How to prevent yeast infections? Generally, taking time out of relax (helpful to avoid stress), nutritious meals, and well-balanced eating style are some of great healthy lifestyle approaches that can be effective option to keep well the performance of your immune system -- which eventually will be also helpful for your body to prevent all kinds of infections (including vaginal yeast
How to Prevent Yeast Infections (9 Simple Tips)
How to prevent yeast infections? Generally, taking time out of relax (helpful to avoid stress), nutritious meals, and well-balanced eating style are some of great healthy lifestyle approaches that can be effective option to keep well the performance of your immune system -- which eventually will be also helpful for your body to prevent all kinds of infections (including vaginal yeast
Yeast Infections in Men (Causes and Symptoms)
(Image credit to shutterstock)
Yeast infection is relatively more common in women (or familiar known as vaginal yeast infection). But this doesn’t mean that it is only restricted to women, in other words we can say that there are also yeast infections in men!
Like in vaginal yeast infections, ‘Candida yeasts’ are still the major reason of yeast infections in men. These yeasts not only
If you give a mouse a placebo...
...It might ask for some cocaine. Or it might feel the effects of cocaine anyway.
The "Placebo Effect" occurs when someone takes a functionally ineffectual drug, but feels the effects anyway. There are many examples of this: Someone in pain takes a sugar pill, but is told that it is a painkiller might report 'feeling much less pain'. A Parkinson's patient takes a sugar pill having been told it was their 'L-dopa' medication and can suddenly move more fluidly. The "Placebo Effect" is so strong that most experiments testing the effectiveness of a drug in healing anything use a placebo control. The researchers want to make sure that the drug has an actual effect that is greater than the placebo effect. (It has been proposed that homeopathic remedies are entirely due to the placebo effect)
One problem with deeply understanding the physical mechanisms which underlie the placebo effect is that all the experiments must be on humans. You can't simply tell a mouse it's getting a 'cure' and give it a fake pill. However, scientists at the National Institute on Drug Abuse (NIDA) have conducted an ingenious experiment that involves giving a mouse what is essentially a placebo. Better still, they published it in PLoS One, so everyone can read the paper for free!
Before we dive into the placebo aspect of this paper, we need to back up and learn a little about as the addiction and reward system works in the brain.
In 1954, James Olds and Peter Milner published a paper showing that a rat would press a lever to receive an electrical stimulation in certain areas of its brain.
This was a huge discovery showing that 'reward' could be activated directly.
Later studies found that when this electrode stimulates the dopamine system of a rat, the rat will press and press and press this lever, even forgoing food when it is famished. Incidentally, a mouse/rat will also compulsively press a lever to get injections of cocaine (which acts by stimulating the dopamine system). You can do all sorts of experiments on drug addiction using this cocaine self-injection system. You can test how long it takes the mouse to become addicted, you can test the effect of drug concentration, you can test how other drugs interact with self-injection of cocaine, and you can even test aspects of withdrawal and relapse.
Which brings up back to our placebo. Wise et al., (2008) investigated the mechanisms underlying this self-administration. What was happening in the mouse brain when they got a dose of cocaine? They found that when the mouse pressed the lever and got the cocaine there was a surge of dopamine almost immediately after. There is a center in the brain called the VTA that contains neurons which release dopamine. When these neurons are active, other areas of the brain are flushed with dopamine and the person/rat/mouse 'feels reward'. But what makes these neurons active?
This brings up a problem we discussed a while ago, about the never ending cycle of neuronal firing. The dopamine neurons fire, but why? what neurons are firing onto them to make them fire, and then, what neurons are making those neurons fire and which ones are firing before that...so forth into forever.
To go one step up in this firing-chain, Wise et al. cleverly looked at 'brain juice' in the VTA and found that when the cocaine is administered, the mouse gets a surge of glutamate there. (Glutamate activates cells, so this would cause the dopamine neurons of the VTA to fire and release dopamine onto other cells).
So what does all this mean, and how does it get us to a placebo for a rat?
Here's the thing: the surge of glutamate that stimulates the VTA only shows up in mice that have already learned that a lever press gives them cocaine. (That is, this glutamate surge doesn't occur the very first time the mouse gets cocaine)
Here is the figure showing this glutamate surge in the VTA. The vertical dotted gray line is when the mouse presses the lever for the cocaine. The red and yellow traces are the condition where the mouse actually gets cocaine in response to the lever press. the blue and green traces are the condition where the mouse gets saline instead (a control), and the gray trace is the first time the rat gets cocaine in response to the lever press.
Another peculiar aspect of this glutamate surge is that it is probably too fast a response to be a result of the cocaine acting in the brain. So how is the injection of cocaine causing a glutamate surge if it is not even acting on the brain yet? This is quite the puzzle. Wise et al., wanted to make sure that this glutamate surge was absolutely not due to the cocaine reaching the brain, so they invented the rat placebo! They altered the cocaine molecule, so it was mostly the same shape as normal cocaine, except it couldn't cross the blood brain barrier. That is, when it is injected into the mouse, it can be detected in the blood and in the peripheral body, but it won't be detected in the brain, and the cocaine will not be able to act directly on the neurons.
When they run the test with this molecule injected instead of cocaine, the figure looks like this:
Pretty similar! This cocaine molecule can't reach the brain, but it causes the same glutamate surge as the real stuff! This shows that glutamate surge is somehow due to the cocaine being felt by the body, but not being felt by the brain. Although they don't call it a placebo in the paper, that is essentially what it is. It is tricking the brain into thinking it has just received cocaine. (In a stronger way than context can, as evidenced by the lack of response to saline.)
So there you have it, a way to trick a rat into thinking it has just received a 'real drug' when it has actually received an ineffectual drug. I think this technique could be adapted to actually study the physiological mechanisms governing the placebo effect.
© TheCellularScale
Wise RA, Wang B, & You ZB (2008). Cocaine serves as a peripheral interoceptive conditioned stimulus for central glutamate and dopamine release. PloS one, 3 (8) PMID: 18682722
reade more...
 |
| Just say no, Rat (source) |
The "Placebo Effect" occurs when someone takes a functionally ineffectual drug, but feels the effects anyway. There are many examples of this: Someone in pain takes a sugar pill, but is told that it is a painkiller might report 'feeling much less pain'. A Parkinson's patient takes a sugar pill having been told it was their 'L-dopa' medication and can suddenly move more fluidly. The "Placebo Effect" is so strong that most experiments testing the effectiveness of a drug in healing anything use a placebo control. The researchers want to make sure that the drug has an actual effect that is greater than the placebo effect. (It has been proposed that homeopathic remedies are entirely due to the placebo effect)
One problem with deeply understanding the physical mechanisms which underlie the placebo effect is that all the experiments must be on humans. You can't simply tell a mouse it's getting a 'cure' and give it a fake pill. However, scientists at the National Institute on Drug Abuse (NIDA) have conducted an ingenious experiment that involves giving a mouse what is essentially a placebo. Better still, they published it in PLoS One, so everyone can read the paper for free!
Before we dive into the placebo aspect of this paper, we need to back up and learn a little about as the addiction and reward system works in the brain.
In 1954, James Olds and Peter Milner published a paper showing that a rat would press a lever to receive an electrical stimulation in certain areas of its brain.
 |
| Olds and Milner, 1954 Figure 2, Xray of rat |
Later studies found that when this electrode stimulates the dopamine system of a rat, the rat will press and press and press this lever, even forgoing food when it is famished. Incidentally, a mouse/rat will also compulsively press a lever to get injections of cocaine (which acts by stimulating the dopamine system). You can do all sorts of experiments on drug addiction using this cocaine self-injection system. You can test how long it takes the mouse to become addicted, you can test the effect of drug concentration, you can test how other drugs interact with self-injection of cocaine, and you can even test aspects of withdrawal and relapse.
Which brings up back to our placebo. Wise et al., (2008) investigated the mechanisms underlying this self-administration. What was happening in the mouse brain when they got a dose of cocaine? They found that when the mouse pressed the lever and got the cocaine there was a surge of dopamine almost immediately after. There is a center in the brain called the VTA that contains neurons which release dopamine. When these neurons are active, other areas of the brain are flushed with dopamine and the person/rat/mouse 'feels reward'. But what makes these neurons active?
