All posts from Last Month

April 20, 2013
08:17 AM
52 views

Eosinophils trigger stem cells to repair damaged muscle tissue

Eosinophil granulocytes, or simply Eosinophils, are white blood cells responsible for combating multicellular parasites and certain infections. However, a new study on mice, by researchers at the University of California, San Francisco (UCSF) suggests that they may also be crucial for muscle regeneration.Read More... Read more »

Heredia, J., Mukundan, L., Chen, F., Mueller, A., Deo, R., Locksley, R., Rando, T., & Chawla, A. (2013) Type 2 Innate Signals Stimulate Fibro/Adipogenic Progenitors to Facilitate Muscle Regeneration. Cell, 153(2), 376-388. DOI: 10.1016/j.cell.2013.02.053

April 20, 2013
04:00 AM
32 views

Will the droids take academic jobs?

by Artem Kaznatcheev in Evolutionary Games Group

As a researcher, one of the biggest challenges I face is keeping up with the scientific literature. This is further exasperated by working in several disciplines, and without a more senior advisor or formal training in most of them. The Evolutionary Game Theory Reading Group, and later this blog, started as an attempt to help [...]... Read more »

Davis, A., Wiegers, T., Johnson, R., Lay, J., Lennon-Hopkins, K., Saraceni-Richards, C., Sciaky, D., Murphy, C., & Mattingly, C. (2013) Text Mining Effectively Scores and Ranks the Literature for Improving Chemical-Gene-Disease Curation at the Comparative Toxicogenomics Database. PLoS ONE, 8(4). DOI: 10.1371/journal.pone.0058201

April 20, 2013
03:17 AM
82 views

Probabilities reveal shape of climate change

by Andy Extance in Simple Climate

David Stainforth from the London School of Economics and his colleagues have developed a new way to analyse weather data and understand which aspects of climate have changed most on a local level, showing European trends with less than a 2% chance of happening at random.... Read more »

Chapman, S., Stainforth, D., & Watkins, N. (2013) On estimating local long-term climate trends. Philosophical Transactions of the Royal Society A: Mathematical, Physical and Engineering Sciences, 371(1991), 20120287-20120287. DOI: 10.1098/rsta.2012.0287

April 19, 2013
11:13 PM
90 views

Potential benefits of an ET-1 signaling antagonist in multiple sclerosis

by Aurelie in The Immuno Blog

Multiple sclerosis (MS) is an immune-mediated inflammatory disease characterized by demyelination in the central nervous system, which leads to a variety of neurological symptoms. Although there is currently no cure for MS, several drugs are available to try and modify … Continue reading →... Read more »

D'haeseleer M, Beelen R, Fierens Y, Cambron M, Vanbinst AM, Verborgh C, Demey J, & De Keyser J. (2013) Cerebral hypoperfusion in multiple sclerosis is reversible and mediated by endothelin-1. Proceedings of the National Academy of Sciences of the United States of America, 110(14), 5654-8. PMID: 23509249

April 19, 2013
08:25 PM
70 views

Does Tylenol Exert its Analgesic Effects via the Spinal Cord?

