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  • January 26, 2015
  • 09:54 PM
  • 7 views

Why are American Atheists Disagreeable and Unconscientious?

by Tom Rees in Epiphenom

There’s a popular model of personality that splits it into five components: openness to experience, conscientiousness, extroversion, agreeableness, and neuroticism. And it’s well known that, while atheists tend to score high on openness, they tend to get low scores on conscientiousness and agreeableness. Back in 2010, Vincent Saroglou and colleagues assembled data from all the [Read More...]... Read more »

Gebauer, J., Bleidorn, W., Gosling, S., Rentfrow, P., Lamb, M., & Potter, J. (2014) Cross-cultural variations in Big Five relationships with religiosity: A sociocultural motives perspective. Journal of Personality and Social Psychology, 107(6), 1064-1091. DOI: 10.1037/a0037683  

  • January 26, 2015
  • 09:21 PM
  • 1 view

High-Dose Statin May Protect Heart Surgery Patients’ Kidney Health

by Wiley Asia Blog in Wiley Asia Blog - Health Sciences

Acute kidney injury often arises after major surgery because the kidneys can be deprived of normal blood flow during the procedure. The use of contrast media, or dyes, can contribute to this problem. In patients undergoing coronary angiography or percutaneous coronary intervention, which are heart procedures that use dyes to help surgeons visualize the arteries, a high dose of the statin atorvastatin was linked with a reduction in blood levels of creatinine, a marker of kidney injury, as well as a lower incidence of acute kidney injury compared with a low dose of the statin.... Read more »

  • January 26, 2015
  • 05:36 PM
  • 9 views

You can’t unboil an egg? Well… now you can

by Gabriel in Lunatic Laboratories

There is a saying, “you can’t unboil an egg.” Usually this is just illustrating cause and effect; you can’t turn back time, or what’s done is done. Well now scientists have successfully unboiled an egg, so suck it thermodynamics. An international team of chemists have accomplished this feat – an innovation that could dramatically reduce costs for cancer treatments, food production and other segments of the $160 billion global biotechnology industry, according to the findings.... Read more »

Yuan, T., Ormonde, C., Kudlacek, S., Kunche, S., Smith, J., Brown, W., Pugliese, K., Olsen, T., Iftikhar, M., Raston, C.... (2015) Shear-Stress-Mediated Refolding of Proteins from Aggregates and Inclusion Bodies. ChemBioChem. DOI: 10.1002/cbic.201402427  

  • January 26, 2015
  • 04:42 PM
  • 8 views

More Complexity = More Disruptions?

by Andreas Wieland in Supply Chain Management Research

Trends in management towards a concentration on core competencies and outsourcing of non-core activities have created complex networks, i.e., global supply chains. At the same time, it has been discussed that this increased complexity has also made companies more vulnerable. An interesting paper, Structural Drivers of Upstream Supply Chain Complexity and the Frequency of Supply […]... Read more »

