MEU MUITO OBRIGADA A TODOS...AMO CADA UM QUE PASSA POR AQUI!!!!

AGRADEÇO DE CORAÇÃO AS PESSOAS QUE PASSARAM PELO MEU BLOG. SEI QUE ESTÁ UM POUCO DIFÍCIL PARA MIM VISITAR A TODOS. NESTA SEMANA QUE PASSOU NÃO TIVE TEMPO PARA NADA.
MUITO TRABALHO, REUNIÃO E ENCONTRO PEDAGÓGICO EM FLORIPA. TEMA" DISLEXIA - AO PÉ DA LETRA- VALEU MUITO A PENA TER IDO. MAS CHEGUEI A MEIA NOITE E SAI AS TRÊS DA MANHA DE CASA.
ALÉM DO CURSO ONTEM A TARDE. POR ISSO NÃO PUDE VISITAR NINGUÉM. MAS ASSIM QUE PUDER DURANTE A SEMANA IREI TE VISITAR. ADORO VOCÊ . ENQUANTO ISSO DEIXO MEUS BLOGS PARA A VOCÊ VISITAR.

AGRADEÇO O PRESENTE DO TOQUE DE AMOR ..

UM LINDO PRESENTE RECEBIDO..

OBRIGADA MINHA CHARA.

TEM UM GRANDE ABRAÇO PARA VOCÊ!!!
MEUS MIMOS
RECEBIDOS/OFERECIDOS.

SINAL DE LIBERDADE

This Is Your Brain's Anti-Drug

What's your anti-drug? Well, it might well be hemopressin. At least, that's probably your anti-marijuana.

Hemopressin is a small protein that was discovered in the brains of rodents in 2003: its name comes from the fact that it's a breakdown product of hemoglobin and that it can lower blood pressure.

No-one seems to have looked to see whether hemopressin is found in humans, yet, but it seems very likely. Almost everything that's in your brain is in a mouse's brain, and vice versa.

Pharmacologically, hemopressin's literally an anti-marijuana molecule: it's an inverse agonist at CB1 receptors, which are the ones targeted by the psychoactive compounds in marijuana, and also by the neurotransmitters known as endocannabinoids. Cannabinoids turn CB1 receptors on, hemopressin turns them off.

Artificial CB1 blockers were developed as weight loss drugs, and one of them, rimonabant, made it onto the market - but it was banned after it turned out that it caused depression and anxiety in many people.

So hemopressin is Nature's rimonabant: in which case, it ought to do what rimonabant does, which is to reduce appetite. And indeed a Journal of Neuroscience paper just out from Godd et al shows that it does just that, in rats and mice: injections of hemopressin reduced feeding.

Interestingly, this worked even when it was injected by the standard route under the skin - many proteins can't enter the brain if they're given this way, because they can't cross the blood-brain barrier, meaning that they have to be injected directly into the brain, which makes researching them much harder. So hemopressin, with any luck, will be pretty easy to study. Any volunteers for the first human trial...?

Dodd, G., Mancini, G., Lutz, B., & Luckman, S. (2010). The Peptide Hemopressin Acts through CB1 Cannabinoid Receptors to Reduce Food Intake in Rats and Mice Journal of Neuroscience, 30 (21), 7369-7376 DOI: 10.1523/JNEUROSCI.5455-09.2010

This Is Your Brain's Anti-Drug

What's your anti-drug? Well, it might well be hemopressin. At least, that's probably your anti-marijuana.

Hemopressin is a small protein that was discovered in the brains of rodents in 2003: its name comes from the fact that it's a breakdown product of hemoglobin and that it can lower blood pressure.

No-one seems to have looked to see whether hemopressin is found in humans, yet, but it seems very likely. Almost everything that's in your brain is in a mouse's brain, and vice versa.

Pharmacologically, hemopressin's literally an anti-marijuana molecule: it's an inverse agonist at CB1 receptors, which are the ones targeted by the psychoactive compounds in marijuana, and also by the neurotransmitters known as endocannabinoids. Cannabinoids turn CB1 receptors on, hemopressin turns them off.

Artificial CB1 blockers were developed as weight loss drugs, and one of them, rimonabant, made it onto the market - but it was banned after it turned out that it caused depression and anxiety in many people.

So hemopressin is Nature's rimonabant: in which case, it ought to do what rimonabant does, which is to reduce appetite. And indeed a Journal of Neuroscience paper just out from Godd et al shows that it does just that, in rats and mice: injections of hemopressin reduced feeding.

Interestingly, this worked even when it was injected by the standard route under the skin - many proteins can't enter the brain if they're given this way, because they can't cross the blood-brain barrier, meaning that they have to be injected directly into the brain, which makes researching them much harder. So hemopressin, with any luck, will be pretty easy to study. Any volunteers for the first human trial...?

Dodd, G., Mancini, G., Lutz, B., & Luckman, S. (2010). The Peptide Hemopressin Acts through CB1 Cannabinoid Receptors to Reduce Food Intake in Rats and Mice Journal of Neuroscience, 30 (21), 7369-7376 DOI: 10.1523/JNEUROSCI.5455-09.2010

Do Genes Remember?

Almost all neuroscientists believe that memories are stored in the connections between neurons: synapses. Learning, then, consists of the strengthening of some synapses, the weakening of others, and maybe even the formation of entirely new ones. But a paper from Catherine Miller and colleagues suggests that changes to DNA are also involved: Cortical DNA methylation maintains remote memory.