by The Neurocritic in The Neurocritic

What do we (not) know about how paracetamol (acetaminophen) works? (Toussaint et al., 2010). . .From the beginning, the focus of the search for paracetamol’s analgesic mechanism has concentrated on the central nervous system. When administered intraventricularly [i.e., directly into the ventricular system of the brain], acetaminophen produces no significant analgesia (115, 132). This finding lead to attempts to inject acetaminophen into the spinal cord (i.t.), which produced marked dose-related antinociception (132).Yesterday’s post about Tylenol as a cure for mortality salience and existential dread got me a little worked up. The first author’s public endorsement of acetaminophen as a possible treatment for chronic anxiety disorders was too much to handle (along with the less than stellar experimental rigor). Is watching a 4 min clip of a David Lynch film really the same thing as a clinically diagnosed psychiatric disorder (Randles et al., 2013)? Why Tylenol and not other pain relievers? What is the hypothesized mechanism of action? Wouldn’t we already know by now, from epidemiological studies at the very least, if Tylenol was an effective anti-anxiety medication?So I started wondering about acetaminophen's actual mechanism of action. I was quite surprised that it's somewhat mysterious. Randles et al. cited one paper on this:Second, acetaminophen affects a number of brain regions, some of which are not directly related to physical or social distress (Toussaint et al., 2010).This led me to believe there was evidence from human neuroimaging studies. Turns out there isn't, beyond the Dewall et al. (2010) paper, which states:Although the precise mechanisms by which acetaminophen exerts an analgesic effect are still unclear, it is widely accepted that acetaminophen reduces pain through central, rather than peripheral, nervous system mechanisms (Anderson, 2008; H.S. Smith, 2009).I would like to point out that the spinal cord is part of the central nervous system. So if it's really true that acetaminophen exerts its pain-relieving effects through synapses in the spinal cord, then what does this say about providing relief from the angst of social exclusion, mortality salience, and existential dread? That it's based on nociceptive spinal cord neurons in laminae I, II, and V? For a visual illustration of this pathway, I highly recommend viewing the animation, Dissection of DLF blocks analgesia, at Neuroscience Online. One hypothesis is that Tylenol (acetaminophen) may act on descending serotonergic pathways (purple projection) at the level of the spinal cord (red synapses). Figure modified from Neuroscience Online.However, it's not that simple. The review paper by Toussaint et al. (2010) concluded, "No one mechanism has been definitively shown to account for its analgesic activity." For its proposed mechanisms of action, they presented evidence both for and against Cyclooxygenase (EC 1.14.99.1, COX) inhibition, COX-1, COX-2, 'COX-3', peroxidase, nitric oxide synthase, cannabinoid receptors, and of course serotonin:There is substantial evidence that paracetamol’s mechanism of analgesia in some manner involves the descending serotonergical pathway. 5-HT neurons, largely originating in raphe nuclei located in the brain stem (117, 118) send projections down to the spinal cord that synapse on afferent neurons entering the spinal cord. These descending projections exert an inhibitory (analgesic) effect on the incoming pain signal before it is transmited to higher CNS centres.Note that these are not the same serotonergic pathways often implicated in depression. The terminal synapses for the latter are indeed located in the brain and not the spinal cord.Last night, in real life, I followed the Watertown news live via @sethmnookin and @taylordobbs (like many others).This morning I dreamt that my workplace had transformed into an institutional fortress taken over by a gang of murderous criminals. The actual law enforcement authorities were too busy watching television talk shows to do anything about it. The thugs were threatening and torturing and killing people in the building. I managed to escape down a balcony exit and hid out for a while, avoiding detection but fearful that the thugs would find me and kill me. They were unstoppable, and there seemed to be no way out. I informed an old West-style sheriff, who managed to detain a carload of the evildoers. While continuing to hide, I wondered whether I would be able to shoot them all dead with a fully automatic weapon before they shot and killed me.Then an early morning doorbell rang and woke me up. It was an unexpected FedEx delivery. In my barely awake state, I thought it might be a bomb.Why am I telling you all this?? Because I find it very hard to believe that Tylenol, a drug that's relatively ineffective for my own headache pain, could possibly alleviate the anxiety caused by this nightmare. Or by the real life nightmare that's affected so many people in Boston.ReferencesDewall CN, Macdonald G, Webster GD, Masten CL, Baumeister RF, Powell C, Combs D, Schurtz DR, Stillman TF, Tice DM, Eisenberger NI. (2010). Acetaminophen reduces social pain: behavioral and neural evidence. Psychol Sci. 21:931-7. Randles, D., Heine, S., & Santos, N. (2013). The Common Pain of Surrealism and Death: Acetaminophen Reduces Compensatory Affirmation Following Meaning Threats. Psychological Science DOI: 10.1177/0956797612464786... Read more »

Toussaint, K., Yang, X., Zielinski, M., Reigle, K., Sacavage, S., Nagar, S., & Raffa, R. (2010) What do we (not) know about how paracetamol (acetaminophen) works?. Journal of Clinical Pharmacy and Therapeutics, 35(6), 617-638. DOI: 10.1111/j.1365-2710.2009.01143.x

April 19, 2013
04:03 PM
100 views

Alice and Bob communicate without transferring a single photon

by Perikis Livas in Tracing Knowledge

If physical particles did not carry information between sender and receiver then what did?... Read more »

Edwin Cartlidge. (2013) Alice and Bob communicate without transferring a single photon. Physicsworld.com. info:/