  • January 26, 2015
  • 04:32 PM
  • 10 views

The secret for a longer life? Kill your unfit cells

by Isabel Torres in Science in the clouds

If you had the choice, would you like to live until you’re 130 years old? New research in fruit flies shows that manipulating a single gene can extend their lifespan up to 60%, suggesting that living well into your hundreds might become a reality in the foreseeable future.Dying of old age is a strange thing. Why does our health decline just because we’re old? Although the answer might at first seem obvious or simple, it really isn’t. There are countless theories of ageing, a few popular even outside the scientific community. Take ‘superfoods’, for example. The miracle properties credited to these antioxidant-rich foods stem from the free radical theory of ageing—older cells produce more of a toxic form of oxygen that gradually poisons them. Antioxidants like vitamin C or D counteract this deleterious effect and prevent ageing (and the appearance of wrinkles), superfood advocates claim.A common denominator in these theories is that we age—and ultimately die—because our cells deteriorate with time (for whatever reason). As tissues and organs mount up more and more of these damaged cells, they begin to malfunction and eventually stop working. This raises an interesting assumption. What if we could get rid of these unfit cells and keep only the healthy ones? Would we live longer? Jeanne Louise Calment had the longest confirmed human lifespan on record (122 years and 164 days).It’s well known that sick cells such as cancerous cells, are eliminated by our bodies, either by immune cells or by committing suicide. However, our ‘old’ unfit cells are still healthy enough to bypass this quality-control checkpoint. Or so it was thought. A few years ago, Eduardo Moreno and colleagues at the University of Bern, Switzerland, showed that healthy but less fit cells are also culled from tissues, by a mechanism they called “fitness fingerprints”. Each cell has a molecular fingerprint on its surface that tells its neighbours how healthy it is. When a given cell has a fingerprint that is worse than its neighbours', it kills itself. But the researchers didn’t know the importance of this cell elimination process for the organism. For example, would we age faster if those cells could not kill themselves? To answer these questions, Moreno’s team genetically engineered fruit flies to control a newly found gene essential for marking unfit cells for culling. “If you put an extra copy of this gene you have better selection of the [unfit] cells, they are eliminated faster and therefore the animals can live longer”, says Moreno.When the gene, which Moreno named azot, was removed from flies, they became sick and died prematurely. On the other hand, flies with an extra copy of the azot gene lived up to 60% longer. Previously, only caloric restriction had been shown to prolong lifespan to such an extent in flies. In fact, reducing the amount of daily calorie input increases longevity in flies, nematodes, fish, mice and rats (data from studies with primates remain controversial). Could it be then, that starved flies with an extra copy of the azot gene live even longer? Indeed, these flies lived about 80% longer, Moreno’s team showed. In human time this would be equivalent to living up to 150 years! The question remains whether these findings could be relevant for our species. Humans have the azotgene, in fact most organisms do, so potentially it should be possible to increase life expectancy in people by altering azot protein levels.“You could start thinking of how to manipulate these mechanisms with drugs, for example, to treat ageing or diseases like neurodegeneration or myocardial infarction,” says Moreno, “I’m totally convinced it will be possible to delay aging and prolong lifespan in humans.” Would we want to live longer though, if we spend most of our life old and sick? “Our long-term challenge will be to understand the biology of aging to address problems associated with steadily increasing life expectancy, such as metabolic disease and neurodegeneration”, says Martin Denzel, a researcher at the Max Planck Institute for Biology of Ageing in Cologne, Germany. With this in mind, Moreno’s team tested whether the long-living azot flies remained healthy as they aged. When the researchers looked in these flies’ brains, they found that their neurons accumulated fewer ageing cellular markers. Azot not only prolongs lifespan, but it also delays ageing. In the future the team wants to understand what azot is actually doing. This gene encodes for a protein of unknown function, but the researchers know that when “the azot gene is activated, it triggers the normal cell death apoptosis pathway”, Moreno concludes. The team will also investigate the function of azot in mice, and collaborate with medical doctors to see if the azot-dependent cell elimination pathways are present in ageing-related diseases like Alzheimers. “I have high hopes that eventually basic research into the aging process will yield treatments that extend the span of healthy living and that improve the quality of life in advanced age”, Denzel explains. “However, it will take a lot of additional work to investigate if this mechanism might be beneficial in mammals.”Reference:... 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  • January 26, 2015
  • 01:26 PM
  • 15 views

The Bed Bug’s Piercing Penis (A Guest Post)

by Miss Behavior in The Scorpion and the Frog

By Rachael Pahl Sex is a dangerous, but necessary, part of life. Across the animal kingdom, there are a multitude of things that can go wrong. You could be injured in a fight by someone who wants to steal your mate, or maybe your partner eats you because you’re taking too long. Either way, nature must have a pretty good reason for the traumatizing effects of sex. A male bed bug traumatically inseminates a female. Image by Rickard Ignell at the Swedish University of Agricultural Sciencesposted at Wikimedia Commons. Bed bugs have a particularly risky way of having sex. When a male bed bug wants to mate, he will pierce the female’s abdomen with his penis (called a lanceolate) and release sperm directly into her body cavity. Talk about forceful! This mode of reproduction in bed bugs is known as traumatic insemination; aptly named. With what seems like a horrific way of reproducing, it’s hard to imagine that there are any benefits for the female. I’m sure you can come up with a plethora of things that could go wrong: infection, damage of major organs, bleeding, even death. Researchers Edward Morrow and Göran Arnqvist with Uppsala University in Sweden, argue that the female has a counter-adaptation to this antagonistic strategy. The area of the abdomen that the male pierces has been modified into a pocket lined with specialized tissues to prevent serious damage to the female. This area is termed the spermalege. Edward and Göran hypothesized that sex is not harmful to the female if the spermalege is punctured, but can be dangerous if any other area is pierced. They also hypothesized that more mating occurrences and improper punctures would reduce the lifespan of the female.To test their hypotheses, Edward and Göran observed the number of times a female was inseminated and where she was pierced (on the spermalege or somewhere else). They had two set-ups to observe mating rate: (1) a female was placed with four males where lots of mating would take place and (2) a female was placed with four males, three of which had their penis glued to their abdomen so that they could not mate. These two set-ups allowed the researchers to observe the differences in female life span between those who had a high mating rate and those who had a low mating rate. Then, the researchers wanted to see where the female was being pierced and how that affected her life span. In addition to traumatic insemination by male bed bugs, the researchers used a pin to pierce the spermalege or an area outside the spermalege and then compared the damage. The study produced two big results. First, females who mated more had a shorter lifespan than those who mated less. This was because the sperm and other fluids deposited caused an immune response as they were seen as foreign objects; too much of these foreign substances can have negative effects on the organism. Second, females that were pierced through the spermalege lived longer than those who were pierced outside the spermalege, suggesting that the spermalege functions to reduce damage and/or infection during insemination. So what are the benefits of traumatic insemination and how does the spermalege reduce the costs to the female? Well, there is a lot of paternal ambiguity in the animal kingdom. The direct deposition of sperm into the abdomen may ensure paternity by getting the sperm as close to the ovaries as possible before another male bed bug can mate with her. This method also reduces courtship time and avoids female resistance, meaning that other males may not have the chance to steal the female away. The spermalege protects females from traumatic insemination by localizing damage to one area that can easily repair itself. Since the spermalege is lined with cuticle, it prevents the leakage of blood and sperm from the wound. The spermalege may also function to prevent entry of pathogens into the bloodstream. In the end, this traumatic insemination is no more dangerous than any other kind of sex, however painful and horrible it sounds. It may even be less risky if done correctly. For more information, check out:Morrow, E., & Arnqvist, G. (2003). Costly traumatic insemination and a female counter-adaptation in bed bugs Proceedings of the Royal Society B: Biological Sciences, 270 (1531), 2377-2381 DOI: 10.1098/rspb.2003.2514 ... Read more »

