Post List

Biology posts

(Modify Search »)

  • April 7, 2016
  • 05:19 PM
  • 189 views

Manufacturing human tissue from textiles

by Dr.Jekyll in Lunatic Laboratories

Until we can figure out our lack of regenerating our bodies, or can convince more people to donate organs, we are at mercy of either luck or technology. Bio 3-D printing offers hope that we can print personalized organs as need and rejection free. But the technology relies almost solely with tissue engineers, there job is to find processes using novel bio-materials seeded with stem cells to grow and replace missing tissues.

... Read more »

  • April 7, 2016
  • 07:28 AM
  • 189 views

Some fungi are into dead bodies and waste piles

by Rosin Cerate in Rosin Cerate

For the past couple of years now, a fungus called Xylaria polymorpha has been munching on the buried roots of a beheaded tree on my parents' front lawn. In the grass surrounding the stump, X. polymorpha sends up a thicket of charcoal club-like mushrooms every summer. They look kinda like a dead man's fingers, which not coincidentally happens to be a common name for the fungus.... Read more »

  • April 7, 2016
  • 04:18 AM
  • 201 views

On genes, environment, broccoli and autism (again)

by Paul Whiteley in Questioning Answers

Picture: Carl Warner: http://www.carlwarner.com/I'm serving up two peer-reviewed papers for your reading delight today which draw attention to the ideas that (a) the 'causes' of autism are likely complex and as heterogeneous as the label itself, (b) gene x environment interactions affecting risk of autism are starting to get some good scientific research airtime and (c) don't 'dis the broccoli [chemical] autism connection just yet...The first paper by Brandon Pearson and colleagues [1] (open-access) has already found some media interest as per the Guardian headline: 'Agricultural fungicides are 'bad news for neurons', study suggests'. Exposing mouse neurons - "cortical neuron-enriched cultures" - to several hundred chemicals (careful of that word) found in the modern environment, researchers concluded that several compounds "produce transcriptional changes in vitro that are similar to those seen in brain samples from humans with autism, advanced age and neurodegeneration (Alzheimer’s disease and Huntington’s disease)." That is, several types of chemicals quite commonly found in the modern environment seemed to alter gene expression in those mouse neuron enriched cultures that weren't a million miles away from that noted previously in conditions such as autism for example.Mouse neurons, you might be thinking? Well, obviously one has to be a little cautious about extrapolating from mouse to humans (see here) but researchers did include some comparison analysis looking at "the gene expression profile of our cultures with brain cell-type-specific expression data sets and human brain gene expression data sets." The result: "cortical cultures show strong transcriptional similarities to the human brain."Clustering chemicals based on "concordant gene expression changes", six groups emerged. Cluster 2 chemicals, containing such pesticides as rotenone, pyridaben and fenpyroximate  and also various compounds under the heading of the strobilurins seemed show some particularly interesting results insofar as they "mimicked the transcriptional changes of two post-mortem ASD [autism spectrum disorder] brain expression data sets in a bidirectional manner." The effects of this cluster of compounds also seemed to unite various conditions with autism including Alzheimer’s disease and Huntington’s disease and the "aging brain". My interest was particularly piqued by that last association in light of other research results (see here).When it came to the 'effects' of those chemicals in terms of genetic and biological processes, researchers put forward some not unfamiliar potential roles: "These chemicals, most of which inhibit mitochondrial complex I or III, stimulated free radical production and disrupted microtubules." Words like 'oxidative stress' start to emerge as they have done in previous autism research (see here) and yet again, inflammation or inflammatory processes seem also to be indicated. Indeed, the authors also make mention of how effects such as free radical production "can be reduced by pretreating with a microtubule stabilizer, an antioxidant, or with sulforaphane." Yes indeed, sulforaphane - the chemical found in broccoli - might indeed be moving back up the autism research agenda (see here for some previous background).There is obviously lots more work to do in this area before anyone gets too carried away. The authors note: "While usage and residue levels of cluster 2 chemicals on conventionally grown foods are increasing, in the absence of causality, it is premature to draw correlations with the increased prevalence of ASD and other brain disorders." Lessons could be learned from other blanket suggestions about 'chemicals' and autism (see here) as well as an appreciation for the concept of the the plural autisms (see here). Then there are the practicalities of whether ingesting such compounds on food or in water is the same as direct exposure to cortical neuron-enriched cultures? Or indeed, whether there may be other routes of contact? I might also suggest that further studies should focus on looking for the metabolites of such agents too [2] bearing in mind the concept of statistically significant thresholds...If you're still here after all that, the second paper I want to talk about is that from Sarah Wong and colleagues [3] that has also received a bit of media attention. The focus this time was on a gene called p53 (see here for some background) and how issues with this gene might be 'over-represented' when it comes to autism following on from other work by some of the same authors [3]. First of all, please don't get too fixated by mention of the words 'cancer gene' when it comes to p53 given it's [protein] tumour suppressing capabilities. As I've discussed before, the risk of cancer does not seem to be elevated any more than the general population risk when it comes to autism (see here). Perhaps of greater relevance to the Wong findings is the idea that p53 has other 'activities' such as that related to oxidative stress (yes, that again) and "DNA repair, bioenergetics and mitochondrial DNA (mtDNA) copy number maintenance."Based on data from CHARGE (beincharge!), researchers garnered blood samples from 66 children diagnosed with an autism spectrum disorder (ASD) and "race-, gender-, and age-matched typically neurodeveloping children (n = 46)" (authors words not mine). They analysed for mtDNA copy number and deletions and p53 gene copy ratios and found them to be "more common in children with AU [autism] and their fathers." The authors translate their findings as pointing to "a role for deficient DNA repair capacity not driven by paternal age." They also suggest that environment might intersect with genetics in relation to 'severity' scores of autism obtained for their cohort: "gene x environment interaction seems to play a greater role in children with autism with less severe symptoms."Taken together the Pearson and Wong findings point to some interesting 'associations' potentially relevant to [some] autism. The idea that certain components of the modern-day environment might increase the risk of autism is nothing new but th... Read more »