April 19, 2013
03:55 PM
115 views

Researchers discover new promising drug for amyotrophic lateral sclerosis

by beredim in Stem Cells Freak

Researchers from the Harvard University reported today that by using a new, stem cell-based, drug-screening technology they have found a compound, called kenpaullone, that is cost-effective and more efficient than current drugs are in treating patients suffering from Amyotrophic Lateral Sclerosis (ALS).Read More... Read more »

Yang, Y., Gupta, S., Kim, K., Powers, B., Cerqueira, A., Wainger, B., Ngo, H., Rosowski, K., Schein, P., Ackeifi, C.... (2013) A Small Molecule Screen in Stem-Cell-Derived Motor Neurons Identifies a Kinase Inhibitor as a Candidate Therapeutic for ALS. Cell Stem Cell. DOI: 10.1016/j.stem.2013.04.003

April 19, 2013
03:16 PM
70 views

The Curious Case of the Earworm (Part 1)

by Melissa Chernick in Science Storiented

I have had “Thrift Shop” stuck in my head for what seems like days.Yes, it is always on the radio, and yes, I usually listen to it when it is playing. Don't judge me. But why (*Stella scream* wwhhhhyyyyy!) has it established a permanent residence in my brain? I’m going to use a few studies to make the case that it isn’t my fault; I’m led around by my biochemistry. Basically, I’m blaming it on my neurons.Hmmm…where to start. Let’s try to figure out why we like a song (or music in general) in the first place. A study by Valorie Salimpoor et al. in 2011 suggests that it comes down to the biochemistry of pleasure. We, as humans, as animals, find many things in our lives to be pleasurable. Why is this? Well, our brain tells us so. Pleasure is, in essence, a reward for a good stimulus. In the brain, it is largely mediated by dopamine, which also works to reinforce and motivate these behaviors. Now, most people will agree that music is a pleasurable stimulus, but as an abstract stimulus (one not directly related to survival) is it regulated by the same dopamine pathways? In this 2011 study, subjects were asked to select their own “highly pleasurable music” to play for these tests (since musical preferences are so individualized). Then the researchers used PET scanning to estimate dopamine release. Since there are physiological changes that occur during moments of extreme pleasure, they also used the “chills” or “musical frission” response, an objective phychophysiological measurement of clear and discrete patterns of autonomic nervous system arousal. To tease out the response to the music versus the anticipation of the music, they combined the temporal specificity of functional MRI (through the temporal profile of blood oxygenation level - BOLD) with the neurochemical specificity of the PET scan.Salimpoor's group found that the pleasure experienced when listening to music is associated with dopamine activity, that there was a positive correlation between the intensity of “chills” and dopamine release, and an increased BOLD response. In fact, dopamine levels surge during key passages of favorite music and just in anticipation of it. This release is pivotal for establishing and maintaining the behavior, making listening to music a valued experience.Ok, biochemistry…check. Let’s go bigger: What parts of your brain light up when you hear music you like? Salimpoor et al. has published a new study in the April 2013 edition of Science that looks at neural processes active when this pleasurable musical event is happening. Specifically, they look at the reward value the first time a song is heard. We now know that dopamine is involved in familiar music, so what about previously unheard music? To test this, the researchers recruited people, asked them to share their musical tastes (“indie” and “electronic” were the most popular), and used music excerpts selected from a music-recommendation software to pick a unheard song within that preference. To assess reward value, to see if participants liked a song enough that they wanted to hear it again, they were given the option purchase the music with their own money (I know if I have to use my own money then I make sure I love it). Then the participants underwent fMRI scans while listening to musical excerpts and were asked to provide bids of how much they were willing to spend for each song.The researchers found that the reward value (amount of the bid) was directly related to the region of the brain associated with positive prediction error (the NAcc for you brain folks), or pleasant surprises. Increased functional connectivity with this region was made with the auditory cortices, the region known to play a role in the retrieval of previously stored sound information (STG), and the areas implicated in beat processing (caudate and premotor areas). Additionally, increased connectivity was found in regions associated with emotional processing and value-guided decision-making (VMPFC, OFC, and amygdala), but only when sounds gain reward values. When added to the dopamine findings, the activity in these brain regions suggests that when you hear new music your brain looks at its stored information about sound relationships and makes a decision on whether or not to like it based on previous listening experiences and the expectations of tonal events associated with that type of music. If you like it, then your brain gives you a pleasure reward and you end up using your money to buy the song (or otherwise find ways to hear it again). If you like it better than you expected, you get even more delight.Now we know why we like the song and want to hear it again (and again and again…).In the next post we will go further and explore what turns this likeable song into an earworm. Or is it its likeablity at all? (insert cliffhanger music here…dun dun duuuunnnn…)Salimpoor, V., Benovoy, M., Larcher, K., Dagher, A., & Zatorre, R. (2011). Anatomically distinct dopamine release during anticipation and experience of peak emotion to music Nature Neuroscience, 14 (2), 257-262 DOI: 10.1038/nn.2726Salimpoor, V., van den Bosch, I., Kovacevic, N., McIntosh, A., Dagher, A., & Zatorre, R. (2013). Interactions Between the Nucleus Accumbens and Auditory Cortices Predict Music Reward Value Science, 340 (6129), 216-219 DOI: 10.1126/science.1231059...and an article in ScienceNOW "Why Your Brain Loves That New Song"(image via rockandtheology) ... Read more »

