemptions was particularly prevalent at private schools, it reported.

Medical experts have expressed alarm.

“Measles is still common in many parts of the world including some countries in Europe, Asia, the Pacific, and Africa, travellers with measles continue to bring the disease into the US,” said a release from the CDC’s National Centre for Immunisation and Respiratory Diseases. “Measles can spread when it reaches a community in the US where groups of people are unvaccinated.”

The highly contagious viral respiratory disease is often accompanied by a blotchy rash, fever, runny nose, cough, body aches, watery eyes or pink eye and tiny white spots in the mouth.

Around the world, about 20 million people are infected each year, and 122,000 die, according to the CDC.

Measles was nearly eradicated in the US; in 2012, 55 cases were reported.

Before vaccines were introduced nearly every child in the US contracted the disease by the age of 15. About three million to four million people were infected annually. Of those, the disease killed between 450 and 500 people each year, put 48,000 in the hospital, caused 7,000 to have seizures and left 1,000 with permanent hearing or brain damage.

Infants and children under one-year-old are at greater risk of developing serious cases of measles. The CDC recommends children over 12 months old receive what is known as the “MMR”, or measles, mumps and rubella, vaccinations. The CDC recommends children older than six months old who will travel abroad receive the vaccines.

Ultraviolet light-induced mutation drives many skin cancers, researchers find .


A genetic mutation caused by ultraviolet light is likely the driving force behind millions of human skin cancers, according to researchers. The mutation occurs in a gene called KNSTRN, which is involved in helping cells divide their DNA equally during cell division.

Paul Khavari and his team found that sunlight triggered a genetic mutation linked to a common type of skin cancer.

A genetic mutation caused by ultraviolet light is likely the driving force behind millions of human skin cancers, according to researchers at the Stanford University School of Medicine.

The mutation occurs in a gene called KNSTRN, which is involved in helping cells divide their DNA equally during cell division.

Genes that cause cancer when mutated are known as oncogenes. Although KNSTRN hasn’t been previously implicated as a cause of human cancers, the research suggests it may be one of the most commonly mutated oncogenes in the world.

“This previously unknown oncogene is activated by sunlight and drives the development of cutaneous squamous cell carcinomas,” said Paul Khavari, MD, PhD, the Carl J. Herzog Professor in Dermatology in the School of Medicine and chair of the Department of Dermatology. “Our research shows that skin cancers arise differently from other cancers, and that a single mutation can cause genomic catastrophe.”

Cutaneous squamous cell carcinoma is the second most common cancer in humans. More than 1 million new cases are diagnosed globally each year. The researchers found that a particular region of KNSTRN is mutated in about 20 percent of cutaneous squamous cell carcinomas and in about 5 percent of melanomas.

A paper describing the research will be published online Sept. 7 in Nature Genetics. Khavari, who is also a member of the Stanford Cancer Institute and chief of the dermatology service at the Veterans Affairs Palo Alto Health Care System, is the senior author of the paper. Postdoctoral scholar Carolyn Lee, MD, PhD, is the lead author.

Lee and Khavari made the discovery while investigating the genetic causes of cutaneous squamous cell carcinoma. They compared the DNA sequences of genes from the tumor cells with those of normal skin and looked for mutations that occurred only in the tumors. They found 336 candidate genes for further study, including some familiar culprits. The top two most commonly mutated genes were CDKN2A and TP53, which were already known to be associated with squamous cell carcinoma.

The third most commonly mutated gene, KNSTRN, was a surprise. It encodes a protein that helps to form the kinetochore — a structure that serves as a kind of handle used to pull pairs of newly replicated chromosomes to either end of the cell during cell division. Sequestering the DNA at either end of the cell allows the cell to split along the middle to form two daughter cells, each with the proper complement of chromosomes.

If the chromosomes don’t separate correctly, the daughter cells will have abnormal amounts of DNA. These cells with extra or missing chromosomes are known as aneuploid, and they are often severely dysfunctional. They tend to misread cellular cues and to behave erratically. Aneuploidy is a critical early step toward the development of many types of cancer.

The mutation in the KNSTRN gene was caused by the replacement of a single nucleotide, called a cytosine, with another, called a thymine, within a specific, short stretch of DNA. The swap is indicative of a cell’s attempt to repair damage from high-energy ultraviolet rays, such as those found in sunlight.

“Mutations at this UV hotspot are not found in any of the other cancers we investigated,” said Khavari. “They occur only in skin cancers.”