Morrow, E., & Arnqvist, G. (2003) Costly traumatic insemination and a female counter-adaptation in bed bugs. Proceedings of the Royal Society B: Biological Sciences, 270(1531), 2377-2381. DOI: 10.1098/rspb.2003.2514  

  • January 26, 2015
  • 07:02 AM
  • 23 views

His brain made him do it” and so I feel much less empathy for him 

by Rita Handrich in The Jury Room

We’ve written about the brain based defenses a lot here. And here’s an article that may shed light on how the presentation of neural defenses could backfire on defense attorneys. First, let’s look at the research. The researchers wondered how the biological explanation of mental illness might affect the empathy of mental health clinicians toward […]

Related posts:
Which jurors most “feel” your client’s pain?
Empathy: Paving the road to preferential treatment with good intentions
A new question for the jury: Did my brain implant make me do it?


... Read more »

Lebowitz MS, & Ahn WK. (2014) Effects of biological explanations for mental disorders on clinicians' empathy. Proceedings of the National Academy of Sciences of the United States of America, 111(50), 17786-90. PMID: 25453068  

  • January 26, 2015
  • 06:27 AM
  • 32 views

We're more likely to cheat when we're anxious

by BPS Research Digest in BPS Research Digest

When we’re stressed out and feeling threatened, our priority becomes self-preservation. According to new research, this defensive mode even affects our morality, making us more likely to cheat and excuse our own unethical behaviour.Maryam Kouchaki and Sreedhari Desai demonstrated this through six experiments. In the clearest example, 63 student participants spent three minutes listening to either calm music, or in the anxiety condition, to Bernard Herrmann's Psycho score. Those freaked out by Hermann's definitive ode to unease declared they were more anxious at the end of the study, and they had threat on their mind (this was confirmed through a word matching task - the Psycho group more often selected words with connotations of threat).Anxious? Check. Threatened? Check. Unethical? Kouchaki and Desai went hunting for cheaters. Their participants next completed a simple computer task for money, for which there was an obvious way to cheat. The non-anxious students made an average of 19 "clear cheats", whereas the anxious ramped this up to 24. The more threatened the anxious felt, the more they cheated.The researchers think this probably happened because threat provokes us to grab resources, status ... anything to buffer the self. An alternative explanation is that anxiety somehow frazzles our apparatus for moral judgment in general. The researchers showed this wasn’t the case in a further experiment where an unethical act - secretly copying a password that gave access to the questions for the next day's fictional job interview - was either posed as something that the participant had done, or a third party named Steve. Participants who had been put into an anxious state judged Steve's infraction just as severely as their non-anxious counterparts, yet they were more likely to let themselves off the hook.When we’re anxious, our sympathetic nervous system floods us with noradrenaline, activating our fight-or-flight pathways. How can I look after me, now? With this imperative looming large, it's unsurprising that we no longer have bandwidth available for our higher principles. It tallies with evidence that, when threatened, people are more likely to consume scarce communal resources, without regard to fair distribution or the long-term. The new findings may not extend to more severe violations such as willingness to harm others, but they do suggest we’re quick to forget lofty notions such as "fair play' when we feel under threat._________________________________ Kouchaki, M., & Desai, S. (2014). Anxious, Threatened, and Also Unethical: How Anxiety Makes Individuals Feel Threatened and Commit Unethical Acts. Journal of Applied Psychology DOI: 10.1037/a0037796 Post written by Alex Fradera (@alexfradera) for the BPS Research Digest.