Salimpoor, V., Benovoy, M., Larcher, K., Dagher, A., & Zatorre, R. (2011) Anatomically distinct dopamine release during anticipation and experience of peak emotion to music. Nature Neuroscience, 14(2), 257-262. DOI: 10.1038/nn.2726

Salimpoor, V., van den Bosch, I., Kovacevic, N., McIntosh, A., Dagher, A., & Zatorre, R. (2013) Interactions Between the Nucleus Accumbens and Auditory Cortices Predict Music Reward Value. Science, 340(6129), 216-219. DOI: 10.1126/science.1231059

April 19, 2013
01:38 PM
85 views

Researchers discover stem cell senescence is linked to aging

by beredim in Stem Cells Freak

As animals age, humans included, the levels of the "Mitotic checkpoint serine/threonine-protein kinase BUB1 beta" protein (BubR1) drop. Past studies, clearly show that declined BubR1 levels are associated with cell senescence (ageing), weight loss, muscle atrophy and cataracts. Now, a new study by researchers at the Mayo Clinic sheds new light in how stem cell senescence is linked to BubR1 decline and how age-related tissue deterioration may be partially reversed by removing stem cells affected by the BubR1 protein.Read More... Read more »

Baker, D., Weaver, R., & van Deursen, J. (2013) p21 Both Attenuates and Drives Senescence and Aging in BubR1 Progeroid Mice. Cell Reports. DOI: 10.1016/j.celrep.2013.03.028

April 19, 2013
01:20 PM
79 views

Google Promises We'll Feel Better in the Summer

by Elizabeth Preston in Inkfish

Shakespeare wasn't kidding about the "winter of our discontent." In the colder and darker months, people do more internet searches for mental health terms, from anxiety and ADHD all the way to suicide. Search patterns also promise that like a refreshed browser window, better times are due to arrive soon.

John Ayers, of the Center for Behavioral Epidemiology and Community Health in San Diego, and other researchers dove into Google Trends to explore whether certain searches vary by season. "Seasonal affective disorder is one of the most studied phenomena in mental health," Ayers says, "with many individuals suffering mood changes from summer to winter due to changes in solar intensity." He wanted to find out whether any other mental health complaints changed with the seasons, as some studies had hinted.

Since Google Trends breaks down searches by category, the researchers started in the "mental health" section. Looking at all mental health searches in the United States between 2006 and 2011, they saw a consistent cycle with peaks in the winter and troughs in the summer. (If you do this search yourself, you'll see that there's also a dip around the December holidays—but the curve reliably bottoms out in July of each year.)

The team did some statistical smoothing and found that mental health searches overall were about 14% higher in the winter than in the summer. To confirm that the difference was due to the season, they ran the same analysis on data from Australia. Searches cycled in the same way—about 11% higher in winter than summer—but the peaks in the southern-hemisphere country were almost exactly 6 months out of sync with the United States.

