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  • September 17, 2014
  • 08:30 AM
  • 8 views

Does Your Cat Sniff New Food?

by CAPB in Companion Animal Psychology Blog

New research investigates which feline behaviours show that cats find food tasty. Photo: FreeBirdPhotos / ShutterstockThere are certain things we can take for granted when feeding the cat: the pitiful miaows that become increasingly strident, the anticipatory purring when you move towards the cat food, and the way the cat wraps herself around your leg as if you’re her best friend ever. But when you put the food down, is there any guarantee she will eat it? Cat food manufacturers have teams of cats that work as food testers, to make sure new foods are as tasty as can be. This study, by Aurélie Becques et al (in press) took place at the Panelis Diana Pet Food Division. Here, cats are housed in groups in an indoor environment with access to the outdoors. Two such groups of cats (17 cats in total) took part in this study.The cats are given free access to kibble for twenty hours of the day, to mimic the most common way of feeding cats in the home. They are fed via a feeding station, which only one cat can enter at a time. The length of time they spend in the station and the amount of food they eat is all measured. A video camera captures their behaviour.The study investigated feline behaviour when eating a Very Palatable Kibble (VPK) compared to a Less Palatable Kibble. In fact, both kibbles were the same (Royal Canin), but different coatings were applied. The coatings were both made of poultry fat and had the same number of calories, but one was previously shown to be very tasty to cats and the other less so. Both sets of cats had in fact been fed these two foods at some point in the past. To further enhance the tastiness of the Very Palatable Kibble, it was mixed with some tuna. This combination was something the cats had not experienced before. It also had the effect of making the VPK slightly less calorie dense.The cats were given a two day test of each type of food. Since this is a working cat food testing environment, in between the sessions reported here, they were given a different food according to the current rotation.The results showed that when cats were offered the Very Palatable Kibble, they ate more each day (81g on average compared to 53g). Because cats made different numbers of visits to the feeding station each day, the researchers compared the first three visits and the last visit of each day. With the exception of the last visit on the first day, the cats ate more of the VPK every time they went to the feeding station.Cats are good at regulating their food intake, and so it is surprising that they ate more calories when fed the VPK. However, since the study only had two days per food, it is possible the cats would have adjusted their food intake over time.Whether the cat was eating in a sitting or standing position, the speed at which it ate, the length of time from approaching the bowl to starting to eat, and the total amount of licking, was the same for the two foods. Previous research has suggested that licking the lips and grooming the face is associated with finding food tasty, whereas cats lick their nose when they don’t like it so much. The researchers sometimes couldn’t tell whether the cat was licking its lips or its nose, especially at night when it was dark, so this remains a question for future research.Sniffing behaviour turns out to be an indicator of a new food’s perceived tastiness. On the first day of LPK, the cats spent a lot more time sniffing the food on the first two visits to the feeding station. The researchers say, “One may have expected that the novelty of the diet should have caused more sniffing. On the contrary the cats tended to sniff more LPK, a diet that they have already experienced, than VPK that they have previously experienced but without the addition of tuna. The tuna was very odorant and it seemed that this odor was attractive enough to elicit eating in a short lapse of time. On the other hand the longer duration of sniffing the LPK diet may correspond to a hesitation to consume a less palatable diet.”The researchers say the cat’s behaviour is an indication of how tasty it finds the food. So if you offer a new food and your cat is sniffing at it, it’s probably not a good sign.Is your cat fussy about food?ReferenceBecques, A., Larose, C., Baron, C., Niceron, C., Feron, C., & Gouat, P. (2014). Behaviour in order to evaluate the palatability of pet food in domestic cats Applied Animal Behaviour Science , 159, 55-61 : 10.1016/j.applanim.2014.07.003 ... Read more »

Becques, A., Larose, C., Baron, C., Niceron, C., Feron, C., & Gouat, P. (2014) Behaviour in order to evaluate the palatability of pet food in domestic cats. Applied Animal Behaviour Science , 55-61. info:/10.1016/j.applanim.2014.07.003