DNA is a series of bases, and fundamentally there are just four: C, A, T and G. However, the Cs and the As can be methylated, i.e. modified by the addition of a very simple methyl chemical group. They then stay that way until they get demethylated in the reverse process. Methylating a gene generally reduces its expression.

It's a bit like writing notes in pencil on top of a printed document: it doesn't change the underlying genetic sequence, but it's a semi-permanent change and it can be inherited by dividing cells. Methylation is a classic example of an epigenetic change, and epigenetics is very hot right now.Miller et al found that learning induces the methylation of a gene called calcineurin (CaN) in the cells of the frontal cortex of rats. These changes appeared within 1 day of the learning event, and they persisted for at least 30 days (the longest time studied - they could well last much longer). Methylation of another gene, reelin, was also increased, but only for a few hours.

When they blocked these changes by injecting a DNA methylation inhibitor into the frontal cortex, it caused amnesia - even if the drug was given 30 days after the learning had taken place. In other words, the methylation inhibitors somehow erased the memory traces. These authors have previously reported that the same kind of learning causes a short-lived increase in methylation in the hippocampus. Taken together with these data, this fits with the well-known theory that memory traces start off being stored in the hippocampus and are then somehow transferred to the cortex later.

This kind of research has a bit of a history. The idea that memories are stored in DNA has led some to theorize that memories can be inherited. It also reminds me of the work of psychologist and Unabomber-victim James McConnell, who claimed that planarian worms can learn information by eating the ground-up remains of other worms who knew something...

These data are very interesting, but they don't imply anything quite so exciting. The pattern of methylation seemed entirely random (except in the sense that it was targeted at certain genes) - so rather than encoding information per se, the DNA changes were acting as a way of reducing CaN gene expression. Most likely, the reduction in CaN was limited to certain cells, and these were the cells that formed the connections that encoded the information.

Miller, C., Gavin, C., White, J., Parrish, R., Honasoge, A., Yancey, C., Rivera, I., Rubio, M., Rumbaugh, G., & Sweatt, J. (2010). Cortical DNA methylation maintains remote memory Nature Neuroscience, 13 (6), 664-666 DOI: 10.1038/nn.2560

Do Genes Remember?

Almost all neuroscientists believe that memories are stored in the connections between neurons: synapses. Learning, then, consists of the strengthening of some synapses, the weakening of others, and maybe even the formation of entirely new ones. But a paper from Catherine Miller and colleagues suggests that changes to DNA are also involved: Cortical DNA methylation maintains remote memory.


DNA is a series of bases, and fundamentally there are just four: C, A, T and G. However, the Cs and the As can be methylated, i.e. modified by the addition of a very simple methyl chemical group. They then stay that way until they get demethylated in the reverse process. Methylating a gene generally reduces its expression.

It's a bit like writing notes in pencil on top of a printed document: it doesn't change the underlying genetic sequence, but it's a semi-permanent change and it can be inherited by dividing cells. Methylation is a classic example of an epigenetic change, and epigenetics is very hot right now.Miller et al found that learning induces the methylation of a gene called calcineurin (CaN) in the cells of the frontal cortex of rats. These changes appeared within 1 day of the learning event, and they persisted for at least 30 days (the longest time studied - they could well last much longer). Methylation of another gene, reelin, was also increased, but only for a few hours.

When they blocked these changes by injecting a DNA methylation inhibitor into the frontal cortex, it caused amnesia - even if the drug was given 30 days after the learning had taken place. In other words, the methylation inhibitors somehow erased the memory traces. These authors have previously reported that the same kind of learning causes a short-lived increase in methylation in the hippocampus. Taken together with these data, this fits with the well-known theory that memory traces start off being stored in the hippocampus and are then somehow transferred to the cortex later.

This kind of research has a bit of a history. The idea that memories are stored in DNA has led some to theorize that memories can be inherited. It also reminds me of the work of psychologist and Unabomber-victim James McConnell, who claimed that planarian worms can learn information by eating the ground-up remains of other worms who knew something...

These data are very interesting, but they don't imply anything quite so exciting. The pattern of methylation seemed entirely random (except in the sense that it was targeted at certain genes) - so rather than encoding information per se, the DNA changes were acting as a way of reducing CaN gene expression. Most likely, the reduction in CaN was limited to certain cells, and these were the cells that formed the connections that encoded the information.

Miller, C., Gavin, C., White, J., Parrish, R., Honasoge, A., Yancey, C., Rivera, I., Rubio, M., Rumbaugh, G., & Sweatt, J. (2010). Cortical DNA methylation maintains remote memory Nature Neuroscience, 13 (6), 664-666 DOI: 10.1038/nn.2560

Much Love Illy Giveaway

I really do like everything in Much Love Illy. It's a really pretty shop. Everything is so colorful! Cakies is giving away 3 things from Much Love Illy! I hope I win this giveaway! You can enter the giveaway here. :) C

Brown Hair Blonde Highlights.

back ...

long without appear by this, my little place, right?