When the scientists broke down searches by specific symptoms or illnesses, the seasonal cycle remained—and in some cases got much stronger. "We were very surprised" to see this, Ayers says. Searches including the terms ADHD, anxiety, bipolar, depression, anorexia or bulimia, OCD, schizophrenia, and suicide all rose in the winter and fell in the summer.

One of the most dramatically cycling search terms was schizophrenia, at 37% higher in the winter. Eating disorder terms varied just as strongly. (The smallest seasonal difference was for anxiety, which was just 7% higher in the winter in the United States, and 15% in Australia.)

Some of this seasonality might be due to the schedule of the school year, Ayers points out. Referrals for kids with ADHD and eating disorders may come from their schools.

Other explanations involve winter itself. The effect of shorter days on our circadian rhythms and hormone levels might be a factor, the authors write, as in seasonal affective disorder. They speculate that a lack of vitamin D (which we make using sunlight) in the winter might contribute. Even omega 3 fatty acids might matter: we consume less of them in winter, and omega 3 deficiency has been linked to some mental illnesses.

There's also the question of what we're doing all season. People hunkered indoors during the colder months may have fewer chances for socializing, which is "a well-known health emollient," the authors write. The same goes for physical activity.

"There is a lot more we need to learn about mental health and seasonality," Ayers says. "For instance, is there a universal mechanism that impacts our mental health?"

Of course, sometimes our malaise isn't about the season.

Whatever portion of mental health is predictable, though, doctors would love to know about it and use that information to help.

This study doesn't give reveal much about low-income or elderly populations who aren't online. And knowing what people are searching for isn't exactly the same as knowing what symptoms they're experiencing. "We are actively working to address these limitations," Ayers says. Working with Google.org, the charitable branch of Google, he hopes to develop systems similar to Google Flu Trends that can track a population's mental health.

"Intuition suggests that these results are reflective of an important link between the seasons and mental health," Ayers says. For now, we have the reassurance of computer algorithms that skies will be clearer soon.

Ayers, J., Althouse, B., Allem, J., Rosenquist, J., & Ford, D. (2013). Seasonality in Seeking Mental Health Information on Google American Journal of Preventive Medicine, 44 (5), 520-525 DOI: 10.1016/j.amepre.2013.01.012

Image: Skaneateles, NY, by me.

... Read more »

Ayers, J., Althouse, B., Allem, J., Rosenquist, J., & Ford, D. (2013) Seasonality in Seeking Mental Health Information on Google. American Journal of Preventive Medicine, 44(5), 520-525. DOI: 10.1016/j.amepre.2013.01.012

April 19, 2013
11:32 AM
69 views

UCLA researchers identify molecule that reduces malignancy risk in stem cell therapies

by beredim in Stem Cells Freak

One of the major problems researchers face when culturing stem cells for therapeutic purposes, is the possibility of malignant cells arising from stem cells that have failed to differentiate properly. However, researchers at the University of California, Los Angeles (UCLA), may have solved this problem, as they have discovered a new agent that can be used to remove any undifferentiated stem cells from the rest of the specialized cells.Read More... Read more »

Dabir, D., Hasson, S., Setoguchi, K., Johnson, M., Wongkongkathep, P., Douglas, C., Zimmerman, J., Damoiseaux, R., Teitell, M., & Koehler, C. (2013) A Small Molecule Inhibitor of Redox-Regulated Protein Translocation into Mitochondria. Developmental Cell, 25(1), 81-92. DOI: 10.1016/j.devcel.2013.03.006

April 19, 2013
09:02 AM
140 views

Gary, diets don't work including yours!

by Daniel Bassett in Chew the Fat

In a recent essay by Gary

Taubes in BMJ he discusses the issues with the current scientific

approach to weight loss and how this can be remedied. Gary Taubes is

an exceptional writer, he is eloquent and articulate, and this fact

alone makes what he claims believable. The problem I find is he does

such a good job refuting the 'calories matter' hypothesis that you

tend to just believe what he says afterwards. But what he fails to do

is shine the same light of criticism on his own cherished hypothesis,

and under this light it also tends to look more like fallacy than

fact. Let me explain.