This brings up a problem we discussed a while ago, about the never ending cycle of neuronal firing. The dopamine neurons fire, but why? what neurons are firing onto them to make them fire, and then, what neurons are making those neurons fire and which ones are firing before that...so forth into forever.
To go one step up in this firing-chain, Wise et al. cleverly looked at 'brain juice' in the VTA and found that when the cocaine is administered, the mouse gets a surge of glutamate there. (Glutamate activates cells, so this would cause the dopamine neurons of the VTA to fire and release dopamine onto other cells).
So what does all this mean, and how does it get us to a placebo for a rat?
Here's the thing: the surge of glutamate that stimulates the VTA only shows up in mice that have already learned that a lever press gives them cocaine. (That is, this glutamate surge doesn't occur the very first time the mouse gets cocaine)
 |
| Wise et al., 2008 (figure1B) |
Another peculiar aspect of this glutamate surge is that it is probably too fast a response to be a result of the cocaine acting in the brain. So how is the injection of cocaine causing a glutamate surge if it is not even acting on the brain yet? This is quite the puzzle. Wise et al., wanted to make sure that this glutamate surge was absolutely not due to the cocaine reaching the brain, so they invented the rat placebo! They altered the cocaine molecule, so it was mostly the same shape as normal cocaine, except it couldn't cross the blood brain barrier. That is, when it is injected into the mouse, it can be detected in the blood and in the peripheral body, but it won't be detected in the brain, and the cocaine will not be able to act directly on the neurons.
When they run the test with this molecule injected instead of cocaine, the figure looks like this:
 |
| Wise et al., 2008 (figure1E) |
So there you have it, a way to trick a rat into thinking it has just received a 'real drug' when it has actually received an ineffectual drug. I think this technique could be adapted to actually study the physiological mechanisms governing the placebo effect.
© TheCellularScale
Wise RA, Wang B, & You ZB (2008). Cocaine serves as a peripheral interoceptive conditioned stimulus for central glutamate and dopamine release. PloS one, 3 (8) PMID: 18682722How to Cure Yeast Infection (self-treatment)?
(Image credit to shutterstock)
After knowing causes and symptoms of vaginal yeast infections, now you may be looking for information about how to cure yeast infection! There are a number of treatment choices to choose from, and the best choice should be based to your condition. Some popular treatment options are nonprescription vaginal boric acid capsules, vaginal medicine (prescription oral)
Causes of Yeast Infections in Women
(image credit to Getty Images)
If you ask about yeast infections in women, then it is often referred to vaginal yeast infection! In fact, 3 of 4 women have this disorder at least 1 time during their lives, which also become the second most common cause of vaginal discharge, itching and burning. The next question ‘What are causes of yeast infections in women?”
You may also like to know about
March 1st is International Self Injury Awareness Day
What do these high profile individuals have in common? Singer, Fiona Apple; Comedian, Russell Brand; Actress, Drew Barrymore; Actor, Johnny Depp; Actor, Colin Farrell; Actress, Megan Fox; Actress, Angelina Jolie; Singer, Demi Lovato and Princess Diana....
Before finding emotional health, they struggled with self-injury.
Self-Injury is a deliberate, non-suicidal behavior that inflicts physical harm on one's body to relieve emotional distress. Self-injury has a paradoxical effect in that the pain self-inflicted actually sets off an endorphin rush, relieving the self-harmer from deep distress. It's important to note that self-injury does not involve a conscious intent to commit suicide - and as such, the clinical term for this behavior is called Non-Suicidal Self Injury (NSSI), NSSI can take many forms from cutting, picking, burning, bruising, puncturing, embedding, scratching or hitting one's self, just to name a few.
In its simplest form, NSSI is a physical solution to an emotional wound. Generally, it is a deliberate, private act that is habitual in occurrence, not attention-seeking behavior, nor meant to be manipulative. Self-injurers are often secretive about their behaviors, rarely letting others know, and often cover up their wounds with clothing, bandages, or jewelry.
Symbolically speaking, deliberately injuring one's self can be viewed as a method to communicate what cannot be spoken. With self-harm, the skin is the canvas and the cut, burn or bruise is the paint that illustrates the picture. Most individuals who self-injure are struggling with emotional expression. This clinical experience is known as Alexithymia - the inability to recognize emotions and their subtleties and to understand or describe thoughts and feelings. Many other self-harmers are struggling with internal conflicts, may have anxiety, depression, may have experienced physical or sexual abuse, or other more serious psychological concerns.
Statistically speaking, approximately 4% of the population in the United States uses NSSI as a way of coping. Individuals who self-injure are represented in all SES brackets in the United States with the behavior usually starting in adolescence. Girls and women tend to self-injure more than boys and men, but this may be represented by the fact that females tend to turn to professional help more than males.
Those Who Self-Injure Are Often Trying To:
* Distract themselves from emotional pain
* End feelings of numbness
* Offset feelings of low self-esteem
* Control helplessness or powerlessness
* Calm overwhelming or unmanageable feelings
* Maintaining control in chaotic situations
* Self-punish, self-shame or self-hate
* Express negative thoughts or feelings that cannot be put into words
* Self-nurture or self-care
10 Tips for Reducing Self-Injury
1) Create an Emergency Kit. Place positive things in your kit like photos of people you love, notes to yourself or from friends or family, a journal for writing, markers or art supplies for artistic expression, an inspirational poem, beloved stuffed animal, upbeat music, favorite scents, things like that.
2) Use positive imagery. Visualize yourself moving through your painful moment without self-harming. Research shows that using positive visualization can keep you in-the-moment which is a key tool for recovery.
3) Hold your ground. Sensory Grounding experiences like holding something soft, listening to soothing music, drawing or writing, for example, can interrupt the trance-like state that often comes with self-harm, shifting you towards more positive behaviors.
4) Reboot your mind. Reframe your thoughts toward helpful statements, also known as Cognitive Grounding Skills, like "Who am I really mad at?""What is setting me off?" or "I am safe and I am in control." These can re-orient you to the here-and-now.
5) Know your triggers. Become aware of what issues bend or break you. Try to dilute your exposure to them, call upon others to help you move through them and remind yourself that you can emerge from them successfully.
6) Take a detour. Reroute self-harm by using less severe forms of sensations. Holding an ice cube, tearing or shredding paper or a sheet, snapping a rubber band against your skin, sucking a lemon peel are ways to dilute the need to experience pain.
7) Move your body. Consider the adrenaline rush of running, dancing, holding a yoga pose, jumping rope to offset urges to self-harm. The rush of adrenaline has been known to produce the similar chemical surge that comes from self-injury.
8) Forgive yourself. As you try to interrupt your self-harming behaviors, know that it may not come as easily some days as others. Should you find that you've lapsed into self-harming, remind yourself that change is a process. Learn to forgive and be kind to yourself as you start anew.
9) Be supportive. If you know someone who may be self-injuring, offer support and try not to shame or criticize the NSSI behavior. Self-injury behaviors can be successfully treated, so help your friend or family member by encouraging them to seek help.
10) Consider calling a therapist. Remember that having an urge to self harm is not the same as actually self harming. If you can distract yourself from self-injury, you are well on your way to recovery. However, if the urges win out, not allowing you to reduce your self-harm behaviors, consider working with a professional.
References
Froeschle, J. & Moyer, M. (2004). Just cut it out: Legal and ethical challenges in counseling students who self-mutilate. Professional School Counseling. 7(4), 231-235.
Kress White, V.E. (2003). Self-injurious behaviors: Assessment and diagnosis. Journal of Counseling & Development. 81(4), 490-496.
Lee, Y. et al. (2010). Direct and indirect effects of the temperament and character on Alexithymia: A pathway analysis with mood and anxiety. Comprehensive Psychiatry, 51 (2), 201-206.
Levenkron, S. (1999). Cutting: Understanding and overcoming self-mutilation. New York: W.W. Norton & Company.
Self-Injury is a deliberate, non-suicidal behavior that inflicts physical harm on one's body to relieve emotional distress. Self-injury has a paradoxical effect in that the pain self-inflicted actually sets off an endorphin rush, relieving the self-harmer from deep distress. It's important to note that self-injury does not involve a conscious intent to commit suicide - and as such, the clinical term for this behavior is called Non-Suicidal Self Injury (NSSI), NSSI can take many forms from cutting, picking, burning, bruising, puncturing, embedding, scratching or hitting one's self, just to name a few.