Thanks to all who cared for me to think if I had suddenly swallowed by the earth and they contacted me through facebook, MJE a mail or text. As I always say, it's amazing the things that got in my life from the creation of this blog dedicated to my son. I gained great friends, who are madrasas and incredible human beings and those who appreciate their friendship forever, because they are each of you help me to continue, make me feel I'm not alone and I can have my moments too loneliness, times when your baby is also present through a word or a hug container in the distance.
And so, those moments invaded my life.
Sometimes it's good step back to gain new energy.
As I said in my previous post, I always try to be positive and see the glass half full rather than half empty, but it is impossible to get up in the morning. But if one wants to maintain this position of "Wonder Woman" at all times and be positive and face life, it is often difficult and everything costs more.
is a long road I've traveled with my son and it is even longer that I have to go. And he needs me whole I need ya, now and not when the anguish finally decides to let me breathe.
few days ago were met two years the date when they received their diagnosis.
was something that I already sensed, because when I started to notice some strange things in his behavior poured my doubts in the Internet browser and all the books and took me to a single destination to a single word: AUTISM.
What words harder and harder to afford. But we did, we swallow that knot so great that we formed in the throat and heart and decided (as the day we look at the three for the first time), go ahead, to struggle together, to do battle with this ghost horible came to scare us. In part he did, of course we were scared!, But instead decided to run face. And we do so every day that cuddles and kisses from our son up every morning.
We spend a lot, too, and I know that's not all, it does not end here, there is still more.
estimate that the thought of all this I again felt this knot in my heart, that desire to mourn contained (because I hate mourn), but I understood that often does, to be able to download, dry your tears and go back to life . I understood that it is okay to do, which is part of the fight, and that those tears are part of the road.
We do many things along these two years, and I thank God and my mom (who is that illuminates the steps from above) for each of them.
is also very encouraging to look back and be able to see far beyond what was our starting point and see today and the giant steps we took, steps that cost much, much effort, much anguish, but also much hope and faith that at some point and rhythm Valen was going to achieve: your connection, her smile, her first words, first sentences, the representative game, the pleasure of playing with other kids his age, full of love links who managed to establish with each of his therapists and people in the garden, boobs, dires, and inclusive teachers (Leti in 2008 and 2009 and now Lucia).
View photos of those years where no left smiling, always with his sightless eyes, as looking beyond us, locked in his bubble, not allowing entry.
and see how little, over the passing time, we arrived at the photos in which her smile and mischievous eyes are the main protagonists.
look back and remember that before did not call us "Mom" or "dada" or trying to communicate with us, as if we needed it. And to the day when we hear these beautiful words left his mouth. Simple words and perhaps for other dads are a normal part of their growth and maturity children, but for us to hear and witness to all who came after them, was like a miracle itself.
Remember back when we gave him a pencil to draw, he made them roll on the floor, or pulling the table over and over again, and reach the day when we saw him draw a line for the first time. Getting to this day that draws beautiful dolls, the slides of the square and its garden patio. Power
admire your great capacity for learning and memory and with great enthusiasm to see how he learned to write each letter of the alphabet, whole words and even numbers. How he learned to play complex games such as dominoes, memotest, bingo and lottery we can realize how fast you learn things. Surely this ability was always there, but we could not realize it, because it would not let us get to where he was hiding. Remember
distressed think we would achieve certain things as normal in the growth of any child and get to the day he finally quit diapers, her beloved pacifier, his cup with a spout, the day he managed to brush one's teeth ... things that cost much more than usual (especially diapers, lol!), but already got them and fills us with great pride. Remember
his first months in the Garden, in which we wept, wandered from one side to another room nonsense, did not approach the other kids, it was impossible to keep him in his chair doing some work like painting or play dough, because beyond his lack of concentration and hyperactivity prevented it, it was disgusting and made tremendous fit dirty if this happened, and get after it already has its handful of belonging to some of the boys who enjoy playing with them, that look, that the name, to have my hands full of odd jobs folders made with their own hands , seeing him so happy every morning eager to get to your garden. Recalling
and seeing the small steps we see that he was giving it all worth it. Her smile, her love, her kisses and hugs make it all worthwhile.
Always with a smile to your lips, always happy. Although many times what I get out of his blessed nap to go to some therapy, he always stands in a good mood, and knowing that Rachel, his neurolinguist, Agus, his psychology of TCC, Leo, his occupational therapist, Flavia, her music therapist are there to help you succeed.
My son is a fighter, a brave man. As you once told me a mommy friend, not we who have to perform well in therapy to make every minute of them may be, are they.

I'm back, ready to continue sharing experiences, joys, feelings of every kind and color, because that is covered this way we travel, no?.
I have many things to tell, many pictures that go up and many blogs to visit, lol!. Little by little I will be putting a day ...

School is Almost Over

Tomorrow is my last day of school. I'm a little bit sad. I'm going to miss seeing all my friends every day. And being in school. I like to learn. But this summer is going to be fun. I'm going to go spend some time with my Nono. He lives in FL. And we already planned our trip. We're going to Disney and to the beach. :)

But I get to leave for NC on Thursday. My Dad has been working there. And I'm excited to get to see him again! My abuelitas are going to stay home. Because we're only going to be gone until Tuesday. I'm excited to see my Nana too! And we might get to go see my friend Sarita. She is in the hospital. :) C

Rhino Shield Paint Customer Complaints

Feliz cumpleaños Mere

Merengada, Mere for friends, turns ten great years.
Our protagonist is a dog released, famous diva. His adventures far and wide in this world, along with his brother Lince, have become so famous that great painters have sought to immortalize in his canvases.
currently Mere naked dog is more valued. Is displayed, with their natural size, or to be habitually in the main art galleries in the world.

If you want to know the adventures that stars in this funny and crazy Merengue visit her flog Mere and Lince. Recommended!

Photo Taken at the International Gallery of Art Royal Canin, just before the inauguration.