The researchers found the UV-induced KNSTRN mutation in about 20 percent of actinic keratoses — a premalignant skin condition that often progresses to squamous cell carcinoma — but never in 122 samples of normal skin, indicating the mutation is likely to be an early event in the development of squamous cell carcinomas.

Furthermore, overexpression of mutant KNSTRN in laboratory-grown human skin cells disrupted their ability to segregate their DNA during cell division and enhanced the growth of cancer cells in a mouse model of squamous cell carcinoma.

Finally, Lee compared five patient-derived squamous cell carcinomas that had the KNSTRN mutation with five samples that did not have the mutation. Although both sets of cells were aneuploid, those with the mutation had the most severely abnormal genomes.

The identification of a new oncogene will allow researchers to better understand how these types of skin cancers develop. It may also give them clues about how to develop new therapies for the disease. In this case, it also neatly connects the dots between sun exposure and skin cancer.

“Essentially, one ultraviolet-mediated mutation in this region promotes aneuploidy and subsequent tumorigenesis,” said Khavari. “It is critical to protect the skin from the sun.”


Story Source:

The above story is based on materials provided by Stanford University Medical Center. The original article was written by Krista Conger. Note: Materials may be edited for content and length.


Journal Reference:

  1. Carolyn S Lee, Aparna Bhaduri, Angela Mah, Whitney L Johnson, Alexander Ungewickell, Cody J Aros, Christie B Nguyen, Eon J Rios, Zurab Siprashvili, Aaron Straight, Jinah Kim, Sumaira Z Aasi, Paul A Khavari. Recurrent point mutations in the kinetochore gene KNSTRN in cutaneous squamous cell carcinoma.Nature Genetics, 2014; DOI: 10.1038/ng.3091

Dynamic duo takes out cellular trash: Research finds how dead cells are removed from body .


Scientists have identified how immune cells use two critical receptors to clear dead cells from the body, pointing the way to new autoimmune and cancer therapies. “This basic research focus allowed us to discover a completely new aspect of immune regulation that no one -— including any immunologist—had known about before,” said one researcher.


In an inflammatory environment (left) and normal environment (right) macrophages (green) engulf dead cells (pink).

In most of the tissues of the body, specialized immune cells are entrusted with the task of engulfing the billions of dead cells that are generated every day. When these garbage disposals don’t do their job, dead cells and their waste products rapidly pile up, destroying healthy tissue and leading to autoimmune diseases such as lupus and rheumatoid arthritis.

Now, Salk scientists have discovered how two critical receptors on these garbage-eating cells identify and engulf dead cells in very different environments, as detailed in Nature Immunology.

“To target these receptors as treatments for autoimmune disease and cancer, it’s important to know exactly which receptor is doing what. And this discovery tells us that,” says senior author of the work Greg Lemke, Salk professor of molecular neurobiology and the holder of Salk’s Françoise Gilot-Salk Chair.

The garbage-disposing cells, known as macrophages, have arrays of receptors on their surface, two of which — called Mer and Axl — are responsible for recognizing dead cells in normal environments and inflamed environments, respectively. Mer operates as a “steady-as-she-goes” receptor, clearing out dead cells in healthy tissues on a daily basis. Axl, in contrast, acts as an “all-hands-on-deck” receptor, kicking macrophages into action in inflammatory settings that result from infection or tissue trauma. These inflamed environments have many more dead cells.

“We thought Axl and Mer were doing the same job, and they are: they both recognize a so-called ‘eat me’ signal displayed on the surface of dead cells. But it turns out that they work in very different settings,” says Lemke, whose lab first discovered the two receptors — which, along with a third, make up the TAM family — two decades ago. Lemke and colleagues explored the roles of TAM receptors in the brain initially, but observed that the absence of these receptors had dramatic effects on the immune system, including the development of autoimmune disease. The receptors have since become a growing focus for cancer and autoimmune research, and previous work has found that these three receptors are important in other areas, including the intestines, reproductive organs, and vision.

“This basic research focus allowed us to discover a completely new aspect of immune regulation that no one — including any immunologist — had known about before,” adds Lemke.

In the new work, the researchers found multiple critical differences between Axl and Mer. For example, the receptors use different molecules — called ligands — to be activated: Axl has a single such ligand and, once engaged, is quickly cleaved off of the surface of the macrophage. Levels of the free-floating Axl in the blood have turned out to be an accurate, general biomarker for inflammation, quickly showing up in the circulation after tissue trauma or injury.