In its simplest form, NSSI is a physical solution to an emotional wound. Generally, it is a deliberate, private act that is habitual in occurrence, not attention-seeking behavior, nor meant to be manipulative. Self-injurers are often secretive about their behaviors, rarely letting others know, and often cover up their wounds with clothing, bandages, or jewelry.
Symbolically speaking, deliberately injuring one's self can be viewed as a method to communicate what cannot be spoken. With self-harm, the skin is the canvas and the cut, burn or bruise is the paint that illustrates the picture. Most individuals who self-injure are struggling with emotional expression. This clinical experience is known as Alexithymia - the inability to recognize emotions and their subtleties and to understand or describe thoughts and feelings. Many other self-harmers are struggling with internal conflicts, may have anxiety, depression, may have experienced physical or sexual abuse, or other more serious psychological concerns.
Statistically speaking, approximately 4% of the population in the United States uses NSSI as a way of coping. Individuals who self-injure are represented in all SES brackets in the United States with the behavior usually starting in adolescence. Girls and women tend to self-injure more than boys and men, but this may be represented by the fact that females tend to turn to professional help more than males.
Those Who Self-Injure Are Often Trying To:
* Distract themselves from emotional pain
* End feelings of numbness
* Offset feelings of low self-esteem
* Control helplessness or powerlessness
* Calm overwhelming or unmanageable feelings
* Maintaining control in chaotic situations
* Self-punish, self-shame or self-hate
* Express negative thoughts or feelings that cannot be put into words
* Self-nurture or self-care
10 Tips for Reducing Self-Injury
1) Create an Emergency Kit. Place positive things in your kit like photos of people you love, notes to yourself or from friends or family, a journal for writing, markers or art supplies for artistic expression, an inspirational poem, beloved stuffed animal, upbeat music, favorite scents, things like that.
2) Use positive imagery. Visualize yourself moving through your painful moment without self-harming. Research shows that using positive visualization can keep you in-the-moment which is a key tool for recovery.
3) Hold your ground. Sensory Grounding experiences like holding something soft, listening to soothing music, drawing or writing, for example, can interrupt the trance-like state that often comes with self-harm, shifting you towards more positive behaviors.
4) Reboot your mind. Reframe your thoughts toward helpful statements, also known as Cognitive Grounding Skills, like "Who am I really mad at?""What is setting me off?" or "I am safe and I am in control." These can re-orient you to the here-and-now.
5) Know your triggers. Become aware of what issues bend or break you. Try to dilute your exposure to them, call upon others to help you move through them and remind yourself that you can emerge from them successfully.
6) Take a detour. Reroute self-harm by using less severe forms of sensations. Holding an ice cube, tearing or shredding paper or a sheet, snapping a rubber band against your skin, sucking a lemon peel are ways to dilute the need to experience pain.
7) Move your body. Consider the adrenaline rush of running, dancing, holding a yoga pose, jumping rope to offset urges to self-harm. The rush of adrenaline has been known to produce the similar chemical surge that comes from self-injury.
8) Forgive yourself. As you try to interrupt your self-harming behaviors, know that it may not come as easily some days as others. Should you find that you've lapsed into self-harming, remind yourself that change is a process. Learn to forgive and be kind to yourself as you start anew.
9) Be supportive. If you know someone who may be self-injuring, offer support and try not to shame or criticize the NSSI behavior. Self-injury behaviors can be successfully treated, so help your friend or family member by encouraging them to seek help.
10) Consider calling a therapist. Remember that having an urge to self harm is not the same as actually self harming. If you can distract yourself from self-injury, you are well on your way to recovery. However, if the urges win out, not allowing you to reduce your self-harm behaviors, consider working with a professional.
References
Froeschle, J. & Moyer, M. (2004). Just cut it out: Legal and ethical challenges in counseling students who self-mutilate. Professional School Counseling. 7(4), 231-235.
Kress White, V.E. (2003). Self-injurious behaviors: Assessment and diagnosis. Journal of Counseling & Development. 81(4), 490-496.
Lee, Y. et al. (2010). Direct and indirect effects of the temperament and character on Alexithymia: A pathway analysis with mood and anxiety. Comprehensive Psychiatry, 51 (2), 201-206.
Levenkron, S. (1999). Cutting: Understanding and overcoming self-mutilation. New York: W.W. Norton & Company.
How and When to Test Blood Sugar after Eating?
One of frequently asked questions about blood sugar testing is how and when to test blood sugar after eating! Well, you should clearly know that the food that you eat before and after your test can influence the test result. -- You may also like to know the correlation between overweight and diabetes!
Most of food you eat will be digested by your digestive system and then can contribute to
Type 2 Diabetes Diet (Carbohydrate and Fiber Counting)
A healthy diet is so important to maintain the weight and blood sugar level (especially for people with diabetes). And as well we know that type 2 diabetes is the more common than type-1 and gestational diabetes (only in pregnancy) -- read also the related previous posts about “type 2 diabetes symptoms and risk factors”!
A proper type 2 diabetes is not only useful for people with diabetes
Type 2 Diabetes Risk Factors
(Image credit to ‘Corbis’)
It is so important to know about type-2 diabetes risk factors, so thus if you have one or some of these risk factors you can consider getting a diabetes test immediately for better prevention by asking and discussing more with your doctor!
Fortunately, unlike type-1 diabetes, there are some modifiable risk factors of type-2 diabetes that can be helpful enough to
Type-2 Diabetes Causes (The Role of Insulin)
What you should know about type 2 diabetes causes, especially about the role of insulin in the reason of type 2 diabetes? As well we know that it is the most common type of diabetes, even approximately effecting up to 85-90 percent (or more) of all individuals with diabetes!
You may also like to read appropriately diet for people with type-2 diabetes, before continuing!
And although older
Difference between Type 1 and Type 2 Diabetes!
What is the difference between type-1 and type-2 diabetes? As well we know that one of the most common disorders & health problems of the endocrine (hormone) system is diabetes (or also familiar known as diabetes mellitus for the formal name). It can occur when the levels of blood sugar are consistently above the level of normal!
Read also factors or conditions that increase your risk of
Know thyself, Cell: Neuronal self-recognition
A neuron's shape is important for its function, but how does it get its shape in the first place? As we've discussed before, dendrites grow out of the cell body (soma) and follow a somewhat pre-described pattern. A Purkinje cell always has a general corral-like shape, but each individual neuron is shaped a little differently. (Just like an oak tree looks different from a pine tree, while at the same time no two oak trees are exactly the same.)
And just as trees branch and grow based on where the sunlight is coming from, dendrites can branch and grow depending on external factors. Of course dendrites don't care about sunlight, but they do want to efficiently 'cover space' to receive lots of incoming signals.
So how do they do it?
Some neurons have dendrites that repulse eachother. As in, if two dendrites are rooted to the same soma, those two dendrites will avoid eachother. This is one way that the dendrite can 'cover space' very efficiently, it will branch and grow until it sees 'itself' and then it will stop and grow in a different direction.
In 1998, Wang and Macagno published a fascinating study using the mechanosensory neurons in the leech. These particular neurons show 'self-avoidance' (the dendrites of the same neuron do not overlap), but they don't show 'class-avoidance' (Dendrites from the same class of neurons do overlap).
Wang and Macagno wanted to test what exactly was so self-repulsive about these dendrites.
There are two ways the cell could recognize itself:
1. Through the use of external signals (such as a chemical marker on the surface of the dendrites that sibling dendrites can detect)
2. Through the use of internal signals (such as the voltage activity transmitted within the cell)
To find out what method the dendrites are using to recognize themselves, Wang and Macagno used a laser to separate a small section of dendrite from the rest of the neuron. Would the other dendrites still avoid this severed dendrite, or would they suddenly see it as a stranger and start to overlap with it?
The attached dendrites start to treat the severed dendrite as a stranger, growing into its area and overlapping with it. Figure 4 from Wang and Macagno shows the intact cell (A), the location of the cut (star in B), and the regrowth of both the severed dendrite and the still attached dendrite (arrow in D).