... Read more »

  • January 26, 2015
  • 06:23 AM
  • 32 views

Is it necessary to use brain imaging to understand teen girls' sexual decision making?

by The Neurocritic in The Neurocritic

“It is feasible to recruit and retain a cohort of female participants to perform a functional magnetic resonance imaging [fMRI] task focused on making decisions about sex, on the basis of varying levels of hypothetical sexual risk, and to complete longitudinal prospective diaries following this task. Preliminary evidence suggests that risk level differentially impacts brain activity related to sexual decision making in these women [i.e., girls aged 14-15 yrs], which may be related to past and future sexual behaviors.”-Hensel et al. (2015) Can the brain activity of adolescents predict whether they are likely to make risky sexual decisions in the future?  I think this is the goal of a new pilot study by researchers at Indiana University and the Kinsey Institute (Hensel et al., 2015). While I have no reason to doubt the good intentions of the project, certain aspects of it make me uncomfortable.But first, I have a confession to make. I'm not an expert in adolescent sexual health like first author Dr. Devon Hensel. Nor do I know much about pediatrics, adolescent medicine, health risk behaviors, sexually transmitted diseases, or the epidemiology of risk, like senior author Dr. J. Dennis Fortenberry (who has over 300 publications on these topics).  His papers include titles such as Time from first intercourse to first sexually transmitted infection diagnosis among adolescent women and Sexual learning, sexual experience, and healthy adolescent sex. Clearly, these are very important topics with serious personal and public health implications. But are fMRI studies of a potentially vulnerable population the best way to address these societal problems?The study recruited 14 adolescent girls (mean age = 14.7 yrs) from health clinics in lower- to middle-income neighborhoods. Most of the participants (12 of the 14) were African-American, most did not drink or do drugs, and most had not yet engaged in sexual activity.  However, the clinics served areas with “high rates of early childbearing and sexually transmitted infection” so the implication is that these young women are at greater risk of poor outcomes than those who live in different neighborhoods.Detailed sexual histories were obtained from the girls upon enrollment (see below). They also kept a diary of sexual thoughts and behaviors for 30 days. Given the sensitive nature of the information revealed by minors, it's especially important to outline the informed consent procedures and the precautions taken to protect privacy. Yes, a parent or guardian gave their approval, and the girls completed informed consent documents that were approved by the local IRB. But I wanted to see more about this in the Methods. For example, did the parent or guardian have access to their daughters' answers and/or diaries, or was that private? This could have influenced the willingness of the girls to disclose potentially embarrassing behavior or “verboten” activities (prohibited by parental mores, church teachings, legal age of consent,1 etc.).  I don't know, maybe the standard procedures are obvious to those within the field of sexual health behavior, but they weren't to me.Turning to more familiar territory, the experimental design for the neuroimaging study involved presentation of four different types of stimuli: (1) faces of adolescent males; (2) alcoholic beverages; (3) restaurant food; (4) household items (e.g., frying pan). My made-up examples of the stimuli are shown below.Each picture was presented with information that indicated the item's risk level (“high” or “low”):Adolescent male faces: number of previous sexual partners and typical condom use (yes/no)Alcoholic beverages: number of alcohol units and whether there was a designated driver (yes/no)Food: calorie content and whether the restaurant serving the food had been cited in the past year for health code violations (yes/no) Household items: whether the object could be returned to the store (yes/no)For each picture, participants rated how likely they were to: (1) have sex with the male, (2) drink the beverage, (3) eat the food, or (4) purchase the product (1 = very unlikely to 4 = very likely). There were 35 exemplars of each category, and each stimulus was presented in both “high” and “low” risk contexts. So oddly, the pizza was 100 calories and from a clean restaurant on one trial, compared to 1,000 calories and from a roach-infested dump on another trial.The faces task was adapted from a study in adult women (Rupp et al., 2009) where the participants gave a mean likelihood rating of 2.45 for sex with low risk men vs. 1.41 for high risk men (significantly less likely for the latter). The teen girls showed the opposite result: 2.85 for low risk teen boys vs. 3.85 for high risk teen boys (significantly more likely) — the “bad boy” effect?But the actual values were quite confusing. At one point the authors say they omitted the alcohol condition: “The present study focused on the legal behaviors (e.g., sexual behavior, buying item, and eating food) in which adolescents could participate.”But in the Fig. 1 legend, they say the opposite (that the alcohol condition was included):Panel (A) provides the average likelihood of young women's endorsing low- and high-risk decisions in the boy, alcohol, food, and household item (control) stimulus categories. Then they say that the low-risk male faces were rated as the most unlikely (i.e., least preferred) of all stimuli.  But Fig. 1 itself shows that the low-risk food stimuli were rated as the most unlikely...Regardless of the precise ratings, the young women were more drawn to all stimuli when they were in the high risk condition. The authors tried to make a case for more "risky" sexual choices among participants with higher levels of overt or covert sexual reporting, but the numbers were either impossibly low (for behavior) or thought-crimes only (for dreams/fantasy). So it's really hard to see how brain activity of any sort could be diagnostic of actual behavior at this point in their lives.And the neuroimaging results were confusing as well. First, the less desirable low-risk stimuli elicited greater responses in cognitive and emotional control regions:Neural activity in a cognitive-affective network, including prefrontal and anterior cingulate (ACC) regions, was significantly greater during low-risk decisions. But then, we see that the more desirable high-risk sexual stimuli elicited greater responses in cognitive/emotional control regions:Compared with other decisions, high-risk sexual decisions elicited greater activity in the anterior cingulate, and low-risk sexual decision elicited greater activity in regions of the visual cortex.&... Read more »

  • January 26, 2015
  • 04:44 AM
  • 26 views

What factors are linked to behavioural crises in autism?