  • September 17, 2014
  • 06:29 AM
  • 16 views

Autoimmune disease risk and eating disorders

by Paul Whiteley in Questioning Answers

"We were set up. The cops were waiting for us.""We observed an association between eating disorders and several autoimmune diseases with different genetic backgrounds. Our findings support the link between immune-mediated mechanisms and development of eating disorders".So said the paper by Anu Raevuori and colleagues [1] (open-access) based on an analysis of over 2300 people "treated at the Eating Disorder Unit of Helsinki University Central Hospital between 1995 and 2010" compared with nearly 10,000 control participants (so yes, this was quite a well-powered study).The Raevuori paper is open-access but if you want a few choice details, here goes...Based on a body of research literature looking at a possible association between eating disorders and autoimmune conditions like type 1 diabetes [2], authors set about testing the hypothesis on a large scale on whether "the risk of autoimmune diseases would be increased in individuals with eating disorders both prior and after the onset of the treatment for an eating disorder".Having already mentioned how large a scale the authors' participants groups were, various eating disorder diagnoses were confirmed based on ICD-10 criteria [3] and both research and control populations were assessed for some 30 autoimmune conditions based on existing hospital discharge registry. "Period and lifetime prevalences" were calculated from the data. Results: "Participants with BN [bulimia nervosa] made up the largest patient group (54.0%), followed by those with AN [anorexia nervosa] (38.8%), and those with BED [binge eating disorder] (7.3%)". Over 5% of those diagnosed with an eating disorder had been diagnosed with one or more autoimmune conditions compared with just under 3% of controls when it came to looking at period prevalence (at the onset of treatment). Long quote coming up... "The risk of prior diagnosis of endocrinological autoimmune diseases (OR 3.3, 95% CI 2.4–4.6, P<0.001), of gastroenterological immune-mediated diseases (OR 2.0, 95% CI 1.3–3.1, P = 0.002), and of autoimmune diseases combined (OR 2.1 95% CI 1.7–2.7, P<0.001) was significantly higher among patients than among matched controls".With regards to lifetime prevalence (over the whole study period) "8.9% (N = 209) of patients and 5.4% of control individuals (N = 509) had ever been diagnosed with one or more autoimmune disease". Whilst only looking like a relatively small percentage difference in the rates of autoimmune conditions between the groups, it is the scale of the Raevuori study in terms of participant numbers which gives the data some 'edge'. As the authors also note, their use of the category BED - binge eating disorder - is also another plus to their study given it's recent inclusion into DSM-5 (see here).As I always seem to be about papers mentioned on this blog, I was really quite interested in the results presented by Raevuori et al and their potential implications for how we describe eating disorders and the potential mechanisms involved in onset. Research into autoimmune conditions has recently been producing some rather important associations as per my covering of things like a [possible] link between autoimmune disorders following trauma and PTSD (see here) and even a suggested connection with some epilepsy (see here).Raevuori and colleagues discuss several pertinent mechanisms potentially linking their findings including the ever-present issue of inflammation and: "Pro-inflammatory cytokines and antibodies/autoantibodies against neuronal antigens". They also mention some possible role for "intestinal microflora contributing to the development of cross-reactive neuronal autoantibodies [providing] a link between gut and brain" and the growing fascination with all-things gut microbiome. Their finding of a greater frequency of the inflammatory bowel disease (IBD), Crohn's disease in their eating disorder cohort offers some evidence for this assertion as a function of the growing interest in gut bacteria and IBDs [4].Without hopefully going too far off tangent from the Raevuori paper, I started to think about how these results might also fit in with some of the research done on autism and whether there may be a bigger picture here. Eating disorders have been mentioned alongside the label autism quite a few times in the research literature [5]. My previous discussions on signs of autism in cases of eating disorders (see here) is one example. Likewise, autoimmune conditions and autism also seem to have something of a connection (see here) alongside presented data on markers of autoimmunity in cases of autism (see here and see here). One can perhaps see how the various elements - immune function, inflammation, gut bacteria, gut permeability? - might be intertwined, albeit in a rather complex fashion...?Music then, and Naive by The Kooks.----------[1] Raevuori A. et al. The increased risk for autoimmune diseases in patients with eating disorders. PLoS One. 2014 Aug 22;9(8):e104845.[2] Young V. et al. Eating problems in adolescents with Type 1 diabetes: a systematic review with meta-analysis. Diabet Med. 2013 Feb;30(2):189-98.[3] Herpetz S. et al. The Diagnosis and Treatment of Eating Disorders. Dtsch Arztebl Int. Oct 2011; 108(40): 678–685.[4] Manichanh C. et al. The gut microbiota in IBD. Nat Rev Gastroenterol Hepatol. 2012 Oct;9(10):599-608.[5] Huke V. et al. Autism spectrum disorders in eating disorder populations: a systematic review. Eur Eat Disord Rev. 2013 Sep;21(5):345-51.----------Raevuori A, Haukka J, Vaarala O, Suvisaari JM, Gissler M, Grainger M, Linna MS, & Suokas JT (2014). The increased risk for autoimmune diseases in patients with eating disorders. PloS one, 9 (8) PMID: 25147950... Read more »

Raevuori A, Haukka J, Vaarala O, Suvisaari JM, Gissler M, Grainger M, Linna MS, & Suokas JT. (2014) The increased risk for autoimmune diseases in patients with eating disorders. PloS one, 9(8). PMID: 25147950  

  • September 16, 2014
  • 02:50 AM
  • 62 views

The schizophrenias (plural)

by Paul Whiteley in Questioning Answers

A micropost if you will, to draw your attention to the paper by Javier Arnedo and colleagues [1] mentioning the concept of 'the schizophrenias' (plural). Some media coverage of this paper can be found here and here. The crux of the paper is that although currently unified by a diagnostic label, schizophrenia seems to be comprised of various conditions: "caused by a moderate number of separate genotypic networks associated with several distinct clinical syndromes"."... dogs and cats living together... mass hysteria!"I'm going to say little else about this findings aside from stressing how (a) this re-conceptualisation of schizophrenia into a more plural condition is not a million miles away from moves in other areas of psychiatry (see here) and (b) the reliance on genetic mutation (SNPs) in the paper whilst interesting, perhaps overlooks other non-structural genomic factors potentially implicated in cases of the schizophrenias (see here). That also there may be some 'common ground' between the schizophrenias and other conditions (see here) might also be important for this growing tide of psychiatric plurality.Music to close. Mr Blue Sky (live).----------[1] Arnedo J. et al. Uncovering the Hidden Risk Architecture of the Schizophrenias: Confirmation in Three Independent Genome-Wide Association Studies. Am J Psychiatry. 2014. September 15.----------Javier Arnedo, Dragan M. Svrakic, Coral del Val, Rocío Romero-Zaliz, Helena Hernández-Cuervo, Molecular Genetics of Schizophrenia Consortium, Ayman H. Fanous, Michele T. Pato, Carlos N. Pato, Gabriel A. de Erausquin, C. Robert Cloninger, & Igor Zwir (2014). Uncovering the Hidden Risk Architecture of the Schizophrenias: Confirmation in Three Independent Genome-Wide Association Studies The American Journal of Psychiatry : doi:10.1176/appi.ajp.2014.14040435... Read more »

Javier Arnedo, Dragan M. Svrakic, Coral del Val, Rocío Romero-Zaliz, Helena Hernández-Cuervo, Molecular Genetics of Schizophrenia Consortium, Ayman H. Fanous, Michele T. Pato, Carlos N. Pato, Gabriel A. de Erausquin.... (2014) Uncovering the Hidden Risk Architecture of the Schizophrenias: Confirmation in Three Independent Genome-Wide Association Studies. The American Journal of Psychiatry. info:/doi:10.1176/appi.ajp.2014.14040435

  • September 15, 2014
  • 04:50 PM
  • 71 views

Religion And Morality: Belief Isn't Better

by Alexis Delanoir in How to Paint Your Panda

It's no secret that when it comes to what the public thinks, atheists are usually at the bottom of the "nice" list. A survey in 2006 found that atheists were the least trusted minority group in America. Similar studies find that atheists are mistrusted and are seen as more immoral than their religious counterparts. But are these views justified? A new study by Hofmann et al. (2014) suggests they aren't, and this conclusion is consistent with other available data.... Read more »

Gervais WM, Shariff AF, & Norenzayan A. (2011) Do you believe in atheists? Distrust is central to anti-atheist prejudice. Journal of personality and social psychology, 101(6), 1189-206. PMID: 22059841  

Hofmann W, Wisneski DC, Brandt MJ, & Skitka LJ. (2014) Morality in everyday life. Science (New York, N.Y.), 345(6202), 1340-3. PMID: 25214626  