The authors offer several possible explanations for why a severed dendrite would appear to be a stranger to the rest of the dendrites, but all are speculative. Maybe the electrical signal prevents gap junctions from forming. Maybe there are channels (such as NMDA receptors) that repulse each other when they are both active at the same time. Maybe there is some cytoplasmic molecule that diffuses between the dendrites and prevents overlap (though the authors admit this mechanism sound too slow to do the job.) The authors even find a problem with the electrical signal hypothesis in that:
Since no one has tested a blockade of electrical activity on these neurons, the mechanism underlying the self-repulsive nature of these dendrites is still a mystery.
© TheCellularScale
Wang H, & Macagno ER (1998). A detached branch stops being recognized as self by other branches of a neuron. Journal of neurobiology, 35 (1), 53-64 PMID: 9552166
reade more...
 |
| branching tree at sunset, San Diego: taken by me |
And just as trees branch and grow based on where the sunlight is coming from, dendrites can branch and grow depending on external factors. Of course dendrites don't care about sunlight, but they do want to efficiently 'cover space' to receive lots of incoming signals.
So how do they do it?
Some neurons have dendrites that repulse eachother. As in, if two dendrites are rooted to the same soma, those two dendrites will avoid eachother. This is one way that the dendrite can 'cover space' very efficiently, it will branch and grow until it sees 'itself' and then it will stop and grow in a different direction.
 |
| (source) The Leech: yuck. |
In 1998, Wang and Macagno published a fascinating study using the mechanosensory neurons in the leech. These particular neurons show 'self-avoidance' (the dendrites of the same neuron do not overlap), but they don't show 'class-avoidance' (Dendrites from the same class of neurons do overlap).
Wang and Macagno wanted to test what exactly was so self-repulsive about these dendrites.
There are two ways the cell could recognize itself:
1. Through the use of external signals (such as a chemical marker on the surface of the dendrites that sibling dendrites can detect)
2. Through the use of internal signals (such as the voltage activity transmitted within the cell)
To find out what method the dendrites are using to recognize themselves, Wang and Macagno used a laser to separate a small section of dendrite from the rest of the neuron. Would the other dendrites still avoid this severed dendrite, or would they suddenly see it as a stranger and start to overlap with it?
 |
| Wang and Macagno, 1998 Figure 4 |
The attached dendrites start to treat the severed dendrite as a stranger, growing into its area and overlapping with it. Figure 4 from Wang and Macagno shows the intact cell (A), the location of the cut (star in B), and the regrowth of both the severed dendrite and the still attached dendrite (arrow in D).
The authors offer several possible explanations for why a severed dendrite would appear to be a stranger to the rest of the dendrites, but all are speculative. Maybe the electrical signal prevents gap junctions from forming. Maybe there are channels (such as NMDA receptors) that repulse each other when they are both active at the same time. Maybe there is some cytoplasmic molecule that diffuses between the dendrites and prevents overlap (though the authors admit this mechanism sound too slow to do the job.) The authors even find a problem with the electrical signal hypothesis in that:
"In some systems the blockade of electrical activity does not affect morphogenesis."
Since no one has tested a blockade of electrical activity on these neurons, the mechanism underlying the self-repulsive nature of these dendrites is still a mystery.
© TheCellularScale
Wang H, & Macagno ER (1998). A detached branch stops being recognized as self by other branches of a neuron. Journal of neurobiology, 35 (1), 53-64 PMID: 9552166
Type 2 Diabetes Symptoms (Signs)
What are type 2 diabetes symptoms (signs)? There are many symptoms, but before discussing about these signs, you should first clearly understand that the diagnosis of this disease is not easy in many cases which often will only be able to be diagnosed clearly if the other health complications have occurred!
Read also a related article about type-1 vs. type-2 diabetes!
In almost 2/3 of all
Gestational Diabetes Test Preparation
What you should know about gestational diabetes test preparation? Like written in the previous article about gestational diabetes symptoms and causes, there are no clearly causes of this disease. Therefore, you need to get a proper screening test to find a clearly diagnosis, particularly after 24-28th of your pregnancy!
Understanding what you should prepare before going to test will be
Gestational Diabetes Symptoms and Causes!
What are gestational diabetes symptoms and causes? A condition of a pregnant woman (first recognized during pregnancy), which characterized by the high level of blood sugar (or familiar known as ‘glucose’) is the definition of gestational diabetes! It can occur about 4 percent of all pregnancies.
You might also like know about gestational diabetes test preparation tips, before continuing!
Neurosexism and Delusions of Gender
On the cellular scale, it is very difficult, if not impossible, to tell the brains of men and women apart. That is, if you zoom in on a part of the brain (like the hippocampus, cortex or striatum) and look at the morphology of a single neuron or the electrical characteristics of that neuron, you would be hard pressed to tell if the neuron you are looking at belongs to a male or a female. This is not very surprising since it is also difficult to tell if the neuron you are looking at is from a human, ape, or elephant. That is a cellular introduction to the non-cellular book that I am reviewing today: Delusions of Gender: How our minds, society, and neurosexism create difference by Cordelia Fine.
My friend from undergrad who is now a philosophy professor recommend this book to me and described it in such a way that I suspected I would hate it. Upon actually reading it however, I was quite surprised at how informative and entertaining it was.
Let's get to it!
Delusions of Gender is a book written in response to the idea that there are inherent differences between men and women that are hard-wired into the brain by evolution and that make women naturally suited for certain activities and men naturally suited for others.
In other words, Cordelia Fine claims that this is NOT the case, or at least that it is not nearly as much the case as people currently believe. This is a difficult claim to make. It's so easy to see that men and women are different in body, so why wouldn't their brains be different? And doesn't evolution make the sexes of many species 'inherently' different? For examples, look at the praying mantis, the zebra finch, and the stickleback.
So what I found amazing is that Cordelia Fine argued this impossible claim so well that I was thoroughly convinced that everything I had heard about the differences between male and female brains and abilities was at best uncertain, and at worst completely wrong.
Let me summarize some of the exact points that she makes:
- You are bound to find differences when you are looking for them.
- Differences are more likely to be reported and publicized than similarities.
- There are glaring flaws in many neuroscience studies showing brain differences between men and women.
- Even if all the studies showing brain differences between men and women were taken as true, that still wouldn't mean that the differences are 'hard wired' or 'inherent' or 'because of evolution'
- Even if all the brain differences are real, and even if they are 'hard wired', that still doesn't mean that women and men actually think differently.
To explain a little further:
Claim 1 says that when there is one difference between two groups, it is easy to think of a scientific study to determine if something else is different between these two groups. This is important because of the 'obvious' differences between men and women (yeah, they have different junk). Since everyone knows men and women are different re: genitalia, let's test whether they are different in brain or behavior. This may seem totally reasonable, but a counter example is finger-print pattern. People can be grouped by their fingerprint pattern into 'loop-shape' or 'swirl-shape' people. This fingerprint pattern is determined genetically, but since it is not an obvious difference (you probably don't even know which group you belong to), no one has ever tested whether 'loop-shape' people have bigger hippocampi than 'swirl-shape' people.
Claim 2 says that for every newspaper headline shouting "Women are inherently totally whacked" (see also this post) there might be several studies quietly showing "Women and men are pretty similar" This problem, research showing differences getting published and hyped, while research showing 'no difference' getting ignored or not even published to begin with is not a problem new to science, nor is it specific to gender issues. It is always more exciting and always has a 'higher impact' as they say, to show that two things are different.
A recent paper by De Liberto et al., (2012) shows that male and female mice show no difference in the amount of DAT (dopamine transporter) in the striatum.
 |
| De Liberto et al., 2012 figure1C |
Let's do a quick thought experiment: Imagine that the researchers had found a difference here, say "male mice have less DAT than female mice." This could have 'meant' that men have more dopamine at the synapse (as the DAT is responsible for cleaning up excess dopamine there), and this could have been 'translated' into the idea that men are happier or women are more moody and prone to depression (Dopamine levels are implicated in moodiness and depression). Wow! what an exciting finding! Front cover of Time magazine: "The Secret Science Behind Moody Women." However, here in reality, these results showed no difference, so they became just a small figure panel in paper about the effects of estrogen.
