Medical News Today: Innovative gene editing method may prevent deafness

For the first time, researchers have used an innovative, state-of-the-art genome editing technique to prevent deafness in mice. There is hope that, in the future, they will be able to use this method to stop the loss of hearing in humans.
man cupping his ear
Could gene editing procedures be used to prevent hereditary deafness?

According to data from the National Institute on Deafness and Other Communication Disorders, around two to three children in every 1,000 in the United States are born with a hearing impairment in one or both ears, and about 15 percent of adults have hearing problems.

Moreover, the Centers for Disease Control and Prevention (CDC) note that 50 to 60 percent of hearing loss cases in babies are due to genetic factors, caused by the mutation of genes that “program” hearing.

Recently, scientists have been experimenting with genome editing methods in the hope that they would be able to manipulate it so as to prevent the onset of total deafness due to genetic factors.

Researchers at the Howard Hughes Medical Institute in Chevy Chase, MD, have now used precise genome editing technology called CRISPR-Cas9 on a mouse model to remove a gene variant that can lead to total loss of hearing.

“We hope that the work will one day inform the development of a cure for certain forms of genetic deafness in people,” says David Liu, one of the researchers involved with the study.

Liu and colleagues detail the process and their findings in a paper published in the journal Nature.

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Prevention by removal of faulty gene copy

One gene that has been associated with hearing is Tmc1. Mutations in this gene have been known to cause deafness, since they trigger the loss of hair cells in the cochlea, a part of the inner ear.

Cochlear hair cells play an important role in hearing; they pick up vibrations and communicate with brain cells, thereby allowing the sensation to be processed. Mutated Tmc1 causes gradual hearing loss in both humans and mice, which allowed Liu and team to use the mouse model in their research.

The scientists hypothesized that, if they could remove the mutated copy of the gene, they would be able to prevent total loss of hearing in the animals.

Working with young mice, the researchers used CRISPR-Cas9, which is a new genome editing technology that allows scientists to intervene with precision within the DNA.

“Cas9” stands for “CRISPR-associated protein 9,” an enzyme that can be used as a tool to remove copies of genes from the genome.

What Liu and team struggled with was getting Cas9 to only “snip off” the mutated copy of Tmc1 and prevent it from also disrupting the healthy copy. This struggle arose from the fact that the mutated and healthy copy differ in only one spot, making it more difficult for the enzyme to differentiate between the two.

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Advancements in CRISPR technology

The solution chosen by the researchers was to deliver Cas9, as well as the guide RNA that is used to direct it, encapsulated in a lipid-based compound. This is a method previously described by Liu and other investigators.

Lipid-encapsulated Cas9 is more efficient, as it can find its way to the targeted gene copy more easily and has a reduced chance of lingering for long enough to interfere with other DNA segments.

The researchers injected the lipid-encapsulated Cas9 and guide RNA complex into the cochlea of newborn mice with a faulty copy of Tmc1, with the effect that, after 8 weeks, the animals’ cochlear hair cells remained mostly intact.

By contrast, the animals that hadn’t been injected with the Cas9-guide RNA complex lost their cochlear hair to a great extent in that period.

Using electrodes, Liu and colleagues proceeded to test the mice’s hearing capacity by monitoring brain activity in the regions associated with processing sound. They discovered that the animals that had not received the CRISPR-Cas9 intervention needed louder stimuli to react.

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Around 4 weeks after the procedure, the mice that were injected with the Cas9 complex were able to perceive sounds that were 15 decibels lower than the ones needed to elicit a reaction from the control animals.

According to Liu, “That’s roughly the difference between a quiet conversation and a garbage disposal.”

Although this technique cannot yet be used to treat human cases, the researchers are hopeful that, in the future, this method will prevent total loss of hearing in many people exposed to hereditary risk factors for deafness.

Liu suggests that this treatment should be applied during childhood, to prevent the loss of cochlear hair as early as possible, since the damage, once done, is not usually reversible. “The conventional thinking in the field is that once you’ve lost your hair cells, it’s difficult to get them back,” he says.

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Medical News Today: All you need to know about agitated depression

Depression is a persistent state of feeling hopeless, sad, or helpless. While there are some common symptoms associated with depression, people can experience depression differently.

One such example is agitated depression. Medical experts may also describe agitated depression as anxious depression or distraught depression.

Though agitated depression is not a distinct type of depression, psychiatric professionals recognize that some people have symptoms of depression as well as agitation.


Agitated depression
Depression with agitation, is known as a “mixed episode” of depression.

Mental health professionals use a manual called the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) to diagnose mental health disorders, including depression.

By using the same criteria, doctors across America can diagnose depressive symptoms in the same way.

For a doctor to diagnose someone with depression, the person must have experienced depressed mood or a loss of interest or pleasure in life (anhedonia) for at least 2 weeks.

Also, a person will also have experienced at least five of the following symptoms:

  • Feelings of sadness, hopelessness, or irritability on a nearly daily basis.
  • Lack of interest or pleasure in activities almost every day.
  • Experiencing significant weight loss or appetite loss that results in weight loss.
  • Difficulty sleeping or sleeping excessively.
  • Experiencing psychomotor agitation, restlessness, or feelings of being “slowed down.”
  • Feeling fatigued or having a lack of energy nearly every day.
  • Feeling worthless or having excessive and unexplained guilt almost every day.
  • Difficulty thinking clearly, concentrating, or making decisions on a daily basis.
  • Experiencing thoughts of death, thinking of harming one’s self, or creating a specific plan for committing suicide.