  • September 15, 2014
  • 04:01 PM
  • 42 views

Humanized FoxP2 and the timing of habits

by Björn Brembs in bjoern.brembs.blog

Last week, Elizabeth Pennisi asked me to comment on the recent paper from Schreiweis et al. entitled “Humanized FoxP2 accelerates learning by enhancing transitions from declarative to procedural performance”. Since I don’t know how much, if anything, of my answers […] ↓ Read the rest of this entry...... Read more »

Schreiweis, C., Bornschein, U., Burguiere, E., Kerimoglu, C., Schreiter, S., Dannemann, M., Goyal, S., Rea, E., French, C., Puliyadi, R.... (2014) Humanized Foxp2 accelerates learning by enhancing transitions from declarative to procedural performance. Proceedings of the National Academy of Sciences. DOI: 10.1073/pnas.1414542111  

  • September 15, 2014
  • 12:58 PM
  • 69 views

The Genetic Roots of Schizophrenia

by Gabriel in Lunatic Laboratories

I have a friend who lost an eye — not in a war zone like you might suspect given my background — but to his brother. Yes, you read that correctly, his brother tried to kill him and in the process he lost his eye. I’ve told this story before, but whenever new schizophrenia research comes out I feel the need to tell it again. While he has forgiven his brother (partly because not long after, he was diagnosed as schizophrenic), he will not be able to see him again until he is released from prison. A tragedy that could’ve been avoided had he been diagnosed sooner.... Read more »

avier Arnedo, M.S.; Dragan M. Svrakic, M.D., Ph.D.; Coral del Val, Ph.D.; Rocío Romero-Zaliz, Ph.D.; Helena Hernández-Cuervo, M.D.; Molecular Genetics of Schizophrenia Consortium; Ayman H. Fanous, M.D.; Michele T. Pato, M.D.; Carlos N. Pato, M.D., Ph.D. (2014) Uncovering the Hidden Risk Architecture of the Schizophrenias: Confirmation in Three Independent Genome-Wide Association Studies. The American Journal of Psychiatry. info:/10.1176/appi.ajp.2014.14040435

  • September 15, 2014
  • 09:49 AM
  • 44 views

Great Apes Share Our Ability to Predict Goal-Oriented Actions

by amikulak in Daily Observations

Within a year after birth, human infants develop the ability to direct their attention to the anticipated goal of another person’s movement, before it has occurred.  So, for example, our […]... Read more »

  • September 15, 2014
  • 08:13 AM
  • 62 views

Pupils benefit from praise, but should teachers give it to them publicly or privately?

by BPS Research Digest in BPS Research Digest

There's a best practice guide for teachers, produced by the Association of School Psychologists in the US, that states praise is best given to pupils in private. This advice is not based on experimental research - there hasn't been any - but on surveys of student preferences, and on the rationale that pupils could be embarrassed by receiving praise in public.Now, in the first study of its kind, John Blaze and his colleagues have systematically compared the effect of public and private praise (also known as "loud" and "quiet" praise) on classroom behaviour. They found that praise had a dramatic beneficial effect on pupils' behaviour, and it didn't matter whether the praise was private or public.The research was conducted at four high-school public classrooms in rural south-eastern United States (the equivalent to state schools in the UK). The classes were mixed-sex, with a mixture of mostly Caucasian and African American pupils, with between 16 and 25 pupils in each class. The children were aged 14 to 16. Three of the teachers were teaching English, the other taught Transition to Algebra.The teachers were given training in appropriate praise: it must be contingent on good behaviour; make clear to the pupil why they are being praised; immediate; and effort-based. During the test sessions of teaching, the teachers carried a buzzer on their belt that prompted them, once every two minutes, to deliver praise to one of their pupils, either loudly so the whole class could hear (in the loud condition) or discreetly, by a whisper in the ear or pat on the shoulder, so that hopefully only the child knew they were being praised (in the quiet condition). For comparison, there were also baseline teaching sessions in which the teachers simply carried out their teaching in their usual style.Trained observers stationed for 20-minute sessions in the classrooms monitored the teachers' praise-giving and the behaviour of the pupils across the different conditions. They found that frequent praise increased pupils' on-task behaviours, such as reading or listening to the teacher, by 31 per cent compared with baseline, and this improvement didn't vary according to whether the praise was private or public. Frequent praise of either manner also reduced naughty behaviours by nearly 20 per cent.Blaze and his team said that the debate over praise will likely continue, but they stated their results are clear: "both loud and quiet forms of praise are effective tools that can have dramatic effects at the secondary level." A weakness of the study is that the researchers didn't monitor the teachers' use of reprimands, which likely reduced as they spent more time delivering praise._________________________________ Blaze JT, Olmi DJ, Mercer SH, Dufrene BA, & Tingstom DH (2014). Loud versus quiet praise: A direct behavioral comparison in secondary classrooms. Journal of school psychology, 52 (4), 349-60 PMID: 25107408 Post written by Christian Jarrett (@psych_writer) for the BPS Research Digest.

... Read more »

Blaze JT, Olmi DJ, Mercer SH, Dufrene BA, & Tingstom DH. (2014) Loud versus quiet praise: A direct behavioral comparison in secondary classrooms. Journal of school psychology, 52(4), 349-60. PMID: 25107408  

  • September 15, 2014
  • 04:57 AM
  • 57 views

How to increase children’s patience in 5 seconds

by Richard Kunert in Brain's Idea

A single act increases adults’ compliance with researchers. The same act makes students more likely to volunteer to solve math problems in front of others. Moreover, it makes four-year-olds more patient. What sounds like a miracle cure to everyday problems is actually the oldest trick in the book: human touch. How do researchers know this? […]... Read more »