by Paul Whiteley in Questioning Answers

The question posed in the title of this post was asked and [partly] answered by the paper by Vincent Guinchat and colleagues [1] based on the analysis of 58 adolescents diagnosed with an autism spectrum disorder (ASD) and "hospitalized for severe challenging behaviors." Challenging behaviours, by the way, refers to a whole spectrum of presentations which doesn't just include aggressive or violent behaviours (see here). Indeed, I recently talked about irritability and autism (see here), which might also fall into this category under certain circumstances.Guinchat and colleagues "aimed to assess risk factors associated with very acute behavioral crises in adolescents with ASD" by way of collecting various data on participants (both retrospectively and prospectively) including the severity of their presentation, the presence of "comorbid organic conditions" and assessing "predictors of Global Assessment Functioning Scale (GAFS) score and duration of hospitalization at discharge."Results: well, an inpatient stay did seem to have a positive effect on participants as per the findings that: "During the inpatient stay... patients doubled on average their GAFS scores." A higher score translates as better outcome. Comorbid psychiatric conditions, known and unknown, was the most frequently cited reason for behavioural crises, with depressive episode and schizophrenia representing the known conditions cited most. Organic causes, including epilepsy and "painful medical conditions" followed in frequency, with environmental causes "including lack of treatment... and adjustment disorder" bringing up the rear. The authors also suggest that the severity of autism presentation (I draw back from using the idea of 'functioning') had a negative effect on GAFS scores at discharge. This point may also tie into some recent findings reported by Rattaz and colleagues [2] where symptom severity of autism might be a risk factor for the presence of self-injurious behaviours.The authors conclude: "Challenging behaviors among adolescents with ASD may stem from diverse risk factors, including environmental problems, comorbid acute psychiatric conditions, or somatic illness such as epilepsy or acute pain. The management of these behavioral challenges requires a unified, multidisciplinary approach."I know that some people might look at this data, shrug and say 'what did you expect', but I'm not one of them. Challenging behaviours can occur in relation to autism for all-manner of reasons but as per other discussions on this topic, one should never assume that challenging behaviours are just 'part and parcel' of a diagnosis of autism. They aren't, even if some of the signs and symptoms of autism may make a person more likely to present with such issues at certain times (including puberty).I've talked before about some of the circumstances around challenging behaviours and autism as per the idea that pain and discomfort for example, might sometimes facilitate the presence of such issues (see here) particularly in the absence of functional language use. Indeed, a lack of communicative abilities (or rather suitable ways or avenues to communicate) can be a real obstacle to health equality more generally when it comes to autism (see here). Epilepsy or seizure-type disorders have also figured on the autism landscape (see here) and potentially contribute as an important factor when it comes to challenging behaviours for some [3]. Ideas on the possibility of overlap between autism and conditions like certain types of depression and/or schizophrenia are gaining traction in recent times (see here and see here respectively) and again, suggest that 'diagnostic vigilance' are the keywords (see here).To close: Take on Me by Harry Hill (and others)?----------[1] Guinchat V. et al. Acute behavioral crises in psychiatric inpatients with autism spectrum disorder (ASD): Recognition of concomitant medical or non-ASD psychiatric conditions predicts enhanced improvement. Research in Developmental Disabilities. 2015; 38: 242-255.[2] Rattaz C. et al. Symptom severity as a risk factor for self-injurious behaviours in adolescents with autism spectrum disorders. J Intellect Disabil Res. 2015 Jan 12.[3] Ito M. et al. Subacute postictal aggression in patients with epilepsy. Epilepsy Behav. 2007 Jun;10(4):611-4.----------Guinchat V, Cravero C, Diaz L, Périsse D, Xavier J, Amiet C, Gourfinkel-An I, Bodeau N, Wachtel L, Cohen D, & Consoli A (2015). Acute behavioral crises in psychiatric inpatients with autism spectrum disorder (ASD): Recognition of concomitant medical or non-ASD psychiatric conditions predicts enhanced improvement. Research in developmental disabilities, 38C, 242-255 PMID: 25575287... Read more »

  • January 26, 2015
  • 12:05 AM
  • 20 views

Minding the Gap: Connecting Pre-season Screenings with Prospective Injury Data

by Laura McDonald in Sports Medicine Research (SMR): In the Lab & In the Field

Anterior reach asymmetry larger than 4 cm on the Y Balance test was associated with increased risk of non-contact injury in a sample of collegiate athletes.... Read more »

  • January 25, 2015
  • 09:19 PM
  • 31 views

Coding Responsibly Part I: Version Control

by Geoffrey Hannigan in Prophage

As a result of the growing number of resources allowing everyone to learn how to code, as well as numerous other awesome educational efforts, programming is steadily growing in popularity and accessibility...... Read more »

Perkel, J. (2011) Coding your way out of a problem. Nature Methods, 8(7), 541-543. DOI: 10.1038/nmeth.1631  

  • January 25, 2015
  • 05:17 PM
  • 27 views

Transferring primary symbionts: a missed link?