  • April 6, 2016
  • 05:02 PM
  • 212 views

Uncovering the genetic elements that drive regeneration

by Dr. Jekyll in Lunatic Laboratories

Lose a hand or a leg? It will grow back… oh wait, it won’t, but why not? Trace our evolution — long before the shedding of gills or the development of opposable thumbs — and you will likely find a common ancestor with the amazing ability to regenerate lost body parts. There is theoretically no reason why we shouldn’t be able to regenerate, not quite like in the movie Deadpool, but come on, would you really complain at that point?

... Read more »

Kang, J., Hu, J., Karra, R., Dickson, A., Tornini, V., Nachtrab, G., Gemberling, M., Goldman, J., Black, B., & Poss, K. (2016) Modulation of tissue repair by regeneration enhancer elements. Nature. DOI: 10.1038/nature17644  

  • April 6, 2016
  • 12:03 PM
  • 239 views

Words We Say to Dogs (and Other Things Scientists Learned Watching People Play with Pets)

by Elizabeth Preston in Inkfish



"Who wants to generate some DATA??" are probably not words you've ever said while taking your dog's leash and tennis ball from the closet. But thanks to videos of people playing with their dogs, scientists now know what words you are likely to use. They also discovered how women's tussling and tug-of-war are different from men's—and what the professionals do better.

The scientists are Alexandra Horowitz and Julie Hecht of Barnard College's Dog Cognition Lab. They asked members of the publ... Read more »

  • April 6, 2016
  • 09:54 AM
  • 174 views

Video Tip of the Week: RGD’s OLGA tool, Object List Generator and Analyzer

by Mary in OpenHelix

One of the really persistent issues in genomics is how to either get a list of things, or handle a list of things. or the overlap among the things. I think that was one of the most popular topics we dealt with in the early days of OpenHelix, but it’s still a issue that people need to […]... Read more »

Shimoyama, M., De Pons, J., Hayman, G., Laulederkind, S., Liu, W., Nigam, R., Petri, V., Smith, J., Tutaj, M., Wang, S.... (2014) The Rat Genome Database 2015: genomic, phenotypic and environmental variations and disease. Nucleic Acids Research, 43(D1). DOI: 10.1093/nar/gku1026  

  • April 6, 2016
  • 09:00 AM
  • 220 views

I’ll Fly Home—Or Not

by Mark Lasbury in As Many Exceptions As Rules

Why do some birds migrate and others don’t? It’s not that simple. The reason isn’t genetics, it isn’t necessarily food or weather either. There are birds that can allow their feet to go to one degree above freezing while keeping the rest of the body toasty – so they don’t need to migrate, yet other birds that are close to them genetically will fly thousands of miles. Other birds species only have a few of the adults migrate – who decides which ones make the trip?... Read more »