On this note of humor so the friend Mere, Brennan, his human mom and Wildcat, his companion dog, a:

HAPPY HAPPY BIRTHDAY !

Do My Symptoms Suggest

Rita Gachi cumpleañera

congratulate for the second year our little friend Rita birthday today thirteenth.

Rita was not born on May 25, that date coincides with the date of its adoption and rescue of an abandoned gas station. The year was 1997 and should have two months old. Since then, Rita shares her life with a large family of cats and dogs Gachimascoteros known.

To learn more about Rita and family, we let you link to your flog: Gachiimascotera .

Congratulations on your 13th birthday Rita !

CURIOSA- DUPLAMENTE FELIZ!!!!!

CURIOSA COMEMORA 65 MIL VISITAS E TAMBÉM 400 SEGUIDORES.. MUITO OBRIGADA PELO SEU CARINHO,
PELA SUA AMIZADE.
ESTOU MUITO FELIZ.
ESTE PRESENTE É PARA VOCÊ TAMBÉM...

AGRADEÇO EM ESPECIAL AO MAURO DO BLOG http://koisasecoisas.blogspot.com/



MEU SEGUIDOR DE Nº 400.

Where Can I Get Money Off The Biolife Card

Candy Bambi cumple dos años de adopcion

Candy, our amigata, today celebrates its second anniversary of the adoption by the Herd Bambi, her cat family.

When Candy had about three months , Cris
his human, found abandoned on the street, was injured and had a broken leg. Spent two weeks hospitalized, had surgery on the leg so he could walk and went ahead thanks to the care he received: " because -Cris tells mom in her family flog , Candy was strong and fought .

Although his leg was stiff and develops Candy walks normally, is happy with his human and feline family and shows signs of having a strong character, possessive, and he knows to be noticed.

Photos: Cris, Bambi Herd



! amigata Congratulations!

fMRI In 1000 Words

I thought I'd write a short and simple intro to how fMRI works. Most such explanations start with the physics of Magnetic Resonance Imaging and eventually explain how it lets you look at brain activity. I'm doing it the other way round, because I like brains more than physics.

So - everyone knows that fMRI is a way of measuring neural activation. But what does it mean for a neuron to be active? All brain cells are "active": they're alive, firing electrical action potentials, and sending out neurotransmitters to other cells at synapses. If a certain cell gets more activated, that means that it's firing action potentials faster, or sending out more chemical signals. It's mostly synaptic activity which fMRI picks up.


How do you measure neural activation? You can do it directly by sticking in an electrode to measure action potentials, or use a glass tube to measure neurotransmitter levels. You can put electrodes on the scalp to pick up the electrical fields created by lots of neurons firing. But fMRI relies on an indirect approach: when a brain cell is firing hard, it uses more energy than when it's not.

Cells make energy from sugar and oxygen; oxygen is transported in the blood. So when a given cell is working hard, it uses more oxygen, and the oxygen content of nearby blood falls. Synaptic activity, in particular, uses loads of oxygen. So you might expect that highly active parts of the brain would have less oxygen. Counter-intuitively, they actually show an increase in blood oxygen, which is probably a kind of "overcompensation" for the activity (although there may be an "initial dip" in oxygen, it's very brief.)

So blood oxygen is a proxy for activation. How do you measure it? Oxygen in blood binds to haemoglobin, a protein that contains iron (which is why blood is red, like rust, and tastes metallic...like iron). By a nice coincidence, haemoglobin with oxygen is red; haemoglobin without oxygen is blueish or purple. This is why your veins, containing deoxygenated blood, are blue and why you turn blue if you're suffocating.

You could measure neural activity by literally looking to see how red the brain is. This is actually possible, but obviously it's a bit impractical. Luckily, as well as being blue, deoxygenated haemoglobin acts as a magnet. So blood is magnetic, and the strength of its magnetic field depends on how oxygenated it is. That's really useful, but how do you measure those magnetic fields?

Using an extremely strong magnet - like the liquid-helium-cooled superconducting coil at the heart of every MRI scanner, for example - you can make some of the protons in the body align in a special way. If you then fire some radio waves at these aligned protons, they can absorb them ("resonate"). As soon as you stop the radio waves, they'll release them back at you, like an echo - which is why the most common form of fMRI scan is called Echo-Planar Imaging (EPI). All matter contains protons; in the human body, most of them are found in water.

Each proton only responds to a specific frequency of radio waves. This frequency is determined by the strength of the magnetic field in which it sits - stronger fields, higher frequencies. Crucially, the magnetic fields surrounding deoxygenated blood therefore shift the radio frequency at which nearby protons respond. Suppose a certain bit of the brain resonates at frequency X. If some deoxygenated blood appears nearby, it will stop them from responding to that frequency - by making them respond to a different one.

fMRI is essentially a way of measuring the degree to which protons in each part of the brain don't respond at the "expected" resonant frequency X, due to interference from nearby deoxygenated haemoglobin. But how do you know what resonant frequency to expect? This is the clever bit: simply by varying the magnetic field across different parts of the brain.

Say you make the magnetic field at the left side of the head slightly stronger than the one at the right - a magnetic gradient. The resonant frequency will therefore vary across the head: the further left, the higher the frequency. This is what the "gradient coils" in an MRI machine do.

Gradient coils therefore translate spatial location into magnetic field strength. And as we know, magnetic field strength = resonant frequency. So spatial location = magnetic field strength = resonant frequency. All you then need to do is to hit the brain with a burst of radio waves of all different frequencies - a kind of white noise called the "RF Pulse" - and record the waves you get back.