Agitation is a symptom that can cause a person to experience feelings of uneasiness and anxiety. Some of the symptoms associated with agitation include:

  • angry outbursts
  • clenching fists
  • disruptive behavior
  • excessive talking
  • feeling as if a person cannot sit still or focus
  • pacing or shuffling feet
  • tension
  • wringing of the hands
  • violent outbursts

A person who has agitated depression experiences feelings of helplessness that can make them feel out of control.

As a result, they can then feel hopeless, which may lead to depressive thoughts. Agitation can cause a person with depression to act impulsively. This could cause a person to hurt themselves or others and engage in harmful behavior.

How is agitated depression different from bipolar?

A person with bipolar disorder may experience fluctuating symptoms of depression and mania (an elevated state of being).

Mania is different from agitation because mania causes a person to feel hyper, “high,” or overly energetic. A person may only sleep a couple of hours each night and stay awake for extended periods.

Mania does not feel good or euphoric to every person, but it can to some people.

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women holding hands across table
Depression may be caused by a significant life event, such as the loss of a family member.

Agitation is often a symptom of an underlying mood disorder and is not a condition of its own. The causes of depression itself can be varied and can occur if:

  • the brain does not regulate mood appropriately
  • a person has a family history of depression and is more vulnerable to the condition
  • a person has experienced significant life events that are especially stressful or sad, such as the loss of a family member or divorce
  • a person has several chronic medical problems

Several of these factors can contribute to depression. However, doctors do not know why a person may experience agitated depression.

A person’s temperament that affects their behavior may increase the likelihood that they will experience agitation related to depression.

How is it diagnosed?

Doctors diagnose agitated depression by asking a person to describe the symptoms they are experiencing.

They may ask questions, such as when the symptoms first began, what makes the symptoms better, or what makes the symptoms worse. Sometimes a person’s loved ones may also describe the changes they have observed in a person’s personality.

A doctor will use the criteria from the DSM-5 to diagnose a person with major depressive disorder, but agitated depression is not diagnosed using DSM-5 criteria. A doctor will also try to rule out other similar conditions, including bipolar disorder.

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How is agitated depression treated?

senior man discussing depression with a counsellor
A psychiatrist or other mental health professional may help to treat agitated depression.

Doctors treat agitated depression with a variety of approaches.

In the first instance, a doctor may prescribe medications called sedatives or benzodiazepines.

Examples may include diazepam (Xanax) or lorazepam (Ativan). These medications work quickly to help a person feel calmer and can temporarily relieve agitation.

Additional steps include:

  • Medications to relieve depression: Doctors may prescribe a variety of drugs to relieve depression, including anti-depressants. If a person does not respond to these medicines, a doctor may add another drug or prescribe a different medication type entirely. Examples can include anti-anxiety medications or mood stabilizers.
  • Counseling: Seeing a psychiatrist or other mental health professional can help a person identify thoughts and feelings that can signal the start of agitation or depressive symptoms. Therapy can help a person focus on thoughts and behaviors that can help them feel better when they struggle with agitated depression.
  • Stress-relieving techniques: Relieving stress and depression through physical activity, meditation, deep breathing, and journaling can all help a person cope with feelings agitated depression.

There is no one single solution to treating agitated depression. A doctor must consider a person’s unique symptoms.

They will likely take a variety of approaches, including prescribing medications and recommending therapy.

Sometimes it can take several months or even years for a person to find the right combination of medications, therapy, and stress-relieving techniques that help them live better with their agitated depression.


While there is no cure for agitated depression, there are many treatments that can help a person live a healthier, happier life. Although finding the right combination of treatments can take time, help is available.

If a person experiences suicidal thoughts or thoughts of self-harm, they should seek emergency medical attention. Medical professionals can help identify ways to stabilize the person medically, and reduce the risks of them injuring themselves.

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Medical News Today: Window blinds injure two children each day in America

Window blind cords are a known strangulation hazard for young children. Despite this common knowledge, research shows that the problem is far from fixed.
Child looking through blinds
Window blind cords still pose a significant threat to child safety.

Window blinds, as innocuous as they seem, are listed by the United States Consumer Product Safety Commission (CPSC) in “the top five hidden hazards in U.S. homes.”

This is not a new issue. In fact, the potential for injury by window blind cords first entered the scientific literature in 1945.

Back in 1994, the CPSC and Window Covering Manufacturers Association, Inc. hatched a plan to eliminate loops from most window blind pull cords and provide consumers with free repair kits to alter their existing products.

Again, in 2000, a similar plan was rolled out to address loops in the inner cords of window blinds. But the threat continues: in 1981–1995, 183 children died due to window blind cords in the U.S.

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Window cord injuries in the U.S.

Recently, Dr. Gary A. Smith and a team from Nationwide Children’s Hospital in Columbus, OH, set out investigate whether these types of injury were still occurring. Their findings are published this month in the journal Pediatrics.

The data showed that between 1990 and 2015, there were around 16,827 window blind-related injuries in children under 6 years old who were treated in U.S. emergency rooms. That’s almost two per day.