  • April 6, 2016
  • 03:13 AM
  • 216 views

Age at autism diagnosis has not decreased in the UK over the past decade

by Paul Whiteley in Questioning Answers

"This study of over 2000 children shows that the median age of ASD [autism spectrum disorder] diagnosis in the UK has not reduced in the last decade."That was the rather important message included in the study by Denise Brett and colleagues [1] (open-access) reporting combined results from the Daslne (Database of Children with ASD Living in the North East of England) and ASD-UK (Autism Spectrum Database-UK) initiatives. Including data from over 2100 children and families, researchers set about examining the mean and median age at diagnosis according to year from 2004 to 2014.Alongside looking at the number and proportion of children per year who were diagnosed below 3 years and 5 years of age, they suggested that "increased publicity, clinical initiatives and awareness of ASD, and the knowledge that some phenotypes are strongly associated with ASD" has seemingly done little to reduce the age at diagnosis for this cohort. As a result, there are consequences: "For children, delayed diagnosis can result in lack of early intervention, suboptimal school placement, and lack of access to the strategies helpful for children with ASD" and "For parents, delays in diagnosis mean they are missing out on understanding their child’s difficulties, and receiving the appropriate support, help and management strategies they need." Indeed, there may be lots of consequences (see here).There are some other important findings reported by Brett et al that also require comment. So: "Children with additional diagnoses were diagnosed with ASD later than children without other diagnoses" as over-represented diagnoses such as attention-deficit hyperactivity disorder (ADHD) are mentioned (see here). In light of the diagnostic 'interference' suggested by conditions such as ADHD, I might direct your attention to the important work coming out of the Wall/Duda lab as being potentially relevant (see here).Also: "Contrary to our hypothesis, and previous research... having a sibling with ASD did not result in an earlier age at diagnosis." This is an odd finding given the wealth of knowledge on the topic of autism familial recurrence (see here) and idea that observation and perhaps even preferential screening might follow when one diagnosis is received. The authors explain this by suggesting that the presentation of autism can (and does) differ from one child (person) to the next. "For example, the first child may have autism and language regression, whereas the sibling’s language may have developed in line with age expectations but social communication difficulties only become clearer at school age." Appreciating the concepts such as the broader autism phenotype (BAP) can fuzzy the boundaries of what is and isn't [clinically] autism (see here), it seems that still there are lessons to be learned here. I'd also suggest that the issue of regression when it comes to the onset of autism is still deserving of a lot more scrutiny (see here)."Factors associated with earlier age of diagnosis were autism diagnosis (compared with other ASD), language regression, language delay, lower socioeconomic status, and greater degree of support required." The authors provide some important details about which factors might affect age at diagnosis that should be added to what is already known (see here). That 'lower socioeconomic status' (SES) was associated with an earlier age of diagnosis might also seem surprising to some readers. The authors rightly highlight our National Health Service ('free at the point of use') and how this "may lessen the impact of SES on access to services in comparison with the US and some other countries." But still, the suggestion that lower SES might facilitate an earlier age of diagnosis does require more study, particularly when conditions like ADHD have also been linked to SES status in the UK (see here). I'm also wondering whether factors such as all that extra pupil premium money (when you can get it) given to schools/academies might also be contributory to earlier identification and diagnosis as a function of SES?The findings from Brett et al suggest that here in the UK, we still have some way to go in order to progress early identification and diagnosis when it comes to autism. I'd like to think that changes are being made to elements contributory to earlier diagnosis as per the introduction of the ASQ-3 to the Healthy Child Program (see here) for example. But, and it is an important point, earlier diagnosis is really only going to be achieved when more money and resources are put into the mechanisms of screening and assessment (see here) and when headlines like 'we waited 6 years for an autism diagnosis' are seen no longer. Indeed, with all the talk about increasing autism awareness (which have been going on for quite a few years now), that awareness counts for nothing if the systems aren't in place to cope with the increasing numbers of people waiting for assessment (see here). And when it comes to autism screening and assessments, we might also want to listen to parents and primary caregivers a little more too (see here).Now, how about also looking at the state of diagnosis and diagnostic delays when it comes to adults too including how 'self-diagnosis' might fit into the picture [2]? Y'know, among the various other changes that could improve the lives of those with autism...To close, for those of us who understand the context of the words 'It's a trap!' it is indeed a sad day...----------[1] Brett D. et al. Factors Affecting Age at ASD Diagnosis in UK: No Evidence that Diagnosis Age has Decreased Between 2004 and 2014. Journal of Autism and Developmental Disorders. 2016. March 31.[2] Foran Lewis L. Exploring the Experience of Self-Diagnosis of Autism Spectrum Disorder in Adults. Archives of Psychiatric Nursing. 2016. 1 April.----------... Read more »

  • April 5, 2016
  • 05:17 PM
  • 204 views

Suicidal thinking and US veterans

by Dr. Jekyll in Lunatic Laboratories

Something very personal about me, the thought of suicide is never too far behind. It is to the point that I need to qualify it to my counselor when I am asked if I have thoughts of suicide, I always do. A new study shows that I am far from alone Nearly 14 percent of military veterans reported suicidal thinking at one or both phases of a two-year Veterans Affairs (VA) study.... Read more »

  • April 5, 2016
  • 06:43 AM
  • 213 views

Coffee’s Guilty Pleasure

by Chiara Civardi in United Academics

Eco-friendly behaviors, such as recycling coffee pods, are associated with a sense of pride.... Read more »

  • April 5, 2016
  • 03:29 AM
  • 162 views

A web service to facilitate orthology benchmarking

by Christophe Dessimoz in Open Reading Frame

Our latest paper, “Standardized Benchmarking in the Quest for Orthologs”, just came out in Nature Methods. This is a brief overview and story behind the paper.