The strength of the radio waves at a given frequency therefore corresponds to the amount of protons in the appropriate place - so you can work out the density of matter in the brain based on the frequencies you get. Also, different kinds of tissues in the body respond differently to excitation; bone responds differently to brain grey matter, for example. So you can build up an image of brain structure by using magnetic gradients.


Of course you can't scan the whole brain at once: you scan it in slices, divided up into roughly cubic units called voxels. Typically in fMRI these are 3x3x3 mm or so, but they can be much smaller for specialized applications. The smaller the voxels, the longer the scan takes because it requires more gradient shifting. The loud noises that occur during MRI scans are caused by the gradient coils changing the gradients extremely quickly in order to scan the whole brain. Modern scanners typically image the whole brain once every 3 seconds, but you can go even faster.

As we've seen, deoxygenated blood degrades the image nearby, in what's called the Blood Oxygenation Level Dependent (BOLD) response. Neural activation increases oxygen and literally makes the brain light up; you could, in theory, see the changes with the naked eye. In fact, they're tiny, and there is always a lot of background noise as well, so you need statistical analysis to determine which parts light up, and then map this onto the brain as colored blobs. But that's another story...

fMRI In 1000 Words

I thought I'd write a short and simple intro to how fMRI works. Most such explanations start with the physics of Magnetic Resonance Imaging and eventually explain how it lets you look at brain activity. I'm doing it the other way round, because I like brains more than physics.

So - everyone knows that fMRI is a way of measuring neural activation. But what does it mean for a neuron to be active? All brain cells are "active": they're alive, firing electrical action potentials, and sending out neurotransmitters to other cells at synapses. If a certain cell gets more activated, that means that it's firing action potentials faster, or sending out more chemical signals. It's mostly synaptic activity which fMRI picks up.


How do you measure neural activation? You can do it directly by sticking in an electrode to measure action potentials, or use a glass tube to measure neurotransmitter levels. You can put electrodes on the scalp to pick up the electrical fields created by lots of neurons firing. But fMRI relies on an indirect approach: when a brain cell is firing hard, it uses more energy than when it's not.

Cells make energy from sugar and oxygen; oxygen is transported in the blood. So when a given cell is working hard, it uses more oxygen, and the oxygen content of nearby blood falls. Synaptic activity, in particular, uses loads of oxygen. So you might expect that highly active parts of the brain would have less oxygen. Counter-intuitively, they actually show an increase in blood oxygen, which is probably a kind of "overcompensation" for the activity (although there may be an "initial dip" in oxygen, it's very brief.)

So blood oxygen is a proxy for activation. How do you measure it? Oxygen in blood binds to haemoglobin, a protein that contains iron (which is why blood is red, like rust, and tastes metallic...like iron). By a nice coincidence, haemoglobin with oxygen is red; haemoglobin without oxygen is blueish or purple. This is why your veins, containing deoxygenated blood, are blue and why you turn blue if you're suffocating.

You could measure neural activity by literally looking to see how red the brain is. This is actually possible, but obviously it's a bit impractical. Luckily, as well as being blue, deoxygenated haemoglobin acts as a magnet. So blood is magnetic, and the strength of its magnetic field depends on how oxygenated it is. That's really useful, but how do you measure those magnetic fields?

Using an extremely strong magnet - like the liquid-helium-cooled superconducting coil at the heart of every MRI scanner, for example - you can make some of the protons in the body align in a special way. If you then fire some radio waves at these aligned protons, they can absorb them ("resonate"). As soon as you stop the radio waves, they'll release them back at you, like an echo - which is why the most common form of fMRI scan is called Echo-Planar Imaging (EPI). All matter contains protons; in the human body, most of them are found in water.

Each proton only responds to a specific frequency of radio waves. This frequency is determined by the strength of the magnetic field in which it sits - stronger fields, higher frequencies. Crucially, the magnetic fields surrounding deoxygenated blood therefore shift the radio frequency at which nearby protons respond. Suppose a certain bit of the brain resonates at frequency X. If some deoxygenated blood appears nearby, it will stop them from responding to that frequency - by making them respond to a different one.

fMRI is essentially a way of measuring the degree to which protons in each part of the brain don't respond at the "expected" resonant frequency X, due to interference from nearby deoxygenated haemoglobin. But how do you know what resonant frequency to expect? This is the clever bit: simply by varying the magnetic field across different parts of the brain.

Say you make the magnetic field at the left side of the head slightly stronger than the one at the right - a magnetic gradient. The resonant frequency will therefore vary across the head: the further left, the higher the frequency. This is what the "gradient coils" in an MRI machine do.

Gradient coils therefore translate spatial location into magnetic field strength. And as we know, magnetic field strength = resonant frequency. So spatial location = magnetic field strength = resonant frequency. All you then need to do is to hit the brain with a burst of radio waves of all different frequencies - a kind of white noise called the "RF Pulse" - and record the waves you get back.

The strength of the radio waves at a given frequency therefore corresponds to the amount of protons in the appropriate place - so you can work out the density of matter in the brain based on the frequencies you get. Also, different kinds of tissues in the body respond differently to excitation; bone responds differently to brain grey matter, for example. So you can build up an image of brain structure by using magnetic gradients.


Of course you can't scan the whole brain at once: you scan it in slices, divided up into roughly cubic units called voxels. Typically in fMRI these are 3x3x3 mm or so, but they can be much smaller for specialized applications. The smaller the voxels, the longer the scan takes because it requires more gradient shifting. The loud noises that occur during MRI scans are caused by the gradient coils changing the gradients extremely quickly in order to scan the whole brain. Modern scanners typically image the whole brain once every 3 seconds, but you can go even faster.