Around 12 percent were due to entanglement. Children who became entangled in the cords were, most often, under the care of a parent and had been left alone for under 10 minutes. More than 93 percent were treatable at the first appointment, and the children were released without further care.

But sadly, on average, around one child per month died from a window blind cord injury.

Medical News Today recently spoke with Dr. Smith, director of the Center for Injury Research and Policy at Nationwide Children’s Hospital. We asked what motivated him to study these types of injury, and his answer was rightfully impassioned.

“I have been deeply concerned about this injury problem for years,” he noted. “Child deaths due to strangulation on window blind cords are unacceptable […] we have known about this problem since the 1940s and have safe and affordable window blinds already widely available on the market that do not have accessible cords.”

“We have had a voluntary safety standard in this country since the mid-1990s, and we’ve had product recalls, and yet we continue to see these deaths,” he added.

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What’s next?

Dr. Smith believes that previous attempts to minimize these injuries fell short of the mark because they were voluntary. He told MNT that, if industry is not prepared to voluntarily make the products safe, “A mandatory federal safety standard should be adopted prohibiting the sale of products with accessible cords.”

We are not waiting for a cure — we have the solution and simply need the political will to implement it.”

Dr. Gary A. Smith, Center for Injury Research and Policy, Nationwide Children’s Hospital

Dr. Smith told MNT that some parents are not aware of all of the dangers, particularly surrounding “the inner cords of the blinds that are harder to see.”

He explains, “Young children are quick, curious, and unable to recognize danger. Many parents underestimate these factors […] There is a misperception that if we just watch our kids carefully, they will be safe.”

As worrying and tragic as these findings are, the solution is a relatively simple one. As Dr. Smith told MNT, safe blinds are available.

“It is time,” he said, “to require that only these products that do not have accessible cords are the only ones sold in the U.S. […] We live in a world designed by adults for the convenience of adults, and, unfortunately, child safety is often an afterthought. It is time to put child safety first.”

Hopefully, this increase in visibility might be the push needed to change policy for the better. When children are being injured despite the existence of a perfectly good solution, it simply must be time for change.

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Medical News Today: All you need to know about varicose vein pain

Varicose veins are swollen and enlarged veins. They are often blue or dark purple and lumpy, bulging, and twisted in appearance. They occur on the legs and feet.

Not all varicose veins bulge to the surface; sometimes they can be invisible and buried deep in the body. Therefore, some people experience pain and discomfort for a long time before discovering the cause.

Almost anyone can have varicose veins, and according to the Society for Vascular Surgery, they affect around 35 percent of people in America.

What are the symptoms?

Varicose veins on backs of legs.
Varicose veins may not always cause symptoms, and symptoms may only be present in certain conditions, such as warm weather.

Sometimes, varicose veins cause no symptoms, while other times, they produce a range of symptoms. Common symptoms include:

  • aching and uncomfortable legs
  • swollen feet and ankles
  • burning or throbbing
  • muscle cramps, particularly at night
  • itchy skin over the affected area
  • skin discoloration
  • heaviness or fatigue in the legs

Symptoms tend to be worse during warm weather, late in the day, or when a person has been standing up for extended periods.


Varicose veins are a common cause of leg pain. People often describe the pain as heaviness or a deep ache.

There are varying degrees of pain associated with varicose veins, and some people experience severe symptoms.

One condition that can cause pain is known as phlebitis, which occurs when varicose veins become inflamed and form blood clots. Signs that a person may have phlebitis include:

  • pain
  • heat
  • hardness
  • discoloration

If a vein bursts, blood can pool around the affected area and pressure and toxins may build up. Sometimes an ulcer may develop, or a person’s skin may tear as a result of a varicose vein, which can be extremely painful.

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What other issues affect varicose vein pain?


Mature female patient speaking to female doctor,
Identifying varicose veins, and taking steps to treat them, may help to prevent complications, such as lymphedema.

Varicose veins can also cause problems elsewhere in the body — specifically the lymphatic system.

The lymphatic system is a network of vessels that help transport and remove waste products and toxins. It plays a major role in immune system function.

Sometimes, varicose veins can damage the lymphatic system and lead to a condition called lymphedema, which causes swelling, often in the feet and toes.

Some people who have lymphedema may also develop cellulitis — a serious skin infection that causes inflammation to the soft tissue of the skin.

Other people may develop venous stasis dermatitis, where the skin becomes leathery and ruddy-brown. Sometimes clear-yellow fluid weeps through the skin.


Varicose veins can also lead to dermatitis, which is an itchy, inflamed rash. When caused by varicose veins, the rash will often appear on the lower leg or ankle.

Dermatitis can cause bleeding, skin ulcers, or sores that can be painful and become infected if scratched or irritated.

Superficial thrombophlebitis

Varicose veins can also lead to inflammation and the formation of a clot in the vein. Often this clot will be close to the surface of the skin in a condition known as superficial thrombophlebitis.

This can cause pain and lead to other problems in the affected area.


Unfortunately, there is little evidence that people can prevent varicose veins from occurring, but they can make various lifestyle changes that may help lessen symptoms and possibly prevent varicose veins from worsening.