Claim 3 is the one I had the hardest time reading. It is true that there is a lot of sloppy science out there, but I think she goes a little too far in her distrust of science. For example, she brings up the dead fish in an MRI study as evidence for fMRI studies being flawed. It is true that in all scientific studies there is a risk of falsely identifying a difference when there is none, but that is exactly what the correction for multiple comparisons is for. This is a statistical correction that all scientist should know about and apply, but sometimes (maybe even often) they don't. However, there are plenty of fMRI studies that do correct for this multiple testing problem and are scientifically sound.
Claims 4 and 5 are my favorite. I thought I would hate this book when I thought that her claim was going to be 'men and women are not different, and neuroscience is flawed and stupid.' However, when I saw that she was actually claiming 'we don't know enough about the brain to draw the conclusions people are drawing' I got right on board. There is way too much "the amygdala lit up therefore the person was frightened" and "the hippocampus is bigger so the person must navigate space better" going around. These claims can get ridiculous and most are just not supported. We don't have a full understanding of the brain, or even of any part of the brain. We don't even have a full understanding of the single neurons that make up the brain (as you well know from reading The Cellular Scale).
In conclusion, there may be (and probably are) brain differences between men and women, some of these differences might be 'hard wired' and 'inherent' and some of them might develop as a child grows up in a gender-difference driven culture. (By the time you get a kid into an MRI machine, s/he has done a lot of developing.) These (possible/probable) brain differences might mean that men and women think differently, or they might not.
We just don't know enough about it, yet.
© TheCellularScale
There are many excellent reviews of this book out there, here are just a few:
SevenDeadlySynapses
NeuroSkeptic (who is actually cited in this book)
TheThinkingMeatProject
GenderAccrossBorders
Di Liberto V, Mäkelä J, Korhonen L, Olivieri M, Tselykh T, Mälkiä A, Do Thi H, Belluardo N, Lindholm D, & Mudò G (2012). Involvement of estrogen receptors in the resveratrol-mediated increase in dopamine transporter in human dopaminergic neurons and in striatum of female mice. Neuropharmacology, 62 (2), 1011-8 PMID: 22041555What Does It Mean to Have an Irregular Period?
What does it mean to have an irregular period? Well, menstrual periods from month to month that can vary more than a few days in length are often considered irregular. Most intervals of women’s menstrual cycle occur between 24-35 days (the normal range). -- You may also like to know about reasons of late period!
How to count the interval of the menstruation? Star or begin counting from the
Irregular Period Causes and Spotting
Looking for irregular period causes and spotting (bleeding)? In fact, there is still no clearly link or correlation between irregular period and bleeding (or spotting between periods)! But in many cases, many women will get higher chance to get irregular period if they get bleeding between their periods.
The vaginal spotting or bleeding between your periods can be categorized into abnormal
Random Acts of Kindness Week
Random Acts of Kindness Week is February 13th thru the 19th here in the United States and Canada.
The Random Acts of Kindness™ Foundation is the official organization of the kindness movement , whose aim is to help everyone create a better world by spreading awareness and increasing engagement in kind actions.
The Random Acts of Kindness™ Foundation is international, with kindness days and weeks sponsored around the globe. They provide free educational and community ideas, guidance, and other resources to promote kindness.
Research shows that tiny acts of kindness ripple exponentially across social experiences - essentially sparking a contagiousness of generosity and cooperativeness. Simple stated, a single kind act influences dozens more.
So be kind and pay it forward!
Citation:
Fowler, H. & Christakis, N. (2010). Cooperative behavior cascades in human social networks. Proceedings of the National Academy of Sciences, Vol. 107(10): 5334-5338
Early Signs of Pregnancy First 2 Weeks
(Image credit to shutterstock)
As well we know that there are several symptoms in early pregnancy, including for the early signs of pregnancy first 2 weeks! One of the clearly symptoms in the first 2 weeks, you may begin to notice your missed period (especially if you have regular period with 28 days of cycle).
You may also like to know about pregnancy symptoms before missed period,
8 Days after Conception (Ovulation): Pregnancy Symptoms
(Image credit to shutterstock)
Looking for 8 days after conception symptoms? There are some early pregnancy symptoms after conception. Some of these signs are vivid dreams, changes in breasts, elevated cervical fluid, nausea, bloating, flatulence, mild cramps, or even exhaustion (fatigue).
You may also be interested to know about early signs of pregnancy first 2 weeks, before continuing!
Sound localization: form meets function in the BirdBrain
In the last post, we introduced the special football-shaped cells of the bird Nucleus Laminaris (NL).
Today we look at how the dendritic length of these neurons dictates the frequencies they are most sensitive to. But first we need to understand what the NL does.
When you hear a noise, you can tell what direction it is coming from (for the most part).
There are several ways the brain can hone in on the direction of a sound. One of those ways is called the 'inter-aural time difference.' That means the difference between when a sound hits one ear and when it hits the other.
For example, imagine you are on a hike in a quiet woods and you hear a leaf-rustling sound to your right. The sound waves from that leaf-rustling actually reach your right ear a fraction of a second before they reach your left ear. The brain can process this time difference and compute the direction of the sound.
Incidentally, birds like the boring-old-chicken and the pretty-cool-barn-owl are particularly good at sound localization. The NL in these birds is where this computation takes place.
Above is a diagram of the bird auditory brain stem. the NL is the line-like structure on either side. The dendrites on the top of the NL neurons receive input from one ear (the ear on the same side of the head), and the dendrites on the bottom of the NL receive input from the other ear (the one on the opposite side of the head). In the picture above, inputs from one ear are in black and inputs from the other are in red. Since a sound from a particular direction hits one ear first, and then the other ear, the top dendrites of a cell will receive inputs at a slightly different time than the bottom dendrites of that cell.
If you remember our last post, you know that the dendrites in the NL are longer near the outside edges of the brain and shorter near the middle. You also will remember that the short-dendrite neurons are sensitive to high frequency sound waves and the long-dendrite neurons are sensitive to lower frequency sound waves. So how do the frequency-tuning properties relate to the dendritic gradient properties?
In a computational study, published in Biological Cybernetics, Grau-Serrat et al., (2003) try to answer this question.
First a quick introduction to computational neuroscience (I plan to write a whole post about this someday):
Now back to the BirdBrain!
So to answer the 'form and function' question inherent in the NL cells, Grau-Serrat et al. create model NL neurons in a computer program and test them with simulated inputs. Because it is a computational model, they have complete control over the conditions. They can put either short or long dendrites on these cells, and can send in high or low frequency sound waves. They also can send an input to the top layer of dendrites at one time and then send an input to the bottom layer of dendrites milliseconds afterwards. Controlling all these factors, they can test whether the size of the dendrites in these cells helps them accurately detect the timing difference between ears. They can also test whether the frequency of the sound (high or low) has anything to do with timing difference detection.
They found a remarkably simple answer:
The lower the frequency, the longer the dendrites need to be to show good time discrimination.
In their computational model, making the dendrites longer generally improved time discrimination, but for every frequency there was a certain dendritic length that was 'long enough'. Adding more dendrite after a certain length didn't improve the time discrimination.
So there you have it, the mystery of the NL dendritic gradient, solved by computational neuroscience.
Note: I know this is a pretty complex system, and I am definitely simplifying. If you know a lot about the auditory brainstem, please don't hesitate to correct/expand on what I've written here in a comment. Also if you don't know a lot about this system and have a question, write it in the comments section and I'll try my best to answer it.
© TheCellularScale
Grau-Serrat V, Carr CE, & Simon JZ (2003). Modeling coincidence detection in nucleus laminaris. Biological cybernetics, 89 (5), 388-96 PMID: 14669019
Wang Y, & Rubel EW (2008). Rapid regulation of microtubule-associated protein 2 in dendrites of nucleus laminaris of the chick following deprivation of afferent activity. Neuroscience, 154 (1), 381-9 PMID: 18440716
reade more...
Today we look at how the dendritic length of these neurons dictates the frequencies they are most sensitive to. But first we need to understand what the NL does.
 |
| (source) |
When you hear a noise, you can tell what direction it is coming from (for the most part).
