We just got rid of our cat and so the mice are coming around. Shortly after the departure of our cat my nose became stuffy, my eyes were watery, my throat became scratchy and I coughed.

My little toddler now is sneezing, her eyes are watery, and her nose is stuffy.

I think this might be allergy symptoms since it sort of comes and goes, it ping-pongs around, unlike when she gets a cold it comes and then goes away.

So how do I know if it is a cold or allergies?

I have allergies but I don't ever get a scratchy throat nor do I cough. (I do get red, itchy eyes. And itchy nose.)

I would guess the two of you have a cold. Colds tend to come and go this time of year. The only way to know for sure is to be allergy tested.

Take care.

Washington, Mar 8 : Researchers at the Washington University School of Medicine have managed to block the development of multiple sclerosis-like symptoms using a mouse model of the disease.

When scientists gave mice a drug that suppressed the activity of a key molecule, immune cells lined up at the boundaries of the spine instead of going in. Scientists have blocked harmful immune cells from entering the brain in mice with a condition similar to multiple sclerosis (MS).

It is important because MS is apparently caused by misdirected immune cells that enter the brain and damage myelin-an insulating material on the branches of neurons that conduct nerve impulses, said researchers.

“the results were so dramatic that we ended up producing early evidence that this compound might be helpful as a drug for MS. the harmful immune cells were unable to gain access to the brain tissue, and the mice that received the highest dosage were protected from disease,” said Robyn Klein.

Klein and her colleagues discovered a chemical stairway that immune cells have to climb down to enter the brain. Immune cells that exit the blood remain along the vessels on the tissue side, climbing down from the meninges into the brain where they can then cross additional barriers and attack myelin on the branches of neurons.

“the effect of immune cell entry into the brain depends on context. in the case of viral infection, immune cell entry is required to clear the virus. but in autoimmune diseases like multiple sclerosis, their entry is associated with damage so we need to find ways to keep them out,” said Klein.

The stairway is located on the tissue side of the microvasculature, tiny vessels that carry blood into the central nervous system. the steps are made of a molecule called CXCL12 that localizes immune cells, acting like stairs that slow them down so that they can be evaluated to determine if they are allowed to enter the brain.

Klein’s lab previously discovered that the blood vessel cells of the microvasculature display copies of this molecule on their surfaces.

Klein also found that MS causes CXCL12 to be pulled inside blood vessel cells in humans and mice, removing the stairway’s steps and the checkpoints they provide.

In the new paper, she showed that blocking the internalization of the molecule prevented immune cells from getting into the brain and doing harm.

Work by another lab called Klein’s attention to CXCR7, a receptor that binds to CXCL12. she showed that the receptor is made by the same cells in the microvasculature that display CXCL12. they watched the receptor take copies of CXCL12 and dump them in the cells’ lysosomes, pockets for breakdown and recycling of molecules the cell no longer needs.

Klein contacted researchers at ChemoCentryx, who were developing a blocker of the CXCR7 receptor as a cancer treatment. When they gave it to the mouse model of MS, immune cells stopped at the meninges.

The findings have been published in the Journal of Experimental Medicine. (ANI)

From Emax Health:

One of the most frustrating characteristics of autism is the individual’s disinterest in or difficulty with social interactions. Researchers have now identified a possible treatment to improve social skills in people with autism, and it involves a drug originally developed to treat TB (tuberculosis).

Researchers at Eastern Virginia Medical School (EVMS) used a specific mouse model (BALB/c) that mimics limited sociability characteristic of autism spectrum disorder to test whether the TB drug, cycloserine, could change social behavior in the mice. Previous research has shown that cycloserine has this potential.

Cycloserine is an antibiotic that is most commonly prescribed to treat TB. It is also used to treat urinary tract infections and other infections that have not responded to treatment.

Normally, BALB/c mice are antisocial: when presented with other mice they move away and do not interact as normal mice do. This behavior is similar to that of people with autism who commonly avoid social contact and eye contact with others.

When the BALB/c mice were administered cycloserine, they acted as normal mice do when they were placed near other mice. This response led the researchers to suggest that the TB drug could reduce the antisocial behavior of people who have autism, including avoiding eye contact and interacting with others in a social setting, behaviors that place them at a decided disadvantage in society.

Autism spectrum disorder affects 110 children out of 10,000, or roughly one in 91 children in the United States, according to the American Academy of Pediatrics. because the disorder is about four to five times more common among boys than girls, autism affects roughly one in every 58 boys.

Study author Stephen I. Deutsch, MD, PhD, the Ann Robinson Chair and professor of psychiatry and behavioral sciences at EVMS, noted that “persons with autism spectrum disorders are often painfully aware of their limited sociability, which can lead to profound feelings of sadness and frustration.”

Maria R. Urbano, MD, associate professor of psychiatry and behavioral sciences, adds that their findings are important because “you might have someone with a 125 or 130 IQ who’s unemployable” because they have poor social skills. Dr. Urbano is already initiating a pilot clinical trial of the TB drug in adolescents and young adults with autism spectrum disorders.

You might recognize that anxiety is often accompanied by depression, but did you know there is a biological link between the two?  Using mice, scientists may have determined exactly how stress and anxiety can lead to depression in the brain.  The research, led by Stephen Ferguson at the University of Western Ontario, may allow for new and improved treatments for anxiety, depression, and other related disorders.  This is good news since depression and anxiety are considered the most common cause of chronic illness.

The scientists’ research determined precisely how stress, anxiety, and depression pathways connect through specific processes in the brain. Molecular experiments revealed a link between two brain chemicals: one which leads to anxiety in response to stress, and another which lead to depression. in a behavioral mouse model, it was found that the presence of the anxiety chemicals increases the number of depressive on the surface of brain cells, which can cause abnormal signals.

Furthermore, the scientists developed an inhibitor that will block the pathway responsible for the connection, effectively blocking anxiety – and potentially depression. This could result in a new, more effective pharmaceutical agent that selectively targets depression and has fewer negative effects. the results are published in the journal Nature Neuroscience.

Anxiety and depression often go hand in hand, and the causes are strongly associated with stressful events. Stressful experiences can also make the symptoms of anxiety and depression more severe. however, molecular biology is the key to understanding why such symptoms arise and how to effectively combat them. by identifying the distinct processes in the brain that link anxiety and depression, researchers have provided new findings that may improve the lives of those coping with these chemical imbalances.