Prevention and symptom relief methods include:

  • avoiding standing or sitting for extended periods
  • trying to move around at least every 30 minutes
  • raising the affected area raised above the level of the heart when sitting, resting, or sleeping
  • doing regular exercise to improve circulation
  • losing weight if overweight
  • avoiding tight-fitting clothes, particularly those that are tight around the waist, groin, and legs
  • avoiding wearing high-heeled shoes for long periods

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Woman putting compression stocking on to treat varicose veins.
Compression stocking are a non-surgical and economical option for treating varicose veins.

Varicose veins do not always require treatment. However, if they are causing pain, there are various treatment options available.

If symptoms are minimal to mild, the doctor will likely advise the person to try the prevention methods mentioned above first to see if they help reduce pain and discomfort.

If they do not help, then a doctor might recommend the following treatment methods:

Compression stockings

In the first instance, a doctor will likely suggest compression stockings combined with elevating the legs and exercising regularly. A person may need to wear the stockings for around 6 months before they feel the full effect.

Compression stockings compress the leg tissue around the veins to prevent blood from pooling. They are designed to help reduce associated aching and swelling.


Ablation uses heat to seal the affected veins either by a laser or radiofrequency.

Ablation treatment is often administered in the doctor’s office and takes around 20 minutes. The doctor uses a local anesthetic to numb the affected area, so the procedure is painless. Once the ablation is complete, the doctor will wrap the area in a compression bandage.


This procedure involves injecting a foam called sclerosant into a varicose vein. The foam causes the vein to spasm, scar, and clot, which will then close the vein off.

This type of clot is not dangerous and, over time, the varicose vein will disappear.


Some people may require surgery, which can include ligation — where the veins are tied to stop the blood pooling — or stripping, where a surgeon removes the vein.

When to see a doctor

Doctors do not consider varicose veins to be a serious condition, and people who have them without any discomfort do not need to see a doctor.

However, if they are causing pain, discomfort, or irritation — particularly at night — then people should seek medical treatment.

It is worth remembering that because varicose veins are not always visible, anyone who experiences aching, swelling, or fatigue should still see their doctor for evaluation.

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Medical News Today: Scientists reverse genetic aging, memory decline in rats

As we age, memory function tends to suffer. Understanding and preventing this creeping deficit is a priority for many scientists. Now, a recently published study brings us one step closer.
Older adult looking at a brain
A recent study investigates a protein in the hippocampus that may be involved in cognitive decline as we age.

With age comes a decline in certain aspects of our cognitive ability. It may not be the case for everyone, and not everyone is affected in the same way, but memory generally worsens.

As our average lifespan increases, so too does interest in the negative impacts that aging has on the mind — and how to prevent or slow them, of course.

To date, researchers have identified hundreds of genes that are involved in the aging process. For instance, in 1988, scientists discovered that a certain gene mutation in Caenorhabditis elegans (a type of worm) could extend maximum lifespan by up to 110 percent.

Since then, more than 800 individual genes have been identified that influence the lifespan of C. elegans, and many more in other species. Although the genes involved in aging are slowly being unfurled, understanding what they do and how to influence them is another challenge entirely.

The hippocampus, aging, and calcium

Recently, Philip Landfield, John Gant, Eric Blalock, and colleagues from the University of Kentucky in Lexington carried out a multipronged study. They wanted to understand the role of a specific protein in age-related memory decline in rats, and how it influences age-related gene changes.

The protein, called FK506-Binding Protein 12.6/1b (FKBP1b), regulates calcium homeostasis in the neurons of the hippocampus, which is a region of the brain involved in spatial memory and converting short-term memories into long-term ones.

When researchers look for changes in the way that the aging brain works, they consistently find alterations in the way that calcium carries out physiological roles.

Earlier work by the same team found that disrupting FKBP1b interfered with hippocampal calcium usage. The study authors also found that expression of the FKBP1b gene was down-regulated in the hippocampus of aging rats and humans with early stage Alzheimer’s disease.

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A deeper look at FKBP1b

For their latest study, they wanted to examine how FKBP1b treatment in aging rats might influence memory performance and age-related genetic changes.

They injected rats with viral vectors that expressed FKBP1b, causing a rise in overall expression of the protein. The injections were given either at 13 months old, before cognitive decline begins (referred to as long-term), or at 19 months old, once decline had begun (called short-term).

Their findings are published this week in The Journal of Neuroscience.

Both long- and short-term treatment improved the performance of aging rats in a water maze task: FKBP1b was able to prevent cognitive decline in long-term rats and reverse it in short-term rats.

The treated rats completed memory tasks better than untreated rats of the same age, and their scores were more in line with young, untreated rats.

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Gene changes overturned

Next, the researchers carried out transcriptional profiling. They identified 2,342 genes expressed differently in young and old animals. Treatment with FKBP1b restored activity in 876 of these age-affected genes. In fact, levels were similar to those of untreated young rats.

The genes that showed changes might “represent a new genomic network” involved in regulating the structure and function of the hippocampus that falls into disrepair with age. The authors conclude:

[T]his genomic evidence adds strong new support for the hypothesis that FKBP1b is a linchpin of neuronal homeostasis that functions at multiple levels, including regulation of [calcium], maintenance of structural integrity, and preservation of cognitive function.”

These recent findings provide further evidence that FKBP1b plays a significant role in cognitive aging and, in particular, memory decline. Because calcium dysfunction appears to play a role in Alzheimer’s disease, the results may also be useful for researchers in that field.