As we've seen, deoxygenated blood degrades the image nearby, in what's called the Blood Oxygenation Level Dependent (BOLD) response. Neural activation increases oxygen and literally makes the brain light up; you could, in theory, see the changes with the naked eye. In fact, they're tiny, and there is always a lot of background noise as well, so you need statistical analysis to determine which parts light up, and then map this onto the brain as colored blobs. But that's another story...

Giveaway Winner!

My winner is #60, Sally. Congratulations! If you can send me your address information I can send you your bows tomorrow. Thank you to everyone who entered! I had so much fun doing this giveaway. I can't wait to do another giveaway on my blog. :) C

How Much Cement For Half A Basketball Court

Feliz cumpleaños Pogo

This Rubiales called Pogo, is celebrating its first birthday. He is from La Plata , Buenos Aires, Argentina and belongs to a large cat family known for Herd

STARS

Simba. Chiquito. Linda. Pinino. Angel Manchita, Saby Porotita, Ruby, Light and Chuck are the gatohermanos of Pogo. You can know the whole pack in your family flog Penelope 8.

WISH YOUR FAMILY AND POGO

feline and human

A GREAT DAY

UM OLHAR NO HORIZONTE...

A VIDA É UM OLHAR DIFERENTE PARA O HORIZONTE.
É VIVER IMENSAMENTE.
É SABER CONVIVER NA SUA PLENITUDE.
A VIDA É VIVER CADA MOMENTO..SIMPLESMENTE VIVER.

É OLHAR NO HORIZONTE E ENCONTRAR A BELEZA DA VIDA LOGO ALI, BEM PERTINHO DE NÓS.
MUITO OBRIGADA POR VOCÊ EXISTIR NA MINHA VIDA.
CARINHOSAMENTE.
EU ESTOU INDO TE VISITAR..NESTE HORIZONTE UNIVERSAL. ONDE AS FRONTEIRAS NÃO TEM LIMITES. SÓ DESAFIOS...
AQUI NOS ENCONTRAMOS E COMPARTILHAMOS.

VENHA CONHECER E INTERAGIR COM ELES.

VENHA CONHECER O MUSEU DE JARAGUÁ DO SUL....


TEM UM GRANDE ABRAÇO E UM SELO MUITO ESPECIAL PARA VOCÊ!!! VOU TE ESPERAR....
MEUS MIMOS
RECEBIDOS/OFERECIDOS.

SINAL DE LIBERDADE

OBRIGADA MARCIA PELO CARINHO..
AMEI O PRESENTE.
REPASSO ESTE CARINHO A TODAS AS MULHERES ESPECIAIS QUE PASSAM POR AQUI.


PARA MEU QUERIDO AMIGOS MASCULINHOS O MEU ABRAÇO...
PEGUE SEU ABRAÇO E MEUS MIMOS..

BOM DIA...FELIZ FINAL DE SEMANA!!

ATRAVÉS DESTA IMAGEM QUERO DEMONSTRAR O MEU CARINHO A TODOS VOCÊS E DIZER QUE ESTOU VISITANDO A TODOS. AGRADEÇO IMENSAMENTE OS NOVOS AMIGOS(AS), QUE AQUI ESTÃO CHEGANDO E DIZER QUE SOU MUITO FELIZ COMA SUA COMPANHIA.

VENHA CONHECER E INTERAGIR COM ELES.

UMA LIÇÃO MUITO ESPECIAL..VEJA...


TEM UM GRANDE ABRAÇO PARA VOCÊ!!!
MEUS MIMOS
RECEBIDOS/OFERECIDOS.

SINAL DE LIBERDADE

Peonies

Aren't these pretty? They're peonies. When my Dad and I went shopping for our plants for the garden, I asked him for these flowers. They only came in bulbs. We bought 2 packs. And I planted them. That was in March.

I went to go check on our plants after school today. The peonies are green, with lots of leaves. They're bigger than last week. But there are still no flowers. I'm excited to see them bloom. But I know it takes a long time for them to grow. I'm just glad that we planted them! :) C

OLA MEU AMIGOS FOFOS. AGRADEÇO O SEU AFETO.

ANTES DE POSTAR QUERO AGRADECER A TODOS PELAS VISITAS. MUITO OBRIGADA.
SEI QUE MUITOS RECADINHOS ESTÃO NA POSTAGEM ANTERIOR. MAS LOGO IREI RETRIBUIR. MUITO OBRIGADA PELO SEU CARINHO.

ESTAMOS AI PARTICIPANDO...CONTO COM O SEU VOTO!!!
MUITO OBRIGADA PELO SEU CARINHO...

A CURIOSA, está participando da enquete

realizada pela Lidia Ferreira

do blog - http://simplythebest01.blogspot.com

cuja finalidade é:

divulgar, homenagear e motivar os blogs a uma maior interação

A CURIOSA está classificado na Categoria - Variedades

A Enquete, teve inicio no dia 13/0 5/2010

e será encerrada no dia 22/05/2010

Conto, com o voto de vocês.

DE AMIGOS.

VENHA INTERAGIR COM
ESTE BLOG.

