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  • July 4, 2014
  • 08:44 PM
  • 77 views

The Bigfoot Question: A Genetic Analysis of Yeti Hair

by Melissa Chernick in Science Storiented

It’s been a while since I’ve written about Bigfoot, and that’s a shame because he’s pretty fun to write about. As with many things, I like to keep it in a scientific context. That’s why I was pretty stoked to see a recent Sasquatch paper in Proceedings of the Royal Society B. A paper that takes an interesting approach: genetics. Right off the bat the paper does not assume non-existence, both pointing out that there are numerous reports and sightings yet no bodies or recent fossils. Theories abound about what these animals are, ranging from surviving populations of collateral hominids to unlikely hybrids. As a general rule, modern science shies away from the yeti-finding field, to the point that they make believers feel rejected. Admittedly, believers have point in that science should not accept or reject anything without examining the evidence and testing hypotheses. Pretty much the definition of science, right? So that's what authors Sykes et al. do, take a scientific approach.The researchers collected a total of 57 Bigfoot hair samples submissions from museum and individual collections. They went about it all officially with a joint press release in May 2012 by Museum of Zoology, Lausanne and the University of Oxford. Then, to eliminate obvious non-hairs, they subjected the samples to macroscopic, microscopic and infrared fluorescence examination. Based on provenance or historic interest, thirty-seven of the samples were selected for genetic analysis. Hairs were first cleaned to remove surface contamination - just consider how many people had handled a sample, so you need to eliminate known human DNA to leave just sample DNA. The meticulously cleaned hair samples were then ground in a buffer to homogenate, incubated with proteinase K, and extracted for PCR amplification. This amplification was of the ribosomal mitrochondrial DNA 12S fragment corresponding to bps 1093-1196 of the human mitrochondrial genome, using a permissive primer combination that allows for a wide range of mammalian DNA. The results were then compared to GenBank accessions for species identification.Perhaps it is important to point out what the 12S mitochondrial DNA is and how it works. Even within fur-bearing species, there is a large amount of variation in hair appearance that can be identified under the microscope to determine species. But, in the absence of an experienced hair examiner (yes, those exist), a reliable, alternative analysis must be used. This analysis comes in the form of highly conserved mitochondrial DNA regions, these are particular sequences that have been maintained by evolution despite speciation, probably because they are functional. Mitochondrial 12S ribosomal RNA has an amplification size that renders it useful for even problematic and/or degraded samples. Highly conserved primer regions and the high nucleotide species diversity present within the portion of the 12S gene examined allows for identification at least to genus and often species. Studies examining the extent of 12S homology within and between species have shown a high degree of confidence in the test's ability to match species from biological samples, usually hair. This includes primate homologies like the chimpanzee, who shares a 98% homology with the human 12S region, Gorilla (97%) and rhesus macaque (90%). These studies have shown that it is unlikely that a non-human primate hair could be confused with human hair using this system.Now knowing all of this, back to the results of the Bigfoot study. Despite multiple attempts, seven of the samples yielded no DNA sequences, leaving the researchers with 30 samples. These 30 samples were each matched to a known species. Ten belonged to various bear species, four were cows, four were horse, four were wolves/dogs, two were raccoons, one was a deer, one a Malaysian tapir, one a sheep, one a serow, and one was human (exact match).There has been quite a few articles in the news about this study, and that’s good because this paper is a nice example of using hard science to test a theory. It is also works towards bridging the gap between two rather disparate groups of people. So kudos to you Sykes et al. Sykes, B., Mullis, R., Hagenmuller, C., Melton, T., & Sartori, M. (2014). Genetic analysis of hair samples attributed to yeti, bigfoot and other anomalous primates Proceedings of the Royal Society B: Biological Sciences, 281 (1789), 20140161-20140161 DOI: 10.1098/rspb.2014.0161A nice write-up from Science News "'Bigfoot' samples analyzed in lab"For more on 12S see an article in Forensic Magazine titled "Easy Species DNA Identification for the Forensic Laboratory Using 12S Mitochondrial DNA"(images via WhoFortedBlog, NewEngland BioLabs, Nature Reviews Genetic paper DOI:10.1038/nrg1606, respectively)... Read more »