There are several ways the brain can hone in on the direction of a sound. One of those ways is called the 'inter-aural time difference.' That means the difference between when a sound hits one ear and when it hits the other.
For example, imagine you are on a hike in a quiet woods and you hear a leaf-rustling sound to your right. The sound waves from that leaf-rustling actually reach your right ear a fraction of a second before they reach your left ear. The brain can process this time difference and compute the direction of the sound.
Incidentally, birds like the boring-old-chicken and the pretty-cool-barn-owl are particularly good at sound localization. The NL in these birds is where this computation takes place.
 |
| Figure 1a, Wang and Rubel (2008) |
Above is a diagram of the bird auditory brain stem. the NL is the line-like structure on either side. The dendrites on the top of the NL neurons receive input from one ear (the ear on the same side of the head), and the dendrites on the bottom of the NL receive input from the other ear (the one on the opposite side of the head). In the picture above, inputs from one ear are in black and inputs from the other are in red. Since a sound from a particular direction hits one ear first, and then the other ear, the top dendrites of a cell will receive inputs at a slightly different time than the bottom dendrites of that cell.
 |
| Figure 2a, Wang and Rubel (2008) |
If you remember our last post, you know that the dendrites in the NL are longer near the outside edges of the brain and shorter near the middle. You also will remember that the short-dendrite neurons are sensitive to high frequency sound waves and the long-dendrite neurons are sensitive to lower frequency sound waves. So how do the frequency-tuning properties relate to the dendritic gradient properties?
In a computational study, published in Biological Cybernetics, Grau-Serrat et al., (2003) try to answer this question.
First a quick introduction to computational neuroscience (I plan to write a whole post about this someday):
"Computational neuroscience is a discipline that aims to understand how information is processed in the nervous system by developing formal models at many different structural scales...The end product of an computational analysis should be a sufficiently specified model, internally consistent and complete enough to enable formal mathematical characterization or computer simulation." Grau-Serrat et. al., 2003I thought these passages from their introduction made an excellent summary of computational neuroscience.
Now back to the BirdBrain!
So to answer the 'form and function' question inherent in the NL cells, Grau-Serrat et al. create model NL neurons in a computer program and test them with simulated inputs. Because it is a computational model, they have complete control over the conditions. They can put either short or long dendrites on these cells, and can send in high or low frequency sound waves. They also can send an input to the top layer of dendrites at one time and then send an input to the bottom layer of dendrites milliseconds afterwards. Controlling all these factors, they can test whether the size of the dendrites in these cells helps them accurately detect the timing difference between ears. They can also test whether the frequency of the sound (high or low) has anything to do with timing difference detection.
They found a remarkably simple answer:
The lower the frequency, the longer the dendrites need to be to show good time discrimination.
In their computational model, making the dendrites longer generally improved time discrimination, but for every frequency there was a certain dendritic length that was 'long enough'. Adding more dendrite after a certain length didn't improve the time discrimination.
 |
| Figure 3, Grau-Serrat et al., 2003 |
In summary, the dendritic gradient of the NL is predicted if the system follws two rules:
- Keep the dendrites as short as possible.
- Make the dendrites long enough to accurately discriminate time differences.
So there you have it, the mystery of the NL dendritic gradient, solved by computational neuroscience.
Note: I know this is a pretty complex system, and I am definitely simplifying. If you know a lot about the auditory brainstem, please don't hesitate to correct/expand on what I've written here in a comment. Also if you don't know a lot about this system and have a question, write it in the comments section and I'll try my best to answer it.
© TheCellularScale
Grau-Serrat V, Carr CE, & Simon JZ (2003). Modeling coincidence detection in nucleus laminaris. Biological cybernetics, 89 (5), 388-96 PMID: 14669019Wang Y, & Rubel EW (2008). Rapid regulation of microtubule-associated protein 2 in dendrites of nucleus laminaris of the chick following deprivation of afferent activity. Neuroscience, 154 (1), 381-9 PMID: 18440716Missed Period Negative Pregnancy Test on Birth Control
(Image credit to shutterstock)
If you get missed period with negative pregnancy test on birth control, your chance to get pregnant is still very lower. There are some women who experience this situation and then they are scared that they are pregnant, especially for some of them who are beginner on taking a form of birth control.
If you are one of them you may need to read the previous
Pregnancy Symptoms before Missed Period
(image credit to shutterstock)
Missed period is one of the early signs of pregnancy, but there are also some earlier pregnancy symptoms before missed period which usually closely associated to hormonal shifts in your body before you note your late period. And these earlier signs of your pregnancy before late period are largely and once again dependent on your hormonal shifts.
You may also like
Missed Period with Negative Test
Do you get a missed period with negative test? Absolutely this is the bad news particularly if you are trying to have a baby or have a plan for pregnancy. But there might be other reasons that you should clearly understand, especially for reasons of late period that can cause some health problems.
Or you can retry your test in next a couple of days, because your body may not produce adequate
Late Period on Birth Control
Late period on birth control is something that often scared for some women. This is one of the most frequently asked questions if you are trying a new medicine or some methods of birth control. Even the late period can take more than 5-6 weeks, which usually known as amenorrhea.
If you are not on a birth control, a missed period can be the strong indication or early symptoms of pregnancy
Late Period (Top 5 Reasons)
Late period or missed period is something that can strike fear into the heart of women, unless some of them who are trying to have a baby or get pregnant. There are some factors or reasons that can cause a missed period. -- You may also like to read about late period on birth control!
As well we know that a later period is one of the most popular early signs of pregnancy, even it can be
Neurons tuned like the strings of a harp
The auditory brainstem of the boring-old-chicken is actually home to some fascinating neurons.
The Nucleus Laminaris (NL) is a group of coincidence-detecting neurons which receive indirect input from both ears and is located in the bird auditory brainstem.
NL neurons show a peculiar dendrite pattern. These bipolar neurons fall into the particular category of football shaped cells which have dendrites coming out the top and bottom of their cell body. The cell body (soma) of these neurons are about the same size, but depending on where they are in the NL, the cells have either short, medium or long dendrites.
The ones near the midline have a bunch of short stubby little dendrites.
If they are a little further out from the midline, they have longer dendrites.
and finally if they are furthest from the middle, they have fewer and much longer dendrites.
all together this makes a gradient from short to long dendrites.
The big question here is "Why?"
What is the purpose of having stubby or extended dendrites like this? Well, even in 1979 when Smith and Rubel reconstructed these neurons, they knew that these neurons had a special answer to the "form and function" question.
The amazing thing about these neurons is that they are 'tuned' to respond maximally to specific frequencies (sound waves). And just like strings on an instrument, the cells with shorter dendrites respond to higher frequencies and the cells with longer dendrites respond to lower frequencies.
Why is this? Dendrites don't actually vibrate like strings, but there must be some reason for a cell with short dendrites to respond to higher frquencies and a cell with long dendrites to respond to low frequencies.
The answer lies in what the Nucleus Laminaris actually does. In the next post we'll venture into the wilds of computational neuroscience and explore the reason behind this strange connection between dendrite shape and cell function.
Smith DJ, & Rubel EW (1979). Organization and development of brain stem auditory nuclei of the chicken: dendritic gradients in nucleus laminaris. The Journal of comparative neurology, 186 (2), 213-39 PMID: 447882
reade more...
 |
| Key West rooster, taken by me. |
The Nucleus Laminaris (NL) is a group of coincidence-detecting neurons which receive indirect input from both ears and is located in the bird auditory brainstem.
NL neurons show a peculiar dendrite pattern. These bipolar neurons fall into the particular category of football shaped cells which have dendrites coming out the top and bottom of their cell body. The cell body (soma) of these neurons are about the same size, but depending on where they are in the NL, the cells have either short, medium or long dendrites.
The ones near the midline have a bunch of short stubby little dendrites.
 |
| Figure 2B from Smith and Rubel, 1979 |
If they are a little further out from the midline, they have longer dendrites.
 |
| Figure 3B from Smith and Rubel, 1979 |
 |
| Figure 10A Smith and Rubel 1979 |
 |
| From Figure6 Smith and Rubel 1979 |
What is the purpose of having stubby or extended dendrites like this? Well, even in 1979 when Smith and Rubel reconstructed these neurons, they knew that these neurons had a special answer to the "form and function" question.