CONTO COM SEU VOTO AINDA NO TOPBLOG. CURIOSA E INTERAÇÃO ESTÃO INDICADOS.
CARINHOSAMENTE, EU AGRADEÇO O SEU VOTO E A SUA VISITA.
UM FORTE ABRAÇO A TODOS. SANDRA

My Dad is Working

My Dad left today. He went to work on some gigs with my Nana. I already miss him. But I'm glad I got to stay with my abuelitas. It's fun that they both live with us. I think that we are going to have a lot of fun together!

We only have a week of school left. Then I'm going to fly to meet my Dad and my Nana. This is going to be a lot of fun! We're going to a race while I'm there. And my Dad said we might get to stop and visit Sarita on our way home. :) C

How to Be A PubMed Historian

Quite a lot of people seem to like those graphs I sometimes make showing the number of papers published about a certain topic in any given year, based on the number of PubMed hits.

But how do I do it? Surely I don't sit there manually searching PubMed for each term, for each year, right? That would mean dozens, maybe hundreds, of manual searches. Well, unfortunately, that is exactly how I've done it in the past. I really am that cool, see.


Actually it doesn't take very long once you get into the swing of it, but I've now worked out a better way. See below for a bash script which repeatedly searches PubMed for a given sequence of years, downloads the first page of the results, picks out the bit where it tells you how many hits you got, and puts it all into a single output text file ready to be pasted into Excel or whatever. This comes with no guarantees whatsoever, but it seems to work. Enjoy...

Edit 29/06/2010: Vastly improved version that searches for multiple different terms sequentially, accepts terms that include spaces, and outputs the data into a sensible format. The search term text file should be a plain text file containing one search term per line. e.g:

serotonin depression
dopamine depression
GABA depression

Would search for each of those terms and output the data for each year into a single text file - with three data columns in this case - good for comparing the relative popularity of many different terms across time.

---
#! /bin/bash
# 29 . 06 . 2010
#PubMedHistory script by Neuroskeptic http://neuroskeptic.blogspot.com
# script to find out how many PubMed hits for a certain string in a given year range.

# usage: script (search term text file) (start year) (end year) (output file)
# e.g script list_of_terms.txt 2000 2005 dope.txt
#first, print the HEADER line of the output file.

printf "YEAR\t" > $4
cat $1 | while read subject
do
#pre-format the subject to remove spaces
ffa=${subject/' '/%20}
echo -n "$ffa" >> $4
printf "\t" >> $4
done
#and a newline
printf "\n" >> $4

#Now the real thing. The main loop is a YEAR loop:

for (( yearz=$2; yearz<=$3; yearz++ )) do #For each year, create a temporary file t.txt containing the output for this line.
#First, the year, then a tab.

printf "$yearz\t" > t.txt

#now, a second loop to go through the list of searches
cat $1 | while read subject
do
one=${subject/' '/%20}
wget -O $yearz.txt http://www.ncbi.nlm.nih.gov/sites/entrez?term="$one"+"$yearz"'[Publication Date]'

#find the line in the output with what we're interested in
output=`cat $yearz.txt | grep ncbi_resultcount | awk '{print}'`
#now, change it to get rid of the bit containing the search term
#as this will screw up the next step if it contains spaces!
output=${output/content*publication/LOL}
#print to a temp file
echo $output > temp$one$2$3$4.txt
#find the bit we want using awk
output=`awk '{ print $22 }' temp$one$2$3$4.txt`
rm temp$one$2$3$4.txt
rm $yearz.txt
#trim output
trimmedout=${output#content\=\"}
trimmedoutB=${trimmedout%\"}
#replace "false" with 0 because that's what "false" means
trimmedoutC=${trimmedoutB/'false'/0}
echo in year $yearz , I got $trimmedoutC. Saving to temp file t.txt
#write the result, and a tab, to the TEMPORARY output file
printf "$trimmedoutC\t" >> t.txt
done
#Now we've done all the search terms for this YEAR, so send the temporary data to the final file
cat t.txt >> $4
#and give it a newline
printf "\n" >> $4
done
rm t.txt

How to Be A PubMed Historian

Quite a lot of people seem to like those graphs I sometimes make showing the number of papers published about a certain topic in any given year, based on the number of PubMed hits.

But how do I do it? Surely I don't sit there manually searching PubMed for each term, for each year, right? That would mean dozens, maybe hundreds, of manual searches. Well, unfortunately, that is exactly how I've done it in the past. I really am that cool, see.


Actually it doesn't take very long once you get into the swing of it, but I've now worked out a better way. See below for a bash script which repeatedly searches PubMed for a given sequence of years, downloads the first page of the results, picks out the bit where it tells you how many hits you got, and puts it all into a single output text file ready to be pasted into Excel or whatever. This comes with no guarantees whatsoever, but it seems to work. Enjoy...

Edit 29/06/2010: Vastly improved version that searches for multiple different terms sequentially, accepts terms that include spaces, and outputs the data into a sensible format. The search term text file should be a plain text file containing one search term per line. e.g:

serotonin depression
dopamine depression
GABA depression

Would search for each of those terms and output the data for each year into a single text file - with three data columns in this case - good for comparing the relative popularity of many different terms across time.

---
#! /bin/bash
# 29 . 06 . 2010
#PubMedHistory script by Neuroskeptic http://neuroskeptic.blogspot.com
# script to find out how many PubMed hits for a certain string in a given year range.