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Medical News Today: Can an existing drug win against aggressive breast cancer?

Triple-negative breast cancer, which is a particularly aggressive form of the disease, often has very poor outcomes; it is resilient in the face of current treatments. But scientists now say that an existing form of antimicrobial therapy is where we should look next in the fight against this form of breast cancer.
dictionary definition of breast cancer
Researchers are investigating the potential of an existing treatment in the fight against triple-negative breast cancer.

According to recent studies, breast cancers are the second most commonly diagnosed type of cancer among women in the United States.

Triple-negative breast cancer is a resilient and especially aggressive subtype, accounting for approximately 15 percent of all diagnoses of breast cancer.

Triple-negative breast cancer is resistant to the commonest type of therapy currently applied: chemotherapy. This is partly due to the sheer endurance of stem-like cancer cells, which promote the formation of new tumors.

For this reason, scientists are permanently on the lookout for better, more effective treatment options that will prevent the migration of cancer cells within the body.

Now, researchers at the Case Comprehensive Cancer Center at Case Western Reserve University School of Medicine in Cleveland, OH, have revealed that triple-negative breast cancer cells may respond to an existing therapy used to treat other conditions, including multiple sclerosis (MS), called interferon-β.

We demonstrate that interferon-β reverses some of the more aggressive features of triple-negative breast cancer, which are responsible for metastasis and therapy-failure. “

First study author Mary Doherty, graduate student at Case Western Reserve School of Medicine

“Moreover,” she adds, “we found that evidence of interferon-β in triple-negative breast cancer tumors correlates with improved patient survival following chemotherapy.”

The researchers’ findings have recently been published in the journal PNAS.

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Interferon-β targets cancer stem cells

Interferon-β is a cytokine, which is a type of protein involved in cell signaling. It has an antimicrobial effect and a complex immune-regulatory impact, which is why it has, so far, been used in the treatment of autoimmune diseases such as MS.

Doherty now explains that interferon-β also acts on the stem-like properties of breast cancer cells, impairing their ability to migrate and thus preventing the formation of metastatic tumors.

“While chemotherapy kills the majority of tumor cells, it fails to eliminate a subset of cancer cells, called cancer stem cells,” Doherty explains.

“The survival of these cancer stem cells following therapy is believed to be responsible for therapy failure in patients,” she notes. This is why interferon-β’s suppression of these cells’ activity could lead to improved treatment outcomes in the future.

In an in vitro study using human triple-negative cancer tissue, the team noted that interferon-β targeted cancer stem-like cells directly. The cytokine had a marked effect on the cancer tissue exposed to it, even after the researchers interrupted the exposure.

For the cancerous tissue that was treated with interferon-β in vitro, the migrating cells had halved, compared with the control tissues that had not been exposed to this treatment.

Moreover, cancer cells treated with interferon-β had a significantly reduced tendency for tumor sphere formation.

Analyzing data sourced from cancer tissue databases, the team also notes that, post-treatment, the breast cancer patients with the longest survival rates, as well as the lowest tumor recurrence rates, exhibited high levels of interferon-β.

More specifically, individuals with high interferon-β levels had an approximately 25 percent lower risk of tumor recurrence compared with the individuals with low levels of interferon-β.

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Next steps on path to new treatment

Following these promising findings, Doherty and team are taking a closer look at the role played by interferon-β in immune-regulation, targeting its potential in boosting the body’s immune response against cancer.

They are also hoping to start clinical trials for a possible interferon-β therapy and explore its effects on its own, or as a complementary pathway to chemotherapy.

One challenge that the scientists will face will be that of finding an effective way of delivering the interferon-β.

“Our future studies will examine improved methods of interferon-β delivery to the tumor site incorporating nanoparticle technology,” Doherty explains.

The recent advances in medical technology, paired with the scientists’ search for ever more effective treatments, deliver fresh hope in the fight against aggressive forms of cancer.

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Medical News Today: What is keratitis?

Keratitis is a painful inflammation of the eye. It can be caused by an infection or an injury. There are many different types of keratitis, and each type needs different treatment.

The eye is highly sensitive, and there are several ways in which it protects itself from damage. The eyelid covers the eye, and tears and fluid protect it from infection. The cornea is the outermost layer of the eye and provides a barrier against dirt, germs, and disease.

Because the cornea is one of the first lines of defense, it can be irritated and become inflamed. This is known as keratitis.

Keratitis and the eye

woman touching her eye
Keratitis is a painful inflammation of the cornea and can have various causes.

Keratitis is a condition affecting the cornea, which is the transparent outer layer at the front of the eye. The cornea helps the eye to focus so that it can see objects clearly.

Keratitis causes the cornea to become inflamed. This can be very painful, cause problems with vision, and make the eye more sensitive to light.

Keratitis does not have one single cause. There is a range of different types of keratitis, and each type needs different treatment.

Causes and risk factors

Keratitis usually happens because something has irritated the eye, for example, an infection or injury. Certain risk factors make it more likely for keratitis to develop.

Wearing contact lenses is a risk, especially if a person wears them overnight. Failing to keep contact lenses or a contact lens case clean increases the chance of getting keratitis.

A person who has recently had an eye disease or injury might mean that they are more likely to develop the condition. People who have the herpes simplex virus are at risk of developing viral keratitis.