The amazing thing about these neurons is that they are 'tuned' to respond maximally to specific frequencies (sound waves). And just like strings on an instrument, the cells with shorter dendrites respond to higher frequencies and the cells with longer dendrites respond to lower frequencies.
Why is this? Dendrites don't actually vibrate like strings, but there must be some reason for a cell with short dendrites to respond to higher frquencies and a cell with long dendrites to respond to low frequencies.
The answer lies in what the Nucleus Laminaris actually does. In the next post we'll venture into the wilds of computational neuroscience and explore the reason behind this strange connection between dendrite shape and cell function.
Smith DJ, & Rubel EW (1979). Organization and development of brain stem auditory nuclei of the chicken: dendritic gradients in nucleus laminaris. The Journal of comparative neurology, 186 (2), 213-39 PMID: 447882Norovirus Gastroenteritis: Incubation Period
-- Credit image to ‘IST’
The illness like nausea, vomiting and diarrhea that caused by noroviruses are usually referred to norovirus gastroenteritis. What actually is norovirus! You can find the answer about the definition of noroviruses in here!
The symptoms of the infection usually can be used to diagnose whether or not someone has this infection. Therefore, the doctor usually will give
Broken Heart Syndrome
Valentine’s Day is not always a candy coated day of love and romance. For many who've lost a loved one, suffered a break up or are on the brink of separation or divorce, this day is anything but sweet. Learning about Broken Heart Syndrome can help you heal from your love trauma and make it through emotional calendar events like this.Facts about Broken Heart Syndrome
•Profound emotional sadness doesn't just weigh heavy on your mind. It significantly impacts your body.
•The depths of being heart-broken lowers your immune system, increases blood pressure and heart rate and causes significant muscle weakness, just to name a few.
•Stress from heartbreak grief can flood the body with hormones, specifically Cortisol, which causes that heavy-achy-feeling you get in your chest area.
•The heartache that comes from lost love can increase the likelihood of a heart attack. In fact, a recent study showed that a person who has a tendency to be depressed and has recently suffered a love trauma was 5 times more likely to die than a person with depression alone or a heart condition alone.
•The actual medical term for this deeply emotional mind/body experience is called Stress Cardiomyopathy also known as Takotsubo Cardiomyopathy. The colloquial term: A broken heart.
•Women are ten times more likely to suffer from Broken Heart Syndrome than men.
Tips for preventing “Broken Heart Syndrome”
•Take control. Prepare yourself for the holiday crush that comes from television, radio, online and in print. Limit your exposure to such things if the overblown seasonal attention becomes too much.
•Take stock in knowing that you’re not alone in feeling lonely, letdown or unhappy during this time. Many are quietly suffering through just like you.
•Don't hold in your emotional pain. Studies show that expressing emotions greatly reduces the body's stress response.
•Don't put a time limit on your grief. And don't let others set one for you either. Your healing time for this love trauma is uniquely yours.
•Make sure you tend to your physical needs. Softness, warmth and touch can be healing. Feed your other senses too – music, scents, beauty - don’t forget to taste the world.
•Don't ignore chronic aches or pains. Check in with your physician to make sure that you’re medically fit.
•Make sure you eat well, choosing healthy foods to keep you nourished during difficult times.
•Keep a routine sleep schedule. If you require medication to help you with sleeping, or to regulate moods or for cardiac management, don't feel ashamed. You're going through a significantly stressful time.
•A broken heart leaves many people feeling stunned and stuck. Move. Get out of bed. Take a shower. Go for a walk. Feel the sun on your face.
•If you feel fragile, limit your exposure to emotionally driven holiday events. That doesn't mean you should avoid people completely. Decide what social connections will give you support, and which ones may be too taxing.
•Don't forget your spiritual side. Prayer, even meditation, has been shown to comfort a broken heart.
•Above all, remember: A broken heart doesn’t make you unlovable. At this moment in time, you are healing. But remind yourself to be open when love presents itself again.
References
Behrens, C.B . et. al. (2010). Major depression as a potential trigger for Takitsubo Cardiomyopathy. International Journal of Cardiology, 15;140(2):e40-2.
Bybee, K.A. & Prasaad, A. (2008). Stress related cardiomyopathy syndromes. Circulation: Journal of the American Heart Association, 118-397-409.
Norovirus Infections and Children (Symptoms and Treatment)
Norovirus can attack anyone, including children. So what you should know about norovirus infections in children? Here are pieces of helpful information for you. Read also about norovirus and pregnancy and incubation period of the infection!
These infections can give a significant impact for the health of the body. Even around more than half of food-borne diseases is caused by noroviruses –
Norovirus and Pregnancy: What You Should Know?
Norovirus infections and pregnancy? What you should clearly understand about them? If you search on internet, there are not too many researches published that discuss about this issue specifically, but one thing that you should know, about 50 percent of the gastroenteritis-cases may be caused by norovirus infection (gastroenteritis includes diarrhea, vomiting and abdominal pain). This suggests
LTP and LTD at the same time? Adventures in Functional Compartmentalization
On Monday we talked about LTP and LTD on a basic level, today we are discussing how they interact with each other. In a recent Open Access paper, Pavlowsky and Alarcon ask the question: Can some synapses on a neuron strengthen while at the same time others weaken? And if so, how do the two processes interact with each other?
First let's get some background. Synapse strengthening (LTP) and synapse weakening (LTD) both require new proteins to be synthesized at the soma* (*in this particular situation, sometimes they don't require it, but those details are too deep to dive into here). So what happens if LTP is induced at some synapses and LTD is induced at others on the same neuron? There are three possibilities:
To determine which of these possibilities actually happen in a neuron, Pavlowsky and Alarcon induce LTP and LTD on the same cells, but in different places.
They induced LTP in one spot (S2) and then induced LTD in another (S1). And lo and behold! the LTP happening first prevented the LTD (favoring the compete hypothesis above).
So this shows that LTP and LTD compete in the neuron. But what are they competing for?
There are two steps in protein synthesis where LTP and LTD might compete: translation (getting a protein from an mRNA) and transcription (creating more mRNA from the DNA).
To test whether translation or transcription is important for this competition, the researchers induced LTP at S2 in the presence of either a translation blocker (anisomycin) or a transcription blocker (actinomycin-D). Then they washed away the blocker and induced LTD at S2.
The translation blocker allowed for subsequent LTD at S1 (top left of figure), while the transcription blocker didn't (top right of figure), even though both prevented the initial LTP at S2 (bottom panels of figure). This is evidence that the translation phase of protein synthesis is important for determining which form of plasticity gets induced (LTP or LTD).
So what does all this mean? The results support the compete hypothesis, that the first plasticity induction (LTP or LTD) gets dibs on most of the plasticity-related protein synthesis machinery and prevents the other from happening. However, if the first induction can't access the protein translation machinery (because it is blocked with anisomycin), then the second induction is able to use it just as it normally would.
The authors do a thorough job investigating this phenomenon, testing different time intervals between LTP and LTD induction, testing location of the stimuli, and have some interesting discussion about what this might mean for learning and memory. If you are interested in the details, I highly recommend this paper, it's in PLoS One, so it is open access.
copyright TheCellularScale
Pavlowsky A, & Alarcon JM (2012). Interaction between Long-Term Potentiation and Depression in CA1 Synapses: Temporal Constrains, Functional Compartmentalization and Protein Synthesis. PloS one, 7 (1) PMID: 22272255
reade more...
 |
| neurons firing (source) |
First let's get some background. Synapse strengthening (LTP) and synapse weakening (LTD) both require new proteins to be synthesized at the soma* (*in this particular situation, sometimes they don't require it, but those details are too deep to dive into here). So what happens if LTP is induced at some synapses and LTD is induced at others on the same neuron? There are three possibilities:
- They compete for protein synthesis at the soma, one using up all the precious protein synthesis machinery and impairing the development of the other
- They cooperate, one starting up the protein synthesis engine at the soma so it's ready to go, helping the other.
- They don't interact and just do their own thing like normal.