  • September 15, 2014
  • 04:47 AM
  • 48 views

Zinc and copper and autism

by Paul Whiteley in Questioning Answers

The paper by Li and colleagues [1] looking at serum copper (Cu) and zinc (Zn) levels in a group of participants diagnosed with an autism spectrum disorder (ASD) is the source material for today's post. Highlighting how "mean serum Zn levels and Zn/Cu ratio were significantly lower in children with ASD compared with normal cases... whereas serum Cu levels were significantly higher" the continued focus on the metallome in autism carries on at a pace. I should at this point out that I'm not in favour of the use of the word 'normal' in this or any context (anyone who feels that they are normal, please make themselves known to the population at large)."Bring me... the bore worms!"Anyhow... I've talked zinc and autism / other conditions on this blog quite a few times (see here and see here). Alongside other more recent data [2] there is a growing realisation that zinc deficiency present in at least some diagnosed on the autism spectrum might have quite a few implications. With this thought in mind, I might also draw your attention to the recent paper by Chaves-Kirsten and colleagues [3] talking about how zinc might also show some connection to the protein kinase of the hour, mTOR (see here) and in particular reducing mTOR levels in a rodent model of autism. This follows other work in this area [4].The Li paper alongside looking at individual levels of zinc and copper and how they seemed to correlate with presented symptoms according to the Childhood Autism Rating Scale (CARS) also talks about the zinc/copper ratio which is something that has been previously discussed in the peer-reviewed literature with reference to autism and various other conditions as per the excellent review by Osredkar & Sustar [5] (open-access). The paper by Faber and colleagues [6] for example, indicated that a low Zn/Cu ratio may "indicate decrement in metallothionein system functioning". They also talked about how issues with this ratio "may be a biomarker of heavy metal, particularly mercury, toxicity in children with ASDs" as per the various biological uses of metallothionein [7]. I know this moves discussions into some quite uncomfortable realms but science is science (see here) and one should not be afraid to have scientific discourse on any topic. Importantly too, the Faber results also seemed to show more than a passing similarity to those presented by Li et al. Same goes for the paper by Russo and colleagues [8].The other interesting point recorded by Li and colleagues was their use of the good 'ole ROC curve as a means to indicate an "auxiliary diagnosis of autism". More frequently linked to a certain Egyptian-Saudi autism research group (see here), ROC curves - "a fundamental tool for diagnostic test evaluation" - basically plots the true positive rate against the false positive rate for a test. Li et al projected the cut-off value for the Zn/Cu ratio to be 0.665 for a diagnosis, with "a sensitivity of 90.0% and a specificity of 91.7%". Bearing in mind the relatively small participants included for analysis (n=60), those aren't bad figures for sensitivity and specificity remembering my recent discussions on the observation-based classifier (OBC) from Wall and colleagues [9] (see here) and what they got.There's little more for me to say about the Li data that I haven't already said here and in other posts on this topic. If you want to read a little more about the possible role of zinc and copper in cases of autism, the report by Bjorklund [10] covers quite a bit of the literature on possible links. The next question is what might we be able to do about any issues in this area? [11]So then, The Last of the Famous International Playboys? (not me of course..)----------[1] Li SO. et al. Serum copper and zinc levels in individuals with autism spectrum disorders. Neuroreport. 2014 Aug 26.[2] Grabrucker S. et al. Zinc deficiency dysregulates the synaptic ProSAP/Shank scaffold and might contribute to autism spectrum disorders. Brain. 2014 Jan;137(Pt 1):137-52.[3] Chaves-Kirsten GP. et al. Prenatal zinc prevents mTOR disturbance in a rat model of autism induced by prenatal lipopolysaccharide. Brain, Behavior & Immunity. 2014; 40: e11-e12.[4] McClung JP. et al. Effect of supplemental dietary zinc on the mTOR signaling pathway in skeletal muscle from post-absorptive mice. FASEB J. 2006; 20 (Meeting Abstract Supplement) A627.[5] Osredkar J. & Sustar N. Copper and Zinc, Biological Role and Significance of Copper/ZincImbalance. Journal of Clinical Toxicology. 2011; S3.[6] Faber S. et al. The plasma zinc/serum copper ratio as a biomarker in children with autism spectrum disorders. Biomarkers. 2009 May;14(3):171-80.[7] Coyle P. et al. Metallothionein: the multipurpose protein. Cell Mol Life Sci. 2002 Apr;59(4):627-47.[8] Russo AJ. et al. Plasma copper and zinc concentration in individuals with autism correlate with selected symptom severity. Nutr Metab Insights. 2012 Feb 28;5:41-7.[9] Duda M. et al. Testing the accuracy of an observation-based classifier for rapid detection of autism risk. Transl Psychiatry. 2014 Aug 12;4:e424.[10] Bjorklund G. The role of zinc and copper in autism spectrum disorders. Acta Neurobiol Exp (Wars). 2013;73(2):225-36.[11] Russo AJ. & Devito R. Analysis of Copper and Zinc Plasma Concentration and the Efficacy of Zinc Therapy in Individuals with Asperger's Syndrome, Pervasive Developmental Disorder Not Otherwise Specified (PDD-NOS) and Autism. Biomark Insights. 2011;6:127-33.----------... Read more »

  • September 14, 2014
  • 06:57 PM
  • 58 views

JUST PUBLISHED: The Dance of Communication: Retaining Family Membership Despite Non-Speech Dementia

by Mark Rubin in The University of Newcastle's School of Psychology Newsline

As the majority of people in developed countries will be touched in some way by dementia in the 21st century, current ways of interacting in dementia care may no longer be acceptable. In particular, when people with dementia appear uncommunicative, their retained awareness and ability to interact is often dismissed or overlooked. Facing social isolation and further decline, many languish with unmet needs for human interaction. However, the intimacies of family interaction in dementia care settings point to a brighter future. A recently published article by Bruce Walmsley and Lynne McCormack filmed speech and non-speech relational communication within families that included a member with severe dementia and limited or absent speech. Exploring the phenomenon of retained awareness, the researchers sought to understand the reciprocal efforts used by all family members to engage in alternative patterns of communication. Interactive patterns revealed ‘in-step’ interactions that stimulated spontaneity and reciprocity and ‘out-of-step’ interactions that heightened frustration and anxiety. Family interactions could be ‘in-step’ and ‘out-of-step’ depending on relatives’ presumptions of awareness, timing of response, perceived interpretation, and what appeared to be pre-existing relational patterns. This study also found that retained awareness may exist at a level previously unrecognised in people with minimal or absent speech as a result of severe dementia. Awareness fluctuated from sensory and perceptual levels to complex movement, goal directed behaviour and self-awareness. This study recognised the difficulty of interpreting awareness related to individual experience, especially in light of minimal speech. However, interactions and expressions of emotion were considered to represent underlying awareness in light of the observed family interactions. By exploring the lived experience of families, it revealed the efforts and willingness of all family members to retain family membership. As a pilot study, it offered a platform for future studies exploring changes in awareness and communication as individuals move from moderate to severe dementia. Importantly, this study reminds us that people with dementia may be more aware and communicative than first assumed.  For more information about this work please see the following journal article:Walmsley, B., & McCormack, L. (2013). The dance of communication: Retaining family membership despite severe non-speech dementia Dementia, 13 (5), 626-641 DOI: 10.1177/1471301213480359 or contact Dr Lynne McCormack at Lynne.McCormack@newcastle.edu.au... Read more »