Sykes, B., Mullis, R., Hagenmuller, C., Melton, T., & Sartori, M. (2014) Genetic analysis of hair samples attributed to yeti, bigfoot and other anomalous primates. Proceedings of the Royal Society B: Biological Sciences, 281(1789), 20140161-20140161. DOI: 10.1098/rspb.2014.0161  

  • July 4, 2014
  • 01:00 PM
  • 128 views

Finally! A Definite Cause of Autism: Hint it isn’t Vaccines

by Gabriel in Lunatic Laboratories

Autism, not caused by vaccines. In fact I’ve written several posts on the genetic clues to autism, now a new study offers more proof that it is purely genetic [at […]... Read more »

Bernier, R., Golzio, C., Xiong, B., Stessman, H., Coe, B., Penn, O., Witherspoon, K., Gerdts, J., Baker, C., Vulto-van Silfhout, A.... (2014) Disruptive CHD8 Mutations Define a Subtype of Autism Early in Development. Cell. DOI: 10.1016/j.cell.2014.06.017  

  • July 4, 2014
  • 10:48 AM
  • 120 views

Parents’ Income Poorly Predicts SAT Score

by nooffensebut in The Unsilenced Science

Here I publish my original study that disproves family income as an important influence on SAT scores, shows race as having its greatest influence on scores at the highest education and income levels, and provides some preliminary evidence for a hereditary influence.... Read more »

nooffensebut. (2014) Parents’ Income is a Poor Predictor of SAT Score. Open Differential Psychology, 1-19. info:other/

Bartels M, Rietveld MJ, Van Baal GC, & Boomsma DI. (2002) Heritability of educational achievement in 12-year-olds and the overlap with cognitive ability. Twin research : the official journal of the International Society for Twin Studies, 5(6), 544-53. PMID: 12573186  

Duckworth AL, Quinn PD, Lynam DR, Loeber R, & Stouthamer-Loeber M. (2011) Role of test motivation in intelligence testing. Proceedings of the National Academy of Sciences of the United States of America, 108(19), 7716-20. PMID: 21518867  

Duncan, J., Seitz, R.J., Kolodny, J., Bor, D., Herzog, H., Ahmed, A., Newell, F.N., & Emslie, H. (2000) A Neural Basis for General Intelligence. Science, 289(5478), 457-460. DOI: 10.1126/science.289.5478.457  

MacCallum RC, Wegener DT, Uchino BN, & Fabrigar LR. (1993) The problem of equivalent models in applications of covariance structure analysis. Psychological bulletin, 114(1), 185-99. PMID: 8346326  

Marioni RE, Davies G, Hayward C, Liewald D, Kerr SM, Campbell A, Luciano M, Smith BH, Padmanabhan S, Hocking LJ.... (2014) Molecular genetic contributions to socioeconomic status and intelligence. Intelligence, 44(100), 26-32. PMID: 24944428  

Trzaskowski M, Harlaar N, Arden R, Krapohl E, Rimfeld K, McMillan A, Dale PS, & Plomin R. (2014) Genetic influence on family socioeconomic status and children's intelligence. Intelligence, 42(100), 83-88. PMID: 24489417  

  • July 4, 2014
  • 05:10 AM
  • 92 views

Public awareness of cancer and federal funding of research in the US is affected by how cancer is reported in the American media

by Lizzie Perdeaux in BHD Research Blog

The link between having a good understanding of your health and of disease (health literacy) and health outcomes is well documented (Berkman et al., 2011). However, access to accurate and unbiased information is required for the public to be able … Continue reading →... Read more »