Orthology benchmarking

Orthology, which formalises the concept of “same” genes in different species, is a foundation of genomics. Last year alone, more than 13,000 scientific papers were published with keyword “ortholog”. To satisfy this enormous demand, many methods and resources for ortholog inference have been proposed. Yet because orthology is defined from the evolutionary history of genes, which usually cannot be known with certainty, benchmarking orthology is hard. There are also practical challenges in comparing complex computational pipelines, many of which are not available as standalone software.

Identifier mapping: the bane of bioinformatics

Back in 2009, Adrian Altenhoff and I published a paper on ortholog benchmarking in PLOS Computational Biology. At the time, this was the first benchmark study with phylogeny-based tests. It also investigated an unprecedented number of methods. One of the most challenging aspect of this work—and by far the most tedious—was to compare inferences performed by different methods on only partly overlapping sets of genomes, often with inconsistent identifiers and releases—giving right to the cynics’s view that “bioinformatics is ninety percent identifier mapping…”

Enter the Quest for Orthologs consortium

Around that time, Eric Sonnhammer and Albert Vilella organised the first Quest for Orthologs (QfO) meeting at the beautiful Genome Campus in Hinxton, UK—the first of a series of collaborative meetings. We have published detailed reports on these meetings (2009, 2011, 2013; stay tuned for the 2015 meeting report…).

Out of these interactions, the Quest for Orthologs consortium was born, with the mission to benchmark, improve and standardise orthology predictions through collaboration, the use of shared reference datasets, and evaluation of emerging new methods.

The consortium is open to all interested parties and now includes over 60 researchers from 40 institutions worldwide, with representatives from many resources, such as UniProt, Ensembl, NCBI COGs, PANTHER, Inparanoid, PhylomeDB, EggNOG, PLAZA, OrthoDB and our own OMA resource.

The orthology benchmark service and other contributions of the paper

The consortium is organised in working groups. One of them is the benchmarking working group, in which Adrian and I have been very involved. This new paper presents several key outcome of the benchmarking working group.

First and foremost, we present a publicly-available, automated, web-based benchmark service. Accessible at http://orthology.benchmarkservice.org, the service lets method developers evaluate predictions performed on the 2011 QfO reference proteome set of 66 species. Within a few hours after submitting their predictions, they obtain detailed feedback on the performance of their method on various benchmarks compared with other methods. Optionally, they can make the results publicly available.



Conceptual overview of the benchmark service (Fig 1 of the paper; click to enlarge)

Second, we discuss the performance of 14 orthology methods on a battery of 20 different tests on a common dataset across all of life.

Third, one of the benchmark, the generalised species discordance test, is new and provides a way for testing pairwise orthology based on trusted species trees of arbitrary size and shape.

Implications

For developers of orthology prediction methods, this work sets minimum standards in orthology benchmarking. Methodological innovations should be reflected in competitive performance in at least a subset of the benchmarks (we recognise that different applications entail different trade-offs). Publication of new or update methods in journals should ideally be accompanied by publication of the associated results in the orthology benchmark service.

For end-users of orthology predictions, the benchmark service provides the most comprehensive survey of methods to date. And because it can process new submissions automatically and continuously, it holds the promise of remaining current and relevant over time. The benchmark service thus enables users to gauge the quality of the orthology calls upon which they depend, and to identify the methods most appropriate to the problem at hand.

 

References

Altenhoff, A., Boeckmann, B., Capella-Gutierrez, S., Dalquen, D., DeLuca, T., Forslund, K., Huerta-Cepas, J., Linard, B., Pereira, C., Pryszcz, L., Schreiber, F., da Silva, A., Szklarczyk, D., Train, C., Bork, P., Lecompte, O., von Mering, C., Xenarios, I., Sjölander, K., Jensen, L., Martin, M., Muffato, M., Altenhoff, A., Boeckmann, B., Capella-Gutierrez, S., DeLuca, T., Forslund, K., Huerta-Cepas, J., Linard, B., Pereira, C., Pryszcz, L., Schreiber, F., da Silva, A., Szklarczyk, D., Train, C., Lecompte, O., Xenarios, I., Sjölander, K., Martin, M., Muffato, M., Quest for Orthologs consortium, Gabaldón, T., Lewis, S., Thomas, P., Sonnhammer, E., Dessimoz, C., Gabaldón, T., Lewis, S., Thomas, P., Sonnhammer, E., & Dessimoz, C. (2016). Standardized benchmarking in the quest for orthologs Nature Methods DOI: 10.1038/nmeth.3830