Keratitis can be caused by the eyes drying out. A problem with the eyelids or tear ducts can mean that a person’s eye is not as moist as it needs to be.

Fungal keratitis occurs when part of a tree or plant, such as a twig, injures the eye, so those people who work with plants are more at risk.

Exposing the eyes to water — such as when swimming or in a hot tub — is a high risk for keratitis.

A person should always clean their contact lenses with a contact lens solution, not wash them in water.


young woman putting in contact lense
Keeping contact lenses and lens cases clean will help reduce the risk of developing keratitis.

There are two main types of keratitis: infectious and noninfectious. Within these two categories, there are other forms of the condition.

Noninfectious causes of keratitis include:

  • wearing contact lenses for too long
  • the eye drying out, sometimes if the eye does not produce enough tears
  • an allergy, for example to cosmetics or pollution
  • something in the eye that should not be there
  • injury to the cornea
  • exposure to intense sunlight, for example from water or snow
  • vitamin A deficiency

Infectious types of keratitis include:

  • bacterial, usually from unclean contact lenses
  • fungal, most often from an eye injury by a tree branch or plant
  • viral, from infection with the herpes simplex virus or herpes zoster virus
  • parasitic, caused by a tiny organism often found in lakes and rivers

The best treatment for keratitis will depend on which type of the condition someone has.

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Pain in the eye is the key symptom of keratitis. Because the cornea is the part of the eye that helps to focus sight, vision may be blurred.

Someone may also feel that they have something in their eye, even if they do not, and the eye may water more than usual. The eye can also appear red, and there may be some discharge.

A person with keratitis may be sensitive to light, which is known as photophobia. They may dislike looking toward a light, having a bright light on in the house, or being outside in strong sunlight.


Keratitis can be serious and may cause loss of vision or blindness if left untreated. The condition is usually treatable if diagnosed early enough.

Complications can include permanent scarring, ulcers on the cornea, or less commonly glaucoma. This is a condition where pressure inside the eye can cause problems with vision.

A person should see a doctor or eye doctor if they have symptoms of keratitis.


An eye doctor will examine the eye and ask questions about what may have caused keratitis.

A doctor may diagnose bacterial or fungal keratitis by taking a small scraping from the cornea to send to a laboratory to be tested.

Viral keratitis does not need laboratory testing, but a doctor will ask for information about a person’s medical history.

Parasitic keratitis may need a more detailed examination of the eye so that the doctor can see the parasite causing the condition.


man using eye drops
Antibacterial eye drops may be prescribed for mild bacterial keratitis.

If a person has keratitis and wears contact lenses, they should take them out as soon as they develop any symptoms of infection or irritation. Contact lenses should not be used again until the condition has gone away.

If a person has is mild bacterial keratitis, a doctor may recommend they use antibacterial eye drops.

In more serious cases, the person may need antibiotics. Steroid eye drops can reduce inflammation if the keratitis is particularly severe.

People can apply eye drops at home and will need to use them regularly. As the condition improves, individuals can use the medication less often.

People who have fungal keratitis will need to use antifungal medication for some months. If this does not resolve the condition, surgery may be necessary in extreme cases.

Eye drops or antiviral medication are used to treat viral keratitis. As there is no cure for the herpes simplex virus that can cause viral keratitis, the condition can happen again.

Parasitic keratitis is the most difficult type to treat and requires urgent medical treatment as well as surgery.

During treatment, someone should see an eye doctor if:

  • the condition is not improving with the use of eye drops
  • their sight becomes blurred
  • the eye becomes more painful, or redder
  • a white spot on the cornea grows in size

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Apart from viral keratitis, most people can avoid other forms of the condition by following good contact lens hygiene.

People can help to prevent keratitis by:

  • following the advice of their eye doctor about how to wear, replace, store, and clean contact lenses
  • washing and drying hands with soap and water before touching the eyes or contact lenses
  • avoiding sleeping in contact lenses
  • keeping water away from contact lenses, such as when showering or swimming
  • cleaning contact lenses with contact lens solution
  • visiting an eye doctor regularly, and contacting them with any symptoms that give concern

Keratitis can affect people who do not wear contact lenses. It is important to protect the eyes from damage that can cause the condition.

Steps to protect the eyes include:

  • wearing protective eyewear if working with plants or trees
  • wearing sunglasses when exposed to bright sunlight
  • being aware of anything that can cause an allergy, and avoiding them if possible
  • eating a diet that includes vitamin A, which can be found in milk and eggs

It may also be possible to reduce the risk of viral keratitis. People should take care not to touch the eyes or the area around them, and only use eye drops that have been prescribed by a doctor.


Keratitis is treatable, but it is important to stop wearing contact lenses as soon as the eye becomes inflamed.

A person should seek medical advice to find the cause of the condition, as treatment can vary depending on the root of the problem.

Those who wear contact lenses are most at risk of infection. Following advice on cleaning and storing contact lenses should prevent keratitis in most cases.

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Medical News Today: Is erectile dysfunction an early sign of CVD?

Erectile dysfunction may be an early indicator of cardiovascular disease, and men with the condition should be subject to more rigorous cardiovascular assessment. This is the conclusion of a new study published in the journal Vascular Medicine.
a man with chest pain
Researchers say that men with ED may have early markers of cardiovascular disease.