  • July 4, 2014
  • 04:53 AM
  • 92 views

DNA methylation patterns and autism: buccal up

by Paul Whiteley in Questioning Answers

"The results indicate the presence of a mosaic subpopulation of epigenetically-dysregulated, ectodermally-derived cells in subjects with ASD [autism spectrum disorder]". That was the very clinical primary conclusion reached in the study by Esther Berko and colleagues [1] (open-access here). They looked at DNA methylation patterns in cheek cell samples for a small sample of children diagnosed with an ASD (n=47) "born to mothers aged 35 and over" compared with samples from an asymptomatic control group (n=48) and found some potentially important differences.Cheek of it.. @ Wikipedia Some of the accompanying press for this paper can be found here. As per the headline: "Study shows environmental influences may cause autism in some cases" the results have been suggested to further add to the notion that genetics may not be the be-all-and-end-all of autism, at least some cases of autism. We'll see about that. That alongside the body of research which seems to suggest that offspring of older mums might be at increased risk of being diagnosed with autism (see here) makes for some interesting reading.Before going on, I should perhaps define a few terms which have or will crop up in this post. So, buccal swabs refers to a way of collecting cells and DNA [non-invasively] from the inside of a person's cheek. Ectoderm refers to the outer layer of germ cells which eventually give rise to hair, skin, the lens of the eye and importantly, the nervous system including neurons and glial cells, as well as the mucus membrane of the mouth. DNA methylation is something which has been covered a few times on this blog (see here and see here) and is part of that wonderful concept of epigenetics and one of the ways that genes are turned on or off depending on their methylation status.The Berko paper is open-access but a few pointers might be useful:Buccal cells were examined as a sort of proxy for brain cells (which generally aren't harvested from live donors). As per the description previously, the ectodermal origins of buccal cells cross that proxy bridge. DNA was extracted from the buccal cells and subjected to various genetic and epigenetic analyses.Researchers used the Mosaic Alteration Detection (MAD) algorithm [2] to test "for abnormal chromosome numbers as well as other chromosomal defects". No evidence of chromosome aneuploidy was detected in either cases or controls which kinda ruled out more traditional genetic effects being related to advancing maternal age.Methylation was then the name of the game, and as I've talked about on a previous post (see here) various ways and means of looking at the methylation status of those little genetic islands: CpG sites. Results:  "a first pass" approach looking at DNA methylation patterns between the groups identified "3560 differentially methylated GCs". Researchers then further refined their analysis by means of something called bump-hunting which took into account age and ancestry as potential effectors of DNA methylation and something called co-methylation network analysis. They were then left with 15 differentially methylated regions (DMRs) on 14 genes "distinguishing the ASD and TD [typically developing] samples". Even further refinement taking into account the overlapping presence of copy number variations (CNVs) (see here for an explanation) boiled the total down and looked at which genes might be associated with DMRs."The candidate DMRs from the genome-wide analysis were associated with genes, of which many have already been implicated in previous studies with ASD" shown in Table 1 of the paper. Further: "The model that results is of mosaic epigenetic dysregulation affecting the same networks and pathways targeted by mutational mechanisms, creating comparable deleterious effects on neuronal function". In other words, the more traditional genetic mutations noted in other work on some genes in relation to autism might also be complemented by epigenetic changes affecting those gene functions too. I found the results of this paper to be absolutely fascinating. Not only that the emphasis was on cells which share some source commonality with those found in the grey-pink matter which has been a primary focus of autism research but also that genetic mutations and epigenetic changes may potentially work synergistically in cases of autism. The added detail that this tied into the seemingly enhanced risk of autism in older mothers [3] (at conception) adds further interest to this work. As the authors noted: "The epigenetic dysregulation observed in these ASD subjects born to older mothers may be associated with aging parental gametes, environmental influences during embryogenesis or could be the consequence of mutations of the chromatin regulatory genes increasingly implicated in ASD". Chromatin by the way, is something of an upcoming star in autism research [4] (open-access here).Obviously there is quite a bit more work to do in this area not least to test whether the Berko findings are also applicable to children with autism born to younger mothers and any influence from the various overlapping conditions which can and do occur in cases of autism such as epilepsy (see here) or intellectual disability. I also hark back to some interesting work presented at IMFAR this year (2014) by Feinberg and colleagues who talked about age-related methylation changes found in semen as being something to watch when it comes to the older dads and autism risk work (see here) which might point to a cumulative effect. Combined with what is already being reported about methylation status and something like those HERVs in relation to autism (see here) and even ADHD (see here), epigenetics is certainly continuing its rise and rise in autism research [5].Music then to close. Hey Ya!----------[1] Berko ER. et al. Mosaic epigenetic dysregulation of ectodermal cells in autism spectrum disorder. PLoS Genet. 2014 May 29;10(5):e1004402.[2] González JR. et al. A fast and accurate method to detect allelic genomic imbalances under... Read more »