Gary Taubes convincingly,

and correctly, argues that a calorie restriction approach to weight

loss is incorrect. I remember one of my favourite quotes from Gary

Taubes (and I am basing this off memory) “if you spend a century

testing a hypothesis, spend millions of dollars to prove that

hypothesis, have millions of people try what you propose, and yet you

don't get any results that prove your claim then it's time to look

for a new hypothesis”. He is right.....after all this time calorie

restricted weight loss studies simply don't work. No study has been

able to show permanent and substantial weight loss. Calories is a

simplistic, and reductionist, way of viewing things and it does not

account for the complex organism that we are. Many animal studies

such as ones that observe squirrels putting on weight as they go into

hibernation, despite severe calorie restriction, indicate that weight

gain is a bit more complex.

He then argues that a

competing hypothesis, one that was mainstream within Germany and

Austria in the first half of the 20th century, took this

into account and opposed the calorie restriction hypothesis held

generally by English and American scientists. This was all pre-WWII

and after the war people tended to have a bit of a grudge against

anything German sounding, and so they simply stopped paying attention

to the theory. What this alternative hypothesis proposes is that fat

deposition is a hormonal issue and just like hormones determine where

hair grows, they also determine where fat is stored. Because insulin

is the grandaddy of fat storage hormones it is logical then that

insulin is what needs to be lowered to prevent fat gain. Thus, Gary

Taubes, and all proponents of the insulin hypothesis, propose that

consuming a diet low in carbohydrates will lead to weight loss.

The problem he says is

history. After WWII calorie restriction became the norm and was

institutionilised. Anyone who tried to say that fat was not

unhealthy, and that calorie restriction was a waste of time was

shunned by academics, funding agencies, and the general public at

large. I don't disagree with this. But here is where me and Gary go

our seperate ways. This is where I feel he needs to look at the

insulin hypothesis with the same criticisms he did for calorie

restriction. Firstly, the fact that calorie restriction is wrong does

not make the alternative true. So just because his theory was

oppressed by those evil calorie restriction monsters does not mean it

was valid.

However, my main point is

this. He admits that this insulin theory has been around for almost a

century, if not longer. He admits that it was mainstream, and then

was lost until Atkins hit the scene in the 60's. So a relatively small hiatus of 20 years. Low carbohydrate

diets then existed in one form or another until this current day. So

these diets have been tried by millions of people and yet have had

little success. I'm sure everyone has heard of weight loss success

stories, but that is the fun thing about stories they are fiction and

you get to make stuff up. The fact is if low carbohydrate diets

worked, and caused substantial weight loss permanently, we would know

about it and be doing it. Enough people have tried!!! The reason I

know this is because when I heard about all the 'success' I also

jumped the bandwagon and gave it a go. We know that no government

agency, or grant funding agency, or mass media hype is going to

prevent the public from trying what seems like a whacky fad diet if

that diet takes a hold, and by god did Atkins take a hold.

My last point is that he

states clinical trials have shown that low carbohydrate diets

convincingly beat low calorie diets in terms of weight loss. Again

this is true but it doesn't make them effective. Low calorie diets

are shockingly ineffective, so all that is required is for low

carbohydrate diets to be less shockingly ineffective. In a recent

study on low carbohydrate diets the authors looked at over 23 clinical trials on over 1000 obese

patients and they found that the mean weight loss was 7kg. Even if you

considered that everyone of those patients was merely borderline

obese, weighing in at 200 pounds, this is only 15 pounds, or a 7.5%

weight loss. For the majority of obese people, and for nearly all the

obese people in those studies, this weight loss percentage would be

much less, and not nearly enough to move them from obese to even just

fat. It is a minimal amount of weight loss and it is still failure.

Low carbohydrate diets simply do not work.

If I was to bump into

Gary Taubes, and after I had told him how I do appreciate his work I

would like to ask him this one question “if after almost a century

of study, with millions of dollars and people thrown at the insulin

hypothesis with little result, isn't it high time that we just admit

that diets don't goddam work!”Taubes, G. (2013). The science of obesity: what do we really know about what makes us fat? An essay by Gary Taubes BMJ, 346 (apr15 5) DOI: 10.1136/bmj.f1050Santos FL, Esteves SS, da Costa Pereira A, Yancy WS Jr, & Nunes JP (2012). Systematic review and meta-analysis of clinical trials of the effects of low carbohydrate diets on cardiovascular risk factors. Obesity reviews : an official journal of the International Association for the Study of Obesity, 13 (11), 1048-66 PMID: 22905670... Read more »