Altenhoff, A., & Dessimoz, C. (2009). Phylogenetic and Functional Assessment of Orthologs Inference Projects and Methods PLoS Computational Biology, 5 (1) DOI: 10.1371/journal.pcbi.1000262

... Read more »

Altenhoff, A., Boeckmann, B., Capella-Gutierrez, S., Dalquen, D., DeLuca, T., Forslund, K., Huerta-Cepas, J., Linard, B., Pereira, C., Pryszcz, L.... (2016) Standardized benchmarking in the quest for orthologs. Nature Methods. DOI: 10.1038/nmeth.3830  

Gabaldón, T., Dessimoz, C., Huxley-Jones, J., Vilella, A., Sonnhammer, E., & Lewis, S. (2009) Joining forces in the quest for orthologs. Genome Biology, 10(9), 403. DOI: 10.1186/gb-2009-10-9-403  

Dessimoz, C., Gabaldon, T., Roos, D., Sonnhammer, E., Herrero, J., & Quest for Orthologs Consortium. (2012) Toward community standards in the quest for orthologs. Bioinformatics, 28(6), 900-904. DOI: 10.1093/bioinformatics/bts050  

Sonnhammer, E., Gabaldon, T., Sousa da Silva, A., Martin, M., Robinson-Rechavi, M., Boeckmann, B., Thomas, P., Dessimoz, C., & , . (2014) Big data and other challenges in the quest for orthologs. Bioinformatics, 30(21), 2993-2998. DOI: 10.1093/bioinformatics/btu492  

  • April 5, 2016
  • 02:49 AM
  • 173 views

Folate receptor autoantibodies (FRAAs) and a 'type' of autism?

by Paul Whiteley in Questioning Answers

"This study suggests that FRAAs [folate receptor α (FRα) autoantibodies] are associated with specific physiological and behavioral characteristics in children with ASD [autism spectrum disorder] and provides support for the notion that these biomarkers may be useful for subgrouping children with ASD, especially with respect to targeted treatments."So said the study findings published by Richard Frye and colleagues [1] (open-access) who continued a research theme looking at FRAAs and their manifestation in 'some' autism. If you've already clicked that link in the last paragraph, you should have something of a flavour for what FRAAs are and what has already been discussed with autism in mind. If you didn't, the long and short of it is FRAAs describing the possibility of issues with folate transport as noted in the condition cerebral folate deficiency (CFD) are also being reported alongside some autism. The subsequent use of folinic acid (a vitamer of folic acid) to compensate might be something to consider for at least some on the autism spectrum bearing in mind my not giving any medical or clinical advice. I might also direct readers to a previous post with a helpful graphic on how the folate cycle also links in to some other important metabolic processes (see here) which is particularly timely in light of more publications on the topic of 'MTHFR'. I'll come back to this shortly.This time around, Dr Frye and colleagues set about looking at whether those with autism also with issues around FRAAs present with a 'specific type' of autism, also taking into account different types of FRAAs - blocking and blinding. Serum samples for 94 children diagnosed with an ASD were analysed for blocking and binding FRAAs. At the same time, various markers covering redox, methylation, immune function and vitamin status were also determined and various measures of behaviour examined.Results: "Fifty seven percent of the participants were positive for either the blocking or binding FRAAs, with 17% positive for blocking FRAA and 51% positive for the binding FRAA; 11% were positive for both FRAAs." From a behavioural/psychometric perspective: "ASD children positive for the blocking FRAA demonstrated better communication on the Vineland Adaptive Behavior Scale, stereotyped behavior on the Aberrant Behavioral Checklist and mannerisms on the Social Responsiveness Scale." In other words, those children with evidence of FRAAs, particularly blocking FRAAs, seemed to "have less severe ASD symptoms." The authors make mention of the term 'optimal outcome' with regards to this group, which is interesting when you consider the status of this often contentious line of research (see here).The results of the various biological assays employed showed some interesting results. So: "ASD children with the blocking FRAA appear to have a more favorable redox and inflammation profile with relatively better glutathione and CT [3-Chlorotyrosine] indices than FRAA blocking negative children." Further, although folate levels were not significantly different between the groups on the basis of the presence of blocking or binding FRAAs (or neither), levels of vitamin B12 did show some differences: "Children positive for the binding FRAA were found to have higher serum B12 levels as compared to those negative for binding FRAAs."Appreciating that it is still early days when it comes to FRAAs and autism, this and other research is crying out for independent replication with some appropriate cautions that FRAAs are not seemingly just confined to a diagnosis of autism (see here). The idea that those with autism with a specific type of FRAA (blocking) might present with a more favourable ASD profile in terms of symptoms and also biochemistry invites the question of whether the presence of such biology might actually be 'beneficial' bearing in mind the limited participant numbers included in the Frye study. I know that this might sound at odds with the whole folate-autism link that has been built up over the years, but as I've said before on this blog, folate metabolism and autism is a mighty complicated topic (see here). Likewise, is the idea that the presence of binding FRAAs might be something to 'target' given their seemingly less favourable biological and behavioural profile.I do have one or two other points to make before I leave you. First, although mention is made of serum levels of the various biological analytes under investigation, one should be mindful of how representative these values are across the body. High serum vitamin B12 does not necessarily mean high brain levels of vitamin B12 for example (and alongside vitamin B12 I would have liked to have seen some data on the compound that is methylmalonic acid). Second, although mention is made of "methylenetetrahydrofolate reductase" (MTHFR), it would be interesting to see how many of the group presented with genetic issues with the production of this enzyme in light of previous findings (see here) and onwards the nature of any connection with FRAAs and autism.This is interesting work but lots more investigation is implied.----------[1] Frye RE. et al. Blocking and Binding Folate Receptor Alpha Autoantibodies Identify Novel Autism Spectrum Disorder Subgroups. Front. Neurosci. 2016. March 9.----------Frye, R., Delhey, L., Slattery, J., Tippett, M., Wynne, R., Rose, S., Kahler, S., Bennuri, S., Melnyk, S., Sequeira, J., & Quadros, E. (2016). Blocking and Binding Folate Receptor Alpha Autoantibodies Identify Novel Autism Spectrum Disorder Subgroups Frontiers in Neuroscience, 10 DOI: 10.3389/fnins.2016.00080... Read more »