  • September 14, 2014
  • 10:03 AM
  • 54 views

Sound Aggression

by Rodney Steadman in Gravity's Pull

Maybe it was all the Who noise that made the Grinch so aggressive. Recent research out of Bulgaria suggests a link between noise pollution and displaced aggression.... Read more »

  • September 12, 2014
  • 11:47 AM
  • 64 views

Insulin, growth hormone and risk of schizophrenia?

by Paul Whiteley in Questioning Answers

"Overall, the present findings suggest that metabolic and hormonal disturbances such as effects on insulin and growth hormone may represent a vulnerability factor to develop mental disorders". That was the conclusion reported by van Beveren and colleagues [1] (open-access) looking at "disruption of insulin and growth factor signaling pathways as an increased risk factor for schizophrenia"."Years ago you served my father in the Clone Wars"Drawing on data derived from participants taking part in the Genetic Risk and Outcome of Psychoses (GROUP) study [2] researchers looked at blood serum samples "to measure the levels of 184 molecules in serum from 112 schizophrenia patients, 133 siblings and 87 unrelated controls". Multiplex immunoassay was the analytical weapon of choice.The results indicated that "10 proteins were present at significantly different levels between schizophrenia patients and controls" which can be seen here. The insulin synthesis pathway showed more than a passing connection to group differences as per the appearance of insulin and precursor molecules such as proinsulin and C-peptide (connecting peptide). Some of these pathway molecules were also reported to be altered in the sibling group(s) too. Growth hormone also featured as a potentially distinguishing marker, as did adiponectin among others.The authors conclude (again) their findings for "the presence of a molecular endophenotype involving disruption of insulin and growth factor signaling pathways as an increased risk factor for schizophrenia". Perhaps even more interesting is their view of the body of work [3] suggesting that "antipsychotic drugs are known to increase peripheral glucose levels" and how, in light of their findings, "these effects may be intrinsically related to the therapeutic mechanism of action by increasing the peripheral blood glucose levels and thereby increasing glucose availability in the brain".As the authors point out, there is still quite a bit more to do in this area including examining larger samples sizes and importantly, looking at blood glucose levels as a measure of insulin resistance to further complement their findings. I note however that issues with insulin function being potentially related to mood and other psychiatric conditions are nothing new as per the various literature in this area. Anderson and colleagues [4] for example, talked about a diagnosis of diabetes doubling the odds of comorbid depression. Bearing in mind, the possible interfering effect of medication, Verma and colleagues [5] found that in drug-naive (unmedicated) patients with first-episode psychosis there was a significantly increased likelihood of diabetes to be present compared with age and sex-matched asymptomatic control participants. I don't doubt however, that any relationship is going to be complicated.Finally, and bearing in mind the prime directive of this blog (no medical or clinical advice given or intended), there is the question of how this research might translate into therapeutic intervention. A final quote from the authors on this and the possibility of: "novel disease prevention approaches, which could involve nutrition modification, stress reduction and pharmaco-therapeutic interventions, including the application of well-tolerated drugs that combat insulin resistance". Alongside the dietary aspect (which is something very favourable to this blog for lots of reasons), I am wondering whether we could also learn something from times gone by [6]? Perhaps even the appliance of prophylactic psychiatry [7]?Music to close and Andrea Bocelli sings Funiculì, Funiculà...----------[1] van Beveren NJM. et al. Evidence for disturbed insulin and growth hormone signaling as potential risk factors in the development of schizophrenia. Translational Psychiatry. 2014; 4: e430.[2] Korver N. et al. Genetic Risk and Outcome of Psychosis (GROUP), a multi-site longitudinal cohort study focused on gene-environment interaction: objectives, sample characteristics, recruitment and assessment methods. Int J Methods Psychiatr Res. 2012 Sep;21(3):205-21.[3] Wirshing DA. et al. The effects of novel antipsychotics on glucose and lipid levels. J Clin Psychiatry. 2002 Oct;63(10):856-65.[4] Anderson RJ. et al. The prevalence of comorbid depression in adults with diabetes: a meta-analysis. Diabetes Care. 2001 Jun;24(6):1069-78.[5] Verma SK. et al. Metabolic risk factors in drug-naive patients with first-episode psychosis. J Clin Psychiatry. 2009 Jul;70(7):997-1000.[6] Anderson K. et al. Salsalate, an old, inexpensive drug with potential new indications: a review of the evidence from 3 recent studies. Am Health Drug Benefits. 2014 Jun;7(4):231-5.[7] Sawa A. & Seidman LJ. Is Prophylactic Psychiatry around the Corner? Combating Adolescent Oxidative Stress for Adult Psychosis and Schizophrenia. Neuron. 2014; 83: 991-993.----------van Beveren NJ, Schwarz E, Noll R, Guest PC, Meijer C, de Haan L, & Bahn S (2014). Evidence for disturbed insulin and growth hormone signaling as potential risk factors in the development of schizophrenia. Translational psychiatry, 4 PMID: 25158005... Read more »

  • September 12, 2014
  • 11:18 AM
  • 83 views

Psychologists have compared the mental abilities of Scrabble and crossword champions