Taubes, G. (2013) The science of obesity: what do we really know about what makes us fat? An essay by Gary Taubes. BMJ, 346(apr15 5). DOI: 10.1136/bmj.f1050

Santos FL, Esteves SS, da Costa Pereira A, Yancy WS Jr, & Nunes JP. (2012) Systematic review and meta-analysis of clinical trials of the effects of low carbohydrate diets on cardiovascular risk factors. Obesity reviews : an official journal of the International Association for the Study of Obesity, 13(11), 1048-66. PMID: 22905670

April 19, 2013
07:21 AM
89 views

Depression: Watch Out For Contagion

by Katja Keuchenius in United Academics

If you’re vulnerable to depression it doesn’t necessarily mean that you have certain unlucky genes or just experienced a traumatic event. What also makes you vulnerable for the mental disorder is the way you think. And even if you don’t yet have this style of thought, you could pick it up from your roommate, a new study suggests.... Read more »

Haeffel, G., & Hames, J. (2013) Cognitive Vulnerability to Depression Can Be Contagious. Clinical Psychological Science. DOI: 10.1177/2167702613485075

Psychology

April 19, 2013
07:15 AM
96 views

Queen’s chemists discover simpler method of making ‘wonder material’

by Perikis Livas in Tracing Knowledge

Researchers at Queen’s University have discovered a cheaper method for making a substance similar to graphene, a wonder material discovered in 2004.... Read more »

Queen’s University. (2013) Queen's chemists discover simpler method of making 'wonder material'. Queen’s University News. info:/

April 19, 2013
06:55 AM
17 views

Loss of FLCN increases longevity in C. elegans

by Lizzie Perdeaux in BHD Research Blog

Several signalling pathways – namely the mTOR, HIF and insulin signalling pathways – are known to slow ageing and increase longevity under certain conditions. This is a topic of much research, and was discussed at the recent “Talks about TORCs” … Continue reading →... Read more »

Gharbi H, Fabretti F, Bharill P, Rinschen M, Brinkkötter S, Frommolt P, Burst V, Schermer B, Benzing T, & Müller RU. (2013) Loss of the Birt-Hogg-Dubé gene product Folliculin induces longevity in a hypoxia-inducible factor dependent manner. Aging cell. PMID: 23566034

Biology

April 19, 2013
05:18 AM
88 views

‘Living fossil’ genome unlocked

by Perikis Livas in Tracing Knowledge

Like lungfish, the other surviving lineage of lobe-finned fishes, coelacanths are actually more closely related to humans and other mammals than to ray-finned fishes such as tuna and trout. Ancient lobe fins were the first vertebrates to brave the land, and the coelacanth genome is expected to reveal much about the origins of tetrapods, the evolutionary line that gave rise to amphibians, reptiles, birds and mammals, says lead author Chris Amemiya, a biologist at the University of Washington in Seattle. “The coelacanth is a cornerstone for our attempt to understand tetrapod evolution,” he says.... Read more »

Woolston, C. (2013) ‘Living fossil’ genome unlocked. Nature, 496(7445), 283-283. DOI: 10.1038/496283a

April 19, 2013
05:16 AM
91 views

Lazarus sign - A natural yet weird-looking phenomenon

by Usman Paracha in SayPeople

Main point:

Lazarus sign, also known as Lazarus reflex, is a complex form of reflex movement of the arms in brain dead patients.

Study Further:

In this phenomenon, the arms of the brain dead patients or the patients with brainstem failure raises to the chest and often fall crossed on to the body (in a place that you may have seen in some of the Egyptian mummies). “The arms flex quickly to the chest from the patient's side, the shoulders adduct, and in some patients, the hands cross or oppose just below the chin. The limbs then return to the patient's side, sometimes asymmetrically,” Researchers reported.

Even weirder is the presence of minor shaky movements of the arms of the patients or the presence of goose bumps on the arms and torso in some cases. Researchers have also reported "respiratory-like movement in a patient with brain death" along with Lazarus sign.

This reflex is a kind of reflex arc generated by the spine that is why it can occur even after brain death, while the other organs are still working. Researchers have found that this phenomenon occurs after several minutes of the removal of the medical ventilators that helped to pump air in and out of brain-dead patients, so that the bodies of the patients would stay alive.