Berko ER, Suzuki M, Beren F, Lemetre C, Alaimo CM, Calder RB, Ballaban-Gil K, Gounder B, Kampf K, Kirschen J.... (2014) Mosaic epigenetic dysregulation of ectodermal cells in autism spectrum disorder. PLoS genetics, 10(5). PMID: 24875834  

  • July 3, 2014
  • 07:44 PM
  • 82 views

This Month in Blastocystis Research (JUN 2014) - IMECs Edition

by Christen Rune Stensvold in Blastocystis Parasite Blog

A rare and extremely timely study using NGS tools to sequence DNA from intestinal microbial eukaryotic communities has been published in June 2014 in Frontiers in Microbiology; here's a small review.... Read more »

Parfrey, L., Walters, W., Lauber, C., Clemente, J., Berg-Lyons, D., Teiling, C., Kodira, C., Mohiuddin, M., Brunelle, J., Driscoll, M.... (2014) Communities of microbial eukaryotes in the mammalian gut within the context of environmental eukaryotic diversity. Frontiers in Microbiology. DOI: 10.3389/fmicb.2014.00298  

  • July 3, 2014
  • 01:00 PM
  • 111 views

Why you Should Not Fear Testosterone Therapy

by Gabriel in Lunatic Laboratories

Testosterone, to some it’s a bad word, bringing crazy images like “roid rage” and the like. To others with more than just a pop culture understanding it is a lifesaver. […]... Read more »

  • July 3, 2014
  • 09:59 AM
  • 98 views

What’s the Answer? (mutation nomenclature)

by Mary in OpenHelix

Biostars is a site for asking, answering and discussing bioinformatics questions and issues. We are members of the community and find it very useful. Often questions and answers arise at Biostars that are germane to our readers (end users of genomics resources). Every Thursday we will be highlighting one of those items or discussions here […]... Read more »

  • July 3, 2014
  • 07:55 AM
  • 96 views

Goalward-bound: why biological research is like football

by Christele Gonneau in the Node

The 2014 FIFA World Cup has mesmerised football fans all around the world over the past weeks, but besides just the fancy footwork on display, we’ve also seen some amazing athleticism. Many of the matches have taken place under scorching, highly humid conditions! Though this might not be foremost in our minds as marvel at […]... Read more »

  • July 3, 2014
  • 02:25 AM
  • 46 views

Journal Club: DNA analysis indicates Bigfoot may be a big fake

by GrrlScientist in Maniraptora

SUMMARY: A new genetic analysis of 'yeti' hair samples reveals they actually originated from dogs, horses, bears or other known mammals. ... Read more »

  • July 2, 2014
  • 05:54 PM
  • 93 views

Heather Can Help UK Meet Bioenergy Targets

by dailyfusion in The Daily Fusion

Harvesting energy from heather could reduce carbon dioxide emissions and help the UK meet its bioenergy targets, according to new research by scientists at Durham and Manchester Universities.... Read more »

  • July 2, 2014
  • 03:54 PM
  • 106 views

Plant = Pill?

by Viputheshwar Sitaraman in Draw Science

E. Longfolia: an aphrodisiac, anti-inflammatory, and anti-malarial miracle plant.... Read more »

Tran TV, Malainer C, Schwaiger S, Atanasov AG, Heiss EH, Dirsch VM, & Stuppner H. (2014) NF-κB inhibitors from Eurycoma longifolia. Journal of natural products, 77(3), 483-8. PMID: 24467387  