by BPS Research Digest in BPS Research Digest

Completed Scrabble (left) and crossword grids (image from Toma et al 2014).Every year, hundreds of word lovers arrive from across the US to compete in the American Crossword Puzzle tournament. They solve clues (e.g. "caught some Z's") and place the answers (e.g. "sleep") in a grid. Meanwhile, a separate group of wordsmiths gather regularly to compete at Scrabble, the game that involves forming words out of letter tiles and finding a suitable place for them on the board.Both sets of players have exceptional abilities, but how exactly do they differ from each other and from non-players of matched academic ability? Some answers are provided by Michael Toma and his colleagues, who have performed the first detailed comparison of the mental skills of the most elite crossword and Scrabble players in the US. Previous studies on gaming expertise have mostly involved chess players, so this is a refreshing new research angle.Toma's team recruited 26 elite Scrabble players (in the top two per cent of competitive players, on average; 20 men) and 31 elite crossword players (in the top 7 per cent, on average; 22 men) to complete several tests of working memory - the kind of memory that we use to juggle and use information over short time-scales.For example, there was a visuospatial task that involved judging whether images were symmetrical, while also remembering highlighted locations in a series of grids that always appeared after each symmetry image. Another challenge was the reading span task (a test of verbal working memory), which involved judging the grammatical sense of sentences, while also remembering the order of individual letters that were flashed on-screen after each grammatical challenge.The researchers anticipated that the Scrabble players would outperform the crossworders on visuospatial working memory, whereas they thought the crossword players might be superior on verbal working memory. These predictions were based on the contrasting skills demanded by the two games. Scrabble players often spend hours learning lists of words that are legal in the game, but unlike crossword players, they don't need to know their meaning. In fact many Scrabble players admit to not knowing the meaning of many of the words they play. On the other hand, Scrabble players need skills to rearrange letters and to find a place for their words on the board (a visuospatial skill), whereas crossword players do not need these skills so much because the grid is prearranged for them.The researchers actually uncovered no group differences on any of the measures of visuospatial and verbal working memory. However, in line with predictions, the crossword competitors outperformed the Scrabble players on an analogies-based word task - identifying a pair of words that have the same relation to each other as a target pair - and the crossworders also had higher (self-reported) verbal SAT scores than the Scrabble players (SAT is a standardised school test used in the US). The two groups also differed drastically in the most important strategies they said they used during game play - for instance, mental flexibility was far more important for crossworders, whereas anagramming was important for Scrabble players but not mentioned by crossworders.Both expert groups far outperformed a control group of high-achieving students on all measures of verbal and visuospatial working memory. This was despite the fact the students had similar verbal SAT levels to the expert players. So it seems the elite players of both games have highly superior working memory relative to controls, but this enhancement is not tailored to their different games.Toma and his team said that by looking beyond chess and studying experts in cognitively demanding verbal games, their research "helps to build a more general understanding of the cognitive mechanisms that underlie elite performance." From a theoretical perspective, their finding of no working memory differences between Scrabble and crossword competitors is supportive of a domain general account of working memory - the idea that there exists a single mechanism that supports the processing of verbal and visuospatial information. _________________________________ Toma, M., Halpern, D., & Berger, D. (2014). Cognitive Abilities of Elite Nationally Ranked SCRABBLE and Crossword Experts Applied Cognitive Psychology DOI: 10.1002/acp.3059 Post written by Christian Jarrett (@psych_writer) for the BPS Research Digest.

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  • September 11, 2014
  • 12:45 PM
  • 87 views

The Origami Brain and a new marker for Schizophrenia

by Gabriel in Lunatic Laboratories

Anyone who has seen pictures or models of the human brain (like the one above) is aware that the outside layer, or cortex, of the brain is folded in an intricate pattern of “hills”, called gyri, and “valleys”, called sulci which give the brain it’s distinctive look. It turns out that the patterns of cortical folding are largely consistent across healthy humans, broadly speaking. However, disturbances in cortical folding patterns suggest deeper disturbances in brain structure and function.... Read more »

Nanda P, Tandon N, Mathew IT, Giakoumatos CI, Abhishekh HA, Clementz BA, Pearlson GD, Sweeney J, Tamminga CA, & Keshavan MS. (2014) Local gyrification index in probands with psychotic disorders and their first-degree relatives. Biological psychiatry, 76(6), 447-55. PMID: 24369266  

  • September 11, 2014
  • 10:42 AM
  • 55 views

The illusion that gives you sensations in a rubber tongue

by BPS Research Digest in BPS Research Digest

Our sense of where our bodies begin and end usually feels consistent and reliable. However psychologists have been having fun for decades, exposing just how malleable the body concept can be.You may have heard of the "rubber hand illusion" (video). By visibly stroking a rubber hand in time with stroking a participant's hidden real hand, you can induce for them the feeling of sensation in the rubber hand.The rubber hand illusion is thought to occur because the brain tends to bind together information arising from different sensory modalities. The stroking sensation arrives at one's real hand, but the stroking is seen occurring at the same time at the rubber hand. The brain binds these two experiences and the visual modality wins, transferring the felt sensation to the rubber appendage.Because the rubber hand illusion depends on the dominance of vision, Charles Michel and his colleagues wondered if a similar illusion would still occur for the tongue - one of our own body parts that we feel but rarely see.  The researchers purchased a fake tongue from a magic shop (see pic), and for forty seconds they stroked this tongue with a cotton bud (Q-tip) at the same time as they stroked each participant's real tongue. The participants could see the stroking of the fake tongue, but the stroking of their own tongue was hidden from view.Averaging responses from the 32 student participants, there was an overall sense among the students of being stroked on the rubber tongue, "thus demonstrating," the researchers said, "visual capture over the felt position of the tongue for the very first time." Further evidence for an illusory effect came from the fact that sensation in the rubber tongue was stronger when the stroking of the fake and real tongues was performed in synchrony as opposed to out of time. This synchronous stroking also led to more agreement from the students that they felt as though they could move the fake tongue, and that the fake tongue was their own.Next, the researchers shone a laser pointer on the fake tongue as the participants watched. Twenty-two of the participants said that this triggered sensations in their real tongue - some said it felt cold, others warm, tactile and/or tingly. "I felt vibrations on my tongue moving in synchrony with the light movement," one student said.The researchers say their results have shown that an illusion, similar to the rubber hand illusion, can be experienced with the tongue. We call this "the Butcher's Tongue Illusion," they said._________________________________ Michel, C., Velasco, C., Salgado-Montejo, A., & Spence, C. (2014). The Butcher’s Tongue Illusion Perception, 43 (8), 818-824 DOI: 10.1068/p7733 Post written by Christian Jarrett (@psych_writer) for the BPS Research Digest.

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Michel, C., Velasco, C., Salgado-Montejo, A., & Spence, C. (2014) The Butcher’s Tongue Illusion. Perception, 43(8), 818-824. DOI: 10.1068/p7733  