To determine which of these possibilities actually happen in a neuron, Pavlowsky and Alarcon induce LTP and LTD on the same cells, but in different places.
 |
| Showing stimulation on the same side of the soma From Figure 2 Pavlowsky and Alarcon 2012 |
They induced LTP in one spot (S2) and then induced LTD in another (S1). And lo and behold! the LTP happening first prevented the LTD (favoring the compete hypothesis above).
So this shows that LTP and LTD compete in the neuron. But what are they competing for?
There are two steps in protein synthesis where LTP and LTD might compete: translation (getting a protein from an mRNA) and transcription (creating more mRNA from the DNA).
To test whether translation or transcription is important for this competition, the researchers induced LTP at S2 in the presence of either a translation blocker (anisomycin) or a transcription blocker (actinomycin-D). Then they washed away the blocker and induced LTD at S2.
 |
| From Figure 6 Pavlowsky and Alarcon 2012 |
The translation blocker allowed for subsequent LTD at S1 (top left of figure), while the transcription blocker didn't (top right of figure), even though both prevented the initial LTP at S2 (bottom panels of figure). This is evidence that the translation phase of protein synthesis is important for determining which form of plasticity gets induced (LTP or LTD).
So what does all this mean? The results support the compete hypothesis, that the first plasticity induction (LTP or LTD) gets dibs on most of the plasticity-related protein synthesis machinery and prevents the other from happening. However, if the first induction can't access the protein translation machinery (because it is blocked with anisomycin), then the second induction is able to use it just as it normally would.
The authors do a thorough job investigating this phenomenon, testing different time intervals between LTP and LTD induction, testing location of the stimuli, and have some interesting discussion about what this might mean for learning and memory. If you are interested in the details, I highly recommend this paper, it's in PLoS One, so it is open access.
copyright TheCellularScale
Pavlowsky A, & Alarcon JM (2012). Interaction between Long-Term Potentiation and Depression in CA1 Synapses: Temporal Constrains, Functional Compartmentalization and Protein Synthesis. PloS one, 7 (1) PMID: 22272255Weight Loss Ideas: 4 Bad Habits You Should Avoid!
You do your exercise regularly and properly, and you have a tight diet to control your fat intake but why you still not find a pleasant result of your weight loss program? There might be something wrong that you should find and resolve immediately!
You may also like to read how to lose weight in 2 weeks with simple secrets, before continuing!
And below are pieces of helpful information about
Hidden Causes of Fatigue in Women
Well, do you know that there are some hidden causes of fatigue in women? Fatigue may be a symptom of an illness, even a serious illness, which mostly caused by minor problems.
You do your routine exercise properly and you have adequate sleep (sleep well) but you feel easy to get tired, why? Even your fatigue may go on for more than seven days (a week) and you don’t know the clearly answer
5 Celebrities with Breast Cancer (Battled It)!
Below are some famous women or celebrities who diagnosed and battled breast cancer, which can be one of our inspirations for ‘breast cancer-fighting’! You may also like to read top myths of breast cancer, before continuing!
Christina Applegate
She was diagnosed with breast cancer at the age of 36 or in 2008. Well, it is unimaginable for most women when the only one choice is the thought
the synapse: where the magic happens
What is a synapse?
The synapse is the junction between two neurons, usually between an axon, which gives the signal, and a dendrite, which receives the signal.
They found that when you stimulated the nerve fibers with certain frequencies (100 Hz is now a commonly used frequency for this), the signal from the group of neurons grew, and stayed large for hours. (They tracked at least one experiment for 10 hours!)
The concept that activity patterns between cells could strengthen the connection between them fundamentally changed the way people thought about information processing in the brain. Now there is a huge branch of neuroscience devoted to connecting LTP and LTD to behavior and investigating the mechanisms which underlie synaptic plasticity.
In a retrospective paper, Lomo describes how the discovery came about. I found this quote particularly interesting:
Bliss TV, & Lomo T (1973). Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. The Journal of physiology, 232 (2), 331-56 PMID: 4727084
Lømo T (2003). The discovery of long-term potentiation. Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 358 (1432), 617-20 PMID: 12740104
reade more...
The synapse is the junction between two neurons, usually between an axon, which gives the signal, and a dendrite, which receives the signal.
This meeting of neurons is absolutely essential to how the brain works. It is where the information gets passed on from one neuron to the next.
The 'magic' at the synapse
When someone talks about neuronal pathways being strengthened, they usually mean a strengthening of this synaptic connection. This strengthening (or weakening) is referred to as "synaptic plasticity." Specifically, when the connection between two neurons is strengthened, it is often referred to as Long Term Potentiation (LTP) and when it is weakened it is is often called Long Term Depression (LTD). Synaptic plasticity is so exciting because it is a feasible biological mechanism for memory formation and storage.
How this 'magic' was discovered
The first paper to show that the connections between neurons could be strengthened was Bliss and Lomo 1973. They were studying the hippocampus, the region that underlies episodic memory and spatial learning.
 |
| Bliss and Lomo, 1973 Fig1a |
 |
| Bliss and Lomo, 1973 Fig4c |
In this figure, the dots represent the size of the signal at each point in time. The arrows represent the high frequency stimulation (here they stimulated 4 times). After each stimulation, the signal grows.
The black dots are the pathway that was stimulated and the open circles are an unstimulated pathway that they used as a control.
"Why did I not pursue and publish a fuller account of my findings in 1966? Because I was overcome by the complexity of the system and my lack of understanding of what was behind the findings. There was also no sense of urgency. Thus, when Tim and I published a full account in 1973 (Bliss & Lømo 1973), it still took years for the significance of the findings to be generally appreciated. "It's hard to imagine 'no rush' to publish something like this and it is refreshing to see a scientist who is hesitant about publishing something that s/he does not fully understand.
Bliss TV, & Lomo T (1973). Long-lasting potentiation of synaptic transmission in the dentate area of the anaesthetized rabbit following stimulation of the perforant path. The Journal of physiology, 232 (2), 331-56 PMID: 4727084Lømo T (2003). The discovery of long-term potentiation. Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 358 (1432), 617-20 PMID: 12740104February is Eating Disorder Awareness Month
Canada, The United Kingdom and The United States use the month of February to bring awareness to Eating Disorders.
Generally, eating disorders involve self-critical, negative thoughts and feelings about body weight and food, and eating habits that disrupts normal body function, and daily life activities.
What causes eating disorders is not entirely clear, though a combination of psychological, genetic, social and family factors are thought to contribute to the disorder.
Types of Eating Disorders
Anorexia Nervosa~ Essentially self-starvation, this disorder involves a refusal to maintain a minimally normal body weight. In severe cases, anorexia can be life-threatening
Bulimia Nervosa ~ This involves repeated episodes of binge eating, followed by ways of trying to purge the food from the body or prevent expected weight gain. People can have this condition and be of normal weight.
Binge-eating Disorder~ This is characterized by frequent episodes of overeating without purging.
Eating Disorders Not Otherwise Specified (EDNOS) ~ A range of other disordered eating patterns don’t fit into the other types of eating disorders. These eating patterns are still serious, and intervention and attention are necessary.
Generally, eating disorders involve self-critical, negative thoughts and feelings about body weight and food, and eating habits that disrupts normal body function, and daily life activities.
What causes eating disorders is not entirely clear, though a combination of psychological, genetic, social and family factors are thought to contribute to the disorder.
Types of Eating Disorders
Anorexia Nervosa~ Essentially self-starvation, this disorder involves a refusal to maintain a minimally normal body weight. In severe cases, anorexia can be life-threatening
Bulimia Nervosa ~ This involves repeated episodes of binge eating, followed by ways of trying to purge the food from the body or prevent expected weight gain. People can have this condition and be of normal weight.
Binge-eating Disorder~ This is characterized by frequent episodes of overeating without purging.
Eating Disorders Not Otherwise Specified (EDNOS) ~ A range of other disordered eating patterns don’t fit into the other types of eating disorders. These eating patterns are still serious, and intervention and attention are necessary.
Eating disorders can affect functioning in every system of the body, especially the heart and kidneys, and may cause lasting damage and even death. Because of the urgency of the risks associated with eating disorders, getting high-quality eating disorder treatment early on is the best way to combat the mental and physical consequences of these devastating mental illnesses.
Left unattended, eating disorders can lead to serious health problems or even death. For more information, go to the National Eating Disorders Association and to the International Association of Eating Disorders.