  • July 2, 2014
  • 01:13 PM
  • 102 views

Saving the Rainforest and the Consequences

by Gabriel in Lunatic Laboratories

The road to hell is paved with good intentions. This seems even more true when a new study came out that shows, when it comes to fixing deforestation and forest degradation, […]... Read more »

Putz, F., & Romero, C. (2014) Futures of Tropical Forests . Biotropica, 46(4), 495-505. DOI: 10.1111/btp.12124  

  • July 2, 2014
  • 10:09 AM
  • 168 views

Vitamin C and Pregnant Women Who Smoke

by Dirk Hanson in Addiction Inbox

Improving pulmonary function in newborns. 500 mg of daily vitamin C given to pregnant smoking women “decreased the effects of in-utero nicotine” and “improved measures of pulmonary function” in their newborns, according to a study  by Cindy T. McEvoy and others at the Oregon Health and Science University in Portland, published in a recent issue of the Journal of the American Medical Association (JAMA). Researchers have long known that smoking during pregnancy can harm the respiratory health of newborns. Maternal smoking during pregnancy can interfere with normal lung development, resulting in lifelong increases in asthma risk and other pulmonary complications. The researchers note that “more than 50% of smokers who become pregnant continue to smoke, corresponding to 12% of all pregnancies.” That adds up to a lot of newborns each year who will start off with more wheezing, respiratory infections, and childhood asthma than their counterparts born to non-smoking mothers. McEvoy and her colleagues wanted to find out whether a daily dose of vitamin C would improve the results of pulmonary function tests in newborns exposed to tobacco in utero. It did. In an accompanying editorial, Graham L. Hall calls the randomized, double-blind, placebo-controlled clinical trial “well-conceived and executed…. Lung function during the first week of life was statistically significantly better (by approximately 10%) among infants born to mothers randomized to receive Vitamin C compared with infants born to mothers randomized to received placebo.” Moreover, the prevalence of wheezing in the first year was reduced from 40% in the placebo group to 21% in the Vitamin C group.The decreases in asthma and wheezing in the Vitamin C newborns were documented through the first year of life.  A 10% reduction does not sound like a lot, but, as Hall writes, “small population-level changes in lung function may lead to significant public health benefits, and the improvements in lung function reported here could be associated with future benefit.” In their paper, the researchers conclude: “Vitamin C supplementation in pregnant smokers may be an inexpensive and simple approach (with continued smoking cessation counseling) to decrease some of the effects of smoking in pregnancy on newborn pulmonary function and ultimately infant respiratory morbidities, but further study is required.” Pregnant women should not smoke, and quitting is by far the healthiest option.  As Hall writes: “By preventing her developing fetus and newborn infant from becoming exposed to tobacco smoke, a pregnant woman can do more for the respiratory health and overall health of her child than any amount of vitamin C may be able to accomplish.” McEvoy C.T.,  Nakia Clay,  Keith Jackson,  Mitzi D. Go,  Patricia Spitale,  Carol Bunten,  Maria Leiva,  David Gonzales,  Julie Hollister-Smith &  Manuel Durand &  (2014). Vitamin C Supplementation for Pregnant Smoking Women and Pulmonary Function in Their Newborn Infants, JAMA, 311 (20) 2074. DOI: http://dx.doi.org/10.1001/jama.2014.5217Graphics Credit: http://www.quitguide.com/... Read more »

McEvoy Cindy T., Nakia Clay, Keith Jackson, Mitzi D. Go, Patricia Spitale, Carol Bunten, Maria Leiva, David Gonzales, Julie Hollister-Smith, & Manuel Durand. (2014) Vitamin C Supplementation for Pregnant Smoking Women and Pulmonary Function in Their Newborn Infants. JAMA, 311(20), 2074. DOI: http://dx.doi.org/10.1001/jama.2014.5217  

  • July 2, 2014
  • 09:36 AM
  • 83 views

Video Tip of the Week: NCBI Variation Viewer

by Mary in OpenHelix

The folks at NCBI recently hosted a webinar that covered a number of resources: GTR, ClinVar, and MedGen. It was a nice introduction to these resources using a case study of exploring information about a 9-year-old child who needed to get clearance for participation in sports. So they follow the course of some details about […]... Read more »