Erectile dysfunction (ED) is defined as the inability to get or maintain an erection.

It is believed that approximately 30 million men in the United States are affected by ED, and the risk of developing the condition increases with age.

Unsurprisingly, ED can have a range of negative implications for a man’s psychological health; it may give rise to low self-esteem, anxiety, and depression. But ED may pose risks for physical health, too.

Previous research has suggested that men with ED are at greater risk of developing cardiovascular disease (CVD), an umbrella term for conditions that affect the heart and blood vessels.

But according to the researchers of a new study, the association between ED and subclinical CVD — that is, CVD that is not severe enough to present observable symptoms — has been unclear.

“Particularly, it is unknown which markers of subclinical CVD have the greatest or most consistent association with ED,” say the researchers, including Dr. Chukwuemeka Osondu, of Baptist Health South Florida in Miami-Dade County.

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ED linked to endothelial dysfunction

For their study, Dr. Osondu and colleagues carried out a systematic review and meta-analysis of 28 studies that investigated the link between ED and early signs of CVD.

They identified a strong association between ED and poor endothelial function, wherein blood vessels are unable to fully dilate and allow blood to flow through. Endothelial dysfunction is an early sign of atherosclerosis, a condition in which plaque builds up in the arteries, raising the risk of heart attack and stroke.

What is more, the researchers found that ED was linked with an increase in carotid intimal medial thickness, which is also an early marker of atherosclerosis.

“These relationships remained consistent within age, study quality, methods of assessing ED, and publication year subgroups,” the researchers report.

The team says that these findings are particularly important for younger men, who are less likely to be assessed for subclinical CVD than older men, and who may be visiting the doctor for the first time due to ED-related symptoms.

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“Our study findings indicate that such men are at greater risk of having identifiable subclinical CVD and will benefit from an active CVD work-up,” the authors write, adding:

Our study supports a more aggressive CV disease risk assessment and management for persons with erectile dysfunction, including young men who may otherwise be categorized as low-risk due to their young ages.”

In an editorial linked to the study, Drs. Naomi Hamburg and Matt Kluge, from Boston University in Massachusetts, say that the findings of Dr. Osondu and colleagues emphasize the importance of ED in determining a man’s risk of CVD.

“A simple standardized ED screening may identify early vascular dysfunction. Similarly, vascular dysfunction may serve as a surrogate marker to evaluate the efficacy of cardiovascular-targeted therapies in men with ED,” they write.

“The presence of ED,” they add, “portends a higher risk of future cardiovascular events, particularly in intermediate-risk men, and may serve as an opportunity for intensification of cardiovascular risk prevention strategies.”

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Medical News Today: How to identify papular urticaria

Papular urticaria is the medical term for an allergic skin reaction or hypersensitivity to insect bites. The word papule refers to a solid bump on the skin. Urticaria is another word for hives, which are round, red welts on the skin that itch severely.

One unique characteristic of this skin disorder is that scratching an area affected by a bug bite can trigger the inflammation of old bites. As a result, it can appear as though there are more new bites than there really are.

Symptoms and appearance

Papular urticaria. Image credit: Alborz Fallah, (2013, December 16)
Papular urticaria appears as clusters of red bumps on the skin.
Image credit: Alborz Fallah, (2013, December 16)

The symptoms of papular urticaria include numerous reddened skin bumps, which usually appear in clusters. The bumps tend to be around 1/12 to 3/4 of an inch in diameter.

At times, the bumps may form scabs or fluid-filled blisters.

The bumps may appear in a curve shape, or in a line, particularly when caused by bed bugs or fleas.

These bumps erupt every few days. They appear most often on the legs, forearms, and face, but have been known to occur in small clusters all over the body.

Some people may notice a central and very small round spot differing in color and appearance from the surrounding tissues. This kind of spot is known as a punctum.

As the result of continuous bug bites, an increase or decrease in the color of the skin may occur.

This type of skin breakout is long-term and comes back repeatedly

The skin bumps are usually accompanied by intense itching, which can lead to severe infections and scarring from constant scratching. When the bumps are scratched, they may become infected, painful, and can become full of pus.

Each bump usually remains on the skin for a few days and up to several weeks.

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Causes and risk factors

Close up of a flea.
Fleabites are one of the most common causes of papular urticaria.

The most prevalent types of insect bites involved in the disorder come from fleas and mosquitoes.

Other insects that have been known to cause papular urticaria include:

  • carpet beetles
  • bed bugs
  • bird mites
  • caterpillars
  • caddisflies
  • insects that live in masonry
  • other insects

A recent study of 2,437 children, published in the World Allergy Organization Journal, revealed that 20 percent of the children in the study had papular urticaria.

In 50 percent of the children, fleabites caused the condition. Other major risk factors identified in the study included:

  • presence of fleas in the home
  • having household pets
  • using a mattress without springs
  • daily use of public transportation
  • living in a warm, tropical climate
  • living in a geographic area heavily infested with insects
  • having siblings with a history of atopic dermatitis
  • being aged under 7 years
  • being raised in poverty

Sometimes, symptoms of papular urticaria improve when a family takes a vacation or moves to a new home. When this happens, it suggests that the cause of the problem is most likely an infestation in the living environment.

Papular urticaria in children

Although adults can be affected, papular urticaria is more common in children than in adults. It most commonly occurs in children aged from 2 to 7 years.