# usage: script (search term text file) (start year) (end year) (output file)
# e.g script list_of_terms.txt 2000 2005 dope.txt
#first, print the HEADER line of the output file.

printf "YEAR\t" > $4
cat $1 | while read subject
do
#pre-format the subject to remove spaces
ffa=${subject/' '/%20}
echo -n "$ffa" >> $4
printf "\t" >> $4
done
#and a newline
printf "\n" >> $4

#Now the real thing. The main loop is a YEAR loop:

for (( yearz=$2; yearz<=$3; yearz++ )) do #For each year, create a temporary file t.txt containing the output for this line.
#First, the year, then a tab.

printf "$yearz\t" > t.txt

#now, a second loop to go through the list of searches
cat $1 | while read subject
do
one=${subject/' '/%20}
wget -O $yearz.txt http://www.ncbi.nlm.nih.gov/sites/entrez?term="$one"+"$yearz"'[Publication Date]'

#find the line in the output with what we're interested in
output=`cat $yearz.txt | grep ncbi_resultcount | awk '{print}'`
#now, change it to get rid of the bit containing the search term
#as this will screw up the next step if it contains spaces!
output=${output/content*publication/LOL}
#print to a temp file
echo $output > temp$one$2$3$4.txt
#find the bit we want using awk
output=`awk '{ print $22 }' temp$one$2$3$4.txt`
rm temp$one$2$3$4.txt
rm $yearz.txt
#trim output
trimmedout=${output#content\=\"}
trimmedoutB=${trimmedout%\"}
#replace "false" with 0 because that's what "false" means
trimmedoutC=${trimmedoutB/'false'/0}
echo in year $yearz , I got $trimmedoutC. Saving to temp file t.txt
#write the result, and a tab, to the TEMPORARY output file
printf "$trimmedoutC\t" >> t.txt
done
#Now we've done all the search terms for this YEAR, so send the temporary data to the final file
cat t.txt >> $4
#and give it a newline
printf "\n" >> $4
done
rm t.txt

Going Rogue

A lot of people are going rogue at the moment. Sarah Palin started it, of course, when she went rogue during the Presidential campaign and then wrote a book about it.

But everyone's at it now. Facebook's gone rogue, Wall Street's gone rogue, even someone's goldfish may have gone rogue.

Or did they? To say that someone's gone rogue is to say that they've done something they shouldn't have, because they were committed to playing by some set of rules. Which means that if you think someone's gone rogue, you're implying that you trusted them in the first place.

When Rudolf Hess, Hitler's Deputy Führer, stole a plane and flew to Scotland in the middle of WW2 in a crazy bid to make peace with Britain, that was going rogue. But Palin, Facebook, and Wall Street didn't so much go rogue, as stay rogue. They were just being themselves.

When John McCain picked Palin as his running mate, either he should have known how she'd act, or (more likely) he should have realized that he didn't know, that she was an unknown quantity. When you gave a private, for-profit company access to all your personal details, you shouldn't be surprised when it turns out that they're using them to make profit.

That's all pretty minor stuff, but there's more: if you voted for the politicians whose policy was to deregulate finance and let banks speculate wildly with your money (i.e. pretty much all mainstream parties), you can hardly blame the banks for speculating wildly with your money. Banks exist to try and make a profit, with your money. They don't owe you anything. If you don't want them to take certain risks with your money, that's a political issue.

Likewise, all too often you hear people bemoaning Big Pharma for pushing drugs at people who don't need them, or suppressing the results of trials, or whatever. But unless a drug company is actually breaking the law, you have no grounds for complaint: they're just trying to make a profit, which is what they're for, being private companies. They're rogues by design.

If you don't like drug companies pushing drugs at consumers, get your politicians to ban direct-to-consumer advertising. If you don't want them hiding the results of clinical trials, get your politicians to force them to reveal all their data (like this). It's a political issue.

Going Rogue

A lot of people are going rogue at the moment. Sarah Palin started it, of course, when she went rogue during the Presidential campaign and then wrote a book about it.

But everyone's at it now. Facebook's gone rogue, Wall Street's gone rogue, even someone's goldfish may have gone rogue.

Or did they? To say that someone's gone rogue is to say that they've done something they shouldn't have, because they were committed to playing by some set of rules. Which means that if you think someone's gone rogue, you're implying that you trusted them in the first place.

When Rudolf Hess, Hitler's Deputy Führer, stole a plane and flew to Scotland in the middle of WW2 in a crazy bid to make peace with Britain, that was going rogue. But Palin, Facebook, and Wall Street didn't so much go rogue, as stay rogue. They were just being themselves.

When John McCain picked Palin as his running mate, either he should have known how she'd act, or (more likely) he should have realized that he didn't know, that she was an unknown quantity. When you gave a private, for-profit company access to all your personal details, you shouldn't be surprised when it turns out that they're using them to make profit.

That's all pretty minor stuff, but there's more: if you voted for the politicians whose policy was to deregulate finance and let banks speculate wildly with your money (i.e. pretty much all mainstream parties), you can hardly blame the banks for speculating wildly with your money. Banks exist to try and make a profit, with your money. They don't owe you anything. If you don't want them to take certain risks with your money, that's a political issue.

Likewise, all too often you hear people bemoaning Big Pharma for pushing drugs at people who don't need them, or suppressing the results of trials, or whatever. But unless a drug company is actually breaking the law, you have no grounds for complaint: they're just trying to make a profit, which is what they're for, being private companies. They're rogues by design.

If you don't like drug companies pushing drugs at consumers, get your politicians to ban direct-to-consumer advertising. If you don't want them hiding the results of clinical trials, get your politicians to force them to reveal all their data (like this). It's a political issue.