Landrum M. J., G. R. Riley, W. Jang, W. S. Rubinstein, D. M. Church, & D. R. Maglott. (2014) ClinVar: public archive of relationships among sequence variation and human phenotype. Nucleic Acids Research, 42(D1). DOI: http://dx.doi.org/10.1093/nar/gkt1113  

  • July 2, 2014
  • 08:25 AM
  • 110 views

How Do Mosquitoes Find You?

by Mark Lasbury in As Many Exceptions As Rules

Spend much time outside in the summer and you will have to deal with mosquitoes. The mechanisms that females use to find a blood meal are becoming better understood. New research shows how the proboscis probes for a blood vessel, perhaps using the TRPA1 heat sensing ion channel as a signal for nearby blood.

Once they feed, females lay eggs. New research indicates that they actually prefer water that contains the dead larvae of similar mosquitoes, dead from predators. The presence of predator parasites by reducing competitors and increasing nutrients in the water.
... Read more »

  • July 2, 2014
  • 03:40 AM
  • 82 views

Quality of life and autism

by Paul Whiteley in Questioning Answers

The BBC ran an interesting article on their website recently titled: Happiness and disability. Discussions about the disability paradox - whereby some people with often significant and persistent disability report experiencing a good or excellent quality of life (QoL) - got me thinking about QoL and in particular, how it might relate to the very wide and very heterogeneous autism spectrum. I might add that I am not insinuating that everyone diagnosed on the autism spectrum are 'disabled' but rather that as per the UK definition of the word (see here), "a ‘substantial’ and ‘long-term’ negative effect on your ability to do normal daily activities" is a hallmark for quite a proportion of people on the autism spectrum.At the same time, the findings from the literature review by Chiang and Wineman [1] should really be making people sit up and take note: "The majority of the individuals with ASD [autism spectrum disorder] had poor QoL [quality of life]". Indeed, not for the first time have such sentiments been voiced in the research literature as per another meta-analysis by van Heijst & Geurts [2] who reported: "Across the lifespan, people with autism experience a much lower quality of life compared to people without autism".What a view... @ Wikipedia Quality of life by the way, can mean quite a few things but for the purposes of this post I'm talking about overall wellbeing including things like life satisfaction and health including mental and physical health.As stated, QoL is often a very subjective thing influenced by all manner of variables, some social, some biological and some psychological. As one example I'd draw your attention to the concept of resilience [3] and the effect that can have but there are many others.QoL is also a dynamic concept which can and does change for everyone following life's ebbs and flows. If I happened to scoop the lottery tomorrow I'd wager that my QoL would probably increase a few points (albeit with potential caveats). Likewise, when it comes to one of the most important influences on QoL, physical health, some people will know what happens to QoL when health deteriorates or when faced with the prospect of even short-term restrictions to normal activities.I should also mention that just because I'm talking about research in the most part suggesting poorer QoL in relation to autism, I'm not trying to stigmatise or anything like that. Poor QoL is not an exclusively autism-related feature; just as I appreciate that for some people on the autism spectrum, QoL is actually pretty good.A trawl through some of the research literature in this area highlights a few common themes.Social contact and networksI've talked before on this blog about issues such as loneliness and how detrimental it might potentially be for one's health (see here). Loneliness or a lack of friends or social support can be an issue for some on the autism spectrum, although I'd hasten to add that sweeping generalisations about everyone with autism craving lots of social contact might be misplaced; not everyone wants to be the life and soul of the party. There has been some focus on how loneliness and social isolation can and do impact on QoL with autism in mind. The paper by Renty & Roeyers [4] talked about how the availability of a "supportive social network" seemed to be an important factor when it came to QoL in high-functioning adults with autism. Just as an aside, I didn't pick the term 'high-functioning', the authors did.The paper by Micah Mazurek [5] (a favourite researcher on this blog) similarly pointed to the detrimental effects that loneliness seemed to have in cases of autism on subsequent QoL. Based on self-report (something which I'll be coming to shortly) "loneliness was associated with increased depression and anxiety and decreased life satisfaction and self-esteem, even after controlling for symptoms of autism spectrum disorders". A "greater quantity and quality of friendships were associated with decreased loneliness" was another rather obvious finding, implying one possible target for possible intervention. Perhaps also relevant to the whole issue of QoL and autism was the focus on comorbidity in this paper: "number of friends provided unique independent effects in predicting self-esteem, depression, and anxiety above and beyond the effects of loneliness".Social contact / participation issues were also addressed in the paper by Lee and colleagues [6] looking children with autism with QoL in mind. They reported: "Children with autism were significantly less likely to attend religious services, more likely to miss school, and less likely to participate in organized activities". Likewise, Orsmond and colleagues [7] reported similar things: "Young adults with an ASD were significantly more likely to never see friends, never get called by friends, never be invited to activities, and be socially isolated". I could go on but I won't. Suffice to say that social contact and participation seem to be big influencers on QoL in quite a few cases of autism.ComorbidityHaving already mentioned how certain comorbidity might also be linked to measures of QoL it's also worthwhile going through some of the other research in this area. I'm pretty enthusiastic that comorbidity when it comes to autism is something deserving of a lot more investigation (see here). By comorbidity, I'm talking about both psychological comorbidity such as depression and anxiety (especially anxiety) all the way up to something like psychosis (see here) or schizophrenia (see here) and the other more somatic comorbidity reported in some cases of autism (see here). I don't also doubt that there is a relationship between psychologically-manifesting comorbidity and physiological comorbidity with autism in mind (see here).Anyhow, I start this section with reference to the paper by Bauman [8] who very succinctly described how medical comorbidity can be a "challenge to diagnosis and treatment" when it comes to autism. Perhaps most relevant to the topic of this post was the assertion: "Many of these medical conditions are treatable, often resulting in improved developmental gains and quality of life for the patient and family". Certainly looking back to a post I did fairly recently on undetected medical comorbidity and autism (see here) I wouldn't argue with such a sentence. Included in the area of health and medical comorbidity potentially impacting on QoL in autism is the various research looking at ... Read more »