“We compared the behavior and regulation of the receptors, and the results were very striking,” says first author Anna Zagórska. “In response to many different pro-inflammatory stimuli, Axl was upregulated and Mer was not. In contrast, immunosuppressive corticosteroids, which are widely used to suppress inflammation in people, upregulated Mer and suppressed Axl. These differences were our entry point to the study.”

Next, the researchers are looking into each receptor’s activity in more detail. The team is finding that these receptors are unusual in that they have a three-step binding procedure, whereas most cell receptors bind in one step. Exploring and understanding this process will help to lead to more targeted therapeutics for cancers and other diseases in which the receptors are thought to act.


Story Source:

The above story is based on materials provided by Salk Institute for Biological Studies. Note: Materials may be edited for content and length.


Journal Reference:

  1. Anna Zagórska, Paqui G Través, Erin D Lew, Ian Dransfield, Greg Lemke.Diversification of TAM receptor tyrosine kinase function. Nature Immunology, 2014; DOI: 10.1038/ni.2986

Why You Forget: 5 Strange Facts About Memory


Memory can be a playful thing. It collects minute details from childhood events, yet leaves us wondering where we left our keys.
There are several types of memories, and the brain has a unique way of forgetting each kind. Psychologists have classified various ways by which we forget, and biologists have studied forgetting mechanisms at the cellular level.
They’ve found that forgetting is normal, and actually vital to how the brain works. Here is a look at the strange facts about how people forget things.

How doorways destroy memory
In one common but mysterious short-term memory failure, people find themselves in a room, without remembering why they ended up there. Researchers say, in these circumstances, the doorway may be to blame. The very act of walking through a doorway may hint to the brain that a new scene has started and it should store prior memories away, thereby causing strange memory lapses. [Top 10 Mysteries of the Mind]
“Entering or exiting through a doorway serves as an ‘event boundary’ in the mind, which separates episodes of activity and files them away,” Gabriel Radvansky, a psychologist at the University of Notre Dame, told Live Science in a 2011 interview. “Recalling the decision or activity that was made in a different room is difficult because it has been compartmentalized.”
But still, mental event-boundaries are useful, because they help us organize our mental timelines and remember not just where, but when a particular event happened.

 

Mind-erasing activities
Although rare, certain activities can result in a temporary memory loss and brain fog, called transient global amnesia. For example, sex has been reported to cause this memory problem, with patients forgetting the past day or so, and having difficulty forming new memories.
People with transient global amnesia suffer no serious side effects, and the memory problems usually disappear in a few hours. But it’s not clear how this happens, and brain scans of patients who have had this type of amnesia show no signs of damage to the brain, or signs of stroke.
Memories can live on, even if we can’t access them
Could forgotten songs continue to live on inside our heads, without us knowing?
In a 2013 report of a strange case in the journal Frontiers in Neurology, researchers described a woman who had musical hallucinations of song that she didn’t recognize, but others did.
“To our knowledge, this is the first report of musical hallucinations of non-recognizable songs that were recognized by others in the patient’s environment,” the researchers wrote.
The scientists said the woman had likely known the song at some point, but forgot it. The case raises the question of what happens to forgotten memories, they said, and suggests that memories can be stored in some form in the brain that renders them accessible, and yet unrecognizable.
It is possible that the woman had fragmented preservation of musical memories, with key portions of those memories lost. As a result, she couldn’t recognize those memories, the researchers said.
Brains may be programmed to forget infancy
Our earliest childhood memories fade, and there’s likely a reason for that, researchers say. Most often, people don’t recall any memories from their earliest years of life, usually before age 3 or 4. This is called infantile amnesia.
Scientists previously thought that early memories were there, but children just didn’t have the language skills to verbalize them.
However, recent research shows that children do make memories during their early years, but then forget through deliberate mechanisms. One possible explanation for this is that the developing brain, while growing exponentially and generating cells, wipes out stored memories.
Brain injuries may cause forgetting
It is possible to lose memories before they even have a chance to become stored, due to injuries in the brain’s structures that are specifically involved in handling memory formation, maintenance and recall. Damage to these areas can result in curious forms of amnesia.
In one of the most-studied cases of such amnesia, Patient H.M. lost the ability to form any new memories after a part of his brain, the hippocampus, was removed during a surgery to treat his epilepsy.