by Mauro Mandrioli in The aphid room

One of the most studied example of symbiotic interaction is related to aphids and their symbiont Buchnera aphidicola  that they host in specialized cells called bacteriocytes. Each aphid may host about 6 millions of Buchnera cells that are involved in the continuous overproduction of tryptophan and other amino acids. In addition to obligate symbionts, exemplified […]... Read more »

Moran NA, & Yun Y. (2015) Experimental replacement of an obligate insect symbiont. Proceedings of the National Academy of Sciences of the United States of America. PMID: 25561531  

  • January 25, 2015
  • 03:41 PM
  • 30 views

The unsolved mysteries of protein misfolding in common neurodegenerative diseases

by neurosci in Neuroscientifically Challenged

Throughout the 1970s, biochemist Stanley Prusiner was obsessed with trying to find the causative agent for a mysterious group of diseases. The diseases, which included kuru and Creutzfeldt–Jakob disease in humans and scrapie in sheep, were characterized by slowly-developing symptoms and neurodegeneration so severe it eventually caused the brain to take on the appearance of a sponge (due to myriad little holes that developed where grey matter was lost). By the time Prusiner began studying these diseases, they had all been experimentally transmitted to chimpanzees or other animals by injecting the animals with biological material from an infected host. So, the diseases seemed to be spread in an infectious manner, but scientists were still trying to identify the agents (e.g. viruses, bacteria, etc.) responsible for their transmission.Prusiner focused on trying to identify the agent behind the transmission of scrapie. He expected the agent to be a virus, but was confused when his tests repeatedly suggested it was composed of protein rather than the nucleic acids that would make up viral DNA. For, although there were others before Prusiner who had proposed ways proteins might be involved in the transmission of infectious diseases, these ideas had not been widely embraced by the scientific community. If Prusiner were to accept what his tests were indicating it would mean challenging the conventional understanding of the nature of infectious agents--which were considered to at least possess DNA or RNA--as well as the fundamental characteristics of proteins, which were not previously known to have infectious capabilities.In 1982, Prusiner published a manuscript outlining a hypothesis that scrapie was caused by a protein that had infectious qualities. He termed this protein a prion, for "proteinaceous infectious particle." Prusiner's ideas were considered somewhat heretical to virologists and others studying these diseases, and Prusiner was faced with criticism from scientists and non-scientists alike. But eventually Prusiner isolated the prion responsible for the transmission of scrapie, confirming his suspicions and silencing the naysayers. In 1997, he was awarded the Nobel Prize in Medicine for his discovery.Now it is well established that prions are agents of disease, in that they can spread from host to host just like typical pathogens. Once inside their host, however, they also have a unique capability of "infecting" other proteins. This results in the spreading of pathology through different regions of the brain, eventually leading to widespread neurodegeneration. But the story of infectious proteins does not end with the rare group of diseases studied by Prusiner. What we are coming to learn now is that this prion-like transmission of pathology between proteins may be a characteristic of other--much more common--diseases that involve neurodegeneration. While these diseases are very different from prion diseases in that they are not spread between individuals, the evidence suggests that the pathophysiology of neurodegenerative diseases like Alzheimer's disease (AD) and Parkinson's disease (PD) may involve proteins that behave like prions in their ability to infect other proteins within the brain of an affected individual.Alzheimer's, Parkinson's, and protein misfoldingThere are a number of diseases that are characterized by neurodegeneration, but AD and PD are the two neurodegenerative diseases that have the greatest impact on our society today in terms of mortality, disability, and economic burden. While both diseases involve neurodegeneration, however, they differ in the areas of the brain most affected (which plays a large role in determining their different symptomatic profiles). In AD, neurodegeneration becomes extensive in several areas of the brain, including areas of the cortex and hippocampus. These are areas that are especially important to cognition and memory, which helps to explain some of the cognitive deficits seen in the disease. In PD, neurons in structures that are part of the basal ganglia--a group of nuclei that play an important role in facilitating movement--are severely affected. The substantia nigra is particularly impacted, with somewhere between 50 and 70% of the neurons in this area being lost by the time of death. While the mechanisms underlying the large-scale neurodegeneration that occurs in AD and PD are not yet fully understood, in both diseases the neurodegeneration is associated with the accumulation of misfolded proteins in or around neurons.Proteins are essential to an extensive list of biological functions, including many vital processes like cellular metabolism, DNA replication, and cell signaling. When a protein is formed from a chain of amino acids, one of the final steps in its synthesis is to undergo a process of folding. The chain of amino acids (known as a polypeptide) that came together to create the protein is folded into a three-dimensional structure, and it is this three-dimensional structure--known as the tertiary structure--that decides the protein's eventual function. In other words, the folding--not simply the amino acid chain that makes up the protein--is what determines the role the protein will play in the body.Thus, protein folding is essential to synthesizing functional proteins. In AD and PD, however, proteins seem to fold incorrectly. This creates proteins with abnormal conformations composed of filaments that are pathologically twisted together instead of folded into a typical three-dimensional structure. These proteins are said to be in an amyloid state, because when this abnormal configuration was first noticed by renowned scientist Rudolf Virchow, he mistakenly identified them as starch (amyloid means starch-like). Once they have formed, these amyloid proteins have a tendency to aggregate into insoluble clumps.AD is characterized by aggregations of two types of proteins, called amyloid beta and tau, respectively. Amyloid beta is always present in the brain in the extracellular space around neurons, although its function has yet to be elucidated. In AD, however, it accumulates into clusters called amyloid plaques (aka senile plaques) that form outside and around neurons. These amyloid plaques often begin to form in the cortex in earlier stages of the disease, but propagate and eventually spread to the brainstem in the later stages. Tau is found within neurons, and is normally involved in maintaining the structure of the neuron through the stabilization of microtubules. When tau becomes misfolded, it can accumulate inside neurons into clusters called neurofibrillary tangles. In AD, these tangles generally begin to form in the brainstem, then spread to the temporal lobes and cortex.PD is characterized by the aggregation of a protein called alpha-synuclein. Alpha-synuclein is found within neurons, and may play various roles in regulating neurotransmitter release. In PD, it clumps into clusters called Lewy bodies (named for Frederic Lewy, who discovered them in 1912), which form inside the neuron. There is no consistent site of origin for Lewy bodies in the brain, but often they are first seen in the brainstem or olfactory bulb.Just like prions, misfolded proteins in neurodegenerative diseases like AD and PD seem to be able to influence previously healthy proteins to also undergo a process of misfolding, causing them to be transformed into an amyloid state. In one of the earliest studies to provide experimental evidence of this, amyloid plaque formation was induced in the brains of monkeys after brain tissue from human AD patients was injected into the monkeys' brains. This process of the spread of pathological misfolding from one protein to the next is referred to as seeded aggregation.Misfolding can be spread not only from protein to protein, but also from neuron to neuron. The way this happens is also still not very clear, but it is suspected that misfolded proteins may be taken up from the extracellular space into neurons or glial cells, where they begin to infect susceptible proteins... Read more »