  • September 11, 2014
  • 09:55 AM
  • 89 views

Treating autism in the first year of life

by Paul Whiteley in Questioning Answers

I had been waiting y'know. Waiting a while for the paper by Sally Rogers and colleagues [1] to finally appear quite a few days after the media headlines about 'reducing', 'reversing' and even 'eliminating' the signs and symptoms of autism in early infancy had appeared. Personally, I prefer the New Scientist headline: 'Early autism intervention speeds infant development' given the text of the paper. I should perhaps also add the words 'for some' to that sentence as you will hopefully see...I'm sure most people have already read about the study ins and outs: take an intervention called 'Infant Start' (IS), a relation of the Early Start Denver Model (ESDM), and apply it with a small (very small) group of "symptomatic" young infants (n=7, aged between 6-15 months old) showing signs and symptoms of autism. Plot baseline measures and progress of those children under IS using various psychometric tools including something like the Autism Observation Scale for Infants (AOSI) and old reliable: the ADOS (the Autism Diagnostic Observation Schedule) compared against four comparison groups. One of those control groups included those with similar early autism symptoms as judged by "elevated AOSI scores and clinician concerns" but who did not receive IS; a so-called "declined referral (DR) group" (n=4). Record results and report outcome based on said 12-week program and added extra sessions a few months down the line.The headline conclusion: "At 36 months, the treated group had much lower rates of both ASD [autism spectrum disorder] and DQs [developmental quotients] under 70 than a similarly symptomatic group who did not enroll in the treatment study". Further: "the pilot study outcomes are promising". I should add that when it came to the "final visit" and "based on standardized assessments and clinical judgement" 2 of the 7 children in the IS group did eventually receive a diagnosis of ASD/PDD-NOS (pervasive developmental disorder not otherwise specified). This compared with 3 of the 4 children in the DR group who met criteria for ASD/PDD-NOS (the other child "presented with intellectual disability"). Insofar as DQ - specifically "overall DQ at or below 70 at 36 months" - well, one child in the IS group fell into this category compared with 3 children in the DR group (note to authors, you've called this the 'DE' group... sorry to be pedantic). You can um-and-ah about the links between ASD and PDD-NOS for example, but suffice to say that any effect from IS was not universal across all participants included in the trial. If you'd like a few more details about the trial and results, I'll refer you to the press release from UC Davis (see here).Of course this is not the first time that this type of very early intervention has been discussed in the peer-reviewed domain. Take for example another paper by Rogers and colleagues [2] (open-access) talking about the use of ESDM with a cohort of 14-24 month old toddlers "at risk for autism spectrum disorders". The results on that occasions were slightly less dramatic than the more recent ones with the caveat that "both younger child age at the start of intervention and a greater number of intervention hours were positively related to the degree of improvement in children's behavior for most variables". I talked about this in a previous post (see here). Indeed it appears that age at start of intervention might be an important variable after all.So, where next with this research? Well, aside from some discussions reiterating how useful it would be to have something to aid early diagnosis (see here) bearing in mind that it has not been conclusively proven that all autism is present from birth (see here), discussions have turned to why such early intervention might have had the effect that it had. Brain plasticity has been mentioned, and how critical periods in early development might be particularly amenable to such intensive intervention. Of course, without the all-important "testing the treatment’s efficacy" under more controlled conditions and with larger groups, one cannot discount some role for chance in the recent findings. Not buying that as an answer? How about differing developmental trajectories then?----------[1] Rogers SJ. et al. Autism Treatment in the First Year of Life: A Pilot Study of Infant Start, a Parent-Implemented Intervention for Symptomatic Infants. Journal of Autism and Developmental Disorders. 2014. 12 September.[2] Rogers SJ. et al. Effects of a brief Early Start Denver model (ESDM)-based parent intervention on toddlers at risk for autism spectrum disorders: a randomized controlled trial. J Am Acad Child Adolesc Psychiatry. 2012 Oct;51(10):1052-65.----------S. J. Rogers, L. Vismara, A. L. Wagner, C. McCormick, G. Young, & S. Ozonoff (2014). Autism Treatment in the First Year of Life: A Pilot Study of Infant Start, a Parent-Implemented Intervention for Symptomatic Infants Journal of Autism and Developmental Disorders : 10.1007/s10803-014-2202-y... Read more »

S. J. Rogers, L. Vismara, A. L. Wagner, C. McCormick, G. Young, & S. Ozonoff. (2014) Autism Treatment in the First Year of Life: A Pilot Study of Infant Start, a Parent-Implemented Intervention for Symptomatic Infants. Journal of Autism and Developmental Disorders. info:/10.1007/s10803-014-2202-y

  • September 11, 2014
  • 04:42 AM
  • 78 views

Omega-3 fatty acids rescues Fragile X phenotypes in Fmr1-Ko mice

by Paul Whiteley in Questioning Answers

"These results demonstrate that n-3 PUFAs dietary supplementation, although not a panacea, has a considerable therapeutic value for FXS [Fragile X syndrome] and potentially for ASD [autism spectrum disorder], suggesting a major mediating role of neuroinflammatory mechanisms".A view @ Wikipedia That was the conclusion reached by Susanna Pietropaolo and colleagues [1] who "evaluated the impact of n-3 PUFA dietary supplementation in a mouse model of fragile X syndrome (FXS), i.e., a major developmental disease and the most frequent monogenic cause of ASD". Looking at the Fmr1-KO mouse model of FXS, a mouse specifically bred to mimic the silencing of the FMR1 gene noted in FXS (see here) with onwards adverse effects for the production of FMRP, researchers looked at what happened when diets were "enriched or not with n-3 PUFAs from weaning until adulthood when they were tested for multiple FXS-like behaviors". The results seemed to indicate that "n-3 PUFA supplementation rescued most of the behavioral abnormalities displayed by Fmr1-KO mice, including alterations in emotionality, social interaction and non-spatial memory, although not their deficits in social recognition and spatial memory". Neuroinflammatory imbalances noted in the knock-out mice were also positively affected by omega-3 supplementation.I don't need to remind you that the Pietropaolo study was a study of mice and one needs to be quite careful about extrapolating animal results when it comes to humans. That being said, given the quite extensive work that has been done on FXS and the detailing of it's molecular background, one might assume that the current results are treated with a little less scepticism than in relation to other more idiopathic 'types' of autism. Still, proper trials with people are indicated as per other research.Omega-3 fatty acids have been discussed before on this blog with autism in mind (see here). The collected literature on their usefulness as supplements for autism is rather mixed at present [2] despite some emerging evidence on their involvement in various biological processes in cases of autism (see here). That being said, I'm not getting too down on omega-3 fatty acids in light of some associations being made with specific skills over and above any condition-specific relationship and some new light being shed on their use in other conditions [3]. I'm yet to find anything like an experimental trial of fatty acids in real people with FXS but did chance(!) upon the study by Lachance and colleagues [4] (open-access) talking about the use of fenretinide (N-(4-hydroxyphenyl) retinamide (4HPR)) in the test-tube and effects "associated with the normalization of arachidonic acid/docosahexaenoic acid ratio in macrophages". The effect talked about translates as a down-regulation in the "production of arachidonic acid (AA), a pro-inflammatory omega-6 polyunsaturated fatty acid, and to increase levels of omega-3 polyunsaturated docosahexaenoic acid (DHA), which has an anti-inflammatory effect". Mmm... possibly some new targets to replace quite a few disappointments when it comes to FXS therapeutics (see here).Music to close. Fontella Bass and Rescue Me.----------[1] Pietropaolo S. et al. Dietary supplementation of omega-3 fatty acids rescues fragile X phenotypes in Fmr1-Ko mice. Psychoneuroendocrinology. 2014 Jul 9;49C:119-129.[2] James S. et al. Omega-3 fatty acids supplementation for autism spectrum disorders (ASD). Cochrane Database Syst Rev. 2011 Nov 9;(11):CD007992.[3] Hawkey E. & Nigg JT. Omega-3 fatty acid and ADHD: Blood level analysis and meta-analytic extension of supplementation trials. Clin Psychol Rev. 2014 Jun 2;34(6):496-505.[4] Lachance C. et al. Fenretinide corrects the imbalance between omega-6 to omega-3 polyunsaturated fatty acids and inhibits macrophage inflammatory mediators via the ERK pathway. PLoS One. 2013 Sep 12;8(9):e74875.----------Pietropaolo S, Goubran MG, Joffre C, Aubert A, Lemaire-Mayo V, Crusio WE, & Layé S (2014). Dietary supplementation of omega-3 fatty acids rescues fragile X phenotypes in Fmr1-Ko mice. Psychoneuroendocrinology, 49C, 119-129 PMID: 25080404... Read more »