Children often outgrow the disease because they become desensitized, which is a process of becoming immune to an allergen after repeated exposure.

When to see the doctor

As soon as a person detects signs and symptoms, it is time to see a healthcare professional. They might carry out some testing to rule out other causes of the itchy bumps and prescribe medication to treat the symptoms.

More serious diseases might be the underlying cause of skin bumps. These include:

It is essential to visit the doctor who can rule out other, more serious disorders.

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Treatment and prevention

Person applying topical ointment to their skin
Steroid cream may be recommended to treat itchy spots.

There are several ways of treating papular urticaria. A person who has the condition can take the following steps:

  • Apply moderately strong steroid cream to the effected itchy spots right away.
  • Take oral antihistamine medication at night to reduce itching and promote sleep.
  • Apply antibiotic cream or give oral systemic antibiotics to treat or prevent secondary infection caused by scratching.
  • Cover exposed skin and use an insect repellent when outside.

It is also important to get rid of the source of the infestation that has caused the problem. People who want to remove an infestation can take the following steps:

  • Treat all household pets with flea medication.
  • Treat pet bedding with flea spray.
  • Spray the home, classroom, or bus with insecticide, being sure to follow instructions carefully.
  • Treat carpets and upholstery with a pyrethroid spray, being sure to vacuum afterward.
  • Check mattresses for signs of bed bugs.
  • Contact certified pest control agency to treat bed bug infestations.


To recap, the three most common appearances of papular urticaria are:

  • small, raised red patches on the skin that may or may not be fluid-filled
  • bumps appearing mostly in clusters, that erupt at old insect bite sites
  • itchy bumps that may last from several days to several weeks

Papular urticaria is a preventable condition. The best way to prevent popular urticaria is to implement a plan to control the presence of fleas and other insects in the home, classroom, and on public transport.

Over time, most children and adults will eventually become desensitized to papular urticaria.

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Medical News Today: Parkinson’s disease: How toxic proteins damage healthy brain cells

For the first time, researchers have spied toxic proteins at work in Parkinson’s disease and identified key features that enable them to drill holes through the walls of healthy brain cells to disrupt their function.
magnifying glass on a brain
New findings show that ‘oligomers’ harm the integrity of cell membranes.

A report on the new discovery — by researchers from the United Kingdom, Spain, and Italy and published in the journal Science — describes what happens when the proteins come into contact with cells.

First study author Dr. Giuliana Fusco — of both Imperial College London and the University of Cambridge, both in the U.K. — says that the scientists hope that the findings will lead to improved drugs for Parkinson’s disease that stop the toxic proteins from getting into healthy brain cells.

Parkinson’s is a disease that gradually destroys the brain cells that produce a messenger chemical called dopamine, which is important for controlling movement.

The symptoms — which develop slowly and get worse over time — include impaired balance, rigidity, slowness of movement, tremors, and problems with speaking and swallowing.

Researchers have also discovered that Parkinson’s affects non-dopamine brain cells, which may explain why the disease often has symptoms that are not to do with movement, such as anxiety, depression, fatigue, and sleep disruption.

It is thought that more than 10 million people worldwide are living with Parkinson’s disease, including an estimated 1 million in the United States.

Although it most often strikes after the age of 50, around 10 percent of cases of Parkinson’s disease are diagnosed in people of a younger age.

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Oligomers ‘disrupt cell membrane integrity’

In the new study, the researchers observed what happens when a protein called alpha synuclein malfunctions and forms into clusters called oligomers, which are toxic to brain cells.

They used solid-state nuclear magnetic resonance spectroscopy to characterize different structural features of the oligomers and then examined how the features influenced their interaction with the cells. They used brain cells from rats as well as brain cells sampled from human brain tumors.

The study is significant because the team found a way to keep the normally unstable oligomers stable for long enough to observe a level of detail that has not been seen before. Once they form, oligomers very quickly either enter cells, dissolve, or turn into long fibers.

By keeping the oligomers stable, the researchers were able to identify two features that are key to their toxicity: one that allows them to stick to the cell wall, and another that lets them penetrate the membrane and disrupt cell function.

“It is a bit like if you put a piece of extremely hot metal on to a plastic surface,” explains co-senior study author Dr. Alfonso De Simone, of the Department of Life Sciences at Imperial College London. “In a fairly short space of time it will burn a hole through the plastic.”

He suggests that the oligomer’s ability to “disrupt the integrity of the membrane” is a crucial step in the process that eventually kills the brain cell.

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Both similar and different to viruses

In further experiments, the team found a way that might reduce oligomer toxicity. They found that altering its protein sequence made the oligomer less able to stick to the cell membrane.

The researchers likened the behavior of the oligomers and their propensity to stick to the walls of brain cells as similar to the way that viruses enter cells. The difference is that while a virus then adapts the cell machinery to its own end, the oligomer just disrupts it.

Dr. De Simone also suggests that oligomers are able to attach themselves to cell membranes because of “an accident of nature” that gives them the same features as normal membrane proteins that help with brain signaling.

Just having this information doesn’t mean that we can now go and make a drug, but obviously if we can understand why these clumps of proteins behave the way they do, we can make faster scientific progress towards treating Parkinson’s disease.”

Dr. Giuliana Fusco

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