Brettschneider, J., Tredici, K., Lee, V., & Trojanowski, J. (2015) Spreading of pathology in neurodegenerative diseases: a focus on human studies. Nature Reviews Neuroscience, 16(2), 109-120. DOI: 10.1038/nrn3887  

  • January 25, 2015
  • 03:36 PM
  • 29 views

Will the ocean follow the land? Marine ecosystems at a tipping point to follow terrestrial defaunation

by Jonathan Trinastic in Goodnight Earth

Data suggests that marine life may soon follow the mass extinctions seen in terrestrial ecosystems - similarities and differences discussed here!... Read more »

McCauley, D., Pinsky, M., Palumbi, S., Estes, J., Joyce, F., & Warner, R. (2015) Marine defaunation: Animal loss in the global ocean. Science, 347(6219), 1255641-1255641. DOI: 10.1126/science.1255641  

  • January 25, 2015
  • 09:13 AM
  • 31 views

Whose Culture is it Anyway? Disentangling Culture and Eating Disorders - Part 3

by Andrea in Science of Eating Disorders

The articles I’ve looked at so far in this series (Becker, in part 1, and Keel and Klump in part 2) give us some insight into the idea that the link between “Western” societies and eating disorders is more complex than a simple matter of media exposure. But, having read these studies, I was still left a bit wanting in terms of unpacking that black box of “culture” that gets tossed around in scholarly and popular literature. What, exactly, are we talking about when we talk culture in eating disorders?... Read more »

  • January 24, 2015
  • 01:39 PM
  • 70 views

Lucid dreaming: The similarities between dreaming and wakefulness

by Gabriel in Lunatic Laboratories

To control one’s dreams and to live out there what is impossible in real life — a truly tempting idea. Some people — so-called lucid dreamers — can do this. Researchers have discovered that the brain area which enables self-reflection is larger in lucid dreamers. Thus, lucid dreamers are possibly also more self-reflecting when they are awake.... Read more »

Filevich E, Dresler M, Brick TR, & Kühn S. (2015) Metacognitive mechanisms underlying lucid dreaming. The Journal of neuroscience : the official journal of the Society for Neuroscience, 35(3), 1082-8. PMID: 25609624  

  • January 24, 2015
  • 09:39 AM
  • 50 views

Urban Legends In The World of Clinical Trials

by Neuroskeptic in Neuroskeptic_Discover

Ethnographer Jill A. Fisher offers a fascinating look at the rumors and urban legends that circulate among the volunteers who get paid to take part in medical research: Stopped hearts, amputated toes and NASA




Fisher visited six clinical trial facilities across the USA. All of these facilities were exclusively devoted to running phase I trials, testing new drugs to see if they are safe in humans. She spent a total of 450 hours in the field, getting to know the 'guinea pigs', and the staf... Read more »

  • January 24, 2015
  • 05:34 AM
  • 52 views

Hartnup disease in coeliac disease: lessons for 'some' autism?