Frye, R., Delhey, L., Slattery, J., Tippett, M., Wynne, R., Rose, S., Kahler, S., Bennuri, S., Melnyk, S., Sequeira, J.... (2016) Blocking and Binding Folate Receptor Alpha Autoantibodies Identify Novel Autism Spectrum Disorder Subgroups. Frontiers in Neuroscience. DOI: 10.3389/fnins.2016.00080  

  • April 4, 2016
  • 08:58 PM
  • 164 views

Big Bird: Unusual Nesting in the Ostrich

by Emily Makowski in Sextraordinary!

I discuss the unique courtship and nesting behaviors of the ostrich and how these behaviors relate to ostrich farming.... Read more »

  • April 4, 2016
  • 03:57 PM
  • 173 views

Your brain has an altered response to desirable foods

by Dr. Jekyll in Lunatic Laboratories

Hungry? Well, let’s face it, that pizza looks much better than the salad. Don’t deny it salad lovers, we all know behind closed doors you look at plenty of food porn to satiate your desires. Understanding the motivations that drive us to eat is important when we talk about weight loss and how we attempt to structure diets. Now a new study shows that for overweight individuals, the brain responses differently to desirable foods., but hold that thought, because there is hope.

... Read more »

  • April 4, 2016
  • 02:41 PM
  • 167 views

Imaging with CRISPR/Cas9

by Gal Haimovich in Green Fluorescent Blog

The hottest buzz-word in biology today is CRISPR: an adaptive immune system in bacteria and archea. At its basis is a nuclease, named Cas9, which is targeted to DNA by a short single-guide RNA (sgRNA). This turned out to be … Continue reading →... Read more »

Deng W, Shi X, Tjian R, Lionnet T, & Singer RH. (2015) CASFISH: CRISPR/Cas9-mediated in situ labeling of genomic loci in fixed cells. Proceedings of the National Academy of Sciences of the United States of America, 112(38), 11870-5. PMID: 26324940  

Nelles DA, Fang MY, O'Connell MR, Xu JL, Markmiller SJ, Doudna JA, & Yeo GW. (2016) Programmable RNA Tracking in Live Cells with CRISPR/Cas9. Cell, 1-9. PMID: 26997482  