  • July 1, 2014
  • 09:37 PM
  • 89 views

DNA analysis indicates Bigfoot may be a big fake | @GrrlScientist

by GrrlScientist in GrrlScientist

A newly-published genetic analysis of hair samples suspected as being from a cryptic primate known by various names such as "bigfoot" or "yeti", has revealed they actually originated from dogs, horses, bears or other well known mammals. ... Read more »

  • July 1, 2014
  • 01:18 PM
  • 107 views

St. Johns Wart and the Dangers of “Alternative” Medicine

by Gabriel in Lunatic Laboratories

Grapefruit juice, I hate the stuff. But did you know that if you drink as little as 8 oz. of it when you take certain medications it could dramatically increase […]... Read more »

Davis SA, Feldman SR, & Taylor SL. (2014) Use of St. John's Wort in Potentially Dangerous Combinations. Journal of alternative and complementary medicine (New York, N.Y.). PMID: 24956073  

Bailey, D., Malcolm, J., Arnold, O., & David Spence, J. (2002) Grapefruit juice-drug interactions. British Journal of Clinical Pharmacology, 46(2), 101-110. DOI: 10.1046/j.1365-2125.1998.00764.x  

  • July 1, 2014
  • 01:18 PM
  • 62 views

St. Johns Wort and the Dangers of “Alternative” Medicine

by Gabriel in Lunatic Laboratories

Grapefruit juice, I hate the stuff. But did you know that if you drink as little as 8 oz. of it when you take certain medications it could dramatically increase […]... Read more »

Davis SA, Feldman SR, & Taylor SL. (2014) Use of St. John's Wort in Potentially Dangerous Combinations. Journal of alternative and complementary medicine (New York, N.Y.). PMID: 24956073  

Bailey, D., Malcolm, J., Arnold, O., & David Spence, J. (2002) Grapefruit juice-drug interactions. British Journal of Clinical Pharmacology, 46(2), 101-110. DOI: 10.1046/j.1365-2125.1998.00764.x  

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