by Paul Whiteley in Questioning Answers

The paper by Thomas Ciecierega and colleagues [1] (open-access) talking about 'refractory' coeliac disease (CD) - a lack of, or diminished response to a gluten-free diet (the primary management option for CD) - and the subsequent diagnosis of Hartnup disease in a young girl is fodder for today's brief post.I already had a big bowl of curly-toed weirdo for breakfast.Describing how authors first diagnosed her with CD but witnessed "only mild clinical and laboratory improvement" following a regime of implementing a gluten-free diet and supplementation with various other nutrients via Total Parental Nutrition among other things, further examinations led to a suspicion of a niacin deficiency. The quite remarkable turn-around in clinical fortunes witnessed following the use of "oral niacin (50 mg three times daily)" led to the final diagnosis of Hartnup disease. This was confirmed by some bog-standard chromatography of a urine specimen which "showed increased levels of excreted neutral amino acids (glutamine, valine, phenylalanine, leucine, asparagine, citrulline, isoleucine, threonine, alanine, serine, histidine, tyrosine, tryptophan)." The authors conclude: "Co-occurrence of Hartnup disease and CD is extremely rare." I'd be minded to say, rare yes, but not unheard of in the peer-reviewed domain [2].This case report stuck out to me for a few reasons. Coeliac disease and the broader spectrum of non-coeliac gluten sensitivity (NCGS) or non-coeliac wheat sensitivity if you wish, are quite a regular feature on this blog; even more so with the news that rates of CD are increasing [3]. Treatment of said 'gluten spectrum conditions' involves the use of a diet devoid of gluten which is found in various cereal products. Said diet also seemingly overlapping with other areas/conditions outside of CD including autism (see here). This is not however, the first time that a gluten-free diet has been talked about as not cutting the mustard in cases of something that initially looked like typical CD (see here).Hartnup disease is something I came across quite early on in my autism research career. One of the compounds that I had some interest in called trans-indolyl-acryloylglycine (IAG) (see here) was thought to be derived from that ever so versatile aromatic amino acid called tryptophan. Whilst IAG turned out not to be the 'autism biomarker' that we initially thought it might be, one of the other clinical occasions that this compound cropped up in was, yes you guessed it, Hartnup disease. Hartnup disease and tryptophan have an interesting association [4].Although not wishing to make connections where none may exist, the presentation of Hartnup disease might also manifest in behaviour as well as the more typical skin symptoms which can present [5]. I stumbled across an interesting BBC news article on the condition that mentions Hartnup disease in the same breath as 'the symptoms of autism' which, although rare, is something I've often thought merits further research attention. I'm not necessarily saying that autism = refractory coeliac disease = Hartnup disease - don't be silly - but it strikes me that there may be more to see in connecting some individual cases based on some biological overlap...So: Paolo Nutini with Candy.----------[1] Ciecierega T. et al. Severe persistent unremitting dermatitis, chronic diarrhea and hypoalbuminemia in a child; Hartnup disease in setting of celiac disease. BMC Pediatrics 2014, 14:311 .[2] Coudray-Lucas C. et al. Association of celiac disease and Hartnup's disease? Value of the tryptophan loading test. Gastroenterol Clin Biol. 1986 Feb;10(2):187-8.[3] Zingone F. et al. Socioeconomic variation in the incidence of childhood coeliac disease in the UK. Arch Dis Child. 2015. 22 Jan.[4] Milovanović DD. A clinicobiochemical study of tryptophan and other plasma and urinary amino acids in the family with Hartnup disease. Adv Exp Med Biol. 2003;527:325-35.[5] Patel AB. & Prabhu AS. Hartnup disease. Indian J Dermatol. 2008 Jan;53(1):31-2.----------Ciecierega, T., Dweikat, I., Awar, M., Shahrour, M., Libdeh, B., & Sultan, M. (2014). Severe persistent unremitting dermatitis, chronic diarrhea and hypoalbuminemia in a child; Hartnup disease in setting of celiac disease BMC Pediatrics, 14 (1) DOI: 10.1186/s12887-014-0311-6... Read more »

  • January 23, 2015
  • 07:16 PM
  • 85 views

Mothers don’t speak clearly to their babies

by Gabriel in Lunatic Laboratories

People have a distinctive way of talking to babies and small children: We speak more slowly, using a sing-song voice, and tend to use cutesy words like "tummy". While we might be inclined to think that we talk this way because it is easier for children to understand, new research suggests that, surprisingly, mothers may actually speak less clearly to their infants than they do to adults.... Read more »

Andrew Martin, Thomas Schatz, Maarten Versteegh, Kouki Miyazawa, Reiko Mazuka, Emmanuel Dupoux, and Alejandrina Cristia. (2015) Kouki Miyazawa, Reiko Mazuka, Emmanuel Dupoux, and Alejandrina Cristia. Mothers Speak Less Clearly to Infants Than to Adults: A Comprehensive Test of the Hyperarticulation Hypothesis. Psychological Science. info:/10.1177/0956797614562453

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