  • April 4, 2016
  • 02:37 AM
  • 174 views

Relative age and ADHD

by Paul Whiteley in Questioning Answers

"ADHD children may just be immature, research suggests".So went the recent BBC headline with reference to the findings reported by Mu-Hong Chen and colleagues [1] (open-access) and the idea that: "Relative age, as an indicator of neurocognitive maturity, is crucial in the risk of being diagnosed with ADHD [attention-deficit hyperactivity disorder] and receiving ADHD medication among children and adolescents."Chen et al are not unfamiliar names discussed on this blog (see here for example) in light of the rise and rise of data emerging from the Taiwan National Health Insurance Research Database (NHIRD) covering all-manner of associations linked to diagnoses such as ADHD and autism. Indeed, not so long ago I was discussing the idea the atopic dermatitis *might* be implicated in one or other diagnosis (see here). This time around the NHIRD was used to test a different hypothesis: "those born in August are more likely to be diagnosed with ADHD and receive a prescription for ADHD treatment than those born in September."An important detail first that many parents with a child born around late August / early September will probably have considered before their child starts school - "The cut-off birthdate for entry to school in Taiwan is August 31, and consequently, those born in August are typically the youngest in their grades." From a starting population of 1 million - "approximately 4.3% of the population of Taiwan" - who were randomly selected from the NHIRD, researchers whittled the numbers down to just under 400,000 aged 4-17 years who were "categorized on the basis of their birth month." The prevalence of ADHD and receipt of "a prescription for ADHD medication (methylphenidate or atomoxetine)" were examined by month, and various statistics were produced.Results: an interesting pattern of diagnosis by birth month emerged. "The prevalence of subjects receiving ADHD diagnosis or medication increased with each birth month from September (1.8% and 1.2%) to August (2.9% and 2.1%)." In other words, those born in August were almost twice as likely to be diagnosed with ADHD as those born the previous September. This increased 'risk' mostly held true when analysis was also done on the basis of specific years starting 1997-1998 through to 2010-2011 and also crossed the genders.The idea that relative immaturity compared to class peers might influence ADHD diagnosis is not a new one. Halldner and colleagues [2] reported on a smaller yet still pretty large cohort of children looking at ADHD diagnosis and medication treatment in Sweden. They reported that "ADHD diagnoses and medication treatment were both significantly more common in individuals born in November/December versus January/February" but also "no corresponding differences in parent- or self-reported ADHD symptoms by calendar birth month." Other authors [3] have arrived at similar conclusions including during recent research.Some commentators have already cautioned about reading too much into the Chen results as a function of them being exclusively based on ADHD diagnosis and medication data without reference to important variables such as family history and environmental influences. I agree that further investigation is indicated before anyone heads down the 'it's all due to immaturity' route and perhaps over-simplifying what can often be a complicated diagnosis/presentation. This also perhaps ties into some important discussions on the increasing rate of ADHD being noted worldwide (see here).That all being said, the idea that perceptions of classroom behaviour may not fully take into account age in comparison to peers perhaps suggests that further education and training should be offered to education providers in order to highlight this issue. That other more social factors such as level of economic deprivation (see here) may also influence decisions about using the label ADHD provides a timely reminder that psychiatric labels do not exist outside of social context.Finally, readers might also entertain the idea that conception in the winter months leading to a late summer birth might also play a role in the results obtained and more than one environmental factor could play a role in the findings. That includes the continuing interest in the overlap between asthma and ADHD (see here). Science in this area might also learn a thing or two from some other recent research findings too...----------[1] Chen M-H. et al. Influence of Relative Age on Diagnosis and Treatment of Attention-Deficit Hyperactivity Disorder in Taiwanese Children. The Journal of Pediatrics. 2016. 10 March.[2] Halldner L. et al. Relative immaturity and ADHD: findings from nationwide registers, parent- and self-reports. J Child Psychol Psychiatry. 2014 Aug;55(8):897-904.[3] Elder TE. The importance of relative standards in ADHD diagnoses: evidence based on exact birth dates. J Health Econ. 2010 Sep;29(5):641-56.----------Chen, M., Lan, W., Bai, Y., Huang, K., Su, T., Tsai, S., Li, C., Lin, W., Chang, W., Pan, T., Chen, T., & Hsu, J. (2016). Influence of Relative Age on Diagnosis and Treatment of Attention-Deficit Hyperactivity Disorder in Taiwanese Children The Journal of Pediatrics DOI: 10.1016/j.jpeds.2016.02.012... Read more »

  • April 3, 2016
  • 09:20 PM
  • 126 views

The Illumina Error Profile for Metagenomic Sequencing

by Geoffrey Hannigan in Prophage

Microbiology, and especially microbial ecology, has become increasingly dependent on advanced DNA and RNA sequencing technologies. This is most evident with the increasing popularity of the human microbiome and its various impacts on human health...... Read more »

  • April 3, 2016
  • 03:17 PM
  • 186 views

Early detection of dementia in Parkinson’s disease might be key to treatment

by Dr. Jekyll in Lunatic Laboratories

If Parkinson’s disease wasn’t bad enough for families to have to learn to deal with, about 80% of patients also develop dementia. That’s the problem with the brain; while it has the amazing ability to adapt to just about anything, it can’t fix everything. There are no particularly good solutions to Parkinson’s or dementia, however, early detection of dementia is key to keeping it at bay and a new study may have a way to do just that.