Pietropaolo S, Goubran MG, Joffre C, Aubert A, Lemaire-Mayo V, Crusio WE, & Layé S. (2014) Dietary supplementation of omega-3 fatty acids rescues fragile X phenotypes in Fmr1-Ko mice. Psychoneuroendocrinology, 119-129. PMID: 25080404  

  • September 10, 2014
  • 11:49 AM
  • 63 views

Are Deaf Dogs and Blind Dogs just like other Dogs?

by CAPB in Companion Animal Psychology Blog

Do dogs that are deaf and/or blind have specific behavioural traits? New research sets out to investigate – and finds they are very similar to dogs with normal hearing and vision.Photo: Amy Rene / ShutterstockNo one knows exactly how many dogs have hearing or vision problems. Congenital deafness and/or blindness occur in several breeds. In some cases this is related to coat colours – for example the double merle gene in Australian Shepherds is linked to deafness and blindness– and at other times not, as with inherited cataracts in many breeds. Very little is known about how dogs with inherited or acquired vision or hearing disorders behave, which was the motivation for this study by Valeri Farmer-Dougan et al (in press) of Ilinois State University.The results showed many similarities between dogs with a hearing or vision impairment (HVI) and those without. This shows that HVI dogs can make good family pets. In fact, the non-HVI dogs were rated as more aggressive and more excitable than those with HVI. There were also some differences in specific behaviours: non-HVI dogs were more likely to chase rabbits, and to eat faeces or roll in it, whereas the HVI dogs were more likely to bark too much, lick a lot, or chew unsuitable objects. The scientists say, “The increased chewing, excessive barking and increased self-licking reported in the HVI dogs may be due to differences in sensory input compared to non-HVI dogs. Indeed, all the excesses in behaviour appear to be self-stimulatory in nature.” Because they asked owners about any other health issues, they do not think health is the cause of this difference. Instead, they think the dogs are making up for the lack of input from their ears or eyes with behaviours that engage their other senses. This suggests that owners of dogs with hearing or vision problems should make an explicit effort to make sure their dog has enough sensory input. Farmer-Duggan et al suggest enrichment with toys, including vibrating toys, Kongs, and chew toys, as well as training sessions to engage the dog’s brain. Many such dogs can also attend agility, flyball, obedience or even dog dance classes.The HVI dogs were more likely to have had formal training, perhaps because their owners thought they would need it more, or perhaps because their owners were more likely to think training is important in general. The lower levels of aggression and excitability in this group could be due to this training, and this is something that future research can investigate. Owners of HVI dogs made adjustments to their training, for example in using more hand signs and physical prompts for deaf dogs. The survey was completed by the owners of 461 dogs. The hearing-impaired and vision-impaired dogs (HVI) were considered as one group since there were no differences between them. 98 dogs were deaf or had a hearing impairment, 32 dogs were blind or partially-sighted, and 53 dogs were both deaf and blind (183 dogs in total). The remainder were a comparison group of dogs without such impairments. The survey asked owners to complete the C-BARQ, a widely-used tool to assess the behavioural traits of dogs. In addition, there were questions about the breed, training methods used, and information about any disabilities the dog had.There are implications for vets, who should be aware of potential problems with chewing, licking and barking in deaf and/or blind dogs. But the results are also encouraging because they do not support the idea that such dogs exhibit problem behaviours in general. Blind and deaf dogs are excluded from many rally and obedience programs (with notable exceptions). The authors say, “Given that no evidence was found for increased aggression, it seems that HVI dogs could successfully participate in these additional socialization opportunities. Opening up these opportunities would increase the available activities for HVI dogs. Increased opportunities for training and competition increase the general health and well-being of all dogs.”The authors conclude that “Through cooperative partnerships between veterinarians, behaviorists and owners, HVI dogs can, indeed, be excellent and well-loved companion dogs.” These results will be especially helpful to owners and potential owners of dogs with hearing or vision impairments.The Canine Inherited Disorders Database has further information on congenital blindnessand deafness in dogs.Do you know a dog with a hearing or vision impairment?ReferenceFarmer-Dougan, V., Quick, A., Harper, K., Schmidt, K., & Campbell, D. (2014). Behavior of Hearing or Vision Impaired and Normal Hearing and Vision Dogs (Canis lupus familiaris): Not the same but not that different Journal of Veterinary Behavior... Read more »

Farmer-Dougan, V., Quick, A., Harper, K., Schmidt, K., & Campbell, D. (2014) Behavior of Hearing or Vision Impaired and Normal Hearing and Vision Dogs (Canis lupus familiaris): Not the same but not that different . Journal of Veterinary Behavior. info:/

  • September 10, 2014
  • 09:40 AM
  • 82 views

Midi-chlorians gave Jedi knights their power. Is there something like this on Earth?

by Bill Sullivan in The 'Scope

A strange and provocative paper by Alexander Panchin and colleagues proposes an unorthodox new idea called the “biomeme hypothesis”, which posits that the impulse behind some religious rituals could be driven by mind-altering parasites.... Read more »

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