Researchers have also found the presence of Lazarus sign during the testing for apnea - brief pause in breathing - that is one of the criteria for the determination of brain death used by the neurologists.

You can see a video of this reflex here.

Further Reading:

Calixto Machado (2007). Brain death: a reappraisal. Springer. p. 79. ISBN 978-0-387-38975-2.

"Practice Parameters: Determining Brain Death in Adults". American Academy of Neurology. 1994. Retrieved 12 July 2009.

Urasaki E, Fukumura A, Itho Y, Itoyama Y, Yamada M, Ushio Y, Wada S, Yokota A, (1988). [Lazarus' sign and respiratory-like movement in a patient with brain death]. [Article in Japanese]. No To Shinkei, 40(12):1111-1116.

Ropper, A. (1984). Unusual spontaneous movements in brain-dead patients Neurology, 34 (8), 1089-1089 DOI: 10.1212/WNL.34.8.1089... Read more »

Ropper, A. (1984) Unusual spontaneous movements in brain-dead patients. Neurology, 34(8), 1089-1089. DOI: 10.1212/WNL.34.8.1089

April 19, 2013
03:53 AM
76 views

Decoding the structure of bone

by Perikis Livas in Tracing Knowledge

[...] a team of researchers at MIT has finally unraveled the structure of bone with almost atom-by-atom precision, after many years of analysis by some of the world’s most powerful computers and comparison with laboratory experiments to confirm the computed results [...]... Read more »

David L. Chandler. (2013) Decoding the structure of bone. MIT News Office. info:/

April 19, 2013
03:44 AM
72 views

Highly extraverted sales people perform more poorly

by Alex Fradera in BPS Occupational Digest

What sales manager wouldn't hire extraverts? They tend to be comfortable in interactions, naturally display enthusiasm and confidence for their own ideas, and can be firm and persistent when they meet with resistance to their agenda. Scrutinise many sales forces and you'll probably spot this reasoning at work.Yet research finds weak and sometimes inconsistent relationships between sales performance and extraversion, with three meta-analyses finding the summed effects to amount to .07 - a non-significant finding. A new study by Adam Grant from the Wharton School, Pennsylvania, suggests that the sweet spot for sales performance might instead be balanced between extraversion and introversion. Grant looked at week-on-week sales performance (revenue earned) for 340 outbound sales executives over three months. All completed a big-five personality inventory beforehand, comprising extraversion along with the other four primary personality dimensions; the inventory required them to rate their agreement with various items using a seven-point Likert scale. Regression analysis on the data revealed no linear relationship between extraversion and sales performance, instead finding a quadratic effect. Specifically, performance rose with extraversion until a peak at 4.5, well before the maximum of seven. From this point, performance actually decreased.In hard numbers, the performers at the peak made on average $151 per hour, versus $127 for those whose extraversion was a standard deviation below, and a more meagre $115 for those a standard deviation above. Grant's analysis confirmed that the findings were not being driven by a confound from other personality factors, for instance a toxic combination of low agreeableness and high extraversion which might invite conflicts.Why might those falling more towards the middle of the scale perform better? Grant dubs these 'ambiverts' and suggests that they are more likely to engage in give and take with clients, falling back to listening as introverts tend to, but then being willing to act and engage. Meanwhile, the strongly extraverted may fall into a range of traps - the dark underbelly of their strengths - by dominating others, projecting overconfidence, and sending obvious 'influence' signals that may lead to prospective customers raising their defences. Grant concludes that organisations may want to look harder at the relationship between personality and sales performance to guide recruitment strategies, and that they may 'benefit from training highly extraverted salespeople to model some of the quiet, reserved tendencies of their more introverted peers'. Grant, A. (2013). Rethinking the Extraverted Sales Ideal: The Ambivert Advantage Psychological Science DOI: 10.1177/0956797612463706Further reading: Barrick, M. R., Mount, M. K., & Judge, T. A. (2001). Personality and performance at the beginning of the new millennium: What do we know and where do we go next? International Journal of Selection and Assessment, 9, 9–30. DOI: 10.1111/1468-2389.00160... Read more »

Grant, A. (2013) Rethinking the Extraverted Sales Ideal: The Ambivert Advantage. Psychological Science. DOI: 10.1177/0956797612463706

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