... Read more »

Bertrand, J., McIntosh, A., Postuma, R., Kovacevic, N., Latreille, V., Panisset, M., Chouinard, S., & Gagnon, J. (2016) Brain Connectivity Alterations Are Associated with the Development of Dementia in Parkinson's Disease. Brain Connectivity, 6(3), 216-224. DOI: 10.1089/brain.2015.0390  

  • April 2, 2016
  • 04:43 PM
  • 202 views

Born to run? Love of exercise may start in the womb

by Dr. Jekyll in Lunatic Laboratories

If you see me on the street and I am running, there is a good chance you should be running as well, because something dangerous is coming. I don’t run, I hate to run, I loathe running, did I mention I don’t like to run? Maybe it’s all the running I did in the military, or if a new study is correct, it may have to do with my mother. Which is good, because now I can blame someone else for my hatred of running.

... Read more »

Eclarinal, J., Zhu, S., Baker, M., Piyarathna, D., Coarfa, C., Fiorotto, M., & Waterland, R. (2016) Maternal exercise during pregnancy promotes physical activity in adult offspring. The FASEB Journal. DOI: 10.1096/fj.201500018R  

  • April 2, 2016
  • 04:05 AM
  • 195 views

Joint attention interventions for children with autism (mostly) work

by Paul Whiteley in Questioning Answers

Today (April 2nd) is World Autism Awareness Day. The theme this year is on inclusion and as the United Nations note: "Mainstreaming disability" insofar as recognising that: "Autism and other forms of disability are part of the human experience that contributes to human diversity." A noble cause indeed; not forgetting that for many on the autism spectrum, long-term outcome remains poor (see here) and awareness about human diversity really needs to go hand-in-hand with real action to change prospects and truly bring equality to the ENTIRE autism spectrum. Indeed, 'life-changing' is a word that should spring to mind...Today I'd like to bring your attention to the findings reported by Kimberly Murza and colleagues [1] which perhaps go some way towards illustrating how relatively simple early intervention can bring about quite big gains onwards to potentially improving future prospects for those on the autism spectrum. The topic of the "systematic review and meta-analysis" carried out by Murza et al was joint attention - whereby two people, often a child and an adult, use various strategies to share attention of an object or event of some interest. Joint attention with autism in mind, has been of some interest for quite a few years.Looking at 15 "randomized experimental studies" where various types of interventions were used to improve joint attention, researchers concluded that there was quite a bit of support "for explicit joint attention interventions for young children with ASD [autism spectrum disorder]." Yes, there is more to do in terms of "which children with ASD respond to which type of intervention" but work in other areas on best- and non-responders should teach us a few lessons about how to go about doing this.There are a multitude of options when it comes to intervening in relation to joint attention, many of which are covered in a recent publication by the group Treating Autism (see here). JASPER (Joint Attention Symbolic Play Engagement Regulation) seems to be making quite a few scientific waves recently [2] but there are others; this bearing in mind the need to improve the quality of trials looking at such behaviours (indeed reviews are only as good as the trials included) and the understanding that behavioural intervention often does little to solve the more 'somatic ' comorbidity that can and does also impact on autism (see here).I might also add that given the depressing news that not much has changed over the past decade insofar as age at diagnosis here in the UK [3], early intervention including that targeting joint attention does not necessarily have to wait until a diagnosis is formally received...----------[1] Murza KA. et al. Joint attention interventions for children with autism spectrum disorder: a systematic review and meta-analysis. Int J Lang Commun Disord. 2016 Mar 8.[2] Goods KS. et al. Preschool based JASPER intervention in minimally verbal children with autism: pilot RCT. J Autism Dev Disord. 2013 May;43(5):1050-6.[3] Brett D. et al. Factors Affecting Age at ASD Diagnosis in UK: No Evidence that Diagnosis Age has Decreased Between 2004 and 2014. Journal of Autism and Developmental Disorders. 2016. March 31.----------Murza KA, Schwartz JB, Hahs-Vaughn DL, & Nye C (2016). Joint attention interventions for children with autism spectrum disorder: a systematic review and meta-analysis. International journal of language & communication disorders / Royal College of Speech & Language Therapists PMID: 26952136... Read more »

join us!

Do you write about peer-reviewed research in your blog? Use ResearchBlogging.org to make it easy for your readers — and others from around the world — to find your serious posts about academic research.

If you don't have a blog, you can still use our site to learn about fascinating developments in cutting-edge research from around the world.

Register Now

Research Blogging is powered by SMG Technology.

To learn more, visit seedmediagroup.com.